,text,id,label
0,<< Androgen >> antagonistic effect of estramustine phosphate (EMP) metabolites on wild-type and mutated [[ androgen receptor ]].,0,1
1,Androgen antagonistic effect of << estramustine phosphate >> (EMP) metabolites on wild-type and mutated [[ androgen receptor ]].,1,1
2,Androgen antagonistic effect of estramustine phosphate (<< EMP >>) metabolites on wild-type and mutated [[ androgen receptor ]].,2,1
3,"Down-regulation of << prostate-specific antigen >> (PSA) expression, an AR-target gene, by [[ estramustine ]] and bicalutamide was accompanied by the blockade of the mutated androgen receptor.",3,8
4,"Down-regulation of prostate-specific antigen (<< PSA >>) expression, an AR-target gene, by [[ estramustine ]] and bicalutamide was accompanied by the blockade of the mutated androgen receptor.",4,8
5,"Down-regulation of prostate-specific antigen (PSA) expression, an << AR >>-target gene, by [[ estramustine ]] and bicalutamide was accompanied by the blockade of the mutated androgen receptor.",5,8
6,"Down-regulation of << prostate-specific antigen >> (PSA) expression, an AR-target gene, by estramustine and [[ bicalutamide ]] was accompanied by the blockade of the mutated androgen receptor.",6,8
7,"Down-regulation of prostate-specific antigen (<< PSA >>) expression, an AR-target gene, by estramustine and [[ bicalutamide ]] was accompanied by the blockade of the mutated androgen receptor.",7,8
8,"Down-regulation of prostate-specific antigen (PSA) expression, an << AR >>-target gene, by estramustine and [[ bicalutamide ]] was accompanied by the blockade of the mutated androgen receptor.",8,8
9,"Down-regulation of prostate-specific antigen (PSA) expression, an AR-target gene, by << estramustine >> and bicalutamide was accompanied by the blockade of the mutated [[ androgen receptor ]].",9,0
10,"Down-regulation of prostate-specific antigen (PSA) expression, an AR-target gene, by estramustine and << bicalutamide >> was accompanied by the blockade of the mutated [[ androgen receptor ]].",10,0
11,Exposure of LNCaP cells to << estramustine >> for 24 hr caused transcriptional inhibition of [[ PSA ]] in a concentration-dependent manner.,11,0
12,"The levels of << PSA >> mRNA decreased 56 and 90% when LNCaP cells were treated with 5 and 10 microM of [[ estramustine ]], respectively (IC50 = 10.97 +/- 1.68 microM).",12,8
13,"Binding of << hydroxyflutamide >> to m-AR in LNCaP cells resulted in a concentration-dependent stimulation of [[ PSA ]] expression, suggesting that hydroxyflutamide acted as an agonist of the m-AR.",13,6
14,"Binding of hydroxyflutamide to m-AR in LNCaP cells resulted in a concentration-dependent stimulation of PSA expression, suggesting that << hydroxyflutamide >> acted as an agonist of the m-[[ AR ]].",14,2
15,"Our data indicate that << estramustine phosphate >> metabolites perform as androgen antagonists of [[ AR ]], an additional mechanism involved in the therapeutic effect of estramustine phosphate in patients with prostate cancer.",15,1
16,"Our data indicate that estramustine phosphate metabolites perform as << androgen >> antagonists of [[ AR ]], an additional mechanism involved in the therapeutic effect of estramustine phosphate in patients with prostate cancer.",16,1
17,"In order to address one aspect of the feasibility of performing time-resolved studies on AChE, a data set has been collected using the Laue technique on a trigonal crystal of << Torpedo californica AChE >> soaked with the reversible inhibitor [[ edrophonium ]], using a total X-ray exposure time of 24 ms.",17,0
18,Selective inhibition of << cyclooxygenase 2 >> spares renal function and [[ prostaglandin ]] synthesis in cirrhotic rats with ascites.,18,4
19,The current study evaluates the effects of a selective << COX-2 >> inhibitor ([[ SC-236 ]]) on renal function in cirrhotic rats with ascites.,19,0
20,"RESULTS: Administration of SC-236 to cirrhotic animals did not produce significant renal effects, whereas administration of the nonselective << COX-1 >>/COX-2 inhibitor, [[ ketorolac ]], resulted in a marked reduction in urine volume, urinary excretion of prostaglandins, and glomerular filtration rate and in a significant impairment in renal water metabolism.",20,0
21,"RESULTS: Administration of SC-236 to cirrhotic animals did not produce significant renal effects, whereas administration of the nonselective COX-1/<< COX-2 >> inhibitor, [[ ketorolac ]], resulted in a marked reduction in urine volume, urinary excretion of prostaglandins, and glomerular filtration rate and in a significant impairment in renal water metabolism.",21,0
22,"RESULTS: Administration of SC-236 to cirrhotic animals did not produce significant renal effects, whereas administration of the nonselective << COX-1 >>/COX-2 inhibitor, ketorolac, resulted in a marked reduction in urine volume, urinary excretion of [[ prostaglandins ]], and glomerular filtration rate and in a significant impairment in renal water metabolism.",22,4
23,"RESULTS: Administration of SC-236 to cirrhotic animals did not produce significant renal effects, whereas administration of the nonselective COX-1/<< COX-2 >> inhibitor, ketorolac, resulted in a marked reduction in urine volume, urinary excretion of [[ prostaglandins ]], and glomerular filtration rate and in a significant impairment in renal water metabolism.",23,4
24,Inhibition of << cPLA2 >> translocation and leukotriene C4 secretion by [[ fluticasone propionate ]] in exogenously activated human eosinophils.,24,8
25,FMLP/CB-stimulated translocation of << cPLA2 >> to the nuclear envelope assessed by specific immunohistochemical staining also was blocked by [[ FP ]].,25,8
26,We find that << FP >> causes a decrease in stimulated eosinophil secretion of LTC4 that is regulated by [[ phospholipase A2 ]] (PLA2).,26,8
27,We find that FP causes a decrease in stimulated eosinophil secretion of << LTC4 >> that is regulated by [[ phospholipase A2 ]] (PLA2).,27,4
28,We find that FP causes a decrease in stimulated eosinophil secretion of << LTC4 >> that is regulated by phospholipase A2 ([[ PLA2 ]]).,28,4
29,Inhibition of LTC4 synthesis precedes the global cytotoxic effects of << FP >> as indicated by the simultaneous upregulation of [[ annexin-1 ]] expression.,29,6
30,<< Desipramine >> treatment decreases 3H-nisoxetine binding and [[ norepinephrine transporter ]] mRNA in SK-N-SHSY5Y cells.,30,8
31,"The antidepressant << desipramine >> has been shown to decrease synaptic membrane concentrations of the norepinephrine re-uptake transporter ([[ NET ]]) in vivo and in vitro, on both an acute and a chronic basis.",31,8
32,"The antidepressant << desipramine >> has been shown to decrease synaptic membrane concentrations of the [[ norepinephrine re-uptake transporter ]] (NET) in vivo and in vitro, on both an acute and a chronic basis.",32,8
33,"We conclude that decreased NET synthesis may contribute to the chronic, but not acute, effect of << desipramine >> to downregulate the [[ NET ]].",33,3
34,Inhibition of the << human ether-a-go-go-related gene (HERG) potassium channel >> by [[ cisapride ]]: affinity for open and inactivated states.,34,0
35,"2 In a chronic transfection model using CHO-K1 cells, << cisapride >> inhibited [[ HERG ]] tail currents after a step to +25 mV with similar potency at room and physiological temperatures (IC50 16. 4 nM at 20-22 degrees C and 23.6 nM at 37 degrees C).",35,0
36,"6 In conclusion, << HERG >> channel inhibition by [[ cisapride ]] exhibits features consistent with open and inactivated state binding and is sensitive to external potassium concentration.",36,0
37,"While it is an antagonist at these latter receptors, << ziprasidone >> behaves as a [[ 5-HT1A ]] agonist in vitro in adenylate cyclase measurements.",37,2
38,"Pretreatment with the << 5-HT1A >> antagonist [[ WAY-100,635 ]] (10 micrograms/kg i.v.) prevented the ziprasidone-induced inhibition; the same dose of WAY-100,635 had little effect on the inhibition produced by clozapine and olanzapine.",38,1
39,"Pretreatment with the << 5-HT1A >> antagonist WAY-100,635 (10 micrograms/kg i.v.) prevented the ziprasidone-induced inhibition; the same dose of [[ WAY-100,635 ]] had little effect on the inhibition produced by clozapine and olanzapine.",39,1
40,"These profiles suggest a mechanism of action for each agent, << 5-HT1A >> agonism for [[ ziprasidone ]] and alpha 1 antagonism for clozapine and olanzapine.",40,2
41,The << 5-HT1A >> agonist activity reported here clearly distinguishes [[ ziprasidone ]] from currently available antipsychotic agents and suggests that this property may play a significant role in its pharmacologic actions.,41,2
42,"The nonselective and irreversible << MAO >> inhibitors, [[ phenelzine ]] (3-10 mg/kg), tranylcypromine (1-3 mg/kg), and nialamide (30 mg/kg), decreased rates of responding maintained by ethanol reinforcement.",42,0
43,"The nonselective and irreversible << MAO >> inhibitors, phenelzine (3-10 mg/kg), [[ tranylcypromine ]] (1-3 mg/kg), and nialamide (30 mg/kg), decreased rates of responding maintained by ethanol reinforcement.",43,0
44,"The nonselective and irreversible << MAO >> inhibitors, phenelzine (3-10 mg/kg), tranylcypromine (1-3 mg/kg), and [[ nialamide ]] (30 mg/kg), decreased rates of responding maintained by ethanol reinforcement.",44,0
45,"The reversible << MAO-A >> inhibitor, [[ befloxatone ]] (0.3-3 mg/kg), and the irreversible MAO-A inhibitor, clorgyline (10-30 mg/kg), also reduced ethanol self-administration.",45,0
46,"The reversible MAO-A inhibitor, befloxatone (0.3-3 mg/kg), and the irreversible << MAO-A >> inhibitor, [[ clorgyline ]] (10-30 mg/kg), also reduced ethanol self-administration.",46,0
47,"The irreversible << MAO-B >> inhibitors, [[ pargyline ]] (30 mg/kg) and l-deprenyl (3-10 mg/kg) also decreased responding maintained by ethanol reinforcement; these results are consistent with previous findings that both drugs decreased ethanol intake in mice.",47,0
48,"The irreversible << MAO-B >> inhibitors, pargyline (30 mg/kg) and [[ l-deprenyl ]] (3-10 mg/kg) also decreased responding maintained by ethanol reinforcement; these results are consistent with previous findings that both drugs decreased ethanol intake in mice.",48,0
49,"<< Dicumarol >>, a potent inhibitor of [[ quinone oxidoreductase ]], at high concentration (500 microm ) caused only a 72% decrease in the utilization of resorufin.",49,0
50,"Activity of the mutant << delta-aminolevulinate synthase >> protein expressed in vitro was 15.1% compared with the normal control, but was increased up to 34.5% by the addition of [[ pyridoxal 5'-phosphate ]], consistent with the clinical response of the patient to pyridoxine treatment.",50,9
51,Preferential cerebrospinal fluid << acetylcholinesterase >> inhibition by [[ rivastigmine ]] in humans.,51,0
52,Inhibition of << AChE >> in the CSF after [[ rivastigmine ]] administration was significantly greater than after placebo for up to 8.4 hours after the dose and was maximal (40%) at 2.4 hours.,52,0
53,"Plasma << BuChE >> activity was significantly lower after [[ rivastigmine ]] than after placebo, but this was not clinically relevant.",53,0
54,"<< BuChE >> activity in CSF was significantly lower after [[ rivastigmine ]] than after placebo for up to 3.6 hours after dosing, but this difference was not sustained.",54,0
55,"This study confirms the feasibility of using continuous measurement of AChE activity in CSF over prolonged periods, that << rivastigmine >> markedly inhibits CSF [[ AChE ]] after a single oral dose of 3 mg, and that the inhibition of central AChE is substantially greater than that of peripheral AChE or BuChE.",55,0
56,"This study confirms the feasibility of using continuous measurement of AChE activity in CSF over prolonged periods, that << rivastigmine >> markedly inhibits CSF AChE after a single oral dose of 3 mg, and that the inhibition of central [[ AChE ]] is substantially greater than that of peripheral AChE or BuChE.",56,0
57,"This study confirms the feasibility of using continuous measurement of AChE activity in CSF over prolonged periods, that << rivastigmine >> markedly inhibits CSF AChE after a single oral dose of 3 mg, and that the inhibition of central AChE is substantially greater than that of peripheral [[ AChE ]] or BuChE.",57,0
58,"This study confirms the feasibility of using continuous measurement of AChE activity in CSF over prolonged periods, that << rivastigmine >> markedly inhibits CSF AChE after a single oral dose of 3 mg, and that the inhibition of central AChE is substantially greater than that of peripheral AChE or [[ BuChE ]].",58,0
59,"Agonist and antagonist actions of << yohimbine >> as compared to fluparoxan at alpha(2)-adrenergic receptors [[ (AR)s ]], serotonin (5-HT)(1A), 5-HT(1B), 5-HT(1D) and dopamine D(2) and D(3) receptors.",59,2
60,"Agonist and antagonist actions of << yohimbine >> as compared to fluparoxan at alpha(2)-adrenergic receptors (AR)s, serotonin [[ (5-HT)(1A) ]], 5-HT(1B), 5-HT(1D) and dopamine D(2) and D(3) receptors.",60,2
61,"Agonist and antagonist actions of << yohimbine >> as compared to fluparoxan at alpha(2)-adrenergic receptors (AR)s, serotonin (5-HT)(1A), [[ 5-HT(1B) ]], 5-HT(1D) and dopamine D(2) and D(3) receptors.",61,2
62,"Agonist and antagonist actions of << yohimbine >> as compared to fluparoxan at alpha(2)-adrenergic receptors (AR)s, serotonin (5-HT)(1A), 5-HT(1B), [[ 5-HT(1D) ]] and dopamine D(2) and D(3) receptors.",62,2
63,"Agonist and antagonist actions of << yohimbine >> as compared to fluparoxan at [[ alpha(2)-adrenergic receptors ]] (AR)s, serotonin (5-HT)(1A), 5-HT(1B), 5-HT(1D) and dopamine D(2) and D(3) receptors.",63,2
64,"Agonist and antagonist actions of yohimbine as compared to << fluparoxan >> at alpha(2)-adrenergic receptors [[ (AR)s ]], serotonin (5-HT)(1A), 5-HT(1B), 5-HT(1D) and dopamine D(2) and D(3) receptors.",64,2
65,"Agonist and antagonist actions of yohimbine as compared to << fluparoxan >> at [[ alpha(2)-adrenergic receptors ]] (AR)s, serotonin (5-HT)(1A), 5-HT(1B), 5-HT(1D) and dopamine D(2) and D(3) receptors.",65,2
66,"Agonist and antagonist actions of << yohimbine >> as compared to fluparoxan at alpha(2)-adrenergic receptors [[ (AR)s ]], serotonin (5-HT)(1A), 5-HT(1B), 5-HT(1D) and dopamine D(2) and D(3) receptors.",66,1
67,"Agonist and antagonist actions of << yohimbine >> as compared to fluparoxan at alpha(2)-adrenergic receptors (AR)s, serotonin [[ (5-HT)(1A) ]], 5-HT(1B), 5-HT(1D) and dopamine D(2) and D(3) receptors.",67,1
68,"Agonist and antagonist actions of << yohimbine >> as compared to fluparoxan at alpha(2)-adrenergic receptors (AR)s, serotonin (5-HT)(1A), [[ 5-HT(1B) ]], 5-HT(1D) and dopamine D(2) and D(3) receptors.",68,1
69,"Agonist and antagonist actions of << yohimbine >> as compared to fluparoxan at alpha(2)-adrenergic receptors (AR)s, serotonin (5-HT)(1A), 5-HT(1B), [[ 5-HT(1D) ]] and dopamine D(2) and D(3) receptors.",69,1
70,"Agonist and antagonist actions of << yohimbine >> as compared to fluparoxan at [[ alpha(2)-adrenergic receptors ]] (AR)s, serotonin (5-HT)(1A), 5-HT(1B), 5-HT(1D) and dopamine D(2) and D(3) receptors.",70,1
71,"Agonist and antagonist actions of yohimbine as compared to << fluparoxan >> at alpha(2)-adrenergic receptors [[ (AR)s ]], serotonin (5-HT)(1A), 5-HT(1B), 5-HT(1D) and dopamine D(2) and D(3) receptors.",71,1
72,"Agonist and antagonist actions of yohimbine as compared to << fluparoxan >> at [[ alpha(2)-adrenergic receptors ]] (AR)s, serotonin (5-HT)(1A), 5-HT(1B), 5-HT(1D) and dopamine D(2) and D(3) receptors.",72,1
73,"Herein, we evaluate the interaction of the << alpha(2)-AR antagonist >>, [[ yohimbine ]], as compared to fluparoxan, at multiple monoaminergic receptors and examine their roles in the modulation of adrenergic, dopaminergic and serotonergic transmission in freely-moving rats.",73,1
74,"Herein, we evaluate the interaction of the << alpha(2)-AR antagonist >>, yohimbine, as compared to [[ fluparoxan ]], at multiple monoaminergic receptors and examine their roles in the modulation of adrenergic, dopaminergic and serotonergic transmission in freely-moving rats.",74,1
75,"In [(35)S]GTPgammaS binding protocols, << yohimbine >> exerts antagonist actions at halpha(2A)-AR, h5-HT(1B), h5-HT(1D), and hD(2) sites, yet partial agonist actions at [[ h5-HT(1A) ]] sites.",75,2
76,"In [(35)S]GTPgammaS binding protocols, << yohimbine >> exerts antagonist actions at [[ halpha(2A)-AR ]], h5-HT(1B), h5-HT(1D), and hD(2) sites, yet partial agonist actions at h5-HT(1A) sites.",76,1
77,"In [(35)S]GTPgammaS binding protocols, << yohimbine >> exerts antagonist actions at halpha(2A)-AR, [[ h5-HT(1B) ]], h5-HT(1D), and hD(2) sites, yet partial agonist actions at h5-HT(1A) sites.",77,1
78,"In [(35)S]GTPgammaS binding protocols, << yohimbine >> exerts antagonist actions at halpha(2A)-AR, h5-HT(1B), [[ h5-HT(1D) ]], and hD(2) sites, yet partial agonist actions at h5-HT(1A) sites.",78,1
79,"In [(35)S]GTPgammaS binding protocols, << yohimbine >> exerts antagonist actions at halpha(2A)-AR, h5-HT(1B), h5-HT(1D), and [[ hD(2) ]] sites, yet partial agonist actions at h5-HT(1A) sites.",79,1
80,"In vivo, agonist actions of << yohimbine >> at [[ 5-HT(1A) ]] sites are revealed by WAY100,635-reversible induction of hypothermia in the rat.",80,2
81,"In vivo, agonist actions of yohimbine at << 5-HT(1A) >> sites are revealed by [[ WAY100,635 ]]-reversible induction of hypothermia in the rat.",81,1
82,"In guinea pigs, antagonist actions of yohimbine at 5-HT(1B) receptors are revealed by blockade of hypothermia evoked by the << 5-HT(1B) >> agonist, [[ GR46,611 ]].",82,2
83,"In guinea pigs, antagonist actions of << yohimbine >> at [[ 5-HT(1B) ]] receptors are revealed by blockade of hypothermia evoked by the 5-HT(1B) agonist, GR46,611.",83,1
84,"In distinction to << yohimbine >>, fluparoxan shows only modest partial agonist actions at [[ h5-HT(1A) ]] sites versus marked antagonist actions at halpha(2)-ARs.",84,2
85,"In distinction to yohimbine, << fluparoxan >> shows only modest partial agonist actions at [[ h5-HT(1A) ]] sites versus marked antagonist actions at halpha(2)-ARs.",85,2
86,"In distinction to << yohimbine >>, fluparoxan shows only modest partial agonist actions at h5-HT(1A) sites versus marked antagonist actions at [[ halpha(2)-ARs ]].",86,1
87,"In distinction to yohimbine, << fluparoxan >> shows only modest partial agonist actions at h5-HT(1A) sites versus marked antagonist actions at [[ halpha(2)-ARs ]].",87,1
88,"In conclusion, the << alpha(2)-AR >> antagonist properties of [[ yohimbine ]] increase DA and NAD levels both alone and in association with fluoxetine.",88,1
89,"However, in contrast to the selective alpha(2)-AR antagonist, fluparoxan, the << 5-HT(1A) >> agonist actions of [[ yohimbine ]] suppress 5-HT levels alone and underlie its inability to augment the influence of fluoxetine upon 5-HT levels.",89,2
90,"However, in contrast to the selective << alpha(2)-AR >> antagonist, [[ fluparoxan ]], the 5-HT(1A) agonist actions of yohimbine suppress 5-HT levels alone and underlie its inability to augment the influence of fluoxetine upon 5-HT levels.",90,1
91,"In this study, the activity of the << delta-opioid receptor >> subtype-selective agonist, [[ SB 227122 ]], was investigated in a guinea pig model of citric acid-induced cough.",91,2
92,"Parenteral administration of selective agonists of the delta-opioid receptor (SB 227122), mu-opioid receptor (codeine and hydrocodone), and << kappa-opioid receptor >> ([[ BRL 52974 ]]) produced dose-related inhibition of citric acid-induced cough with ED(50) values of 7.3, 5.2, 5.1, and 5.3 mg/kg, respectively.",92,2
93,"Parenteral administration of selective agonists of the << delta-opioid receptor >> ([[ SB 227122 ]]), mu-opioid receptor (codeine and hydrocodone), and kappa-opioid receptor (BRL 52974) produced dose-related inhibition of citric acid-induced cough with ED(50) values of 7.3, 5.2, 5.1, and 5.3 mg/kg, respectively.",93,2
94,"Parenteral administration of selective agonists of the delta-opioid receptor (SB 227122), << mu-opioid receptor >> ([[ codeine ]] and hydrocodone), and kappa-opioid receptor (BRL 52974) produced dose-related inhibition of citric acid-induced cough with ED(50) values of 7.3, 5.2, 5.1, and 5.3 mg/kg, respectively.",94,2
95,"Parenteral administration of selective agonists of the delta-opioid receptor (SB 227122), << mu-opioid receptor >> (codeine and [[ hydrocodone ]]), and kappa-opioid receptor (BRL 52974) produced dose-related inhibition of citric acid-induced cough with ED(50) values of 7.3, 5.2, 5.1, and 5.3 mg/kg, respectively.",95,2
96,"The nonselective << opioid receptor >> antagonist, naloxone (3 mg/kg, i.m.), attenuated the antitussive effects of [[ codeine ]] or SB 227122, indicating that the antitussive activity of both compounds is opioid receptor-mediated.",96,2
97,"The nonselective opioid receptor antagonist, naloxone (3 mg/kg, i.m.), attenuated the antitussive effects of << codeine >> or SB 227122, indicating that the antitussive activity of both compounds is [[ opioid receptor ]]-mediated.",97,2
98,"The nonselective << opioid receptor >> antagonist, naloxone (3 mg/kg, i.m.), attenuated the antitussive effects of codeine or [[ SB 227122 ]], indicating that the antitussive activity of both compounds is opioid receptor-mediated.",98,2
99,"The nonselective opioid receptor antagonist, naloxone (3 mg/kg, i.m.), attenuated the antitussive effects of codeine or << SB 227122 >>, indicating that the antitussive activity of both compounds is [[ opioid receptor ]]-mediated.",99,2
100,"The nonselective << opioid receptor >> antagonist, [[ naloxone ]] (3 mg/kg, i.m.), attenuated the antitussive effects of codeine or SB 227122, indicating that the antitussive activity of both compounds is opioid receptor-mediated.",100,1
101,"The << delta-receptor >> antagonist, SB 244525 (10 mg/kg, i.p.), inhibited the antitussive effect of [[ SB 227122 ]] (20 mg/kg, i.p.).",101,2
102,"The << delta-receptor >> antagonist, [[ SB 244525 ]] (10 mg/kg, i.p.), inhibited the antitussive effect of SB 227122 (20 mg/kg, i.p.).",102,1
103,"In contrast, combined pretreatment with << beta-funaltrexamine >> ([[ mu-receptor ]] antagonist; 20 mg/kg, s.c.) and norbinaltorphimine (kappa-receptor antagonist; 20 mg/kg, s.c.), at doses that inhibited the antitussive activity of mu- and kappa-receptor agonists, respectively, was without effect on the antitussive response of SB 227122 (20 mg/kg, i.p.).",103,1
104,"In contrast, combined pretreatment with beta-funaltrexamine (mu-receptor antagonist; 20 mg/kg, s.c.) and << norbinaltorphimine >> ([[ kappa-receptor ]] antagonist; 20 mg/kg, s.c.), at doses that inhibited the antitussive activity of mu- and kappa-receptor agonists, respectively, was without effect on the antitussive response of SB 227122 (20 mg/kg, i.p.).",104,1
105,"The << sigma-receptor >> antagonist rimcazole (3 mg/kg, i.p.) inhibited the antitussive effect of [[ dextromethorphan ]] (30 mg/kg, i.p.), a sigma-receptor agonist, but not that of SB 227122.",105,2
106,"The << sigma-receptor >> antagonist [[ rimcazole ]] (3 mg/kg, i.p.) inhibited the antitussive effect of dextromethorphan (30 mg/kg, i.p.), a sigma-receptor agonist, but not that of SB 227122.",106,1
107,These studies provide compelling evidence that the antitussive effects of << SB 227122 >> in this guinea pig cough model are mediated by agonist activity at the [[ delta-opioid receptor ]].,107,2
108,"New modes of therapy have recently been introduced, and data on the << cyclooxygenase-2 >> (COX-2)-specific inhibitors [[ celecoxib ]] and rofecoxib suggest that these agents will meet the need for safe and effective therapeutic alternatives to conventional NSAIDs.",108,0
109,"New modes of therapy have recently been introduced, and data on the cyclooxygenase-2 (<< COX-2 >>)-specific inhibitors [[ celecoxib ]] and rofecoxib suggest that these agents will meet the need for safe and effective therapeutic alternatives to conventional NSAIDs.",109,0
110,"New modes of therapy have recently been introduced, and data on the << cyclooxygenase-2 >> (COX-2)-specific inhibitors celecoxib and [[ rofecoxib ]] suggest that these agents will meet the need for safe and effective therapeutic alternatives to conventional NSAIDs.",110,0
111,"New modes of therapy have recently been introduced, and data on the cyclooxygenase-2 (<< COX-2 >>)-specific inhibitors celecoxib and [[ rofecoxib ]] suggest that these agents will meet the need for safe and effective therapeutic alternatives to conventional NSAIDs.",111,0
112,"Kinetics of inhibition of << human and rat dihydroorotate dehydrogenase >> by atovaquone, lawsone derivatives, [[ brequinar sodium ]] and polyporic acid.",112,0
113,"Kinetics of inhibition of << human and rat dihydroorotate dehydrogenase >> by atovaquone, lawsone derivatives, brequinar sodium and [[ polyporic acid ]].",113,0
114,"Kinetics of inhibition of << human and rat dihydroorotate dehydrogenase >> by [[ atovaquone ]], lawsone derivatives, brequinar sodium and polyporic acid.",114,0
115,"Kinetics of inhibition of << human and rat dihydroorotate dehydrogenase >> by atovaquone, [[ lawsone ]] derivatives, brequinar sodium and polyporic acid.",115,0
116,Mitochondrially-bound << dihydroorotate dehydrogenase >> (EC 1.3.99.11) catalyzes the fourth sequential step in the de novo synthesis of [[ uridine monophosphate ]].,116,4
117,Mitochondrially-bound dihydroorotate dehydrogenase (<< EC 1.3.99.11 >>) catalyzes the fourth sequential step in the de novo synthesis of [[ uridine monophosphate ]].,117,4
118,"With respect to the quinone co-substrate of the dihydroorotate dehydrogenase, << atovaquone >> (Kic = 2.7 microM) and dichloroally-lawsone (Kic = 9.8 nM) were shown to be competitive inhibitors of [[ human dihydroorotate dehydrogenase ]].",118,0
119,"With respect to the quinone co-substrate of the dihydroorotate dehydrogenase, atovaquone (Kic = 2.7 microM) and << dichloroally-lawsone >> (Kic = 9.8 nM) were shown to be competitive inhibitors of [[ human dihydroorotate dehydrogenase ]].",119,0
120,"With respect to the << quinone >> co-substrate of the [[ dihydroorotate dehydrogenase ]], atovaquone (Kic = 2.7 microM) and dichloroally-lawsone (Kic = 9.8 nM) were shown to be competitive inhibitors of human dihydroorotate dehydrogenase.",120,5
121,"<< Dichloroally]-lawsone >> was found to be a time-dependent inhibitor of the rat enzyme, with the lowest inhibition constant (Ki* = 0.77 nM) determined so far for [[ mammalian dihydroorotate dehydrogenases ]].",121,0
122,"Another inhibitor, << brequinar >> was previously reported to be a slow-binding inhibitor of the [[ human dihydroorotate dehydrogenase ]] [W. Knecht, M. Loffler, Species-related inhibition of human and rat dihyroorotate dehydrogenase by immunosuppressive isoxazol and cinchoninic acid derivatives, Biochem. Pharmacol. 56 (1998) 1259-1264].",122,0
123,"Another inhibitor, brequinar was previously reported to be a slow-binding inhibitor of the human dihydroorotate dehydrogenase [W. Knecht, M. Loffler, Species-related inhibition of << human and rat dihyroorotate dehydrogenase >> by immunosuppressive [[ isoxazol ]] and cinchoninic acid derivatives, Biochem. Pharmacol. 56 (1998) 1259-1264].",123,0
124,"Another inhibitor, brequinar was previously reported to be a slow-binding inhibitor of the human dihydroorotate dehydrogenase [W. Knecht, M. Loffler, Species-related inhibition of << human and rat dihyroorotate dehydrogenase >> by immunosuppressive isoxazol and [[ cinchoninic acid ]] derivatives, Biochem. Pharmacol. 56 (1998) 1259-1264].",124,0
125,"With respect to the substrate << dihydroorotate >>, atovaquone was an uncompetitive inhibitor of [[ human dihydroorotate dehydrogenase ]] (Kiu = 11.6 microM) and a non-competitive inhibitor of the rat enzyme (Kiu = 905/ Kic = 1,012 nM).",125,0
126,"With respect to the substrate dihydroorotate, << atovaquone >> was an uncompetitive inhibitor of [[ human dihydroorotate dehydrogenase ]] (Kiu = 11.6 microM) and a non-competitive inhibitor of the rat enzyme (Kiu = 905/ Kic = 1,012 nM).",126,0
127,Determinants of voltage-dependent inactivation affect << Mibefradil >> block of [[ calcium channels ]].,127,0
128,<< Mibefradil >> (Ro 40-5967) belongs to a new chemical class of these molecules which differs from other Ca2+ antagonists by its ability to potently block [[ T-type Ca2+ channels ]].,128,0
129,Mibefradil (<< Ro 40-5967 >>) belongs to a new chemical class of these molecules which differs from other Ca2+ antagonists by its ability to potently block [[ T-type Ca2+ channels ]].,129,0
130,"<< Mibefradil >> blocked alpha1A and alpha1E with a Kd comparable to that reported for [[ T-type channels ]], but had a lower affinity (approximately 30-fold) for alpha1C.",130,0
131,Postoperative concentrations of << plasminogen >> were decreased significantly in the [[ tranexamic acid ]] group (P < 0.001).,131,8
132,"Iontophoresis of << +/- propranolol >>, whose serotonergic actions include antagonism and partial agonism at [[ 5-HT1 ]] receptors, also increased serotonin and decreased firing (n=4).",132,2
133,"Iontophoresis of << +/- propranolol >>, whose serotonergic actions include antagonism and partial agonism at [[ 5-HT1 ]] receptors, also increased serotonin and decreased firing (n=4).",133,1
134,"<< Methiothepin >> (intravenous, 1 mg/kg), whose serotonergic actions include [[ 5-HT1 ]] and 5-HT2 antagonism, typically raised serotonin levels (four of five cells) and always blocked inhibition by clomipramine (n = 3).",134,1
135,"<< Methiothepin >> (intravenous, 1 mg/kg), whose serotonergic actions include 5-HT1 and [[ 5-HT2 ]] antagonism, typically raised serotonin levels (four of five cells) and always blocked inhibition by clomipramine (n = 3).",135,1
136,The << Hsp90 >>-specific inhibitor [[ geldanamycin ]] selectively disrupts kinase-mediated signaling events of T-lymphocyte activation.,136,0
137,The Hsp90-specific inhibitor << geldanamycin >> selectively disrupts [[ kinase ]]-mediated signaling events of T-lymphocyte activation.,137,0
138,Improper function of these proteins can be induced by selective disruption of their complexes with << Hsp90 >> using the [[ benzoquinonoid ansamycin ]] geldanamycin.,138,0
139,Improper function of these proteins can be induced by selective disruption of their complexes with << Hsp90 >> using the benzoquinonoid ansamycin [[ geldanamycin ]].,139,0
140,"In this study, we demonstrate that << geldanamycin >> treatment blocks [[ interleukin (IL)-2 ]] secretion, IL-2 receptor expression, and proliferation of stimulated T-lymphocytes.",140,8
141,"In this study, we demonstrate that << geldanamycin >> treatment blocks interleukin (IL)-2 secretion, [[ IL-2 receptor ]] expression, and proliferation of stimulated T-lymphocytes.",141,8
142,"Moreover, << geldanamycin >> decreases the amount and phosphorylation of [[ Lck ]] and Raf-1 kinases and prevents activation of the extracellular signal regulated kinase (ERK)-2 kinase.",142,8
143,"Moreover, << geldanamycin >> decreases the amount and phosphorylation of Lck and [[ Raf-1 ]] kinases and prevents activation of the extracellular signal regulated kinase (ERK)-2 kinase.",143,8
144,"Moreover, << geldanamycin >> decreases the amount and phosphorylation of Lck and Raf-1 [[ kinases ]] and prevents activation of the extracellular signal regulated kinase (ERK)-2 kinase.",144,8
145,"Moreover, << geldanamycin >> decreases the amount and phosphorylation of [[ Lck ]] and Raf-1 kinases and prevents activation of the extracellular signal regulated kinase (ERK)-2 kinase.",145,0
146,"Moreover, << geldanamycin >> decreases the amount and phosphorylation of Lck and [[ Raf-1 ]] kinases and prevents activation of the extracellular signal regulated kinase (ERK)-2 kinase.",146,0
147,"Moreover, << geldanamycin >> decreases the amount and phosphorylation of Lck and Raf-1 [[ kinases ]] and prevents activation of the extracellular signal regulated kinase (ERK)-2 kinase.",147,0
148,"Moreover, << geldanamycin >> decreases the amount and phosphorylation of Lck and Raf-1 kinases and prevents activation of the [[ extracellular signal regulated kinase (ERK)-2 ]] kinase.",148,0
149,"Moreover, << geldanamycin >> decreases the amount and phosphorylation of Lck and Raf-1 kinases and prevents activation of the extracellular signal regulated kinase (ERK)-2 [[ kinase ]].",149,0
150,<< Geldanamycin >> also disrupts the [[ T-cell receptor ]]-mediated activation of nuclear factor of activated T-cells (NF-AT).,150,0
151,<< Geldanamycin >> also disrupts the T-cell receptor-mediated activation of [[ nuclear factor of activated T-cells ]] (NF-AT).,151,0
152,<< Geldanamycin >> also disrupts the T-cell receptor-mediated activation of nuclear factor of activated T-cells ([[ NF-AT ]]).,152,0
153,"Through demonstrating the selective inhibition of << kinase >>-related T-lymphocyte responses by [[ geldanamycin ]], our results emphasize the substantial role of Hsp90-kinase complexes in T-cell activation.",153,0
154,"<< gamma-Butyrobetaine hydroxylase >> catalyse the last step in [[ carnitine ]] biosynthesis, the formation of L-carnitine from gamma-butyrobetaine, a reaction dependent on Fe2+, alpha-ketoglutarate, ascorbate and oxygen.",154,4
155,"<< gamma-Butyrobetaine hydroxylase >> catalyse the last step in carnitine biosynthesis, the formation of [[ L-carnitine ]] from gamma-butyrobetaine, a reaction dependent on Fe2+, alpha-ketoglutarate, ascorbate and oxygen.",155,4
156,"<< gamma-Butyrobetaine hydroxylase >> catalyse the last step in carnitine biosynthesis, the formation of L-carnitine from [[ gamma-butyrobetaine ]], a reaction dependent on Fe2+, alpha-ketoglutarate, ascorbate and oxygen.",156,5
157,Inhibition of the actions of << ET-1 >> by [[ salicylates ]] is apparently competitive.,157,0
158,A unique cytosolic activity related but distinct from << NQO1 >> catalyses metabolic activation of [[ mitomycin C ]].,158,5
159,"Among the various enzymes, << dicoumarol >> inhibitable cytosolic [[ NAD(P)H:quinone oxidoreductase1 ]] (NQO1) was shown to catalyse bioreductive activation of MMC leading to cross-linking of the DNA and cytotoxicity.",159,0
160,"Among the various enzymes, << dicoumarol >> inhibitable cytosolic NAD(P)H:quinone oxidoreductase1 ([[ NQO1 ]]) was shown to catalyse bioreductive activation of MMC leading to cross-linking of the DNA and cytotoxicity.",160,0
161,"Among the various enzymes, dicoumarol inhibitable cytosolic << NAD(P)H:quinone oxidoreductase1 >> (NQO1) was shown to catalyse bioreductive activation of [[ MMC ]] leading to cross-linking of the DNA and cytotoxicity.",161,5
162,"Among the various enzymes, dicoumarol inhibitable cytosolic NAD(P)H:quinone oxidoreductase1 (<< NQO1 >>) was shown to catalyse bioreductive activation of [[ MMC ]] leading to cross-linking of the DNA and cytotoxicity.",162,5
163,"However, the role of << NQO1 >> in metabolic activation of [[ MMC ]] has been disputed.",163,5
164,"In this report, we present cellular and animal models to demonstrate that << NQO1 >> may play only a minor role in metabolic activation of [[ MMC ]].",164,5
165,"This activity, like << NQO1 >>, was inhibited by [[ dicoumarol ]] and immunologically related to NQO1.",165,0
166,<< Troglitazone >> reduces [[ plasminogen activator inhibitor-1 ]] expression and secretion in cultured human adipocytes.,166,8
167,RESULTS: Exposure of in vitro differentiated subcutaneous adipocytes from young normal-weight females to 1 microgram/ml << troglitazone >> for 72 h caused a reduction of both [[ PAI-1 ]] secretion (by 29 +/- 5%; p < 0.01) and PAI-1 mRNA expression (by 26 +/- 3%; p < 0.05).,167,8
168,RESULTS: Exposure of in vitro differentiated subcutaneous adipocytes from young normal-weight females to 1 microgram/ml << troglitazone >> for 72 h caused a reduction of both PAI-1 secretion (by 29 +/- 5%; p < 0.01) and [[ PAI-1 ]] mRNA expression (by 26 +/- 3%; p < 0.05).,168,8
169,"In cultures from severely obese subjects, << troglitazone >> induced a decrease of [[ PAI-1 ]] antigen secretion from newly differentiated omental adipocytes by 49 +/- 8% (p < 0.01) and from subcutaneous adipocytes by 30 +/- 7% (p < 0.05).",169,8
170,"Exposure of freshly isolated subcutaneous and omental adipocytes in suspension culture to << troglitazone >> induced a similar reduction of [[ PAI-1 ]] concentration in the culture medium (by 35 +/- 11%, p < 0.05, and 33 +/- 8%, p < 0.05 compared with control, respectively).",170,8
171,"CONCLUSION/INTERPRETATION: This study provides evidence that << troglitazone >> reduces [[ PAI-1 ]] production in human adipocytes, probably at the transcriptional level.",171,8
172,"We examined the effect of JTH-601 (3- inverted question mark<< N-[2-(4-hydroxy-2-isopropyl-5-methylphenoxy)ethyl]-N-methylaminom >> ethyl inverted question mark-4-methoxy-2,5,6-trimethylphenol hemifumarate), a new [[ alpha(1L)-adrenoceptor ]] antagonist, on prostatic function in isolated canine prostate and in anesthetized dogs.",172,1
173,"We examined the effect of JTH-601 (3- inverted question markN-[2-(4-hydroxy-2-isopropyl-5-methylphenoxy)ethyl]-N-methylaminom << ethyl >> inverted question mark-4-methoxy-2,5,6-trimethylphenol hemifumarate), a new [[ alpha(1L)-adrenoceptor ]] antagonist, on prostatic function in isolated canine prostate and in anesthetized dogs.",173,1
174,"We examined the effect of JTH-601 (3- inverted question markN-[2-(4-hydroxy-2-isopropyl-5-methylphenoxy)ethyl]-N-methylaminom ethyl inverted question mark-<< 4-methoxy-2,5,6-trimethylphenol hemifumarate >>), a new [[ alpha(1L)-adrenoceptor ]] antagonist, on prostatic function in isolated canine prostate and in anesthetized dogs.",174,1
175,"We examined the effect of << JTH-601 >> (3- inverted question markN-[2-(4-hydroxy-2-isopropyl-5-methylphenoxy)ethyl]-N-methylaminom ethyl inverted question mark-4-methoxy-2,5,6-trimethylphenol hemifumarate), a new [[ alpha(1L)-adrenoceptor ]] antagonist, on prostatic function in isolated canine prostate and in anesthetized dogs.",175,1
176,"In these tissues, << JTH-601 >>, prazosin (a non-selective [[ alpha(1)-adrenoceptor ]] antagonist), and tamsulosin (an alpha(1A)-adrenoceptor antagonist) competitively antagonized contraction in a concentration-dependent manner.",176,1
177,"In these tissues, JTH-601, << prazosin >> (a non-selective [[ alpha(1)-adrenoceptor ]] antagonist), and tamsulosin (an alpha(1A)-adrenoceptor antagonist) competitively antagonized contraction in a concentration-dependent manner.",177,1
178,"In these tissues, JTH-601, prazosin (a non-selective alpha(1)-adrenoceptor antagonist), and << tamsulosin >> (an [[ alpha(1A)-adrenoceptor ]] antagonist) competitively antagonized contraction in a concentration-dependent manner.",178,1
179,<< JTH-601 >> is expected to be an effective [[ alpha(1)-adrenoceptor ]] antagonist for the treatment of urinary outlet obstruction by benign prostatic hypertrophy with a minimum effect on the cardiovascular system.,179,1
180,The salivary fluid secretory mechanism is thought to require << Na(+)/K(+)/2Cl(-) cotransporter >>-mediated [[ Cl(-) ]] uptake.,180,5
181,These data directly demonstrate that << NKCC1 >> is the major [[ Cl(-) ]] uptake mechanism across the basolateral membrane of acinar cells and is critical for driving saliva secretion in vivo.,181,5
182,"UNLABELLED: Apparent << muscarinic acetylcholine (mAch) receptor >> occupancy in mouse cerebral cortex, hippocampus, and striatum by [[ scopolamine ]], an antagonist, and biperiden, a relatively selective M1 antagonist, was estimated with competitive binding studies using two different radioligands: 3H-N-methyl piperidyl benzilate (3H-NMPB) and 3H-quinuclidinyl benzilate (3H-QNB).",182,1
183,"UNLABELLED: Apparent muscarinic acetylcholine (mAch) receptor occupancy in mouse cerebral cortex, hippocampus, and striatum by scopolamine, an antagonist, and << biperiden >>, a relatively selective [[ M1 ]] antagonist, was estimated with competitive binding studies using two different radioligands: 3H-N-methyl piperidyl benzilate (3H-NMPB) and 3H-quinuclidinyl benzilate (3H-QNB).",183,1
184,Impaired expression of the uncoupling protein-3 gene in skeletal muscle during lactation: fibrates and << troglitazone >> reverse lactation-induced downregulation of the [[ uncoupling protein-3 ]] gene.,184,6
185,"Treatment of lactating mice with a single injection of << bezafibrate >>, an activator of the [[ peroxisome proliferator-activated receptor ]] (PPAR), raises UCP-3 mRNA in skeletal muscle to levels similar to those in virgin mice.",185,9
186,"Treatment of lactating mice with a single injection of << bezafibrate >>, an activator of the peroxisome proliferator-activated receptor ([[ PPAR ]]), raises UCP-3 mRNA in skeletal muscle to levels similar to those in virgin mice.",186,9
187,"Treatment of lactating mice with a single injection of << bezafibrate >>, an activator of the peroxisome proliferator-activated receptor (PPAR), raises [[ UCP-3 ]] mRNA in skeletal muscle to levels similar to those in virgin mice.",187,6
188,"4-chloro-6-[(2,3-xylidine)-pirimidinylthio] acetic acid (WY-14,643), a specific ligand of the PPAR-alpha subtype, causes the most dramatic increase in UCP-3 mRNA, whereas << troglitazone >>, a specific activator of [[ PPAR-gamma ]], also significantly increases UCP-3 mRNA abundance in skeletal muscle of lactating mice.",188,9
189,"<< 4-chloro-6-[(2,3-xylidine)-pirimidinylthio] acetic acid >> (WY-14,643), a specific ligand of the PPAR-alpha subtype, causes the most dramatic increase in [[ UCP-3 ]] mRNA, whereas troglitazone, a specific activator of PPAR-gamma, also significantly increases UCP-3 mRNA abundance in skeletal muscle of lactating mice.",189,6
190,"4-chloro-6-[(2,3-xylidine)-pirimidinylthio] acetic acid (<< WY-14,643 >>), a specific ligand of the PPAR-alpha subtype, causes the most dramatic increase in [[ UCP-3 ]] mRNA, whereas troglitazone, a specific activator of PPAR-gamma, also significantly increases UCP-3 mRNA abundance in skeletal muscle of lactating mice.",190,6
191,"4-chloro-6-[(2,3-xylidine)-pirimidinylthio] acetic acid (WY-14,643), a specific ligand of the PPAR-alpha subtype, causes the most dramatic increase in UCP-3 mRNA, whereas << troglitazone >>, a specific activator of PPAR-gamma, also significantly increases [[ UCP-3 ]] mRNA abundance in skeletal muscle of lactating mice.",191,6
192,It is proposed that the UCP-3 gene is regulated in skeletal muscle during lactation in response to changes in circulating free << fatty acids >> by mechanisms involving activation of [[ PPARs ]].,192,9
193,"<< Retigabine >>, a novel anti-convulsant, enhances activation of KCNQ2/Q3 [[ potassium channels ]].",193,9
194,Suppression of << NF-kappaB >> activity by [[ sulfasalazine ]] is mediated by direct inhibition of IkappaB kinases alpha and beta.,194,0
195,The aim of this study was to define the molecular mechanism by which << sulfasalazine >> inhibits [[ NF-kappaB ]] activation.,195,0
196,"RESULTS: << NF-kappaB >>/Rel activity induced by tumor necrosis factor alpha, [[ 12-O-tetradecanoylphorbol-13-acetate ]], or overexpression of NF-kappaB-inducing kinase, IKK-alpha, IKK-beta, or constitutively active IKK-alpha and IKK-beta mutants was inhibited dose dependently by sulfasalazine.",196,9
197,"RESULTS: NF-kappaB/<< Rel >> activity induced by tumor necrosis factor alpha, [[ 12-O-tetradecanoylphorbol-13-acetate ]], or overexpression of NF-kappaB-inducing kinase, IKK-alpha, IKK-beta, or constitutively active IKK-alpha and IKK-beta mutants was inhibited dose dependently by sulfasalazine.",197,9
198,"RESULTS: << NF-kappaB >>/Rel activity induced by tumor necrosis factor alpha, 12-O-tetradecanoylphorbol-13-acetate, or overexpression of NF-kappaB-inducing kinase, IKK-alpha, IKK-beta, or constitutively active IKK-alpha and IKK-beta mutants was inhibited dose dependently by [[ sulfasalazine ]].",198,0
199,"RESULTS: NF-kappaB/<< Rel >> activity induced by tumor necrosis factor alpha, 12-O-tetradecanoylphorbol-13-acetate, or overexpression of NF-kappaB-inducing kinase, IKK-alpha, IKK-beta, or constitutively active IKK-alpha and IKK-beta mutants was inhibited dose dependently by [[ sulfasalazine ]].",199,0
200,"RESULTS: NF-kappaB/Rel activity induced by tumor necrosis factor alpha, 12-O-tetradecanoylphorbol-13-acetate, or overexpression of << NF-kappaB-inducing kinase >>, IKK-alpha, IKK-beta, or constitutively active IKK-alpha and IKK-beta mutants was inhibited dose dependently by [[ sulfasalazine ]].",200,0
201,"RESULTS: NF-kappaB/Rel activity induced by tumor necrosis factor alpha, 12-O-tetradecanoylphorbol-13-acetate, or overexpression of NF-kappaB-inducing kinase, << IKK-alpha >>, IKK-beta, or constitutively active IKK-alpha and IKK-beta mutants was inhibited dose dependently by [[ sulfasalazine ]].",201,0
202,"RESULTS: NF-kappaB/Rel activity induced by tumor necrosis factor alpha, 12-O-tetradecanoylphorbol-13-acetate, or overexpression of NF-kappaB-inducing kinase, IKK-alpha, << IKK-beta >>, or constitutively active IKK-alpha and IKK-beta mutants was inhibited dose dependently by [[ sulfasalazine ]].",202,0
203,"RESULTS: NF-kappaB/Rel activity induced by tumor necrosis factor alpha, 12-O-tetradecanoylphorbol-13-acetate, or overexpression of NF-kappaB-inducing kinase, IKK-alpha, IKK-beta, or constitutively active << IKK-alpha >> and IKK-beta mutants was inhibited dose dependently by [[ sulfasalazine ]].",203,0
204,"RESULTS: NF-kappaB/Rel activity induced by tumor necrosis factor alpha, 12-O-tetradecanoylphorbol-13-acetate, or overexpression of NF-kappaB-inducing kinase, IKK-alpha, IKK-beta, or constitutively active IKK-alpha and << IKK-beta >> mutants was inhibited dose dependently by [[ sulfasalazine ]].",204,0
205,"<< Sulfasalazine >> inhibited [[ tumor necrosis factor alpha ]]-induced activation of endogenous IKK in Jurkat T cells and SW620 colon cells, as well as the catalytic activity of purified IKK-alpha and IKK-beta in vitro.",205,0
206,"<< Sulfasalazine >> inhibited tumor necrosis factor alpha-induced activation of endogenous [[ IKK ]] in Jurkat T cells and SW620 colon cells, as well as the catalytic activity of purified IKK-alpha and IKK-beta in vitro.",206,0
207,"<< Sulfasalazine >> inhibited tumor necrosis factor alpha-induced activation of endogenous IKK in Jurkat T cells and SW620 colon cells, as well as the catalytic activity of purified [[ IKK-alpha ]] and IKK-beta in vitro.",207,0
208,"<< Sulfasalazine >> inhibited tumor necrosis factor alpha-induced activation of endogenous IKK in Jurkat T cells and SW620 colon cells, as well as the catalytic activity of purified IKK-alpha and [[ IKK-beta ]] in vitro.",208,0
209,The decrease in substrate phosphorylation by IKK-alpha and -beta is associated with a decrease in autophosphorylation of << IKKs >> and can be antagonized by excess [[ adenosine triphosphate ]].,209,0
210,The suppression of << NF-kappaB >> activation by inhibition of the IKKs contributes to the well-known anti-inflammatory and immunosuppressive effects of [[ sulfasalazine ]].,210,0
211,The suppression of NF-kappaB activation by inhibition of the << IKKs >> contributes to the well-known anti-inflammatory and immunosuppressive effects of [[ sulfasalazine ]].,211,0
212,<< COX-2 >> produces [[ prostaglandins ]] that inhibit apoptosis and stimulate angiogenesis and invasiveness.,212,4
213,"In contrast, aspirin-like nonselective NSAIDs such as sulindac and << indomethacin >> inhibit not only the enzymatic action of the highly inducible, proinflammatory [[ COX-2 ]] but the constitutively expressed, cytoprotective COX-1 as well.",213,0
214,"In contrast, aspirin-like nonselective NSAIDs such as sulindac and << indomethacin >> inhibit not only the enzymatic action of the highly inducible, proinflammatory COX-2 but the constitutively expressed, cytoprotective [[ COX-1 ]] as well.",214,0
215,"In contrast, << aspirin >>-like nonselective NSAIDs such as sulindac and indomethacin inhibit not only the enzymatic action of the highly inducible, proinflammatory [[ COX-2 ]] but the constitutively expressed, cytoprotective COX-1 as well.",215,0
216,"In contrast, << aspirin >>-like nonselective NSAIDs such as sulindac and indomethacin inhibit not only the enzymatic action of the highly inducible, proinflammatory COX-2 but the constitutively expressed, cytoprotective [[ COX-1 ]] as well.",216,0
217,"In contrast, aspirin-like nonselective NSAIDs such as << sulindac >> and indomethacin inhibit not only the enzymatic action of the highly inducible, proinflammatory [[ COX-2 ]] but the constitutively expressed, cytoprotective COX-1 as well.",217,0
218,"In contrast, aspirin-like nonselective NSAIDs such as << sulindac >> and indomethacin inhibit not only the enzymatic action of the highly inducible, proinflammatory COX-2 but the constitutively expressed, cytoprotective [[ COX-1 ]] as well.",218,0
219,"Selective COX-2 inhibitors, such as << meloxicam >>, celecoxib (SC-58635), and rofecoxib (MK-0966), are NSAIDs that have been modified chemically to preferentially inhibit [[ COX-2 ]] but not COX-1.",219,0
220,"Selective << COX-2 >> inhibitors, such as [[ meloxicam ]], celecoxib (SC-58635), and rofecoxib (MK-0966), are NSAIDs that have been modified chemically to preferentially inhibit COX-2 but not COX-1.",220,0
221,"Selective COX-2 inhibitors, such as meloxicam, << celecoxib >> (SC-58635), and rofecoxib (MK-0966), are NSAIDs that have been modified chemically to preferentially inhibit [[ COX-2 ]] but not COX-1.",221,0
222,"Selective << COX-2 >> inhibitors, such as meloxicam, [[ celecoxib ]] (SC-58635), and rofecoxib (MK-0966), are NSAIDs that have been modified chemically to preferentially inhibit COX-2 but not COX-1.",222,0
223,"Selective COX-2 inhibitors, such as meloxicam, celecoxib (<< SC-58635 >>), and rofecoxib (MK-0966), are NSAIDs that have been modified chemically to preferentially inhibit [[ COX-2 ]] but not COX-1.",223,0
224,"Selective << COX-2 >> inhibitors, such as meloxicam, celecoxib ([[ SC-58635 ]]), and rofecoxib (MK-0966), are NSAIDs that have been modified chemically to preferentially inhibit COX-2 but not COX-1.",224,0
225,"Selective COX-2 inhibitors, such as meloxicam, celecoxib (SC-58635), and << rofecoxib >> (MK-0966), are NSAIDs that have been modified chemically to preferentially inhibit [[ COX-2 ]] but not COX-1.",225,0
226,"Selective << COX-2 >> inhibitors, such as meloxicam, celecoxib (SC-58635), and [[ rofecoxib ]] (MK-0966), are NSAIDs that have been modified chemically to preferentially inhibit COX-2 but not COX-1.",226,0
227,"Selective COX-2 inhibitors, such as meloxicam, celecoxib (SC-58635), and rofecoxib (<< MK-0966 >>), are NSAIDs that have been modified chemically to preferentially inhibit [[ COX-2 ]] but not COX-1.",227,0
228,"Selective << COX-2 >> inhibitors, such as meloxicam, celecoxib (SC-58635), and rofecoxib ([[ MK-0966 ]]), are NSAIDs that have been modified chemically to preferentially inhibit COX-2 but not COX-1.",228,0
229,"For instance, << meloxicam >> inhibits the growth of cultured colon cancer cells (HCA-7 and Moser-S) that express [[ COX-2 ]] but has no effect on HCT-116 tumor cells that do not express COX-2.",229,0
230,"This effect may due to induction of apoptosis through uncoupling of oxidative phosphorylation and down-regulation of << Bcl-2 >>, as has been demonstrated for some nonselective NSAIDs, for instance, [[ flurbiprofen ]].",230,8
231,"To assess the feasibility of targeting these high AAAD levels for chemotherapy, << AAAD >> inhibitors [[ carbidopa ]] (alpha-methyl-dopahydrazine), alpha-monofluoromethyldopa (MFMD), and 3-hydroxybenzylhydrazine (NSD-1015) were incubated (72 h) with NCI-H727 human lung carcinoid cells.",231,0
232,"To assess the feasibility of targeting these high AAAD levels for chemotherapy, << AAAD >> inhibitors carbidopa ([[ alpha-methyl-dopahydrazine ]]), alpha-monofluoromethyldopa (MFMD), and 3-hydroxybenzylhydrazine (NSD-1015) were incubated (72 h) with NCI-H727 human lung carcinoid cells.",232,0
233,"To assess the feasibility of targeting these high AAAD levels for chemotherapy, << AAAD >> inhibitors carbidopa (alpha-methyl-dopahydrazine), [[ alpha-monofluoromethyldopa ]] (MFMD), and 3-hydroxybenzylhydrazine (NSD-1015) were incubated (72 h) with NCI-H727 human lung carcinoid cells.",233,0
234,"To assess the feasibility of targeting these high AAAD levels for chemotherapy, << AAAD >> inhibitors carbidopa (alpha-methyl-dopahydrazine), alpha-monofluoromethyldopa ([[ MFMD ]]), and 3-hydroxybenzylhydrazine (NSD-1015) were incubated (72 h) with NCI-H727 human lung carcinoid cells.",234,0
235,"To assess the feasibility of targeting these high AAAD levels for chemotherapy, << AAAD >> inhibitors carbidopa (alpha-methyl-dopahydrazine), alpha-monofluoromethyldopa (MFMD), and [[ 3-hydroxybenzylhydrazine ]] (NSD-1015) were incubated (72 h) with NCI-H727 human lung carcinoid cells.",235,0
236,"To assess the feasibility of targeting these high AAAD levels for chemotherapy, << AAAD >> inhibitors carbidopa (alpha-methyl-dopahydrazine), alpha-monofluoromethyldopa (MFMD), and 3-hydroxybenzylhydrazine ([[ NSD-1015 ]]) were incubated (72 h) with NCI-H727 human lung carcinoid cells.",236,0
237,"<< Hexahydrochromeno[4,3-b]pyrrole >> derivatives as [[ acetylcholinesterase ]] inhibitors.",237,0
238,"Since this compound retains good << AChE >> inhibitory activity and its [[ hexahydrochromeno[4,3-b]pyrrole ]] moiety is reminiscent of the hexahydropyrrolo[2,3-b]indole of physostigmine (3), we have designed and synthesized carbamates 4-6, and their biological evaluation has been assessed in vitro against human AChE and BChE.",238,0
239,"Since this compound retains good << AChE >> inhibitory activity and its hexahydrochromeno[4,3-b]pyrrole moiety is reminiscent of the [[ hexahydropyrrolo[2,3-b]indole of physostigmine ]] (3), we have designed and synthesized carbamates 4-6, and their biological evaluation has been assessed in vitro against human AChE and BChE.",239,0
240,"When the anti-corticosterone drug << aminoglutethimide >> (CYP11A1 inhibitor) was administered to B16F10 mice, corticosterone levels in splenic tissue or serum and [[ CYP11A1 ]] mRNA expression were decreased at 14 days after tumor inoculation.",240,8
241,"When the anti-corticosterone drug << aminoglutethimide >> ([[ CYP11A1 ]] inhibitor) was administered to B16F10 mice, corticosterone levels in splenic tissue or serum and CYP11A1 mRNA expression were decreased at 14 days after tumor inoculation.",241,0
242,"We report here that a human degradation-resistant GLP-2 analogue, h[Gly2]-GLP-2 significantly improves survival, reduces bacteremia, attenuates epithelial injury, and inhibits crypt apoptosis in the murine gastrointestinal tract after administration of << topoisomerase I >> inhibitor [[ irinotecan hydrochloride ]] or the antimetabolite 5-fluorouracil.",242,0
243,"Furthermore, h[<< Gly2 >>]-GLP-2 reduced chemotherapy-induced apoptosis, decreased activation of caspase-8 and -3, and inhibited [[ poly(ADP-ribose) polymerase ]] cleavage in heterologous cells transfected with the GLP-2 receptor.",243,0
244,OBJECTIVES: The hypothesis of the present study was that differences among << dopamine transporter >> (DAT) ligands in potency and effectiveness as a positive reinforcers were related to potency and effectiveness as [[ DA ]] uptake inhibitors.,244,5
245,OBJECTIVES: The hypothesis of the present study was that differences among dopamine transporter (<< DAT >>) ligands in potency and effectiveness as a positive reinforcers were related to potency and effectiveness as [[ DA ]] uptake inhibitors.,245,5
246,"Accordingly, self-administration of a group of local anesthetics that are << DAT >> ligands was compared to their effects as [[ DA ]] uptake blockers in vitro in brain tissue.",246,5
247,Contribution of the << Na+-K+-2Cl- cotransporter >> NKCC1 to [[ Cl- ]] secretion in rat OMCD.,247,5
248,Contribution of the Na+-K+-2Cl- cotransporter << NKCC1 >> to [[ Cl- ]] secretion in rat OMCD.,248,5
249,"The purpose of this study was to determine whether rat outer medullary collecting duct (OMCD) secretes Cl- and whether transepithelial Cl- transport occurs, in part, through << Cl- >> uptake across the basolateral membrane mediated by [[ NKCC1 ]] in series with Cl- efflux across the apical membrane.",249,5
250,"The purpose of this study was to determine whether rat outer medullary collecting duct (OMCD) secretes Cl- and whether transepithelial Cl- transport occurs, in part, through Cl- uptake across the basolateral membrane mediated by << NKCC1 >> in series with [[ Cl- ]] efflux across the apical membrane.",250,5
251,"Bumetanide-sensitive Cl- secretion was dependent on extracellular Na+ and either K+ or NH, consistent with the ion dependency of << NKCC1 >>-mediated [[ Cl- ]] transport.",251,5
252,"In conclusion, OMCD tubules from deoxycorticosterone pivalate-treated rats secrete << Cl- >> into the luminal fluid through [[ NKCC1 ]]-mediated Cl- uptake across the basolateral membrane in series with Cl- efflux across the apical membrane.",252,5
253,"In conclusion, OMCD tubules from deoxycorticosterone pivalate-treated rats secrete Cl- into the luminal fluid through << NKCC1 >>-mediated [[ Cl- ]] uptake across the basolateral membrane in series with Cl- efflux across the apical membrane.",253,5
254,"In conclusion, OMCD tubules from deoxycorticosterone pivalate-treated rats secrete Cl- into the luminal fluid through << NKCC1 >>-mediated Cl- uptake across the basolateral membrane in series with [[ Cl- ]] efflux across the apical membrane.",254,5
255,The physiological role of << NKCC1 >>-mediated [[ Cl- ]] uptake remains to be determined.,255,5
256,"The broad-spectrum anti-emetic activity of << AS-8112 >>, a novel dopamine D2, D3 and [[ 5-HT3 receptors ]] antagonist.",256,1
257,"In guinea-pig isolated colon, AS-8112 produced a rightward shift of the concentration-response curves of << 2-methyl-5HT >>, a [[ 5-HT3 receptor ]] agonist (pA2 value of 7.04).",257,2
258,"In guinea-pig isolated colon, << AS-8112 >> produced a rightward shift of the concentration-response curves of 2-methyl-5HT, a [[ 5-HT3 receptor ]] agonist (pA2 value of 7.04).",258,1
259,Other << 5-HT3 receptor >> antagonists also produced such a shift in the following antagonistic-potency order: [[ granisetron ]]> ondansetron=AS-8112>>metoclopramide.,259,1
260,Other << 5-HT3 receptor >> antagonists also produced such a shift in the following antagonistic-potency order: granisetron> [[ ondansetron ]]=AS-8112>>metoclopramide.,260,1
261,Other << 5-HT3 receptor >> antagonists also produced such a shift in the following antagonistic-potency order: granisetron> ondansetron=[[ AS-8112 ]]>>metoclopramide.,261,1
262,Other << 5-HT3 receptor >> antagonists also produced such a shift in the following antagonistic-potency order: granisetron> ondansetron=AS-8112>>[[ metoclopramide ]].,262,1
263,"In mice, << AS-8112 >> (1.0 - 3.0 mg kg(-1) s.c.) potently inhibited hypothermia induced by the [[ dopamine D3 receptor ]] agonist; R(+)-7-OH-DPAT (R(+)-7-hydroxy-2-(N,N-di-n-propylamino)tetraline) (0.3 mg kg(-1) s.c.).",263,0
264,"In mice, AS-8112 (1.0 - 3.0 mg kg(-1) s.c.) potently inhibited hypothermia induced by the << dopamine D3 receptor >> agonist; [[ R(+)-7-OH-DPAT ]] (R(+)-7-hydroxy-2-(N,N-di-n-propylamino)tetraline) (0.3 mg kg(-1) s.c.).",264,2
265,"In mice, AS-8112 (1.0 - 3.0 mg kg(-1) s.c.) potently inhibited hypothermia induced by the << dopamine D3 receptor >> agonist; R(+)-7-OH-DPAT ([[ R(+)-7-hydroxy-2-(N,N-di-n-propylamino)tetraline ]]) (0.3 mg kg(-1) s.c.).",265,2
266,"In conclusion, << AS-8112 >> is a potent dopamine D2, D3 and [[ 5-HT3 receptors ]] antagonist, and a novel anti-emetic agent with a broad-spectrum of anti-emetic activity.",266,1
267,<< Rofecoxib >> is a selective [[ cyclo-oxygenase (COX)-2 ]] inhibitor which has little or no effect on the COX-1 isoenzyme at doses up to 1000 mg/day.,267,0
268,"<< Rofecoxib >> has greater selectivity for [[ COX-2 ]] than celecoxib, meloxicam, diclofenac and indomethacin.",268,0
269,<< Fenofibrate >> and GW2331 induced expression of [[ acyl-coenzyme A (CoA) oxidase ]] and enoyl-CoA hydratase and reduced apolipoprotein C-III and phosphoenolpyruvate carboxykinase mRNAs.,269,6
270,<< Fenofibrate >> and GW2331 induced expression of acyl-coenzyme A (CoA) oxidase and [[ enoyl-CoA hydratase ]] and reduced apolipoprotein C-III and phosphoenolpyruvate carboxykinase mRNAs.,270,6
271,Fenofibrate and << GW2331 >> induced expression of [[ acyl-coenzyme A (CoA) oxidase ]] and enoyl-CoA hydratase and reduced apolipoprotein C-III and phosphoenolpyruvate carboxykinase mRNAs.,271,6
272,Fenofibrate and << GW2331 >> induced expression of acyl-coenzyme A (CoA) oxidase and [[ enoyl-CoA hydratase ]] and reduced apolipoprotein C-III and phosphoenolpyruvate carboxykinase mRNAs.,272,6
273,<< Fenofibrate >> and GW2331 induced expression of acyl-coenzyme A (CoA) oxidase and enoyl-CoA hydratase and reduced [[ apolipoprotein C-III ]] and phosphoenolpyruvate carboxykinase mRNAs.,273,8
274,<< Fenofibrate >> and GW2331 induced expression of acyl-coenzyme A (CoA) oxidase and enoyl-CoA hydratase and reduced apolipoprotein C-III and [[ phosphoenolpyruvate carboxykinase ]] mRNAs.,274,8
275,Fenofibrate and << GW2331 >> induced expression of acyl-coenzyme A (CoA) oxidase and enoyl-CoA hydratase and reduced [[ apolipoprotein C-III ]] and phosphoenolpyruvate carboxykinase mRNAs.,275,8
276,Fenofibrate and << GW2331 >> induced expression of acyl-coenzyme A (CoA) oxidase and enoyl-CoA hydratase and reduced apolipoprotein C-III and [[ phosphoenolpyruvate carboxykinase ]] mRNAs.,276,8
277,<< Rosiglitazone >> modestly increased apolipoprotein C-III mRNA and had no effect on expression of the other 2 genes in the liver but increased the expression of [[ glucose transporter 4 ]] and phosphoenolpyruvate carboxykinase in adipose tissue.,277,6
278,<< Rosiglitazone >> modestly increased apolipoprotein C-III mRNA and had no effect on expression of the other 2 genes in the liver but increased the expression of glucose transporter 4 and [[ phosphoenolpyruvate carboxykinase ]] in adipose tissue.,278,6
279,<< Rosiglitazone >> modestly increased [[ apolipoprotein C-III ]] mRNA and had no effect on expression of the other 2 genes in the liver but increased the expression of glucose transporter 4 and phosphoenolpyruvate carboxykinase in adipose tissue.,279,6
280,<< Long-chain alkanols >> are general anesthetics which can also act as uncharged noncompetitive inhibitors of the peripheral [[ nicotinic acetylcholine receptor ]] (AChR) by binding to one or more specific sites on the AChR.,280,0
281,"<< Cembranoids >> are naturally occurring, uncharged noncompetitive inhibitors of peripheral and neuronal [[ AChRs ]], which have no demonstrable general anesthetic activity in vivo.",281,0
282,"<< Sulfasalazine >>, a potent suppressor of lymphoma growth by inhibition of the [[ x(c)- cystine transporter ]]: a new action for an old drug.",282,0
283,"<< Sulfasalazine >> was fortuitously found to be a novel, potent inhibitor of the [[ x(c)- transporter ]].",283,0
284,"It showed high rat lymphoma growth-inhibitory and lytic activity in vitro (IC50 = 0.16 mM), based specifically on inhibition of << x(c) >>--mediated cystine uptake, in contrast to its colonic metabolites, [[ sulfapyridine ]] and 5-aminosalicylic acid.",284,0
285,"It showed high rat lymphoma growth-inhibitory and lytic activity in vitro (IC50 = 0.16 mM), based specifically on inhibition of << x(c) >>--mediated cystine uptake, in contrast to its colonic metabolites, sulfapyridine and [[ 5-aminosalicylic acid ]].",285,0
286,"It showed high rat lymphoma growth-inhibitory and lytic activity in vitro (IC50 = 0.16 mM), based specifically on inhibition of << x(c) >>--mediated [[ cystine ]] uptake, in contrast to its colonic metabolites, sulfapyridine and 5-aminosalicylic acid.",286,5
287,The << x(c)- cystine transporter >> represents a novel target for sulfasalazine-like drugs with high potential for application in therapy of lymphoblastic and other malignancies dependent on extracellular [[ cyst(e)ine ]].,287,5
288,"Advances in antihypertensive combination therapy: benefits of low-dose thiazide diuretics in conjunction with << omapatrilat >>, a [[ vasopeptidase ]] inhibitor.",288,0
289,"<< Omapatrilat >>, the prototypical [[ vasopeptidase ]] inhibitor, inhibits not only ACE but also neutral endopeptidase.",289,0
290,"<< Omapatrilat >>, the prototypical vasopeptidase inhibitor, inhibits not only [[ ACE ]] but also neutral endopeptidase.",290,0
291,"<< Omapatrilat >>, the prototypical vasopeptidase inhibitor, inhibits not only ACE but also [[ neutral endopeptidase ]].",291,0
292,"Like conventional ACE inhibitors, << omapatrilat >> causes extracellular volume reduction and vasodilatation; moreover, it increases levels of [[ atrial and brain natriuretic peptides ]] and bradykinin.",292,6
293,"Like conventional ACE inhibitors, << omapatrilat >> causes extracellular volume reduction and vasodilatation; moreover, it increases levels of atrial and brain natriuretic peptides and [[ bradykinin ]].",293,6
294,"Like conventional << ACE >> inhibitors, [[ omapatrilat ]] causes extracellular volume reduction and vasodilatation; moreover, it increases levels of atrial and brain natriuretic peptides and bradykinin.",294,0
295,"The transport amiloride-sensitive mechanism, that decreased the acidic intracellular pH change occurring in this medium, would correspond to << Na+ >>-H+ exchange ([[ NHE1 ]] isoform).",295,5
296,"The transport amiloride-sensitive mechanism, that decreased the acidic intracellular pH change occurring in this medium, would correspond to Na+-<< H+ >> exchange ([[ NHE1 ]] isoform).",296,5
297,<< Aspirin >> and salicylate bind to immunoglobulin heavy chain binding protein (BiP) and inhibit its [[ ATPase ]] activity in human fibroblasts.,297,0
298,Aspirin and << salicylate >> bind to immunoglobulin heavy chain binding protein (BiP) and inhibit its [[ ATPase ]] activity in human fibroblasts.,298,0
299,<< Salicylates >> inhibited [[ ATPase ]] activity stimulated by this specific heptapeptide but did not block ATP binding or induce BiP expression.,299,0
300,"The specific activity of only << ornithine aminotransferase >> (OAT), the rate-limiting enzyme in the conversion of ornithine to [[ proline ]], increased in 2 weeks of hypertrophy.",300,4
301,"The specific activity of only ornithine aminotransferase (<< OAT >>), the rate-limiting enzyme in the conversion of ornithine to [[ proline ]], increased in 2 weeks of hypertrophy.",301,4
302,"The specific activity of only << ornithine aminotransferase >> (OAT), the rate-limiting enzyme in the conversion of [[ ornithine ]] to proline, increased in 2 weeks of hypertrophy.",302,5
303,"The specific activity of only ornithine aminotransferase (<< OAT >>), the rate-limiting enzyme in the conversion of [[ ornithine ]] to proline, increased in 2 weeks of hypertrophy.",303,5
304,"A series of studies is reviewed that assesses the relationship between cytokines released at the site of tissue injury and NSAID analgesia, and the in vivo selectivity of a selective << cyclooxygenase (COX)-2 >> inhibitor ([[ celecoxib ]]) in comparison to a dual COX-1/COX-2 inhibitor (ketorolac).",304,0
305,"A series of studies is reviewed that assesses the relationship between cytokines released at the site of tissue injury and NSAID analgesia, and the in vivo selectivity of a selective cyclooxygenase (COX)-2 inhibitor (celecoxib) in comparison to a dual << COX-1 >>/COX-2 inhibitor ([[ ketorolac ]]).",305,0
306,"A series of studies is reviewed that assesses the relationship between cytokines released at the site of tissue injury and NSAID analgesia, and the in vivo selectivity of a selective cyclooxygenase (COX)-2 inhibitor (celecoxib) in comparison to a dual COX-1/<< COX-2 >> inhibitor ([[ ketorolac ]]).",306,0
307,Three replicate studies in the oral surgery model of acute pain used submucosal microdialysis sample collection for the measurement of << prostaglandin E2 >> (PGE2; a product of both [[ COX-1 ]] and COX-2) and thromboxane B2 (as a biomarker for COX-1 activity) with parallel assessments of pain.,307,4
308,Three replicate studies in the oral surgery model of acute pain used submucosal microdialysis sample collection for the measurement of << prostaglandin E2 >> (PGE2; a product of both COX-1 and [[ COX-2 ]]) and thromboxane B2 (as a biomarker for COX-1 activity) with parallel assessments of pain.,308,4
309,Three replicate studies in the oral surgery model of acute pain used submucosal microdialysis sample collection for the measurement of prostaglandin E2 (<< PGE2 >>; a product of both [[ COX-1 ]] and COX-2) and thromboxane B2 (as a biomarker for COX-1 activity) with parallel assessments of pain.,309,4
310,Three replicate studies in the oral surgery model of acute pain used submucosal microdialysis sample collection for the measurement of prostaglandin E2 (<< PGE2 >>; a product of both COX-1 and [[ COX-2 ]]) and thromboxane B2 (as a biomarker for COX-1 activity) with parallel assessments of pain.,310,4
311,"The time course of << PGE2 >> production was consistent with early release due to [[ COX-1 ]] activity followed by increased production 2-3 hours after surgery, consistent with COX-2 expression.",311,4
312,"The time course of << PGE2 >> production was consistent with early release due to COX-1 activity followed by increased production 2-3 hours after surgery, consistent with [[ COX-2 ]] expression.",312,4
313,"<< Celecoxib >> selectively suppressed PGE2 but not TxB2 at time points consistent with [[ COX-2 ]] activity, while producing analgesia.",313,0
314,"Celecoxib selectively suppressed << PGE2 >> but not TxB2 at time points consistent with [[ COX-2 ]] activity, while producing analgesia.",314,4
315,These studies demonstrate the ability to assess the time course and selective effects of COX-2 inhibitors in vivo and suggest that suppression of << COX-2 >> mediated [[ PGE2 ]] is temporally related to NSAID analgesia.,315,4
316,"Acute and chronic << PLZ >> administration increase brain GABA levels, an effect due, at least in part, to an inhibition of the activity of the GABA metabolizing enzyme, [[ GABA transaminase ]] (GABA-T).",316,0
317,"Acute and chronic << PLZ >> administration increase brain GABA levels, an effect due, at least in part, to an inhibition of the activity of the GABA metabolizing enzyme, GABA transaminase ([[ GABA-T ]]).",317,0
318,"Acute and chronic PLZ administration increase brain GABA levels, an effect due, at least in part, to an inhibition of the activity of the << GABA >> metabolizing enzyme, [[ GABA transaminase ]] (GABA-T).",318,5
319,"Acute and chronic PLZ administration increase brain GABA levels, an effect due, at least in part, to an inhibition of the activity of the << GABA >> metabolizing enzyme, GABA transaminase ([[ GABA-T ]]).",319,5
320,"As with GABA, the metabolism of << alanine >> involves a [[ pyridoxal phosphate-dependent transaminase ]].",320,5
321,"In the study reported here, the effects of acute PLZ treatment on the levels of various << amino acids >>, some of which are also metabolized by [[ pyridoxal phosphate-dependent transaminases ]] were compared in rat whole brain.",321,5
322,"The elevation in brain alanine levels could be explained, at least in part, by a time- and dose-dependent inhibitory effect of << PLZ >> on [[ alanine transaminase ]] (ALA-T), although as with GABA the increases are higher than expected from the degree of enzyme inhibition produced.",322,0
323,"The elevation in brain alanine levels could be explained, at least in part, by a time- and dose-dependent inhibitory effect of << PLZ >> on alanine transaminase ([[ ALA-T ]]), although as with GABA the increases are higher than expected from the degree of enzyme inhibition produced.",323,0
324,"The elevation in brain << alanine >> levels could be explained, at least in part, by a time- and dose-dependent inhibitory effect of PLZ on [[ alanine transaminase ]] (ALA-T), although as with GABA the increases are higher than expected from the degree of enzyme inhibition produced.",324,5
325,"The elevation in brain << alanine >> levels could be explained, at least in part, by a time- and dose-dependent inhibitory effect of PLZ on alanine transaminase ([[ ALA-T ]]), although as with GABA the increases are higher than expected from the degree of enzyme inhibition produced.",325,5
326,"In addition, we also showed that the elevation in alanine levels and the inhibition of << alanine transaminase >> in the brain are retained after 14 days of [[ PLZ ]] treatment, and that PLZ produces a marked increase in extracellular levels of alanine.",326,0
327,"In addition, we also showed that the elevation in << alanine >> levels and the inhibition of [[ alanine transaminase ]] in the brain are retained after 14 days of PLZ treatment, and that PLZ produces a marked increase in extracellular levels of alanine.",327,5
328,"<< Cyclooxygenase-1 >> (COX-1) inhibitors ([[ flurbiprofen ]], ketoprofen and ketrolack) attenuated the nicotine-induced contraction in a concentration-dependent manner, and cyclooxygenase-2 (COX-2) inhibitors at high concentrations (nimesulide and NS-389) slightly attenuated the contraction.",328,0
329,"Cyclooxygenase-1 (<< COX-1 >>) inhibitors ([[ flurbiprofen ]], ketoprofen and ketrolack) attenuated the nicotine-induced contraction in a concentration-dependent manner, and cyclooxygenase-2 (COX-2) inhibitors at high concentrations (nimesulide and NS-389) slightly attenuated the contraction.",329,0
330,"<< Cyclooxygenase-1 >> (COX-1) inhibitors (flurbiprofen, [[ ketoprofen ]] and ketrolack) attenuated the nicotine-induced contraction in a concentration-dependent manner, and cyclooxygenase-2 (COX-2) inhibitors at high concentrations (nimesulide and NS-389) slightly attenuated the contraction.",330,0
331,"Cyclooxygenase-1 (<< COX-1 >>) inhibitors (flurbiprofen, [[ ketoprofen ]] and ketrolack) attenuated the nicotine-induced contraction in a concentration-dependent manner, and cyclooxygenase-2 (COX-2) inhibitors at high concentrations (nimesulide and NS-389) slightly attenuated the contraction.",331,0
332,"<< Cyclooxygenase-1 >> (COX-1) inhibitors (flurbiprofen, ketoprofen and [[ ketrolack ]]) attenuated the nicotine-induced contraction in a concentration-dependent manner, and cyclooxygenase-2 (COX-2) inhibitors at high concentrations (nimesulide and NS-389) slightly attenuated the contraction.",332,0
333,"Cyclooxygenase-1 (<< COX-1 >>) inhibitors (flurbiprofen, ketoprofen and [[ ketrolack ]]) attenuated the nicotine-induced contraction in a concentration-dependent manner, and cyclooxygenase-2 (COX-2) inhibitors at high concentrations (nimesulide and NS-389) slightly attenuated the contraction.",333,0
334,"Cyclooxygenase-1 (COX-1) inhibitors (flurbiprofen, ketoprofen and ketrolack) attenuated the nicotine-induced contraction in a concentration-dependent manner, and << cyclooxygenase-2 >> (COX-2) inhibitors at high concentrations ([[ nimesulide ]] and NS-389) slightly attenuated the contraction.",334,0
335,"Cyclooxygenase-1 (COX-1) inhibitors (flurbiprofen, ketoprofen and ketrolack) attenuated the nicotine-induced contraction in a concentration-dependent manner, and cyclooxygenase-2 (<< COX-2 >>) inhibitors at high concentrations ([[ nimesulide ]] and NS-389) slightly attenuated the contraction.",335,0
336,"Cyclooxygenase-1 (COX-1) inhibitors (flurbiprofen, ketoprofen and ketrolack) attenuated the nicotine-induced contraction in a concentration-dependent manner, and << cyclooxygenase-2 >> (COX-2) inhibitors at high concentrations (nimesulide and [[ NS-389 ]]) slightly attenuated the contraction.",336,0
337,"Cyclooxygenase-1 (COX-1) inhibitors (flurbiprofen, ketoprofen and ketrolack) attenuated the nicotine-induced contraction in a concentration-dependent manner, and cyclooxygenase-2 (<< COX-2 >>) inhibitors at high concentrations (nimesulide and [[ NS-389 ]]) slightly attenuated the contraction.",337,0
338,A << TXA2 synthetase >> inhibitor ([[ OKY-046 ]]) attenuated the contraction to a small extent only at high concentrations.,338,0
339,A << TXA2 receptor >> antagonist ([[ S-1452 ]]) attenuated the contraction in a concentration-dependent manner.,339,1
340,A << nicotinic receptor >> antagonist ([[ hexamethonium ]]) attenuated the contraction in part and an alpha-adrenoceptor antagonist (prazosin) nearly abolished the contraction.,340,1
341,A nicotinic receptor antagonist (hexamethonium) attenuated the contraction in part and an << alpha-adrenoceptor >> antagonist ([[ prazosin ]]) nearly abolished the contraction.,341,1
342,"Non-<< steroidal >> anti-inflammatory drugs (NSAIDs) are competitive inhibitors of [[ cyclooxygenase ]] (COX), the enzyme that mediates biosynthesis of prostaglandins and thromboxanes from arachidonic acid.",342,0
343,"Non-<< steroidal >> anti-inflammatory drugs (NSAIDs) are competitive inhibitors of cyclooxygenase ([[ COX ]]), the enzyme that mediates biosynthesis of prostaglandins and thromboxanes from arachidonic acid.",343,0
344,"Non-steroidal anti-inflammatory drugs (NSAIDs) are competitive inhibitors of << cyclooxygenase >> (COX), the enzyme that mediates biosynthesis of [[ prostaglandins ]] and thromboxanes from arachidonic acid.",344,4
345,"Non-steroidal anti-inflammatory drugs (NSAIDs) are competitive inhibitors of cyclooxygenase (<< COX >>), the enzyme that mediates biosynthesis of [[ prostaglandins ]] and thromboxanes from arachidonic acid.",345,4
346,"Non-steroidal anti-inflammatory drugs (NSAIDs) are competitive inhibitors of << cyclooxygenase >> (COX), the enzyme that mediates biosynthesis of prostaglandins and [[ thromboxanes ]] from arachidonic acid.",346,4
347,"Non-steroidal anti-inflammatory drugs (NSAIDs) are competitive inhibitors of cyclooxygenase (<< COX >>), the enzyme that mediates biosynthesis of prostaglandins and [[ thromboxanes ]] from arachidonic acid.",347,4
348,"Non-steroidal anti-inflammatory drugs (NSAIDs) are competitive inhibitors of << cyclooxygenase >> (COX), the enzyme that mediates biosynthesis of prostaglandins and thromboxanes from [[ arachidonic acid ]].",348,5
349,"Non-steroidal anti-inflammatory drugs (NSAIDs) are competitive inhibitors of cyclooxygenase (<< COX >>), the enzyme that mediates biosynthesis of prostaglandins and thromboxanes from [[ arachidonic acid ]].",349,5
350,"Accordingly, docking of different << COX >> inhibitors, including selective and non-selective ligands: rofecoxib, ketoprofen, suprofen, carprofen, [[ zomepirac ]], indomethacin, diclofenac and meclofenamic acid were undertaken using the AMBER program.",350,0
351,"Accordingly, docking of different << COX >> inhibitors, including selective and non-selective ligands: rofecoxib, ketoprofen, suprofen, carprofen, zomepirac, [[ indomethacin ]], diclofenac and meclofenamic acid were undertaken using the AMBER program.",351,0
352,"Accordingly, docking of different << COX >> inhibitors, including selective and non-selective ligands: rofecoxib, ketoprofen, suprofen, carprofen, zomepirac, indomethacin, [[ diclofenac ]] and meclofenamic acid were undertaken using the AMBER program.",352,0
353,"Accordingly, docking of different << COX >> inhibitors, including selective and non-selective ligands: rofecoxib, ketoprofen, suprofen, carprofen, zomepirac, indomethacin, diclofenac and [[ meclofenamic acid ]] were undertaken using the AMBER program.",353,0
354,"Accordingly, docking of different << COX >> inhibitors, including selective and non-selective ligands: [[ rofecoxib ]], ketoprofen, suprofen, carprofen, zomepirac, indomethacin, diclofenac and meclofenamic acid were undertaken using the AMBER program.",354,0
355,"Accordingly, docking of different << COX >> inhibitors, including selective and non-selective ligands: rofecoxib, [[ ketoprofen ]], suprofen, carprofen, zomepirac, indomethacin, diclofenac and meclofenamic acid were undertaken using the AMBER program.",355,0
356,"Accordingly, docking of different << COX >> inhibitors, including selective and non-selective ligands: rofecoxib, ketoprofen, [[ suprofen ]], carprofen, zomepirac, indomethacin, diclofenac and meclofenamic acid were undertaken using the AMBER program.",356,0
357,"Accordingly, docking of different << COX >> inhibitors, including selective and non-selective ligands: rofecoxib, ketoprofen, suprofen, [[ carprofen ]], zomepirac, indomethacin, diclofenac and meclofenamic acid were undertaken using the AMBER program.",357,0
358,"Olopatadine hydrochloride (<< olopatadine >>, 11-[(Z)-3-(dimethylamino)propylidene]-6,11-dihydrodibenz[b,e]oxepin-2-acetic acid monohydrochloride) is a novel antiallergic/[[ histamine H1-receptor ]] antagonistic drug that was synthesized and evaluated in our laboratories.",358,1
359,"Olopatadine hydrochloride (olopatadine, << 11-[(Z)-3-(dimethylamino)propylidene]-6,11-dihydrodibenz[b,e]oxepin-2-acetic acid monohydrochloride >>) is a novel antiallergic/[[ histamine H1-receptor ]] antagonistic drug that was synthesized and evaluated in our laboratories.",359,1
360,"<< Olopatadine hydrochloride >> (olopatadine, 11-[(Z)-3-(dimethylamino)propylidene]-6,11-dihydrodibenz[b,e]oxepin-2-acetic acid monohydrochloride) is a novel antiallergic/[[ histamine H1-receptor ]] antagonistic drug that was synthesized and evaluated in our laboratories.",360,1
361,<< Olopatadine >> is a selective [[ histamine H1-receptor ]] antagonist possessing inhibitory effects on the release of inflammatory lipid mediators such as leukotriene and thromboxane from human polymorphonuclear leukocytes and eosinophils.,361,1
362,A molecular mechanism of action of << theophylline >>: Induction of [[ histone deacetylase ]] activity to decrease inflammatory gene expression.,362,9
363,We show both in vitro and in vivo that low-dose << theophylline >> enhances [[ HDAC ]] activity in epithelial cells and macrophages.,363,9
364,Thus we have shown that low-dose << theophylline >> exerts an anti-asthma effect through increasing activation of [[ HDAC ]] which is subsequently recruited by corticosteroids to suppress inflammatory genes.,364,9
365,"In rats, << rifamycin SV >> and rifampicin were shown to interfere with hepatic organic anion uptake by inhibition of the [[ organic anion transporting polypeptides ]] Oatp1 and Oatp2.",365,0
366,"In rats, << rifamycin SV >> and rifampicin were shown to interfere with hepatic organic anion uptake by inhibition of the organic anion transporting polypeptides [[ Oatp1 ]] and Oatp2.",366,0
367,"In rats, << rifamycin SV >> and rifampicin were shown to interfere with hepatic organic anion uptake by inhibition of the organic anion transporting polypeptides Oatp1 and [[ Oatp2 ]].",367,0
368,"In rats, rifamycin SV and << rifampicin >> were shown to interfere with hepatic organic anion uptake by inhibition of the [[ organic anion transporting polypeptides ]] Oatp1 and Oatp2.",368,0
369,"In rats, rifamycin SV and << rifampicin >> were shown to interfere with hepatic organic anion uptake by inhibition of the organic anion transporting polypeptides [[ Oatp1 ]] and Oatp2.",369,0
370,"In rats, rifamycin SV and << rifampicin >> were shown to interfere with hepatic organic anion uptake by inhibition of the organic anion transporting polypeptides Oatp1 and [[ Oatp2 ]].",370,0
371,"In complementary RNA (cRNA)-injected Xenopus laevis oocytes, << rifamycin SV >> (10 micromol/L) cis-inhibited [[ human organic anion transporting polypeptide C ]] (SLC21A6) (OATP-C), human organic anion transporting polypeptide 8 (SLC21A8) (OATP8), human organic anion transporting polypeptide B (SLC21A9) (OATP-B), and human organic anion transporting polypeptide A (SLC21A3) (OATP-A) mediated BSP uptake by 69%, 79%, 89%, and 57%, respectively, as compared with uptake into control oocytes.",371,0
372,"In complementary RNA (cRNA)-injected Xenopus laevis oocytes, << rifamycin SV >> (10 micromol/L) cis-inhibited human organic anion transporting polypeptide C ([[ SLC21A6 ]]) (OATP-C), human organic anion transporting polypeptide 8 (SLC21A8) (OATP8), human organic anion transporting polypeptide B (SLC21A9) (OATP-B), and human organic anion transporting polypeptide A (SLC21A3) (OATP-A) mediated BSP uptake by 69%, 79%, 89%, and 57%, respectively, as compared with uptake into control oocytes.",372,0
373,"In complementary RNA (cRNA)-injected Xenopus laevis oocytes, << rifamycin SV >> (10 micromol/L) cis-inhibited human organic anion transporting polypeptide C (SLC21A6) ([[ OATP-C ]]), human organic anion transporting polypeptide 8 (SLC21A8) (OATP8), human organic anion transporting polypeptide B (SLC21A9) (OATP-B), and human organic anion transporting polypeptide A (SLC21A3) (OATP-A) mediated BSP uptake by 69%, 79%, 89%, and 57%, respectively, as compared with uptake into control oocytes.",373,0
374,"In complementary RNA (cRNA)-injected Xenopus laevis oocytes, << rifamycin SV >> (10 micromol/L) cis-inhibited human organic anion transporting polypeptide C (SLC21A6) (OATP-C), [[ human organic anion transporting polypeptide 8 ]] (SLC21A8) (OATP8), human organic anion transporting polypeptide B (SLC21A9) (OATP-B), and human organic anion transporting polypeptide A (SLC21A3) (OATP-A) mediated BSP uptake by 69%, 79%, 89%, and 57%, respectively, as compared with uptake into control oocytes.",374,0
375,"In complementary RNA (cRNA)-injected Xenopus laevis oocytes, << rifamycin SV >> (10 micromol/L) cis-inhibited human organic anion transporting polypeptide C (SLC21A6) (OATP-C), human organic anion transporting polypeptide 8 ([[ SLC21A8 ]]) (OATP8), human organic anion transporting polypeptide B (SLC21A9) (OATP-B), and human organic anion transporting polypeptide A (SLC21A3) (OATP-A) mediated BSP uptake by 69%, 79%, 89%, and 57%, respectively, as compared with uptake into control oocytes.",375,0
376,"In complementary RNA (cRNA)-injected Xenopus laevis oocytes, << rifamycin SV >> (10 micromol/L) cis-inhibited human organic anion transporting polypeptide C (SLC21A6) (OATP-C), human organic anion transporting polypeptide 8 (SLC21A8) ([[ OATP8 ]]), human organic anion transporting polypeptide B (SLC21A9) (OATP-B), and human organic anion transporting polypeptide A (SLC21A3) (OATP-A) mediated BSP uptake by 69%, 79%, 89%, and 57%, respectively, as compared with uptake into control oocytes.",376,0
377,"In complementary RNA (cRNA)-injected Xenopus laevis oocytes, << rifamycin SV >> (10 micromol/L) cis-inhibited human organic anion transporting polypeptide C (SLC21A6) (OATP-C), human organic anion transporting polypeptide 8 (SLC21A8) (OATP8), [[ human organic anion transporting polypeptide B ]] (SLC21A9) (OATP-B), and human organic anion transporting polypeptide A (SLC21A3) (OATP-A) mediated BSP uptake by 69%, 79%, 89%, and 57%, respectively, as compared with uptake into control oocytes.",377,0
378,"In complementary RNA (cRNA)-injected Xenopus laevis oocytes, << rifamycin SV >> (10 micromol/L) cis-inhibited human organic anion transporting polypeptide C (SLC21A6) (OATP-C), human organic anion transporting polypeptide 8 (SLC21A8) (OATP8), human organic anion transporting polypeptide B ([[ SLC21A9 ]]) (OATP-B), and human organic anion transporting polypeptide A (SLC21A3) (OATP-A) mediated BSP uptake by 69%, 79%, 89%, and 57%, respectively, as compared with uptake into control oocytes.",378,0
379,"In complementary RNA (cRNA)-injected Xenopus laevis oocytes, << rifamycin SV >> (10 micromol/L) cis-inhibited human organic anion transporting polypeptide C (SLC21A6) (OATP-C), human organic anion transporting polypeptide 8 (SLC21A8) (OATP8), human organic anion transporting polypeptide B (SLC21A9) ([[ OATP-B ]]), and human organic anion transporting polypeptide A (SLC21A3) (OATP-A) mediated BSP uptake by 69%, 79%, 89%, and 57%, respectively, as compared with uptake into control oocytes.",379,0
380,"In complementary RNA (cRNA)-injected Xenopus laevis oocytes, << rifamycin SV >> (10 micromol/L) cis-inhibited human organic anion transporting polypeptide C (SLC21A6) (OATP-C), human organic anion transporting polypeptide 8 (SLC21A8) (OATP8), human organic anion transporting polypeptide B (SLC21A9) (OATP-B), and [[ human organic anion transporting polypeptide A ]] (SLC21A3) (OATP-A) mediated BSP uptake by 69%, 79%, 89%, and 57%, respectively, as compared with uptake into control oocytes.",380,0
381,"In complementary RNA (cRNA)-injected Xenopus laevis oocytes, << rifamycin SV >> (10 micromol/L) cis-inhibited human organic anion transporting polypeptide C (SLC21A6) (OATP-C), human organic anion transporting polypeptide 8 (SLC21A8) (OATP8), human organic anion transporting polypeptide B (SLC21A9) (OATP-B), and human organic anion transporting polypeptide A ([[ SLC21A3 ]]) (OATP-A) mediated BSP uptake by 69%, 79%, 89%, and 57%, respectively, as compared with uptake into control oocytes.",381,0
382,"In complementary RNA (cRNA)-injected Xenopus laevis oocytes, << rifamycin SV >> (10 micromol/L) cis-inhibited human organic anion transporting polypeptide C (SLC21A6) (OATP-C), human organic anion transporting polypeptide 8 (SLC21A8) (OATP8), human organic anion transporting polypeptide B (SLC21A9) (OATP-B), and human organic anion transporting polypeptide A (SLC21A3) ([[ OATP-A ]]) mediated BSP uptake by 69%, 79%, 89%, and 57%, respectively, as compared with uptake into control oocytes.",382,0
383,"<< Rifampicin >> (10 micromol/L) inhibited [[ OATP8 ]]-mediated BSP uptake by 50%, whereas inhibition of OATP-C-, OATP-B-, and OATP-A-mediated BSP transport was below 15%.",383,0
384,"<< Rifampicin >> (10 micromol/L) inhibited OATP8-mediated BSP uptake by 50%, whereas inhibition of [[ OATP-C ]]-, OATP-B-, and OATP-A-mediated BSP transport was below 15%.",384,0
385,"<< Rifampicin >> (10 micromol/L) inhibited OATP8-mediated BSP uptake by 50%, whereas inhibition of OATP-C-, [[ OATP-B ]]-, and OATP-A-mediated BSP transport was below 15%.",385,0
386,"<< Rifampicin >> (10 micromol/L) inhibited OATP8-mediated BSP uptake by 50%, whereas inhibition of OATP-C-, OATP-B-, and [[ OATP-A ]]-mediated BSP transport was below 15%.",386,0
387,"Rifampicin (10 micromol/L) inhibited << OATP8 >>-mediated [[ BSP ]] uptake by 50%, whereas inhibition of OATP-C-, OATP-B-, and OATP-A-mediated BSP transport was below 15%.",387,5
388,"Rifampicin (10 micromol/L) inhibited OATP8-mediated BSP uptake by 50%, whereas inhibition of << OATP-C >>-, OATP-B-, and OATP-A-mediated [[ BSP ]] transport was below 15%.",388,5
389,"Rifampicin (10 micromol/L) inhibited OATP8-mediated BSP uptake by 50%, whereas inhibition of OATP-C-, << OATP-B >>-, and OATP-A-mediated [[ BSP ]] transport was below 15%.",389,5
390,"Rifampicin (10 micromol/L) inhibited OATP8-mediated BSP uptake by 50%, whereas inhibition of OATP-C-, OATP-B-, and << OATP-A >>-mediated [[ BSP ]] transport was below 15%.",390,5
391,"100 micromol/L << rifampicin >> inhibited [[ OATP-C ]]- and OATP8-, OATP-B- and OATP-A-mediated BSP uptake by 66%, 96%, 25%, and 49%, respectively.",391,0
392,"100 micromol/L << rifampicin >> inhibited OATP-C- and [[ OATP8 ]]-, OATP-B- and OATP-A-mediated BSP uptake by 66%, 96%, 25%, and 49%, respectively.",392,0
393,"100 micromol/L << rifampicin >> inhibited OATP-C- and OATP8-, [[ OATP-B ]]- and OATP-A-mediated BSP uptake by 66%, 96%, 25%, and 49%, respectively.",393,0
394,"100 micromol/L << rifampicin >> inhibited OATP-C- and OATP8-, OATP-B- and [[ OATP-A ]]-mediated BSP uptake by 66%, 96%, 25%, and 49%, respectively.",394,0
395,"100 micromol/L rifampicin inhibited << OATP-C >>- and OATP8-, OATP-B- and OATP-A-mediated [[ BSP ]] uptake by 66%, 96%, 25%, and 49%, respectively.",395,5
396,"100 micromol/L rifampicin inhibited OATP-C- and << OATP8 >>-, OATP-B- and OATP-A-mediated [[ BSP ]] uptake by 66%, 96%, 25%, and 49%, respectively.",396,5
397,"100 micromol/L rifampicin inhibited OATP-C- and OATP8-, << OATP-B >>- and OATP-A-mediated [[ BSP ]] uptake by 66%, 96%, 25%, and 49%, respectively.",397,5
398,"100 micromol/L rifampicin inhibited OATP-C- and OATP8-, OATP-B- and << OATP-A >>-mediated [[ BSP ]] uptake by 66%, 96%, 25%, and 49%, respectively.",398,5
399,Direct transport of << rifampicin >> could be shown for [[ OATP-C ]] (apparent K(m) value 13 micromol/L) and OATP8 (2.3 micromol/L).,399,5
400,Direct transport of << rifampicin >> could be shown for OATP-C (apparent K(m) value 13 micromol/L) and [[ OATP8 ]] (2.3 micromol/L).,400,5
401,Inhibition of << human liver OATPs >> can explain the previously observed effects of [[ rifamycin SV ]] and rifampicin on hepatic organic anion elimination.,401,0
402,Inhibition of << human liver OATPs >> can explain the previously observed effects of rifamycin SV and [[ rifampicin ]] on hepatic organic anion elimination.,402,0
403,<< Metformin >> increases [[ AMP-activated protein kinase ]] activity in skeletal muscle of subjects with type 2 diabetes.,403,9
404,"<< AMP-activated protein kinase >> (AMPK) activity increases in response to depletion of cellular energy stores, and this enzyme has been implicated in the stimulation of [[ glucose ]] uptake into skeletal muscle and the inhibition of liver gluconeogenesis.",404,5
405,"AMP-activated protein kinase (<< AMPK >>) activity increases in response to depletion of cellular energy stores, and this enzyme has been implicated in the stimulation of [[ glucose ]] uptake into skeletal muscle and the inhibition of liver gluconeogenesis.",405,5
406,"We recently reported that << AMPK >> is activated by [[ metformin ]] in cultured rat hepatocytes, mediating the inhibitory effects of the drug on hepatic glucose production.",406,9
407,"In the present study, we evaluated whether therapeutic doses of << metformin >> increase [[ AMPK ]] activity in vivo in subjects with type 2 diabetes.",407,9
408,"<< Metformin >> treatment for 10 weeks significantly increased [[ AMPK alpha2 ]] activity in the skeletal muscle, and this was associated with increased phosphorylation of AMPK on Thr172 and decreased acetyl-CoA carboxylase-2 activity.",408,9
409,"<< Metformin >> treatment for 10 weeks significantly increased AMPK alpha2 activity in the skeletal muscle, and this was associated with increased phosphorylation of [[ AMPK ]] on Thr172 and decreased acetyl-CoA carboxylase-2 activity.",409,9
410,"<< Metformin >> treatment for 10 weeks significantly increased AMPK alpha2 activity in the skeletal muscle, and this was associated with increased phosphorylation of AMPK on Thr172 and decreased [[ acetyl-CoA carboxylase-2 ]] activity.",410,0
411,The increase in << AMPK alpha2 >> activity was likely due to a change in muscle energy status because ATP and phosphocreatine concentrations were lower after [[ metformin ]] treatment.,411,9
412,<< Metformin >>-induced increases in [[ AMPK ]] activity were associated with higher rates of glucose disposal and muscle glycogen concentrations.,412,9
413,<< Thalidomide >> prevents alcoholic liver injury in rats through suppression of Kupffer cell sensitization and [[ TNF-alpha ]] production.,413,8
414,<< Thalidomide >> has been shown to suppress [[ TNF-alpha ]] production from macrophages.,414,8
415,"Furthermore, << thalidomide >> abolished the LPS-induced increase in [[ CD14 ]] expression and [Ca2+]i elevation in KCs.",415,8
416,"Moreover, << thalidomide >> reduced the LPS-induced [[ TNF-alpha ]] production by KCs by decreasing TNF-alpha messenger RNA.",416,8
417,"Moreover, << thalidomide >> reduced the LPS-induced TNF-alpha production by KCs by decreasing [[ TNF-alpha ]] messenger RNA.",417,8
418,CONCLUSIONS: These results collectively indicate that << thalidomide >> prevents alcoholic liver injury through suppression of [[ TNF-alpha ]] production and abolishment of KC sensitization.,418,8
419,"During polyamine catabolism, spermine and spermidine are first acetylated by spermidine/spermine N(1)-acetyltransferase (SSAT) and subsequently oxidized by << polyamine oxidase >> (PAO) to produce [[ spermidine ]] and putrescine, respectively.",419,4
420,"During polyamine catabolism, spermine and spermidine are first acetylated by spermidine/spermine N(1)-acetyltransferase (SSAT) and subsequently oxidized by polyamine oxidase (<< PAO >>) to produce [[ spermidine ]] and putrescine, respectively.",420,4
421,"During polyamine catabolism, spermine and spermidine are first acetylated by spermidine/spermine N(1)-acetyltransferase (SSAT) and subsequently oxidized by << polyamine oxidase >> (PAO) to produce spermidine and [[ putrescine ]], respectively.",421,4
422,"During polyamine catabolism, spermine and spermidine are first acetylated by spermidine/spermine N(1)-acetyltransferase (SSAT) and subsequently oxidized by polyamine oxidase (<< PAO >>) to produce spermidine and [[ putrescine ]], respectively.",422,4
423,"During polyamine catabolism, << spermine >> and spermidine are first acetylated by spermidine/spermine N(1)-acetyltransferase ([[ SSAT ]]) and subsequently oxidized by polyamine oxidase (PAO) to produce spermidine and putrescine, respectively.",423,5
424,"During polyamine catabolism, << spermine >> and spermidine are first acetylated by [[ spermidine/spermine N(1)-acetyltransferase ]] (SSAT) and subsequently oxidized by polyamine oxidase (PAO) to produce spermidine and putrescine, respectively.",424,5
425,"During polyamine catabolism, spermine and << spermidine >> are first acetylated by spermidine/spermine N(1)-acetyltransferase ([[ SSAT ]]) and subsequently oxidized by polyamine oxidase (PAO) to produce spermidine and putrescine, respectively.",425,5
426,"During polyamine catabolism, spermine and << spermidine >> are first acetylated by [[ spermidine/spermine N(1)-acetyltransferase ]] (SSAT) and subsequently oxidized by polyamine oxidase (PAO) to produce spermidine and putrescine, respectively.",426,5
427,"During << polyamine >> catabolism, spermine and spermidine are first acetylated by spermidine/spermine N(1)-acetyltransferase ([[ SSAT ]]) and subsequently oxidized by polyamine oxidase (PAO) to produce spermidine and putrescine, respectively.",427,5
428,"During << polyamine >> catabolism, spermine and spermidine are first acetylated by [[ spermidine/spermine N(1)-acetyltransferase ]] (SSAT) and subsequently oxidized by polyamine oxidase (PAO) to produce spermidine and putrescine, respectively.",428,5
429,"In attempting to clone the PAO involved in this back-conversion pathway, we encountered an oxidase that preferentially cleaves << spermine >> in the absence of prior acetylation by [[ SSAT ]].",429,5
430,"Substrate specificity using lysates of oxidase-transfected HEK-293 cells revealed that the newly identified << oxidase >> strongly favoured [[ spermine ]] over N (1)-acetylspermine and that it failed to act on N (1)-acetylspermidine, spermidine or the preferred PAO substrate, N (1), N (12)-diacetylspermine.",430,5
431,"Substrate specificity using lysates of oxidase-transfected HEK-293 cells revealed that the newly identified << oxidase >> strongly favoured spermine over [[ N (1)-acetylspermine ]] and that it failed to act on N (1)-acetylspermidine, spermidine or the preferred PAO substrate, N (1), N (12)-diacetylspermine.",431,5
432,"Substrate specificity using lysates of oxidase-transfected HEK-293 cells revealed that the newly identified oxidase strongly favoured spermine over N (1)-acetylspermine and that it failed to act on N (1)-acetylspermidine, spermidine or the preferred << PAO >> substrate, [[ N (1), N (12)-diacetylspermine ]].",432,5
433,"The << PAO >> inhibitor, [[ MDL-72,527 ]], only partially blocked oxidation of spermine while a previously reported PAO substrate, N (1)-( n -octanesulphonyl)spermine, potently inhibited the reaction.",433,0
434,"The PAO inhibitor, MDL-72,527, only partially blocked oxidation of spermine while a previously reported << PAO >> substrate, [[ N (1)-( n -octanesulphonyl)spermine ]], potently inhibited the reaction.",434,5
435,"Although a significant platelet hyperreactivity was observed in the patients, the HPA-1 genotype did not influence basal or << ADP >>-induced [[ CD62P ]] expression.",435,6
436,In no other subject any activation of platelets by GP IIb/IIIa inhibitors was observed and there were no statistically significant differences between HPA-1 genotypes with respect to the effects of GP IIb/IIIa inhibitors on basal or << ADP >>-stimulated [[ CD62P ]] expression.,436,6
437,"Most halogenated cysteine S-conjugates are metabolized by cysteine S-conjugate << beta-lyases >> to [[ pyruvate ]], ammonia, and an alpha-chloroenethiolate (with DCVC) or an alpha-difluoroalkylthiolate (with TFEC) that may eliminate halide to give a thioacyl halide, which reacts with epsilon-amino groups of lysine residues in proteins.",437,4
438,"Most halogenated cysteine S-conjugates are metabolized by cysteine S-conjugate << beta-lyases >> to pyruvate, [[ ammonia ]], and an alpha-chloroenethiolate (with DCVC) or an alpha-difluoroalkylthiolate (with TFEC) that may eliminate halide to give a thioacyl halide, which reacts with epsilon-amino groups of lysine residues in proteins.",438,4
439,"Most halogenated cysteine S-conjugates are metabolized by cysteine S-conjugate << beta-lyases >> to pyruvate, ammonia, and an [[ alpha-chloroenethiolate ]] (with DCVC) or an alpha-difluoroalkylthiolate (with TFEC) that may eliminate halide to give a thioacyl halide, which reacts with epsilon-amino groups of lysine residues in proteins.",439,4
440,"Most halogenated cysteine S-conjugates are metabolized by cysteine S-conjugate << beta-lyases >> to pyruvate, ammonia, and an alpha-chloroenethiolate (with [[ DCVC ]]) or an alpha-difluoroalkylthiolate (with TFEC) that may eliminate halide to give a thioacyl halide, which reacts with epsilon-amino groups of lysine residues in proteins.",440,4
441,"Most halogenated cysteine S-conjugates are metabolized by cysteine S-conjugate << beta-lyases >> to pyruvate, ammonia, and an alpha-chloroenethiolate (with DCVC) or an [[ alpha-difluoroalkylthiolate ]] (with TFEC) that may eliminate halide to give a thioacyl halide, which reacts with epsilon-amino groups of lysine residues in proteins.",441,4
442,"Most halogenated cysteine S-conjugates are metabolized by cysteine S-conjugate << beta-lyases >> to pyruvate, ammonia, and an alpha-chloroenethiolate (with DCVC) or an alpha-difluoroalkylthiolate (with [[ TFEC ]]) that may eliminate halide to give a thioacyl halide, which reacts with epsilon-amino groups of lysine residues in proteins.",442,4
443,"Most halogenated << cysteine S-conjugates >> are metabolized by cysteine S-conjugate [[ beta-lyases ]] to pyruvate, ammonia, and an alpha-chloroenethiolate (with DCVC) or an alpha-difluoroalkylthiolate (with TFEC) that may eliminate halide to give a thioacyl halide, which reacts with epsilon-amino groups of lysine residues in proteins.",443,5
444,"The juvenile visceral steatosis (jvs) mouse, having a mutation in the << carnitine >> transporter gene [[ Octn2 ]], is a model of primary systemic carnitine deficiency in humans (SCD, OMIM 212140).",444,5
445,"Reuptake of extracellular << noradrenaline >> (NA) into superior cervical ganglion (SCG) neurones is mediated by means of the [[ noradrenaline transporter ]] (NAT, uptake 1).",445,5
446,"Reuptake of extracellular << noradrenaline >> (NA) into superior cervical ganglion (SCG) neurones is mediated by means of the noradrenaline transporter ([[ NAT ]], uptake 1).",446,5
447,"Reuptake of extracellular noradrenaline (<< NA >>) into superior cervical ganglion (SCG) neurones is mediated by means of the [[ noradrenaline transporter ]] (NAT, uptake 1).",447,5
448,"Reuptake of extracellular noradrenaline (<< NA >>) into superior cervical ganglion (SCG) neurones is mediated by means of the noradrenaline transporter ([[ NAT ]], uptake 1).",448,5
449,"The ensuing radioactive outflow from these cultures was enhanced by desipramine and reserpine, but reduced (in the presence of desipramine) by the << OCT3 >> inhibitors cyanine 863, [[ oestradiol ]] and corticosterone.",449,0
450,"The ensuing radioactive outflow from these cultures was enhanced by desipramine and reserpine, but reduced (in the presence of desipramine) by the << OCT3 >> inhibitors cyanine 863, oestradiol and [[ corticosterone ]].",450,0
451,"The outflow of << [3H]-MPP+ >> was significantly enhanced by MPP+, guanidine, choline and amantadine as potential substrates for [[ OCT ]]-related transmembrane transporters.",451,5
452,"The outflow of << [3H]-MPP+ >> was significantly enhanced by MPP+, guanidine, choline and amantadine as potential substrates for OCT-related [[ transmembrane transporters ]].",452,5
453,"The outflow of [3H]-MPP+ was significantly enhanced by << MPP+ >>, guanidine, choline and amantadine as potential substrates for [[ OCT ]]-related transmembrane transporters.",453,5
454,"The outflow of [3H]-MPP+ was significantly enhanced by << MPP+ >>, guanidine, choline and amantadine as potential substrates for OCT-related [[ transmembrane transporters ]].",454,5
455,"The outflow of [3H]-MPP+ was significantly enhanced by MPP+, << guanidine >>, choline and amantadine as potential substrates for [[ OCT ]]-related transmembrane transporters.",455,5
456,"The outflow of [3H]-MPP+ was significantly enhanced by MPP+, << guanidine >>, choline and amantadine as potential substrates for OCT-related [[ transmembrane transporters ]].",456,5
457,"The outflow of [3H]-MPP+ was significantly enhanced by MPP+, guanidine, << choline >> and amantadine as potential substrates for [[ OCT ]]-related transmembrane transporters.",457,5
458,"The outflow of [3H]-MPP+ was significantly enhanced by MPP+, guanidine, << choline >> and amantadine as potential substrates for OCT-related [[ transmembrane transporters ]].",458,5
459,"The outflow of [3H]-MPP+ was significantly enhanced by MPP+, guanidine, choline and << amantadine >> as potential substrates for [[ OCT ]]-related transmembrane transporters.",459,5
460,"The outflow of [3H]-MPP+ was significantly enhanced by MPP+, guanidine, choline and << amantadine >> as potential substrates for OCT-related [[ transmembrane transporters ]].",460,5
461,"However, desipramine at a low concentration essentially blocked the radioactive outflow induced by all of these substances with the exception of << MPP+ >>, indicating the [[ NAT ]] and not an OCT as their primary site of action.",461,5
462,Our observations indicate an << OCT >>-mediated transmembrane transport of [[ [3H]-MPP+ ]].,462,5
463,"Amongst the three << OCTs >> expressed in the SCG, OCT3 best fits the profile of substrates and antagonists that cause trans-stimulation and trans-inhibition, respectively, of [[ [3H]-MPP+ ]] release.",463,5
464,"Amongst the three OCTs expressed in the SCG, << OCT3 >> best fits the profile of substrates and antagonists that cause trans-stimulation and trans-inhibition, respectively, of [[ [3H]-MPP+ ]] release.",464,5
465,"An inhibitor of << type B monoamine oxidase >> (MAO-B), [[ (-)deprenyl ]] (selegiline), was reported to have neuroprotective activity, but clinical trials failed to confirm it.",465,0
466,"An inhibitor of type B monoamine oxidase (<< MAO-B >>), [[ (-)deprenyl ]] (selegiline), was reported to have neuroprotective activity, but clinical trials failed to confirm it.",466,0
467,"An inhibitor of << type B monoamine oxidase >> (MAO-B), (-)deprenyl ([[ selegiline ]]), was reported to have neuroprotective activity, but clinical trials failed to confirm it.",467,0
468,"An inhibitor of type B monoamine oxidase (<< MAO-B >>), (-)deprenyl ([[ selegiline ]]), was reported to have neuroprotective activity, but clinical trials failed to confirm it.",468,0
469,"<< Rasagiline >> prevented the PT in mitochondria directly and also indirectly through induction of antiapoptotic [[ Bcl-2 ]] and a neurotrophic factor, glial cell line-derived neurotrophic factor (GDNF).",469,6
470,"<< Rasagiline >> prevented the PT in mitochondria directly and also indirectly through induction of antiapoptotic Bcl-2 and a [[ neurotrophic factor ]], glial cell line-derived neurotrophic factor (GDNF).",470,6
471,"<< Rasagiline >> prevented the PT in mitochondria directly and also indirectly through induction of antiapoptotic Bcl-2 and a neurotrophic factor, [[ glial cell line-derived neurotrophic factor ]] (GDNF).",471,6
472,"<< Rasagiline >> prevented the PT in mitochondria directly and also indirectly through induction of antiapoptotic Bcl-2 and a neurotrophic factor, glial cell line-derived neurotrophic factor ([[ GDNF ]]).",472,6
473,Long-term administration of << propargylamines >> to rats increased the activities of antioxidative enzymes [[ superoxide dismutase ]] (SOD) and catalase in the brain regions containing dopamine neurons.,473,9
474,Long-term administration of << propargylamines >> to rats increased the activities of antioxidative enzymes superoxide dismutase ([[ SOD ]]) and catalase in the brain regions containing dopamine neurons.,474,9
475,Long-term administration of << propargylamines >> to rats increased the activities of antioxidative enzymes superoxide dismutase (SOD) and [[ catalase ]] in the brain regions containing dopamine neurons.,475,9
476,"Practical asymmetric synthesis of << aprepitant >>, a potent human [[ NK-1 receptor ]] antagonist, via a stereoselective Lewis acid-catalyzed trans acetalization reaction.",476,1
477,"A streamlined and high-yielding synthesis of << aprepitant >> (1), a potent [[ substance P (SP) receptor ]] antagonist, is described.",477,1
478,Pentosan polysulfate << sodium >> (PPS) has been shown to exert antitumor activity by antagonizing the binding of [[ bFGF ]] to cell surface receptors.,478,1
479,These findings suggest that << RhBG >> and RhCG may play important and cell-specific roles in [[ ammonium ]] transport and signaling in these regions of the kidney.,479,5
480,These findings suggest that RhBG and << RhCG >> may play important and cell-specific roles in [[ ammonium ]] transport and signaling in these regions of the kidney.,480,5
481,"<< PDE5 >> is the predominant PDE in the corpus cavernosum, and [[ cGMP ]] is its primary substrate.",481,5
482,"PDE5 is the predominant << PDE >> in the corpus cavernosum, and [[ cGMP ]] is its primary substrate.",482,5
483,"Therefore, in men with ED, elevation of cGMP in corpus cavernosal tissue via selective inhibition of << cGMP >>-specific [[ PDE5 ]] is a means of improving erectile function at minimal risk of adverse events.",483,0
484,"This approach is validated by the clinical efficacy and safety of << sildenafil >>, the pioneering drug for selective [[ PDE5 ]] inhibitor therapy for ED.",484,0
485,"<< Sildenafil >> exhibits inhibitory potency against PDE5 and a 10-fold lower dose-related inhibitory potency against rod outer segment PDE6, the predominant [[ PDE ]] in the phototransduction cascade in rods.",485,0
486,"<< Sildenafil >> exhibits inhibitory potency against [[ PDE5 ]] and a 10-fold lower dose-related inhibitory potency against rod outer segment PDE6, the predominant PDE in the phototransduction cascade in rods.",486,0
487,"<< Sildenafil >> exhibits inhibitory potency against PDE5 and a 10-fold lower dose-related inhibitory potency against rod outer segment [[ PDE6 ]], the predominant PDE in the phototransduction cascade in rods.",487,0
488,"As free << sildenafil >> plasma concentrations approach concentrations sufficient to inhibit retinal [[ PDE6 ]], usually at higher therapeutic doses, transient, reversible visual adverse events can occur, albeit infrequently.",488,0
489,"Selective inhibition of << PDE5 >> is a rational therapeutic approach in ED, as proved by the clinical success of [[ sildenafil ]].",489,0
490,"However, when coapplied with 10 micro m GABA, << ivermectin >> potentiated the GABA-evoked current of the [[ GAB-1 ]]/HG1A receptor, but attenuated the GABA response of the GAB-1/HG1E receptor.",490,7
491,"However, when coapplied with 10 micro m GABA, << ivermectin >> potentiated the GABA-evoked current of the GAB-1/[[ HG1A ]] receptor, but attenuated the GABA response of the GAB-1/HG1E receptor.",491,7
492,"However, when coapplied with 10 micro m GABA, << ivermectin >> potentiated the GABA-evoked current of the GAB-1/HG1A receptor, but attenuated the GABA response of the [[ GAB-1 ]]/HG1E receptor.",492,3
493,"However, when coapplied with 10 micro m GABA, << ivermectin >> potentiated the GABA-evoked current of the GAB-1/HG1A receptor, but attenuated the GABA response of the GAB-1/[[ HG1E ]] receptor.",493,3
494,<< Yohimbine >> is a potent and selective [[ alpha2- versus alpha1-adrenoceptor ]] antagonist.,494,1
495,"Plasmacytoid dendritic cells produce cytokines and mature in response to the << TLR7 >> agonists, imiquimod and [[ resiquimod ]].",495,2
496,"Plasmacytoid dendritic cells produce cytokines and mature in response to the << TLR7 >> agonists, [[ imiquimod ]] and resiquimod.",496,2
497,"The immune response modifiers, << imiquimod >> and resiquimod, are TLR7 agonists that induce [[ type I interferon ]] in numerous species, including humans.",497,6
498,"The immune response modifiers, imiquimod and << resiquimod >>, are TLR7 agonists that induce [[ type I interferon ]] in numerous species, including humans.",498,6
499,"The immune response modifiers, << imiquimod >> and resiquimod, are [[ TLR7 ]] agonists that induce type I interferon in numerous species, including humans.",499,2
500,"The immune response modifiers, imiquimod and << resiquimod >>, are [[ TLR7 ]] agonists that induce type I interferon in numerous species, including humans.",500,2
501,"Here, we characterize the activation of human pDC with the << TLR7 >> agonists [[ imiquimod ]] and resiquimod.",501,2
502,"Here, we characterize the activation of human pDC with the << TLR7 >> agonists imiquimod and [[ resiquimod ]].",502,2
503,"Results indicate that << imiquimod >> and resiquimod induce [[ IFN-alpha ]] and IFN-omega from purified pDC, and pDC are the principle IFN-producing cells in the blood.",503,6
504,"Results indicate that << imiquimod >> and resiquimod induce IFN-alpha and [[ IFN-omega ]] from purified pDC, and pDC are the principle IFN-producing cells in the blood.",504,6
505,<< Resiquimod >>-stimulated pDC also produce a number of other [[ cytokines ]] including TNF-alpha and IP-10.,505,6
506,<< Resiquimod >>-stimulated pDC also produce a number of other cytokines including [[ TNF-alpha ]] and IP-10.,506,6
507,<< Resiquimod >>-stimulated pDC also produce a number of other cytokines including TNF-alpha and [[ IP-10 ]].,507,6
508,"<< Resiquimod >> enhances co-stimulatory marker expression, [[ CCR7 ]] expression, and pDC viability.",508,6
509,"These results demonstrate that << imidazoquinoline >> molecules directly induce pDC maturation as determined by [[ cytokine ]] induction, CCR7 and co-stimulatory marker expression and prolonging viability.",509,6
510,Induction of << heat shock proteins >> (HSPs) by [[ sodium arsenite ]] in cultured astrocytes and reduction of hydrogen peroxide-induced cell death.,510,7
511,Induction of heat shock proteins (<< HSPs >>) by [[ sodium arsenite ]] in cultured astrocytes and reduction of hydrogen peroxide-induced cell death.,511,7
512,"<< Arsenite >> triggered strong induction of [[ HSPs ]], which was prevented by 1 micro g/mL cycloheximide (CXH).",512,7
513,"Arsenite triggered strong induction of << HSPs >>, which was prevented by 1 micro g/mL [[ cycloheximide ]] (CXH).",513,3
514,"Arsenite triggered strong induction of << HSPs >>, which was prevented by 1 micro g/mL cycloheximide ([[ CXH ]]).",514,3
515,"<< H2O2 >> caused cell loss and increased cell death with features of apoptosis, i.e. TdT-mediated dUTP nick-end labelling (TUNEL) reaction and [[ caspase-3 ]] activation.",515,9
516,Pre-treatment with arsenite increased << protein kinase B >> (Akt) and extracellular signal regulated kinase 1/2 (ERK1/2) phosphorylation after [[ H2O2 ]].,516,9
517,Pre-treatment with arsenite increased protein kinase B (<< Akt >>) and extracellular signal regulated kinase 1/2 (ERK1/2) phosphorylation after [[ H2O2 ]].,517,9
518,"However, while << Akt >> phosphorylation was prevented by CHX, Erk1/2 phosphorylation was further enhanced by [[ CHX ]].",518,0
519,"The results show that transient << arsenite >> pre-treatment induces Hsp72, HO-1 and, to a lesser extent, Hsp27; it reduces H2O2-induced astrocyte death; and it causes selective activation of [[ Akt ]] following H2O2.",519,9
520,"The results show that transient arsenite pre-treatment induces Hsp72, HO-1 and, to a lesser extent, Hsp27; it reduces H2O2-induced astrocyte death; and it causes selective activation of << Akt >> following [[ H2O2 ]].",520,9
521,"The results show that transient << arsenite >> pre-treatment induces [[ Hsp72 ]], HO-1 and, to a lesser extent, Hsp27; it reduces H2O2-induced astrocyte death; and it causes selective activation of Akt following H2O2.",521,7
522,"The results show that transient << arsenite >> pre-treatment induces Hsp72, [[ HO-1 ]] and, to a lesser extent, Hsp27; it reduces H2O2-induced astrocyte death; and it causes selective activation of Akt following H2O2.",522,7
523,"The results show that transient << arsenite >> pre-treatment induces Hsp72, HO-1 and, to a lesser extent, [[ Hsp27 ]]; it reduces H2O2-induced astrocyte death; and it causes selective activation of Akt following H2O2.",523,7
524,Investigation of bradykinin metabolism in human and rat plasma in the presence of the dual << ACE >>/NEP inhibitors [[ GW660511X ]] and omapatrilat.,524,0
525,Investigation of bradykinin metabolism in human and rat plasma in the presence of the dual ACE/<< NEP >> inhibitors [[ GW660511X ]] and omapatrilat.,525,0
526,Investigation of bradykinin metabolism in human and rat plasma in the presence of the dual << ACE >>/NEP inhibitors GW660511X and [[ omapatrilat ]].,526,0
527,Investigation of bradykinin metabolism in human and rat plasma in the presence of the dual ACE/<< NEP >> inhibitors GW660511X and [[ omapatrilat ]].,527,0
528,In this work a novel approach combining HPLC-UV on-line with oaTOF-MS and ICPMS was applied to investigate in human and rat plasma the metabolism of labelled BK (79/81 Br-Phe5) BrBK in the presence of two new dual << ACE >>/NEP inhibitors ([[ GW660511X ]] and omapatrilat) currently under clinical trial.,528,0
529,In this work a novel approach combining HPLC-UV on-line with oaTOF-MS and ICPMS was applied to investigate in human and rat plasma the metabolism of labelled BK (79/81 Br-Phe5) BrBK in the presence of two new dual ACE/<< NEP >> inhibitors ([[ GW660511X ]] and omapatrilat) currently under clinical trial.,529,0
530,In this work a novel approach combining HPLC-UV on-line with oaTOF-MS and ICPMS was applied to investigate in human and rat plasma the metabolism of labelled BK (79/81 Br-Phe5) BrBK in the presence of two new dual << ACE >>/NEP inhibitors (GW660511X and [[ omapatrilat ]]) currently under clinical trial.,530,0
531,In this work a novel approach combining HPLC-UV on-line with oaTOF-MS and ICPMS was applied to investigate in human and rat plasma the metabolism of labelled BK (79/81 Br-Phe5) BrBK in the presence of two new dual ACE/<< NEP >> inhibitors (GW660511X and [[ omapatrilat ]]) currently under clinical trial.,531,0
532,"Unlike GW660511X, << omapatrilat >> abolished the production of [[ BrBK1-5 ]] and BrBK1-7, suggesting a better ACE inhibition effect over GW660511X as no NEP activity was found.",532,8
533,"Unlike GW660511X, << omapatrilat >> abolished the production of BrBK1-5 and [[ BrBK1-7 ]], suggesting a better ACE inhibition effect over GW660511X as no NEP activity was found.",533,8
534,"Unlike GW660511X, << omapatrilat >> abolished the production of BrBK1-5 and BrBK1-7, suggesting a better [[ ACE ]] inhibition effect over GW660511X as no NEP activity was found.",534,0
535,"Unlike GW660511X, omapatrilat abolished the production of BrBK1-5 and BrBK1-7, suggesting a better << ACE >> inhibition effect over [[ GW660511X ]] as no NEP activity was found.",535,0
536,In addition the production of << BrBK1-8 >> was enhanced in the presence of these inhibitors with a greater accumulation being observed with [[ omapatrilat ]].,536,6
537,The production of << Br-Phe5 >> was reduced with [[ GW660511X ]] while no significant change was observed with omapatrilat after 4 h of incubation.,537,8
538,<< GW660511X >> and omapatrilat reduced the production of [[ BrBK1-5 ]] and BrBK1-7 with more effect being observed with omapatrilat.,538,8
539,<< GW660511X >> and omapatrilat reduced the production of BrBK1-5 and [[ BrBK1-7 ]] with more effect being observed with omapatrilat.,539,8
540,GW660511X and << omapatrilat >> reduced the production of [[ BrBK1-5 ]] and BrBK1-7 with more effect being observed with omapatrilat.,540,8
541,GW660511X and << omapatrilat >> reduced the production of BrBK1-5 and [[ BrBK1-7 ]] with more effect being observed with omapatrilat.,541,8
542,GW660511X and omapatrilat reduced the production of << BrBK1-5 >> and BrBK1-7 with more effect being observed with [[ omapatrilat ]].,542,8
543,GW660511X and omapatrilat reduced the production of BrBK1-5 and << BrBK1-7 >> with more effect being observed with [[ omapatrilat ]].,543,8
544,<< GW660511X >> and omapatrilat increased the production of both [[ BrBK1-8 ]] and Br-Phe5 but not that of BrBK4-8 and BrBK2-8.,544,6
545,<< GW660511X >> and omapatrilat increased the production of both BrBK1-8 and [[ Br-Phe5 ]] but not that of BrBK4-8 and BrBK2-8.,545,6
546,GW660511X and << omapatrilat >> increased the production of both [[ BrBK1-8 ]] and Br-Phe5 but not that of BrBK4-8 and BrBK2-8.,546,6
547,GW660511X and << omapatrilat >> increased the production of both BrBK1-8 and [[ Br-Phe5 ]] but not that of BrBK4-8 and BrBK2-8.,547,6
548,"This study shows that the potency of << GW660511X >> in comparison with omapatrilat is more than 100-fold lower in human, but less than 10-fold lower in rat plasma, suggesting that rat may not be a suitable in vivo model for the evaluation of [[ ACE ]]/NEP inhibition in relation to effects in humans.",548,0
549,"This study shows that the potency of << GW660511X >> in comparison with omapatrilat is more than 100-fold lower in human, but less than 10-fold lower in rat plasma, suggesting that rat may not be a suitable in vivo model for the evaluation of ACE/[[ NEP ]] inhibition in relation to effects in humans.",549,0
550,"This study shows that the potency of GW660511X in comparison with << omapatrilat >> is more than 100-fold lower in human, but less than 10-fold lower in rat plasma, suggesting that rat may not be a suitable in vivo model for the evaluation of ACE/[[ NEP ]] inhibition in relation to effects in humans.",550,0
551,"Acetylcholinesterase (<< AChE >>) predominates in the healthy brain, with butyrylcholinesterase (BuChE) considered to play a minor role in regulating brain [[ acetylcholine ]] (ACh) levels.",551,5
552,"Acetylcholinesterase (AChE) predominates in the healthy brain, with << butyrylcholinesterase >> (BuChE) considered to play a minor role in regulating brain [[ acetylcholine ]] (ACh) levels.",552,5
553,"Acetylcholinesterase (AChE) predominates in the healthy brain, with butyrylcholinesterase (<< BuChE >>) considered to play a minor role in regulating brain [[ acetylcholine ]] (ACh) levels.",553,5
554,"<< Acetylcholinesterase >> (AChE) predominates in the healthy brain, with butyrylcholinesterase (BuChE) considered to play a minor role in regulating brain [[ acetylcholine ]] (ACh) levels.",554,5
555,"Acetylcholinesterase (<< AChE >>) predominates in the healthy brain, with butyrylcholinesterase (BuChE) considered to play a minor role in regulating brain acetylcholine ([[ ACh ]]) levels.",555,5
556,"Acetylcholinesterase (AChE) predominates in the healthy brain, with << butyrylcholinesterase >> (BuChE) considered to play a minor role in regulating brain acetylcholine ([[ ACh ]]) levels.",556,5
557,"Acetylcholinesterase (AChE) predominates in the healthy brain, with butyrylcholinesterase (<< BuChE >>) considered to play a minor role in regulating brain acetylcholine ([[ ACh ]]) levels.",557,5
558,"<< Acetylcholinesterase >> (AChE) predominates in the healthy brain, with butyrylcholinesterase (BuChE) considered to play a minor role in regulating brain acetylcholine ([[ ACh ]]) levels.",558,5
559,"Experimental evidence from the use of agents with enhanced selectivity for BuChE (cymserine analogues, MF-8622) and the dual inhibitor of both << AChE >> and BuChE, [[ rivastigmine ]], indicates potential therapeutic benefits of inhibiting both AChE and BuChE in AD and related dementias.",559,0
560,"Experimental evidence from the use of agents with enhanced selectivity for BuChE (cymserine analogues, MF-8622) and the dual inhibitor of both AChE and << BuChE >>, [[ rivastigmine ]], indicates potential therapeutic benefits of inhibiting both AChE and BuChE in AD and related dementias.",560,0
561,"Experimental evidence from the use of agents with enhanced selectivity for BuChE (cymserine analogues, MF-8622) and the dual inhibitor of both AChE and BuChE, << rivastigmine >>, indicates potential therapeutic benefits of inhibiting both [[ AChE ]] and BuChE in AD and related dementias.",561,0
562,"Experimental evidence from the use of agents with enhanced selectivity for BuChE (cymserine analogues, MF-8622) and the dual inhibitor of both AChE and BuChE, << rivastigmine >>, indicates potential therapeutic benefits of inhibiting both AChE and [[ BuChE ]] in AD and related dementias.",562,0
563,The development of specific << BuChE >> inhibitors and further experience with the dual enzyme inhibitor [[ rivastigmine ]] will improve understanding of the aetiology of AD and should lead to a wider variety of potent treatment options.,563,0
564,"Agents which have recently been shown to block << cyclin D1 >> translation by regulating calcium levels are the [[ unsaturated essential fatty acid ]], eicosapentaenoic acid (EPA), the antidiabetic thiazolidinediones, and the antifungal agent, clotrimazole.",564,8
565,"Agents which have recently been shown to block << cyclin D1 >> translation by regulating calcium levels are the unsaturated essential fatty acid, [[ eicosapentaenoic acid ]] (EPA), the antidiabetic thiazolidinediones, and the antifungal agent, clotrimazole.",565,8
566,"Agents which have recently been shown to block << cyclin D1 >> translation by regulating calcium levels are the unsaturated essential fatty acid, eicosapentaenoic acid ([[ EPA ]]), the antidiabetic thiazolidinediones, and the antifungal agent, clotrimazole.",566,8
567,"Agents which have recently been shown to block << cyclin D1 >> translation by regulating calcium levels are the unsaturated essential fatty acid, eicosapentaenoic acid (EPA), the antidiabetic [[ thiazolidinediones ]], and the antifungal agent, clotrimazole.",567,8
568,"Agents which have recently been shown to block << cyclin D1 >> translation by regulating calcium levels are the unsaturated essential fatty acid, eicosapentaenoic acid (EPA), the antidiabetic thiazolidinediones, and the antifungal agent, [[ clotrimazole ]].",568,8
569,<< Angiotensin AT1 receptor >> antagonist [[ losartan ]] and the defence reaction in the anaesthetised rat.,569,1
570,We investigated the effect of << AT1 receptor >> blockade in the NTS on the response to stimulation of HDA in anaesthetised rats treated with the neuromuscular blocking agent [[ pancuronium bromide ]].,570,0
571,Blockade of << LTC4 >> synthesis caused by additive inhibition of [[ gIV-PLA2 ]] phosphorylation: Effect of salmeterol and PDE4 inhibition in human eosinophils.,571,4
572,"OBJECTIVE: To determine (a) whether << PDE4 >> inhibition alone with [[ rolipram ]] blocked secretions of arachidonic acid (AA) and leukotriene C(4) (LTC(4)) caused by activation of eosinophils with formyl-met-leu-phe plus cytochalasin B (FMLP/B), (b) to determine if PDE4 inhibition plus beta(2)-adrenoceptor agonist act additively to augment endogenous cAMP concentration, and (c) to determine the mechanism by which additive inhibition of AA and LTC(4) synthesis is regulated by cAMP.",572,0
573,RESULTS: Rolipram unmasked the inhibitory effect of << beta(2)-adrenoceptor >> stimulation with [[ salmeterol ]] and significantly attenuated the stimulated release of AA and subsequent LTC(4).,573,9
574,Inhibition corresponded to increased cAMP production caused by rolipram alone or << rolipram >> plus salmeterol and blocked proportionately the phosphorylation and activation of [[ gIV-PLA(2) ]] in FMLP/B-activated eosinophils.,574,0
575,Inhibition corresponded to increased cAMP production caused by rolipram alone or rolipram plus << salmeterol >> and blocked proportionately the phosphorylation and activation of [[ gIV-PLA(2) ]] in FMLP/B-activated eosinophils.,575,0
576,CONCLUSIONS: Inhibition of << PDE4 >> by [[ rolipram ]] unmasks beta(2)-adrenergic blockade of LTC(4) synthesis caused by FMLP/B.,576,0
577,Anabolic effects of << clenbuterol >> on skeletal muscle are mediated by [[ beta 2-adrenoceptor ]] activation.,577,9
578,The potent anabolic effects of the << beta 2-adrenoceptor >> agonist [[ clenbuterol ]] on skeletal muscle have been reported to be independent of actions on beta-adrenoceptors.,578,2
579,"These effects were not mimicked by oral administration of the << beta 2-adrenoceptor >> agonist [[ salbutamol ]] even at high dose (52 mg/kg diet), and the effects of clenbuterol were not inhibited by addition of DL-propranolol (200 mg/kg diet).",579,2
580,"These effects were not mimicked by oral administration of the << beta 2-adrenoceptor >> agonist salbutamol even at high dose (52 mg/kg diet), and the effects of [[ clenbuterol ]] were not inhibited by addition of DL-propranolol (200 mg/kg diet).",580,2
581,"In the hot-plate test in mice, the antinociceptive action of the << alpha 2-adrenoceptor >> agonist, [[ UK 14,304 ]], was abolished by the alpha 2-adrenoceptor antagonist, idazoxan, the potent alpha 2A-adrenoceptor antagonist, RX 821002 and the preferential alpha 2A-adrenoceptor antagonist, BRL 44408.",581,2
582,"In the hot-plate test in mice, the antinociceptive action of the alpha 2-adrenoceptor agonist, UK 14,304, was abolished by the << alpha 2-adrenoceptor >> antagonist, [[ idazoxan ]], the potent alpha 2A-adrenoceptor antagonist, RX 821002 and the preferential alpha 2A-adrenoceptor antagonist, BRL 44408.",582,1
583,"In the hot-plate test in mice, the antinociceptive action of the alpha 2-adrenoceptor agonist, UK 14,304, was abolished by the alpha 2-adrenoceptor antagonist, idazoxan, the potent << alpha 2A-adrenoceptor >> antagonist, [[ RX 821002 ]] and the preferential alpha 2A-adrenoceptor antagonist, BRL 44408.",583,1
584,"In the hot-plate test in mice, the antinociceptive action of the alpha 2-adrenoceptor agonist, UK 14,304, was abolished by the alpha 2-adrenoceptor antagonist, idazoxan, the potent alpha 2A-adrenoceptor antagonist, RX 821002 and the preferential << alpha 2A-adrenoceptor >> antagonist, [[ BRL 44408 ]].",584,1
585,"The preferential << alpha 2A-adrenoceptor >> partial agonist, [[ guanfacine ]], partially inhibited UK 14,304-induced antinociception.",585,2
586,"The preferential << alpha 2A-adrenoceptor >> partial agonist, guanfacine, partially inhibited [[ UK 14,304 ]]-induced antinociception.",586,2
587,"<< SDH >> (L-serine dehydratase, EC 4.3.1.17) catalyzes the pyridoxal 5'-phosphate (PLP)-dependent dehydration of L-serine to yield [[ pyruvate ]] and ammonia.",587,4
588,"SDH (L-serine dehydratase, << EC 4.3.1.17 >>) catalyzes the pyridoxal 5'-phosphate (PLP)-dependent dehydration of L-serine to yield [[ pyruvate ]] and ammonia.",588,4
589,"SDH << (L-serine dehydratase >>, EC 4.3.1.17) catalyzes the pyridoxal 5'-phosphate (PLP)-dependent dehydration of L-serine to yield [[ pyruvate ]] and ammonia.",589,4
590,"<< SDH >> (L-serine dehydratase, EC 4.3.1.17) catalyzes the pyridoxal 5'-phosphate (PLP)-dependent dehydration of L-serine to yield pyruvate and [[ ammonia ]].",590,4
591,"SDH (L-serine dehydratase, << EC 4.3.1.17 >>) catalyzes the pyridoxal 5'-phosphate (PLP)-dependent dehydration of L-serine to yield pyruvate and [[ ammonia ]].",591,4
592,"SDH << (L-serine dehydratase >>, EC 4.3.1.17) catalyzes the pyridoxal 5'-phosphate (PLP)-dependent dehydration of L-serine to yield pyruvate and [[ ammonia ]].",592,4
593,"<< SDH >> (L-serine dehydratase, EC 4.3.1.17) catalyzes the pyridoxal 5'-phosphate (PLP)-dependent dehydration of [[ L-serine ]] to yield pyruvate and ammonia.",593,5
594,"SDH (L-serine dehydratase, << EC 4.3.1.17 >>) catalyzes the pyridoxal 5'-phosphate (PLP)-dependent dehydration of [[ L-serine ]] to yield pyruvate and ammonia.",594,5
595,"SDH << (L-serine dehydratase >>, EC 4.3.1.17) catalyzes the pyridoxal 5'-phosphate (PLP)-dependent dehydration of [[ L-serine ]] to yield pyruvate and ammonia.",595,5
596,"Formation of << pyruvate >> by [[ SDH ]] is a two-step reaction in which the hydroxyl group of serine is cleaved to produce aminoacrylate, and then the aminoacrylate is deaminated by nonenzymatic hydrolysis to produce pyruvate.",596,4
597,"Formation of pyruvate by << SDH >> is a two-step reaction in which the hydroxyl group of serine is cleaved to produce aminoacrylate, and then the aminoacrylate is deaminated by nonenzymatic hydrolysis to produce [[ pyruvate ]].",597,4
598,"Formation of pyruvate by << SDH >> is a two-step reaction in which the hydroxyl group of serine is cleaved to produce [[ aminoacrylate ]], and then the aminoacrylate is deaminated by nonenzymatic hydrolysis to produce pyruvate.",598,5
599,Blocking EGFR signaling with the EGFR/HER-2 kinase inhibitor (KI) << GW572016 >> decreased the postradiation survival of irradiated [[ Ras ]]-transformed cells and normal cells but had no effect on the survival of unirradiated cells.,599,8
600,Blocking << EGFR >> signaling with the EGFR/HER-2 kinase inhibitor (KI) [[ GW572016 ]] decreased the postradiation survival of irradiated Ras-transformed cells and normal cells but had no effect on the survival of unirradiated cells.,600,8
601,Blocking EGFR signaling with the << EGFR >>/HER-2 kinase inhibitor (KI) [[ GW572016 ]] decreased the postradiation survival of irradiated Ras-transformed cells and normal cells but had no effect on the survival of unirradiated cells.,601,0
602,Blocking EGFR signaling with the EGFR/<< HER-2 >> kinase inhibitor (KI) [[ GW572016 ]] decreased the postradiation survival of irradiated Ras-transformed cells and normal cells but had no effect on the survival of unirradiated cells.,602,0
603,"Ras-CM and TGF-alpha also increase << PI3-K >> activity downstream of the EGFR and increase postradiation survival, both of which are abrogated by [[ GW572016 ]].",603,0
604,"Ras-CM and TGF-alpha also increase PI3-K activity downstream of the << EGFR >> and increase postradiation survival, both of which are abrogated by [[ GW572016 ]].",604,0
605,"Thus, << Ras >> utilizes autocrine signaling through EGFR to increase radioresistance, and the EGFR KI [[ GW572016 ]] acts as a radiosensitizer.",605,8
606,"Thus, Ras utilizes autocrine signaling through EGFR to increase radioresistance, and the << EGFR >> KI [[ GW572016 ]] acts as a radiosensitizer.",606,0
607,The observation that << Ras >>-transformed cells can be sensitized to killing by ionizing radiation with [[ GW572016 ]] demonstrates that EGFR KIs could potentially be used to radiosensitize tumors in which radioresistance is dependent on Ras-driven autocrine signaling through EGFR.,607,8
608,The observation that Ras-transformed cells can be sensitized to killing by ionizing radiation with << GW572016 >> demonstrates that [[ EGFR ]] KIs could potentially be used to radiosensitize tumors in which radioresistance is dependent on Ras-driven autocrine signaling through EGFR.,608,0
609,"(-)-Isoprenaline and a nonconventional << beta(3)-adrenoceptor >> agonist, [[ (+/-)-[4-[3-[(1,1-dimethylethyl)amino]-2-hydroxypropoxy]-1,3-dihydro-2H-benzimida zol-2-one] hydrochloride ]] ((+/-)-CGP12177A), induced concentration-dependent relaxation of (-)-phenylephrine (0.3 microM) preconstricted spiral preparations.",609,2
610,"(-)-Isoprenaline and a nonconventional << beta(3)-adrenoceptor >> agonist, (+/-)-[4-[3-[(1,1-dimethylethyl)amino]-2-hydroxypropoxy]-1,3-dihydro-2H-benzimida zol-2-one] hydrochloride ([[ (+/-)-CGP12177A ]]), induced concentration-dependent relaxation of (-)-phenylephrine (0.3 microM) preconstricted spiral preparations.",610,2
611,"Pretreatment with a combination of << (+/-)-2-hydroxy-5-[2-[[2-hydroxy-3-[4-[1-methyl-4-(trifluoromethyl)-1H-imidazol-2 -yl]phenoxy]propyl]amino]ethoxy]-benzamide methanesulfonate >> (CGP20712A, a selective [[ beta(1)-adrenoceptor ]] antagonist) and (+/-)-1-[2,3-(dihydro-7-methyl-1H-inden-4-yl)oxy]-3-[(1-methylethyl)amino]-2-buta nol hydrochloride (ICI-118,5511, a selective beta(2)-adrenoceptor antagonist) (0.1 microM for each) produced a 14-fold rightward shift of the concentration-response curve for (-)-isoprenaline; however, the relaxation in response to (+/-)-CGP12177A was unaffected by the blockade of beta(1)- and beta(2)-adrenoceptors.",611,1
612,"Pretreatment with a combination of (+/-)-2-hydroxy-5-[2-[[2-hydroxy-3-[4-[1-methyl-4-(trifluoromethyl)-1H-imidazol-2 -yl]phenoxy]propyl]amino]ethoxy]-benzamide methanesulfonate (<< CGP20712A >>, a selective [[ beta(1)-adrenoceptor ]] antagonist) and (+/-)-1-[2,3-(dihydro-7-methyl-1H-inden-4-yl)oxy]-3-[(1-methylethyl)amino]-2-buta nol hydrochloride (ICI-118,5511, a selective beta(2)-adrenoceptor antagonist) (0.1 microM for each) produced a 14-fold rightward shift of the concentration-response curve for (-)-isoprenaline; however, the relaxation in response to (+/-)-CGP12177A was unaffected by the blockade of beta(1)- and beta(2)-adrenoceptors.",612,1
613,"Pretreatment with a combination of (+/-)-2-hydroxy-5-[2-[[2-hydroxy-3-[4-[1-methyl-4-(trifluoromethyl)-1H-imidazol-2 -yl]phenoxy]propyl]amino]ethoxy]-benzamide methanesulfonate (CGP20712A, a selective beta(1)-adrenoceptor antagonist) and << (+/-)-1-[2,3-(dihydro-7-methyl-1H-inden-4-yl)oxy]-3-[(1-methylethyl)amino]-2-buta nol hydrochloride >> (ICI-118,5511, a selective [[ beta(2)-adrenoceptor ]] antagonist) (0.1 microM for each) produced a 14-fold rightward shift of the concentration-response curve for (-)-isoprenaline; however, the relaxation in response to (+/-)-CGP12177A was unaffected by the blockade of beta(1)- and beta(2)-adrenoceptors.",613,1
614,"Pretreatment with a combination of (+/-)-2-hydroxy-5-[2-[[2-hydroxy-3-[4-[1-methyl-4-(trifluoromethyl)-1H-imidazol-2 -yl]phenoxy]propyl]amino]ethoxy]-benzamide methanesulfonate (CGP20712A, a selective beta(1)-adrenoceptor antagonist) and (+/-)-1-[2,3-(dihydro-7-methyl-1H-inden-4-yl)oxy]-3-[(1-methylethyl)amino]-2-buta nol hydrochloride (<< ICI-118,5511 >>, a selective [[ beta(2)-adrenoceptor ]] antagonist) (0.1 microM for each) produced a 14-fold rightward shift of the concentration-response curve for (-)-isoprenaline; however, the relaxation in response to (+/-)-CGP12177A was unaffected by the blockade of beta(1)- and beta(2)-adrenoceptors.",614,1
615,The specificity of tracer uptake was determined by adding the << NET >> inhibitor [[ imipramine ]].,615,0
616,"<< [(131)I]MIBG >> uptake in PC12 cells, which express the [[ NET ]] endogenously, was 20- to 28-fold lower than in transduced cells.",616,5
617,"In vivo, A431<< NET >> tumors demonstrated a 33-fold higher [[ [(123)I]MIBG ]] uptake than parental tumors.",617,5
618,"The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, << formoterol >>, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.",618,2
619,"The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, << broxaterol >>) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.",619,2
620,"The aim of this study was, therefore, to provide comparative binding characteristics of agonists (<< epinephrine >>, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.",620,2
621,"The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, << norepinephrine >>, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.",621,2
622,"The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, << isoproterenol >>, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.",622,2
623,"The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, << fenoterol >>, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.",623,2
624,"The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, << salbutamol >>, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.",624,2
625,"The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, << salmeterol >>, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.",625,2
626,"The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, << terbutalin >>, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.",626,2
627,"The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (<< propranolol >>, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.",627,1
628,"The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, << alprenolol >>, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.",628,1
629,"The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, << atenolol >>, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.",629,1
630,"The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, << metoprolol >>, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.",630,1
631,"The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, << bisoprolol >>, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.",631,1
632,"The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, << carvedilol >>, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.",632,1
633,"The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, << pindolol >>, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.",633,1
634,"The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, << BRL 37344 >>, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.",634,1
635,"The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, << CGP 20712 >>, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.",635,1
636,"The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, << SR 59230A >>, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.",636,1
637,"The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, << CGP 12177 >>, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.",637,1
638,"The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, << ICI 118551 >>) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.",638,1
639,Manipulation of kinetic profiles in << 2-aryl propionic acid >> [[ cyclooxygenase ]] inhibitors.,639,0
640,"Effects of the << EGFR >>/HER2 kinase inhibitor [[ GW572016 ]] on EGFR- and HER2-overexpressing breast cancer cell line proliferation, radiosensitization, and resistance.",640,0
641,"Effects of the EGFR/<< HER2 >> kinase inhibitor [[ GW572016 ]] on EGFR- and HER2-overexpressing breast cancer cell line proliferation, radiosensitization, and resistance.",641,0
642,"Effects of the EGFR/HER2 << kinase >> inhibitor [[ GW572016 ]] on EGFR- and HER2-overexpressing breast cancer cell line proliferation, radiosensitization, and resistance.",642,0
643,"To gauge the potential clinical utility of targeting both EGFR and HER2 to control growth and radiosensitize human breast cancers, we examined the effect of a dual << EGFR >>/HER2 inhibitor, [[ GW572016 ]], on the proliferation and radiation response of either EGFR- or HER2-overexpressing human breast cancer cell lines.",643,0
644,"To gauge the potential clinical utility of targeting both EGFR and HER2 to control growth and radiosensitize human breast cancers, we examined the effect of a dual EGFR/<< HER2 >> inhibitor, [[ GW572016 ]], on the proliferation and radiation response of either EGFR- or HER2-overexpressing human breast cancer cell lines.",644,0
645,"RESULTS: << GW572016 >> inhibited constitutive and/or ligand-induced [[ EGFR ]] or HER2 tyrosine phosphorylation of all five cell lines, which correlated with the antiproliferative response in all but one cell line.",645,0
646,"RESULTS: << GW572016 >> inhibited constitutive and/or ligand-induced EGFR or [[ HER2 ]] tyrosine phosphorylation of all five cell lines, which correlated with the antiproliferative response in all but one cell line.",646,0
647,"Exploration of potential mechanisms of resistance in SUM185 cells revealed failure of << GW572016 >> to inhibit downstream ERK and Akt activation, despite inhibition of [[ HER2 ]] phosphorylation.",647,0
648,CONCLUSION: << GW572016 >> potently inhibits receptor phosphorylation in either [[ EGFR ]]- or HER2-overexpressing cell lines and has both antiproliferative and radiosensitizing effects.,648,0
649,CONCLUSION: << GW572016 >> potently inhibits receptor phosphorylation in either EGFR- or [[ HER2 ]]-overexpressing cell lines and has both antiproliferative and radiosensitizing effects.,649,0
650,"Metformin, but not leptin, regulates AMP-activated protein kinase in pancreatic islets: impact on << glucose >>-stimulated [[ insulin ]] secretion.",650,6
651,"<< Metformin >>, a drug widely used in the treatment of type 2 diabetes, has recently been shown to act on skeletal muscle and liver in part through the activation of [[ AMP-activated protein kinase ]] (AMPK).",651,9
652,"<< Metformin >>, a drug widely used in the treatment of type 2 diabetes, has recently been shown to act on skeletal muscle and liver in part through the activation of AMP-activated protein kinase ([[ AMPK ]]).",652,9
653,"Whether << metformin >> or the satiety factor leptin, which also stimulates [[ AMPK ]] in muscle, regulates this enzyme in pancreatic islets is unknown.",653,9
654,"Increases in << glucose >> concentration from 0 to 3 and from 3 to 17 mM inhibited [[ AMPK ]] activity in primary islets from mouse, rat, and human, confirming previous findings in insulinoma cells.",654,0
655,"Incubation with << metformin >> (0.2-1 mM) activated [[ AMPK ]] in both human islets and MIN6 beta-cells in parallel with an inhibition of insulin secretion, whereas leptin (10-100 nM) was without effect in MIN6 cells.",655,9
656,"Incubation with << metformin >> (0.2-1 mM) activated AMPK in both human islets and MIN6 beta-cells in parallel with an inhibition of [[ insulin ]] secretion, whereas leptin (10-100 nM) was without effect in MIN6 cells.",656,8
657,The inhibitory effects of << metformin >> on [[ insulin ]] secretion may therefore need to be considered with respect to the use of this drug for the treatment of type 2 diabetes.,657,8
658,A novel retinoic acid-responsive element regulates << retinoic acid >>-induced [[ BLR1 ]] expression.,658,6
659,"RA is known to induce expression of the Burkitt's lymphoma receptor 1 (BLR1) gene which propels RA-induced cell cycle arrest and differentiation of HL-60 human myeloblastic leukemia cells, motivating the present analysis of transcriptional regulation of << blr1 >> expression by [[ RA ]].",659,6
660,"<< RA >> is known to induce expression of the [[ Burkitt's lymphoma receptor 1 ]] (BLR1) gene which propels RA-induced cell cycle arrest and differentiation of HL-60 human myeloblastic leukemia cells, motivating the present analysis of transcriptional regulation of blr1 expression by RA.",660,6
661,"<< RA >> is known to induce expression of the Burkitt's lymphoma receptor 1 ([[ BLR1 ]]) gene which propels RA-induced cell cycle arrest and differentiation of HL-60 human myeloblastic leukemia cells, motivating the present analysis of transcriptional regulation of blr1 expression by RA.",661,6
662,A 5'-flanking region capable of supporting << RA >>-induced [[ blr1 ]] activation in HL-60 cells was found to contain a 205-bp sequence in the distal portion that was necessary for transcriptional activation by RA.,662,9
663,"The ability of this cis-acting RAR-RXR binding element to activate transcription in response to << RA >> also depended on downstream sequences where an octamer transcription factor 1 (Oct1) site and a [[ nuclear factor of activated T cells ]] (NFATc) site between this element and the transcriptional start, as well as a cyclic AMP response element binding factor (CREB) site between the transcriptional start and first exon of the blr1 gene, were necessary.",663,8
664,In sum the results of the present study indicate that << RA >>-induced expression of [[ blr1 ]] expression depends on a novel RA response element.,664,6
665,The persistent membrane retention of << desipramine >> causes lasting inhibition of [[ norepinephrine transporter ]] function.,665,0
666,"[3H]DMI trapped in membranes was displaceable by the structurally unrelated << NET >> inhibitor, [[ nisoxetine ]], in a concentration-dependent manner, implying interaction of retained [3H]DMI with the NET.",666,0
667,<< Irbesartan >> is a long-acting [[ angiotensin II ]] antagonist acting specifically at the level of the Type 1-receptor subtype (AT1-receptor).,667,1
668,<< Irbesartan >> may have antiatherosclerotic properties beyond those expected from blood pressure lowering per se: this AT1-blocker decreases the vascular oxidative stress and prevents the procoagulant as well as the pro-inflammatory effects of [[ angiotensin II ]].,668,3
669,<< Irbesartan >> may have antiatherosclerotic properties beyond those expected from blood pressure lowering per se: this [[ AT1 ]]-blocker decreases the vascular oxidative stress and prevents the procoagulant as well as the pro-inflammatory effects of angiotensin II.,669,0
670,"To verify the hypothesis that the non-conventional partial agonist << (-)-CGP12177 >> binds at two beta(1)-adrenoceptor sites, [[ human beta(1)-adrenoceptors ]], expressed in CHO cells, were labelled with (-)-[(3)H]-CGP12177.",670,2
671,"To verify the hypothesis that the non-conventional partial agonist << (-)-CGP12177 >> binds at two [[ beta(1)-adrenoceptor ]] sites, human beta(1)-adrenoceptors, expressed in CHO cells, were labelled with (-)-[(3)H]-CGP12177.",671,2
672,"<< Imiquimod >>, a Toll-like receptor-7 agonist, induces [[ perforin ]] in cytotoxic T lymphocytes in vitro.",672,7
673,"<< Imiquimod >>, a [[ Toll-like receptor-7 ]] agonist, induces perforin in cytotoxic T lymphocytes in vitro.",673,2
674,"<< Imiquimod >> (IMQ), an activator of [[ Toll-like receptor-7 ]] (TLR-7), induces by several routes a profound anti-viral and anti-tumor effect in vivo.",674,9
675,"<< Imiquimod >> (IMQ), an activator of Toll-like receptor-7 ([[ TLR-7 ]]), induces by several routes a profound anti-viral and anti-tumor effect in vivo.",675,9
676,"Imiquimod (<< IMQ >>), an activator of [[ Toll-like receptor-7 ]] (TLR-7), induces by several routes a profound anti-viral and anti-tumor effect in vivo.",676,9
677,"Imiquimod (<< IMQ >>), an activator of Toll-like receptor-7 ([[ TLR-7 ]]), induces by several routes a profound anti-viral and anti-tumor effect in vivo.",677,9
678,"In peripheral lymphocytes of healthy and diseased subjects, << IMQ >> induced a significant increase of [[ perforin ]](+) CTLs within 12h in all experiments performed.",678,6
679,"This effect was most pronounced in CTLs of patients suffering from atopic dermatitis, a model disorder for subnormal perforin expression: as compared to perforin(+) CTLs detected at time point zero (100%), up to 270% of << perforin >>(+) CTLs were induced by 2.5 microg/ml [corrected] [[ IMQ ]].",679,6
680,"Thus, the biological activity of << IMQ >> appears to exceed its previously known functions, inasmuch as it boosts up significantly the [[ perforin ]]-granule system.",680,6
681,"<< Ang II >> level in plasma and mesenteric arteries in SHR group was the same or lower than that in WKY group, and was higher in [[ irbesartan ]] group and lower in imidapril group.",681,6
682,"<< Ang II >> level in plasma and mesenteric arteries in SHR group was the same or lower than that in WKY group, and was higher in irbesartan group and lower in [[ imidapril ]] group.",682,8
683,"The ratio of << TGF-beta1 >> absorbed light value to GAPDH absorbed light value in the SHR group was 0.887+/-0.019, which was significantly higher than that in WKY group, [[ imidapril ]] group, and irbesartan group with the ratios of 0.780+/-0.018, 0.803+/-0.005, and 0.847+/-0.017, respectively (P<0.01).",683,6
684,"The ratio of TGF-beta1 absorbed light value to << GAPDH >> absorbed light value in the SHR group was 0.887+/-0.019, which was significantly higher than that in WKY group, [[ imidapril ]] group, and irbesartan group with the ratios of 0.780+/-0.018, 0.803+/-0.005, and 0.847+/-0.017, respectively (P<0.01).",684,6
685,"The ratio of << TGF-beta1 >> absorbed light value to GAPDH absorbed light value in the SHR group was 0.887+/-0.019, which was significantly higher than that in WKY group, imidapril group, and [[ irbesartan ]] group with the ratios of 0.780+/-0.018, 0.803+/-0.005, and 0.847+/-0.017, respectively (P<0.01).",685,6
686,"The ratio of TGF-beta1 absorbed light value to << GAPDH >> absorbed light value in the SHR group was 0.887+/-0.019, which was significantly higher than that in WKY group, imidapril group, and [[ irbesartan ]] group with the ratios of 0.780+/-0.018, 0.803+/-0.005, and 0.847+/-0.017, respectively (P<0.01).",686,6
687,<< Ang II >> level in plasma and mesenteric arteries in imidapril group was significantly lower than that in [[ irbesartan ]] group (P<0.05).,687,6
688,<< Ang II >> level in plasma and mesenteric arteries in [[ imidapril ]] group was significantly lower than that in irbesartan group (P<0.05).,688,8
689,"The << c-Jun >> absorbed light value/GAPDH absorbed light value of mesenteric arteries in the SHR group was 0.850+/-0.015, which was significantly higher than that in the WKY, [[ imidapril ]], and irbesartan groups (0.582+/-0.013, 0.743+/-0.012, and 0.789+/-0.013, respectively, P<0.01), and was significantly lower in imidapril group than in irbesartan group (P<0.05).",689,6
690,"The c-Jun absorbed light value/<< GAPDH >> absorbed light value of mesenteric arteries in the SHR group was 0.850+/-0.015, which was significantly higher than that in the WKY, [[ imidapril ]], and irbesartan groups (0.582+/-0.013, 0.743+/-0.012, and 0.789+/-0.013, respectively, P<0.01), and was significantly lower in imidapril group than in irbesartan group (P<0.05).",690,6
691,"The << c-Jun >> absorbed light value/GAPDH absorbed light value of mesenteric arteries in the SHR group was 0.850+/-0.015, which was significantly higher than that in the WKY, imidapril, and [[ irbesartan ]] groups (0.582+/-0.013, 0.743+/-0.012, and 0.789+/-0.013, respectively, P<0.01), and was significantly lower in imidapril group than in irbesartan group (P<0.05).",691,6
692,"The c-Jun absorbed light value/<< GAPDH >> absorbed light value of mesenteric arteries in the SHR group was 0.850+/-0.015, which was significantly higher than that in the WKY, imidapril, and [[ irbesartan ]] groups (0.582+/-0.013, 0.743+/-0.012, and 0.789+/-0.013, respectively, P<0.01), and was significantly lower in imidapril group than in irbesartan group (P<0.05).",692,6
693,"CONCLUSION: << Imidapril >> and irbesartan can not only control blood pressure but also inhibit mesenteric arteries remodeling and mRNA expression of [[ TGF-beta1 ]], c-Jun in SHR.",693,8
694,"CONCLUSION: << Imidapril >> and irbesartan can not only control blood pressure but also inhibit mesenteric arteries remodeling and mRNA expression of TGF-beta1, [[ c-Jun ]] in SHR.",694,8
695,"CONCLUSION: Imidapril and << irbesartan >> can not only control blood pressure but also inhibit mesenteric arteries remodeling and mRNA expression of [[ TGF-beta1 ]], c-Jun in SHR.",695,8
696,"CONCLUSION: Imidapril and << irbesartan >> can not only control blood pressure but also inhibit mesenteric arteries remodeling and mRNA expression of TGF-beta1, [[ c-Jun ]] in SHR.",696,8
697,"BACKGROUND: To assess the sensitivity of biochemical, physiological, and pharmacological markers of peripheral norepinephrine (NE) transporter (NET) function, we chronically antagonized << NET >> by a range of doses of [[ duloxetine ]] [(+)-N-methyl-3-(1-naphthalenyloxy)-2 thiophenepropanamine], which blocks the NE reuptake process.",697,1
698,"BACKGROUND: To assess the sensitivity of biochemical, physiological, and pharmacological markers of peripheral norepinephrine (NE) transporter (NET) function, we chronically antagonized << NET >> by a range of doses of duloxetine [[[ (+)-N-methyl-3-(1-naphthalenyloxy)-2 thiophenepropanamine ]]], which blocks the NE reuptake process.",698,1
699,"BACKGROUND: To assess the sensitivity of biochemical, physiological, and pharmacological markers of peripheral norepinephrine (NE) transporter (NET) function, we chronically antagonized << NET >> by a range of doses of duloxetine [(+)-N-methyl-3-(1-naphthalenyloxy)-2 thiophenepropanamine], which blocks the [[ NE ]] reuptake process.",699,5
700,"<< Auranofin >>, an antirheumatic gold compound, is an inhibitor of selenocysteine enzymes, such as thioredoxin reductase and [[ glutathione peroxidase ]].",700,0
701,"<< Auranofin >>, an antirheumatic gold compound, is an inhibitor of [[ selenocysteine enzymes ]], such as thioredoxin reductase and glutathione peroxidase.",701,0
702,"<< Auranofin >>, an antirheumatic gold compound, is an inhibitor of selenocysteine enzymes, such as [[ thioredoxin reductase ]] and glutathione peroxidase.",702,0
703,"There was significantly less << thioredoxin reductase >> activity in rat liver extracts, whereas the level of glutathione activity remained unchanged, demonstrating that the dose of [[ auranofin ]] used was able to selectively inhibit one of these enzyme systems.",703,0
704,"Furthermore, << gallium >> also seems to affect intracellular availability of iron already taken up via this pathway, probably due to its inhibitory activity on [[ vacuolar-type H(+)-ATPases ]].",704,0
705,"However, some experimental findings raise the question whether these effects resulting from the << iron >>-mimicking properties of gallium are solely responsible for its antineoplastic activity or whether additional mechanisms are involved, such as antimitotic effects which result from its capability of inhibiting [[ tubulin ]] polymerization.",705,0
706,"However, some experimental findings raise the question whether these effects resulting from the iron-mimicking properties of << gallium >> are solely responsible for its antineoplastic activity or whether additional mechanisms are involved, such as antimitotic effects which result from its capability of inhibiting [[ tubulin ]] polymerization.",706,0
707,"GABA-evoked currents were completely and reversibly blocked by the competitive << GABAA receptor >> antagonist [[ bicuculline ]] (IC50 = 1.7 microM), indicating expression of GABAA but not GABAC receptors.",707,1
708,"<< Histamine H1-receptor >> (H1R) antagonists, or [[ antihistamines ]], often induce sedative side effects when used for the treatment of allergic disorders.",708,1
709,"Histamine H1-receptor (<< H1R >>) antagonists, or [[ antihistamines ]], often induce sedative side effects when used for the treatment of allergic disorders.",709,1
710,"A novel membrane sensor for << histamine H1-receptor >> antagonist ""[[ fexofenadine ]]"".",710,1
711,"<< Thymidylate synthase >> (TS) continues to be a critical target for 5-fluorouracil (5-FU) and its prodrugs, UFT/LV (Orzel), capecitabine (Xeloda), and S-1, primarily because this enzyme is essential for the synthesis of [[ 2-deoxythymidine-5-monophosphate ]], a precursor for DNA synthesis.",711,4
712,"Thymidylate synthase (<< TS >>) continues to be a critical target for 5-fluorouracil (5-FU) and its prodrugs, UFT/LV (Orzel), capecitabine (Xeloda), and S-1, primarily because this enzyme is essential for the synthesis of [[ 2-deoxythymidine-5-monophosphate ]], a precursor for DNA synthesis.",712,4
713,"While fluoropyrimidine antimetabolites have other sites of action, antifolates << ZD1694 >> (raltitrexed, Tomudex) and AG337 (Thymitag) are more specific and potent [[ TS ]] inhibitors.",713,0
714,"While fluoropyrimidine antimetabolites have other sites of action, antifolates ZD1694 (<< raltitrexed >>, Tomudex) and AG337 (Thymitag) are more specific and potent [[ TS ]] inhibitors.",714,0
715,"While fluoropyrimidine antimetabolites have other sites of action, antifolates ZD1694 (raltitrexed, << Tomudex >>) and AG337 (Thymitag) are more specific and potent [[ TS ]] inhibitors.",715,0
716,"While fluoropyrimidine antimetabolites have other sites of action, antifolates ZD1694 (raltitrexed, Tomudex) and << AG337 >> (Thymitag) are more specific and potent [[ TS ]] inhibitors.",716,0
717,"While fluoropyrimidine antimetabolites have other sites of action, antifolates ZD1694 (raltitrexed, Tomudex) and AG337 (<< Thymitag >>) are more specific and potent [[ TS ]] inhibitors.",717,0
718,"The availability of the 5-FU prodrugs offers the possibility of greater therapeutic selectivity based on the demonstration that << thymidine phosphorylase >>, the activating enzyme for [[ 5-FU ]], is expressed at a higher level in tumor tissue compared with normal tissue counterparts.",718,5
719,<< Orlistat >> is an inhibitor of [[ pancreatic lipase ]] which is able to block the absorption of 30% of ingested fat.,719,0
720,"<< Troglitazone >>, bosentan and glibenclamide inhibit the [[ bile salt export pump ]] (Bsep) which transports taurocholate into bile.",720,0
721,"<< Troglitazone >>, bosentan and glibenclamide inhibit the bile salt export pump ([[ Bsep ]]) which transports taurocholate into bile.",721,0
722,"Troglitazone, << bosentan >> and glibenclamide inhibit the [[ bile salt export pump ]] (Bsep) which transports taurocholate into bile.",722,0
723,"Troglitazone, << bosentan >> and glibenclamide inhibit the bile salt export pump ([[ Bsep ]]) which transports taurocholate into bile.",723,0
724,"Troglitazone, bosentan and << glibenclamide >> inhibit the [[ bile salt export pump ]] (Bsep) which transports taurocholate into bile.",724,0
725,"Troglitazone, bosentan and << glibenclamide >> inhibit the bile salt export pump ([[ Bsep ]]) which transports taurocholate into bile.",725,0
726,"Troglitazone, bosentan and glibenclamide inhibit the << bile salt export pump >> (Bsep) which transports [[ taurocholate ]] into bile.",726,5
727,"Troglitazone, bosentan and glibenclamide inhibit the bile salt export pump (<< Bsep >>) which transports [[ taurocholate ]] into bile.",727,5
728,The discovery of a second isoform of cyclooxygenase (COX) led to the search for compounds that could selectively inhibit COX-2 in humans while sparing << prostaglandin >> formation from [[ COX-1 ]].,728,4
729,"We report here the pharmacological properties of a third selective << COX-2 >> inhibitor, [[ valdecoxib ]], which is the most potent and in vitro selective of the marketed COX-2 inhibitors that we have studied.",729,0
730,"We report here the pharmacological properties of a third selective COX-2 inhibitor, << valdecoxib >>, which is the most potent and in vitro selective of the marketed [[ COX-2 ]] inhibitors that we have studied.",730,0
731,"<< Valdecoxib >> potently inhibits recombinant [[ COX-2 ]], with an IC(50) of 0.005 microM; this compares with IC values of 0.05 microM for celecoxib, 0.5 microM for rofecoxib, and 5 microM for etoricoxib.",731,0
732,"Valdecoxib potently inhibits recombinant << COX-2 >>, with an IC(50) of 0.005 microM; this compares with IC values of 0.05 microM for [[ celecoxib ]], 0.5 microM for rofecoxib, and 5 microM for etoricoxib.",732,0
733,"Valdecoxib potently inhibits recombinant << COX-2 >>, with an IC(50) of 0.005 microM; this compares with IC values of 0.05 microM for celecoxib, 0.5 microM for [[ rofecoxib ]], and 5 microM for etoricoxib.",733,0
734,"Valdecoxib potently inhibits recombinant << COX-2 >>, with an IC(50) of 0.005 microM; this compares with IC values of 0.05 microM for celecoxib, 0.5 microM for rofecoxib, and 5 microM for [[ etoricoxib ]].",734,0
735,"Unique binding interactions of << valdecoxib >> with COX-2 translate into a fast rate of inactivation of [[ COX-2 ]] (110,000 M/s compared with 7000 M/s for rofecoxib and 80 M/s for etoricoxib).",735,3
736,<< Valdecoxib >> inhibits [[ COX-1 ]] in a competitive fashion only at very high concentrations (IC(50) = 150 microM).,736,0
737,<< Valdecoxib >> showed similar activity in the [[ human whole-blood COX ]] assay (COX-2 IC(50) = 0.24 microM; COX-1 IC(50) = 21.9 microM).,737,0
738,<< Valdecoxib >> showed similar activity in the human whole-blood COX assay ([[ COX-2 ]] IC(50) = 0.24 microM; COX-1 IC(50) = 21.9 microM).,738,0
739,<< Valdecoxib >> showed similar activity in the human whole-blood COX assay (COX-2 IC(50) = 0.24 microM; [[ COX-1 ]] IC(50) = 21.9 microM).,739,0
740,"An angiotensin II AT1 receptor antagonist, << telmisartan >> augments glucose uptake and [[ GLUT4 ]] protein expression in 3T3-L1 adipocytes.",740,6
741,"An << angiotensin II AT1 receptor >> antagonist, [[ telmisartan ]] augments glucose uptake and GLUT4 protein expression in 3T3-L1 adipocytes.",741,1
742,"An angiotensin II AT1 receptor antagonist, telmisartan augments << glucose >> uptake and [[ GLUT4 ]] protein expression in 3T3-L1 adipocytes.",742,5
743,Treatment of both differentiating adipocytes and fully differentiated adipocytes with << telmisartan >> caused a dose-dependent increase in mRNA levels for [[ PPARgamma ]] target genes such as aP2 and adiponectin.,743,6
744,Treatment of both differentiating adipocytes and fully differentiated adipocytes with << telmisartan >> caused a dose-dependent increase in mRNA levels for PPARgamma target genes such as [[ aP2 ]] and adiponectin.,744,6
745,Treatment of both differentiating adipocytes and fully differentiated adipocytes with << telmisartan >> caused a dose-dependent increase in mRNA levels for PPARgamma target genes such as aP2 and [[ adiponectin ]].,745,6
746,"By contrast, << telmisartan >> attenuated [[ 11beta-hydroxysteroid dehydrogenase type 1 ]] mRNA level in differentiated adipocytes.",746,6
747,"Of note, we demonstrated for the first time that << telmisartan >> augmented [[ GLUT4 ]] protein expression and 2-deoxy glucose uptake both in basal and insulin-stimulated state of adipocytes, which may contribute, at least partly, to its insulin-sensitizing ability.",747,6
748,"Of note, we demonstrated for the first time that telmisartan augmented << GLUT4 >> protein expression and [[ 2-deoxy glucose ]] uptake both in basal and insulin-stimulated state of adipocytes, which may contribute, at least partly, to its insulin-sensitizing ability.",748,5
749,"Especially, the compound 1 showed strong inhibition (IC50=1.33 microM) against the enzyme << tyrosinase >>, as compared to the standard tyrosinase inhibitors [[ kojic acid ]] (IC50=16.67 microM) and L-mimosine (IC50=3.68 microM), indicating its potential used for the treatment of hyperpigmentation associated with the high production of melanocytes.",749,0
750,"Especially, the compound 1 showed strong inhibition (IC50=1.33 microM) against the enzyme << tyrosinase >>, as compared to the standard tyrosinase inhibitors kojic acid (IC50=16.67 microM) and [[ L-mimosine ]] (IC50=3.68 microM), indicating its potential used for the treatment of hyperpigmentation associated with the high production of melanocytes.",750,0
751,"Oxytocin antagonist (OTA), << TT-235 >>, was developed by our group and shown to inhibit either spontaneous or [[ oxytocin ]]-induced uterine contractions in primates.",751,0
752,"<< Oxytocin >> antagonist (OTA), [[ TT-235 ]], was developed by our group and shown to inhibit either spontaneous or oxytocin-induced uterine contractions in primates.",752,1
753,The purpose of the present study was to confirm the duration of << TT-235 >> to block [[ oxytocin ]]-induced uterine contractions in estrous rats.,753,0
754,"In Experiment 1, << Antag I >>, Antag II and TT-235 inhibited the integrated uterine response to [[ oxytocin ]] at 5 minutes by 76%, 77% and 80%, respectively, compared to controls (p<0.05).",754,0
755,"In Experiment 1, Antag I, << Antag II >> and TT-235 inhibited the integrated uterine response to [[ oxytocin ]] at 5 minutes by 76%, 77% and 80%, respectively, compared to controls (p<0.05).",755,0
756,"In Experiment 1, Antag I, Antag II and << TT-235 >> inhibited the integrated uterine response to [[ oxytocin ]] at 5 minutes by 76%, 77% and 80%, respectively, compared to controls (p<0.05).",756,0
757,"In Experiment 2, << TT-235 >> induced a significant decrease (p<0.05) in [[ oxytocin receptor ]] number and binding affinity at both 0.5 and 4 hours compared with controls.",757,8
758,"In conclusion, << TT-235 >> may inhibit the uterine response to oxytocin by decreasing [[ oxytocin receptor ]] numbers and oxytocin binding affinity, which might explain the prolonged oxytocin antagonist activity of TT-235.",758,8
759,"In conclusion, << TT-235 >> may inhibit the uterine response to [[ oxytocin ]] by decreasing oxytocin receptor numbers and oxytocin binding affinity, which might explain the prolonged oxytocin antagonist activity of TT-235.",759,0
760,"In conclusion, TT-235 may inhibit the uterine response to oxytocin by decreasing oxytocin receptor numbers and oxytocin binding affinity, which might explain the prolonged << oxytocin >> antagonist activity of [[ TT-235 ]].",760,1
761,Preclinical pharmacology of << lumiracoxib >>: a novel selective inhibitor of [[ cyclooxygenase-2 ]].,761,0
762,"This manuscript presents the preclinical profile of << lumiracoxib >>, a novel [[ cyclooxygenase-2 ]] (COX-2) selective inhibitor.",762,0
763,"This manuscript presents the preclinical profile of << lumiracoxib >>, a novel cyclooxygenase-2 ([[ COX-2 ]]) selective inhibitor.",763,0
764,"<< Lumiracoxib >> inhibited purified [[ COX-1 ]] and COX-2 with K(i) values of 3 and 0.06 microM, respectively.",764,0
765,"<< Lumiracoxib >> inhibited purified COX-1 and [[ COX-2 ]] with K(i) values of 3 and 0.06 microM, respectively.",765,0
766,"In cellular assays, << lumiracoxib >> had an IC(50) of 0.14 microM in [[ COX-2 ]]-expressing dermal fibroblasts, but caused no inhibition of COX-1 at concentrations up to 30 microM (HEK 293 cells transfected with human COX-1).",766,0
767,"In a human whole blood assay, IC(50) values for << lumiracoxib >> were 0.13 microM for [[ COX-2 ]] and 67 microM for COX-1 (COX-1/COX-2 selectivity ratio 515).",767,0
768,"In a human whole blood assay, IC(50) values for << lumiracoxib >> were 0.13 microM for COX-2 and 67 microM for [[ COX-1 ]] (COX-1/COX-2 selectivity ratio 515).",768,0
769,"In a human whole blood assay, IC(50) values for << lumiracoxib >> were 0.13 microM for COX-2 and 67 microM for COX-1 ([[ COX-1 ]]/COX-2 selectivity ratio 515).",769,0
770,"In a human whole blood assay, IC(50) values for << lumiracoxib >> were 0.13 microM for COX-2 and 67 microM for COX-1 (COX-1/[[ COX-2 ]] selectivity ratio 515).",770,0
771,"Ex vivo, << lumiracoxib >> inhibited [[ COX-1 ]]-derived thromboxane B(2) (TxB(2)) generation with an ID(50) of 33 mg kg(-1), whereas COX-2-derived production of prostaglandin E(2) (PGE(2)) in the lipopolysaccharide-stimulated rat air pouch was inhibited with an ID(50) value of 0.24 mg kg(-1).",771,0
772,"Ex vivo, lumiracoxib inhibited << COX-1 >>-derived [[ thromboxane B(2) ]] (TxB(2)) generation with an ID(50) of 33 mg kg(-1), whereas COX-2-derived production of prostaglandin E(2) (PGE(2)) in the lipopolysaccharide-stimulated rat air pouch was inhibited with an ID(50) value of 0.24 mg kg(-1).",772,4
773,"Ex vivo, lumiracoxib inhibited << COX-1 >>-derived thromboxane B(2) ([[ TxB(2) ]]) generation with an ID(50) of 33 mg kg(-1), whereas COX-2-derived production of prostaglandin E(2) (PGE(2)) in the lipopolysaccharide-stimulated rat air pouch was inhibited with an ID(50) value of 0.24 mg kg(-1).",773,4
774,"Ex vivo, lumiracoxib inhibited COX-1-derived thromboxane B(2) (TxB(2)) generation with an ID(50) of 33 mg kg(-1), whereas << COX-2 >>-derived production of [[ prostaglandin E(2) ]] (PGE(2)) in the lipopolysaccharide-stimulated rat air pouch was inhibited with an ID(50) value of 0.24 mg kg(-1).",774,4
775,"Ex vivo, lumiracoxib inhibited COX-1-derived thromboxane B(2) (TxB(2)) generation with an ID(50) of 33 mg kg(-1), whereas << COX-2 >>-derived production of prostaglandin E(2) ([[ PGE(2) ]]) in the lipopolysaccharide-stimulated rat air pouch was inhibited with an ID(50) value of 0.24 mg kg(-1).",775,4
776,"However, consistent with its low << COX-1 >> inhibitory activity, [[ lumiracoxib ]] at a dose of 100 mg kg(-1) orally caused no ulcers and was significantly less ulcerogenic than diclofenac (P<0.05).",776,0
777,"However, consistent with its low << COX-1 >> inhibitory activity, lumiracoxib at a dose of 100 mg kg(-1) orally caused no ulcers and was significantly less ulcerogenic than [[ diclofenac ]] (P<0.05).",777,0
778,"<< Lumiracoxib >> is a highly selective [[ COX-2 ]] inhibitor with anti-inflammatory, analgesic and antipyretic activities comparable with diclofenac, the reference NSAID, but with much improved gastrointestinal safety.",778,0
779,"Lumiracoxib is a highly selective << COX-2 >> inhibitor with anti-inflammatory, analgesic and antipyretic activities comparable with [[ diclofenac ]], the reference NSAID, but with much improved gastrointestinal safety.",779,0
780,"As << thiamine >> metabolism deficiencies have been seen in placental infarcts previously, these indicate that [[ PP20 ]]/hTPK may have a role in placental diseases.",780,5
781,"As << thiamine >> metabolism deficiencies have been seen in placental infarcts previously, these indicate that PP20/[[ hTPK ]] may have a role in placental diseases.",781,5
782,"Safety and tolerability of << denufosol tetrasodium >> inhalation solution, a novel [[ P2Y2 receptor ]] agonist: results of a phase 1/phase 2 multicenter study in mild to moderate cystic fibrosis.",782,2
783,"<< Denufosol tetrasodium >> (INS37217) is a selective [[ P2Y(2) ]] agonist that stimulates ciliary beat frequency and Cl(-) secretion in normal and cystic fibrosis (CF) airway epithelia, and is being investigated as an inhaled treatment for CF.",783,2
784,"Denufosol tetrasodium (<< INS37217 >>) is a selective [[ P2Y(2) ]] agonist that stimulates ciliary beat frequency and Cl(-) secretion in normal and cystic fibrosis (CF) airway epithelia, and is being investigated as an inhaled treatment for CF.",784,2
785,"The << Cl(-) >> secretory response is mediated via a non-[[ CFTR ]] pathway, and the driving force for Cl(-) secretion is enhanced by the effect of P2Y(2) activation to also inhibit epithelial Na(+) transport.",785,5
786,"<< Denufosol >> is metabolically more stable and better tolerated, and may enhance mucociliary clearance for a longer period of time than previously investigated [[ P2Y(2) ]] agonists.",786,2
787,The dextromethorphan analog << dimemorfan >> attenuates kainate-induced seizures via [[ sigma1 receptor ]] activation: comparison with the effects of dextromethorphan.,787,9
788,The << dextromethorphan >> analog dimemorfan attenuates kainate-induced seizures via [[ sigma1 receptor ]] activation: comparison with the effects of dextromethorphan.,788,9
789,"Dimemorfan pre-treatment also attenuated the << KA >>-induced increases in c-fos/c-jun expression, [[ activator protein (AP)-1 ]] DNA-binding activity, and loss of cells in the CA1 and CA3 fields of the hippocampus.",789,9
790,"Dimemorfan pre-treatment also attenuated the << KA >>-induced increases in [[ c-fos ]]/c-jun expression, activator protein (AP)-1 DNA-binding activity, and loss of cells in the CA1 and CA3 fields of the hippocampus.",790,6
791,"Dimemorfan pre-treatment also attenuated the << KA >>-induced increases in c-fos/[[ c-jun ]] expression, activator protein (AP)-1 DNA-binding activity, and loss of cells in the CA1 and CA3 fields of the hippocampus.",791,6
792,"<< Dimemorfan >> pre-treatment also attenuated the KA-induced increases in [[ c-fos ]]/c-jun expression, activator protein (AP)-1 DNA-binding activity, and loss of cells in the CA1 and CA3 fields of the hippocampus.",792,8
793,"<< Dimemorfan >> pre-treatment also attenuated the KA-induced increases in c-fos/[[ c-jun ]] expression, activator protein (AP)-1 DNA-binding activity, and loss of cells in the CA1 and CA3 fields of the hippocampus.",793,8
794,"<< Dimemorfan >> pre-treatment also attenuated the KA-induced increases in c-fos/c-jun expression, [[ activator protein (AP)-1 ]] DNA-binding activity, and loss of cells in the CA1 and CA3 fields of the hippocampus.",794,0
795,"The anticonvulsant action of dextromethorphan or dimemorfan was significantly counteracted by a selective << sigma1 receptor >> antagonist [[ BD 1047 ]], suggesting that the anticonvulsant action of dextromethorphan or dimemorfan is, at least in part, related to sigma1 receptor-activated modulation of AP-1 transcription factors.",795,1
796,Binding domains of the oxytocin receptor for the selective << oxytocin receptor >> antagonist barusiban in comparison to the agonists [[ oxytocin ]] and carbetocin.,796,2
797,Binding domains of the oxytocin receptor for the selective << oxytocin receptor >> antagonist barusiban in comparison to the agonists oxytocin and [[ carbetocin ]].,797,2
798,Binding domains of the oxytocin receptor for the selective << oxytocin receptor >> antagonist [[ barusiban ]] in comparison to the agonists oxytocin and carbetocin.,798,1
799,"We have analyzed binding domains of the oxytocin receptor for barusiban, a highly selective oxytocin receptor antagonist, in comparison to the combined << vasopressin V1A/oxytocin receptor >> antagonist atosiban and the agonists [[ oxytocin ]] and carbetocin.",799,2
800,"We have analyzed binding domains of the oxytocin receptor for barusiban, a highly selective oxytocin receptor antagonist, in comparison to the combined << vasopressin V1A/oxytocin receptor >> antagonist atosiban and the agonists oxytocin and [[ carbetocin ]].",800,2
801,"We have analyzed binding domains of the oxytocin receptor for barusiban, a highly selective oxytocin receptor antagonist, in comparison to the combined << vasopressin V1A/oxytocin receptor >> antagonist [[ atosiban ]] and the agonists oxytocin and carbetocin.",801,1
802,"We have analyzed binding domains of the oxytocin receptor for << barusiban >>, a highly selective [[ oxytocin receptor ]] antagonist, in comparison to the combined vasopressin V1A/oxytocin receptor antagonist atosiban and the agonists oxytocin and carbetocin.",802,1
803,"For the << vasopressin V1A/oxytocin receptor >> antagonist [[ atosiban ]], none of the receptor constructs were able to provide a binding with higher affinity than the starting vasopressin V2 receptor.",803,1
804,"The binding domain of barusiban differs from the binding domain of the agonists and the nonselective << oxytocin receptor >> antagonist [[ d(CH2)5[Tyr-(Me)2,Thr4,Orn8,Tyr9]vasotocin ]] that has been used in previous studies.",804,1
805,"The compounds << 5'-azacytidine >> (AZC) and procainamide (PCA) belong to inhibitors of [[ DNMT1 ]], whose low activity correlates with increase in transcription of various genes.",805,0
806,"The compounds 5'-azacytidine (<< AZC >>) and procainamide (PCA) belong to inhibitors of [[ DNMT1 ]], whose low activity correlates with increase in transcription of various genes.",806,0
807,"The compounds 5'-azacytidine (AZC) and << procainamide >> (PCA) belong to inhibitors of [[ DNMT1 ]], whose low activity correlates with increase in transcription of various genes.",807,0
808,"The compounds 5'-azacytidine (AZC) and procainamide (<< PCA >>) belong to inhibitors of [[ DNMT1 ]], whose low activity correlates with increase in transcription of various genes.",808,0
809,"However, the flowcytometric analysis revealed that << AZC >> and PCA decreased intracellular contents of [[ CD3-zeta chain ]] in these cells in dose dependent manner.",809,8
810,"However, the flowcytometric analysis revealed that AZC and << PCA >> decreased intracellular contents of [[ CD3-zeta chain ]] in these cells in dose dependent manner.",810,8
811,"Clinical studies in cancer patients treated with the new << fluoropyrimidine >> analogue capecitabine (N4-pentoxycarbonyl-5'-5-fluorocytidine) have shown that plasma 2'-deoxyuridine was significantly elevated after 1 week of treatment, consistent with inhibition of [[ thymidylate synthase ]] (TS).",811,0
812,"Clinical studies in cancer patients treated with the new << fluoropyrimidine >> analogue capecitabine (N4-pentoxycarbonyl-5'-5-fluorocytidine) have shown that plasma 2'-deoxyuridine was significantly elevated after 1 week of treatment, consistent with inhibition of thymidylate synthase ([[ TS ]]).",812,0
813,"Clinical studies in cancer patients treated with the new fluoropyrimidine analogue << capecitabine >> (N4-pentoxycarbonyl-5'-5-fluorocytidine) have shown that plasma 2'-deoxyuridine was significantly elevated after 1 week of treatment, consistent with inhibition of [[ thymidylate synthase ]] (TS).",813,0
814,"Clinical studies in cancer patients treated with the new fluoropyrimidine analogue << capecitabine >> (N4-pentoxycarbonyl-5'-5-fluorocytidine) have shown that plasma 2'-deoxyuridine was significantly elevated after 1 week of treatment, consistent with inhibition of thymidylate synthase ([[ TS ]]).",814,0
815,"Clinical studies in cancer patients treated with the new fluoropyrimidine analogue capecitabine (<< N4-pentoxycarbonyl-5'-5-fluorocytidine >>) have shown that plasma 2'-deoxyuridine was significantly elevated after 1 week of treatment, consistent with inhibition of [[ thymidylate synthase ]] (TS).",815,0
816,"Clinical studies in cancer patients treated with the new fluoropyrimidine analogue capecitabine (<< N4-pentoxycarbonyl-5'-5-fluorocytidine >>) have shown that plasma 2'-deoxyuridine was significantly elevated after 1 week of treatment, consistent with inhibition of thymidylate synthase ([[ TS ]]).",816,0
817,"Clinical studies in cancer patients treated with the new fluoropyrimidine analogue capecitabine (N4-pentoxycarbonyl-5'-5-fluorocytidine) have shown that plasma << 2'-deoxyuridine >> was significantly elevated after 1 week of treatment, consistent with inhibition of [[ thymidylate synthase ]] (TS).",817,0
818,"Clinical studies in cancer patients treated with the new fluoropyrimidine analogue capecitabine (N4-pentoxycarbonyl-5'-5-fluorocytidine) have shown that plasma << 2'-deoxyuridine >> was significantly elevated after 1 week of treatment, consistent with inhibition of thymidylate synthase ([[ TS ]]).",818,0
819,These findings suggest that the mechanism of antiproliferative toxicity of capecitabine is at least partly due to << TS >> inhibitory activity of its active metabolite 5-fluoro-2'-deoxyuridine monophosphate ([[ FdUMP ]]).,819,0
820,These findings suggest that the mechanism of antiproliferative toxicity of << capecitabine >> is at least partly due to [[ TS ]] inhibitory activity of its active metabolite 5-fluoro-2'-deoxyuridine monophosphate (FdUMP).,820,0
821,These findings suggest that the mechanism of antiproliferative toxicity of capecitabine is at least partly due to << TS >> inhibitory activity of its active metabolite [[ 5-fluoro-2'-deoxyuridine monophosphate ]] (FdUMP).,821,0
822,Induction of heparin-binding EGF-like growth factor and activation of << EGF receptor >> in [[ imatinib mesylate ]]-treated squamous carcinoma cells.,822,9
823,"<< Imatinib mesylate >> is a tyrosine kinase inhibitor of the ABL, platelet-derived growth factor receptor ([[ PDGFR ]]), and c-kit kinases.",823,0
824,"<< Imatinib mesylate >> is a tyrosine kinase inhibitor of the ABL, platelet-derived growth factor receptor (PDGFR), and [[ c-kit ]] kinases.",824,0
825,"<< Imatinib mesylate >> is a tyrosine kinase inhibitor of the ABL, platelet-derived growth factor receptor (PDGFR), and c-kit [[ kinases ]].",825,0
826,"<< Imatinib mesylate >> is a [[ tyrosine kinase ]] inhibitor of the ABL, platelet-derived growth factor receptor (PDGFR), and c-kit kinases.",826,0
827,"<< Imatinib mesylate >> is a tyrosine kinase inhibitor of the [[ ABL ]], platelet-derived growth factor receptor (PDGFR), and c-kit kinases.",827,0
828,"<< Imatinib mesylate >> is a tyrosine kinase inhibitor of the ABL, [[ platelet-derived growth factor receptor ]] (PDGFR), and c-kit kinases.",828,0
829,Treatment of head and neck squamous carcinoma cells with clinically relevant concentrations of << imatinib >>-induced changes in cell morphology and growth similar to changes associated with [[ epidermal growth factor receptor ]] (EGFR) activation.,829,9
830,Treatment of head and neck squamous carcinoma cells with clinically relevant concentrations of << imatinib >>-induced changes in cell morphology and growth similar to changes associated with epidermal growth factor receptor ([[ EGFR ]]) activation.,830,9
831,"<< Imatinib >>-induced changes were blocked with the EGFR antagonist cetuximab, which suggested direct involvement of [[ EGFR ]] in this process.",831,9
832,"Western blot analysis of cells incubated with << imatinib >> demonstrated activation of [[ EGFR ]] and downstream signaling that was reduced by inhibition of mitogen-activated protein/extracellular signal-regulated kinase kinase 1 (MEK1) and EGFR, but not Her2/ErbB2.",832,9
833,"Western blot analysis of cells incubated with << imatinib >> demonstrated activation of [[ EGFR ]] and downstream signaling that was reduced by inhibition of mitogen-activated protein/extracellular signal-regulated kinase kinase 1 (MEK1) and EGFR, but not Her2/ErbB2.",833,6
834,"Inhibitors and neutralizing antibodies against heparin-binding epidermal growth factor-like growth factor (HB-EGF), and to a lesser extent transforming growth factor-alpha, reduced << imatinib >>-mediated [[ mitogen activated protein kinase ]] (MAPK) activation.",834,9
835,"Inhibitors and neutralizing antibodies against heparin-binding epidermal growth factor-like growth factor (HB-EGF), and to a lesser extent transforming growth factor-alpha, reduced << imatinib >>-mediated mitogen activated protein kinase ([[ MAPK ]]) activation.",835,9
836,"<< Imatinib >> stimulated the rapid release of soluble HB-EGF and the subsequent induction of membrane-bound HB-EGF, which correlated with biphasic [[ MAPK ]] activation.",836,9
837,"<< Imatinib >> stimulated the rapid release of soluble [[ HB-EGF ]] and the subsequent induction of membrane-bound HB-EGF, which correlated with biphasic MAPK activation.",837,6
838,"<< Imatinib >> stimulated the rapid release of soluble HB-EGF and the subsequent induction of membrane-bound [[ HB-EGF ]], which correlated with biphasic MAPK activation.",838,6
839,"Together, these results suggested that << imatinib >> affects EGFR activation and signaling pathways through rapid release and increased expression of endogenous [[ EGFR ]]-activating ligands.",839,6
840,"Although, << imatinib >> primarily inhibits tyrosine kinases, it also stimulates the activity of [[ EGFR ]] tyrosine kinase in head and neck squamous tumors.",840,9
841,"Although, << imatinib >> primarily inhibits tyrosine kinases, it also stimulates the activity of EGFR [[ tyrosine kinase ]] in head and neck squamous tumors.",841,9
842,"Although, << imatinib >> primarily inhibits [[ tyrosine kinases ]], it also stimulates the activity of EGFR tyrosine kinase in head and neck squamous tumors.",842,0
843,"The identity of the lung << beta-ADHs >> was further demonstrated by their characteristic pH-activity profiles for ethanol oxidation, Km values for NAD and ethanol, and inhibition by [[ 4-methylpyrazole ]] or 1,10-phenanthroline.",843,0
844,"The identity of the lung << beta-ADHs >> was further demonstrated by their characteristic pH-activity profiles for ethanol oxidation, Km values for NAD and ethanol, and inhibition by 4-methylpyrazole or [[ 1,10-phenanthroline ]].",844,0
845,"The identity of the lung << beta-ADHs >> was further demonstrated by their characteristic pH-activity profiles for [[ ethanol ]] oxidation, Km values for NAD and ethanol, and inhibition by 4-methylpyrazole or 1,10-phenanthroline.",845,5
846,"The identity of the lung << beta-ADHs >> was further demonstrated by their characteristic pH-activity profiles for ethanol oxidation, Km values for NAD and [[ ethanol ]], and inhibition by 4-methylpyrazole or 1,10-phenanthroline.",846,5
847,These findings indicate that human pulmonary << ethanol >>-metabolizing activities differ significantly with respect to genetic polymorphism at both the [[ ADH2 ]] and the ALDH2 loci.,847,5
848,These findings indicate that human pulmonary << ethanol >>-metabolizing activities differ significantly with respect to genetic polymorphism at both the ADH2 and the [[ ALDH2 ]] loci.,848,5
849,"The results suggest that individuals with high Vmax << beta 2-ADH >> and deficient in low-Km mitochondrial ALDH2, accounting for approximately 45% of the Chinese population, may end up with [[ acetaldehyde ]] accumulation during alcohol consumption, rendering them vulnerable to tissue injury caused by this highly reactive and toxic metabolite.",849,4
850,"The results suggest that individuals with high Vmax beta 2-ADH and deficient in low-Km mitochondrial << ALDH2 >>, accounting for approximately 45% of the Chinese population, may end up with [[ acetaldehyde ]] accumulation during alcohol consumption, rendering them vulnerable to tissue injury caused by this highly reactive and toxic metabolite.",850,4
851,"The results suggest that individuals with high Vmax << beta 2-ADH >> and deficient in low-Km mitochondrial ALDH2, accounting for approximately 45% of the Chinese population, may end up with acetaldehyde accumulation during [[ alcohol ]] consumption, rendering them vulnerable to tissue injury caused by this highly reactive and toxic metabolite.",851,5
852,"The results suggest that individuals with high Vmax beta 2-ADH and deficient in low-Km mitochondrial << ALDH2 >>, accounting for approximately 45% of the Chinese population, may end up with acetaldehyde accumulation during [[ alcohol ]] consumption, rendering them vulnerable to tissue injury caused by this highly reactive and toxic metabolite.",852,5
853,<< Simvastatin >> induces [[ interleukin-18 ]] production in human peripheral blood mononuclear cells.,853,6
854,"<< Simvastatin >>, an HMG-CoA reductase inhibitor with mild inhibition of LFA-1, induced the production of [[ interleukin (IL)-18 ]], tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma in human peripheral blood mononuclear cells (PBMC).",854,6
855,"<< Simvastatin >>, an HMG-CoA reductase inhibitor with mild inhibition of LFA-1, induced the production of interleukin (IL)-18, [[ tumor necrosis factor (TNF)-alpha ]] and interferon (IFN)-gamma in human peripheral blood mononuclear cells (PBMC).",855,6
856,"<< Simvastatin >>, an HMG-CoA reductase inhibitor with mild inhibition of LFA-1, induced the production of interleukin (IL)-18, tumor necrosis factor (TNF)-alpha and [[ interferon (IFN)-gamma ]] in human peripheral blood mononuclear cells (PBMC).",856,6
857,"<< Simvastatin >>, an [[ HMG-CoA reductase ]] inhibitor with mild inhibition of LFA-1, induced the production of interleukin (IL)-18, tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma in human peripheral blood mononuclear cells (PBMC).",857,0
858,"<< Simvastatin >>, an HMG-CoA reductase inhibitor with mild inhibition of [[ LFA-1 ]], induced the production of interleukin (IL)-18, tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma in human peripheral blood mononuclear cells (PBMC).",858,0
859,The IL-18 production is located upstream of the << cytokine >> cascade activated by [[ simvastatin ]].,859,9
860,The << IL-18 >> production is located upstream of the cytokine cascade activated by [[ simvastatin ]].,860,6
861,"Moreover, << simvastatin >> concentration-dependently inhibited the expression of ICAM-1 and induced the expression of [[ CD40 ]] on monocytes.",861,6
862,"Moreover, << simvastatin >> concentration-dependently inhibited the expression of [[ ICAM-1 ]] and induced the expression of CD40 on monocytes.",862,8
863,"In the presence of IL-18, << simvastatin >> suppressed the expression of ICAM-1 and CD40 as well as the production of [[ IL-12 ]], TNF-alpha and IFN-gamma in PBMC, contributing to the anti-inflammatory effect of simvastatin.",863,6
864,"In the presence of IL-18, << simvastatin >> suppressed the expression of ICAM-1 and CD40 as well as the production of IL-12, [[ TNF-alpha ]] and IFN-gamma in PBMC, contributing to the anti-inflammatory effect of simvastatin.",864,6
865,"In the presence of IL-18, << simvastatin >> suppressed the expression of ICAM-1 and CD40 as well as the production of IL-12, TNF-alpha and [[ IFN-gamma ]] in PBMC, contributing to the anti-inflammatory effect of simvastatin.",865,6
866,"In the presence of IL-18, << simvastatin >> suppressed the expression of [[ ICAM-1 ]] and CD40 as well as the production of IL-12, TNF-alpha and IFN-gamma in PBMC, contributing to the anti-inflammatory effect of simvastatin.",866,8
867,"In the presence of IL-18, << simvastatin >> suppressed the expression of ICAM-1 and [[ CD40 ]] as well as the production of IL-12, TNF-alpha and IFN-gamma in PBMC, contributing to the anti-inflammatory effect of simvastatin.",867,8
868,"The effects of simvastatin were abolished by the addition of the product of the << HMG-CoA reductase >>, [[ mevalonate ]], indicating the involvement of HMG-CoA reductase in the action of simvastatin.",868,4
869,"<< COX-1 >> and COX-2 inhibition in horse blood by [[ phenylbutazone ]], flunixin, carprofen and meloxicam: an in vitro analysis.",869,0
870,"COX-1 and << COX-2 >> inhibition in horse blood by [[ phenylbutazone ]], flunixin, carprofen and meloxicam: an in vitro analysis.",870,0
871,"<< COX-1 >> and COX-2 inhibition in horse blood by phenylbutazone, [[ flunixin ]], carprofen and meloxicam: an in vitro analysis.",871,0
872,"COX-1 and << COX-2 >> inhibition in horse blood by phenylbutazone, [[ flunixin ]], carprofen and meloxicam: an in vitro analysis.",872,0
873,"<< COX-1 >> and COX-2 inhibition in horse blood by phenylbutazone, flunixin, [[ carprofen ]] and meloxicam: an in vitro analysis.",873,0
874,"COX-1 and << COX-2 >> inhibition in horse blood by phenylbutazone, flunixin, [[ carprofen ]] and meloxicam: an in vitro analysis.",874,0
875,"<< COX-1 >> and COX-2 inhibition in horse blood by phenylbutazone, flunixin, carprofen and [[ meloxicam ]]: an in vitro analysis.",875,0
876,"COX-1 and << COX-2 >> inhibition in horse blood by phenylbutazone, flunixin, carprofen and [[ meloxicam ]]: an in vitro analysis.",876,0
877,"We report on the inhibitory activity of the NSAIDs meloxicam, << carprofen >>, phenylbutazone and flunixin, on blood [[ cyclooxygenases ]] in the horse using in vitro enzyme-linked assays.",877,0
878,"We report on the inhibitory activity of the NSAIDs meloxicam, carprofen, << phenylbutazone >> and flunixin, on blood [[ cyclooxygenases ]] in the horse using in vitro enzyme-linked assays.",878,0
879,"We report on the inhibitory activity of the NSAIDs meloxicam, carprofen, phenylbutazone and << flunixin >>, on blood [[ cyclooxygenases ]] in the horse using in vitro enzyme-linked assays.",879,0
880,"We report on the inhibitory activity of the NSAIDs << meloxicam >>, carprofen, phenylbutazone and flunixin, on blood [[ cyclooxygenases ]] in the horse using in vitro enzyme-linked assays.",880,0
881,"As expected, comparison of IC50 indicated that << meloxicam >> and carprofen are more selective inhibitors of [[ COX-2 ]] than phenylbutazone and flunixin; meloxicam was the most advantageous for horses of four NSAIDs examined.",881,0
882,"As expected, comparison of IC50 indicated that meloxicam and << carprofen >> are more selective inhibitors of [[ COX-2 ]] than phenylbutazone and flunixin; meloxicam was the most advantageous for horses of four NSAIDs examined.",882,0
883,"As expected, comparison of IC50 indicated that meloxicam and carprofen are more selective inhibitors of << COX-2 >> than [[ phenylbutazone ]] and flunixin; meloxicam was the most advantageous for horses of four NSAIDs examined.",883,0
884,"As expected, comparison of IC50 indicated that meloxicam and carprofen are more selective inhibitors of << COX-2 >> than phenylbutazone and [[ flunixin ]]; meloxicam was the most advantageous for horses of four NSAIDs examined.",884,0
885,"However at IC80, phenylbutazone (+134.4%) and flunixin (+29.7%) had greater COX-2 selectivity than at IC50, and meloxicam (-41.2%) and << carprofen >> (-12.9%) had lower [[ COX-2 ]] selectivity than at IC50.",885,0
886,"However at IC80, << phenylbutazone >> (+134.4%) and flunixin (+29.7%) had greater [[ COX-2 ]] selectivity than at IC50, and meloxicam (-41.2%) and carprofen (-12.9%) had lower COX-2 selectivity than at IC50.",886,0
887,"However at IC80, phenylbutazone (+134.4%) and << flunixin >> (+29.7%) had greater [[ COX-2 ]] selectivity than at IC50, and meloxicam (-41.2%) and carprofen (-12.9%) had lower COX-2 selectivity than at IC50.",887,0
888,"However at IC80, phenylbutazone (+134.4%) and flunixin (+29.7%) had greater COX-2 selectivity than at IC50, and << meloxicam >> (-41.2%) and carprofen (-12.9%) had lower [[ COX-2 ]] selectivity than at IC50.",888,0
889,<< Carvedilol >> prevents cardiac hypertrophy and overexpression of [[ hypoxia-inducible factor-1alpha ]] and vascular endothelial growth factor in pressure-overloaded rat heart.,889,8
890,<< Carvedilol >> prevents cardiac hypertrophy and overexpression of hypoxia-inducible factor-1alpha and [[ vascular endothelial growth factor ]] in pressure-overloaded rat heart.,890,8
891,"Treatment with << carvedilol >> reversed both protein and mRNA of HIF-1alpha, VEGF, BNP, and [[ NGF-beta ]] to the baseline values.",891,6
892,"Treatment with << carvedilol >> reversed both protein and mRNA of [[ HIF-1alpha ]], VEGF, BNP, and NGF-beta to the baseline values.",892,8
893,"Treatment with << carvedilol >> reversed both protein and mRNA of HIF-1alpha, [[ VEGF ]], BNP, and NGF-beta to the baseline values.",893,8
894,"Treatment with << carvedilol >> reversed both protein and mRNA of HIF-1alpha, VEGF, [[ BNP ]], and NGF-beta to the baseline values.",894,8
895,"Increased immunohistochemical labeling of << HIF-1alpha >>, VEGF, and BNP in the ventricular myocardium was observed in the banding group and [[ carvedilol ]] again normalized the labeling.",895,8
896,"Increased immunohistochemical labeling of HIF-1alpha, << VEGF >>, and BNP in the ventricular myocardium was observed in the banding group and [[ carvedilol ]] again normalized the labeling.",896,8
897,"Increased immunohistochemical labeling of HIF-1alpha, VEGF, and << BNP >> in the ventricular myocardium was observed in the banding group and [[ carvedilol ]] again normalized the labeling.",897,8
898,"Treatment with << carvedilol >> is associated with a reversal of abnormal regulation of [[ HIF-1alpha ]], VEGF, BNP, and NGF-beta in the hypertrophic myocardium.",898,8
899,"Treatment with << carvedilol >> is associated with a reversal of abnormal regulation of HIF-1alpha, [[ VEGF ]], BNP, and NGF-beta in the hypertrophic myocardium.",899,8
900,"Treatment with << carvedilol >> is associated with a reversal of abnormal regulation of HIF-1alpha, VEGF, [[ BNP ]], and NGF-beta in the hypertrophic myocardium.",900,8
901,"<< Imatinib >> (STI571, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of [[ KIT ]], ABL, BCR-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.",901,0
902,"<< Imatinib >> (STI571, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, [[ ABL ]], BCR-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.",902,0
903,"<< Imatinib >> (STI571, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, [[ BCR ]]-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.",903,0
904,"<< Imatinib >> (STI571, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-[[ ABL ]], PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.",904,0
905,"<< Imatinib >> (STI571, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-ABL, [[ PDGFRA ]], and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.",905,0
906,"<< Imatinib >> (STI571, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-ABL, PDGFRA, and [[ PDGFRB, ]] represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.",906,0
907,"Imatinib (<< STI571 >>, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of [[ KIT ]], ABL, BCR-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.",907,0
908,"Imatinib (<< STI571 >>, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, [[ ABL ]], BCR-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.",908,0
909,"Imatinib (<< STI571 >>, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, [[ BCR ]]-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.",909,0
910,"Imatinib (<< STI571 >>, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-[[ ABL ]], PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.",910,0
911,"Imatinib (<< STI571 >>, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-ABL, [[ PDGFRA ]], and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.",911,0
912,"Imatinib (<< STI571 >>, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-ABL, PDGFRA, and [[ PDGFRB, ]] represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.",912,0
913,"Imatinib (STI571, << Gleevec >>, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of [[ KIT ]], ABL, BCR-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.",913,0
914,"Imatinib (STI571, << Gleevec >>, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, [[ ABL ]], BCR-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.",914,0
915,"Imatinib (STI571, << Gleevec >>, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, [[ BCR ]]-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.",915,0
916,"Imatinib (STI571, << Gleevec >>, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-[[ ABL ]], PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.",916,0
917,"Imatinib (STI571, << Gleevec >>, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-ABL, [[ PDGFRA ]], and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.",917,0
918,"Imatinib (STI571, << Gleevec >>, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-ABL, PDGFRA, and [[ PDGFRB, ]] represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.",918,0
919,"Imatinib (STI571, Gleevec, << Glivec >>; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of [[ KIT ]], ABL, BCR-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.",919,0
920,"Imatinib (STI571, Gleevec, << Glivec >>; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, [[ ABL ]], BCR-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.",920,0
921,"Imatinib (STI571, Gleevec, << Glivec >>; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, [[ BCR ]]-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.",921,0
922,"Imatinib (STI571, Gleevec, << Glivec >>; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-[[ ABL ]], PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.",922,0
923,"Imatinib (STI571, Gleevec, << Glivec >>; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-ABL, [[ PDGFRA ]], and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.",923,0
924,"Imatinib (STI571, Gleevec, << Glivec >>; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-ABL, PDGFRA, and [[ PDGFRB, ]] represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.",924,0
925,"Evaluation of histamine H1-, H2-, and H3-receptor ligands at the human histamine H4 receptor: identification of << 4-methylhistamine >> as the first potent and selective [[ H4 receptor ]] agonist.",925,2
926,"Most of the tested H(2)R agonists and << imidazole >>-based H(3)R ligands show micromolar-to-nanomolar range hH(4)R affinity, and these ligands exert different intrinsic [[ hH(4)R ]] activities, ranging from full agonists to inverse agonists.",926,10
927,"Most of the tested H(2)R agonists and << imidazole >>-based H(3)R ligands show micromolar-to-nanomolar range hH(4)R affinity, and these ligands exert different intrinsic [[ hH(4)R ]] activities, ranging from full agonists to inverse agonists.",927,11
928,"Moreover, << 4-methylhistamine >> potently activated the [[ hH(4)R ]] (pEC(50) = 7.4 +/- 0.1; alpha = 1), and this response was competitively antagonized by the selective H(4)R antagonist JNJ 7777120 [1-[(5-chloro-1H-indol-2-yl)-carbonyl]-4-methylpiperazine] (pA(2) = 7.8).",928,9
929,"Moreover, 4-methylhistamine potently activated the hH(4)R (pEC(50) = 7.4 +/- 0.1; alpha = 1), and this response was competitively antagonized by the selective << H(4)R >> antagonist [[ JNJ 7777120 ]] [1-[(5-chloro-1H-indol-2-yl)-carbonyl]-4-methylpiperazine] (pA(2) = 7.8).",929,1
930,"Moreover, 4-methylhistamine potently activated the hH(4)R (pEC(50) = 7.4 +/- 0.1; alpha = 1), and this response was competitively antagonized by the selective << H(4)R >> antagonist JNJ 7777120 [[[ 1-[(5-chloro-1H-indol-2-yl)-carbonyl]-4-methylpiperazine ]]] (pA(2) = 7.8).",930,1
931,The identification of << 4-methylhistamine >> as a potent [[ H(4)R ]] agonist is of major importance for future studies to unravel the physiological roles of the H(4)R.,931,2
932,"Irinotecan (CPT-11, << 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin >>) has exhibited clinical activities against a broad spectrum of carcinomas by inhibiting [[ DNA topoisomerase I ]] (Topo I).",932,0
933,"Irinotecan (CPT-11, << 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin >>) has exhibited clinical activities against a broad spectrum of carcinomas by inhibiting DNA topoisomerase I ([[ Topo I ]]).",933,0
934,"<< Irinotecan >> (CPT-11, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin) has exhibited clinical activities against a broad spectrum of carcinomas by inhibiting [[ DNA topoisomerase I ]] (Topo I).",934,0
935,"<< Irinotecan >> (CPT-11, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin) has exhibited clinical activities against a broad spectrum of carcinomas by inhibiting DNA topoisomerase I ([[ Topo I ]]).",935,0
936,"Irinotecan (<< CPT-11 >>, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin) has exhibited clinical activities against a broad spectrum of carcinomas by inhibiting [[ DNA topoisomerase I ]] (Topo I).",936,0
937,"Irinotecan (<< CPT-11 >>, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin) has exhibited clinical activities against a broad spectrum of carcinomas by inhibiting DNA topoisomerase I ([[ Topo I ]]).",937,0
938,"Early-onset diarrhea is observed immediately after CPT-11 infusion and probably due to the inhibition of << acetylcholinesterase >> activity, which can be eliminated by administration of [[ atropine ]].",938,9
939,"Early-onset diarrhea is observed immediately after << CPT-11 >> infusion and probably due to the inhibition of [[ acetylcholinesterase ]] activity, which can be eliminated by administration of atropine.",939,0
940,"<< CPT-11 >> and SN-38 may also stimulate the production of pro-inflammatory [[ cytokines ]] and prostaglandins (PGs), thus inducing the secretion of Na(+) and Cl(-).",940,6
941,"CPT-11 and << SN-38 >> may also stimulate the production of pro-inflammatory [[ cytokines ]] and prostaglandins (PGs), thus inducing the secretion of Na(+) and Cl(-).",941,6
942,"<< Pyridoxal kinase >> (PDXK) catalyzes the phosphorylation of [[ pyridoxal ]], pyridoxamine, and pyridoxine in the presence of ATP and Zn2+.",942,5
943,"Pyridoxal kinase (<< PDXK >>) catalyzes the phosphorylation of [[ pyridoxal ]], pyridoxamine, and pyridoxine in the presence of ATP and Zn2+.",943,5
944,"<< Pyridoxal kinase >> (PDXK) catalyzes the phosphorylation of pyridoxal, [[ pyridoxamine ]], and pyridoxine in the presence of ATP and Zn2+.",944,5
945,"Pyridoxal kinase (<< PDXK >>) catalyzes the phosphorylation of pyridoxal, [[ pyridoxamine ]], and pyridoxine in the presence of ATP and Zn2+.",945,5
946,"<< Pyridoxal kinase >> (PDXK) catalyzes the phosphorylation of pyridoxal, pyridoxamine, and [[ pyridoxine ]] in the presence of ATP and Zn2+.",946,5
947,"Pyridoxal kinase (<< PDXK >>) catalyzes the phosphorylation of pyridoxal, pyridoxamine, and [[ pyridoxine ]] in the presence of ATP and Zn2+.",947,5
948,"<< (R)-Roscovitine >> (CYC202, Seliciclib) is a relatively selective inhibitor of [[ cyclin-dependent kinases ]] (CDKs), currently evaluated for the treatment of cancers, neurodegenerative disorders, renal diseases, and several viral infections.",948,0
949,"<< (R)-Roscovitine >> (CYC202, Seliciclib) is a relatively selective inhibitor of cyclin-dependent kinases ([[ CDKs ]]), currently evaluated for the treatment of cancers, neurodegenerative disorders, renal diseases, and several viral infections.",949,0
950,"(R)-Roscovitine (<< CYC202 >>, Seliciclib) is a relatively selective inhibitor of [[ cyclin-dependent kinases ]] (CDKs), currently evaluated for the treatment of cancers, neurodegenerative disorders, renal diseases, and several viral infections.",950,0
951,"(R)-Roscovitine (<< CYC202 >>, Seliciclib) is a relatively selective inhibitor of cyclin-dependent kinases ([[ CDKs ]]), currently evaluated for the treatment of cancers, neurodegenerative disorders, renal diseases, and several viral infections.",951,0
952,"(R)-Roscovitine (CYC202, << Seliciclib >>) is a relatively selective inhibitor of [[ cyclin-dependent kinases ]] (CDKs), currently evaluated for the treatment of cancers, neurodegenerative disorders, renal diseases, and several viral infections.",952,0
953,"(R)-Roscovitine (CYC202, << Seliciclib >>) is a relatively selective inhibitor of cyclin-dependent kinases ([[ CDKs ]]), currently evaluated for the treatment of cancers, neurodegenerative disorders, renal diseases, and several viral infections.",953,0
954,"Using [(3)H]glucosamine-labeled gastric mucosal cells, we show that stimulatory effect of beta-adrenergic agonist, isoproterenol, on << mucin >> secretion was inhibited by EGFR kinase inhibitor, [[ PD153035 ]], as well as wortmannin, a specific inhibitor of PI3K.",954,8
955,"Using [(3)H]glucosamine-labeled gastric mucosal cells, we show that stimulatory effect of beta-adrenergic agonist, isoproterenol, on << mucin >> secretion was inhibited by EGFR kinase inhibitor, PD153035, as well as [[ wortmannin ]], a specific inhibitor of PI3K.",955,8
956,"Using [(3)H]glucosamine-labeled gastric mucosal cells, we show that stimulatory effect of beta-adrenergic agonist, isoproterenol, on mucin secretion was inhibited by << EGFR >> kinase inhibitor, [[ PD153035 ]], as well as wortmannin, a specific inhibitor of PI3K.",956,0
957,"Using [(3)H]glucosamine-labeled gastric mucosal cells, we show that stimulatory effect of beta-adrenergic agonist, isoproterenol, on mucin secretion was inhibited by EGFR << kinase >> inhibitor, [[ PD153035 ]], as well as wortmannin, a specific inhibitor of PI3K.",957,0
958,"Using [(3)H]glucosamine-labeled gastric mucosal cells, we show that stimulatory effect of beta-adrenergic agonist, isoproterenol, on mucin secretion was inhibited by EGFR kinase inhibitor, PD153035, as well as << wortmannin >>, a specific inhibitor of [[ PI3K ]].",958,0
959,"Both inhibitors, moreover, blunted the mucin secretory responses to beta-adrenergic agonist-generated second messenger, cAMP as well as << adenylate cyclase >> activator, [[ forskolin ]].",959,9
960,"Both inhibitors, moreover, blunted the << mucin >> secretory responses to beta-adrenergic agonist-generated second messenger, cAMP as well as adenylate cyclase activator, [[ forskolin ]].",960,8
961,"Both inhibitors, moreover, blunted the mucin secretory responses to beta-adrenergic agonist-generated second messenger, << cAMP >> as well as [[ adenylate cyclase ]] activator, forskolin.",961,5
962,"The gastric mucin secretory responses to isoproterenol, furthermore, were inhibited by << PP2 >>, a selective inhibitor of tyrosine kinase Src responsible for ligand-independent [[ EGFR ]] autophosphorylation, but not by ERK inhibitor, PD98059.",962,9
963,"The << gastric mucin >> secretory responses to isoproterenol, furthermore, were inhibited by [[ PP2 ]], a selective inhibitor of tyrosine kinase Src responsible for ligand-independent EGFR autophosphorylation, but not by ERK inhibitor, PD98059.",963,8
964,"The gastric mucin secretory responses to isoproterenol, furthermore, were inhibited by << PP2 >>, a selective inhibitor of [[ tyrosine kinase ]] Src responsible for ligand-independent EGFR autophosphorylation, but not by ERK inhibitor, PD98059.",964,0
965,"The gastric mucin secretory responses to isoproterenol, furthermore, were inhibited by << PP2 >>, a selective inhibitor of tyrosine kinase [[ Src ]] responsible for ligand-independent EGFR autophosphorylation, but not by ERK inhibitor, PD98059.",965,0
966,"The gastric mucin secretory responses to isoproterenol, furthermore, were inhibited by PP2, a selective inhibitor of tyrosine kinase Src responsible for ligand-independent EGFR autophosphorylation, but not by << ERK >> inhibitor, [[ PD98059 ]].",966,0
967,"The inhibition of << ERK >>, moreover, did not cause attenuation in mucin secretion in response to [[ cAMP ]] and forskolin.",967,0
968,"The inhibition of << ERK >>, moreover, did not cause attenuation in mucin secretion in response to cAMP and [[ forskolin ]].",968,0
969,<< Losartan >>: a selective [[ angiotensin II type 1 (AT1) receptor ]] antagonist for the treatment of heart failure.,969,1
970,<< Losartan >> (COZAAR) is the prototype of a new class of potent and selective [[ angiotensin II (AII) type 1 (AT(1)) receptor ]] antagonists with the largest published preclinical and clinical data base.,970,1
971,Losartan (<< COZAAR >>) is the prototype of a new class of potent and selective [[ angiotensin II (AII) type 1 (AT(1)) receptor ]] antagonists with the largest published preclinical and clinical data base.,971,1
972,<< Losartan >> is well-absorbed orally as an active drug and is rapidly converted via oxidation in the human liver to a more potent metabolite (designated E3174) with an affinity 20- to 30-times greater for the [[ AT(1) receptor ]] (non-competitive inhibition).,972,0
973,"Clinical experience in heart failure is growing, and recent data suggest an improved survival with << losartan >> versus captopril, a drug from the [[ angiotensin-converting-enzyme ]] inhibitor class with proven benefit in this population.",973,0
974,"Clinical experience in heart failure is growing, and recent data suggest an improved survival with losartan versus << captopril >>, a drug from the [[ angiotensin-converting-enzyme ]] inhibitor class with proven benefit in this population.",974,0
975,"The current comprehensive losartan clinical end-point programme (4 large scale morbidity/mortality trials) should provide evidence regarding the efficacy of direct blockade of the << AT(1) receptor >> with [[ losartan ]] compared to standard therapy: 1) The Losartan Heart Failure Survival Study - ELITE II, 2) The Losartan Post-Myocardial Infarction Survival Study - OPTIMAAL, 3) The Losartan Hypertension Survival Study - LIFE and 4) The Losartan Renal Protection Study - RENAAL.",975,0
976,"We now demonstrate that << amrinone >>, a noncatechol inotrope, strongly inhibits lipopolysaccharide (LPS)-induced [[ TNF ]] production at concentrations readily achieved in vivo.",976,8
977,Combined application of << dexamethasone >> and amrinone caused additive inhibition of [[ TNF ]] biosynthesis in vitro.,977,0
978,Combined application of dexamethasone and << amrinone >> caused additive inhibition of [[ TNF ]] biosynthesis in vitro.,978,0
979,"Abrupt removal of << amrinone >> or pentoxifylline from the culture medium prior to LPS stimulation, however, caused significantly augmented [[ TNF ]] production.",979,6
980,"Abrupt removal of amrinone or << pentoxifylline >> from the culture medium prior to LPS stimulation, however, caused significantly augmented [[ TNF ]] production.",980,6
981,"In the present study, age-related changes of << pyridoxal 5'-phosphate >> (PLP) synthesizing enzymes, pyridoxal kinase ([[ PLK ]]) and pyridoxine 5'-phosphate oxidase (PNPO), their protein contents and activities were examined in the gerbil hippocampus proper.",981,4
982,"In the present study, age-related changes of << pyridoxal 5'-phosphate >> (PLP) synthesizing enzymes, pyridoxal kinase (PLK) and [[ pyridoxine 5'-phosphate oxidase ]] (PNPO), their protein contents and activities were examined in the gerbil hippocampus proper.",982,4
983,"In the present study, age-related changes of << pyridoxal 5'-phosphate >> (PLP) synthesizing enzymes, pyridoxal kinase (PLK) and pyridoxine 5'-phosphate oxidase ([[ PNPO ]]), their protein contents and activities were examined in the gerbil hippocampus proper.",983,4
984,"In the present study, age-related changes of << pyridoxal 5'-phosphate >> (PLP) synthesizing enzymes, [[ pyridoxal kinase ]] (PLK) and pyridoxine 5'-phosphate oxidase (PNPO), their protein contents and activities were examined in the gerbil hippocampus proper.",984,4
985,"In the present study, age-related changes of pyridoxal 5'-phosphate (<< PLP >>) synthesizing enzymes, pyridoxal kinase ([[ PLK ]]) and pyridoxine 5'-phosphate oxidase (PNPO), their protein contents and activities were examined in the gerbil hippocampus proper.",985,4
986,"In the present study, age-related changes of pyridoxal 5'-phosphate (<< PLP >>) synthesizing enzymes, pyridoxal kinase (PLK) and [[ pyridoxine 5'-phosphate oxidase ]] (PNPO), their protein contents and activities were examined in the gerbil hippocampus proper.",986,4
987,"In the present study, age-related changes of pyridoxal 5'-phosphate (<< PLP >>) synthesizing enzymes, pyridoxal kinase (PLK) and pyridoxine 5'-phosphate oxidase ([[ PNPO ]]), their protein contents and activities were examined in the gerbil hippocampus proper.",987,4
988,"In the present study, age-related changes of pyridoxal 5'-phosphate (<< PLP >>) synthesizing enzymes, [[ pyridoxal kinase ]] (PLK) and pyridoxine 5'-phosphate oxidase (PNPO), their protein contents and activities were examined in the gerbil hippocampus proper.",988,4
989,"Therefore, decreases of << PLK >> and PNPO in the hippocampal CA1 region of aged brains may be involved in aging processes related with [[ gamma-aminobutyric acid ]] (GABA) function.",989,8
990,"Therefore, decreases of PLK and << PNPO >> in the hippocampal CA1 region of aged brains may be involved in aging processes related with [[ gamma-aminobutyric acid ]] (GABA) function.",990,8
991,"Therefore, decreases of << PLK >> and PNPO in the hippocampal CA1 region of aged brains may be involved in aging processes related with gamma-aminobutyric acid ([[ GABA ]]) function.",991,8
992,"Therefore, decreases of PLK and << PNPO >> in the hippocampal CA1 region of aged brains may be involved in aging processes related with gamma-aminobutyric acid ([[ GABA ]]) function.",992,8
993,"This process was reduced by a protonophore, carbonylcyanide p-trifluoromethoxyphenylhydrazone, and a typical << monocarboxylate transporter >> (MCT) inhibitor, [[ alpha-cyano-4-hydroxycinnamic acid ]], suggesting that nicotinate uptake by rat astrocytes is mediated by H(+)-coupled monocarboxylate transport system.",993,0
994,"This process was reduced by a protonophore, carbonylcyanide p-trifluoromethoxyphenylhydrazone, and a typical monocarboxylate transporter (<< MCT >>) inhibitor, [[ alpha-cyano-4-hydroxycinnamic acid ]], suggesting that nicotinate uptake by rat astrocytes is mediated by H(+)-coupled monocarboxylate transport system.",994,0
995,"This process was reduced by a protonophore, carbonylcyanide p-trifluoromethoxyphenylhydrazone, and a typical monocarboxylate transporter (MCT) inhibitor, alpha-cyano-4-hydroxycinnamic acid, suggesting that << nicotinate >> uptake by rat astrocytes is mediated by H(+)-coupled [[ monocarboxylate transport system ]].",995,5
996,"Because l-lactate reduced to 67% of the nicotinate uptake even at 10mM, it is unlikely that << nicotinate >> uptake in rat astrocytes is mediated by [[ MCT1 ]] and/or MCT2.",996,5
997,"Because l-lactate reduced to 67% of the nicotinate uptake even at 10mM, it is unlikely that << nicotinate >> uptake in rat astrocytes is mediated by MCT1 and/or [[ MCT2 ]].",997,5
998,"These results provide biochemical evidence of a H(+)-coupled and saturable transport system, presumed to be a << low-affinity monocarboxylate transporter >> MCT4 or other unknown H(+)-coupled monocarboxylate transport system, for [[ nicotinate ]] in rat cerebrocortical astrocytes.",998,5
999,"These results provide biochemical evidence of a H(+)-coupled and saturable transport system, presumed to be a low-affinity monocarboxylate transporter << MCT4 >> or other unknown H(+)-coupled monocarboxylate transport system, for [[ nicotinate ]] in rat cerebrocortical astrocytes.",999,5
1000,"These results provide biochemical evidence of a H(+)-coupled and saturable transport system, presumed to be a low-affinity monocarboxylate transporter MCT4 or other unknown << H(+)-coupled monocarboxylate transport system >>, for [[ nicotinate ]] in rat cerebrocortical astrocytes.",1000,5
1001,"A review of the structural and functional features of << olmesartan medoxomil >>, an [[ angiotensin receptor ]] blocker.",1001,0
1002,"The marked antihypertensive efficacy of << olmesartan medoxomil >> may result from a unique pharmacological interaction of the drug with the AT1 receptor, resulting in a potent, long-lasting, dose-dependent blockade of [[ A-II ]].",1002,0
1003,Effects of << granulocyte colony-stimulating factor >> (G-CSF) and neutrophil elastase inhibitor ([[ ONO-5046 ]]) on acid-induced lung injury in rats.,1003,0
1004,Effects of granulocyte colony-stimulating factor (<< G-CSF >>) and neutrophil elastase inhibitor ([[ ONO-5046 ]]) on acid-induced lung injury in rats.,1004,0
1005,Effects of granulocyte colony-stimulating factor (G-CSF) and << neutrophil elastase >> inhibitor ([[ ONO-5046 ]]) on acid-induced lung injury in rats.,1005,0
1006,"We examined the effects of the high dose of granulocyte-colony stimulating factor (G-CSF), which is capable of increasing peripheral neutrophils, and a specific << neutrophil elastase >> inhibitor ([[ ONO-5046 ]]) on acid lung injury in rats.",1006,0
1007,"<< Miglustat >>, an imino sugar that reversibly inhibits [[ glucosylceramide synthase ]] and reduces intracellular substrate burden, is an oral treatment for patients with type 1 GD that was recently approved in the United States for symptomatic patients with mild to moderate clinical manifestations for whom ERT is not an option.",1007,0
1008,"Miglustat, an << imino sugar >> that reversibly inhibits [[ glucosylceramide synthase ]] and reduces intracellular substrate burden, is an oral treatment for patients with type 1 GD that was recently approved in the United States for symptomatic patients with mild to moderate clinical manifestations for whom ERT is not an option.",1008,0
1009,"Nicotinic-receptor potentiator drugs, huprine X and << galantamine >>, increase ACh release by blocking [[ AChE ]] activity but not acting on nicotinic receptors.",1009,0
1010,"This effect was reverted in the presence of << atropine >> (ATR; 0.1 microM), which blocks the pre-synaptic [[ muscarinic M2 receptor ]].",1010,0
1011,"This effect was reverted in the presence of atropine (<< ATR >>; 0.1 microM), which blocks the pre-synaptic [[ muscarinic M2 receptor ]].",1011,0
1012,"After that, a wide range of concentrations of drugs, concomitantly with ATR (0.1 microM), was studied in the presence of << haloperidol >> (HAL; 0.01 microM), a [[ dopamine D2 ]] antagonist.",1012,1
1013,"After that, a wide range of concentrations of drugs, concomitantly with ATR (0.1 microM), was studied in the presence of haloperidol (<< HAL >>; 0.01 microM), a [[ dopamine D2 ]] antagonist.",1013,1
1014,"To test the role of << nicotinic receptors >> in the drugs' effects on [3H]-ACh release, [[ mecamylamine ]] (MEC) 100 microM was used to block such receptors.",1014,0
1015,"To test the role of << nicotinic receptors >> in the drugs' effects on [3H]-ACh release, mecamylamine ([[ MEC ]]) 100 microM was used to block such receptors.",1015,0
1016,"mRNA levels for << RAR-alpha >>, RAR-beta and RAR-gamma, the nuclear receptors for retinoic acid, decreased during activation of freshly isolated HSC even with [[ retinoid ]] supplementation.",1016,8
1017,"mRNA levels for RAR-alpha, << RAR-beta >> and RAR-gamma, the nuclear receptors for retinoic acid, decreased during activation of freshly isolated HSC even with [[ retinoid ]] supplementation.",1017,8
1018,"mRNA levels for RAR-alpha, RAR-beta and << RAR-gamma >>, the nuclear receptors for retinoic acid, decreased during activation of freshly isolated HSC even with [[ retinoid ]] supplementation.",1018,8
1019,"mRNA levels for RAR-alpha, RAR-beta and RAR-gamma, the << nuclear receptors >> for retinoic acid, decreased during activation of freshly isolated HSC even with [[ retinoid ]] supplementation.",1019,8
1020,"Preincubation (30 min) of bovine tracheal smooth muscle with various concentrations (0.1, 1 and 10 microM) of << fenoterol >> decreased isoprenaline-induced maximal relaxation (E(max)) of methacholine-contracted preparations in a concentration dependent fashion, indicating desensitization of the [[ beta(2)-adrenoceptor ]].",1020,3
1021,"Preincubation (30 min) of bovine tracheal smooth muscle with various concentrations (0.1, 1 and 10 microM) of fenoterol decreased << isoprenaline >>-induced maximal relaxation (E(max)) of methacholine-contracted preparations in a concentration dependent fashion, indicating desensitization of the [[ beta(2)-adrenoceptor ]].",1021,2
1022,"Preincubation with 1 microM of the << protein kinase C >> (PKC) activator phorbol 12-myristate 13-acetate ([[ PMA ]]) caused a small but significant decrease in isoprenaline-induced E(max), indicating activated PKC-mediated heterologous beta(2)-adrenoceptor desensitization.",1022,9
1023,"Preincubation with 1 microM of the protein kinase C (<< PKC >>) activator phorbol 12-myristate 13-acetate ([[ PMA ]]) caused a small but significant decrease in isoprenaline-induced E(max), indicating activated PKC-mediated heterologous beta(2)-adrenoceptor desensitization.",1023,9
1024,"Preincubation with 1 microM of the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (<< PMA >>) caused a small but significant decrease in isoprenaline-induced E(max), indicating activated [[ PKC ]]-mediated heterologous beta(2)-adrenoceptor desensitization.",1024,9
1025,"Preincubation with 1 microM of the << protein kinase C >> (PKC) activator [[ phorbol 12-myristate 13-acetate ]] (PMA) caused a small but significant decrease in isoprenaline-induced E(max), indicating activated PKC-mediated heterologous beta(2)-adrenoceptor desensitization.",1025,9
1026,"Preincubation with 1 microM of the protein kinase C (<< PKC >>) activator [[ phorbol 12-myristate 13-acetate ]] (PMA) caused a small but significant decrease in isoprenaline-induced E(max), indicating activated PKC-mediated heterologous beta(2)-adrenoceptor desensitization.",1026,9
1027,"Preincubation with 1 microM of the protein kinase C (PKC) activator << phorbol 12-myristate 13-acetate >> (PMA) caused a small but significant decrease in isoprenaline-induced E(max), indicating activated [[ PKC ]]-mediated heterologous beta(2)-adrenoceptor desensitization.",1027,9
1028,"Preincubation with 1 microM of the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (<< PMA >>) caused a small but significant decrease in isoprenaline-induced E(max), indicating activated PKC-mediated heterologous [[ beta(2)-adrenoceptor ]] desensitization.",1028,3
1029,"Preincubation with 1 microM of the protein kinase C (PKC) activator << phorbol 12-myristate 13-acetate >> (PMA) caused a small but significant decrease in isoprenaline-induced E(max), indicating activated PKC-mediated heterologous [[ beta(2)-adrenoceptor ]] desensitization.",1029,3
1030,"Preincubation with 1 microM of the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) caused a small but significant decrease in << isoprenaline >>-induced E(max), indicating activated PKC-mediated heterologous [[ beta(2)-adrenoceptor ]] desensitization.",1030,2
1031,"Moreover, the specific << PKC >>-inhibitor [[ 2-[1-(3-dimethylaminopropyl)-1H-indol-3-yl]-3-(1H-indol-3-yl) maleimide ]] (GF 109203X) markedly increased the potency and E(max) of isoprenaline for all conditions used, including control conditions, and the synergistic effects of PMA and fenoterol were completely prevented.",1031,0
1032,"Moreover, the specific << PKC >>-inhibitor 2-[1-(3-dimethylaminopropyl)-1H-indol-3-yl]-3-(1H-indol-3-yl) maleimide ([[ GF 109203X ]]) markedly increased the potency and E(max) of isoprenaline for all conditions used, including control conditions, and the synergistic effects of PMA and fenoterol were completely prevented.",1032,0
1033,"Tyrosine kinase inhibitors are << quinazoline >>-derived, low molecular weight synthetic molecules that can block the intracellular tyrosine kinase domain of several receptors, including EGFR, Erb2, and vascular endothelial growth factor receptor, and thereby inhibit ligand-induced receptor phosphorylation and abrogate the biologic effect of [[ EGFR ]] signaling.",1033,8
1034,"<< Tyrosine kinase >> inhibitors are [[ quinazoline ]]-derived, low molecular weight synthetic molecules that can block the intracellular tyrosine kinase domain of several receptors, including EGFR, Erb2, and vascular endothelial growth factor receptor, and thereby inhibit ligand-induced receptor phosphorylation and abrogate the biologic effect of EGFR signaling.",1034,0
1035,"Tyrosine kinase inhibitors are << quinazoline >>-derived, low molecular weight synthetic molecules that can block the intracellular [[ tyrosine kinase domain ]] of several receptors, including EGFR, Erb2, and vascular endothelial growth factor receptor, and thereby inhibit ligand-induced receptor phosphorylation and abrogate the biologic effect of EGFR signaling.",1035,0
1036,"Tyrosine kinase inhibitors are << quinazoline >>-derived, low molecular weight synthetic molecules that can block the intracellular tyrosine kinase domain of several receptors, including [[ EGFR ]], Erb2, and vascular endothelial growth factor receptor, and thereby inhibit ligand-induced receptor phosphorylation and abrogate the biologic effect of EGFR signaling.",1036,0
1037,"Tyrosine kinase inhibitors are << quinazoline >>-derived, low molecular weight synthetic molecules that can block the intracellular tyrosine kinase domain of several receptors, including EGFR, [[ Erb2 ]], and vascular endothelial growth factor receptor, and thereby inhibit ligand-induced receptor phosphorylation and abrogate the biologic effect of EGFR signaling.",1037,0
1038,"Tyrosine kinase inhibitors are << quinazoline >>-derived, low molecular weight synthetic molecules that can block the intracellular tyrosine kinase domain of several receptors, including EGFR, Erb2, and [[ vascular endothelial growth factor receptor ]], and thereby inhibit ligand-induced receptor phosphorylation and abrogate the biologic effect of EGFR signaling.",1038,0
1039,"When expressed heterologously in a mammalian cell line, << rabbit PAT1 >> mediates pH-dependent, Na(+)-independent uptake of [[ proline ]], glycine, l-alanine and alpha-(methylamino)isobutyric acid.",1039,5
1040,"When expressed heterologously in a mammalian cell line, << rabbit PAT1 >> mediates pH-dependent, Na(+)-independent uptake of proline, [[ glycine ]], l-alanine and alpha-(methylamino)isobutyric acid.",1040,5
1041,"When expressed heterologously in a mammalian cell line, << rabbit PAT1 >> mediates pH-dependent, Na(+)-independent uptake of proline, glycine, [[ l-alanine ]] and alpha-(methylamino)isobutyric acid.",1041,5
1042,"When expressed heterologously in a mammalian cell line, << rabbit PAT1 >> mediates pH-dependent, Na(+)-independent uptake of proline, glycine, l-alanine and [[ alpha-(methylamino)isobutyric acid ]].",1042,5
1043,"In the presence of Na+ and under conditions in which << PAT1 >> transport function was suppressed, a second [[ proline ]] uptake system was detected that exhibited functional characteristics similar to those of the IMINO system.",1043,5
1044,"The functional characteristics of rabbit PAT1 in either mammalian cells or renal BBMV suggest that << PAT1 >> is the low-affinity transporter of [[ proline ]], glycine and hydroxyproline believed to be defective in patients with iminoglycinuria.",1044,5
1045,"The functional characteristics of rabbit PAT1 in either mammalian cells or renal BBMV suggest that << PAT1 >> is the low-affinity transporter of proline, [[ glycine ]] and hydroxyproline believed to be defective in patients with iminoglycinuria.",1045,5
1046,"The functional characteristics of rabbit PAT1 in either mammalian cells or renal BBMV suggest that << PAT1 >> is the low-affinity transporter of proline, glycine and [[ hydroxyproline ]] believed to be defective in patients with iminoglycinuria.",1046,5
1047,The fact that << trimipramine >> also suppressed [[ IFN-gamma ]] production and T-cell proliferation indicates that these immunomodulatory actions of antidepressants are most likely unrelated to inhibition of monoamine reuptake.,1047,8
1048,"The mean body weight at baseline (52.59 kg) did not differ significantly from that at 1 week after treatment (52.84 kg; P > .05), but the mean << leptin >> level after 1 week of treatment with [[ cyproheptadine ]] (3.14 ng/mL) was 14.2% higher than that at baseline (2.75 ng/mL; P < .05).",1048,6
1049,Comparison of << captopril >> and enalapril to study the role of the sulfhydryl-group in improvement of endothelial dysfunction with [[ ACE ]] inhibitors in high dieted methionine mice.,1049,0
1050,Comparison of captopril and << enalapril >> to study the role of the sulfhydryl-group in improvement of endothelial dysfunction with [[ ACE ]] inhibitors in high dieted methionine mice.,1050,0
1051,Comparison of captopril and enalapril to study the role of the << sulfhydryl >>-group in improvement of endothelial dysfunction with [[ ACE ]] inhibitors in high dieted methionine mice.,1051,0
1052,"We compared the effects of << Captopril >> (an [[ ACE ]] inhibitor with -SH group), enalapril (an ACE-inhibitor without -SH group), N-acetylcysteine (only -SH group not ACE inhibitor) on endothelial dysfunction injured by methionine-induced hyperhomocysteinemia (HHcy) in rats.",1052,0
1053,"We compared the effects of Captopril (an << ACE >> inhibitor with -[[ SH ]] group), enalapril (an ACE-inhibitor without -SH group), N-acetylcysteine (only -SH group not ACE inhibitor) on endothelial dysfunction injured by methionine-induced hyperhomocysteinemia (HHcy) in rats.",1053,0
1054,"We compared the effects of Captopril (an ACE inhibitor with -SH group), << enalapril >> (an [[ ACE ]]-inhibitor without -SH group), N-acetylcysteine (only -SH group not ACE inhibitor) on endothelial dysfunction injured by methionine-induced hyperhomocysteinemia (HHcy) in rats.",1054,0
1055,"It was found that a single intragastric gavage by << L-methionine >> resulted in inhibition of endothelium-dependent relaxation, markedly increased the serum level of malondialdehyde and decreased the activity of [[ PON1 ]] and SOD, similarly decreased the level of NO in the serum; but had no effects on endothelium-independent relaxation and angiotensin-converting enzyme activity compared with the control group.",1055,0
1056,"It was found that a single intragastric gavage by << L-methionine >> resulted in inhibition of endothelium-dependent relaxation, markedly increased the serum level of malondialdehyde and decreased the activity of PON1 and [[ SOD ]], similarly decreased the level of NO in the serum; but had no effects on endothelium-independent relaxation and angiotensin-converting enzyme activity compared with the control group.",1056,0
1057,"Given the treatment with three doses of << Captopril >> (15 approximately 45 mg/kg) markedly attenuated inhibition of vasodilator responses to ACh, and eliminated the increased level of malondialdehyde, the decreased level of NO, activity of [[ PON1 ]] and SOD in serum by single intragastric gavaged L-methionine.",1057,9
1058,"Given the treatment with three doses of << Captopril >> (15 approximately 45 mg/kg) markedly attenuated inhibition of vasodilator responses to ACh, and eliminated the increased level of malondialdehyde, the decreased level of NO, activity of PON1 and [[ SOD ]] in serum by single intragastric gavaged L-methionine.",1058,9
1059,"These results suggested that Captopril can protect the vascular endothelium against the damages induced by L-methionine in rats, and the beneficial effects of << Captopril >> may be related to attenuating the decrease in [[ PON1 ]] activity and NO levels.",1059,9
1060,"These results suggested that Captopril can protect the vascular endothelium against the damages induced by << L-methionine >> in rats, and the beneficial effects of Captopril may be related to attenuating the decrease in [[ PON1 ]] activity and NO levels.",1060,0
1061,"<< Sorafenib >>, which belongs chemically to a class that can be described as bis-aryl ureas, was selected for further pharmacologic characterization based on potent inhibition of [[ Raf-1 ]] and its favorable kinase selectivity profile.",1061,0
1062,"<< Sorafenib >>, which belongs chemically to a class that can be described as bis-aryl ureas, was selected for further pharmacologic characterization based on potent inhibition of Raf-1 and its favorable [[ kinase ]] selectivity profile.",1062,0
1063,"Sorafenib, which belongs chemically to a class that can be described as << bis-aryl ureas >>, was selected for further pharmacologic characterization based on potent inhibition of [[ Raf-1 ]] and its favorable kinase selectivity profile.",1063,0
1064,"Sorafenib, which belongs chemically to a class that can be described as << bis-aryl ureas >>, was selected for further pharmacologic characterization based on potent inhibition of Raf-1 and its favorable [[ kinase ]] selectivity profile.",1064,0
1065,Further characterization showed that << sorafenib >> suppresses both wild-type and [[ V599E ]] mutant B-Raf activity in vitro.,1065,0
1066,Further characterization showed that << sorafenib >> suppresses both wild-type and V599E mutant [[ B-Raf ]] activity in vitro.,1066,0
1067,"In addition, << sorafenib >> demonstrated significant activity against several receptor tyrosine kinases involved in neovascularization and tumor progression, including vascular-endothelial growth factor (VEGFR)-2, [[ VEGFR-3 ]], platelet-derived growth factor (PDGFR)-beta Flt-3, and c-KIT.",1067,7
1068,"In addition, << sorafenib >> demonstrated significant activity against several receptor tyrosine kinases involved in neovascularization and tumor progression, including vascular-endothelial growth factor (VEGFR)-2, VEGFR-3, [[ platelet-derived growth factor (PDGFR)-beta ]] Flt-3, and c-KIT.",1068,7
1069,"In addition, << sorafenib >> demonstrated significant activity against several receptor tyrosine kinases involved in neovascularization and tumor progression, including vascular-endothelial growth factor (VEGFR)-2, VEGFR-3, platelet-derived growth factor (PDGFR)-beta [[ Flt-3 ]], and c-KIT.",1069,7
1070,"In addition, << sorafenib >> demonstrated significant activity against several receptor tyrosine kinases involved in neovascularization and tumor progression, including vascular-endothelial growth factor (VEGFR)-2, VEGFR-3, platelet-derived growth factor (PDGFR)-beta Flt-3, and [[ c-KIT ]].",1070,7
1071,"In addition, << sorafenib >> demonstrated significant activity against several [[ receptor tyrosine kinases ]] involved in neovascularization and tumor progression, including vascular-endothelial growth factor (VEGFR)-2, VEGFR-3, platelet-derived growth factor (PDGFR)-beta Flt-3, and c-KIT.",1071,7
1072,"In addition, << sorafenib >> demonstrated significant activity against several receptor tyrosine kinases involved in neovascularization and tumor progression, including [[ vascular-endothelial growth factor (VEGFR)-2 ]], VEGFR-3, platelet-derived growth factor (PDGFR)-beta Flt-3, and c-KIT.",1072,7
1073,"A selective << retinoid X receptor >> agonist [[ bexarotene ]] (LGD1069, targretin) inhibits angiogenesis and metastasis in solid tumours.",1073,2
1074,"A selective << retinoid X receptor >> agonist bexarotene ([[ LGD1069 ]], targretin) inhibits angiogenesis and metastasis in solid tumours.",1074,2
1075,"A selective << retinoid X receptor >> agonist bexarotene (LGD1069, [[ targretin ]]) inhibits angiogenesis and metastasis in solid tumours.",1075,2
1076,The present study determined the influence of a << retinoid X receptor >> agonist [[ bexarotene ]] on angiogenesis and metastasis in solid tumours.,1076,2
1077,Analysis of tumour-conditioned medium indicated that << bexarotene >> decreased the secretion of angiogenic factors and matrix metalloproteinases and increased the tissue inhibitor of [[ matrix metalloproteinases ]].,1077,6
1078,Analysis of tumour-conditioned medium indicated that << bexarotene >> decreased the secretion of angiogenic factors and [[ matrix metalloproteinases ]] and increased the tissue inhibitor of matrix metalloproteinases.,1078,8
1079,The ability of << bexarotene >> to inhibit angiogenesis and metastasis was dependent on activation of its heterodimerisation partner [[ peroxisome proliferator-activated receptor gamma ]].,1079,9
1080,In subjects with dysmenorrhea the increase in pain following the administration of << vasopressin >> was significantly lower during [[ atosiban ]] than during placebo infusion.,1080,8
1081,"CONCLUSIONS: << Atosiban >> reduces [[ vasopressin ]]-induced intrauterine pressure in both healthy volunteers and dysmenorrheics, and reported pain in subjects with dysmenorrhea.",1081,8
1082,"Novel highly affine histamine H3 receptor ligands with additional inhibitory effects on the main histamine metabolizing enzyme in the brain, N-methyltransferase, chemically show structural elements of the << acetylcholinesterase >> inhibitor [[ tacrine ]].",1082,0
1083,"Novel highly affine histamine H3 receptor ligands with additional inhibitory effects on the main << histamine >> metabolizing enzyme in the brain, [[ N-methyltransferase ]], chemically show structural elements of the acetylcholinesterase inhibitor tacrine.",1083,5
1084,Some of the new compounds proved in a slightly modified colorimetric Ellmann's assay to be potent inhibitors of << acetylcholinesterase >> and of butyrylcholinesterase which is another catalytic enzyme hydrolysing [[ acetylcholine ]].,1084,5
1085,Some of the new compounds proved in a slightly modified colorimetric Ellmann's assay to be potent inhibitors of acetylcholinesterase and of << butyrylcholinesterase >> which is another catalytic enzyme hydrolysing [[ acetylcholine ]].,1085,5
1086,"For some, pharmacologic inhibitors are available, including << sorafenib >> for [[ BRAF ]], farnesyltransferase inhibitors for NRAS, PD-0325901 for mitogen-activated protein kinase/extracellular signal-regulated kinase kinase, rapamycin analogues for mammalian target of rapamycin, and agents that inhibit either vascular endothelial growth factor or its receptors.",1086,0
1087,"For some, pharmacologic inhibitors are available, including sorafenib for BRAF, farnesyltransferase inhibitors for NRAS, << PD-0325901 >> for [[ mitogen-activated protein kinase ]]/extracellular signal-regulated kinase kinase, rapamycin analogues for mammalian target of rapamycin, and agents that inhibit either vascular endothelial growth factor or its receptors.",1087,0
1088,"For some, pharmacologic inhibitors are available, including sorafenib for BRAF, farnesyltransferase inhibitors for NRAS, << PD-0325901 >> for mitogen-activated protein kinase/[[ extracellular signal-regulated kinase kinase ]], rapamycin analogues for mammalian target of rapamycin, and agents that inhibit either vascular endothelial growth factor or its receptors.",1088,0
1089,"For some, pharmacologic inhibitors are available, including sorafenib for BRAF, farnesyltransferase inhibitors for NRAS, PD-0325901 for mitogen-activated protein kinase/extracellular signal-regulated kinase kinase, << rapamycin >> analogues for [[ mammalian target of rapamycin ]], and agents that inhibit either vascular endothelial growth factor or its receptors.",1089,0
1090,"This aminophospholipid ""<< flippase >>"" selectively transports [[ PS ]] to the cytosolic leaflet of the bilayer and is sensitive to vanadate, Ca(2+), and modification by sulfhydryl reagents.",1090,5
1091,"The purified << Atp8a1 >> is inactive in detergent micelles or in micelles containing phosphatidylcholine, phosphatidic acid, or phosphatidylinositol, is minimally activated by [[ phosphatidylglycerol ]] or phosphatidylethanolamine (PE), and is maximally activated by PS.",1091,9
1092,"The purified << Atp8a1 >> is inactive in detergent micelles or in micelles containing phosphatidylcholine, phosphatidic acid, or phosphatidylinositol, is minimally activated by phosphatidylglycerol or [[ phosphatidylethanolamine ]] (PE), and is maximally activated by PS.",1092,9
1093,"The purified << Atp8a1 >> is inactive in detergent micelles or in micelles containing phosphatidylcholine, phosphatidic acid, or phosphatidylinositol, is minimally activated by phosphatidylglycerol or phosphatidylethanolamine ([[ PE ]]), and is maximally activated by PS.",1093,9
1094,"The purified << Atp8a1 >> is inactive in detergent micelles or in micelles containing phosphatidylcholine, phosphatidic acid, or phosphatidylinositol, is minimally activated by phosphatidylglycerol or phosphatidylethanolamine (PE), and is maximally activated by [[ PS ]].",1094,9
1095,"Similar to the << plasma membrane PS transporter >>, Atp8a1 is activated only by the naturally occurring [[ sn-1,2-glycerol ]] isomer of PS and not the sn-2,3-glycerol stereoisomer.",1095,9
1096,"Similar to the plasma membrane PS transporter, << Atp8a1 >> is activated only by the naturally occurring [[ sn-1,2-glycerol ]] isomer of PS and not the sn-2,3-glycerol stereoisomer.",1096,9
1097,"Activation of << Atp8a1 >> is also reduced by these modifications; [[ phosphatidylserine-O-methyl ester ]], lysophosphatidylserine, glycerophosphoserine, and phosphoserine, which are not transported by the plasma membrane flippase, do not activate Atp8a1.",1097,3
1098,"Activation of << Atp8a1 >> is also reduced by these modifications; phosphatidylserine-O-methyl ester, [[ lysophosphatidylserine ]], glycerophosphoserine, and phosphoserine, which are not transported by the plasma membrane flippase, do not activate Atp8a1.",1098,3
1099,"Activation of << Atp8a1 >> is also reduced by these modifications; phosphatidylserine-O-methyl ester, lysophosphatidylserine, [[ glycerophosphoserine ]], and phosphoserine, which are not transported by the plasma membrane flippase, do not activate Atp8a1.",1099,3
1100,"Activation of << Atp8a1 >> is also reduced by these modifications; phosphatidylserine-O-methyl ester, lysophosphatidylserine, glycerophosphoserine, and [[ phosphoserine ]], which are not transported by the plasma membrane flippase, do not activate Atp8a1.",1100,3
1101,"Weakly translocated lipids (<< PE >>, phosphatidylhydroxypropionate, and phosphatidylhomoserine) are also weak [[ Atp8a1 ]] activators.",1101,9
1102,"Weakly translocated lipids (PE, << phosphatidylhydroxypropionate >>, and phosphatidylhomoserine) are also weak [[ Atp8a1 ]] activators.",1102,9
1103,"Weakly translocated lipids (PE, phosphatidylhydroxypropionate, and << phosphatidylhomoserine >>) are also weak [[ Atp8a1 ]] activators.",1103,9
1104,"However, << N-methyl-phosphatidylserine >>, which is transported by the plasma membrane [[ flippase ]] at a rate equivalent to PS, is incapable of activating Atp8a1 activity.",1104,5
1105,"These results indicate that the << ATPase >> activity of the secretory granule Atp8a1 is activated by phospholipids binding to a specific site whose properties ([[ PS ]] selectivity, dependence upon glycerol but not serine, stereochemistry, and vanadate sensitivity) are similar to, but distinct from, the properties of the substrate binding site of the plasma membrane flippase.",1105,9
1106,"These results indicate that the ATPase activity of the secretory granule << Atp8a1 >> is activated by phospholipids binding to a specific site whose properties ([[ PS ]] selectivity, dependence upon glycerol but not serine, stereochemistry, and vanadate sensitivity) are similar to, but distinct from, the properties of the substrate binding site of the plasma membrane flippase.",1106,9
1107,<< Sorafenib >> (BAY 43-9006) is a small-molecule inhibitor that has been shown to target members of multiple classes of [[ tyrosine kinases ]] that are known to be involved in tumor cell proliferation and tumor angiogenesis.,1107,0
1108,Sorafenib (<< BAY 43-9006 >>) is a small-molecule inhibitor that has been shown to target members of multiple classes of [[ tyrosine kinases ]] that are known to be involved in tumor cell proliferation and tumor angiogenesis.,1108,0
1109,<< Hydrogen sulfide >> inhibits nitric oxide production and [[ nuclear factor-kappaB ]] via heme oxygenase-1 expression in RAW264.7 macrophages stimulated with lipopolysaccharide.,1109,0
1110,"Hydrogen sulfide (<< H(2)S >>), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase ([[ CSE ]]) and/or cystathionine beta-synthase (CBS) from L-cysteine (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.",1110,4
1111,"Hydrogen sulfide (<< H(2)S >>), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase (CSE) and/or [[ cystathionine beta-synthase ]] (CBS) from L-cysteine (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.",1111,4
1112,"Hydrogen sulfide (<< H(2)S >>), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase (CSE) and/or cystathionine beta-synthase ([[ CBS ]]) from L-cysteine (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.",1112,4
1113,"Hydrogen sulfide (<< H(2)S >>), a regulatory gaseous molecule that is endogenously synthesized by [[ cystathionine gamma-lyase ]] (CSE) and/or cystathionine beta-synthase (CBS) from L-cysteine (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.",1113,4
1114,"<< Hydrogen sulfide >> (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase ([[ CSE ]]) and/or cystathionine beta-synthase (CBS) from L-cysteine (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.",1114,4
1115,"<< Hydrogen sulfide >> (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase (CSE) and/or [[ cystathionine beta-synthase ]] (CBS) from L-cysteine (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.",1115,4
1116,"<< Hydrogen sulfide >> (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase (CSE) and/or cystathionine beta-synthase ([[ CBS ]]) from L-cysteine (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.",1116,4
1117,"<< Hydrogen sulfide >> (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by [[ cystathionine gamma-lyase ]] (CSE) and/or cystathionine beta-synthase (CBS) from L-cysteine (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.",1117,4
1118,"Hydrogen sulfide (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase (<< CSE >>) and/or cystathionine beta-synthase (CBS) from [[ L-cysteine ]] (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.",1118,5
1119,"Hydrogen sulfide (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase (CSE) and/or << cystathionine beta-synthase >> (CBS) from [[ L-cysteine ]] (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.",1119,5
1120,"Hydrogen sulfide (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase (CSE) and/or cystathionine beta-synthase (<< CBS >>) from [[ L-cysteine ]] (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.",1120,5
1121,"Hydrogen sulfide (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by << cystathionine gamma-lyase >> (CSE) and/or cystathionine beta-synthase (CBS) from [[ L-cysteine ]] (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.",1121,5
1122,"Hydrogen sulfide (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase (<< CSE >>) and/or cystathionine beta-synthase (CBS) from L-cysteine ([[ L-Cys ]]) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.",1122,5
1123,"Hydrogen sulfide (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase (CSE) and/or << cystathionine beta-synthase >> (CBS) from L-cysteine ([[ L-Cys ]]) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.",1123,5
1124,"Hydrogen sulfide (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase (CSE) and/or cystathionine beta-synthase (<< CBS >>) from L-cysteine ([[ L-Cys ]]) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.",1124,5
1125,"Hydrogen sulfide (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by << cystathionine gamma-lyase >> (CSE) and/or cystathionine beta-synthase (CBS) from L-cysteine ([[ L-Cys ]]) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.",1125,5
1126,"Here, we show that at noncytotoxic concentrations, << H(2)S >> was able to inhibit NO production and [[ inducible NO synthase ]] (iNOS) expression via heme oxygenase (HO-1) expression in RAW264.7 macrophages stimulated with lipopolysaccharide (LPS).",1126,8
1127,"Here, we show that at noncytotoxic concentrations, << H(2)S >> was able to inhibit NO production and inducible NO synthase ([[ iNOS ]]) expression via heme oxygenase (HO-1) expression in RAW264.7 macrophages stimulated with lipopolysaccharide (LPS).",1127,8
1128,"Here, we show that at noncytotoxic concentrations, H(2)S was able to inhibit << NO >> production and [[ inducible NO synthase ]] (iNOS) expression via heme oxygenase (HO-1) expression in RAW264.7 macrophages stimulated with lipopolysaccharide (LPS).",1128,4
1129,"Here, we show that at noncytotoxic concentrations, H(2)S was able to inhibit << NO >> production and inducible NO synthase ([[ iNOS ]]) expression via heme oxygenase (HO-1) expression in RAW264.7 macrophages stimulated with lipopolysaccharide (LPS).",1129,4
1130,"Both << H(2)S >> solution prepared by bubbling pure H(2)S gas and NaSH, a H(2)S donor, dose dependently induced HO-1 expression through the activation of the [[ extracellular signal-regulated kinase ]] (ERK).",1130,9
1131,"Both << H(2)S >> solution prepared by bubbling pure H(2)S gas and NaSH, a H(2)S donor, dose dependently induced HO-1 expression through the activation of the extracellular signal-regulated kinase ([[ ERK ]]).",1131,9
1132,"Both << H(2)S >> solution prepared by bubbling pure H(2)S gas and NaSH, a H(2)S donor, dose dependently induced [[ HO-1 ]] expression through the activation of the extracellular signal-regulated kinase (ERK).",1132,6
1133,Pretreatment with << H(2)S >> or NaHS significantly inhibited LPS-induced [[ iNOS ]] expression and NO production.,1133,8
1134,Pretreatment with H(2)S or << NaHS >> significantly inhibited LPS-induced [[ iNOS ]] expression and NO production.,1134,8
1135,Pretreatment with H(2)S or NaHS significantly inhibited LPS-induced << iNOS >> expression and [[ NO ]] production.,1135,4
1136,"Moreover, NO production in LPS-stimulated macrophages that are expressing CSE mRNA was significantly reduced by the addition of L-Cys, a substrate for H(2)S, but enhanced by the selective << CSE >> inhibitor [[ beta-cyano-L-alanine ]] but not by the CBS inhibitor aminooxyacetic acid.",1136,0
1137,"Moreover, NO production in LPS-stimulated macrophages that are expressing CSE mRNA was significantly reduced by the addition of L-Cys, a substrate for H(2)S, but enhanced by the selective CSE inhibitor beta-cyano-L-alanine but not by the << CBS >> inhibitor [[ aminooxyacetic acid ]].",1137,0
1138,"Moreover, NO production in LPS-stimulated macrophages that are expressing << CSE >> mRNA was significantly reduced by the addition of [[ L-Cys ]], a substrate for H(2)S, but enhanced by the selective CSE inhibitor beta-cyano-L-alanine but not by the CBS inhibitor aminooxyacetic acid.",1138,5
1139,"While either blockage of HO activity by the HO inhibitor, tin protoporphyrin IX, or down-regulation of HO-1 expression by HO-1 small interfering RNA (siRNA) reversed the inhibitory effects of << H(2)S >> on [[ iNOS ]] expression and NO production, HO-1 overexpression produced the same inhibitory effects of H(2)S.",1139,8
1140,"While either blockage of HO activity by the HO inhibitor, tin protoporphyrin IX, or down-regulation of HO-1 expression by HO-1 small interfering RNA (siRNA) reversed the inhibitory effects of H(2)S on << iNOS >> expression and [[ NO ]] production, HO-1 overexpression produced the same inhibitory effects of H(2)S.",1140,4
1141,"In addition, LPS-induced nuclear factor << (NF)-kappaB >> activation was diminished in RAW264.7 macrophages preincubated with [[ H(2)S ]].",1141,0
1142,"Interestingly, the inhibitory effect of << H(2)S >> on [[ NF-kappaB ]] activation was reversed by the transient transfection with HO-1 siRNA, but was mimicked by either HO-1 gene transfection or treatment with carbon monoxide (CO), an end product of HO-1.",1142,0
1143,"Interestingly, the inhibitory effect of H(2)S on NF-kappaB activation was reversed by the transient transfection with HO-1 siRNA, but was mimicked by either HO-1 gene transfection or treatment with << carbon monoxide >> (CO), an end product of [[ HO-1 ]].",1143,4
1144,"Interestingly, the inhibitory effect of H(2)S on NF-kappaB activation was reversed by the transient transfection with HO-1 siRNA, but was mimicked by either HO-1 gene transfection or treatment with carbon monoxide (<< CO >>), an end product of [[ HO-1 ]].",1144,4
1145,<< CO >> treatment also inhibited LPS-induced NO production and [[ iNOS ]] expression via its inactivation of NF-kappaB.,1145,8
1146,<< CO >> treatment also inhibited LPS-induced NO production and iNOS expression via its inactivation of [[ NF-kappaB ]].,1146,0
1147,CO treatment also inhibited LPS-induced << NO >> production and [[ iNOS ]] expression via its inactivation of NF-kappaB.,1147,4
1148,"Collectively, our results suggest that << H(2)S >> can inhibit NO production and [[ NF-kappaB ]] activation in LPS-stimulated macrophages through a mechanism that involves the action of HO-1/CO.",1148,0
1149,"Collectively, our results suggest that H(2)S can inhibit NO production and NF-kappaB activation in LPS-stimulated macrophages through a mechanism that involves the action of << HO-1 >>/[[ CO ]].",1149,4
1150,Sources of << L-arg >> include dietary proteins and endogenous synthesis by [[ argininosuccinate synthetase ]] and argininosuccinate lyase.,1150,4
1151,Sources of << L-arg >> include dietary proteins and endogenous synthesis by argininosuccinate synthetase and [[ argininosuccinate lyase ]].,1151,4
1152,L-arg is converted to << urea >> by [[ arginase I ]] in the liver and arginase II in the kidney.,1152,4
1153,L-arg is converted to << urea >> by arginase I in the liver and [[ arginase II ]] in the kidney.,1153,4
1154,<< L-arg >> is converted to urea by [[ arginase I ]] in the liver and arginase II in the kidney.,1154,5
1155,<< L-arg >> is converted to urea by arginase I in the liver and [[ arginase II ]] in the kidney.,1155,5
1156,"We hypothesized that preservation of plasma << L-arg >> in CRF may be, partly, due to downregulation/inhibition of [[ arginase ]].",1156,5
1157,"However, in vitro experiments simulating a uremic milieu revealed a marked concentration-dependent inhibition of << arginase >> activity by [[ urea ]] in the tissue lysates.",1157,0
1158,"CONCLUSIONS: Although CRF does not change the abundance or intrinsic properties of << arginase >>, the inherent rise in [[ urea ]] concentration inhibits its enzymatic activity.",1158,0
1159,"However, several promising nonpeptide, << vasopressin receptor >> antagonists have been described; these agents are [[ VPA-985 ]] (lixivaptan), YM-087 (conivaptan), OPC-41061 (tolvaptan), and SR-121463.",1159,1
1160,"However, several promising nonpeptide, << vasopressin receptor >> antagonists have been described; these agents are VPA-985 ([[ lixivaptan ]]), YM-087 (conivaptan), OPC-41061 (tolvaptan), and SR-121463.",1160,1
1161,"However, several promising nonpeptide, << vasopressin receptor >> antagonists have been described; these agents are VPA-985 (lixivaptan), [[ YM-087 ]] (conivaptan), OPC-41061 (tolvaptan), and SR-121463.",1161,1
1162,"However, several promising nonpeptide, << vasopressin receptor >> antagonists have been described; these agents are VPA-985 (lixivaptan), YM-087 ([[ conivaptan ]]), OPC-41061 (tolvaptan), and SR-121463.",1162,1
1163,"However, several promising nonpeptide, << vasopressin receptor >> antagonists have been described; these agents are VPA-985 (lixivaptan), YM-087 (conivaptan), [[ OPC-41061 ]] (tolvaptan), and SR-121463.",1163,1
1164,"However, several promising nonpeptide, << vasopressin receptor >> antagonists have been described; these agents are VPA-985 (lixivaptan), YM-087 (conivaptan), OPC-41061 ([[ tolvaptan ]]), and SR-121463.",1164,1
1165,"However, several promising nonpeptide, << vasopressin receptor >> antagonists have been described; these agents are VPA-985 (lixivaptan), YM-087 (conivaptan), OPC-41061 (tolvaptan), and [[ SR-121463 ]].",1165,1
1166,Sedation and << histamine H1-receptor >> antagonism: studies in man with the enantiomers of chlorpheniramine and [[ dimethindene ]].,1166,1
1167,Sedation and << histamine H1-receptor >> antagonism: studies in man with the enantiomers of [[ chlorpheniramine ]] and dimethindene.,1167,1
1168,"BG also showed a protective effect in the presence of a << DNA polymerase beta >> inhibitor ([[ cytosine arabinoside-3-phosphate ]], Ara-C), demonstrating that BG does not act through an anti-mutagenic mechanism of action involving DNA polymerase beta.",1168,0
1169,"BG also showed a protective effect in the presence of a << DNA polymerase beta >> inhibitor (cytosine arabinoside-3-phosphate, [[ Ara-C ]]), demonstrating that BG does not act through an anti-mutagenic mechanism of action involving DNA polymerase beta.",1169,0
1170,"Reduction of cerebral infarct size by the AT1-receptor blocker candesartan, the << HMG-CoA reductase >> inhibitor [[ rosuvastatin ]] and their combination.",1170,0
1171,"Reduction of cerebral infarct size by the << AT1 >>-receptor blocker [[ candesartan ]], the HMG-CoA reductase inhibitor rosuvastatin and their combination.",1171,0
1172,Our purpose was to test the impact of single and/or combined treatment with the << AT(1) >>-receptor blocker [[ candesartan ]] and the HMG-CoA reductase inhibitor rosuvastatin on infarct size and neuroscore in transient cerebral ischemia in rats.,1172,0
1173,Our purpose was to test the impact of single and/or combined treatment with the AT(1)-receptor blocker candesartan and the << HMG-CoA reductase >> inhibitor [[ rosuvastatin ]] on infarct size and neuroscore in transient cerebral ischemia in rats.,1173,0
1174,Diacylglycerol (DAG) acts as an allosteric activator of protein kinase C (PKC) and is converted to << phosphatidic acid >> by [[ DAG kinase ]] (DGK).,1174,4
1175,Diacylglycerol (DAG) acts as an allosteric activator of protein kinase C (PKC) and is converted to << phosphatidic acid >> by DAG kinase ([[ DGK ]]).,1175,4
1176,<< Diacylglycerol >> (DAG) acts as an allosteric activator of protein kinase C (PKC) and is converted to phosphatidic acid by [[ DAG kinase ]] (DGK).,1176,5
1177,<< Diacylglycerol >> (DAG) acts as an allosteric activator of protein kinase C (PKC) and is converted to phosphatidic acid by DAG kinase ([[ DGK ]]).,1177,5
1178,Diacylglycerol (<< DAG >>) acts as an allosteric activator of protein kinase C (PKC) and is converted to phosphatidic acid by [[ DAG kinase ]] (DGK).,1178,5
1179,Diacylglycerol (<< DAG >>) acts as an allosteric activator of protein kinase C (PKC) and is converted to phosphatidic acid by DAG kinase ([[ DGK ]]).,1179,5
1180,Monoclonal antibody 25B1 generated against << diisopropyl phosphorofluoridate >> inhibited fetal [[ bovine serum acetylcholinesterase ]] has been extensively characterized with respect to its anticholinesterase properties.,1180,0
1181,Monoclonal antibody 25B1 appears to be directed against a conformational epitope located in close proximity to the catalytic center of the enzyme and was found to be most suitable for studying the stabilization of the active site of << acetylcholinesterase >> against denaturation by heat or [[ guanidine ]] following phosphorylation by organophosphorus anticholinesterase compounds.,1181,3
1182,The << sordarins >> group are protein synthesis inhibitors that work by blocking the function of [[ fungal translation elongation factor 2 ]].,1182,0
1183,"Phospholipase C beta (PLC-beta)-coupled G protein-coupled receptor (GPCR) activities traditionally are assessed by measuring Ca2+ triggered by << D-myo-inositol 1,4,5-trisphosphate >> (IP3), a [[ PLC-beta ]] hydrolysis product, or by measuring the production of inositol phosphate using cumbersome radioactive assays.",1183,4
1184,"Phospholipase C beta (PLC-beta)-coupled G protein-coupled receptor (GPCR) activities traditionally are assessed by measuring Ca2+ triggered by D-myo-inositol 1,4,5-trisphosphate (<< IP3 >>), a [[ PLC-beta ]] hydrolysis product, or by measuring the production of inositol phosphate using cumbersome radioactive assays.",1184,4
1185,"Phospholipase C beta (PLC-beta)-coupled G protein-coupled receptor (GPCR) activities traditionally are assessed by measuring Ca2+ triggered by D-myo-inositol 1,4,5-trisphosphate (IP3), a << PLC-beta >> hydrolysis product, or by measuring the production of [[ inositol phosphate ]] using cumbersome radioactive assays.",1185,4
1186,"It has been known for decades that << lithium chloride >> (LiCl) leads to D-myo-inositol 1-phosphate accumulation on [[ GPCR ]] activation by inhibiting inositol monophosphatase, the final enzyme of the IP3 metabolic cascade.",1186,9
1187,"It has been known for decades that lithium chloride (<< LiCl >>) leads to D-myo-inositol 1-phosphate accumulation on [[ GPCR ]] activation by inhibiting inositol monophosphatase, the final enzyme of the IP3 metabolic cascade.",1187,9
1188,"It has been known for decades that << lithium chloride >> (LiCl) leads to D-myo-inositol 1-phosphate accumulation on GPCR activation by inhibiting [[ inositol monophosphatase ]], the final enzyme of the IP3 metabolic cascade.",1188,0
1189,"It has been known for decades that lithium chloride (<< LiCl >>) leads to D-myo-inositol 1-phosphate accumulation on GPCR activation by inhibiting [[ inositol monophosphatase ]], the final enzyme of the IP3 metabolic cascade.",1189,0
1190,"It has been known for decades that lithium chloride (LiCl) leads to << D-myo-inositol 1-phosphate >> accumulation on GPCR activation by inhibiting [[ inositol monophosphatase ]], the final enzyme of the IP3 metabolic cascade.",1190,5
1191,"It has been known for decades that lithium chloride (LiCl) leads to D-myo-inositol 1-phosphate accumulation on GPCR activation by inhibiting << inositol monophosphatase >>, the final enzyme of the [[ IP3 ]] metabolic cascade.",1191,5
1192,"Once formed, the molecule can be converted to << glycine >> by [[ alanine-glyoxylate aminotransferase ]] (AGAT).",1192,4
1193,"Once formed, the molecule can be converted to << glycine >> by alanine-glyoxylate aminotransferase ([[ AGAT ]]).",1193,4
1194,<< 11Beta-HSD1 >> activates cortisone to [[ cortisol ]] to facilitate glucocorticoid receptor (GR)-mediated action.,1194,4
1195,<< 11Beta-HSD1 >> activates [[ cortisone ]] to cortisol to facilitate glucocorticoid receptor (GR)-mediated action.,1195,5
1196,"By contrast, 11beta-HSD2 plays a pivotal role in aldosterone target tissues where it catalyses the opposite reaction (i.e. inactivation of cortisol to cortisone) to prevent activation of the << mineralocorticoid receptor >> (MR) by [[ cortisol ]].",1196,9
1197,"By contrast, 11beta-HSD2 plays a pivotal role in aldosterone target tissues where it catalyses the opposite reaction (i.e. inactivation of cortisol to cortisone) to prevent activation of the mineralocorticoid receptor (<< MR >>) by [[ cortisol ]].",1197,9
1198,"By contrast, << 11beta-HSD2 >> plays a pivotal role in aldosterone target tissues where it catalyses the opposite reaction (i.e. inactivation of cortisol to [[ cortisone ]]) to prevent activation of the mineralocorticoid receptor (MR) by cortisol.",1198,4
1199,"By contrast, << 11beta-HSD2 >> plays a pivotal role in aldosterone target tissues where it catalyses the opposite reaction (i.e. inactivation of [[ cortisol ]] to cortisone) to prevent activation of the mineralocorticoid receptor (MR) by cortisol.",1199,5
1200,"Mutations in the 11beta-HSD2 gene cause a rare form of inherited hypertension, the syndrome of apparent mineralocorticoid excess (AME), in which << cortisol >> activates the [[ MR ]] resulting in severe hypertension and hypokalemia.",1200,9
1201,Ingestion of competitive inhibitors of << 11beta-HSD2 >> such as liquorice and [[ carbenoxolone ]] result in a similar but milder clinical phenotype.,1201,0
1202,"Here we demonstrate that PPARgamma, turns on << retinoic acid >> synthesis by inducing the expression of retinol and retinal metabolizing enzymes such as [[ retinol dehydrogenase 10 ]] and retinaldehyde dehydrogenase type 2 (RALDH2).",1202,4
1203,"Here we demonstrate that PPARgamma, turns on << retinoic acid >> synthesis by inducing the expression of retinol and retinal metabolizing enzymes such as retinol dehydrogenase 10 and [[ retinaldehyde dehydrogenase type 2 ]] (RALDH2).",1203,4
1204,"Here we demonstrate that PPARgamma, turns on << retinoic acid >> synthesis by inducing the expression of retinol and retinal metabolizing enzymes such as retinol dehydrogenase 10 and retinaldehyde dehydrogenase type 2 ([[ RALDH2 ]]).",1204,4
1205,"Here we demonstrate that PPARgamma, turns on retinoic acid synthesis by inducing the expression of << retinol >> and retinal metabolizing enzymes such as [[ retinol dehydrogenase 10 ]] and retinaldehyde dehydrogenase type 2 (RALDH2).",1205,5
1206,"Here we demonstrate that PPARgamma, turns on retinoic acid synthesis by inducing the expression of << retinol >> and retinal metabolizing enzymes such as retinol dehydrogenase 10 and [[ retinaldehyde dehydrogenase type 2 ]] (RALDH2).",1206,5
1207,"Here we demonstrate that PPARgamma, turns on retinoic acid synthesis by inducing the expression of << retinol >> and retinal metabolizing enzymes such as retinol dehydrogenase 10 and retinaldehyde dehydrogenase type 2 ([[ RALDH2 ]]).",1207,5
1208,"Here we demonstrate that PPARgamma, turns on retinoic acid synthesis by inducing the expression of retinol and << retinal >> metabolizing enzymes such as [[ retinol dehydrogenase 10 ]] and retinaldehyde dehydrogenase type 2 (RALDH2).",1208,5
1209,"Here we demonstrate that PPARgamma, turns on retinoic acid synthesis by inducing the expression of retinol and << retinal >> metabolizing enzymes such as retinol dehydrogenase 10 and [[ retinaldehyde dehydrogenase type 2 ]] (RALDH2).",1209,5
1210,"Here we demonstrate that PPARgamma, turns on retinoic acid synthesis by inducing the expression of retinol and << retinal >> metabolizing enzymes such as retinol dehydrogenase 10 and retinaldehyde dehydrogenase type 2 ([[ RALDH2 ]]).",1210,5
1211,"<< ATRA >> regulates gene expression via the activation of the [[ retinoic acid receptor (RAR)alpha ]] in human DCs, and RARalpha acutely regulates CD1d expression.",1211,9
1212,"<< ATRA >> regulates gene expression via the activation of the retinoic acid receptor (RAR)alpha in human DCs, and [[ RARalpha ]] acutely regulates CD1d expression.",1212,9
1213,"<< ATRA >> regulates gene expression via the activation of the retinoic acid receptor (RAR)alpha in human DCs, and RARalpha acutely regulates [[ CD1d ]] expression.",1213,6
1214,The << retinoic acid >>-induced elevated expression of [[ CD1d ]] is coupled to enhanced iNKT cell activation.,1214,6
1215,"Furthermore, in vivo relevant lipids such as oxidized low-density lipoprotein can also elicit << retinoid >> signaling leading to [[ CD1d ]] up-regulation.",1215,6
1216,CONTEXT: << Ramelteon >> is a novel [[ MT1 ]] and MT2 melatonin receptor selective agonist recently approved for insomnia treatment.,1216,2
1217,CONTEXT: << Ramelteon >> is a novel MT1 and [[ MT2 melatonin receptor ]] selective agonist recently approved for insomnia treatment.,1217,2
1218,Late INa induced by the << VGSC >> long QT mutant R1623Q was reduced by [[ resveratrol ]] and quercetin.,1218,8
1219,Late INa induced by the VGSC long QT mutant << R1623Q >> was reduced by [[ resveratrol ]] and quercetin.,1219,8
1220,Late INa induced by the << VGSC >> long QT mutant R1623Q was reduced by resveratrol and [[ quercetin ]].,1220,8
1221,Late INa induced by the VGSC long QT mutant << R1623Q >> was reduced by resveratrol and [[ quercetin ]].,1221,8
1222,"Enhancement of radiosensitivity by << topoisomerase II >> inhibitor, [[ amrubicin ]] and amrubicinol, in human lung adenocarcinoma A549 cells and kinetics of apoptosis and necrosis induction.",1222,0
1223,"Enhancement of radiosensitivity by << topoisomerase II >> inhibitor, amrubicin and [[ amrubicinol ]], in human lung adenocarcinoma A549 cells and kinetics of apoptosis and necrosis induction.",1223,0
1224,"Similar to << AMR >> and AMROH, adriamycin and etoposide (VP-16) are [[ DNA topoisomerase II ]] inhibitors.",1224,0
1225,"Similar to AMR and << AMROH >>, adriamycin and etoposide (VP-16) are [[ DNA topoisomerase II ]] inhibitors.",1225,0
1226,"Similar to AMR and AMROH, << adriamycin >> and etoposide (VP-16) are [[ DNA topoisomerase II ]] inhibitors.",1226,0
1227,"Similar to AMR and AMROH, adriamycin and << etoposide >> (VP-16) are [[ DNA topoisomerase II ]] inhibitors.",1227,0
1228,"Similar to AMR and AMROH, adriamycin and etoposide (<< VP-16 >>) are [[ DNA topoisomerase II ]] inhibitors.",1228,0
1229,"Accumulated evidence in humans and animals shows that both << aspirin >> and H. pylori upregulate the expression of [[ cyclooxygenase (COX)-2 ]] both at mRNA and protein levels at the ulcer margin, but failed to influence significantly that of COX-1.",1229,6
1230,"It was, therefore, proposed that H. pylori may in fact, antagonize, << aspirin >>-induced delay of ulcer healing due to suppression of acid secretion by the enhancement in PGE(2) possibly derived from [[ COX-2 ]] expression and activity and to the overexpression of growth factors such as TGF alpha and VEGF.",1230,9
1231,"It was, therefore, proposed that H. pylori may in fact, antagonize, << aspirin >>-induced delay of ulcer healing due to suppression of acid secretion by the enhancement in PGE(2) possibly derived from COX-2 expression and activity and to the overexpression of growth factors such as [[ TGF alpha ]] and VEGF.",1231,6
1232,"It was, therefore, proposed that H. pylori may in fact, antagonize, << aspirin >>-induced delay of ulcer healing due to suppression of acid secretion by the enhancement in PGE(2) possibly derived from COX-2 expression and activity and to the overexpression of growth factors such as TGF alpha and [[ VEGF ]].",1232,6
1233,"It was, therefore, proposed that H. pylori may in fact, antagonize, << aspirin >>-induced delay of ulcer healing due to suppression of acid secretion by the enhancement in PGE(2) possibly derived from [[ COX-2 ]] expression and activity and to the overexpression of growth factors such as TGF alpha and VEGF.",1233,6
1234,"It was, therefore, proposed that H. pylori may in fact, antagonize, aspirin-induced delay of ulcer healing due to suppression of acid secretion by the enhancement in << PGE(2) >> possibly derived from [[ COX-2 ]] expression and activity and to the overexpression of growth factors such as TGF alpha and VEGF.",1234,4
1235,<< Methylthioadenosine phosphorylase >> (MTAP) salvages purines by releasing [[ adenine ]] from methylthioadenosine and is often deleted in mesothelioma.,1235,4
1236,Methylthioadenosine phosphorylase (<< MTAP >>) salvages purines by releasing [[ adenine ]] from methylthioadenosine and is often deleted in mesothelioma.,1236,4
1237,<< Methylthioadenosine phosphorylase >> (MTAP) salvages purines by releasing adenine from [[ methylthioadenosine ]] and is often deleted in mesothelioma.,1237,5
1238,Methylthioadenosine phosphorylase (<< MTAP >>) salvages purines by releasing adenine from [[ methylthioadenosine ]] and is often deleted in mesothelioma.,1238,5
1239,"Based on selective nucleoside protection, TS was found to be the primary pemetrexed target in both cell lines with << GARFT >> inhibition requiring 20- to 30-fold higher [[ pemetrexed ]] concentrations.",1239,0
1240,"Most drugs currently employed in the treatment of type 2 diabetes either target the sulfonylurea receptor stimulating << insulin >> release ([[ sulfonylureas ]], glinides), or target the peroxisome proliferator-activated receptor (PPARgamma) improving insulin resistance (thiazolidinediones).",1240,6
1241,"Most drugs currently employed in the treatment of type 2 diabetes either target the sulfonylurea receptor stimulating << insulin >> release (sulfonylureas, [[ glinides ]]), or target the peroxisome proliferator-activated receptor (PPARgamma) improving insulin resistance (thiazolidinediones).",1241,6
1242,Our work shows that << sulfonylureas >> and glinides additionally bind to PPARgamma and exhibit [[ PPARgamma ]] agonistic activity.,1242,2
1243,Our work shows that sulfonylureas and << glinides >> additionally bind to PPARgamma and exhibit [[ PPARgamma ]] agonistic activity.,1243,2
1244,"Among the measured compounds, << gliquidone >> and glipizide (two sulfonylureas), as well as nateglinide (a glinide), exhibit [[ PPARgamma ]] agonistic activity at concentrations comparable with those reached under pharmacological treatment.",1244,2
1245,"Among the measured compounds, gliquidone and << glipizide >> (two sulfonylureas), as well as nateglinide (a glinide), exhibit [[ PPARgamma ]] agonistic activity at concentrations comparable with those reached under pharmacological treatment.",1245,2
1246,"Among the measured compounds, gliquidone and glipizide (two << sulfonylureas >>), as well as nateglinide (a glinide), exhibit [[ PPARgamma ]] agonistic activity at concentrations comparable with those reached under pharmacological treatment.",1246,2
1247,"Among the measured compounds, gliquidone and glipizide (two sulfonylureas), as well as << nateglinide >> (a glinide), exhibit [[ PPARgamma ]] agonistic activity at concentrations comparable with those reached under pharmacological treatment.",1247,2
1248,"Among the measured compounds, gliquidone and glipizide (two sulfonylureas), as well as nateglinide (a << glinide >>), exhibit [[ PPARgamma ]] agonistic activity at concentrations comparable with those reached under pharmacological treatment.",1248,2
1249,"The most active of these compounds, << gliquidone >>, is shown to be as potent as pioglitazone at inducing [[ PPARgamma ]] target gene expression.",1249,6
1250,"The most active of these compounds, gliquidone, is shown to be as potent as << pioglitazone >> at inducing [[ PPARgamma ]] target gene expression.",1250,6
1251,"<< Glinides >>, sulfonylureas, and other acidified sulfonamides may be promising leads in the development of new [[ PPARgamma ]] agonists.",1251,2
1252,"Glinides, << sulfonylureas >>, and other acidified sulfonamides may be promising leads in the development of new [[ PPARgamma ]] agonists.",1252,2
1253,"Glinides, sulfonylureas, and other << acidified sulfonamides >> may be promising leads in the development of new [[ PPARgamma ]] agonists.",1253,2
1254,"Such organization results in the local activation of << PKA >> subsets through the generation of confined intracellular gradients of [[ cAMP ]], but the mechanisms responsible for limiting the diffusion of cAMP largely remain to be clarified.",1254,9
1255,"By using pharmacological and genetic manipulation of phosphodiesterases (PDEs), we demonstrate that compartmentalized << PDE4B >> and PDE4D are responsible for selectively modulating the concentration of [[ cAMP ]] in individual subcellular compartments.",1255,5
1256,"By using pharmacological and genetic manipulation of phosphodiesterases (PDEs), we demonstrate that compartmentalized PDE4B and << PDE4D >> are responsible for selectively modulating the concentration of [[ cAMP ]] in individual subcellular compartments.",1256,5
1257,"We propose a model whereby compartmentalized << PDEs >>, rather than representing an enzymatic barrier to cAMP diffusion, act as a sink to drain the second messenger from discrete locations, resulting in multiple and simultaneous domains with different [[ cAMP ]] concentrations irrespective of their distance from the site of cAMP synthesis.",1257,5
1258,"We propose a model whereby compartmentalized << PDEs >>, rather than representing an enzymatic barrier to cAMP diffusion, act as a sink to drain the second messenger from discrete locations, resulting in multiple and simultaneous domains with different cAMP concentrations irrespective of their distance from the site of [[ cAMP ]] synthesis.",1258,5
1259,SK-Br3 cells cultured in the presence of topoisomerase IIalpha (TOP2A) inhibitors << doxorubicin >> and etopoxide (VP-16) demonstrated a 2- to 3-fold increase in [[ FAS promoter ]] activity when compared with control cells growing in drug-free culture conditions.,1259,9
1260,SK-Br3 cells cultured in the presence of topoisomerase IIalpha (TOP2A) inhibitors doxorubicin and << etopoxide >> (VP-16) demonstrated a 2- to 3-fold increase in [[ FAS promoter ]] activity when compared with control cells growing in drug-free culture conditions.,1260,9
1261,SK-Br3 cells cultured in the presence of topoisomerase IIalpha (TOP2A) inhibitors doxorubicin and etopoxide (<< VP-16 >>) demonstrated a 2- to 3-fold increase in [[ FAS promoter ]] activity when compared with control cells growing in drug-free culture conditions.,1261,9
1262,SK-Br3 cells cultured in the presence of << topoisomerase IIalpha >> (TOP2A) inhibitors [[ doxorubicin ]] and etopoxide (VP-16) demonstrated a 2- to 3-fold increase in FAS promoter activity when compared with control cells growing in drug-free culture conditions.,1262,0
1263,SK-Br3 cells cultured in the presence of topoisomerase IIalpha (<< TOP2A >>) inhibitors [[ doxorubicin ]] and etopoxide (VP-16) demonstrated a 2- to 3-fold increase in FAS promoter activity when compared with control cells growing in drug-free culture conditions.,1263,0
1264,SK-Br3 cells cultured in the presence of << topoisomerase IIalpha >> (TOP2A) inhibitors doxorubicin and [[ etopoxide ]] (VP-16) demonstrated a 2- to 3-fold increase in FAS promoter activity when compared with control cells growing in drug-free culture conditions.,1264,0
1265,SK-Br3 cells cultured in the presence of topoisomerase IIalpha (<< TOP2A >>) inhibitors doxorubicin and [[ etopoxide ]] (VP-16) demonstrated a 2- to 3-fold increase in FAS promoter activity when compared with control cells growing in drug-free culture conditions.,1265,0
1266,SK-Br3 cells cultured in the presence of << topoisomerase IIalpha >> (TOP2A) inhibitors doxorubicin and etopoxide ([[ VP-16 ]]) demonstrated a 2- to 3-fold increase in FAS promoter activity when compared with control cells growing in drug-free culture conditions.,1266,0
1267,SK-Br3 cells cultured in the presence of topoisomerase IIalpha (<< TOP2A >>) inhibitors doxorubicin and etopoxide ([[ VP-16 ]]) demonstrated a 2- to 3-fold increase in FAS promoter activity when compared with control cells growing in drug-free culture conditions.,1267,0
1268,"RESULT(S): The expression of endometrial << ERalpha >>, PRAB, PRB, and SRC-1 was increased significantly after 1 week of [[ mifepristone ]], but the increase was no longer seen after 10 weeks.",1268,6
1269,"RESULT(S): The expression of endometrial ERalpha, << PRAB >>, PRB, and SRC-1 was increased significantly after 1 week of [[ mifepristone ]], but the increase was no longer seen after 10 weeks.",1269,6
1270,"RESULT(S): The expression of endometrial ERalpha, PRAB, << PRB >>, and SRC-1 was increased significantly after 1 week of [[ mifepristone ]], but the increase was no longer seen after 10 weeks.",1270,6
1271,"RESULT(S): The expression of endometrial ERalpha, PRAB, PRB, and << SRC-1 >> was increased significantly after 1 week of [[ mifepristone ]], but the increase was no longer seen after 10 weeks.",1271,6
1272,"CONCLUSION(S): Short-term exposure of << mifepristone >> in new starters of DMPA increases the expression of endometrial [[ ERalpha ]], PRAB, PRB, and SRC-1 and promotes cell proliferation.",1272,6
1273,"CONCLUSION(S): Short-term exposure of << mifepristone >> in new starters of DMPA increases the expression of endometrial ERalpha, [[ PRAB ]], PRB, and SRC-1 and promotes cell proliferation.",1273,6
1274,"CONCLUSION(S): Short-term exposure of << mifepristone >> in new starters of DMPA increases the expression of endometrial ERalpha, PRAB, [[ PRB ]], and SRC-1 and promotes cell proliferation.",1274,6
1275,"CONCLUSION(S): Short-term exposure of << mifepristone >> in new starters of DMPA increases the expression of endometrial ERalpha, PRAB, PRB, and [[ SRC-1 ]] and promotes cell proliferation.",1275,6
1276,"In the present study, << glucose >>-stimulated [[ insulin ]] secretion was significantly increased in GalN-treated rats compared to controls.",1276,6
1277,"In the present study, glucose-stimulated << insulin >> secretion was significantly increased in [[ GalN ]]-treated rats compared to controls.",1277,6
1278,"Levels of mRNA encoding << insulin 1 >>, ICA512, and PC1/3 were increased in the pancreatic islets of [[ GalN ]]-treated rats.",1278,6
1279,"Levels of mRNA encoding insulin 1, << ICA512 >>, and PC1/3 were increased in the pancreatic islets of [[ GalN ]]-treated rats.",1279,6
1280,"When the << PTB-binding site >> in insulin 1 mRNA was incubated with the islet cytosolic fraction, the RNA-protein complex level was increased in the cytosolic fraction obtained from [[ GalN ]]-treated rats compared to the level in control rats.",1280,6
1281,"When the PTB-binding site in << insulin 1 >> mRNA was incubated with the islet cytosolic fraction, the RNA-protein complex level was increased in the cytosolic fraction obtained from [[ GalN ]]-treated rats compared to the level in control rats.",1281,6
1282,The cytosolic fraction obtained from pancreatic islets obtained from << GalN >>-treated rats had an increased [[ PTB ]] level compared to the levels obtained from the pancreatic islets of control rats.,1282,6
1283,"The changes in CysLT1 receptor expression 24 h after NMDA injection and the effects of a << CysLT1 receptor >> antagonist, [[ pranlukast ]] (0.01 and 0.1 mg/kg), an NMDA receptor antagonist, ketamine (30 mg/kg), and an antioxidant, edaravone (9 mg/kg) were observed.",1283,1
1284,"The changes in CysLT1 receptor expression 24 h after NMDA injection and the effects of a CysLT1 receptor antagonist, pranlukast (0.01 and 0.1 mg/kg), an << NMDA receptor >> antagonist, [[ ketamine ]] (30 mg/kg), and an antioxidant, edaravone (9 mg/kg) were observed.",1284,1
1285,"RESULTS: In the << NMDA >>-injured brain, the [[ CysLT1 receptor ]] mRNA, and protein expression were upregulated, and the receptor was mainly localized in the neurons and not in the astrocytes.",1285,6
1286,"Pranlukast, ketamine and edaravone decreased NMDA-induced injury; << pranlukast >> (0.1 mg/kg) and ketamine inhibited the upregulated expression of the [[ CysLT1 receptor ]].",1286,8
1287,"Pranlukast, ketamine and edaravone decreased NMDA-induced injury; pranlukast (0.1 mg/kg) and << ketamine >> inhibited the upregulated expression of the [[ CysLT1 receptor ]].",1287,8
1288,"CONCLUSION: << CysLT1 receptor >> expression in neurons is upregulated after [[ NMDA ]] injection, and NMDA-induced responses are inhibited by CysLT1 receptor antagonists, indicating that the increased CysLT1 receptor is involved in NMDA excitotoxicity.",1288,6
1289,"CONCLUSION: CysLT1 receptor expression in neurons is upregulated after NMDA injection, and NMDA-induced responses are inhibited by CysLT1 receptor antagonists, indicating that the increased << CysLT1 receptor >> is involved in [[ NMDA ]] excitotoxicity.",1289,6
1290,"We have previously demonstrated that phosphorylation of << Fas-associated death domain-containing protein >> (FADD) at 194 serine through c-jun NH2-terminal kinase (JNK) activation sensitizes breast cancer cells to chemotherapy through accelerating cell cycle arrest at G2/M, and that Bcl-2 phosphorylation downstream of JNK/FADD plays an important role in cell growth suppression by [[ paclitaxel ]].",1290,9
1291,"We have previously demonstrated that phosphorylation of Fas-associated death domain-containing protein (<< FADD >>) at 194 serine through c-jun NH2-terminal kinase (JNK) activation sensitizes breast cancer cells to chemotherapy through accelerating cell cycle arrest at G2/M, and that Bcl-2 phosphorylation downstream of JNK/FADD plays an important role in cell growth suppression by [[ paclitaxel ]].",1291,9
1292,"We have previously demonstrated that phosphorylation of Fas-associated death domain-containing protein (FADD) at 194 serine through << c-jun NH2-terminal kinase >> (JNK) activation sensitizes breast cancer cells to chemotherapy through accelerating cell cycle arrest at G2/M, and that Bcl-2 phosphorylation downstream of JNK/FADD plays an important role in cell growth suppression by [[ paclitaxel ]].",1292,9
1293,"We have previously demonstrated that phosphorylation of Fas-associated death domain-containing protein (FADD) at 194 serine through c-jun NH2-terminal kinase (<< JNK >>) activation sensitizes breast cancer cells to chemotherapy through accelerating cell cycle arrest at G2/M, and that Bcl-2 phosphorylation downstream of JNK/FADD plays an important role in cell growth suppression by [[ paclitaxel ]].",1293,9
1294,"We have previously demonstrated that phosphorylation of Fas-associated death domain-containing protein (FADD) at 194 serine through c-jun NH2-terminal kinase (JNK) activation sensitizes breast cancer cells to chemotherapy through accelerating cell cycle arrest at G2/M, and that Bcl-2 phosphorylation downstream of << JNK >>/FADD plays an important role in cell growth suppression by [[ paclitaxel ]].",1294,9
1295,"We have previously demonstrated that phosphorylation of Fas-associated death domain-containing protein (FADD) at 194 serine through c-jun NH2-terminal kinase (JNK) activation sensitizes breast cancer cells to chemotherapy through accelerating cell cycle arrest at G2/M, and that Bcl-2 phosphorylation downstream of JNK/<< FADD >> plays an important role in cell growth suppression by [[ paclitaxel ]].",1295,9
1296,"The mechanism(s) responsible for arterial vasodilation observed following acute administration of << racemic carvedilol >>, a novel vasodilator/[[ beta adrenoceptor ]] antagonist, has been investigated in rats.",1296,1
1297,"Carvedilol (0.3 mg/kg, iv) produced a significant inhibition of the << beta 1 adrenoceptor >> mediated positive chronotropic response to [[ isoproterenol ]].",1297,9
1298,"<< Carvedilol >> (0.3 mg/kg, iv) produced a significant inhibition of the [[ beta 1 adrenoceptor ]] mediated positive chronotropic response to isoproterenol.",1298,0
1299,"This same dose of << carvedilol >> also inhibited, but to a lesser degree, the [[ beta 2 adrenoceptor ]] mediated vasodepressor response to salbutamol in pithed rats whose blood pressure was elevated by a constant intravenous infusion of angiotensin II.",1299,0
1300,"Thus, << carvedilol >> blocks both beta 1 and beta 2 adrenoceptors at antihypertensive doses, with modest selectivity being observed for the [[ beta 1 adrenoceptor ]] subtype.",1300,0
1301,"<< Carvedilol >> produced significant inhibition of the [[ alpha 1 adrenoceptor ]] mediated pressor response to cirazoline in the pithed rat, but had no effect on the alpha 2 adrenoceptor mediated pressor response to B-HT 933, suggesting that carvedilol is also an alpha 1 adrenoceptor antagonist at antihypertensive doses.",1301,0
1302,"Carvedilol produced significant inhibition of the alpha 1 adrenoceptor mediated pressor response to cirazoline in the pithed rat, but had no effect on the alpha 2 adrenoceptor mediated pressor response to B-HT 933, suggesting that << carvedilol >> is also an [[ alpha 1 adrenoceptor ]] antagonist at antihypertensive doses.",1302,1
1303,"The vasopressor response to the << calcium channel >> activator, [[ BAY-K-8644 ]], which is mediated through the opening of voltage dependent calcium channels and the subsequent translocation of extracellular calcium, was significantly inhibited by carvedilol (1 mg/kg, iv), suggesting that carvedilol is also a calcium channel antagonist, consistent with our previous in vitro studies.",1303,9
1304,"The vasopressor response to the calcium channel activator, << BAY-K-8644 >>, which is mediated through the opening of [[ voltage dependent calcium channels ]] and the subsequent translocation of extracellular calcium, was significantly inhibited by carvedilol (1 mg/kg, iv), suggesting that carvedilol is also a calcium channel antagonist, consistent with our previous in vitro studies.",1304,9
1305,"The vasopressor response to the calcium channel activator, BAY-K-8644, which is mediated through the opening of << voltage dependent calcium channels >> and the subsequent translocation of extracellular calcium, was significantly inhibited by [[ carvedilol ]] (1 mg/kg, iv), suggesting that carvedilol is also a calcium channel antagonist, consistent with our previous in vitro studies.",1305,0
1306,"The vasopressor response to the calcium channel activator, BAY-K-8644, which is mediated through the opening of voltage dependent calcium channels and the subsequent translocation of extracellular calcium, was significantly inhibited by carvedilol (1 mg/kg, iv), suggesting that << carvedilol >> is also a [[ calcium channel ]] antagonist, consistent with our previous in vitro studies.",1306,1
1307,"The vasopressor response to the calcium channel activator, BAY-K-8644, which is mediated through the opening of << voltage dependent calcium channels >> and the subsequent translocation of extracellular [[ calcium ]], was significantly inhibited by carvedilol (1 mg/kg, iv), suggesting that carvedilol is also a calcium channel antagonist, consistent with our previous in vitro studies.",1307,5
1308,"In anesthetized spontaneously hypertensive rats, the antihypertensive activity of carvedilol was nearly abolished by combined pretreatment of the rats with high doses of the << alpha 1 adrenoceptor >> antagonist, [[ prazosin ]] (1 mg/kg, iv), and the nonselective beta adrenoceptor antagonist, propranolol (3 mg/kg, iv), suggesting that the majority of the antihypertensive response produced by carvedilol may be accounted for by blockade of beta and alpha 1 adrenoceptors.",1308,1
1309,"In anesthetized spontaneously hypertensive rats, the antihypertensive activity of carvedilol was nearly abolished by combined pretreatment of the rats with high doses of the alpha 1 adrenoceptor antagonist, prazosin (1 mg/kg, iv), and the nonselective << beta adrenoceptor >> antagonist, [[ propranolol ]] (3 mg/kg, iv), suggesting that the majority of the antihypertensive response produced by carvedilol may be accounted for by blockade of beta and alpha 1 adrenoceptors.",1309,1
1310,"We therefore conclude that << carvedilol >>, at antihypertensive doses, is an antagonist of beta 1, beta 2, and alpha 1 adrenoceptors, and also of [[ calcium channels ]] in vascular smooth muscle.(ABSTRACT TRUNCATED AT 400 WORDS)",1310,1
1311,<< 5-HT3 receptor >> antagonism with [[ alosetron ]] reduced responses to 5-HT in controls but not during inflammation.,1311,1
1312,"<< Progestin >> activation of [[ Src ]]/MAPK occurred outside the nucleus with the B isoform of PR that was distributed between the cytoplasm and nucleus, but not with PR-A that was predominantly nuclear.",1312,9
1313,"<< Progestin >> activation of Src/[[ MAPK ]] occurred outside the nucleus with the B isoform of PR that was distributed between the cytoplasm and nucleus, but not with PR-A that was predominantly nuclear.",1313,9
1314,"<< Progestin >> induction of the cyclin D1 gene, which lacks a progesterone response element, was dependent on [[ PR ]] activation of the Src/MAPK pathway, whereas induction of the Sgk (serum and glucocorticoid regulated kinase) gene that contains a functional progesterone response element was unaffected by mutations that interfere with PR activation of Src.",1314,9
1315,"<< Progestin >> induction of the cyclin D1 gene, which lacks a progesterone response element, was dependent on PR activation of the [[ Src ]]/MAPK pathway, whereas induction of the Sgk (serum and glucocorticoid regulated kinase) gene that contains a functional progesterone response element was unaffected by mutations that interfere with PR activation of Src.",1315,9
1316,"<< Progestin >> induction of the cyclin D1 gene, which lacks a progesterone response element, was dependent on PR activation of the Src/[[ MAPK ]] pathway, whereas induction of the Sgk (serum and glucocorticoid regulated kinase) gene that contains a functional progesterone response element was unaffected by mutations that interfere with PR activation of Src.",1316,9
1317,These results highlight the importance of << PR >> activation of the Src/MAPK signaling pathway for [[ progesterone ]]-induced transcription of select target genes and cell cycle progression.,1317,9
1318,These results highlight the importance of PR activation of the << Src >>/MAPK signaling pathway for [[ progesterone ]]-induced transcription of select target genes and cell cycle progression.,1318,9
1319,These results highlight the importance of PR activation of the Src/<< MAPK >> signaling pathway for [[ progesterone ]]-induced transcription of select target genes and cell cycle progression.,1319,9
1320,"i.p. injection of a subthreshold dose of << picrotoxin >>, a use-dependent [[ gamma-aminobutyric acid receptor ]] antagonist, reduces cortical electroencephalogram delta power and transiently inhibits spontaneous seizure activity in ADNFLE mutant mice.",1320,1
1321,MicroPET imaging in nonhuman primates with [<< 11C >>]1 and [11C]2 demonstrated that both tracers behave similarly in vivo with high uptake being observed in the [[ SERT ]]-rich brain regions and peak uptake being achieved in about 55 min postinjection.,1321,5
1322,MicroPET imaging in nonhuman primates with [11C]1 and [<< 11C >>]2 demonstrated that both tracers behave similarly in vivo with high uptake being observed in the [[ SERT ]]-rich brain regions and peak uptake being achieved in about 55 min postinjection.,1322,5
1323,This trial investigated the possibility of pharmacokinetic interactions between the << AT1 receptor >> antagonist [[ olmesartan medoxomil ]] and the thiazide diuretic hydrochlorothiazide in healthy subjects.,1323,1
1324,<< SecS >> required selenophosphate and O-phosphoseryl-tRNA([Ser]Sec) as substrates to generate [[ selenocysteyl ]]-tRNA([Ser]Sec).,1324,4
1325,<< SecS >> required selenophosphate and [[ O-phosphoseryl ]]-tRNA([Ser]Sec) as substrates to generate selenocysteyl-tRNA([Ser]Sec).,1325,5
1326,<< SecS >> required [[ selenophosphate ]] and O-phosphoseryl-tRNA([Ser]Sec) as substrates to generate selenocysteyl-tRNA([Ser]Sec).,1326,5
1327,"In addition, we found that << selenophosphate synthetase 2 >> could synthesize [[ monoselenophosphate ]] in vitro but selenophosphate synthetase 1 could not.",1327,4
1328,<< Triflusal >> (30 mg/kg) also significantly decreased the protein levels of [[ IL-Ibeta ]] but not nuclear factor kappa B or tumor necrosis factor-alpha in the cortex ipsilateral to the middle cerebral artery occlusion.,1328,8
1329,<< Glutamate >> stimulates [[ glutamate receptor interacting protein 1 ]] degradation by ubiquitin-proteasome system to regulate surface expression of GluR2.,1329,3
1330,"Here we report that << glutamate >> stimulation caused a rapid reduction in protein levels of [[ GRIP1 ]], but not that of glutamate receptor (GluR) 1, GluR2 and protein interacting with C kinase 1 (PICK1) in rat primary cortical neuron cultures.",1330,8
1331,"Down-regulation of << GRIP1 >> by [[ glutamate ]] was blocked by carbobenzoxyl-leucinyl-leucinyl-leucinal (MG132), a proteasome inhibitor and by expression of K48R-ubiquitin, a dominant negative form of ubiquitin.",1331,3
1332,"Down-regulation of GRIP1 by glutamate was blocked by carbobenzoxyl-leucinyl-leucinyl-leucinal (<< MG132 >>), a [[ proteasome ]] inhibitor and by expression of K48R-ubiquitin, a dominant negative form of ubiquitin.",1332,0
1333,"Down-regulation of GRIP1 by glutamate was blocked by << carbobenzoxyl-leucinyl-leucinyl-leucinal >> (MG132), a [[ proteasome ]] inhibitor and by expression of K48R-ubiquitin, a dominant negative form of ubiquitin.",1333,0
1334,"The << GRIP1 >> reduction was inhibited by [[ MK-801 ]], an N-methyl-d-aspartate (NMDA) receptor antagonist, but not by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), an AMPA receptor antagonist.",1334,9
1335,"The GRIP1 reduction was inhibited by << MK-801 >>, an [[ N-methyl-d-aspartate (NMDA) receptor ]] antagonist, but not by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), an AMPA receptor antagonist.",1335,1
1336,"The GRIP1 reduction was inhibited by MK-801, an N-methyl-d-aspartate (NMDA) receptor antagonist, but not by << 6-cyano-7-nitroquinoxaline-2,3-dione >> (CNQX), an [[ AMPA receptor ]] antagonist.",1336,1
1337,"The GRIP1 reduction was inhibited by MK-801, an N-methyl-d-aspartate (NMDA) receptor antagonist, but not by 6-cyano-7-nitroquinoxaline-2,3-dione (<< CNQX >>), an [[ AMPA receptor ]] antagonist.",1337,1
1338,"<< EGTA >> and 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetra acetic acid tetrakis (BAPTA), two Ca2+ chelators, but not nifedipine, an L-type Ca2+ channel blocker, prevented [[ GRIP1 ]] degradation.",1338,7
1339,"EGTA and << 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetra acetic acid tetrakis >> (BAPTA), two Ca2+ chelators, but not nifedipine, an L-type Ca2+ channel blocker, prevented [[ GRIP1 ]] degradation.",1339,7
1340,"EGTA and 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetra acetic acid tetrakis (<< BAPTA >>), two Ca2+ chelators, but not nifedipine, an L-type Ca2+ channel blocker, prevented [[ GRIP1 ]] degradation.",1340,7
1341,"EGTA and 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetra acetic acid tetrakis (BAPTA), two Ca2+ chelators, but not << nifedipine >>, an [[ L-type Ca2+ channel ]] blocker, prevented GRIP1 degradation.",1341,0
1342,"Furthermore, MG132 prevented << glutamate >>-stimulated reduction in surface amount of [[ GluR2 ]], and knockdown of GRIP1 by RNAi against GRIP1 reduced surface GluR2 in neurons.",1342,8
1343,Our results suggest that << glutamate >> induces [[ GRIP1 ]] degradation by proteasome through an NMDA receptor-Ca2+ pathway and that GRIP1 degradation may play an important role in regulating GluR2 surface expression.,1343,3
1344,Our results suggest that << glutamate >> induces GRIP1 degradation by proteasome through an NMDA receptor-Ca2+ pathway and that [[ GRIP1 ]] degradation may play an important role in regulating GluR2 surface expression.,1344,3
1345,The inhibitory effect of the leukotriene receptor antagonist on << leukotriene D4 >>-induced MUC2/5AC gene expression and [[ mucin ]] secretion in human airway epithelial cells.,1345,6
1346,The inhibitory effect of the leukotriene receptor antagonist on << leukotriene D4 >>-induced [[ MUC2/5AC ]] gene expression and mucin secretion in human airway epithelial cells.,1346,6
1347,"METHODS: The effect of leukotriene D(4) and the << leukotriene receptor >> antagonist, [[ pranlukast hydrate ]] (ONO-1078) on the regulation of MUC2/5AC gene expression and mucin secretion were observed in human airway NCI-H292 epithelial cells.",1347,1
1348,"METHODS: The effect of leukotriene D(4) and the << leukotriene receptor >> antagonist, pranlukast hydrate ([[ ONO-1078 ]]) on the regulation of MUC2/5AC gene expression and mucin secretion were observed in human airway NCI-H292 epithelial cells.",1348,1
1349,RESULTS: << Leukotriene D(4) >> upregulated [[ MUC2/5AC ]] gene expression and mucin secretion in a dose dependent pattern.,1349,6
1350,RESULTS: << Leukotriene D(4) >> upregulated MUC2/5AC gene expression and [[ mucin ]] secretion in a dose dependent pattern.,1350,6
1351,"Pranlukast hydrate (ONO-1078, 100 microM) downregulated the << leukotriene D(4) >>-induced [[ MUC2/5AC ]] gene expression and mucin secretion.",1351,6
1352,"Pranlukast hydrate (ONO-1078, 100 microM) downregulated the << leukotriene D(4) >>-induced MUC2/5AC gene expression and [[ mucin ]] secretion.",1352,6
1353,"<< Pranlukast hydrate >> (ONO-1078, 100 microM) downregulated the leukotriene D(4)-induced [[ MUC2/5AC ]] gene expression and mucin secretion.",1353,8
1354,"<< Pranlukast hydrate >> (ONO-1078, 100 microM) downregulated the leukotriene D(4)-induced MUC2/5AC gene expression and [[ mucin ]] secretion.",1354,8
1355,"Pranlukast hydrate (<< ONO-1078 >>, 100 microM) downregulated the leukotriene D(4)-induced [[ MUC2/5AC ]] gene expression and mucin secretion.",1355,8
1356,"Pranlukast hydrate (<< ONO-1078 >>, 100 microM) downregulated the leukotriene D(4)-induced MUC2/5AC gene expression and [[ mucin ]] secretion.",1356,8
1357,"We studied in a clinical trial whether isolated isoflavone treatment in postmenopausal women could affect reverse cholesterol transport as evaluated by << adenosine triphosphate-binding cassette A1 >>- (ABCA1), dependent [[ cholesterol ]] efflux from macrophages.",1357,5
1358,"We studied in a clinical trial whether isolated isoflavone treatment in postmenopausal women could affect reverse cholesterol transport as evaluated by adenosine triphosphate-binding cassette A1- (<< ABCA1 >>), dependent [[ cholesterol ]] efflux from macrophages.",1358,5
1359,"[H]-Cholesterol-labeled J774 macrophage cells, with and without ABCA1 up-regulation, were incubated with the samples, and << ABCA1 >>-dependent [[ cholesterol ]] efflux and serum lipid and lipoprotein levels were assessed.",1359,5
1360,"Thus, isoflavone supplementation did not affect << ABCA1 >>-dependent [[ cholesterol ]] efflux to serum.",1360,5
1361,"However, as a novel finding, << isoflavone >> treatment increased a subclass of [[ high-density lipoprotein ]], the pre-beta high-density lipoprotein levels by 18% without affecting any other serum lipid concentrations.",1361,6
1362,"However, as a novel finding, << isoflavone >> treatment increased a subclass of high-density lipoprotein, the [[ pre-beta high-density lipoprotein ]] levels by 18% without affecting any other serum lipid concentrations.",1362,6
1363,<< ABCA1 >>-facilitated [[ cholesterol ]] efflux and lipid parameters did not differ between equol-producing and non-equol-producing women.,1363,5
1364,"CONCLUSION: In postmenopausal women, isolated << isoflavone >> treatment does not affect ABCA1-dependent cholesterol efflux potential from macrophages but increases circulating [[ pre-beta high-density lipoprotein ]] level, which could provide beneficial vascular effects.",1364,6
1365,"CONCLUSION: In postmenopausal women, isolated isoflavone treatment does not affect << ABCA1 >>-dependent [[ cholesterol ]] efflux potential from macrophages but increases circulating pre-beta high-density lipoprotein level, which could provide beneficial vascular effects.",1365,5
1366,The ability of << sorafenib >> to inhibit oncogenic [[ PDGFRbeta ]] and FLT3 mutants and overcome resistance to other small molecule inhibitors.,1366,0
1367,The ability of << sorafenib >> to inhibit oncogenic PDGFRbeta and [[ FLT3 ]] mutants and overcome resistance to other small molecule inhibitors.,1367,0
1368,"<< Sorafenib >> (BAY43-9006, Nexavar) is a small molecule [[ B-RAF ]] inhibitor that is used for the treatment of renal cell carcinoma, and has been shown to have activity against receptor tyrosine kinases from the platelet-derived growth factor receptor (PDGFR) and vascular endothelial growth factor receptor (VEGFR) families.",1368,0
1369,"Sorafenib (<< BAY43-9006 >>, Nexavar) is a small molecule [[ B-RAF ]] inhibitor that is used for the treatment of renal cell carcinoma, and has been shown to have activity against receptor tyrosine kinases from the platelet-derived growth factor receptor (PDGFR) and vascular endothelial growth factor receptor (VEGFR) families.",1369,0
1370,"Sorafenib (BAY43-9006, << Nexavar >>) is a small molecule [[ B-RAF ]] inhibitor that is used for the treatment of renal cell carcinoma, and has been shown to have activity against receptor tyrosine kinases from the platelet-derived growth factor receptor (PDGFR) and vascular endothelial growth factor receptor (VEGFR) families.",1370,0
1371,"We investigated the efficacy of << sorafenib >> at inhibiting mutants of the [[ receptor tyrosine kinases ]] PDGFRbeta, KIT, and FLT3, which are implicated in the pathogenesis of myeloid malignancies.",1371,0
1372,"We investigated the efficacy of << sorafenib >> at inhibiting mutants of the receptor tyrosine kinases [[ PDGFRbeta ]], KIT, and FLT3, which are implicated in the pathogenesis of myeloid malignancies.",1372,0
1373,"We investigated the efficacy of << sorafenib >> at inhibiting mutants of the receptor tyrosine kinases PDGFRbeta, [[ KIT ]], and FLT3, which are implicated in the pathogenesis of myeloid malignancies.",1373,0
1374,"We investigated the efficacy of << sorafenib >> at inhibiting mutants of the receptor tyrosine kinases PDGFRbeta, KIT, and [[ FLT3 ]], which are implicated in the pathogenesis of myeloid malignancies.",1374,0
1375,"RESULTS: We show that << sorafenib >> is a potent inhibitor of [[ ETV6 ]]-PDGFRbeta and FLT3 mutants, including some of the mutants that confer resistance to PKC412 and other FLT3 inhibitors.",1375,0
1376,"RESULTS: We show that << sorafenib >> is a potent inhibitor of ETV6-[[ PDGFRbeta ]] and FLT3 mutants, including some of the mutants that confer resistance to PKC412 and other FLT3 inhibitors.",1376,0
1377,"RESULTS: We show that << sorafenib >> is a potent inhibitor of ETV6-PDGFRbeta and [[ FLT3 ]] mutants, including some of the mutants that confer resistance to PKC412 and other FLT3 inhibitors.",1377,0
1378,"RESULTS: We show that << sorafenib >> is a potent inhibitor of ETV6-PDGFRbeta and FLT3 mutants, including some of the mutants that confer resistance to PKC412 and other [[ FLT3 ]] inhibitors.",1378,0
1379,"<< Sorafenib >> induced a cell cycle block and apoptosis in the acute myeloid leukemia cell lines MV4-11 and MOLM-13, both expressing [[ FLT3 ]] with an internal tandem duplication, whereas no effect was observed on four other acute myeloid leukemia cell lines.",1379,0
1380,INTERPRETATION AND CONCLUSIONS: These results warrant further clinical studies of << sorafenib >> for the treatment of myeloid malignancies expressing activated forms of [[ PDGFRbeta ]] and FLT3.,1380,0
1381,INTERPRETATION AND CONCLUSIONS: These results warrant further clinical studies of << sorafenib >> for the treatment of myeloid malignancies expressing activated forms of PDGFRbeta and [[ FLT3 ]].,1381,0
1382,"Exposure to << mifepristone >> (a [[ glucocorticoid receptor ]] antagonist), but not spironolactone (a mineralocorticoid receptor antagonist), precluded both the corticosteroid-induced elevation in amiloride-sensitive I(sc) and the induced changes in beta- and gamma-ENaC mRNA.",1382,1
1383,"Exposure to mifepristone (a glucocorticoid receptor antagonist), but not << spironolactone >> (a [[ mineralocorticoid receptor ]] antagonist), precluded both the corticosteroid-induced elevation in amiloride-sensitive I(sc) and the induced changes in beta- and gamma-ENaC mRNA.",1383,1
1384,Oral << aspirin >> (as a representative of the salicylate family) inhibited diabetes-induced increase in [[ NF-kappaB ]] DNA-binding affinity in electrophoretic mobility shift assay and transcription factor array in nuclear extract isolated from whole retina.,1384,0
1385,Oral aspirin (as a representative of the << salicylate >> family) inhibited diabetes-induced increase in [[ NF-kappaB ]] DNA-binding affinity in electrophoretic mobility shift assay and transcription factor array in nuclear extract isolated from whole retina.,1385,0
1386,"All three << salicylates >> inhibited the diabetes-induced translocation of [[ p50 ]] (a subunit of NF-kappaB) into nuclei of retinal vascular endothelial cells of the isolated retinal vasculature, as well as of p50 and p65 into nuclei of cells in the ganglion cell layer and inner nuclear layer on whole-retinal sections.",1386,8
1387,"All three << salicylates >> inhibited the diabetes-induced translocation of p50 (a subunit of NF-kappaB) into nuclei of retinal vascular endothelial cells of the isolated retinal vasculature, as well as of [[ p50 ]] and p65 into nuclei of cells in the ganglion cell layer and inner nuclear layer on whole-retinal sections.",1387,8
1388,"All three << salicylates >> inhibited the diabetes-induced translocation of p50 (a subunit of NF-kappaB) into nuclei of retinal vascular endothelial cells of the isolated retinal vasculature, as well as of p50 and [[ p65 ]] into nuclei of cells in the ganglion cell layer and inner nuclear layer on whole-retinal sections.",1388,8
1389,"All three << salicylates >> inhibited the diabetes-induced translocation of p50 (a subunit of [[ NF-kappaB ]]) into nuclei of retinal vascular endothelial cells of the isolated retinal vasculature, as well as of p50 and p65 into nuclei of cells in the ganglion cell layer and inner nuclear layer on whole-retinal sections.",1389,0
1390,"<< Sulfasalazine >> (also as a representative of the salicylates) inhibited the diabetes-induced upregulation of several inflammatory gene products, which are regulated by [[ NF-kappaB ]], including vascular cell adhesion molecule, intracellular adhesion molecule-1, inducible nitric oxide synthase, and cyclooxygenase-2 in whole-retinal lysate.",1390,0
1391,"<< Sulfasalazine >> (also as a representative of the salicylates) inhibited the diabetes-induced upregulation of several inflammatory gene products, which are regulated by NF-kappaB, including vascular cell adhesion molecule, [[ intracellular adhesion molecule-1 ]], inducible nitric oxide synthase, and cyclooxygenase-2 in whole-retinal lysate.",1391,0
1392,"<< Sulfasalazine >> (also as a representative of the salicylates) inhibited the diabetes-induced upregulation of several inflammatory gene products, which are regulated by NF-kappaB, including vascular cell adhesion molecule, intracellular adhesion molecule-1, [[ inducible nitric oxide synthase ]], and cyclooxygenase-2 in whole-retinal lysate.",1392,0
1393,"<< Sulfasalazine >> (also as a representative of the salicylates) inhibited the diabetes-induced upregulation of several inflammatory gene products, which are regulated by NF-kappaB, including vascular cell adhesion molecule, intracellular adhesion molecule-1, inducible nitric oxide synthase, and [[ cyclooxygenase-2 ]] in whole-retinal lysate.",1393,0
1394,"Sulfasalazine (also as a representative of the << salicylates >>) inhibited the diabetes-induced upregulation of several inflammatory gene products, which are regulated by [[ NF-kappaB ]], including vascular cell adhesion molecule, intracellular adhesion molecule-1, inducible nitric oxide synthase, and cyclooxygenase-2 in whole-retinal lysate.",1394,0
1395,"<< Salicylates >>, in doses administrated in our experiments, inhibited [[ NF-kappa ]]B and perhaps other transcription factors in the retina, were well tolerated, and offered new tools to investigate and inhibit the development of diabetic retinopathy.",1395,0
1396,"Lymphocytes possess the essential components of a cholinergic system, including acetylcholine (<< ACh >>); [[ choline acetyltransferase ]] (ChAT), its synthesizing enzyme; and both muscarinic and nicotinic ACh receptors (mAChRs and nAChRs, respectively).",1396,4
1397,"Lymphocytes possess the essential components of a cholinergic system, including acetylcholine (<< ACh >>); choline acetyltransferase ([[ ChAT ]]), its synthesizing enzyme; and both muscarinic and nicotinic ACh receptors (mAChRs and nAChRs, respectively).",1397,4
1398,"Lymphocytes possess the essential components of a cholinergic system, including << acetylcholine >> (ACh); [[ choline acetyltransferase ]] (ChAT), its synthesizing enzyme; and both muscarinic and nicotinic ACh receptors (mAChRs and nAChRs, respectively).",1398,4
1399,"Lymphocytes possess the essential components of a cholinergic system, including << acetylcholine >> (ACh); choline acetyltransferase ([[ ChAT ]]), its synthesizing enzyme; and both muscarinic and nicotinic ACh receptors (mAChRs and nAChRs, respectively).",1399,4
1400,"In addition, activation of protein kinase C and increases in intracellular << cAMP >> also enhance cholinergic activity in T cells, and [[ lymphocyte function associated antigen-1 ]] (LFA-1; CD11a/CD18) is an important mediator of leukocyte migration and T cell activation.",1400,6
1401,"In addition, activation of protein kinase C and increases in intracellular << cAMP >> also enhance cholinergic activity in T cells, and lymphocyte function associated antigen-1 ([[ LFA-1 ]]; CD11a/CD18) is an important mediator of leukocyte migration and T cell activation.",1401,6
1402,"In addition, activation of protein kinase C and increases in intracellular << cAMP >> also enhance cholinergic activity in T cells, and lymphocyte function associated antigen-1 (LFA-1; [[ CD11a ]]/CD18) is an important mediator of leukocyte migration and T cell activation.",1402,6
1403,"In addition, activation of protein kinase C and increases in intracellular << cAMP >> also enhance cholinergic activity in T cells, and lymphocyte function associated antigen-1 (LFA-1; CD11a/[[ CD18 ]]) is an important mediator of leukocyte migration and T cell activation.",1403,6
1404,We found that << simvastatin >> abolishes anti-[[ CD11a ]] mAb-induced increases in lymphocytic cholinergic activity in a manner independent of its cholesterol-lowering activity.,1404,3
1405,INTRODUCTION: Medroxyprogesterone acetate (<< MPA >>) induces estrogen receptor (ER)-positive and progesterone receptor ([[ PR ]])-positive ductal invasive mammary carcinomas in BALB/c mice.,1405,7
1406,INTRODUCTION: Medroxyprogesterone acetate (<< MPA >>) induces [[ estrogen receptor ]] (ER)-positive and progesterone receptor (PR)-positive ductal invasive mammary carcinomas in BALB/c mice.,1406,7
1407,INTRODUCTION: Medroxyprogesterone acetate (<< MPA >>) induces estrogen receptor ([[ ER ]])-positive and progesterone receptor (PR)-positive ductal invasive mammary carcinomas in BALB/c mice.,1407,7
1408,INTRODUCTION: << Medroxyprogesterone acetate >> (MPA) induces estrogen receptor (ER)-positive and progesterone receptor ([[ PR ]])-positive ductal invasive mammary carcinomas in BALB/c mice.,1408,7
1409,INTRODUCTION: << Medroxyprogesterone acetate >> (MPA) induces [[ estrogen receptor ]] (ER)-positive and progesterone receptor (PR)-positive ductal invasive mammary carcinomas in BALB/c mice.,1409,7
1410,INTRODUCTION: << Medroxyprogesterone acetate >> (MPA) induces estrogen receptor ([[ ER ]])-positive and progesterone receptor (PR)-positive ductal invasive mammary carcinomas in BALB/c mice.,1410,7
1411,INTRODUCTION: << Medroxyprogesterone acetate >> (MPA) induces estrogen receptor (ER)-positive and [[ progesterone receptor ]] (PR)-positive ductal invasive mammary carcinomas in BALB/c mice.,1411,7
1412,"The expression of << ER-alpha >> and PR isoform A in virgin mice was surprisingly much higher in BALB/c than in C57BL/6 mammary glands, and both receptors were downregulated in [[ progestin ]]-treated BALB/c mice (P < 0.05).",1412,8
1413,"The expression of ER-alpha and << PR isoform A >> in virgin mice was surprisingly much higher in BALB/c than in C57BL/6 mammary glands, and both receptors were downregulated in [[ progestin ]]-treated BALB/c mice (P < 0.05).",1413,8
1414,<< PR isoform B >> levels were low in virgin control mice and increased after [[ progestin ]] treatment in both strains.,1414,6
1415,"Various genes controlled by << estrogen >>, including [[ X-inactive-specific transcript ]], anterior gradient-2, trefoil factor-1, CRP-ductin, ghrelin, and small proline-rich protein-2A, were dramatically over-expressed.",1415,6
1416,"Various genes controlled by << estrogen >>, including X-inactive-specific transcript, [[ anterior gradient-2 ]], trefoil factor-1, CRP-ductin, ghrelin, and small proline-rich protein-2A, were dramatically over-expressed.",1416,6
1417,"Various genes controlled by << estrogen >>, including X-inactive-specific transcript, anterior gradient-2, [[ trefoil factor-1 ]], CRP-ductin, ghrelin, and small proline-rich protein-2A, were dramatically over-expressed.",1417,6
1418,"Various genes controlled by << estrogen >>, including X-inactive-specific transcript, anterior gradient-2, trefoil factor-1, [[ CRP-ductin ]], ghrelin, and small proline-rich protein-2A, were dramatically over-expressed.",1418,6
1419,"Various genes controlled by << estrogen >>, including X-inactive-specific transcript, anterior gradient-2, trefoil factor-1, CRP-ductin, [[ ghrelin ]], and small proline-rich protein-2A, were dramatically over-expressed.",1419,6
1420,"Various genes controlled by << estrogen >>, including X-inactive-specific transcript, anterior gradient-2, trefoil factor-1, CRP-ductin, ghrelin, and [[ small proline-rich protein-2A ]], were dramatically over-expressed.",1420,6
1421,"<< Estrogen >>-regulated genes including cytokeratin 1-19 and [[ Cyp2a4 ]] were over-expressed, although Cyp3a25 was suppressed.",1421,6
1422,"<< Estrogen >>-regulated genes including [[ cytokeratin 1-19 ]] and Cyp2a4 were over-expressed, although Cyp3a25 was suppressed.",1422,6
1423,"<< Estrogen >>-regulated genes including cytokeratin 1-19 and Cyp2a4 were over-expressed, although [[ Cyp3a25 ]] was suppressed.",1423,8
1424,"Several genes involved with steroid metabolism also showed remarkable expression changes, including increased expression of << 17beta-hydroxysteroid dehydrogenase-7 >> (HSD17beta7; involved in [[ estradiol ]] production) and decreased expression of HSD17beta5 (involved in testosterone production).",1424,4
1425,"Several genes involved with steroid metabolism also showed remarkable expression changes, including increased expression of 17beta-hydroxysteroid dehydrogenase-7 (<< HSD17beta7 >>; involved in [[ estradiol ]] production) and decreased expression of HSD17beta5 (involved in testosterone production).",1425,4
1426,"Several genes involved with steroid metabolism also showed remarkable expression changes, including increased expression of 17beta-hydroxysteroid dehydrogenase-7 (HSD17beta7; involved in estradiol production) and decreased expression of << HSD17beta5 >> (involved in [[ testosterone ]] production).",1426,4
1427,"The expression of key genes important in << methionine >> metabolism, such as [[ methionine adenosyltransferase-1a ]], betaine-homocysteine methyltransferase and thioether S-methyltransferase, were suppressed.",1427,4
1428,"The expression of key genes important in << methionine >> metabolism, such as methionine adenosyltransferase-1a, [[ betaine-homocysteine methyltransferase ]] and thioether S-methyltransferase, were suppressed.",1428,4
1429,"The expression of key genes important in << methionine >> metabolism, such as methionine adenosyltransferase-1a, betaine-homocysteine methyltransferase and [[ thioether S-methyltransferase ]], were suppressed.",1429,4
1430,<< Monosodium urate >> crystals stimulate monocytes and macrophages to release [[ IL-1beta ]] through the NALP3 component of the inflammasome.,1430,6
1431,Structural basis of inhibition of the << human NAD+-dependent deacetylase SIRT5 >> by [[ suramin ]].,1431,0
1432,We identified << suramin >> as a compound that binds to human SIRT5 and showed that it inhibits [[ SIRT5 NAD(+)-dependent deacetylase ]] activity with an IC(50) value of 22 microM.,1432,0
1433,"In humans, << methionine synthase >> deficiency results in the accumulation of [[ methyltetrahydrofolate ]] at the expense of folate derivatives required for purine and thymidylate biosynthesis.",1433,5
1434,<< Metformin >> and phenformin activate [[ AMP-activated protein kinase ]] in the heart by increasing cytosolic AMP concentration.,1434,9
1435,Metformin and << phenformin >> activate [[ AMP-activated protein kinase ]] in the heart by increasing cytosolic AMP concentration.,1435,9
1436,"<< Metformin >> and phenformin, which are biguanides, have been reported to increase [[ AMPK ]] activity without increasing AMP/ATP.",1436,9
1437,"Metformin and << phenformin >>, which are biguanides, have been reported to increase [[ AMPK ]] activity without increasing AMP/ATP.",1437,9
1438,"Metformin and phenformin, which are << biguanides >>, have been reported to increase [[ AMPK ]] activity without increasing AMP/ATP.",1438,9
1439,"In hearts treated with << phenformin >> for 18 min and then perfused for 20 min with Krebs-Henseleit buffer, [AMP] began to increase at 26 min and [[ AMPK ]] activity was elevated at 36 min.",1439,9
1440,"In hearts treated with << metformin >>, [AMP] was increased at 50 min and [[ AMPK ]] activity, phosphorylated AMPK, and phosphorylated acetyl-CoA carboxylase were elevated at 61 min.",1440,9
1441,"In hearts treated with << metformin >>, [AMP] was increased at 50 min and AMPK activity, phosphorylated [[ AMPK ]], and phosphorylated acetyl-CoA carboxylase were elevated at 61 min.",1441,9
1442,"In hearts treated with << metformin >>, [AMP] was increased at 50 min and AMPK activity, phosphorylated AMPK, and [[ phosphorylated acetyl-CoA carboxylase ]] were elevated at 61 min.",1442,9
1443,"In summary, << phenformin >> and metformin increase [[ AMPK ]] activity and phosphorylation in the isolated heart.",1443,9
1444,"In summary, phenformin and << metformin >> increase [[ AMPK ]] activity and phosphorylation in the isolated heart.",1444,9
1445,"Cytosolic [AMP] reported metabolically active << AMP >>, which triggered increased [[ AMPK ]] activity, but measures of total AMP did not.",1445,9
1446,<< Histamine H(1) >> blockade is one of the more prominent actions of the multi-receptor acting antipsychotic [[ clozapine ]].,1446,0
1447,It is currently not known how much this << H(1) >> antagonism of [[ clozapine ]] contributes to the therapeutic or adverse side effects of clozapine.,1447,1
1448,"In the current project, we found that the selective << H(1) >> antagonist pyrilamine also reversed the [[ dizocilpine ]]-induced impairment in PPI of tactile startle with an auditory prepulse.",1448,7
1449,"In the current project, we found that the selective << H(1) >> antagonist [[ pyrilamine ]] also reversed the dizocilpine-induced impairment in PPI of tactile startle with an auditory prepulse.",1449,1
1450,"In summary, the therapeutic effect of << clozapine >> in reversing PPI impairment was mimicked by the [[ H(1) ]] antagonist pyrilamine, while pyrilamine had a mixed effect on cognition.",1450,3
1451,"In summary, the therapeutic effect of clozapine in reversing PPI impairment was mimicked by the << H(1) >> antagonist [[ pyrilamine ]], while pyrilamine had a mixed effect on cognition.",1451,1
1452,"In summary, the therapeutic effect of clozapine in reversing PPI impairment was mimicked by the << H(1) >> antagonist pyrilamine, while [[ pyrilamine ]] had a mixed effect on cognition.",1452,1
1453,"Thus, << H(1) >> antagonism seems to play a role in part of the beneficial actions of antipsychotics, such as [[ clozapine ]].",1453,1
1454,"Furthermore, the enzymatic activity of << alanine aminotransferase >> (ALT), which converts the critical gluconeogenic amino acid alanine into [[ pyruvate ]], is decreased (approximately 50%) in KLF15-/- hepatocytes.",1454,4
1455,"Furthermore, the enzymatic activity of alanine aminotransferase (<< ALT >>), which converts the critical gluconeogenic amino acid alanine into [[ pyruvate ]], is decreased (approximately 50%) in KLF15-/- hepatocytes.",1455,4
1456,"Furthermore, the enzymatic activity of << alanine aminotransferase >> (ALT), which converts the critical gluconeogenic [[ amino acid ]] alanine into pyruvate, is decreased (approximately 50%) in KLF15-/- hepatocytes.",1456,5
1457,"Furthermore, the enzymatic activity of alanine aminotransferase (<< ALT >>), which converts the critical gluconeogenic [[ amino acid ]] alanine into pyruvate, is decreased (approximately 50%) in KLF15-/- hepatocytes.",1457,5
1458,"Furthermore, the enzymatic activity of << alanine aminotransferase >> (ALT), which converts the critical gluconeogenic amino acid [[ alanine ]] into pyruvate, is decreased (approximately 50%) in KLF15-/- hepatocytes.",1458,5
1459,"Furthermore, the enzymatic activity of alanine aminotransferase (<< ALT >>), which converts the critical gluconeogenic amino acid [[ alanine ]] into pyruvate, is decreased (approximately 50%) in KLF15-/- hepatocytes.",1459,5
1460,<< D-glucose >> stimulation of L-arginine transport and nitric oxide synthesis results from activation of mitogen-activated protein kinases p42/44 and [[ Smad2 ]] requiring functional type II TGF-beta receptors in human umbilical vein endothelium.,1460,9
1461,Elevated extracellular << D-glucose >> increases [[ transforming growth factor beta1 ]] (TGF-beta1) release from human umbilical vein endothelium (HUVEC).,1461,6
1462,Elevated extracellular << D-glucose >> increases transforming growth factor beta1 ([[ TGF-beta1 ]]) release from human umbilical vein endothelium (HUVEC).,1462,6
1463,<< TGF-beta1 >> release was higher ( approximately 1.6-fold) in 25 mM (high) compared with 5 mM (normal) [[ D-glucose ]].,1463,6
1464,"TGF-beta1 and high << D-glucose >> increased [[ hCAT-1 ]] mRNA expression ( approximately 8-fold) and maximal transport velocity (V(max)), L-[(3)H]citrulline formation from L-[(3)H]arginine (index of NO synthesis) and endothelial NO synthase (eNOS) protein abundance, but did not alter eNOS phosphorylation.",1464,6
1465,"TGF-beta1 and high D-glucose increased hCAT-1 mRNA expression ( approximately 8-fold) and maximal transport velocity (V(max)), L-[(3)H]citrulline formation from L-[(3)H]arginine (index of << NO >> synthesis) and [[ endothelial NO synthase ]] (eNOS) protein abundance, but did not alter eNOS phosphorylation.",1465,4
1466,"TGF-beta1 and high D-glucose increased hCAT-1 mRNA expression ( approximately 8-fold) and maximal transport velocity (V(max)), L-[(3)H]citrulline formation from L-[(3)H]arginine (index of << NO >> synthesis) and endothelial NO synthase ([[ eNOS ]]) protein abundance, but did not alter eNOS phosphorylation.",1466,4
1467,"TGF-beta1 and high << D-glucose >> increased p42/44(mapk) and [[ Smad2 ]] phosphorylation, an effect blocked by PD-98059 (MEK1/2 inhibitor).",1467,9
1468,"TGF-beta1 and high D-glucose increased p42/44(mapk) and << Smad2 >> phosphorylation, an effect blocked by [[ PD-98059 ]] (MEK1/2 inhibitor).",1468,0
1469,High << D-glucose >> increases L-arginine transport and eNOS expression following [[ TbetaRII ]] activation by TGF-beta1 involving p42/44(mapk) and Smad2 in HUVEC.,1469,9
1470,High << D-glucose >> increases L-arginine transport and eNOS expression following TbetaRII activation by TGF-beta1 involving p42/44(mapk) and [[ Smad2 ]] in HUVEC.,1470,9
1471,High << D-glucose >> increases L-arginine transport and [[ eNOS ]] expression following TbetaRII activation by TGF-beta1 involving p42/44(mapk) and Smad2 in HUVEC.,1471,6
1472,<< n-3 and n-6 polyunsaturated fatty acids >> induce the expression of COX-2 via [[ PPARgamma ]] activation in human keratinocyte HaCaT cells.,1472,9
1473,<< n-3 and n-6 polyunsaturated fatty acids >> induce the expression of [[ COX-2 ]] via PPARgamma activation in human keratinocyte HaCaT cells.,1473,6
1474,"We demonstrate that only treatment of HaCaT with << GLA >> and EPA or a PPARgamma ligand (roziglitazone), induced [[ COX-2 ]] expression (protein and mRNA).",1474,6
1475,"We demonstrate that only treatment of HaCaT with GLA and << EPA >> or a PPARgamma ligand (roziglitazone), induced [[ COX-2 ]] expression (protein and mRNA).",1475,6
1476,"We demonstrate that only treatment of HaCaT with GLA and EPA or a PPARgamma ligand (<< roziglitazone >>), induced [[ COX-2 ]] expression (protein and mRNA).",1476,6
1477,Moreover stimulation of << COX-2 promoter >> activity was increased by those [[ PUFAs ]] or rosiglitazone.,1477,9
1478,Moreover stimulation of << COX-2 promoter >> activity was increased by those PUFAs or [[ rosiglitazone ]].,1478,9
1479,"The inhibitory effects of << GW9662 >> and T0070907 ([[ PPARgamma ]] antagonists), on COX-2 expression and on stimulation of COX-2 promoter activity by EPA and GLA suggest that PPARgamma is implicated in COX-2 induction.",1479,1
1480,"The inhibitory effects of GW9662 and << T0070907 >> ([[ PPARgamma ]] antagonists), on COX-2 expression and on stimulation of COX-2 promoter activity by EPA and GLA suggest that PPARgamma is implicated in COX-2 induction.",1480,1
1481,"Finally, PLA2 inhibitor methyl arachidonyl fluorophosphonate blocked the PUFA effects on COX-2 induction, promoter activity and arachidonic acid mobilization suggesting involvement of << AA >> metabolites in [[ PPAR ]] activation.",1481,9
1482,"Finally, << PLA2 >> inhibitor methyl [[ arachidonyl fluorophosphonate ]] blocked the PUFA effects on COX-2 induction, promoter activity and arachidonic acid mobilization suggesting involvement of AA metabolites in PPAR activation.",1482,0
1483,"Finally, PLA2 inhibitor methyl << arachidonyl fluorophosphonate >> blocked the PUFA effects on [[ COX-2 ]] induction, promoter activity and arachidonic acid mobilization suggesting involvement of AA metabolites in PPAR activation.",1483,0
1484,These findings demonstrate that << n-3 and n-6 PUFA >> increased [[ PPARgamma ]] activity is necessary for the COX-2 induction in HaCaT human keratinocyte cells.,1484,9
1485,These findings demonstrate that << n-3 and n-6 PUFA >> increased PPARgamma activity is necessary for the [[ COX-2 ]] induction in HaCaT human keratinocyte cells.,1485,9
1486,"Given the anti-inflammatory properties of EPA, we suggest that induction of << COX-2 >> in keratinocytes may be important in the anti-inflammatory and protective mechanism of action of [[ PUFAs n-3 ]] or n-6.",1486,9
1487,"OBJECTIVE: The aim of this study was to assess the efficacy and tolerability of nebulized arformoterol tartrate (a selective, long-acting << beta(2)-adrenergic >> agonist that is the [[ [R,R] isomer of formoterol ]]) and salmeterol xinafoate versus placebo in patients with chronic obstructive pulmonary disease (COPD).",1487,2
1488,"OBJECTIVE: The aim of this study was to assess the efficacy and tolerability of nebulized << arformoterol tartrate >> (a selective, long-acting [[ beta(2)-adrenergic ]] agonist that is the [R,R] isomer of formoterol) and salmeterol xinafoate versus placebo in patients with chronic obstructive pulmonary disease (COPD).",1488,2
1489,"<< Acetyl-coenzyme A carboxylase >> (ACC) enzymes exist as two isoforms, ACC1 and ACC2, which play critical roles in [[ fatty acid ]] biosynthesis and oxidation.",1489,4
1490,"Acetyl-coenzyme A carboxylase (<< ACC >>) enzymes exist as two isoforms, ACC1 and ACC2, which play critical roles in [[ fatty acid ]] biosynthesis and oxidation.",1490,4
1491,"Acetyl-coenzyme A carboxylase (ACC) enzymes exist as two isoforms, << ACC1 >> and ACC2, which play critical roles in [[ fatty acid ]] biosynthesis and oxidation.",1491,4
1492,"Acetyl-coenzyme A carboxylase (ACC) enzymes exist as two isoforms, ACC1 and << ACC2 >>, which play critical roles in [[ fatty acid ]] biosynthesis and oxidation.",1492,4
1493,"The cytosolic << ACC1 >> is expressed primarily in liver and adipose tissue, and uses malonyl-coenzyme A as a key building block in [[ fatty acid ]] biosynthesis.",1493,4
1494,"The mitochondrial << ACC2 >> is primarily expressed in heart and skeletal muscle, where it is involved in the regulation of [[ fatty acid ]] oxidation.",1494,4
1495,"In contrast, the << RA >> catabolising enzymes [[ Cyp26A1 ]] and Cyp26B1 which are known to be RA-responsive were not expressed at all in the developing eye.",1495,5
1496,"In contrast, the << RA >> catabolising enzymes Cyp26A1 and [[ Cyp26B1 ]] which are known to be RA-responsive were not expressed at all in the developing eye.",1496,5
1497,"Incretin-receptor activation leads to << glucose >>-dependent [[ insulin ]] secretion, induction of beta-cell proliferation, and enhanced resistance to apoptosis.",1497,6
1498,This report reviews published and unpublished data that suggest that << aripiprazole >> acts as a selective partial agonist at the [[ dopamine D(2) receptor ]] and does not affect 5-HT receptors at therapeutic doses.,1498,2
1499,<< Mifepriston'e >> blocks [[ glucocorticoid receptor ]] activation without modifying cortisol synthesis.,1499,0
1500,"[N-(piperidin-1-yl)-5-(4-chlorophenyl)-4-methyl-1H-pyrazole-3-carboxyamide] (<< SR 141716A >>), a selective [[ cannabinoid CB1 receptor ]] antagonist, injected into the paraventricular nucleus of the hypothalamus (PVN) of male rats, induces penile erection.",1500,1
1501,"[<< N-(piperidin-1-yl)-5-(4-chlorophenyl)-4-methyl-1H-pyrazole-3-carboxyamide >>] (SR 141716A), a selective [[ cannabinoid CB1 receptor ]] antagonist, injected into the paraventricular nucleus of the hypothalamus (PVN) of male rats, induces penile erection.",1501,1
1502,"The present findings confirm that PVN CB1 receptors, localized mainly in GABAergic synapses that control in an inhibitory fashion excitatory synapses, exert an inhibitory control on penile erection, demonstrating for the first time that chronic blockade of << CB1 receptors >> by [[ SR 141716A ]] increases the density of these receptors in the PVN.",1502,0
1503,"Modulation of the function of CD36 (CD36-/- mice), << p38 >>(MAPK) ([[ SB203580 ]]), COX-1 (indomethacin), and glycoprotein Ib alpha (Nk-protease, 6D1 antibody) induced approximately 50% inhibition.",1503,0
1504,"Modulation of the function of CD36 (CD36-/- mice), p38(<< MAPK >>) ([[ SB203580 ]]), COX-1 (indomethacin), and glycoprotein Ib alpha (Nk-protease, 6D1 antibody) induced approximately 50% inhibition.",1504,0
1505,"Modulation of the function of CD36 (CD36-/- mice), p38(MAPK) (SB203580), << COX-1 >> ([[ indomethacin ]]), and glycoprotein Ib alpha (Nk-protease, 6D1 antibody) induced approximately 50% inhibition.",1505,0
1506,"We show that murine Rdh12 and human RDH13 do not reveal activity towards the checked steroids, but that << human type 12 RDH >> reduces dihydrotestosterone to [[ androstanediol ]], and is thus also involved in steroid metabolism.",1506,4
1507,"The << sibutramine >> group showed significant retardation in gastric emptying of solids (P = .03), reduced maximum tolerated volume (P = .03), and increased postprandial [[ peptide YY ]] compared with the placebo group.",1507,6
1508,CONCLUSIONS: Weight reduction with << sibutramine >> is associated with altered gastric functions and increased [[ peptide YY ]] and is significantly associated with SLC6A4 genotype.,1508,6
1509,An investigation of the absolute configuration of the potent << histamine H3 receptor >> antagonist [[ GT-2331 ]] using vibrational circular dichroism.,1509,1
1510,"In this study the neuromuscular blocking drug << vecuronium >> and the controls gallamine and pancuronium slowed the rate of atropine induced [(3)H]N-methylscopolamine dissociation from Chinese hamster ovary cells expressing recombinant [[ human muscarinic M2 receptors ]] K(off) values min(-1); vecuronium (125 nM), atropine 0.45+/-0.07+blocker 0.04+/-0.02; gallamine (21 nM), atropine 0.42+/-0.05+blocker 0.15+/-0.04; pancuronium(21 nM), atropine 0.36+/-0.03+blocker 0.03+/-0.01).",1510,3
1511,"In this study the neuromuscular blocking drug vecuronium and the controls << gallamine >> and pancuronium slowed the rate of atropine induced [(3)H]N-methylscopolamine dissociation from Chinese hamster ovary cells expressing recombinant [[ human muscarinic M2 receptors ]] K(off) values min(-1); vecuronium (125 nM), atropine 0.45+/-0.07+blocker 0.04+/-0.02; gallamine (21 nM), atropine 0.42+/-0.05+blocker 0.15+/-0.04; pancuronium(21 nM), atropine 0.36+/-0.03+blocker 0.03+/-0.01).",1511,3
1512,"In this study the neuromuscular blocking drug vecuronium and the controls gallamine and << pancuronium >> slowed the rate of atropine induced [(3)H]N-methylscopolamine dissociation from Chinese hamster ovary cells expressing recombinant [[ human muscarinic M2 receptors ]] K(off) values min(-1); vecuronium (125 nM), atropine 0.45+/-0.07+blocker 0.04+/-0.02; gallamine (21 nM), atropine 0.42+/-0.05+blocker 0.15+/-0.04; pancuronium(21 nM), atropine 0.36+/-0.03+blocker 0.03+/-0.01).",1512,3
1513,Patients with acute vitiligo have low epidermal << catalase >> expression/activities and accumulate 10(-3) M [[ H(2)O(2) ]].,1513,5
1514,<< Mammalian cysteine dioxygenase >> (CDO) is a non-heme iron metalloenzyme that catalyzes the first committed step in oxidative [[ cysteine ]] catabolism.,1514,5
1515,Mammalian cysteine dioxygenase (<< CDO >>) is a non-heme iron metalloenzyme that catalyzes the first committed step in oxidative [[ cysteine ]] catabolism.,1515,5
1516,"However, upon addition of NO to << CDO >> in the presence of substrate [[ l-cysteine ]], a low-spin {FeNO}7 (S = 1/2) signal that accounts for approximately 85% of the iron within the enzyme develops.",1516,5
1517,"The transcriptional activity of torafugu << PPARalpha1 >> was enhanced 4.5- and 11.5-fold by [[ Wy-14643 ]] and 5,8,11,14-eicosatetraynoic acid (ETYA) each at 10 microM, respectively, whereas that of PPARalpha2, 4.5- and 7.3-fold at the same concentration of the respective ligands, respectively.",1517,9
1518,"The transcriptional activity of torafugu PPARalpha1 was enhanced 4.5- and 11.5-fold by << Wy-14643 >> and 5,8,11,14-eicosatetraynoic acid (ETYA) each at 10 microM, respectively, whereas that of [[ PPARalpha2 ]], 4.5- and 7.3-fold at the same concentration of the respective ligands, respectively.",1518,9
1519,"The transcriptional activity of torafugu << PPARalpha1 >> was enhanced 4.5- and 11.5-fold by Wy-14643 and [[ 5,8,11,14-eicosatetraynoic acid ]] (ETYA) each at 10 microM, respectively, whereas that of PPARalpha2, 4.5- and 7.3-fold at the same concentration of the respective ligands, respectively.",1519,9
1520,"The transcriptional activity of torafugu PPARalpha1 was enhanced 4.5- and 11.5-fold by Wy-14643 and << 5,8,11,14-eicosatetraynoic acid >> (ETYA) each at 10 microM, respectively, whereas that of [[ PPARalpha2 ]], 4.5- and 7.3-fold at the same concentration of the respective ligands, respectively.",1520,9
1521,"The transcriptional activity of torafugu << PPARalpha1 >> was enhanced 4.5- and 11.5-fold by Wy-14643 and 5,8,11,14-eicosatetraynoic acid ([[ ETYA ]]) each at 10 microM, respectively, whereas that of PPARalpha2, 4.5- and 7.3-fold at the same concentration of the respective ligands, respectively.",1521,9
1522,"The transcriptional activity of torafugu PPARalpha1 was enhanced 4.5- and 11.5-fold by Wy-14643 and 5,8,11,14-eicosatetraynoic acid (<< ETYA >>) each at 10 microM, respectively, whereas that of [[ PPARalpha2 ]], 4.5- and 7.3-fold at the same concentration of the respective ligands, respectively.",1522,9
1523,"Furthermore, the activities of the two << torafugu PPARalphas >> were enhanced 4.3- and 7.6-fold by [[ arachidonic acid ]], 4.4- and 5.2-fold by docosahexaenoic acid, and 6.7- and 8.0-fold by eicosapentaenoic acid each at 50 microM, respectively.",1523,9
1524,"Furthermore, the activities of the two << torafugu PPARalphas >> were enhanced 4.3- and 7.6-fold by arachidonic acid, 4.4- and 5.2-fold by [[ docosahexaenoic acid ]], and 6.7- and 8.0-fold by eicosapentaenoic acid each at 50 microM, respectively.",1524,9
1525,"Furthermore, the activities of the two << torafugu PPARalphas >> were enhanced 4.3- and 7.6-fold by arachidonic acid, 4.4- and 5.2-fold by docosahexaenoic acid, and 6.7- and 8.0-fold by [[ eicosapentaenoic acid ]] each at 50 microM, respectively.",1525,9
1526,Combination chemotherapy with a << substance P receptor >> antagonist ([[ aprepitant ]]) and melarsoprol in a mouse model of human African trypanosomiasis.,1526,1
1527,Combination chemotherapy with a << substance P receptor >> antagonist (aprepitant) and [[ melarsoprol ]] in a mouse model of human African trypanosomiasis.,1527,1
1528,In this study we investigated the effects of combination chemotherapy with melarsoprol and a << humanised SP receptor >> antagonist [[ aprepitant ]] (EMEND) in this mouse model.,1528,1
1529,In this study we investigated the effects of combination chemotherapy with melarsoprol and a << humanised SP receptor >> antagonist aprepitant ([[ EMEND ]]) in this mouse model.,1529,1
1530,It is thought to play a critical role in the visual cycle by functioning as an acceptor of << 11-cis-retinol >> from the [[ isomerohydrolase ]] reaction.,1530,4
1531,<< Dimethylarginine dimethylaminohydrolase >> (DDAH) metabolizes asymmetric dimethylarginine to generate [[ L-citrulline ]] and is present in large quantities in the kidney.,1531,4
1532,Dimethylarginine dimethylaminohydrolase (<< DDAH >>) metabolizes asymmetric dimethylarginine to generate [[ L-citrulline ]] and is present in large quantities in the kidney.,1532,4
1533,<< Dimethylarginine dimethylaminohydrolase >> (DDAH) metabolizes asymmetric [[ dimethylarginine ]] to generate L-citrulline and is present in large quantities in the kidney.,1533,5
1534,Dimethylarginine dimethylaminohydrolase (<< DDAH >>) metabolizes asymmetric [[ dimethylarginine ]] to generate L-citrulline and is present in large quantities in the kidney.,1534,5
1535,We present a new study that optimizes the Prescott-Jones colorimetric assay to measure << DDAH >>-dependent [[ L-citrulline ]] generation in kidney homogenates.,1535,4
1536,We found that the removal of << urea >> with [[ urease ]] is necessary since urea also produces a positive reaction.,1536,5
1537,Our optimized << L-citrulline >> production assay to measure [[ DDAH ]] activity correlated closely with the direct measure of the rate of asymmetric dimethylarginine consumption.,1537,4
1538,Our optimized L-citrulline production assay to measure << DDAH >> activity correlated closely with the direct measure of the rate of asymmetric [[ dimethylarginine ]] consumption.,1538,5
1539,"Using this assay, we found that both << superoxide >> and nitric oxide inhibit renal cortical [[ DDAH ]] activity in vitro.",1539,0
1540,"Using this assay, we found that both superoxide and << nitric oxide >> inhibit renal cortical [[ DDAH ]] activity in vitro.",1540,0
1541,"The next large phase III adjuvant trial for this subset of breast cancer is an international collaboration designed to evaluate the added or alternative benefit of an oral tyrosine kinase inhibitor targeting << HER2 >>/neu as well as the epidermal growth factor receptor (EGFR), [[ lapatinib ]].",1541,0
1542,"The next large phase III adjuvant trial for this subset of breast cancer is an international collaboration designed to evaluate the added or alternative benefit of an oral tyrosine kinase inhibitor targeting HER2/<< neu >> as well as the epidermal growth factor receptor (EGFR), [[ lapatinib ]].",1542,0
1543,"The next large phase III adjuvant trial for this subset of breast cancer is an international collaboration designed to evaluate the added or alternative benefit of an oral tyrosine kinase inhibitor targeting HER2/neu as well as the << epidermal growth factor receptor >> (EGFR), [[ lapatinib ]].",1543,0
1544,"The next large phase III adjuvant trial for this subset of breast cancer is an international collaboration designed to evaluate the added or alternative benefit of an oral tyrosine kinase inhibitor targeting HER2/neu as well as the epidermal growth factor receptor (<< EGFR >>), [[ lapatinib ]].",1544,0
1545,"Exposure of Jurkat cells to either << (5S,10R)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,b]cyclohepten-5,10-imine >> [(+)-MK 801] or D-(-)-2-amino-5-phosphonopentanoic acid (D-AP5), two selective [[ NMDA receptor ]] antagonists, limited cell growth by inhibiting cell cycle progression and inducing apoptosis, whereas l-glutamate (1 microM) and NMDA (10 microM) significantly increased (137.2+/-22.0%; P<0.01) Jurkat T cell adhesion to fibronectin.",1545,1
1546,"Exposure of Jurkat cells to either (5S,10R)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,b]cyclohepten-5,10-imine [<< (+)-MK 801 >>] or D-(-)-2-amino-5-phosphonopentanoic acid (D-AP5), two selective [[ NMDA receptor ]] antagonists, limited cell growth by inhibiting cell cycle progression and inducing apoptosis, whereas l-glutamate (1 microM) and NMDA (10 microM) significantly increased (137.2+/-22.0%; P<0.01) Jurkat T cell adhesion to fibronectin.",1546,1
1547,"Exposure of Jurkat cells to either (5S,10R)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,b]cyclohepten-5,10-imine [(+)-MK 801] or << D-(-)-2-amino-5-phosphonopentanoic acid >> (D-AP5), two selective [[ NMDA receptor ]] antagonists, limited cell growth by inhibiting cell cycle progression and inducing apoptosis, whereas l-glutamate (1 microM) and NMDA (10 microM) significantly increased (137.2+/-22.0%; P<0.01) Jurkat T cell adhesion to fibronectin.",1547,1
1548,"Exposure of Jurkat cells to either (5S,10R)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,b]cyclohepten-5,10-imine [(+)-MK 801] or D-(-)-2-amino-5-phosphonopentanoic acid (<< D-AP5 >>), two selective [[ NMDA receptor ]] antagonists, limited cell growth by inhibiting cell cycle progression and inducing apoptosis, whereas l-glutamate (1 microM) and NMDA (10 microM) significantly increased (137.2+/-22.0%; P<0.01) Jurkat T cell adhesion to fibronectin.",1548,1
1549,<< Desvenlafaxine succinate >> identifies novel antagonist binding determinants in the [[ human norepinephrine transporter ]].,1549,1
1550,"<< Desvenlafaxine succinate >> (DVS) is a recently introduced antagonist of the human norepinephrine and serotonin transporters ([[ hNET ]] and hSERT, respectively), currently in clinical development for use in the treatment of major depressive disorder and vasomotor symptoms associated with menopause.",1550,1
1551,"<< Desvenlafaxine succinate >> (DVS) is a recently introduced antagonist of the human norepinephrine and serotonin transporters (hNET and [[ hSERT ]], respectively), currently in clinical development for use in the treatment of major depressive disorder and vasomotor symptoms associated with menopause.",1551,1
1552,"Desvenlafaxine succinate (<< DVS >>) is a recently introduced antagonist of the human norepinephrine and serotonin transporters ([[ hNET ]] and hSERT, respectively), currently in clinical development for use in the treatment of major depressive disorder and vasomotor symptoms associated with menopause.",1552,1
1553,"Desvenlafaxine succinate (<< DVS >>) is a recently introduced antagonist of the human norepinephrine and serotonin transporters (hNET and [[ hSERT ]], respectively), currently in clinical development for use in the treatment of major depressive disorder and vasomotor symptoms associated with menopause.",1553,1
1554,"Using << hNET >> in transfected human embryonic kidney-293 cells, this difference in potency for DVS at sites labeled by [(3)H]NIS was found to distinguish DVS, the [[ DVS ]] analog rac-(1-[1-(3-chloro-phenyl)-2-(4-methylpiperazin-1-yl)-ethyl]cyclohexanol (WY-46824), methylphenidate, and the cocaine analog 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester (RTI-55) from other hNET antagonists, such as NIS, mazindol, tricyclic antidepressants, and cocaine.",1554,1
1555,"Using << hNET >> in transfected human embryonic kidney-293 cells, this difference in potency for DVS at sites labeled by [(3)H]NIS was found to distinguish DVS, the DVS analog [[ rac-(1-[1-(3-chloro-phenyl)-2-(4-methylpiperazin-1-yl)-ethyl]cyclohexanol ]] (WY-46824), methylphenidate, and the cocaine analog 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester (RTI-55) from other hNET antagonists, such as NIS, mazindol, tricyclic antidepressants, and cocaine.",1555,1
1556,"Using << hNET >> in transfected human embryonic kidney-293 cells, this difference in potency for DVS at sites labeled by [(3)H]NIS was found to distinguish DVS, the DVS analog rac-(1-[1-(3-chloro-phenyl)-2-(4-methylpiperazin-1-yl)-ethyl]cyclohexanol ([[ WY-46824 ]]), methylphenidate, and the cocaine analog 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester (RTI-55) from other hNET antagonists, such as NIS, mazindol, tricyclic antidepressants, and cocaine.",1556,1
1557,"Using << hNET >> in transfected human embryonic kidney-293 cells, this difference in potency for DVS at sites labeled by [(3)H]NIS was found to distinguish DVS, the DVS analog rac-(1-[1-(3-chloro-phenyl)-2-(4-methylpiperazin-1-yl)-ethyl]cyclohexanol (WY-46824), [[ methylphenidate ]], and the cocaine analog 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester (RTI-55) from other hNET antagonists, such as NIS, mazindol, tricyclic antidepressants, and cocaine.",1557,1
1558,"Using << hNET >> in transfected human embryonic kidney-293 cells, this difference in potency for DVS at sites labeled by [(3)H]NIS was found to distinguish DVS, the DVS analog rac-(1-[1-(3-chloro-phenyl)-2-(4-methylpiperazin-1-yl)-ethyl]cyclohexanol (WY-46824), methylphenidate, and the [[ cocaine ]] analog 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester (RTI-55) from other hNET antagonists, such as NIS, mazindol, tricyclic antidepressants, and cocaine.",1558,1
1559,"Using << hNET >> in transfected human embryonic kidney-293 cells, this difference in potency for DVS at sites labeled by [(3)H]NIS was found to distinguish DVS, the DVS analog rac-(1-[1-(3-chloro-phenyl)-2-(4-methylpiperazin-1-yl)-ethyl]cyclohexanol (WY-46824), methylphenidate, and the cocaine analog [[ 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester ]] (RTI-55) from other hNET antagonists, such as NIS, mazindol, tricyclic antidepressants, and cocaine.",1559,1
1560,"Using << hNET >> in transfected human embryonic kidney-293 cells, this difference in potency for DVS at sites labeled by [(3)H]NIS was found to distinguish DVS, the DVS analog rac-(1-[1-(3-chloro-phenyl)-2-(4-methylpiperazin-1-yl)-ethyl]cyclohexanol (WY-46824), methylphenidate, and the cocaine analog 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester ([[ RTI-55 ]]) from other hNET antagonists, such as NIS, mazindol, tricyclic antidepressants, and cocaine.",1560,1
1561,"Using hNET in transfected human embryonic kidney-293 cells, this difference in potency for DVS at sites labeled by [(3)H]NIS was found to distinguish DVS, the DVS analog rac-(1-[1-(3-chloro-phenyl)-2-(4-methylpiperazin-1-yl)-ethyl]cyclohexanol (WY-46824), methylphenidate, and the cocaine analog 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester (RTI-55) from other << hNET >> antagonists, such as [[ NIS ]], mazindol, tricyclic antidepressants, and cocaine.",1561,1
1562,"Using hNET in transfected human embryonic kidney-293 cells, this difference in potency for DVS at sites labeled by [(3)H]NIS was found to distinguish DVS, the DVS analog rac-(1-[1-(3-chloro-phenyl)-2-(4-methylpiperazin-1-yl)-ethyl]cyclohexanol (WY-46824), methylphenidate, and the cocaine analog 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester (RTI-55) from other << hNET >> antagonists, such as NIS, [[ mazindol ]], tricyclic antidepressants, and cocaine.",1562,1
1563,"Using hNET in transfected human embryonic kidney-293 cells, this difference in potency for DVS at sites labeled by [(3)H]NIS was found to distinguish DVS, the DVS analog rac-(1-[1-(3-chloro-phenyl)-2-(4-methylpiperazin-1-yl)-ethyl]cyclohexanol (WY-46824), methylphenidate, and the cocaine analog 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester (RTI-55) from other << hNET >> antagonists, such as NIS, mazindol, [[ tricyclic ]] antidepressants, and cocaine.",1563,1
1564,"Using hNET in transfected human embryonic kidney-293 cells, this difference in potency for DVS at sites labeled by [(3)H]NIS was found to distinguish DVS, the DVS analog rac-(1-[1-(3-chloro-phenyl)-2-(4-methylpiperazin-1-yl)-ethyl]cyclohexanol (WY-46824), methylphenidate, and the cocaine analog 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester (RTI-55) from other << hNET >> antagonists, such as NIS, mazindol, tricyclic antidepressants, and [[ cocaine ]].",1564,1
1565,"Using << hNET >> in transfected human embryonic kidney-293 cells, this difference in potency for DVS at sites labeled by [(3)H]NIS was found to distinguish [[ DVS ]], the DVS analog rac-(1-[1-(3-chloro-phenyl)-2-(4-methylpiperazin-1-yl)-ethyl]cyclohexanol (WY-46824), methylphenidate, and the cocaine analog 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester (RTI-55) from other hNET antagonists, such as NIS, mazindol, tricyclic antidepressants, and cocaine.",1565,1
1566,"<< Sorafenib >> and sunitinib are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 ([[ VEGFR-2 ]], VEGFR-3) and platelet-derived growth factor receptor beta (PDGFR-beta), while temsirolimus is an mTOR inhibitor.",1566,0
1567,"<< Sorafenib >> and sunitinib are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 (VEGFR-2, [[ VEGFR-3 ]]) and platelet-derived growth factor receptor beta (PDGFR-beta), while temsirolimus is an mTOR inhibitor.",1567,0
1568,"<< Sorafenib >> and sunitinib are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 (VEGFR-2, VEGFR-3) and [[ platelet-derived growth factor receptor beta ]] (PDGFR-beta), while temsirolimus is an mTOR inhibitor.",1568,0
1569,"<< Sorafenib >> and sunitinib are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 (VEGFR-2, VEGFR-3) and platelet-derived growth factor receptor beta ([[ PDGFR-beta ]]), while temsirolimus is an mTOR inhibitor.",1569,0
1570,"Sorafenib and << sunitinib >> are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 ([[ VEGFR-2 ]], VEGFR-3) and platelet-derived growth factor receptor beta (PDGFR-beta), while temsirolimus is an mTOR inhibitor.",1570,0
1571,"Sorafenib and << sunitinib >> are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 (VEGFR-2, [[ VEGFR-3 ]]) and platelet-derived growth factor receptor beta (PDGFR-beta), while temsirolimus is an mTOR inhibitor.",1571,0
1572,"Sorafenib and << sunitinib >> are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 (VEGFR-2, VEGFR-3) and [[ platelet-derived growth factor receptor beta ]] (PDGFR-beta), while temsirolimus is an mTOR inhibitor.",1572,0
1573,"Sorafenib and << sunitinib >> are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 (VEGFR-2, VEGFR-3) and platelet-derived growth factor receptor beta ([[ PDGFR-beta ]]), while temsirolimus is an mTOR inhibitor.",1573,0
1574,"Sorafenib and sunitinib are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 (VEGFR-2, VEGFR-3) and platelet-derived growth factor receptor beta (PDGFR-beta), while << temsirolimus >> is an [[ mTOR ]] inhibitor.",1574,0
1575,"One is that the binding of retinoids to nuclear retinoic acid receptors (RARs) does not match their therapeutic efficacy: acitretin activates the three receptor subtypes, RAR-alpha, -beta and -gamma, without measurable receptor binding, whereas << tazarotene >> preferentially binds to and activates RAR-beta and -gamma in preference to [[ RAR-alpha ]].",1575,9
1576,"Comprehensive review of << rasagiline >>, a second-generation [[ monoamine oxidase ]] inhibitor, for the treatment of Parkinson's disease.",1576,0
1577,Rasagiline [<< N-propargyl-l(R)-aminoindan >>] is a second-generation propargylamine pharmacophore that selectively and irreversibly inhibits brain [[ MAO-B ]] and is specifically designed for the treatment of Parkinson's disease (PD).,1577,0
1578,Rasagiline [N-propargyl-l(R)-aminoindan] is a second-generation << propargylamine >> pharmacophore that selectively and irreversibly inhibits brain [[ MAO-B ]] and is specifically designed for the treatment of Parkinson's disease (PD).,1578,0
1579,<< Rasagiline >> [N-propargyl-l(R)-aminoindan] is a second-generation propargylamine pharmacophore that selectively and irreversibly inhibits brain [[ MAO-B ]] and is specifically designed for the treatment of Parkinson's disease (PD).,1579,0
1580,"Based on the results from those studies, we concluded that << rasagiline >> PO QD, at the therapeutic dosage range of 0.5 to 1 rag/d, is effective and well tolerated and completely, selectively, and specifically inhibited [[ MAO-B ]].",1580,0
1581,This overview focuses on the indirect antithrombin dependent pentasaccharide derivatives of idraparinux and on the most advanced oral direct inhibitors to << factor Xa >> ([[ rivaroxaban ]] and apixaban) and IIa (dabigatran).,1581,0
1582,This overview focuses on the indirect antithrombin dependent pentasaccharide derivatives of idraparinux and on the most advanced oral direct inhibitors to << factor Xa >> (rivaroxaban and [[ apixaban ]]) and IIa (dabigatran).,1582,0
1583,"INTERVENTIONS: In the 8-week run-in period, all participants received the << ACE >> inhibitor [[ cilazapril ]] (5 mg), the ARB telmisartan (80 mg), and the diuretic hydrochlorothiazide (12.5 mg) as double RAAS blockade to achieve the target blood pressure of less than 130/80 mm Hg.",1583,0
1584,"Porcine TLR8 and << TLR7 >> are both activated by a selective TLR7 ligand, [[ imiquimod ]].",1584,9
1585,"Porcine << TLR8 >> and TLR7 are both activated by a selective TLR7 ligand, [[ imiquimod ]].",1585,9
1586,"Two << imidazoquinoline >> molecules, imiquimod and gardiquimod, markedly activated both [[ porcine TLR7 ]] and TLR8 whereas only human TLR7, but not TLR8, was activated by the ligands.",1586,9
1587,"Two << imidazoquinoline >> molecules, imiquimod and gardiquimod, markedly activated both porcine TLR7 and [[ TLR8 ]] whereas only human TLR7, but not TLR8, was activated by the ligands.",1587,9
1588,"Two << imidazoquinoline >> molecules, imiquimod and gardiquimod, markedly activated both porcine TLR7 and TLR8 whereas only [[ human TLR7 ]], but not TLR8, was activated by the ligands.",1588,9
1589,"Two imidazoquinoline molecules, << imiquimod >> and gardiquimod, markedly activated both [[ porcine TLR7 ]] and TLR8 whereas only human TLR7, but not TLR8, was activated by the ligands.",1589,9
1590,"Two imidazoquinoline molecules, << imiquimod >> and gardiquimod, markedly activated both porcine TLR7 and [[ TLR8 ]] whereas only human TLR7, but not TLR8, was activated by the ligands.",1590,9
1591,"Two imidazoquinoline molecules, << imiquimod >> and gardiquimod, markedly activated both porcine TLR7 and TLR8 whereas only [[ human TLR7 ]], but not TLR8, was activated by the ligands.",1591,9
1592,"Two imidazoquinoline molecules, imiquimod and << gardiquimod >>, markedly activated both [[ porcine TLR7 ]] and TLR8 whereas only human TLR7, but not TLR8, was activated by the ligands.",1592,9
1593,"Two imidazoquinoline molecules, imiquimod and << gardiquimod >>, markedly activated both porcine TLR7 and [[ TLR8 ]] whereas only human TLR7, but not TLR8, was activated by the ligands.",1593,9
1594,"Two imidazoquinoline molecules, imiquimod and << gardiquimod >>, markedly activated both porcine TLR7 and TLR8 whereas only [[ human TLR7 ]], but not TLR8, was activated by the ligands.",1594,9
1595,"Moreover, activation of transfected cells and porcine PBMC by << TLR7 >> ligands was inhibited by [[ bafilomycin A(1) ]] indicating the requirement of endosomal/lysosomal acidification for activation of the receptors.",1595,0
1596,High-affinity blockade of << voltage-operated skeletal muscle and neuronal sodium channels >> by [[ halogenated propofol ]] analogues.,1596,0
1597,"The IC(50) for block of resting channels at -150 mV was 2.3, 3.9 and 11.3 microM in Na(V)1.4, respectively, and 29.2 microM for << 4-chloropropofol >> in [[ Na(V)1.2 ]].",1597,0
1598,"Estimated affinities for the fast-inactivated channel state were 81 nM, 312 nM and 227 nM for << 4-iodopropofol >>, 4-bromopropofol and 4-chloropropofol in [[ Na(V)1.4 ]], and 450 nM for 4-chloropropofol in Na(V)1.2.",1598,0
1599,"Estimated affinities for the fast-inactivated channel state were 81 nM, 312 nM and 227 nM for 4-iodopropofol, << 4-bromopropofol >> and 4-chloropropofol in [[ Na(V)1.4 ]], and 450 nM for 4-chloropropofol in Na(V)1.2.",1599,0
1600,"Estimated affinities for the fast-inactivated channel state were 81 nM, 312 nM and 227 nM for 4-iodopropofol, 4-bromopropofol and << 4-chloropropofol >> in [[ Na(V)1.4 ]], and 450 nM for 4-chloropropofol in Na(V)1.2.",1600,0
1601,"Estimated affinities for the fast-inactivated channel state were 81 nM, 312 nM and 227 nM for 4-iodopropofol, 4-bromopropofol and 4-chloropropofol in Na(V)1.4, and 450 nM for << 4-chloropropofol >> in [[ Na(V)1.2 ]].",1601,0
1602,CONCLUSIONS AND IMPLICATIONS: << Halogenated propofol >> analogues constitute a novel class of [[ sodium channel ]]-blocking drugs possessing almost 100-fold higher potency compared with the local anaesthetic and anti-arrhythmic drug lidocaine.,1602,0
1603,"<< Irbesartan >> (Aprovel, Avapro, Irbetan, Karvea), an [[ angiotensin II receptor type 1 ]] antagonist, is approved in many countries worldwide for the treatment of hypertension.",1603,1
1604,"Irbesartan (<< Aprovel >>, Avapro, Irbetan, Karvea), an [[ angiotensin II receptor type 1 ]] antagonist, is approved in many countries worldwide for the treatment of hypertension.",1604,1
1605,"Irbesartan (Aprovel, << Avapro >>, Irbetan, Karvea), an [[ angiotensin II receptor type 1 ]] antagonist, is approved in many countries worldwide for the treatment of hypertension.",1605,1
1606,"Irbesartan (Aprovel, Avapro, << Irbetan >>, Karvea), an [[ angiotensin II receptor type 1 ]] antagonist, is approved in many countries worldwide for the treatment of hypertension.",1606,1
1607,"Irbesartan (Aprovel, Avapro, Irbetan, << Karvea >>), an [[ angiotensin II receptor type 1 ]] antagonist, is approved in many countries worldwide for the treatment of hypertension.",1607,1
1608,"DNA damage is accepted as a consequence of << thymidylate >> deprivation induced by chemotherapeutic inhibitors of [[ thymidylate synthase ]] (TS), but the types of damage and signaling responses remain incompletely understood.",1608,4
1609,"DNA damage is accepted as a consequence of << thymidylate >> deprivation induced by chemotherapeutic inhibitors of thymidylate synthase ([[ TS ]]), but the types of damage and signaling responses remain incompletely understood.",1609,4
1610,"When RAD51, which is a central component of HR, was depleted by siRNA cells were sensitized to raltitrexed (<< RTX >>), which specifically inhibits [[ TS ]].",1610,0
1611,"<< RTX >> treatment also induced foci of [[ RAD51 ]], gamma-H2AX, phospho-Chk1, and phospho-NBS1, although the extent of co-localization with RPA2 foci varied.",1611,6
1612,"<< RTX >> treatment also induced foci of RAD51, [[ gamma-H2AX ]], phospho-Chk1, and phospho-NBS1, although the extent of co-localization with RPA2 foci varied.",1612,6
1613,"<< RTX >> treatment also induced foci of RAD51, gamma-H2AX, [[ phospho-Chk1 ]], and phospho-NBS1, although the extent of co-localization with RPA2 foci varied.",1613,6
1614,"<< RTX >> treatment also induced foci of RAD51, gamma-H2AX, phospho-Chk1, and [[ phospho-NBS1 ]], although the extent of co-localization with RPA2 foci varied.",1614,6
1615,<< Nicotinamide N-methyltransferase >> (NNMT) catalyses the conversion of nicotinamide to [[ 1-methylnicotinamide ]] and plays an important role in hepatic detoxification reactions.,1615,4
1616,Nicotinamide N-methyltransferase (<< NNMT >>) catalyses the conversion of nicotinamide to [[ 1-methylnicotinamide ]] and plays an important role in hepatic detoxification reactions.,1616,4
1617,<< Nicotinamide N-methyltransferase >> (NNMT) catalyses the conversion of [[ nicotinamide ]] to 1-methylnicotinamide and plays an important role in hepatic detoxification reactions.,1617,5
1618,Nicotinamide N-methyltransferase (<< NNMT >>) catalyses the conversion of [[ nicotinamide ]] to 1-methylnicotinamide and plays an important role in hepatic detoxification reactions.,1618,5
1619,"<< Homocysteine >>, the atherogenic product of the [[ NNMT ]]-catalyzed reaction, was secreted from 3T3-L1 cells or adipose tissue cultures.",1619,4
1620,Homocysteine release increased during 3T3-L1 differentiation and was reduced when adipose tissue was treated with the << NNMT >> inhibitor [[ 1-methylnicotinamide ]].,1620,0
1621,"Nicotinic acid (<< NA >>), a widely used drug to lower elevated plasma lipid levels, induced [[ NNMT ]] enzyme activity in white adipose tissue of mice.",1621,9
1622,"<< Nicotinic acid >> (NA), a widely used drug to lower elevated plasma lipid levels, induced [[ NNMT ]] enzyme activity in white adipose tissue of mice.",1622,9
1623,These data support the concept that adipose tissue << NNMT >> contributes to the increased plasma [[ homocysteine ]] levels in patients treated with NA.,1623,4
1624,Global target profile of the << kinase >> inhibitor [[ bosutinib ]] in primary chronic myeloid leukemia cells.,1624,0
1625,"Here, we characterized the target profile of the dual << SRC >>/ABL inhibitor [[ bosutinib ]] employing a two-tiered approach using chemical proteomics to identify natural binders in whole cell lysates of primary CML and K562 cells in parallel to in vitro kinase assays against a large recombinant kinase panel.",1625,0
1626,"Here, we characterized the target profile of the dual SRC/<< ABL >> inhibitor [[ bosutinib ]] employing a two-tiered approach using chemical proteomics to identify natural binders in whole cell lysates of primary CML and K562 cells in parallel to in vitro kinase assays against a large recombinant kinase panel.",1626,0
1627,"A comparison of bosutinib with << dasatinib >> across the whole [[ kinase ]] panel revealed overlapping, but distinct, inhibition profiles.",1627,0
1628,"A comparison of << bosutinib >> with dasatinib across the whole [[ kinase ]] panel revealed overlapping, but distinct, inhibition profiles.",1628,0
1629,"Finally, << bosutinib >> is the first [[ kinase ]] inhibitor shown to target CAMK2G, recently implicated in myeloid leukemia cell proliferation.",1629,0
1630,"Finally, << bosutinib >> is the first kinase inhibitor shown to target [[ CAMK2G ]], recently implicated in myeloid leukemia cell proliferation.",1630,0
1631,Affinity alkylation with 2 alpha-bromoacetoxyprogesterone suggests that the << dehydrogenase >> and isomerase substrate [[ steroids ]] bind at different sites on the same protein.,1631,5
1632,"The affinity labeling << nucleotide >> analog, 5'-[p-(fluorosulfonyl)benzoyl]adenosine (FSA), inactivates the [[ dehydrogenase ]] and isomerase activities at similar rates in an irreversible manner which follows first order kinetics with respect to both time and alkylator concentration (0.2-0.6 mM).",1632,0
1633,"The affinity labeling nucleotide analog, << 5'-[p-(fluorosulfonyl)benzoyl]adenosine >> (FSA), inactivates the [[ dehydrogenase ]] and isomerase activities at similar rates in an irreversible manner which follows first order kinetics with respect to both time and alkylator concentration (0.2-0.6 mM).",1633,0
1634,"The affinity labeling nucleotide analog, 5'-[p-(fluorosulfonyl)benzoyl]adenosine (<< FSA >>), inactivates the [[ dehydrogenase ]] and isomerase activities at similar rates in an irreversible manner which follows first order kinetics with respect to both time and alkylator concentration (0.2-0.6 mM).",1634,0
1635,"The 3 beta-hydroxysteroid substrate, pregnenolone, protects isomerase as well as << dehydrogenase >> from inactivation by [[ FSA ]].",1635,0
1636,"The most successful example of << kinase >> blockers is [[ Imatinib ]] (Imatinib mesylate, Gleevec, STI571), the inhibitor of Bcr/Abl oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.",1636,0
1637,"The most successful example of kinase blockers is << Imatinib >> (Imatinib mesylate, Gleevec, STI571), the inhibitor of [[ Bcr ]]/Abl oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.",1637,0
1638,"The most successful example of kinase blockers is << Imatinib >> (Imatinib mesylate, Gleevec, STI571), the inhibitor of Bcr/[[ Abl ]] oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.",1638,0
1639,"The most successful example of << kinase >> blockers is Imatinib ([[ Imatinib mesylate ]], Gleevec, STI571), the inhibitor of Bcr/Abl oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.",1639,0
1640,"The most successful example of kinase blockers is Imatinib (<< Imatinib mesylate >>, Gleevec, STI571), the inhibitor of [[ Bcr ]]/Abl oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.",1640,0
1641,"The most successful example of kinase blockers is Imatinib (<< Imatinib mesylate >>, Gleevec, STI571), the inhibitor of Bcr/[[ Abl ]] oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.",1641,0
1642,"The most successful example of << kinase >> blockers is Imatinib (Imatinib mesylate, [[ Gleevec ]], STI571), the inhibitor of Bcr/Abl oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.",1642,0
1643,"The most successful example of kinase blockers is Imatinib (Imatinib mesylate, << Gleevec >>, STI571), the inhibitor of [[ Bcr ]]/Abl oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.",1643,0
1644,"The most successful example of kinase blockers is Imatinib (Imatinib mesylate, << Gleevec >>, STI571), the inhibitor of Bcr/[[ Abl ]] oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.",1644,0
1645,"The most successful example of << kinase >> blockers is Imatinib (Imatinib mesylate, Gleevec, [[ STI571 ]]), the inhibitor of Bcr/Abl oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.",1645,0
1646,"The most successful example of kinase blockers is Imatinib (Imatinib mesylate, Gleevec, << STI571 >>), the inhibitor of [[ Bcr ]]/Abl oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.",1646,0
1647,"The most successful example of kinase blockers is Imatinib (Imatinib mesylate, Gleevec, << STI571 >>), the inhibitor of Bcr/[[ Abl ]] oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.",1647,0
1648,"Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (<< SU 11248 >>, Sutent) specific for [[ VEGF receptor ]] kinase, AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.",1648,0
1649,"Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (<< SU 11248 >>, Sutent) specific for VEGF receptor [[ kinase ]], AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.",1649,0
1650,"Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, << Sutent >>) specific for [[ VEGF receptor ]] kinase, AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.",1650,0
1651,"Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, << Sutent >>) specific for VEGF receptor [[ kinase ]], AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.",1651,0
1652,"Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for VEGF receptor kinase, << AMN107 >> (Nilotinib) and INNO-406 (NS-187) specific for [[ c-KIT ]] kinase.",1652,0
1653,"Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for VEGF receptor kinase, AMN107 (<< Nilotinib >>) and INNO-406 (NS-187) specific for [[ c-KIT ]] kinase.",1653,0
1654,"Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for VEGF receptor kinase, AMN107 (Nilotinib) and << INNO-406 >> (NS-187) specific for [[ c-KIT ]] kinase.",1654,0
1655,"Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for VEGF receptor kinase, AMN107 (Nilotinib) and INNO-406 (<< NS-187 >>) specific for [[ c-KIT ]] kinase.",1655,0
1656,"Others kinase inhibitors used recently in cancer therapy include << Dasatinib >> (BMS-354825) specific for [[ ABL ]] non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for VEGF receptor kinase, AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.",1656,0
1657,"Others kinase inhibitors used recently in cancer therapy include << Dasatinib >> (BMS-354825) specific for ABL [[ non-receptor cytoplasmic kinase ]], Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for VEGF receptor kinase, AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.",1657,0
1658,"Others kinase inhibitors used recently in cancer therapy include Dasatinib (<< BMS-354825 >>) specific for [[ ABL ]] non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for VEGF receptor kinase, AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.",1658,0
1659,"Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, << Gefitinib >> (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for [[ VEGF receptor ]] kinase, AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.",1659,0
1660,"Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, << Gefitinib >> (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for VEGF receptor [[ kinase ]], AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.",1660,0
1661,"Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (<< Iressa >>), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for [[ VEGF receptor ]] kinase, AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.",1661,0
1662,"Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (<< Iressa >>), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for VEGF receptor [[ kinase ]], AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.",1662,0
1663,"Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), << Erlotinib >> (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for [[ VEGF receptor ]] kinase, AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.",1663,0
1664,"Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), << Erlotinib >> (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for VEGF receptor [[ kinase ]], AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.",1664,0
1665,"Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (<< OSI-774 >>, Tarceva) and Sunitinib (SU 11248, Sutent) specific for [[ VEGF receptor ]] kinase, AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.",1665,0
1666,"Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (<< OSI-774 >>, Tarceva) and Sunitinib (SU 11248, Sutent) specific for VEGF receptor [[ kinase ]], AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.",1666,0
1667,"Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, << Tarceva >>) and Sunitinib (SU 11248, Sutent) specific for [[ VEGF receptor ]] kinase, AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.",1667,0
1668,"Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, << Tarceva >>) and Sunitinib (SU 11248, Sutent) specific for VEGF receptor [[ kinase ]], AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.",1668,0
1669,"Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and << Sunitinib >> (SU 11248, Sutent) specific for [[ VEGF receptor ]] kinase, AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.",1669,0
1670,"Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and << Sunitinib >> (SU 11248, Sutent) specific for VEGF receptor [[ kinase ]], AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.",1670,0
1671,"The following << TK >> blockers for treatment of various human tumors are in clinical development: [[ Lapatinib ]] (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib (CI-1033), Zactima (ZD6474), Vatalanib (PTK787/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide (SU101, Arava).",1671,0
1672,"The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib ([[ Lapatinib ditosylate ]], Tykerb, GW-572016), Canertinib (CI-1033), Zactima (ZD6474), Vatalanib (PTK787/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide (SU101, Arava).",1672,0
1673,"The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, [[ Tykerb ]], GW-572016), Canertinib (CI-1033), Zactima (ZD6474), Vatalanib (PTK787/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide (SU101, Arava).",1673,0
1674,"The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, [[ GW-572016 ]]), Canertinib (CI-1033), Zactima (ZD6474), Vatalanib (PTK787/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide (SU101, Arava).",1674,0
1675,"The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), [[ Canertinib ]] (CI-1033), Zactima (ZD6474), Vatalanib (PTK787/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide (SU101, Arava).",1675,0
1676,"The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib ([[ CI-1033 ]]), Zactima (ZD6474), Vatalanib (PTK787/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide (SU101, Arava).",1676,0
1677,"The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib (CI-1033), [[ Zactima ]] (ZD6474), Vatalanib (PTK787/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide (SU101, Arava).",1677,0
1678,"The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib (CI-1033), Zactima ([[ ZD6474 ]]), Vatalanib (PTK787/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide (SU101, Arava).",1678,0
1679,"The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib (CI-1033), Zactima (ZD6474), [[ Vatalanib ]] (PTK787/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide (SU101, Arava).",1679,0
1680,"The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib (CI-1033), Zactima (ZD6474), Vatalanib ([[ PTK787 ]]/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide (SU101, Arava).",1680,0
1681,"The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib (CI-1033), Zactima (ZD6474), Vatalanib (PTK787/[[ ZK 222584 ]]), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide (SU101, Arava).",1681,0
1682,"The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib (CI-1033), Zactima (ZD6474), Vatalanib (PTK787/ZK 222584), [[ Sorafenib ]] (Bay 43-9006, Nexavar), and Leflunomide (SU101, Arava).",1682,0
1683,"The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib (CI-1033), Zactima (ZD6474), Vatalanib (PTK787/ZK 222584), Sorafenib ([[ Bay 43-9006 ]], Nexavar), and Leflunomide (SU101, Arava).",1683,0
1684,"The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib (CI-1033), Zactima (ZD6474), Vatalanib (PTK787/ZK 222584), Sorafenib (Bay 43-9006, [[ Nexavar ]]), and Leflunomide (SU101, Arava).",1684,0
1685,"The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib (CI-1033), Zactima (ZD6474), Vatalanib (PTK787/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and [[ Leflunomide ]] (SU101, Arava).",1685,0
1686,"The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib (CI-1033), Zactima (ZD6474), Vatalanib (PTK787/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide ([[ SU101 ]], Arava).",1686,0
1687,"The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib (CI-1033), Zactima (ZD6474), Vatalanib (PTK787/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide (SU101, [[ Arava ]]).",1687,0
1688,"Currently, the use of orally administered << MAO >> inhibitor antidepressants (eg, [[ phenelzine ]], tranylcypromine) is limited by the risk of tyramine-provoked events (eg, acute hypertension and headache, also known as the ""cheese reaction"") when combined with dietary tyramine.",1688,0
1689,"Currently, the use of orally administered << MAO >> inhibitor antidepressants (eg, phenelzine, [[ tranylcypromine ]]) is limited by the risk of tyramine-provoked events (eg, acute hypertension and headache, also known as the ""cheese reaction"") when combined with dietary tyramine.",1689,0
1690,"It undergoes extensive biotransformation, which is affected by poor metabolism by << cytochrome P450 (CYP) 2D6 >> in a small percentage of the population; these patients have greater exposure to and slower elimination of [[ atomoxetine ]] than extensive metabolizers.",1690,5
1691,"<< CYP2D6 >> inhibitors, such as [[ paroxetine ]], are associated with changes in atomoxetine pharmacokinetics similar to those observed among poor CYP2D6 metabolizers.",1691,0
1692,"CYP2D6 inhibitors, such as paroxetine, are associated with changes in << atomoxetine >> pharmacokinetics similar to those observed among poor [[ CYP2D6 ]] metabolizers.",1692,5
1693,<< Atomoxetine >> appeared better tolerated among extensive [[ CYP2D6 ]] metabolizers than among poor metabolizers.,1693,5
1694,<< Mammalian glutamate dehydrogenase >> (GDH) is a homohexameric enzyme that catalyzes the reversible oxidative deamination of l-glutamate to [[ 2-oxoglutarate ]] using NAD(P)(+) as coenzyme.,1694,4
1695,Mammalian glutamate dehydrogenase (<< GDH >>) is a homohexameric enzyme that catalyzes the reversible oxidative deamination of l-glutamate to [[ 2-oxoglutarate ]] using NAD(P)(+) as coenzyme.,1695,4
1696,<< Mammalian glutamate dehydrogenase >> (GDH) is a homohexameric enzyme that catalyzes the reversible oxidative deamination of [[ l-glutamate ]] to 2-oxoglutarate using NAD(P)(+) as coenzyme.,1696,5
1697,Mammalian glutamate dehydrogenase (<< GDH >>) is a homohexameric enzyme that catalyzes the reversible oxidative deamination of [[ l-glutamate ]] to 2-oxoglutarate using NAD(P)(+) as coenzyme.,1697,5
1698,The recently discovered hyperinsulinism/hyperammonemia disorder showed that the loss of allosteric inhibition of GDH by << GTP >> causes excessive secretion of [[ insulin ]].,1698,6
1699,"Subsequent studies demonstrated that wild-type and hyperinsulinemia/hyperammonemia forms of << GDH >> are inhibited by the green tea polyphenols, [[ epigallocatechin gallate ]] and epicatechin gallate.",1699,0
1700,"Subsequent studies demonstrated that wild-type and hyperinsulinemia/hyperammonemia forms of << GDH >> are inhibited by the green tea polyphenols, epigallocatechin gallate and [[ epicatechin gallate ]].",1700,0
1701,"BACKGROUND: Peripheral inflammatory pain is associated with an upregulation of spinal cord << COX-2 >> (cyclooxygenase-2), with a subsequent increase in central [[ prostaglandin E2 ]] (PGE2) levels associated with the development of hyperalgesia.",1701,4
1702,"BACKGROUND: Peripheral inflammatory pain is associated with an upregulation of spinal cord COX-2 (<< cyclooxygenase-2 >>), with a subsequent increase in central [[ prostaglandin E2 ]] (PGE2) levels associated with the development of hyperalgesia.",1702,4
1703,"BACKGROUND: Peripheral inflammatory pain is associated with an upregulation of spinal cord << COX-2 >> (cyclooxygenase-2), with a subsequent increase in central prostaglandin E2 ([[ PGE2 ]]) levels associated with the development of hyperalgesia.",1703,4
1704,"BACKGROUND: Peripheral inflammatory pain is associated with an upregulation of spinal cord COX-2 (<< cyclooxygenase-2 >>), with a subsequent increase in central prostaglandin E2 ([[ PGE2 ]]) levels associated with the development of hyperalgesia.",1704,4
1705,"Using the << alpha 1-adrenoceptor >> subtype-selective antagonists chlorethylclonidine (CEC), WB4101, and [[ 5-methyl-urapidil ]], we have examined the possible heterogeneity in the alpha 1-adrenoceptor populations in rabbit aorta.",1705,1
1706,"Using the << alpha 1-adrenoceptor >> subtype-selective antagonists [[ chlorethylclonidine ]] (CEC), WB4101, and 5-methyl-urapidil, we have examined the possible heterogeneity in the alpha 1-adrenoceptor populations in rabbit aorta.",1706,1
1707,"Using the << alpha 1-adrenoceptor >> subtype-selective antagonists chlorethylclonidine ([[ CEC ]]), WB4101, and 5-methyl-urapidil, we have examined the possible heterogeneity in the alpha 1-adrenoceptor populations in rabbit aorta.",1707,1
1708,"Using the << alpha 1-adrenoceptor >> subtype-selective antagonists chlorethylclonidine (CEC), [[ WB4101 ]], and 5-methyl-urapidil, we have examined the possible heterogeneity in the alpha 1-adrenoceptor populations in rabbit aorta.",1708,1
1709,Radioligand binding studies with the nonselective << alpha 1-adrenoceptor >> antagonist radioligand [[ 125I-BE2254 ]] showed that 73-87% of the binding sites in rabbit aorta are CEC sensitive and they are predominantly low affinity sites both for WB4101 (pKd = 8.1) and for 5-methylurapidil (pKd = 7.1).,1709,1
1710,"The Schild plots for the competitive antagonists WB4101 and 5-methyl-urapidil against << alpha 1a-adrenoceptor >>-selective agonist [[ methoxamine ]]-induced contraction were linear and had slopes not significantly different from unity, with a pA2 of 9.07 +/- 0.07 (n = 5) for WB4101 and 9.09 +/- 0.05 (n = 3) for 5-methyl-urapidil.",1710,2
1711,"The Schild plots for the competitive antagonists WB4101 and 5-methyl-urapidil against << alpha 1a-adrenoceptor >>-selective agonist methoxamine-induced contraction were linear and had slopes not significantly different from unity, with a pA2 of 9.07 +/- 0.07 (n = 5) for [[ WB4101 ]] and 9.09 +/- 0.05 (n = 3) for 5-methyl-urapidil.",1711,1
1712,"The Schild plots for the competitive antagonists WB4101 and 5-methyl-urapidil against << alpha 1a-adrenoceptor >>-selective agonist methoxamine-induced contraction were linear and had slopes not significantly different from unity, with a pA2 of 9.07 +/- 0.07 (n = 5) for WB4101 and 9.09 +/- 0.05 (n = 3) for [[ 5-methyl-urapidil ]].",1712,1
1713,"The Schild plots for the competitive antagonists << WB4101 >> and 5-methyl-urapidil against [[ alpha 1a-adrenoceptor ]]-selective agonist methoxamine-induced contraction were linear and had slopes not significantly different from unity, with a pA2 of 9.07 +/- 0.07 (n = 5) for WB4101 and 9.09 +/- 0.05 (n = 3) for 5-methyl-urapidil.",1713,1
1714,"The Schild plots for the competitive antagonists WB4101 and << 5-methyl-urapidil >> against [[ alpha 1a-adrenoceptor ]]-selective agonist methoxamine-induced contraction were linear and had slopes not significantly different from unity, with a pA2 of 9.07 +/- 0.07 (n = 5) for WB4101 and 9.09 +/- 0.05 (n = 3) for 5-methyl-urapidil.",1714,1
1715,"Computer-assisted analysis of these curvilinear Schild plots in a two-receptor system indicated that << alpha 1-adrenoceptor >> populations responsible for the constrictive response are predominantly (approximately 80-90%) low affinity sites for the two antagonists (pKd approximately 8.1 for [[ WB4101 ]] and pKd approximately 7.1 for 5-methyl-urapidil) and a small population (approximately 10-20%) are high affinity sites (pKd approximately 9.1 for both WB4101 and 5-methyl-urapidil), which was in good agreement with radioligand binding studies.(ABSTRACT TRUNCATED AT 400 WORDS)",1715,1
1716,"Computer-assisted analysis of these curvilinear Schild plots in a two-receptor system indicated that << alpha 1-adrenoceptor >> populations responsible for the constrictive response are predominantly (approximately 80-90%) low affinity sites for the two antagonists (pKd approximately 8.1 for WB4101 and pKd approximately 7.1 for [[ 5-methyl-urapidil ]]) and a small population (approximately 10-20%) are high affinity sites (pKd approximately 9.1 for both WB4101 and 5-methyl-urapidil), which was in good agreement with radioligand binding studies.(ABSTRACT TRUNCATED AT 400 WORDS)",1716,1
1717,<< Ambrisentan >> is an [[ endothelin receptor ]] antagonist (ERA) that was recently approved for treatment of pulmonary arterial hypertension (PAH).,1717,1
1718,<< Ambrisentan >> is the first [[ ET(A) ]] selective ERA approved for use in the US.,1718,1
1719,"As discussed in this review, various progestogens including dydrogesterone and its 20alpha-dihydro-derivative, medrogestone, << promegestone >>, nomegestrol acetate and norelgestromin can reduce intratissular levels of estradiol in breast cancer by blocking [[ sulfatase ]] and 17beta-hydroxysteroid-dehydrogenase type 1 activities.",1719,0
1720,"As discussed in this review, various progestogens including dydrogesterone and its 20alpha-dihydro-derivative, medrogestone, << promegestone >>, nomegestrol acetate and norelgestromin can reduce intratissular levels of estradiol in breast cancer by blocking sulfatase and [[ 17beta-hydroxysteroid-dehydrogenase type 1 ]] activities.",1720,0
1721,"As discussed in this review, various progestogens including dydrogesterone and its 20alpha-dihydro-derivative, medrogestone, promegestone, << nomegestrol acetate >> and norelgestromin can reduce intratissular levels of estradiol in breast cancer by blocking [[ sulfatase ]] and 17beta-hydroxysteroid-dehydrogenase type 1 activities.",1721,0
1722,"As discussed in this review, various progestogens including dydrogesterone and its 20alpha-dihydro-derivative, medrogestone, promegestone, << nomegestrol acetate >> and norelgestromin can reduce intratissular levels of estradiol in breast cancer by blocking sulfatase and [[ 17beta-hydroxysteroid-dehydrogenase type 1 ]] activities.",1722,0
1723,"As discussed in this review, various progestogens including dydrogesterone and its 20alpha-dihydro-derivative, medrogestone, promegestone, nomegestrol acetate and << norelgestromin >> can reduce intratissular levels of estradiol in breast cancer by blocking [[ sulfatase ]] and 17beta-hydroxysteroid-dehydrogenase type 1 activities.",1723,0
1724,"As discussed in this review, various progestogens including dydrogesterone and its 20alpha-dihydro-derivative, medrogestone, promegestone, nomegestrol acetate and << norelgestromin >> can reduce intratissular levels of estradiol in breast cancer by blocking sulfatase and [[ 17beta-hydroxysteroid-dehydrogenase type 1 ]] activities.",1724,0
1725,"As discussed in this review, various << progestogens >> including dydrogesterone and its 20alpha-dihydro-derivative, medrogestone, promegestone, nomegestrol acetate and norelgestromin can reduce intratissular levels of estradiol in breast cancer by blocking [[ sulfatase ]] and 17beta-hydroxysteroid-dehydrogenase type 1 activities.",1725,0
1726,"As discussed in this review, various << progestogens >> including dydrogesterone and its 20alpha-dihydro-derivative, medrogestone, promegestone, nomegestrol acetate and norelgestromin can reduce intratissular levels of estradiol in breast cancer by blocking sulfatase and [[ 17beta-hydroxysteroid-dehydrogenase type 1 ]] activities.",1726,0
1727,"As discussed in this review, various progestogens including << dydrogesterone >> and its 20alpha-dihydro-derivative, medrogestone, promegestone, nomegestrol acetate and norelgestromin can reduce intratissular levels of estradiol in breast cancer by blocking [[ sulfatase ]] and 17beta-hydroxysteroid-dehydrogenase type 1 activities.",1727,0
1728,"As discussed in this review, various progestogens including << dydrogesterone >> and its 20alpha-dihydro-derivative, medrogestone, promegestone, nomegestrol acetate and norelgestromin can reduce intratissular levels of estradiol in breast cancer by blocking sulfatase and [[ 17beta-hydroxysteroid-dehydrogenase type 1 ]] activities.",1728,0
1729,"As discussed in this review, various progestogens including dydrogesterone and its 20alpha-dihydro-derivative, << medrogestone >>, promegestone, nomegestrol acetate and norelgestromin can reduce intratissular levels of estradiol in breast cancer by blocking [[ sulfatase ]] and 17beta-hydroxysteroid-dehydrogenase type 1 activities.",1729,0
1730,"As discussed in this review, various progestogens including dydrogesterone and its 20alpha-dihydro-derivative, << medrogestone >>, promegestone, nomegestrol acetate and norelgestromin can reduce intratissular levels of estradiol in breast cancer by blocking sulfatase and [[ 17beta-hydroxysteroid-dehydrogenase type 1 ]] activities.",1730,0
1731,"As discussed in this review, various progestogens including dydrogesterone and its 20alpha-dihydro-derivative, medrogestone, promegestone, nomegestrol acetate and norelgestromin can reduce intratissular levels of << estradiol >> in breast cancer by blocking [[ sulfatase ]] and 17beta-hydroxysteroid-dehydrogenase type 1 activities.",1731,5
1732,"As discussed in this review, various progestogens including dydrogesterone and its 20alpha-dihydro-derivative, medrogestone, promegestone, nomegestrol acetate and norelgestromin can reduce intratissular levels of << estradiol >> in breast cancer by blocking sulfatase and [[ 17beta-hydroxysteroid-dehydrogenase type 1 ]] activities.",1732,5
1733,<< Mitiglinide >> reduced fasting plasma glucose and [[ GA ]] levels after 4 weeks and Hb(A1c) levels after 8 weeks.,1733,8
1734,<< Mitiglinide >> reduced fasting plasma glucose and GA levels after 4 weeks and [[ Hb(A1c) ]] levels after 8 weeks.,1734,8
1735,A molecular mechanism for << ibuprofen >>-mediated [[ RhoA ]] inhibition in neurons.,1735,0
1736,<< Ibuprofen >> is a nonsteroidal anti-inflammatory drug widely used to relieve pain and inflammation in many disorders via inhibition of [[ cyclooxygenases ]].,1736,0
1737,"Recently, we have demonstrated that << ibuprofen >> inhibits intracellular signaling of [[ RhoA ]] and promotes significant axonal growth and functional recovery following spinal cord lesions in rodents.",1737,8
1738,"In addition, another study suggests that << ibuprofen >> reduces generation of amyloid-beta42 peptide via inactivation of RhoA signaling, although it may also regulate [[ amyloid-beta42 ]] formation by direct inhibition of the gamma-secretase complex.",1738,6
1739,"In addition, another study suggests that << ibuprofen >> reduces generation of [[ amyloid-beta42 ]] peptide via inactivation of RhoA signaling, although it may also regulate amyloid-beta42 formation by direct inhibition of the gamma-secretase complex.",1739,8
1740,"In addition, another study suggests that << ibuprofen >> reduces generation of amyloid-beta42 peptide via inactivation of [[ RhoA ]] signaling, although it may also regulate amyloid-beta42 formation by direct inhibition of the gamma-secretase complex.",1740,8
1741,"In addition, another study suggests that << ibuprofen >> reduces generation of amyloid-beta42 peptide via inactivation of RhoA signaling, although it may also regulate amyloid-beta42 formation by direct inhibition of the [[ gamma-secretase complex ]].",1741,0
1742,"The molecular mechanisms by which << ibuprofen >> inhibits the [[ RhoA ]] signal in neurons, however, remain unclear.",1742,8
1743,"Here, we report that the transcription factor peroxisome proliferator-activated receptor gamma (PPARgamma) is essential for coupling << ibuprofen >> to [[ RhoA ]] inhibition and subsequent neurite growth promotion in neurons.",1743,0
1744,<< Ibuprofen >> activates [[ PPARgamma ]] in neuron-like PC12 and B104 cells.,1744,9
1745,"Activation of PPARgamma with traditional agonists mimics the << RhoA >>-inhibiting properties of [[ ibuprofen ]] in PC12 cells and, like ibuprofen, promotes neurite elongation in primary cultured neurons exposed to axonal growth inhibitors.",1745,0
1746,These findings support that PPARgamma plays an essential role in mediating the << RhoA >>-inhibiting effect of [[ ibuprofen ]].,1746,0
1747,"Elucidation of the novel molecular mechanisms linking << ibuprofen >> to [[ RhoA ]] inhibition may provide additional therapeutic targets to the disorders characterized by RhoA activation, including spinal cord injuries and Alzheimer's disease.",1747,0
1748,"Of these, the << thrombin >> inhibitor [[ dabigatran ]] and factor Xa inhibitor rivaroxaban have recently been licensed for thromboprophylaxis after orthopaedic surgery mainly in Europe.",1748,0
1749,"Of these, the thrombin inhibitor dabigatran and << factor Xa >> inhibitor [[ rivaroxaban ]] have recently been licensed for thromboprophylaxis after orthopaedic surgery mainly in Europe.",1749,0
1750,"In addition, the << factor Xa >> inhibitor [[ apixaban ]] is in late-stage clinical development.",1750,0
1751,<< Captopril >> directly inhibits [[ matrix metalloproteinase-2 ]] activity in continuous ambulatory peritoneal dialysis therapy.,1751,0
1752,"We determined whether an << angiotensin-converting enzyme >> (ACE) inhibitor, [[ captopril ]], inhibits MMP-2 activity in peritoneal effluents from patients on CAPD, and simulated molecular models of the MMP-2-captopril complex.",1752,0
1753,"We determined whether an angiotensin-converting enzyme (<< ACE >>) inhibitor, [[ captopril ]], inhibits MMP-2 activity in peritoneal effluents from patients on CAPD, and simulated molecular models of the MMP-2-captopril complex.",1753,0
1754,METHODS: The inhibitory effect of << captopril >> on [[ MMP-2 ]] activity was measured in peritoneal effluents from 17 patients on CAPD.,1754,0
1755,"RESULTS: << Captopril >> directly inhibited [[ MMP-2 ]] activity in peritoneal effluents from patients on CAPD (IC50; 48 micromol/l), and that captopril binding to the MMP-2 active site could be formed in each complex model without molecular distortion.",1755,0
1756,"CONCLUSION: ACE inhibitors, such as << captopril >>, may be applied as important compounds for [[ MMP-2 ]] inhibition in inflammation caused by CAPD.",1756,0
1757,"CONCLUSION: << ACE >> inhibitors, such as [[ captopril ]], may be applied as important compounds for MMP-2 inhibition in inflammation caused by CAPD.",1757,0
1758,<< Phenformin >> has a direct inhibitory effect on the [[ ATP-sensitive potassium channel ]].,1758,0
1759,<< Phenformin >> but not metformin inhibits a number of variants of [[ K(ATP) ]] including the cloned equivalents of currents present in vascular and non-vascular smooth muscle (Kir6.1/SUR2B and Kir6.2/SUR2B) and pancreatic beta-cells (Kir6.2/SUR1).,1759,0
1760,<< Phenformin >> but not metformin inhibits a number of variants of K(ATP) including the cloned equivalents of currents present in vascular and non-vascular smooth muscle ([[ Kir6.1 ]]/SUR2B and Kir6.2/SUR2B) and pancreatic beta-cells (Kir6.2/SUR1).,1760,0
1761,<< Phenformin >> but not metformin inhibits a number of variants of K(ATP) including the cloned equivalents of currents present in vascular and non-vascular smooth muscle (Kir6.1/[[ SUR2B ]] and Kir6.2/SUR2B) and pancreatic beta-cells (Kir6.2/SUR1).,1761,0
1762,<< Phenformin >> but not metformin inhibits a number of variants of K(ATP) including the cloned equivalents of currents present in vascular and non-vascular smooth muscle (Kir6.1/SUR2B and [[ Kir6.2 ]]/SUR2B) and pancreatic beta-cells (Kir6.2/SUR1).,1762,0
1763,<< Phenformin >> but not metformin inhibits a number of variants of K(ATP) including the cloned equivalents of currents present in vascular and non-vascular smooth muscle (Kir6.1/SUR2B and Kir6.2/[[ SUR2B ]]) and pancreatic beta-cells (Kir6.2/SUR1).,1763,0
1764,<< Phenformin >> but not metformin inhibits a number of variants of K(ATP) including the cloned equivalents of currents present in vascular and non-vascular smooth muscle (Kir6.1/SUR2B and Kir6.2/SUR2B) and pancreatic beta-cells ([[ Kir6.2 ]]/SUR1).,1764,0
1765,<< Phenformin >> but not metformin inhibits a number of variants of K(ATP) including the cloned equivalents of currents present in vascular and non-vascular smooth muscle (Kir6.1/SUR2B and Kir6.2/SUR2B) and pancreatic beta-cells (Kir6.2/[[ SUR1 ]]).,1765,0
1766,The extent and rate of inhibition are similar to that seen with the known << K(ATP) >> blocker [[ PNU 37883A ]].,1766,0
1767,"Additionally, << phenformin >> inhibited the current elicited through the [[ Kir6.2DeltaC26 ]] (functional without SUR) channel with an IC50 of 1.78 mM.",1767,0
1768,<< Phenformin >> reduced the open probability of [[ Kir6.1 ]]/SUR2B channels by approximately 90% in inside-out patches.,1768,3
1769,<< Phenformin >> reduced the open probability of Kir6.1/[[ SUR2B ]] channels by approximately 90% in inside-out patches.,1769,3
1770,"Different VDRAs are known to have differential effects on serum calcium (Ca), which may also affect serum PTH levels since serum << Ca >> regulates [[ PTH ]] secretion mediated by the Ca-sensing receptor (CaSR).",1770,6
1771,"Both drugs at the tested doses (0.042-0.33 mug/kg) suppressed PTH mRNA expression and serum << PTH >> effectively in the 5/6 NX rats, but [[ paricalcitol ]] was less potent in raising serum Ca than doxercalciferol.",1771,3
1772,"Both drugs at the tested doses (0.042-0.33 mug/kg) suppressed PTH mRNA expression and serum << PTH >> effectively in the 5/6 NX rats, but paricalcitol was less potent in raising serum Ca than [[ doxercalciferol ]].",1772,3
1773,"Both drugs at the tested doses (0.042-0.33 mug/kg) suppressed << PTH >> mRNA expression and serum PTH effectively in the 5/6 NX rats, but [[ paricalcitol ]] was less potent in raising serum Ca than doxercalciferol.",1773,8
1774,"Both drugs at the tested doses (0.042-0.33 mug/kg) suppressed << PTH >> mRNA expression and serum PTH effectively in the 5/6 NX rats, but paricalcitol was less potent in raising serum Ca than [[ doxercalciferol ]].",1774,8
1775,"In pig parathyroid cells, paricalcitol and the active form of doxercalciferol induced VDR translocation from the cytoplasm into the nucleus, suppressed PTH mRNA expression and inhibited cell proliferation in a similar manner, although << paricalcitol >> induced the expression of [[ CaSR ]] mRNA more effectively.",1775,6
1776,"In pig parathyroid cells, << paricalcitol >> and the active form of doxercalciferol induced VDR translocation from the cytoplasm into the nucleus, suppressed [[ PTH ]] mRNA expression and inhibited cell proliferation in a similar manner, although paricalcitol induced the expression of CaSR mRNA more effectively.",1776,8
1777,"In pig parathyroid cells, paricalcitol and the active form of << doxercalciferol >> induced VDR translocation from the cytoplasm into the nucleus, suppressed [[ PTH ]] mRNA expression and inhibited cell proliferation in a similar manner, although paricalcitol induced the expression of CaSR mRNA more effectively.",1777,8
1778,<< Thalidomide >> initiates its teratogenic effects by binding to CRBN and inhibiting the associated [[ ubiquitin ligase ]] activity.,1778,0
1779,"<< Telmisartan >> is an [[ angiotensin II receptor ]] blocker (ARB) displaying unique pharmacologic properties, including a longer half life than any other ARB, that result in large and sustained reductions of blood pressure.",1779,0
1780,"Recent studies indicate that << tamoxifen >> initially acts as an antagonist, but later functions as an [[ ER ]] agonist, promoting tumor growth.",1780,2
1781,"Recent studies indicate that << tamoxifen >> initially acts as an antagonist, but later functions as an [[ ER ]] agonist, promoting tumor growth.",1781,1
1782,"With the pentapeptide linked through the C7alpha position of << estradiol >>, the resulting PROTAC shows the most effective [[ ER ]] degradation and highest affinity for the estrogen receptor.",1782,3
1783,"KEY RESULTS: Several agonists were found to be highly subtype selective because of selective affinity (e.g. << salmeterol >> and formoterol, for the [[ beta(2)-adrenoceptor ]] over the beta(1) or beta(3)), while others (e.g. isoprenaline) had little affinity-selectivity.",1783,2
1784,"KEY RESULTS: Several agonists were found to be highly subtype selective because of selective affinity (e.g. << salmeterol >> and formoterol, for the beta(2)-adrenoceptor over the [[ beta(1) ]] or beta(3)), while others (e.g. isoprenaline) had little affinity-selectivity.",1784,2
1785,"KEY RESULTS: Several agonists were found to be highly subtype selective because of selective affinity (e.g. salmeterol and << formoterol >>, for the [[ beta(2)-adrenoceptor ]] over the beta(1) or beta(3)), while others (e.g. isoprenaline) had little affinity-selectivity.",1785,2
1786,"KEY RESULTS: Several agonists were found to be highly subtype selective because of selective affinity (e.g. salmeterol and << formoterol >>, for the beta(2)-adrenoceptor over the beta(1) or [[ beta(3) ]]), while others (e.g. isoprenaline) had little affinity-selectivity.",1786,2
1787,"KEY RESULTS: Several agonists were found to be highly subtype selective because of selective affinity (e.g. salmeterol and formoterol, for the << beta(2)-adrenoceptor >> over the beta(1) or beta(3)), while others (e.g. [[ isoprenaline ]]) had little affinity-selectivity.",1787,2
1788,"KEY RESULTS: Several agonists were found to be highly subtype selective because of selective affinity (e.g. salmeterol and formoterol, for the beta(2)-adrenoceptor over the << beta(1) >> or beta(3)), while others (e.g. [[ isoprenaline ]]) had little affinity-selectivity.",1788,2
1789,"KEY RESULTS: Several agonists were found to be highly subtype selective because of selective affinity (e.g. salmeterol and formoterol, for the beta(2)-adrenoceptor over the beta(1) or << beta(3) >>), while others (e.g. [[ isoprenaline ]]) had little affinity-selectivity.",1789,2
1790,<< Rasagiline >>: a novel anti-Parkinsonian [[ monoamine oxidase-B ]] inhibitor with neuroprotective activity.,1790,0
1791,"<< Rasagiline >> (N-propargyl-1-(R)-aminoindan) is a novel, highly potent irreversible [[ monoamine oxidase (MAO)-B ]] inhibitor, anti-Parkinsonian drug.",1791,0
1792,"Rasagiline (<< N-propargyl-1-(R)-aminoindan >>) is a novel, highly potent irreversible [[ monoamine oxidase (MAO)-B ]] inhibitor, anti-Parkinsonian drug.",1792,0
1793,"Its S-isomer, << TVP1022 >> is thousand times less potent as an [[ MAO-B ]] inhibitor.",1793,0
1794,"However, both compounds have similar molecular mechanisms of neuroprotection in neuronal cell cultures and animal neurodegenerative models, indicating that the neuroprotective effect of rasagiline does not depend on inhibition of MAO-B, but rather is associated with the << N-propargyl >> moiety, which promotes mitochondrial viability and stabilizes permeability transition by regulating [[ Bcl-2 ]] family proteins.",1794,6
1795,"However, both compounds have similar molecular mechanisms of neuroprotection in neuronal cell cultures and animal neurodegenerative models, indicating that the neuroprotective effect of << rasagiline >> does not depend on inhibition of [[ MAO-B ]], but rather is associated with the N-propargyl moiety, which promotes mitochondrial viability and stabilizes permeability transition by regulating Bcl-2 family proteins.",1795,0
1796,"Our findings suggest that R316C causes reduced association with and impaired release of NCoR, resulting in RTH predominantly at the pituitary level, and that slightly elevated serum << TSH >> level with high dose of [[ levothyroxine ]] might be optimum for normal growth.",1796,6
1797,BACKGROUND: Recent epidemiologic and laboratory studies have suggested that non-<< steroidal >> anti-inflammatory drugs (NSAIDs) may reduce the risk of breast cancer through inhibition of [[ cyclooxygenase-2 ]] (COX-2).,1797,0
1798,BACKGROUND: Recent epidemiologic and laboratory studies have suggested that non-<< steroidal >> anti-inflammatory drugs (NSAIDs) may reduce the risk of breast cancer through inhibition of cyclooxygenase-2 ([[ COX-2 ]]).,1798,0
1799,"METHODS: We conducted a case-control study to measure the association between selective << cox-2 >> inhibitors, particularly [[ celecoxib ]], rofecoxib, valdecoxib and non-specific NSAID subgroups, and breast cancer risk.",1799,0
1800,"METHODS: We conducted a case-control study to measure the association between selective << cox-2 >> inhibitors, particularly celecoxib, [[ rofecoxib ]], valdecoxib and non-specific NSAID subgroups, and breast cancer risk.",1800,0
1801,"METHODS: We conducted a case-control study to measure the association between selective << cox-2 >> inhibitors, particularly celecoxib, rofecoxib, [[ valdecoxib ]] and non-specific NSAID subgroups, and breast cancer risk.",1801,0
1802,"With exposure to << rofecoxib >>, a selective [[ COX-2 ]] inhibitor, breast cancer risk reduction was appreciable (46%), suggesting a possible role for selective COX-2 inhibitors in breast cancer prophylaxis.",1802,0
1803,"With exposure to << rofecoxib >>, a selective COX-2 inhibitor, breast cancer risk reduction was appreciable (46%), suggesting a possible role for selective [[ COX-2 ]] inhibitors in breast cancer prophylaxis.",1803,0
1804,"The suppressive effect of << ceruletide >> on barrel rotation could be partially countered by MK-329, a selective peripheral [[ CCK ]] (CCK-A) receptor antagonist.",1804,3
1805,"The suppressive effect of << ceruletide >> on barrel rotation could be partially countered by MK-329, a selective peripheral CCK [[ (CCK-A) receptor ]] antagonist.",1805,3
1806,"The suppressive effect of ceruletide on barrel rotation could be partially countered by << MK-329 >>, a selective peripheral [[ CCK ]] (CCK-A) receptor antagonist.",1806,1
1807,"The suppressive effect of ceruletide on barrel rotation could be partially countered by << MK-329 >>, a selective peripheral CCK [[ (CCK-A) receptor ]] antagonist.",1807,1
1808,These findings suggest that << ceruletide >> specifically suppresses the barrel rotation evoked by SMS 201-995 in a long-lasting manner possibly acting through [[ CCK-A receptor ]].,1808,3
1809,Effects of the << histamine H1 >> antagonist [[ chlorcyclizine ]] on rat fetal palate development.,1809,1
1810,BACKGROUND: The effects of << histamine H1 >> antagonist [[ chlorcyclizine ]] on rat palate development were characterized following in utero exposure.,1810,1
1811,"Removing medium Ca2+, blocking << Ca2+ channels >> with 50 mumol/l [[ verapamil ]], or inhibiting calmodulin activation with 20 mumol/l trifluoperazine, 10 mumol/l chlorpromazine or 10 mumol/l pimozide almost completely blocked hyposmolarity-induced secretion.",1811,0
1812,"Removing medium Ca2+, blocking Ca2+ channels with 50 mumol/l verapamil, or inhibiting << calmodulin >> activation with 20 mumol/l [[ trifluoperazine ]], 10 mumol/l chlorpromazine or 10 mumol/l pimozide almost completely blocked hyposmolarity-induced secretion.",1812,0
1813,"Removing medium Ca2+, blocking Ca2+ channels with 50 mumol/l verapamil, or inhibiting << calmodulin >> activation with 20 mumol/l trifluoperazine, 10 mumol/l [[ chlorpromazine ]] or 10 mumol/l pimozide almost completely blocked hyposmolarity-induced secretion.",1813,0
1814,"Removing medium Ca2+, blocking Ca2+ channels with 50 mumol/l verapamil, or inhibiting << calmodulin >> activation with 20 mumol/l trifluoperazine, 10 mumol/l chlorpromazine or 10 mumol/l [[ pimozide ]] almost completely blocked hyposmolarity-induced secretion.",1814,0
1815,"The smooth muscle relaxant, << W-7 >>, which is believed relatively specific in inhibiting the Ca2(+)-calmodulin interaction, depressed hyposmolarity-induced [[ PRL ]] secretion in a dose-dependent manner (r = -0.991, p less than 0.01).",1815,8
1816,An essential control in experiments using Gy mice is to demonstrate that the abnormal phenotypes exhibited by these mice are abolished by providing replacement << spermine >> and this can be accomplished by breeding with CAG-[[ SMS ]] mice that express SpmS from a ubiquitous promoter.,1816,4
1817,An essential control in experiments using Gy mice is to demonstrate that the abnormal phenotypes exhibited by these mice are abolished by providing replacement << spermine >> and this can be accomplished by breeding with CAG-SMS mice that express [[ SpmS ]] from a ubiquitous promoter.,1817,4
1818,"<< Cabozantinib >> (XL184), a novel [[ MET ]] and VEGFR2 inhibitor, simultaneously suppresses metastasis, angiogenesis, and tumor growth.",1818,0
1819,"<< Cabozantinib >> (XL184), a novel MET and [[ VEGFR2 ]] inhibitor, simultaneously suppresses metastasis, angiogenesis, and tumor growth.",1819,0
1820,"Cabozantinib (<< XL184 >>), a novel [[ MET ]] and VEGFR2 inhibitor, simultaneously suppresses metastasis, angiogenesis, and tumor growth.",1820,0
1821,"Cabozantinib (<< XL184 >>), a novel MET and [[ VEGFR2 ]] inhibitor, simultaneously suppresses metastasis, angiogenesis, and tumor growth.",1821,0
1822,"<< Cabozantinib >> (XL184) is a small-molecule [[ kinase ]] inhibitor with potent activity toward MET and VEGF receptor 2 (VEGFR2), as well as a number of other receptor tyrosine kinases that have also been implicated in tumor pathobiology, including RET, KIT, AXL, and FLT3.",1822,0
1823,"<< Cabozantinib >> (XL184) is a small-molecule kinase inhibitor with potent activity toward [[ MET ]] and VEGF receptor 2 (VEGFR2), as well as a number of other receptor tyrosine kinases that have also been implicated in tumor pathobiology, including RET, KIT, AXL, and FLT3.",1823,0
1824,"<< Cabozantinib >> (XL184) is a small-molecule kinase inhibitor with potent activity toward MET and [[ VEGF receptor 2 ]] (VEGFR2), as well as a number of other receptor tyrosine kinases that have also been implicated in tumor pathobiology, including RET, KIT, AXL, and FLT3.",1824,0
1825,"<< Cabozantinib >> (XL184) is a small-molecule kinase inhibitor with potent activity toward MET and VEGF receptor 2 ([[ VEGFR2 ]]), as well as a number of other receptor tyrosine kinases that have also been implicated in tumor pathobiology, including RET, KIT, AXL, and FLT3.",1825,0
1826,"<< Cabozantinib >> (XL184) is a small-molecule kinase inhibitor with potent activity toward MET and VEGF receptor 2 (VEGFR2), as well as a number of other [[ receptor tyrosine kinases ]] that have also been implicated in tumor pathobiology, including RET, KIT, AXL, and FLT3.",1826,0
1827,"<< Cabozantinib >> (XL184) is a small-molecule kinase inhibitor with potent activity toward MET and VEGF receptor 2 (VEGFR2), as well as a number of other receptor tyrosine kinases that have also been implicated in tumor pathobiology, including [[ RET ]], KIT, AXL, and FLT3.",1827,0
1828,"<< Cabozantinib >> (XL184) is a small-molecule kinase inhibitor with potent activity toward MET and VEGF receptor 2 (VEGFR2), as well as a number of other receptor tyrosine kinases that have also been implicated in tumor pathobiology, including RET, [[ KIT ]], AXL, and FLT3.",1828,0
1829,"<< Cabozantinib >> (XL184) is a small-molecule kinase inhibitor with potent activity toward MET and VEGF receptor 2 (VEGFR2), as well as a number of other receptor tyrosine kinases that have also been implicated in tumor pathobiology, including RET, KIT, [[ AXL ]], and FLT3.",1829,0
1830,"<< Cabozantinib >> (XL184) is a small-molecule kinase inhibitor with potent activity toward MET and VEGF receptor 2 (VEGFR2), as well as a number of other receptor tyrosine kinases that have also been implicated in tumor pathobiology, including RET, KIT, AXL, and [[ FLT3 ]].",1830,0
1831,"Cabozantinib (<< XL184 >>) is a small-molecule [[ kinase ]] inhibitor with potent activity toward MET and VEGF receptor 2 (VEGFR2), as well as a number of other receptor tyrosine kinases that have also been implicated in tumor pathobiology, including RET, KIT, AXL, and FLT3.",1831,0
1832,"Cabozantinib (<< XL184 >>) is a small-molecule kinase inhibitor with potent activity toward [[ MET ]] and VEGF receptor 2 (VEGFR2), as well as a number of other receptor tyrosine kinases that have also been implicated in tumor pathobiology, including RET, KIT, AXL, and FLT3.",1832,0
1833,"Cabozantinib (<< XL184 >>) is a small-molecule kinase inhibitor with potent activity toward MET and [[ VEGF receptor 2 ]] (VEGFR2), as well as a number of other receptor tyrosine kinases that have also been implicated in tumor pathobiology, including RET, KIT, AXL, and FLT3.",1833,0
1834,"Cabozantinib (<< XL184 >>) is a small-molecule kinase inhibitor with potent activity toward MET and VEGF receptor 2 ([[ VEGFR2 ]]), as well as a number of other receptor tyrosine kinases that have also been implicated in tumor pathobiology, including RET, KIT, AXL, and FLT3.",1834,0
1835,"Cabozantinib (<< XL184 >>) is a small-molecule kinase inhibitor with potent activity toward MET and VEGF receptor 2 (VEGFR2), as well as a number of other [[ receptor tyrosine kinases ]] that have also been implicated in tumor pathobiology, including RET, KIT, AXL, and FLT3.",1835,0
1836,"Cabozantinib (<< XL184 >>) is a small-molecule kinase inhibitor with potent activity toward MET and VEGF receptor 2 (VEGFR2), as well as a number of other receptor tyrosine kinases that have also been implicated in tumor pathobiology, including [[ RET ]], KIT, AXL, and FLT3.",1836,0
1837,"Cabozantinib (<< XL184 >>) is a small-molecule kinase inhibitor with potent activity toward MET and VEGF receptor 2 (VEGFR2), as well as a number of other receptor tyrosine kinases that have also been implicated in tumor pathobiology, including RET, [[ KIT ]], AXL, and FLT3.",1837,0
1838,"Cabozantinib (<< XL184 >>) is a small-molecule kinase inhibitor with potent activity toward MET and VEGF receptor 2 (VEGFR2), as well as a number of other receptor tyrosine kinases that have also been implicated in tumor pathobiology, including RET, KIT, [[ AXL ]], and FLT3.",1838,0
1839,"Cabozantinib (<< XL184 >>) is a small-molecule kinase inhibitor with potent activity toward MET and VEGF receptor 2 (VEGFR2), as well as a number of other receptor tyrosine kinases that have also been implicated in tumor pathobiology, including RET, KIT, AXL, and [[ FLT3 ]].",1839,0
1840,Treatment with << cabozantinib >> inhibited [[ MET ]] and VEGFR2 phosphorylation in vitro and in tumor models in vivo and led to significant reductions in cell invasion in vitro.,1840,0
1841,Treatment with << cabozantinib >> inhibited MET and [[ VEGFR2 ]] phosphorylation in vitro and in tumor models in vivo and led to significant reductions in cell invasion in vitro.,1841,0
1842,"Importantly, treatment with << cabozantinib >> did not increase lung tumor burden in an experimental model of metastasis, which has been observed with inhibitors of [[ VEGF ]] signaling that do not target MET.",1842,8
1843,"Collectively, these data suggest that << cabozantinib >> is a promising agent for inhibiting tumor angiogenesis and metastasis in cancers with dysregulated [[ MET ]] and VEGFR signaling.",1843,8
1844,"Collectively, these data suggest that << cabozantinib >> is a promising agent for inhibiting tumor angiogenesis and metastasis in cancers with dysregulated MET and [[ VEGFR ]] signaling.",1844,8
1845,"Inhibition of the NF-kappaB pathway was responsible for this effect since the << colchicoside >> inhibited RANKL-induced [[ NF-kappaB ]] activation, activation of IkappaB kinase (IKK) and suppressed inhibitor of NF-kappaBalpha (IkappaBalpha) phosphorylation and degradation, an inhibitor of NF-kappaB.",1845,0
1846,"Inhibition of the NF-kappaB pathway was responsible for this effect since the << colchicoside >> inhibited RANKL-induced NF-kappaB activation, activation of [[ IkappaB kinase ]] (IKK) and suppressed inhibitor of NF-kappaBalpha (IkappaBalpha) phosphorylation and degradation, an inhibitor of NF-kappaB.",1846,0
1847,"Inhibition of the NF-kappaB pathway was responsible for this effect since the << colchicoside >> inhibited RANKL-induced NF-kappaB activation, activation of IkappaB kinase ([[ IKK ]]) and suppressed inhibitor of NF-kappaBalpha (IkappaBalpha) phosphorylation and degradation, an inhibitor of NF-kappaB.",1847,0
1848,"Inhibition of the NF-kappaB pathway was responsible for this effect since the << colchicoside >> inhibited RANKL-induced NF-kappaB activation, activation of IkappaB kinase (IKK) and suppressed inhibitor of [[ NF-kappaBalpha ]] (IkappaBalpha) phosphorylation and degradation, an inhibitor of NF-kappaB.",1848,0
1849,"Inhibition of the NF-kappaB pathway was responsible for this effect since the << colchicoside >> inhibited RANKL-induced NF-kappaB activation, activation of IkappaB kinase (IKK) and suppressed inhibitor of NF-kappaBalpha ([[ IkappaBalpha ]]) phosphorylation and degradation, an inhibitor of NF-kappaB.",1849,0
1850,"Inhibition of the NF-kappaB pathway was responsible for this effect since the << colchicoside >> inhibited RANKL-induced NF-kappaB activation, activation of IkappaB kinase (IKK) and suppressed inhibitor of NF-kappaBalpha (IkappaBalpha) phosphorylation and degradation, an inhibitor of [[ NF-kappaB ]].",1850,0
1851,"Inhibition of the NF-kappaB pathway was responsible for this effect since the << colchicoside >> inhibited [[ RANKL ]]-induced NF-kappaB activation, activation of IkappaB kinase (IKK) and suppressed inhibitor of NF-kappaBalpha (IkappaBalpha) phosphorylation and degradation, an inhibitor of NF-kappaB.",1851,0
1852,"CONCLUSIONS AND IMPLICATIONS: Together, these data suggest that << thiocolchicoside >> significantly suppressed osteoclastogenesis induced by [[ RANKL ]] and tumour cells via the NF-kappaB signalling pathway.",1852,0
1853,"CONCLUSIONS AND IMPLICATIONS: Together, these data suggest that << thiocolchicoside >> significantly suppressed osteoclastogenesis induced by RANKL and tumour cells via the [[ NF-kappaB ]] signalling pathway.",1853,0
1854,"Although genetic polymorphisms in the endothelial nitric oxide synthase (<< eNOS >>) gene may impair endogenous [[ NO ]] formation, there is little information about how eNOS polymorphisms and haplotypes affect the responses to sildenafil.",1854,4
1855,"Although genetic polymorphisms in the << endothelial nitric oxide synthase >> (eNOS) gene may impair endogenous [[ NO ]] formation, there is little information about how eNOS polymorphisms and haplotypes affect the responses to sildenafil.",1855,4
1856,<< Mercury >> induces the expression of [[ cyclooxygenase-2 ]] and inducible nitric oxide synthase.,1856,6
1857,<< Mercury >> induces the expression of cyclooxygenase-2 and [[ inducible nitric oxide synthase ]].,1857,6
1858,"Here, we report biochemical evidence that << mercury >> alone induces [[ NF-κB ]] activation, resulting in the induced expression of COX-2 and iNOS.",1858,9
1859,"Here, we report biochemical evidence that << mercury >> alone induces NF-κB activation, resulting in the induced expression of [[ COX-2 ]] and iNOS.",1859,6
1860,"Here, we report biochemical evidence that << mercury >> alone induces NF-κB activation, resulting in the induced expression of COX-2 and [[ iNOS ]].",1860,6
1861,"Unexpectedly, both the << mGluR(5) >>specific agonist, [[ CHPG ]], and the group II mGluR (mGlu(2/3)) agonist, LY379268 (LY), induced a TTX-insensitive outward current/hyperpolarization.",1861,2
1862,"Unexpectedly, both the mGluR(5)specific agonist, CHPG, and the << group II mGluR >> (mGlu(2/3)) agonist, [[ LY379268 ]] (LY), induced a TTX-insensitive outward current/hyperpolarization.",1862,2
1863,Both outward currents were significantly reduced by the << mGluR >> antagonist [[ MCPG ]] and the CHPG-induced current was blocked by the specific mGluR(5) antagonist MTEP.,1863,1
1864,Both outward currents were significantly reduced by the mGluR antagonist MCPG and the CHPG-induced current was blocked by the specific << mGluR(5) >> antagonist [[ MTEP ]].,1864,1
1865,"We have examined the effectiveness of two novel << Chk1 >> selective inhibitors, [[ AR323 ]] and AR678, in a panel of melanoma cell lines and normal cell types.",1865,0
1866,"We have examined the effectiveness of two novel << Chk1 >> selective inhibitors, AR323 and [[ AR678 ]], in a panel of melanoma cell lines and normal cell types.",1866,0
1867,"<< Aspirin >> inhibits mTOR signaling, activates [[ AMP-activated protein kinase ]], and induces autophagy in colorectal cancer cells.",1867,9
1868,"<< Aspirin >> inhibits [[ mTOR ]] signaling, activates AMP-activated protein kinase, and induces autophagy in colorectal cancer cells.",1868,8
1869,RESULTS: << Aspirin >> reduced [[ mTOR ]] signaling in CRC cells by inhibiting the mTOR effectors S6K1 and 4E-BP1.,1869,8
1870,RESULTS: << Aspirin >> reduced mTOR signaling in CRC cells by inhibiting the [[ mTOR ]] effectors S6K1 and 4E-BP1.,1870,0
1871,RESULTS: << Aspirin >> reduced mTOR signaling in CRC cells by inhibiting the mTOR effectors [[ S6K1 ]] and 4E-BP1.,1871,0
1872,RESULTS: << Aspirin >> reduced mTOR signaling in CRC cells by inhibiting the mTOR effectors S6K1 and [[ 4E-BP1 ]].,1872,0
1873,<< Aspirin >> changed nucleotide ratios and activated [[ AMPK ]] in CRC cells.,1873,9
1874,"<< mTOR >> was still inhibited by [[ aspirin ]] in CRC cells after siRNA knockdown of AMPKalpha, indicating AMPK-dependent and AMPK-independent mechanisms of aspirin-induced inhibition of mTOR.",1874,0
1875,"mTOR was still inhibited by aspirin in CRC cells after siRNA knockdown of AMPKalpha, indicating AMPK-dependent and AMPK-independent mechanisms of << aspirin >>-induced inhibition of [[ mTOR ]].",1875,0
1876,"<< Aspirin >> induced autophagy, a feature of [[ mTOR ]] inhibition.",1876,0
1877,"Aspirin and << metformin >> (an activator of [[ AMPK ]]) increased inhibition of mTOR and Akt, as well as autophagy in CRC cells.",1877,9
1878,"<< Aspirin >> and metformin (an activator of [[ AMPK ]]) increased inhibition of mTOR and Akt, as well as autophagy in CRC cells.",1878,9
1879,"Aspirin and << metformin >> (an activator of AMPK) increased inhibition of [[ mTOR ]] and Akt, as well as autophagy in CRC cells.",1879,0
1880,"Aspirin and << metformin >> (an activator of AMPK) increased inhibition of mTOR and [[ Akt ]], as well as autophagy in CRC cells.",1880,0
1881,"<< Aspirin >> and metformin (an activator of AMPK) increased inhibition of [[ mTOR ]] and Akt, as well as autophagy in CRC cells.",1881,0
1882,"<< Aspirin >> and metformin (an activator of AMPK) increased inhibition of mTOR and [[ Akt ]], as well as autophagy in CRC cells.",1882,0
1883,Rectal mucosal samples from patients given << aspirin >> had reduced phosphorylation of [[ S6K1 ]] and S6.,1883,0
1884,Rectal mucosal samples from patients given << aspirin >> had reduced phosphorylation of S6K1 and [[ S6 ]].,1884,0
1885,"CONCLUSIONS: << Aspirin >> is an inhibitor of mTOR and an activator of [[ AMPK ]], targeting regulators of intracellular energy homeostasis and metabolism.",1885,9
1886,"CONCLUSIONS: << Aspirin >> is an inhibitor of [[ mTOR ]] and an activator of AMPK, targeting regulators of intracellular energy homeostasis and metabolism.",1886,0
1887,"Exogenous stimulation of << PKA >> activity, achieved by [[ forskolin ]] treatment, protected K-ras-transformed cells from apoptosis induced by glucose deprivation, enhanced complex I activity, intracellular adenosine triphosphate (ATP) levels, mitochondrial fusion and decreased intracellular reactive oxygen species (ROS) levels.",1887,9
1888,"Exogenous stimulation of PKA activity, achieved by << forskolin >> treatment, protected K-ras-transformed cells from apoptosis induced by glucose deprivation, enhanced [[ complex I ]] activity, intracellular adenosine triphosphate (ATP) levels, mitochondrial fusion and decreased intracellular reactive oxygen species (ROS) levels.",1888,9
1889,"Exogenous stimulation of PKA activity, achieved by forskolin treatment, protected << K-ras >>-transformed cells from apoptosis induced by [[ glucose ]] deprivation, enhanced complex I activity, intracellular adenosine triphosphate (ATP) levels, mitochondrial fusion and decreased intracellular reactive oxygen species (ROS) levels.",1889,8
1890,"In << TGF-β1 >>-induced NPDFs, [[ berberine ]] significantly inhibited the expression of α-SMA and collagen type I mRNA and reduced α-SMA and collagen protein levels.",1890,8
1891,"In TGF-β1-induced NPDFs, << berberine >> significantly inhibited the expression of [[ α-SMA ]] and collagen type I mRNA and reduced α-SMA and collagen protein levels.",1891,8
1892,"In TGF-β1-induced NPDFs, << berberine >> significantly inhibited the expression of α-SMA and [[ collagen type I ]] mRNA and reduced α-SMA and collagen protein levels.",1892,8
1893,"In TGF-β1-induced NPDFs, << berberine >> significantly inhibited the expression of α-SMA and collagen type I mRNA and reduced [[ α-SMA ]] and collagen protein levels.",1893,8
1894,"In TGF-β1-induced NPDFs, << berberine >> significantly inhibited the expression of α-SMA and collagen type I mRNA and reduced α-SMA and [[ collagen ]] protein levels.",1894,8
1895,<< Berberine >> only suppressed the expression of [[ pp38 ]] among the evaluated signaling molecules.,1895,8
1896,<< SB203580 >> (a specific inhibitor of p38 kinase) markedly suppressed the increased expression of [[ collagen type I ]] and α-SMA in TGF-β1-induced NPDFs.,1896,8
1897,<< SB203580 >> (a specific inhibitor of p38 kinase) markedly suppressed the increased expression of collagen type I and [[ α-SMA ]] in TGF-β1-induced NPDFs.,1897,8
1898,<< SB203580 >> (a specific inhibitor of p38 kinase) markedly suppressed the increased expression of collagen type I and α-SMA in [[ TGF-β1 ]]-induced NPDFs.,1898,8
1899,<< SB203580 >> (a specific inhibitor of [[ p38 ]] kinase) markedly suppressed the increased expression of collagen type I and α-SMA in TGF-β1-induced NPDFs.,1899,0
1900,<< SB203580 >> (a specific inhibitor of p38 [[ kinase ]]) markedly suppressed the increased expression of collagen type I and α-SMA in TGF-β1-induced NPDFs.,1900,0
1901,"CRBN mediated antiproliferative activities of lenalidomide and pomalidomide in myeloma cells, as well as << lenalidomide >>- and pomalidomide-induced [[ cytokine ]] production in T cells.",1901,6
1902,"CRBN mediated antiproliferative activities of lenalidomide and pomalidomide in myeloma cells, as well as lenalidomide- and << pomalidomide >>-induced [[ cytokine ]] production in T cells.",1902,6
1903,"<< Lenalidomide >> and pomalidomide inhibited autoubiquitination of [[ CRBN ]] in HEK293T cells expressing thalidomide-binding competent wild-type CRBN, but not thalidomide-binding defective CRBN(YW/AA).",1903,0
1904,"<< Lenalidomide >> and pomalidomide inhibited autoubiquitination of CRBN in HEK293T cells expressing thalidomide-binding competent wild-type [[ CRBN ]], but not thalidomide-binding defective CRBN(YW/AA).",1904,0
1905,"Lenalidomide and << pomalidomide >> inhibited autoubiquitination of [[ CRBN ]] in HEK293T cells expressing thalidomide-binding competent wild-type CRBN, but not thalidomide-binding defective CRBN(YW/AA).",1905,0
1906,"Lenalidomide and << pomalidomide >> inhibited autoubiquitination of CRBN in HEK293T cells expressing thalidomide-binding competent wild-type [[ CRBN ]], but not thalidomide-binding defective CRBN(YW/AA).",1906,0
1907,"Overexpression of CRBN wild-type protein, but not CRBN(YW/AA) mutant protein, in KMS12 myeloma cells, amplified << pomalidomide >>-mediated reductions in c-myc and IRF4 expression and increases in p21([[ WAF-1 ]]) expression.",1907,6
1908,"Overexpression of CRBN wild-type protein, but not CRBN(YW/AA) mutant protein, in KMS12 myeloma cells, amplified << pomalidomide >>-mediated reductions in c-myc and IRF4 expression and increases in [[ p21 ]](WAF-1) expression.",1908,6
1909,"Overexpression of CRBN wild-type protein, but not CRBN(YW/AA) mutant protein, in KMS12 myeloma cells, amplified << pomalidomide >>-mediated reductions in [[ c-myc ]] and IRF4 expression and increases in p21(WAF-1) expression.",1909,8
1910,"Overexpression of CRBN wild-type protein, but not CRBN(YW/AA) mutant protein, in KMS12 myeloma cells, amplified << pomalidomide >>-mediated reductions in c-myc and [[ IRF4 ]] expression and increases in p21(WAF-1) expression.",1910,8
1911,"Long-term selection for << lenalidomide >> resistance in H929 myeloma cell lines was accompanied by a reduction in [[ CRBN ]], while in DF15R myeloma cells resistant to both pomalidomide and lenalidomide, CRBN protein was undetectable.",1911,8
1912,"These << polyphenols >>, but not GvEx, showed a certain level of inhibition of human-cDNA-expressed [[ CYPs ]].",1912,0
1913,"<< Crizotinib >> is an oral tyrosine kinase inhibitor (TKI), which silences the protein product of the [[ ALK ]] fusion gene and has recently been approved for the treatment of NSCLC aberrantly expressing ALK.",1913,8
1914,"<< Crizotinib >> is an oral [[ tyrosine kinase ]] inhibitor (TKI), which silences the protein product of the ALK fusion gene and has recently been approved for the treatment of NSCLC aberrantly expressing ALK.",1914,0
1915,"To clarify if the behavioral interaction between ethanol and adenosine reported previously occur centrally or due to a peripheral hemodynamic change, the effect of i.c.v. << adenosine >> agonists, [[ N6-(R-phenylisopropyl)adenosine ]] (R-PIA), N6-(S-phenylisopropyl)adenosine, 5'-(N-cyclopropyl)-carboxamidoadenosine, antagonists, theophylline and 8-p-(sulfophenyl)theophylline as well as enprofylline on ethanol-(i.p.)-induced motor incoordination was evaluated by rotorod.",1915,2
1916,"To clarify if the behavioral interaction between ethanol and adenosine reported previously occur centrally or due to a peripheral hemodynamic change, the effect of i.c.v. << adenosine >> agonists, N6-(R-phenylisopropyl)adenosine ([[ R-PIA ]]), N6-(S-phenylisopropyl)adenosine, 5'-(N-cyclopropyl)-carboxamidoadenosine, antagonists, theophylline and 8-p-(sulfophenyl)theophylline as well as enprofylline on ethanol-(i.p.)-induced motor incoordination was evaluated by rotorod.",1916,2
1917,"To clarify if the behavioral interaction between ethanol and adenosine reported previously occur centrally or due to a peripheral hemodynamic change, the effect of i.c.v. << adenosine >> agonists, N6-(R-phenylisopropyl)adenosine (R-PIA), [[ N6-(S-phenylisopropyl)adenosine ]], 5'-(N-cyclopropyl)-carboxamidoadenosine, antagonists, theophylline and 8-p-(sulfophenyl)theophylline as well as enprofylline on ethanol-(i.p.)-induced motor incoordination was evaluated by rotorod.",1917,2
1918,"To clarify if the behavioral interaction between ethanol and adenosine reported previously occur centrally or due to a peripheral hemodynamic change, the effect of i.c.v. << adenosine >> agonists, N6-(R-phenylisopropyl)adenosine (R-PIA), N6-(S-phenylisopropyl)adenosine, [[ 5'-(N-cyclopropyl)-carboxamidoadenosine ]], antagonists, theophylline and 8-p-(sulfophenyl)theophylline as well as enprofylline on ethanol-(i.p.)-induced motor incoordination was evaluated by rotorod.",1918,2
1919,"To clarify if the behavioral interaction between ethanol and adenosine reported previously occur centrally or due to a peripheral hemodynamic change, the effect of i.c.v. << adenosine >> agonists, N6-(R-phenylisopropyl)adenosine (R-PIA), N6-(S-phenylisopropyl)adenosine, 5'-(N-cyclopropyl)-carboxamidoadenosine, antagonists, [[ theophylline ]] and 8-p-(sulfophenyl)theophylline as well as enprofylline on ethanol-(i.p.)-induced motor incoordination was evaluated by rotorod.",1919,1
1920,"To clarify if the behavioral interaction between ethanol and adenosine reported previously occur centrally or due to a peripheral hemodynamic change, the effect of i.c.v. << adenosine >> agonists, N6-(R-phenylisopropyl)adenosine (R-PIA), N6-(S-phenylisopropyl)adenosine, 5'-(N-cyclopropyl)-carboxamidoadenosine, antagonists, theophylline and [[ 8-p-(sulfophenyl)theophylline ]] as well as enprofylline on ethanol-(i.p.)-induced motor incoordination was evaluated by rotorod.",1920,1
1921,"To clarify if the behavioral interaction between ethanol and adenosine reported previously occur centrally or due to a peripheral hemodynamic change, the effect of i.c.v. << adenosine >> agonists, N6-(R-phenylisopropyl)adenosine (R-PIA), N6-(S-phenylisopropyl)adenosine, 5'-(N-cyclopropyl)-carboxamidoadenosine, antagonists, theophylline and 8-p-(sulfophenyl)theophylline as well as [[ enprofylline ]] on ethanol-(i.p.)-induced motor incoordination was evaluated by rotorod.",1921,1
1922,"<< Enprofylline >>, a weak adenosine antagonist but potent inhibitor of [[ cyclic AMP phosphodiesterase ]], did not alter ethanol's motor incoordination, further supporting involvement of brain adenosine receptor mechanism(s) in ethanol-adenosine interactions.",1922,0
1923,"<< Enprofylline >>, a weak [[ adenosine ]] antagonist but potent inhibitor of cyclic AMP phosphodiesterase, did not alter ethanol's motor incoordination, further supporting involvement of brain adenosine receptor mechanism(s) in ethanol-adenosine interactions.",1923,1
1924,"<< Celastrol >>, a TAK1 inhibitor and anti-inflammatory compound used in traditional Chinese medicine, also decreased [[ TGF-β1 ]]-induced phosphorylation of TAK1 and RELA, and suppressed basal, TGF-β1- and tumor necrosis factor-alpha (TNF-α)-induced NF-κB reporter gene activity.",1924,3
1925,"<< Celastrol >>, a TAK1 inhibitor and anti-inflammatory compound used in traditional Chinese medicine, also decreased TGF-β1-induced phosphorylation of TAK1 and RELA, and suppressed basal, [[ TGF-β1 ]]- and tumor necrosis factor-alpha (TNF-α)-induced NF-κB reporter gene activity.",1925,3
1926,"<< Celastrol >>, a TAK1 inhibitor and anti-inflammatory compound used in traditional Chinese medicine, also decreased TGF-β1-induced phosphorylation of TAK1 and RELA, and suppressed basal, TGF-β1- and [[ tumor necrosis factor-alpha ]] (TNF-α)-induced NF-κB reporter gene activity.",1926,3
1927,"<< Celastrol >>, a [[ TAK1 ]] inhibitor and anti-inflammatory compound used in traditional Chinese medicine, also decreased TGF-β1-induced phosphorylation of TAK1 and RELA, and suppressed basal, TGF-β1- and tumor necrosis factor-alpha (TNF-α)-induced NF-κB reporter gene activity.",1927,0
1928,"<< Celastrol >>, a TAK1 inhibitor and anti-inflammatory compound used in traditional Chinese medicine, also decreased TGF-β1-induced phosphorylation of [[ TAK1 ]] and RELA, and suppressed basal, TGF-β1- and tumor necrosis factor-alpha (TNF-α)-induced NF-κB reporter gene activity.",1928,0
1929,"<< Celastrol >>, a TAK1 inhibitor and anti-inflammatory compound used in traditional Chinese medicine, also decreased TGF-β1-induced phosphorylation of TAK1 and [[ RELA ]], and suppressed basal, TGF-β1- and tumor necrosis factor-alpha (TNF-α)-induced NF-κB reporter gene activity.",1929,0
1930,"<< Celastrol >>, a TAK1 inhibitor and anti-inflammatory compound used in traditional Chinese medicine, also decreased TGF-β1-induced phosphorylation of TAK1 and RELA, and suppressed basal, TGF-β1- and tumor necrosis factor-alpha (TNF-α)-induced [[ NF-κB ]] reporter gene activity.",1930,0
1931,"<< Celastrol >> also inhibited cell proliferation, while increasing sub-G0 DNA fragmentation and [[ Annexin V ]] markers of apoptosis.",1931,6
1932,<< Celastrol >> highlights the therapeutic potential of agents targeting [[ TAK1 ]] as a key node in this pro-oncogenic TGF-β-NF-κB signal pathway.,1932,0
1933,The atypical antidepressant << mianserin >> exhibits agonist activity at [[ kappa-opioid receptors ]].,1933,2
1934,We previously reported that << tricyclic >> antidepressants act as agonists at distinct [[ opioid receptors ]].,1934,2
1935,"In [(35)S]GTPgammaS assays, << mianserin >> selectively activated [[ kappa-opioid receptors ]].",1935,9
1936,The agonist activity was antagonized by the selective << kappa-opioid >> blocker [[ nor-binaltorphimine ]] (nor-BNI).,1936,0
1937,The agonist activity was antagonized by the selective << kappa-opioid >> blocker nor-binaltorphimine ([[ nor-BNI ]]).,1937,0
1938,The agonist activity was antagonized by the selective << kappa-opioid >> blocker [[ nor-binaltorphimine ]] (nor-BNI).,1938,1
1939,The agonist activity was antagonized by the selective << kappa-opioid >> blocker nor-binaltorphimine ([[ nor-BNI ]]).,1939,1
1940,The << mianserin >> analogue mirtazapine also displayed [[ kappa-opioid ]] agonist activity.,1940,2
1941,The mianserin analogue << mirtazapine >> also displayed [[ kappa-opioid ]] agonist activity.,1941,2
1942,"In rat striatum and nucleus accumbens, mianserin stimulated [35S]GTPgammaS binding in a nor-BNI-sensitive manner with maximal effects lower than those of the full << kappa-opioid >> agonists [[ (-)-U50,488 ]] and dynorphin A.",1942,2
1943,"In rat striatum and nucleus accumbens, mianserin stimulated [35S]GTPgammaS binding in a nor-BNI-sensitive manner with maximal effects lower than those of the full << kappa-opioid >> agonists (-)-U50,488 and [[ dynorphin A ]].",1943,2
1944,"When combined, mianserin antagonized the effects of the full kappa-opioid receptor agonists in [(35)S]GTPgammaS assays and reduced the stimulation of << p38 >> MAPK and ERK1/2 phosphorylation by [[ dynorphin A ]].",1944,9
1945,"When combined, mianserin antagonized the effects of the full kappa-opioid receptor agonists in [(35)S]GTPgammaS assays and reduced the stimulation of p38 << MAPK >> and ERK1/2 phosphorylation by [[ dynorphin A ]].",1945,9
1946,"When combined, << mianserin >> antagonized the effects of the full kappa-opioid receptor agonists in [(35)S]GTPgammaS assays and reduced the stimulation of [[ p38 ]] MAPK and ERK1/2 phosphorylation by dynorphin A.",1946,0
1947,"When combined, << mianserin >> antagonized the effects of the full kappa-opioid receptor agonists in [(35)S]GTPgammaS assays and reduced the stimulation of p38 [[ MAPK ]] and ERK1/2 phosphorylation by dynorphin A.",1947,0
1948,"When combined, << mianserin >> antagonized the effects of the full [[ kappa-opioid receptor ]] agonists in [(35)S]GTPgammaS assays and reduced the stimulation of p38 MAPK and ERK1/2 phosphorylation by dynorphin A.",1948,1
1949,"CONCLUSIONS AND IMPLICATIONS: In different cell systems, << mianserin >> directly activates [[ kappa-opioid receptors ]], displaying partial agonist activity at brain receptors.",1949,9
1950,"CONCLUSIONS AND IMPLICATIONS: In different cell systems, << mianserin >> directly activates [[ kappa-opioid receptors ]], displaying partial agonist activity at brain receptors.",1950,2
1951,"In the present study we tested whether << propranolol >>, a [[ β-receptor ]] antagonist commonly used as antihypertensive drug, could ameliorate the cognitive impairments and increases in AD-related markers shown by the senescence-accelerated mouse prone-8 (SAMP8).",1951,1
1952,<< LXRs >> are thought to be activated predominantly by [[ oxysterols ]] generated enzymatically from cholesterol in different cell organelles.,1952,9
1953,Defects resulting in slowed release of cholesterol from late endosomes and lysosomes or reduction in << sterol-27-hydroxylase >> activity lead to specific blocks in [[ oxysterol ]] production and impaired LXR-dependent gene activation.,1953,4
1954,"The purpose of this review is to summarize current knowledge about << oxysterol >>-dependent activation by [[ LXR ]] of genes involved in reverse cholesterol transport, and what these defects of cell cholesterol homeostasis can teach us about the critical pathways of oxysterol generation for expression of LXR-dependent genes.",1954,9
1955,<< CBDP >> irreversibly inhibits [[ butyrylcholinesterase ]] (BChE) in human plasma by forming adducts on the active site serine (Ser-198).,1955,0
1956,<< CBDP >> irreversibly inhibits butyrylcholinesterase ([[ BChE ]]) in human plasma by forming adducts on the active site serine (Ser-198).,1956,0
1957,"Mass spectral analysis of << CBDP >>-inhibited [[ BChE ]] digested with Glu-C showed an o-hydroxybenzyl adduct (+106amu) on lysine 499, a residue far from the active site, but not on His-438.",1957,0
1958,"We previously demonstrated that the somatostatinergic system, implicated in neuronal survival control, can be modulated by << α-tocopherol >> in the rat dentate gyrus, increasing [[ cyclic adenosine monophosphate response element binding protein ]] phosphorylation.",1958,9
1959,"<< Galantamine >> is a reversible, competitive [[ acetylcholinesterase ]] (AChE) inhibitor and allosteric potentiating ligand of nicotinic acetylcholine receptors (nAChR-APL) that shares many common structural elements with morphinan-based opioids.",1959,0
1960,"<< Galantamine >> is a reversible, competitive acetylcholinesterase ([[ AChE ]]) inhibitor and allosteric potentiating ligand of nicotinic acetylcholine receptors (nAChR-APL) that shares many common structural elements with morphinan-based opioids.",1960,0
1961,Modulation of the << nitric oxide >> producing system (demonstrated via the [[ NADPH-diaphorase ]] histochemical reaction) by oestradiol has been established in several structures of the rat brain.,1961,4
1962,"Adult ovariectomised rats were divided into six groups and injected either with vehicle or a single dose of oestradiol, a selective ERα agonist-PPT [4,4',4″-(4-propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol], a selective << ERβ >> agonist-[[ DPN ]] [2,3-bis(4-hydroxyphenyl)-propionitrile], a selective ERα antagonist-MPP [1,3-bis(4-hydroxyphenyl)-4-methyl-5-[4-(2-piperidinylethoxy)phenol]-1H-pyrazole dihydrochloride] or a selective ERβ antagonist-PHTPP (4-[2-phenyl-5,7-bis(trifluoromethyl)pyrazolo[1,5-a]pyrimidin-3-yl]phenol).",1962,2
1963,"Adult ovariectomised rats were divided into six groups and injected either with vehicle or a single dose of oestradiol, a selective ERα agonist-PPT [4,4',4″-(4-propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol], a selective << ERβ >> agonist-DPN [[[ 2,3-bis(4-hydroxyphenyl)-propionitrile ]]], a selective ERα antagonist-MPP [1,3-bis(4-hydroxyphenyl)-4-methyl-5-[4-(2-piperidinylethoxy)phenol]-1H-pyrazole dihydrochloride] or a selective ERβ antagonist-PHTPP (4-[2-phenyl-5,7-bis(trifluoromethyl)pyrazolo[1,5-a]pyrimidin-3-yl]phenol).",1963,2
1964,"Adult ovariectomised rats were divided into six groups and injected either with vehicle or a single dose of oestradiol, a selective << ERα >> agonist-[[ PPT ]] [4,4',4″-(4-propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol], a selective ERβ agonist-DPN [2,3-bis(4-hydroxyphenyl)-propionitrile], a selective ERα antagonist-MPP [1,3-bis(4-hydroxyphenyl)-4-methyl-5-[4-(2-piperidinylethoxy)phenol]-1H-pyrazole dihydrochloride] or a selective ERβ antagonist-PHTPP (4-[2-phenyl-5,7-bis(trifluoromethyl)pyrazolo[1,5-a]pyrimidin-3-yl]phenol).",1964,2
1965,"Adult ovariectomised rats were divided into six groups and injected either with vehicle or a single dose of oestradiol, a selective << ERα >> agonist-PPT [[[ 4,4',4″-(4-propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol ]]], a selective ERβ agonist-DPN [2,3-bis(4-hydroxyphenyl)-propionitrile], a selective ERα antagonist-MPP [1,3-bis(4-hydroxyphenyl)-4-methyl-5-[4-(2-piperidinylethoxy)phenol]-1H-pyrazole dihydrochloride] or a selective ERβ antagonist-PHTPP (4-[2-phenyl-5,7-bis(trifluoromethyl)pyrazolo[1,5-a]pyrimidin-3-yl]phenol).",1965,2
1966,"Adult ovariectomised rats were divided into six groups and injected either with vehicle or a single dose of oestradiol, a selective ERα agonist-PPT [4,4',4″-(4-propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol], a selective ERβ agonist-DPN [2,3-bis(4-hydroxyphenyl)-propionitrile], a selective << ERα >> antagonist-[[ MPP ]] [1,3-bis(4-hydroxyphenyl)-4-methyl-5-[4-(2-piperidinylethoxy)phenol]-1H-pyrazole dihydrochloride] or a selective ERβ antagonist-PHTPP (4-[2-phenyl-5,7-bis(trifluoromethyl)pyrazolo[1,5-a]pyrimidin-3-yl]phenol).",1966,1
1967,"Adult ovariectomised rats were divided into six groups and injected either with vehicle or a single dose of oestradiol, a selective ERα agonist-PPT [4,4',4″-(4-propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol], a selective ERβ agonist-DPN [2,3-bis(4-hydroxyphenyl)-propionitrile], a selective << ERα >> antagonist-MPP [[[ 1,3-bis(4-hydroxyphenyl)-4-methyl-5-[4-(2-piperidinylethoxy)phenol ]]]-1H-pyrazole dihydrochloride] or a selective ERβ antagonist-PHTPP (4-[2-phenyl-5,7-bis(trifluoromethyl)pyrazolo[1,5-a]pyrimidin-3-yl]phenol).",1967,1
1968,"Adult ovariectomised rats were divided into six groups and injected either with vehicle or a single dose of oestradiol, a selective ERα agonist-PPT [4,4',4″-(4-propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol], a selective ERβ agonist-DPN [2,3-bis(4-hydroxyphenyl)-propionitrile], a selective << ERα >> antagonist-MPP [1,3-bis(4-hydroxyphenyl)-4-methyl-5-[4-(2-piperidinylethoxy)phenol]-[[ 1H-pyrazole dihydrochloride ]]] or a selective ERβ antagonist-PHTPP (4-[2-phenyl-5,7-bis(trifluoromethyl)pyrazolo[1,5-a]pyrimidin-3-yl]phenol).",1968,1
1969,"Adult ovariectomised rats were divided into six groups and injected either with vehicle or a single dose of oestradiol, a selective ERα agonist-PPT [4,4',4″-(4-propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol], a selective ERβ agonist-DPN [2,3-bis(4-hydroxyphenyl)-propionitrile], a selective ERα antagonist-MPP [1,3-bis(4-hydroxyphenyl)-4-methyl-5-[4-(2-piperidinylethoxy)phenol]-1H-pyrazole dihydrochloride] or a selective << ERβ >> antagonist-[[ PHTPP ]] (4-[2-phenyl-5,7-bis(trifluoromethyl)pyrazolo[1,5-a]pyrimidin-3-yl]phenol).",1969,1
1970,"Adult ovariectomised rats were divided into six groups and injected either with vehicle or a single dose of oestradiol, a selective ERα agonist-PPT [4,4',4″-(4-propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol], a selective ERβ agonist-DPN [2,3-bis(4-hydroxyphenyl)-propionitrile], a selective ERα antagonist-MPP [1,3-bis(4-hydroxyphenyl)-4-methyl-5-[4-(2-piperidinylethoxy)phenol]-1H-pyrazole dihydrochloride] or a selective << ERβ >> antagonist-PHTPP ([[ 4-[2-phenyl-5,7-bis(trifluoromethyl)pyrazolo[1,5-a]pyrimidin-3-yl]phenol ]]).",1970,1
1971,<< Verrucarin A >> sensitizes TRAIL-induced apoptosis via the upregulation of [[ DR5 ]] in an eIF2α/CHOP-dependent manner.,1971,6
1972,<< Verrucarin A >> sensitizes TRAIL-induced apoptosis via the upregulation of DR5 in an [[ eIF2α ]]/CHOP-dependent manner.,1972,6
1973,<< Verrucarin A >> sensitizes TRAIL-induced apoptosis via the upregulation of DR5 in an eIF2α/[[ CHOP ]]-dependent manner.,1973,6
1974,"Furthermore, << salubrinal >>, a specific [[ eIF2α ]] phosphorylation-inducing agent, increased CHOP and DR5 expression in the presence of VA.",1974,9
1975,"Furthermore, << salubrinal >>, a specific eIF2α phosphorylation-inducing agent, increased [[ CHOP ]] and DR5 expression in the presence of VA.",1975,6
1976,"Furthermore, << salubrinal >>, a specific eIF2α phosphorylation-inducing agent, increased CHOP and [[ DR5 ]] expression in the presence of VA.",1976,6
1977,"Disruption of microtubule prevented insulin-induced actin remodeling and distal insulin signal transduction, with reduction in surface << glucose transporter isoform 4 >> (GLUT4) and [[ glucose ]] uptake.",1977,5
1978,"Disruption of microtubule prevented insulin-induced actin remodeling and distal insulin signal transduction, with reduction in surface glucose transporter isoform 4 (<< GLUT4 >>) and [[ glucose ]] uptake.",1978,5
1979,"Other groups received either an infusion of the selective << NMDA receptor >> antagonist ([[ AP7 ]]; 10 nmol; intra-mPFC) or vehicle, 10 min prior to PILO preceding LFS600, or prior to a supra-threshold LTD protocol (900 pulses, 1 Hz; LFS900).",1979,1
1980,"Our data also indicate that << NMDA receptor >> pre-activation is essential to the muscarinic enhancement of mPFC synaptic depression, since [[ AP7 ]] microinjection into the mPFC blocked the conversion of transient depression into long-lasting LTD produced by PILO.",1980,0
1981,"Metabolism of << triethylenetetramine >> and 1,12-diamino-3,6,9-triazadodecane by the spermidine/spermine-N(1)-acetyltransferase and [[ thialysine acetyltransferase ]].",1981,5
1982,"Metabolism of << triethylenetetramine >> and 1,12-diamino-3,6,9-triazadodecane by the [[ spermidine/spermine-N(1)-acetyltransferase ]] and thialysine acetyltransferase.",1982,5
1983,"Metabolism of triethylenetetramine and << 1,12-diamino-3,6,9-triazadodecane >> by the spermidine/spermine-N(1)-acetyltransferase and [[ thialysine acetyltransferase ]].",1983,5
1984,"Metabolism of triethylenetetramine and << 1,12-diamino-3,6,9-triazadodecane >> by the [[ spermidine/spermine-N(1)-acetyltransferase ]] and thialysine acetyltransferase.",1984,5
1985,We recently showed that << TETA >> is metabolized in vitro by polyamine catabolic enzyme [[ spermidine/spermine-N(1)-acetyltransferase ]] (SSAT1) and by thialysine acetyltransferase (SSAT2) to its monoacetylated derivative (MAT).,1985,5
1986,We recently showed that << TETA >> is metabolized in vitro by polyamine catabolic enzyme spermidine/spermine-N(1)-acetyltransferase ([[ SSAT1 ]]) and by thialysine acetyltransferase (SSAT2) to its monoacetylated derivative (MAT).,1986,5
1987,We recently showed that << TETA >> is metabolized in vitro by polyamine catabolic enzyme spermidine/spermine-N(1)-acetyltransferase (SSAT1) and by [[ thialysine acetyltransferase ]] (SSAT2) to its monoacetylated derivative (MAT).,1987,5
1988,We recently showed that << TETA >> is metabolized in vitro by polyamine catabolic enzyme spermidine/spermine-N(1)-acetyltransferase (SSAT1) and by thialysine acetyltransferase ([[ SSAT2 ]]) to its monoacetylated derivative (MAT).,1988,5
1989,We recently showed that TETA is metabolized in vitro by << polyamine >> catabolic enzyme [[ spermidine/spermine-N(1)-acetyltransferase ]] (SSAT1) and by thialysine acetyltransferase (SSAT2) to its monoacetylated derivative (MAT).,1989,5
1990,We recently showed that TETA is metabolized in vitro by << polyamine >> catabolic enzyme spermidine/spermine-N(1)-acetyltransferase ([[ SSAT1 ]]) and by thialysine acetyltransferase (SSAT2) to its monoacetylated derivative (MAT).,1990,5
1991,The acetylation of << TETA >> is increased in [[ SSAT1 ]]-overexpressing mice compared with wild-type mice.,1991,5
1992,"However, SSAT1-deficient mice metabolize << TETA >> at the same rate as the wild-type mice, indicating the existence of another [[ N-acetylase ]] respons 2ible for its metabolism in mice.",1992,5
1993,"Here, we show that siRNA-mediated knockdown of << SSAT2 >> in HEPG2 cells and in primary hepatocytes from the SSAT1-deficient or wild-type mice reduced the metabolism of [[ TETA ]] to MAT.",1993,5
1994,"By contrast, << 1,12-diamino-3,6,9-triazadodecane >>(SpmTrien), a charge-deficient spermine analog, was an extremely poor substrate of human recombinant SSAT2 and was metabolized by [[ SSAT1 ]] in HEPG2 cells and in wild-type primary hepatocytes.",1994,5
1995,"By contrast, << 1,12-diamino-3,6,9-triazadodecane >>(SpmTrien), a charge-deficient spermine analog, was an extremely poor substrate of [[ human recombinant SSAT2 ]] and was metabolized by SSAT1 in HEPG2 cells and in wild-type primary hepatocytes.",1995,5
1996,"By contrast, 1,12-diamino-3,6,9-triazadodecane(<< SpmTrien >>), a charge-deficient spermine analog, was an extremely poor substrate of human recombinant SSAT2 and was metabolized by [[ SSAT1 ]] in HEPG2 cells and in wild-type primary hepatocytes.",1996,5
1997,"By contrast, 1,12-diamino-3,6,9-triazadodecane(<< SpmTrien >>), a charge-deficient spermine analog, was an extremely poor substrate of [[ human recombinant SSAT2 ]] and was metabolized by SSAT1 in HEPG2 cells and in wild-type primary hepatocytes.",1997,5
1998,"By contrast, 1,12-diamino-3,6,9-triazadodecane(SpmTrien), a charge-deficient << spermine >> analog, was an extremely poor substrate of human recombinant SSAT2 and was metabolized by [[ SSAT1 ]] in HEPG2 cells and in wild-type primary hepatocytes.",1998,5
1999,"By contrast, 1,12-diamino-3,6,9-triazadodecane(SpmTrien), a charge-deficient << spermine >> analog, was an extremely poor substrate of [[ human recombinant SSAT2 ]] and was metabolized by SSAT1 in HEPG2 cells and in wild-type primary hepatocytes.",1999,5
2000,"Thus, despite the similar structures of TETA and SpmTrien, << SSAT2 >> is the main acetylator of [[ TETA ]], whereas SpmTrien is primarily acetylated by SSAT1.",2000,5
2001,"Thus, despite the similar structures of TETA and SpmTrien, SSAT2 is the main acetylator of TETA, whereas << SpmTrien >> is primarily acetylated by [[ SSAT1 ]].",2001,5
2002,In vitro metabolism of the << 5-hydroxytryptamine1B >> receptor antagonist [[ elzasonan ]].,2002,1
2003,The rCYP data was normalized relative to the levels of each CYP form in native human liver microsomes to better assess the contribution of each << rCYP >> in the metabolism of [[ elzasonan ]].,2003,5
2004,Cytochrome b5 has shown to be an essential component in << P450 3A4 >> catalyzed [[ 5-hydroxyelzasonan ]] formation and provides insights on the disconnect between human liver microsomes data and that of rCYP.,2004,4
2005,"In utero exposure to << valproic acid >> (VPA), a [[ histone deacetylase ]] (HDAC) inhibitor, causes neural tube, heart, and limb defects.",2005,0
2006,"In utero exposure to << valproic acid >> (VPA), a histone deacetylase ([[ HDAC ]]) inhibitor, causes neural tube, heart, and limb defects.",2006,0
2007,"In utero exposure to valproic acid (<< VPA >>), a [[ histone deacetylase ]] (HDAC) inhibitor, causes neural tube, heart, and limb defects.",2007,0
2008,"In utero exposure to valproic acid (<< VPA >>), a histone deacetylase ([[ HDAC ]]) inhibitor, causes neural tube, heart, and limb defects.",2008,0
2009,"<< VPA >> caused a significant concentration- dependent increase in limb abnormalities, which was correlated with its [[ HDAC ]] inhibitory effect.",2009,0
2010,"The signaling of both << Sox9 >> and Runx2, key regulators of chondrogenesis, was downregulated by [[ VPA ]].",2010,8
2011,"The signaling of both Sox9 and << Runx2 >>, key regulators of chondrogenesis, was downregulated by [[ VPA ]].",2011,8
2012,<< α-TOCO >> plus a [[ pancaspase ]] inhibitor completely abolished AMD/TNF-induced cytotoxicity.,2012,0
2013,"In summary, activation of << caspases >> and oxidative stress were observed after [[ AMD ]]/TNF cotreatment, and caspase inhibitors and a lipid-soluble free-radical scavenger attenuated AMD/TNF-induced cytotoxicity.",2013,9
2014,Human serum butyrylcholinesterase (<< HuBChE >>) is currently the most suitable bioscavenger for the prophylaxis of highly toxic [[ organophosphate ]] (OP) nerve agents.,2014,5
2015,<< Human serum butyrylcholinesterase >> (HuBChE) is currently the most suitable bioscavenger for the prophylaxis of highly toxic [[ organophosphate ]] (OP) nerve agents.,2015,5
2016,Cu-dependent << tyrosinase >> activity was also markedly reduced in both types of CLDN knockdown cells when incubated with the substrate [[ l-DOPA ]].,2016,5
2017,Protein expression of << Ugt1a6 >> also decreased and corresponded with reduced in vitro glucuronidation of [[ bisphenol A ]] in S9 fractions from livers of pregnant mice.,2017,8
2018,<< Dimethylfumarate >> attenuates renal fibrosis via NF-E2-related factor 2-mediated inhibition of transforming growth factor-beta/[[ Smad ]] signaling.,2018,8
2019,<< Dimethylfumarate >> attenuates renal fibrosis via NF-E2-related factor 2-mediated inhibition of [[ transforming growth factor-beta ]]/Smad signaling.,2019,8
2020,"Results showed that << DMF >> increased nuclear levels of [[ Nrf2 ]], and both DMF and adenovirus-mediated overexpression of Nrf2 (Ad-Nrf2) decreased PAI-1, alpha-smooth muscle actin (alpha-SMA), fibronectin and type 1 collagen expression in TGF-beta-treated rat mesangial cells (RMCs) and renal fibroblast cells (NRK-49F).",2020,6
2021,"Results showed that DMF increased nuclear levels of Nrf2, and both << DMF >> and adenovirus-mediated overexpression of [[ Nrf2 ]] (Ad-Nrf2) decreased PAI-1, alpha-smooth muscle actin (alpha-SMA), fibronectin and type 1 collagen expression in TGF-beta-treated rat mesangial cells (RMCs) and renal fibroblast cells (NRK-49F).",2021,6
2022,"Results showed that DMF increased nuclear levels of Nrf2, and both << DMF >> and adenovirus-mediated overexpression of Nrf2 (Ad-Nrf2) decreased [[ PAI-1 ]], alpha-smooth muscle actin (alpha-SMA), fibronectin and type 1 collagen expression in TGF-beta-treated rat mesangial cells (RMCs) and renal fibroblast cells (NRK-49F).",2022,8
2023,"Results showed that DMF increased nuclear levels of Nrf2, and both << DMF >> and adenovirus-mediated overexpression of Nrf2 (Ad-Nrf2) decreased PAI-1, [[ alpha-smooth muscle actin ]] (alpha-SMA), fibronectin and type 1 collagen expression in TGF-beta-treated rat mesangial cells (RMCs) and renal fibroblast cells (NRK-49F).",2023,8
2024,"Results showed that DMF increased nuclear levels of Nrf2, and both << DMF >> and adenovirus-mediated overexpression of Nrf2 (Ad-Nrf2) decreased PAI-1, alpha-smooth muscle actin ([[ alpha-SMA ]]), fibronectin and type 1 collagen expression in TGF-beta-treated rat mesangial cells (RMCs) and renal fibroblast cells (NRK-49F).",2024,8
2025,"Results showed that DMF increased nuclear levels of Nrf2, and both << DMF >> and adenovirus-mediated overexpression of Nrf2 (Ad-Nrf2) decreased PAI-1, alpha-smooth muscle actin (alpha-SMA), [[ fibronectin ]] and type 1 collagen expression in TGF-beta-treated rat mesangial cells (RMCs) and renal fibroblast cells (NRK-49F).",2025,8
2026,"Results showed that DMF increased nuclear levels of Nrf2, and both << DMF >> and adenovirus-mediated overexpression of Nrf2 (Ad-Nrf2) decreased PAI-1, alpha-smooth muscle actin (alpha-SMA), fibronectin and [[ type 1 collagen ]] expression in TGF-beta-treated rat mesangial cells (RMCs) and renal fibroblast cells (NRK-49F).",2026,8
2027,"Additionally, << DMF >> and Ad-Nrf2 repressed [[ TGF-beta ]]-stimulated Smad3 activity by inhibiting Smad3 phosphorylation, which was restored by siRNA-mediated knockdown of Nrf2 expression.",2027,3
2028,"Additionally, << DMF >> and Ad-Nrf2 repressed TGF-beta-stimulated [[ Smad3 ]] activity by inhibiting Smad3 phosphorylation, which was restored by siRNA-mediated knockdown of Nrf2 expression.",2028,0
2029,"Additionally, << DMF >> and Ad-Nrf2 repressed TGF-beta-stimulated Smad3 activity by inhibiting [[ Smad3 ]] phosphorylation, which was restored by siRNA-mediated knockdown of Nrf2 expression.",2029,0
2030,"However, downregulation of the antioxidant response element (ARE)-driven Nrf2 target genes such as NQO1, HO-1 and glutathione S-transferase (GST) did not reverse the inhibitory effect of << DMF >> on [[ TGF-beta ]]-induced upregulation of profibrotic genes or extracellular matrix proteins, suggesting an ARE-independent anti-fibrotic activity of DMF.",2030,3
2031,"Finally, << DMF >> suppressed unilateral ureteral obstruction (UUO)-induced renal fibrosis and alpha-SMA, fibronectin and type 1 collagen expression in the obstructed kidneys from UUO mice, along with increased and decreased expression of [[ Nrf2 ]] and phospho-Smad3, respectively.",2031,6
2032,"Finally, << DMF >> suppressed unilateral ureteral obstruction (UUO)-induced renal fibrosis and [[ alpha-SMA ]], fibronectin and type 1 collagen expression in the obstructed kidneys from UUO mice, along with increased and decreased expression of Nrf2 and phospho-Smad3, respectively.",2032,8
2033,"Finally, << DMF >> suppressed unilateral ureteral obstruction (UUO)-induced renal fibrosis and alpha-SMA, [[ fibronectin ]] and type 1 collagen expression in the obstructed kidneys from UUO mice, along with increased and decreased expression of Nrf2 and phospho-Smad3, respectively.",2033,8
2034,"Finally, << DMF >> suppressed unilateral ureteral obstruction (UUO)-induced renal fibrosis and alpha-SMA, fibronectin and [[ type 1 collagen ]] expression in the obstructed kidneys from UUO mice, along with increased and decreased expression of Nrf2 and phospho-Smad3, respectively.",2034,8
2035,"Finally, << DMF >> suppressed unilateral ureteral obstruction (UUO)-induced renal fibrosis and alpha-SMA, fibronectin and type 1 collagen expression in the obstructed kidneys from UUO mice, along with increased and decreased expression of Nrf2 and [[ phospho-Smad3 ]], respectively.",2035,8
2036,"In summary, << DMF >> attenuated renal fibrosis via the Nrf2-mediated inhibition of [[ TGF-beta ]]/Smad3 signaling in an ARE-independent manner, suggesting that DMF could be used to treat renal fibrosis.",2036,8
2037,"In summary, << DMF >> attenuated renal fibrosis via the Nrf2-mediated inhibition of TGF-beta/[[ Smad3 ]] signaling in an ARE-independent manner, suggesting that DMF could be used to treat renal fibrosis.",2037,8
2038,Our results showed that bone remodeling was significantly decreased in CCL3(-/-) and CCR1(-/-) mice and in animals treated with << Met >>-RANTES (an antagonist of [[ CCR5 ]] and CCR1).,2038,1
2039,Our results showed that bone remodeling was significantly decreased in CCL3(-/-) and CCR1(-/-) mice and in animals treated with << Met >>-RANTES (an antagonist of CCR5 and [[ CCR1 ]]).,2039,1
2040,"mRNA levels of << receptor activator of nuclear factor kappa-B >> (RANK), its ligand RANKL, tumor necrosis factor alpha (TNF-α) and RANKL/osteoprotegerin (OPG) ratio were diminished in the periodontium of CCL3(-/-) mice and in the group treated with [[ Met ]]-RANTES.",2040,8
2041,"mRNA levels of receptor activator of nuclear factor kappa-B (<< RANK >>), its ligand RANKL, tumor necrosis factor alpha (TNF-α) and RANKL/osteoprotegerin (OPG) ratio were diminished in the periodontium of CCL3(-/-) mice and in the group treated with [[ Met ]]-RANTES.",2041,8
2042,"mRNA levels of receptor activator of nuclear factor kappa-B (RANK), its ligand << RANKL >>, tumor necrosis factor alpha (TNF-α) and RANKL/osteoprotegerin (OPG) ratio were diminished in the periodontium of CCL3(-/-) mice and in the group treated with [[ Met ]]-RANTES.",2042,8
2043,"mRNA levels of receptor activator of nuclear factor kappa-B (RANK), its ligand RANKL, << tumor necrosis factor alpha >> (TNF-α) and RANKL/osteoprotegerin (OPG) ratio were diminished in the periodontium of CCL3(-/-) mice and in the group treated with [[ Met ]]-RANTES.",2043,8
2044,"mRNA levels of receptor activator of nuclear factor kappa-B (RANK), its ligand RANKL, tumor necrosis factor alpha (<< TNF-α >>) and RANKL/osteoprotegerin (OPG) ratio were diminished in the periodontium of CCL3(-/-) mice and in the group treated with [[ Met ]]-RANTES.",2044,8
2045,"mRNA levels of receptor activator of nuclear factor kappa-B (RANK), its ligand RANKL, tumor necrosis factor alpha (TNF-α) and << RANKL >>/osteoprotegerin (OPG) ratio were diminished in the periodontium of CCL3(-/-) mice and in the group treated with [[ Met ]]-RANTES.",2045,8
2046,"mRNA levels of receptor activator of nuclear factor kappa-B (RANK), its ligand RANKL, tumor necrosis factor alpha (TNF-α) and RANKL/<< osteoprotegerin >> (OPG) ratio were diminished in the periodontium of CCL3(-/-) mice and in the group treated with [[ Met ]]-RANTES.",2046,8
2047,"mRNA levels of receptor activator of nuclear factor kappa-B (RANK), its ligand RANKL, tumor necrosis factor alpha (TNF-α) and RANKL/osteoprotegerin (<< OPG >>) ratio were diminished in the periodontium of CCL3(-/-) mice and in the group treated with [[ Met ]]-RANTES.",2047,8
2048,<< Met >>-RANTES treatment also reduced the levels of [[ cathepsin K ]] and metalloproteinase 13 (MMP13).,2048,8
2049,<< Met >>-RANTES treatment also reduced the levels of cathepsin K and [[ metalloproteinase 13 ]] (MMP13).,2049,8
2050,<< Met >>-RANTES treatment also reduced the levels of cathepsin K and metalloproteinase 13 ([[ MMP13 ]]).,2050,8
2051,"The expression of the osteoblast markers runt-related transcription factor 2 (RUNX2) and periostin was decreased, while << osteocalcin >> (OCN) was augmented in CCL3(-/-) and [[ Met ]]-RANTES-treated mice.",2051,6
2052,"The expression of the osteoblast markers runt-related transcription factor 2 (RUNX2) and periostin was decreased, while osteocalcin (<< OCN >>) was augmented in CCL3(-/-) and [[ Met ]]-RANTES-treated mice.",2052,6
2053,"The expression of the osteoblast markers runt-related transcription factor 2 (<< RUNX2 >>) and periostin was decreased, while osteocalcin (OCN) was augmented in CCL3(-/-) and [[ Met ]]-RANTES-treated mice.",2053,8
2054,"The expression of the osteoblast markers runt-related transcription factor 2 (RUNX2) and << periostin >> was decreased, while osteocalcin (OCN) was augmented in CCL3(-/-) and [[ Met ]]-RANTES-treated mice.",2054,8
2055,"The expression of the osteoblast markers << runt-related transcription factor 2 >> (RUNX2) and periostin was decreased, while osteocalcin (OCN) was augmented in CCL3(-/-) and [[ Met ]]-RANTES-treated mice.",2055,8
2056,"The quinolizidine alkaloids (natural products) such as oxymatrine, sophoridine, sophocarpine and << matrine >> carry the common molecular structure of O=C=N-C-C-C-N that possessed positive ionotropic effect and [[ hERG ]] blocking activity.",2056,0
2057,"The quinolizidine alkaloids (natural products) such as oxymatrine, sophoridine, sophocarpine and matrine carry the common molecular structure of << O=C=N-C-C-C-N >> that possessed positive ionotropic effect and [[ hERG ]] blocking activity.",2057,0
2058,"The << quinolizidine alkaloids >> (natural products) such as oxymatrine, sophoridine, sophocarpine and matrine carry the common molecular structure of O=C=N-C-C-C-N that possessed positive ionotropic effect and [[ hERG ]] blocking activity.",2058,0
2059,"The quinolizidine alkaloids (natural products) such as << oxymatrine >>, sophoridine, sophocarpine and matrine carry the common molecular structure of O=C=N-C-C-C-N that possessed positive ionotropic effect and [[ hERG ]] blocking activity.",2059,0
2060,"The quinolizidine alkaloids (natural products) such as oxymatrine, << sophoridine >>, sophocarpine and matrine carry the common molecular structure of O=C=N-C-C-C-N that possessed positive ionotropic effect and [[ hERG ]] blocking activity.",2060,0
2061,"The quinolizidine alkaloids (natural products) such as oxymatrine, sophoridine, << sophocarpine >> and matrine carry the common molecular structure of O=C=N-C-C-C-N that possessed positive ionotropic effect and [[ hERG ]] blocking activity.",2061,0
2062,"Several effects of << polyphenols >> are useful in this scenario, including a reduction in the activities of cytokines and modulation of cellular metabolism through histone deacetylase inhibitors, [[ AMPK ]] activators, calorie-restriction mimetics or epigenetic regulators.",2062,9
2063,"Several effects of << polyphenols >> are useful in this scenario, including a reduction in the activities of [[ cytokines ]] and modulation of cellular metabolism through histone deacetylase inhibitors, AMPK activators, calorie-restriction mimetics or epigenetic regulators.",2063,0
2064,"Several effects of << polyphenols >> are useful in this scenario, including a reduction in the activities of cytokines and modulation of cellular metabolism through [[ histone deacetylase ]] inhibitors, AMPK activators, calorie-restriction mimetics or epigenetic regulators.",2064,0
2065,"Inhibition of << EGF >>/EGFR activation with [[ naphtho[1,2-b]furan-4,5-dione ]] blocks migration and invasion of MDA-MB-231 cells.",2065,0
2066,"Inhibition of EGF/<< EGFR >> activation with [[ naphtho[1,2-b]furan-4,5-dione ]] blocks migration and invasion of MDA-MB-231 cells.",2066,0
2067,"<< NFD >> suppressed [[ EGF ]]-mediated protein levels of c-Jun and c-Fos, and reduced MMP-9 expression and activity, concomitantly with a marked inhibition on cell migration and invasion without obvious cellular cytotoxicity.",2067,3
2068,"<< NFD >> suppressed EGF-mediated protein levels of [[ c-Jun ]] and c-Fos, and reduced MMP-9 expression and activity, concomitantly with a marked inhibition on cell migration and invasion without obvious cellular cytotoxicity.",2068,8
2069,"<< NFD >> suppressed EGF-mediated protein levels of c-Jun and [[ c-Fos ]], and reduced MMP-9 expression and activity, concomitantly with a marked inhibition on cell migration and invasion without obvious cellular cytotoxicity.",2069,8
2070,"<< NFD >> suppressed EGF-mediated protein levels of c-Jun and c-Fos, and reduced [[ MMP-9 ]] expression and activity, concomitantly with a marked inhibition on cell migration and invasion without obvious cellular cytotoxicity.",2070,8
2071,"<< NFD >> suppressed EGF-mediated protein levels of c-Jun and c-Fos, and reduced [[ MMP-9 ]] expression and activity, concomitantly with a marked inhibition on cell migration and invasion without obvious cellular cytotoxicity.",2071,0
2072,<< NFD >> abrogated [[ EGF ]]-induced phosphorylation of EGF receptor (EGFR) and phosphatidylinositol 3-kinase (PI3K)/Akt.,2072,3
2073,<< NFD >> abrogated EGF-induced phosphorylation of [[ EGF receptor ]] (EGFR) and phosphatidylinositol 3-kinase (PI3K)/Akt.,2073,0
2074,<< NFD >> abrogated EGF-induced phosphorylation of EGF receptor ([[ EGFR ]]) and phosphatidylinositol 3-kinase (PI3K)/Akt.,2074,0
2075,<< NFD >> abrogated EGF-induced phosphorylation of EGF receptor (EGFR) and [[ phosphatidylinositol 3-kinase ]] (PI3K)/Akt.,2075,0
2076,<< NFD >> abrogated EGF-induced phosphorylation of EGF receptor (EGFR) and phosphatidylinositol 3-kinase ([[ PI3K ]])/Akt.,2076,0
2077,<< NFD >> abrogated EGF-induced phosphorylation of EGF receptor (EGFR) and phosphatidylinositol 3-kinase (PI3K)/[[ Akt ]].,2077,0
2078,"The specific << PI3K >> inhibitor, [[ wortmannin ]], blocked significantly EGF-induced cell migration and invasion.",2078,0
2079,"The specific PI3K inhibitor, << wortmannin >>, blocked significantly [[ EGF ]]-induced cell migration and invasion.",2079,0
2080,"Furthermore, the EGFR inhibitor << AG1478 >> inhibited EGF-induced [[ MMP-9 ]] expression, cell migration and invasion, as well as the activation of PI3K/Akt, suggesting that PI3K/Akt activation occur downstream of EGFR activation.",2080,8
2081,"Furthermore, the EGFR inhibitor << AG1478 >> inhibited EGF-induced MMP-9 expression, cell migration and invasion, as well as the activation of PI3K/Akt, suggesting that [[ PI3K ]]/Akt activation occur downstream of EGFR activation.",2081,0
2082,"Furthermore, the EGFR inhibitor << AG1478 >> inhibited EGF-induced MMP-9 expression, cell migration and invasion, as well as the activation of PI3K/Akt, suggesting that PI3K/[[ Akt ]] activation occur downstream of EGFR activation.",2082,0
2083,"Furthermore, the EGFR inhibitor << AG1478 >> inhibited EGF-induced MMP-9 expression, cell migration and invasion, as well as the activation of PI3K/Akt, suggesting that PI3K/Akt activation occur downstream of [[ EGFR ]] activation.",2083,0
2084,"Furthermore, the << EGFR >> inhibitor [[ AG1478 ]] inhibited EGF-induced MMP-9 expression, cell migration and invasion, as well as the activation of PI3K/Akt, suggesting that PI3K/Akt activation occur downstream of EGFR activation.",2084,0
2085,"Furthermore, the EGFR inhibitor << AG1478 >> inhibited [[ EGF ]]-induced MMP-9 expression, cell migration and invasion, as well as the activation of PI3K/Akt, suggesting that PI3K/Akt activation occur downstream of EGFR activation.",2085,0
2086,"Furthermore, the EGFR inhibitor << AG1478 >> inhibited EGF-induced MMP-9 expression, cell migration and invasion, as well as the activation of [[ PI3K ]]/Akt, suggesting that PI3K/Akt activation occur downstream of EGFR activation.",2086,0
2087,"Furthermore, the EGFR inhibitor << AG1478 >> inhibited EGF-induced MMP-9 expression, cell migration and invasion, as well as the activation of PI3K/[[ Akt ]], suggesting that PI3K/Akt activation occur downstream of EGFR activation.",2087,0
2088,"These findings suggest that << NFD >> inhibited the EGF-induced invasion and migration of MDA-MB-231 cells via EGFR-dependent [[ PI3K ]]/Akt signaling, leading to the down-regulation of MMP-9 expression.",2088,8
2089,"These findings suggest that << NFD >> inhibited the EGF-induced invasion and migration of MDA-MB-231 cells via EGFR-dependent PI3K/[[ Akt ]] signaling, leading to the down-regulation of MMP-9 expression.",2089,8
2090,"These findings suggest that << NFD >> inhibited the EGF-induced invasion and migration of MDA-MB-231 cells via EGFR-dependent PI3K/Akt signaling, leading to the down-regulation of [[ MMP-9 ]] expression.",2090,8
2091,"These findings suggest that << NFD >> inhibited the [[ EGF ]]-induced invasion and migration of MDA-MB-231 cells via EGFR-dependent PI3K/Akt signaling, leading to the down-regulation of MMP-9 expression.",2091,0
2092,"These findings suggest that << NFD >> inhibited the EGF-induced invasion and migration of MDA-MB-231 cells via [[ EGFR ]]-dependent PI3K/Akt signaling, leading to the down-regulation of MMP-9 expression.",2092,0
2093,"Herein, we report the identification and characterization of << 3-(5-tert-butyl-isoxazol-3-yl)-2-[(3-chloro-phenyl)-hydrazono]-3-oxo-propionitrile >> (ESI-09), a novel noncyclic nucleotide EPAC antagonist that is capable of specifically blocking intracellular EPAC-mediated Rap1 activation and Akt phosphorylation, as well as EPAC-mediated [[ insulin ]] secretion in pancreatic β cells.",2093,8
2094,"Herein, we report the identification and characterization of 3-(5-tert-butyl-isoxazol-3-yl)-2-[(3-chloro-phenyl)-hydrazono]-3-oxo-propionitrile (<< ESI-09 >>), a novel noncyclic nucleotide EPAC antagonist that is capable of specifically blocking intracellular EPAC-mediated Rap1 activation and Akt phosphorylation, as well as EPAC-mediated [[ insulin ]] secretion in pancreatic β cells.",2094,8
2095,"Herein, we report the identification and characterization of 3-(5-tert-butyl-isoxazol-3-yl)-2-[(3-chloro-phenyl)-hydrazono]-3-oxo-propionitrile (ESI-09), a novel noncyclic << nucleotide >> EPAC antagonist that is capable of specifically blocking intracellular EPAC-mediated Rap1 activation and Akt phosphorylation, as well as EPAC-mediated [[ insulin ]] secretion in pancreatic β cells.",2095,8
2096,"Herein, we report the identification and characterization of << 3-(5-tert-butyl-isoxazol-3-yl)-2-[(3-chloro-phenyl)-hydrazono]-3-oxo-propionitrile >> (ESI-09), a novel noncyclic nucleotide EPAC antagonist that is capable of specifically blocking intracellular [[ EPAC ]]-mediated Rap1 activation and Akt phosphorylation, as well as EPAC-mediated insulin secretion in pancreatic β cells.",2096,0
2097,"Herein, we report the identification and characterization of << 3-(5-tert-butyl-isoxazol-3-yl)-2-[(3-chloro-phenyl)-hydrazono]-3-oxo-propionitrile >> (ESI-09), a novel noncyclic nucleotide EPAC antagonist that is capable of specifically blocking intracellular EPAC-mediated [[ Rap1 ]] activation and Akt phosphorylation, as well as EPAC-mediated insulin secretion in pancreatic β cells.",2097,0
2098,"Herein, we report the identification and characterization of << 3-(5-tert-butyl-isoxazol-3-yl)-2-[(3-chloro-phenyl)-hydrazono]-3-oxo-propionitrile >> (ESI-09), a novel noncyclic nucleotide EPAC antagonist that is capable of specifically blocking intracellular EPAC-mediated Rap1 activation and [[ Akt ]] phosphorylation, as well as EPAC-mediated insulin secretion in pancreatic β cells.",2098,0
2099,"Herein, we report the identification and characterization of << 3-(5-tert-butyl-isoxazol-3-yl)-2-[(3-chloro-phenyl)-hydrazono]-3-oxo-propionitrile >> (ESI-09), a novel noncyclic nucleotide EPAC antagonist that is capable of specifically blocking intracellular EPAC-mediated Rap1 activation and Akt phosphorylation, as well as [[ EPAC ]]-mediated insulin secretion in pancreatic β cells.",2099,0
2100,"Herein, we report the identification and characterization of 3-(5-tert-butyl-isoxazol-3-yl)-2-[(3-chloro-phenyl)-hydrazono]-3-oxo-propionitrile (<< ESI-09 >>), a novel noncyclic nucleotide EPAC antagonist that is capable of specifically blocking intracellular [[ EPAC ]]-mediated Rap1 activation and Akt phosphorylation, as well as EPAC-mediated insulin secretion in pancreatic β cells.",2100,0
2101,"Herein, we report the identification and characterization of 3-(5-tert-butyl-isoxazol-3-yl)-2-[(3-chloro-phenyl)-hydrazono]-3-oxo-propionitrile (<< ESI-09 >>), a novel noncyclic nucleotide EPAC antagonist that is capable of specifically blocking intracellular EPAC-mediated [[ Rap1 ]] activation and Akt phosphorylation, as well as EPAC-mediated insulin secretion in pancreatic β cells.",2101,0
2102,"Herein, we report the identification and characterization of 3-(5-tert-butyl-isoxazol-3-yl)-2-[(3-chloro-phenyl)-hydrazono]-3-oxo-propionitrile (<< ESI-09 >>), a novel noncyclic nucleotide EPAC antagonist that is capable of specifically blocking intracellular EPAC-mediated Rap1 activation and [[ Akt ]] phosphorylation, as well as EPAC-mediated insulin secretion in pancreatic β cells.",2102,0
2103,"Herein, we report the identification and characterization of 3-(5-tert-butyl-isoxazol-3-yl)-2-[(3-chloro-phenyl)-hydrazono]-3-oxo-propionitrile (<< ESI-09 >>), a novel noncyclic nucleotide EPAC antagonist that is capable of specifically blocking intracellular EPAC-mediated Rap1 activation and Akt phosphorylation, as well as [[ EPAC ]]-mediated insulin secretion in pancreatic β cells.",2103,0
2104,"Herein, we report the identification and characterization of 3-(5-tert-butyl-isoxazol-3-yl)-2-[(3-chloro-phenyl)-hydrazono]-3-oxo-propionitrile (ESI-09), a novel noncyclic << nucleotide >> EPAC antagonist that is capable of specifically blocking intracellular [[ EPAC ]]-mediated Rap1 activation and Akt phosphorylation, as well as EPAC-mediated insulin secretion in pancreatic β cells.",2104,0
2105,"Herein, we report the identification and characterization of 3-(5-tert-butyl-isoxazol-3-yl)-2-[(3-chloro-phenyl)-hydrazono]-3-oxo-propionitrile (ESI-09), a novel noncyclic << nucleotide >> EPAC antagonist that is capable of specifically blocking intracellular EPAC-mediated [[ Rap1 ]] activation and Akt phosphorylation, as well as EPAC-mediated insulin secretion in pancreatic β cells.",2105,0
2106,"Herein, we report the identification and characterization of 3-(5-tert-butyl-isoxazol-3-yl)-2-[(3-chloro-phenyl)-hydrazono]-3-oxo-propionitrile (ESI-09), a novel noncyclic << nucleotide >> EPAC antagonist that is capable of specifically blocking intracellular EPAC-mediated Rap1 activation and [[ Akt ]] phosphorylation, as well as EPAC-mediated insulin secretion in pancreatic β cells.",2106,0
2107,"Herein, we report the identification and characterization of 3-(5-tert-butyl-isoxazol-3-yl)-2-[(3-chloro-phenyl)-hydrazono]-3-oxo-propionitrile (ESI-09), a novel noncyclic << nucleotide >> EPAC antagonist that is capable of specifically blocking intracellular EPAC-mediated Rap1 activation and Akt phosphorylation, as well as [[ EPAC ]]-mediated insulin secretion in pancreatic β cells.",2107,0
2108,"Herein, we report the identification and characterization of << 3-(5-tert-butyl-isoxazol-3-yl)-2-[(3-chloro-phenyl)-hydrazono]-3-oxo-propionitrile >> (ESI-09), a novel noncyclic nucleotide [[ EPAC ]] antagonist that is capable of specifically blocking intracellular EPAC-mediated Rap1 activation and Akt phosphorylation, as well as EPAC-mediated insulin secretion in pancreatic β cells.",2108,1
2109,"Herein, we report the identification and characterization of 3-(5-tert-butyl-isoxazol-3-yl)-2-[(3-chloro-phenyl)-hydrazono]-3-oxo-propionitrile (<< ESI-09 >>), a novel noncyclic nucleotide [[ EPAC ]] antagonist that is capable of specifically blocking intracellular EPAC-mediated Rap1 activation and Akt phosphorylation, as well as EPAC-mediated insulin secretion in pancreatic β cells.",2109,1
2110,"Herein, we report the identification and characterization of 3-(5-tert-butyl-isoxazol-3-yl)-2-[(3-chloro-phenyl)-hydrazono]-3-oxo-propionitrile (ESI-09), a novel noncyclic << nucleotide >> [[ EPAC ]] antagonist that is capable of specifically blocking intracellular EPAC-mediated Rap1 activation and Akt phosphorylation, as well as EPAC-mediated insulin secretion in pancreatic β cells.",2110,1
2111,<< Metformin >> directly inhibits [[ ghrelin ]] secretion through AMP-activated protein kinase in rat primary gastric cells.,2111,8
2112,<< Metformin >> treatment is also associated with lower circulating levels of the [[ orexigenic hormone ]] ghrelin.,2112,8
2113,<< Metformin >> treatment is also associated with lower circulating levels of the orexigenic hormone [[ ghrelin ]].,2113,8
2114,Metformin significantly reduced << ghrelin >> secretion and proghrelin mRNA production and both these effects were blocked by co-incubation with the AMPK inhibitor [[ compound C ]].,2114,6
2115,Metformin significantly reduced ghrelin secretion and << proghrelin >> mRNA production and both these effects were blocked by co-incubation with the AMPK inhibitor [[ compound C ]].,2115,6
2116,<< Metformin >> significantly reduced [[ ghrelin ]] secretion and proghrelin mRNA production and both these effects were blocked by co-incubation with the AMPK inhibitor compound C.,2116,8
2117,<< Metformin >> significantly reduced ghrelin secretion and [[ proghrelin ]] mRNA production and both these effects were blocked by co-incubation with the AMPK inhibitor compound C.,2117,8
2118,Metformin significantly reduced ghrelin secretion and proghrelin mRNA production and both these effects were blocked by co-incubation with the << AMPK >> inhibitor [[ compound C ]].,2118,0
2119,"Furthermore, the << AMPK >> activator [[ 5-amino-1-β-D-ribofuranosyl-imidazole-4-carboxamide ]] (AICAR) significantly inhibited ghrelin secretion.",2119,9
2120,"Furthermore, the << AMPK >> activator 5-amino-1-β-D-ribofuranosyl-imidazole-4-carboxamide ([[ AICAR ]]) significantly inhibited ghrelin secretion.",2120,9
2121,"Furthermore, the AMPK activator 5-amino-1-β-D-ribofuranosyl-imidazole-4-carboxamide (<< AICAR >>) significantly inhibited [[ ghrelin ]] secretion.",2121,8
2122,"Finally, << Metformin >> treatment caused a significant increase in the level of [[ phosphorylated (active) AMPK ]].",2122,6
2123,Our results show that << Metformin >> directly inhibits stomach [[ ghrelin ]] production and secretion through AMPK.,2123,8
2124,Fungicide << prochloraz >> and environmental pollutant dioxin induce the [[ ABCG2 ]] transporter in bovine mammary epithelial cells by the arylhydrocarbon receptor signaling pathway.,2124,7
2125,Fungicide prochloraz and environmental pollutant << dioxin >> induce the [[ ABCG2 ]] transporter in bovine mammary epithelial cells by the arylhydrocarbon receptor signaling pathway.,2125,7
2126,"As these regulatory motifs mediate regulation of target genes by << AhR >> agonists including [[ TCDD ]] and prochloraz, we have systematically investigated the effect of both contaminants on functional ABCG2 transport activity in primary bovine mammary epithelial cells.",2126,2
2127,"As these regulatory motifs mediate regulation of target genes by << AhR >> agonists including TCDD and [[ prochloraz ]], we have systematically investigated the effect of both contaminants on functional ABCG2 transport activity in primary bovine mammary epithelial cells.",2127,2
2128,TCDD or prochloraz doubled << ABCG2 >>-mediated [[ Hoechst H33342 ]] secretion.,2128,5
2129,This effect was almost completely reversed by specific << ABCG2 >> inhibitor [[ Ko143 ]].,2129,0
2130,Receptor binding was significantly reduced by specific << AhR >> antagonist [[ salicyl amide ]].,2130,1
2131,Induction of AhR by << TCDD >> and prochloraz resulted in a time- and dose-dependent increase of [[ ABCG2 ]] gene expression and transporter protein levels.,2131,6
2132,Induction of AhR by TCDD and << prochloraz >> resulted in a time- and dose-dependent increase of [[ ABCG2 ]] gene expression and transporter protein levels.,2132,6
2133,Induction of << AhR >> by [[ TCDD ]] and prochloraz resulted in a time- and dose-dependent increase of ABCG2 gene expression and transporter protein levels.,2133,7
2134,Induction of << AhR >> by TCDD and [[ prochloraz ]] resulted in a time- and dose-dependent increase of ABCG2 gene expression and transporter protein levels.,2134,7
2135,We found that << Ag >> NPs were highly cytotoxic to hepatocytes (LC(50) lactate dehydrogenase: 2.5 μg/cm(2)) and affected hepatocyte homeostasis by reducing [[ albumin ]] release.,2135,8
2136,"We observed similar effects of << Ag >> NPs on inflammatory mediator expression in vitro and in vivo with increase of [[ interleukin-8 ]] (IL-8)/macrophage inflammatory protein 2, IL-1RI, and tumor necrosis factor-α expression in both models and increased IL-8 protein release in vitro.",2136,6
2137,"We observed similar effects of << Ag >> NPs on inflammatory mediator expression in vitro and in vivo with increase of interleukin-8 ([[ IL-8 ]])/macrophage inflammatory protein 2, IL-1RI, and tumor necrosis factor-α expression in both models and increased IL-8 protein release in vitro.",2137,6
2138,"We observed similar effects of << Ag >> NPs on inflammatory mediator expression in vitro and in vivo with increase of interleukin-8 (IL-8)/[[ macrophage inflammatory protein 2 ]], IL-1RI, and tumor necrosis factor-α expression in both models and increased IL-8 protein release in vitro.",2138,6
2139,"We observed similar effects of << Ag >> NPs on inflammatory mediator expression in vitro and in vivo with increase of interleukin-8 (IL-8)/macrophage inflammatory protein 2, [[ IL-1RI ]], and tumor necrosis factor-α expression in both models and increased IL-8 protein release in vitro.",2139,6
2140,"We observed similar effects of << Ag >> NPs on inflammatory mediator expression in vitro and in vivo with increase of interleukin-8 (IL-8)/macrophage inflammatory protein 2, IL-1RI, and [[ tumor necrosis factor-α ]] expression in both models and increased IL-8 protein release in vitro.",2140,6
2141,"We observed similar effects of << Ag >> NPs on inflammatory mediator expression in vitro and in vivo with increase of interleukin-8 (IL-8)/macrophage inflammatory protein 2, IL-1RI, and tumor necrosis factor-α expression in both models and increased [[ IL-8 ]] protein release in vitro.",2141,6
2142,"Blood pressure was increased in rats exposed to IH, and treatment with the << PDK-1 >> inhibitor [[ OSU-03012 ]] [2-amino-N-{4-[5-(2-phenanthrenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]-phenyl}-acetamide] (33 mg/day) lowered blood pressure in IH but not sham group rats.",2142,0
2143,"Blood pressure was increased in rats exposed to IH, and treatment with the << PDK-1 >> inhibitor OSU-03012 [[[ 2-amino-N-{4-[5-(2-phenanthrenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]-phenyl}-acetamide ]]] (33 mg/day) lowered blood pressure in IH but not sham group rats.",2143,0
2144,"Following << CdCl₂ >> treatment, [[ ICAM2 ]] was found to be upregulated during restructuring of the seminiferous epithelium, with round spermatids becoming increasingly immunoreactive for ICAM2 by 6-16 h.",2144,7
2145,"Interestingly, there was a loss in the binding of ICAM2 to << actin >> during [[ CdCl₂ ]]-induced germ cell loss, suggesting that a loss of ICAM2-actin interactions might have facilitated junction restructuring.",2145,0
2146,The catalytic competence of << cytochrome P450 >> in the synthesis of [[ serotonin ]] from 5-methoxytryptamine in the brain: an in vitro study.,2146,4
2147,The catalytic competence of << cytochrome P450 >> in the synthesis of serotonin from [[ 5-methoxytryptamine ]] in the brain: an in vitro study.,2147,5
2148,"Of the rat CYP isoforms studied, << CYP2D >> isoforms were the most efficient in catalyzing the O-demethylation of 5-methoxytryptamine to [[ serotonin ]], but they were less effective than the human isoform CYP2D6.",2148,4
2149,"Of the rat CYP isoforms studied, CYP2D isoforms were the most efficient in catalyzing the O-demethylation of 5-methoxytryptamine to << serotonin >>, but they were less effective than the [[ human isoform CYP2D6 ]].",2149,4
2150,"Of the rat CYP isoforms studied, << CYP2D >> isoforms were the most efficient in catalyzing the [[ O ]]-demethylation of 5-methoxytryptamine to serotonin, but they were less effective than the human isoform CYP2D6.",2150,5
2151,"Of the rat CYP isoforms studied, CYP2D isoforms were the most efficient in catalyzing the << O >>-demethylation of 5-methoxytryptamine to serotonin, but they were less effective than the [[ human isoform CYP2D6 ]].",2151,5
2152,"Of the rat CYP isoforms studied, << CYP2D >> isoforms were the most efficient in catalyzing the O-demethylation of [[ 5-methoxytryptamine ]] to serotonin, but they were less effective than the human isoform CYP2D6.",2152,5
2153,"Of the rat CYP isoforms studied, CYP2D isoforms were the most efficient in catalyzing the O-demethylation of << 5-methoxytryptamine >> to serotonin, but they were less effective than the [[ human isoform CYP2D6 ]].",2153,5
2154,The reaction was inhibited by the specific << CYP2D >> inhibitors [[ quinine ]] and fluoxetine.,2154,0
2155,The reaction was inhibited by the specific << CYP2D >> inhibitors quinine and [[ fluoxetine ]].,2155,0
2156,Human liver microsomes of the wild-type << CYP2D6 >> metabolized 5-methoxytryptamine to [[ serotonin ]] more effectively than did the defective CYP2D6*4*4 ones.,2156,4
2157,Human liver microsomes of the wild-type CYP2D6 metabolized 5-methoxytryptamine to << serotonin >> more effectively than did the defective [[ CYP2D6 ]]*4*4 ones.,2157,4
2158,Human liver microsomes of the wild-type << CYP2D6 >> metabolized [[ 5-methoxytryptamine ]] to serotonin more effectively than did the defective CYP2D6*4*4 ones.,2158,5
2159,Human liver microsomes of the wild-type CYP2D6 metabolized << 5-methoxytryptamine >> to serotonin more effectively than did the defective [[ CYP2D6 ]]*4*4 ones.,2159,5
2160,"The obtained results indicate that << rat brain CYP2D >> isoforms catalyze the formation of [[ serotonin ]] from 5-methoxytryptamine, and that the deficit or genetic defect of CYP2D may affect serotonin metabolism in the brain.",2160,4
2161,"The obtained results indicate that rat brain CYP2D isoforms catalyze the formation of serotonin from 5-methoxytryptamine, and that the deficit or genetic defect of << CYP2D >> may affect [[ serotonin ]] metabolism in the brain.",2161,4
2162,"The obtained results indicate that << rat brain CYP2D >> isoforms catalyze the formation of serotonin from [[ 5-methoxytryptamine ]], and that the deficit or genetic defect of CYP2D may affect serotonin metabolism in the brain.",2162,5
2163,<< Toosendanin >> induces apoptosis through suppression of [[ JNK ]] signaling pathway in HL-60 cells.,2163,8
2164,Western blot analysis indicated that << TSN >> inhibits the [[ CDC42 ]]/MEKK1/JNK pathway.,2164,0
2165,Western blot analysis indicated that << TSN >> inhibits the CDC42/[[ MEKK1 ]]/JNK pathway.,2165,0
2166,Western blot analysis indicated that << TSN >> inhibits the CDC42/MEKK1/[[ JNK ]] pathway.,2166,0
2167,"Administration of low, but not high, doses of oral << nicotine >> in DSS-treated mice resulted in a significant decrease in disease severity, histologic damage scores, as well as colonic level of [[ tumor necrosis factor-α ]].",2167,6
2168,"Small interfering RNA directed BDNF, orexin-A, and << SB334867 >> [N-(2-methyl-6-benzoxazolyl)-N'-1,5-naphthyridin-4-yl urea; a specific [[ orexin-1 receptor ]] antagonist] were administered directly into the hypothalamus.",2168,1
2169,"Small interfering RNA directed BDNF, orexin-A, and SB334867 [<< N-(2-methyl-6-benzoxazolyl)-N'-1,5-naphthyridin-4-yl urea >>; a specific [[ orexin-1 receptor ]] antagonist] were administered directly into the hypothalamus.",2169,1
2170,"The MCAO-induced decrease in insulin receptor levels in the liver and skeletal muscle on day 1 was recovered to control levels by orexin-A, and this effect of << orexin-A >> was reversed by the administration of [[ SB334867 ]] as well as by hypothalamic BDNF knockdown.",2170,3
2171,"The MCAO-induced decrease in << insulin receptor >> levels in the liver and skeletal muscle on day 1 was recovered to control levels by orexin-A, and this effect of orexin-A was reversed by the administration of [[ SB334867 ]] as well as by hypothalamic BDNF knockdown.",2171,8
2172,<< Mesalamine >> modulates intercellular adhesion through inhibition of [[ p-21 activated kinase-1 ]].,2172,0
2173,"Moreover, << 5-ASA >> treatment restored membranous expression of adhesion molecules [[ E-cadherin ]] and β-catenin.",2173,6
2174,"Moreover, << 5-ASA >> treatment restored membranous expression of adhesion molecules E-cadherin and [[ β-catenin ]].",2174,6
2175,<< PAK1 >> expression was elevated in APC(min) polyps and [[ 5-ASA ]] treatment reduced its expression.,2175,8
2176,We propose that inhibition of << PAK1 >> expression by [[ 5-ASA ]] can impede with neoplastic progression in colorectal carcinogenesis.,2176,8
2177,The mechanism of << PAK1 >> inhibition and induction of membranous translocation of adhesion proteins by [[ 5-ASA ]] might be independent of its known anti-inflammatory action.,2177,0
2178,"In contrast, << EGCG >> markedly downregulated major [[ bile acid transporters ]] (Asbt and Ostα) and regulatory molecules (Shp and Fgf15) in the ileum.",2178,3
2179,"In contrast, << EGCG >> markedly downregulated major bile acid transporters ([[ Asbt ]] and Ostα) and regulatory molecules (Shp and Fgf15) in the ileum.",2179,3
2180,"In contrast, << EGCG >> markedly downregulated major bile acid transporters (Asbt and [[ Ostα ]]) and regulatory molecules (Shp and Fgf15) in the ileum.",2180,3
2181,"In contrast, << EGCG >> markedly downregulated major bile acid transporters (Asbt and Ostα) and regulatory molecules ([[ Shp ]] and Fgf15) in the ileum.",2181,8
2182,"In contrast, << EGCG >> markedly downregulated major bile acid transporters (Asbt and Ostα) and regulatory molecules (Shp and [[ Fgf15 ]]) in the ileum.",2182,8
2183,"This study shows ability of << EGCG >> to raise plasma bile acid concentrations, mainly through [[ Cyp7a1 ]] upregulation, and to decrease bile production through reduction in Mrp2-mediated bile acid-independent bile flow.",2183,6
2184,<< Catalpol >> inhibits LPS plus [[ IFN-γ ]]-induced inflammatory response in astrocytes primary cultures.,2184,0
2185,Biochemical analyses showed that NO and ROS production and << iNOS >> activity were significantly reduced by [[ catalpol ]].,2185,0
2186,"Data at transcriptional level also demonstrated that << catalpol >> potently attenuated gene expressions involved in inflammation, such as [[ iNOS ]], COX-2 and TLR4.",2186,8
2187,"Data at transcriptional level also demonstrated that << catalpol >> potently attenuated gene expressions involved in inflammation, such as iNOS, [[ COX-2 ]] and TLR4.",2187,8
2188,"Data at transcriptional level also demonstrated that << catalpol >> potently attenuated gene expressions involved in inflammation, such as iNOS, COX-2 and [[ TLR4 ]].",2188,8
2189,"In addition, our exploration further revealed that the suppressive action of << catalpol >> on inflammation was mediated via inhibiting nuclear factor-κB ([[ NF-κB ]]) activation.",2189,0
2190,"In addition, our exploration further revealed that the suppressive action of << catalpol >> on inflammation was mediated via inhibiting [[ nuclear factor-κB ]] (NF-κB) activation.",2190,0
2191,"Collectively, these results suggest that << catalpol >> can exert inhibitory effects on the inflammatory reaction in astrocytes and that inactivation of [[ NF-κB ]] could be the major determinant for its anti-inflammatory mechanism.",2191,0
2192,<< Protein tyrosine phosphatase 1B >> inhibitory effect by dammarane-type triterpenes from hydrolyzate of total Gynostemma pentaphyllum [[ saponins ]].,2192,0
2193,<< Protein tyrosine phosphatase 1B >> inhibitory effect by [[ dammarane ]]-type triterpenes from hydrolyzate of total Gynostemma pentaphyllum saponins.,2193,0
2194,<< Protein tyrosine phosphatase 1B >> inhibitory effect by dammarane-type [[ triterpenes ]] from hydrolyzate of total Gynostemma pentaphyllum saponins.,2194,0
2195,"Also, reactive astrogliosis takes part of the early responses to the insult with << (PhTe)(2) >>, evidenced by upregulated [[ GFAP ]] in Western blot, PCR and immunofluorescence analysis.",2195,6
2196,"Six days after (PhTe)(2) injection we found persistent astrogliosis, increased propidium iodide (PI) positive cells in NeuN positive population evidenced by flow cytometry and reduced immunofluorescence for << NeuN >>, suggesting that the in vivo exposure to [[ (PhTe)(2) ]] progressed to neuronal death.",2196,8
2197,"Neurodegeneration was related with decreased [(3)H]glutamate uptake and decreased << Akt >> immunoreactivity, however phospho-GSK-3-β (Ser9) was not altered in [[ (PhTe)(2) ]] injected rat.",2197,8
2198,"Therefore, the present results show that the earlier cerebellar responses to << (PhTe)(2) >> include disruption of cytoskeletal homeostasis that could be related with [[ MAPK ]] and PKA activation and reactive astrogliosis.",2198,9
2199,"Therefore, the present results show that the earlier cerebellar responses to << (PhTe)(2) >> include disruption of cytoskeletal homeostasis that could be related with MAPK and [[ PKA ]] activation and reactive astrogliosis.",2199,9
2200,"Fluorescence of the reporter dye is turned on by rapid removal of the quinone quencher, an event that immediately occurs only after highly selective, two-electron reduction of the sterically and conformationally restricted << quinone >> substrate by the cancer-associated [[ human NAD(P)H:quinone oxidoreductase isozyme 1 ]] (hNQO1).",2200,5
2201,"Fluorescence of the reporter dye is turned on by rapid removal of the quinone quencher, an event that immediately occurs only after highly selective, two-electron reduction of the sterically and conformationally restricted << quinone >> substrate by the cancer-associated human NAD(P)H:quinone oxidoreductase isozyme 1 ([[ hNQO1 ]]).",2201,5
2202,"Synthesis, biological evaluation, and molecular modeling of << glycyrrhizin >> derivatives as potent [[ high-mobility group box-1 ]] inhibitors with anti-heart-failure activity in vivo.",2202,0
2203,"Within the << TPBP >> scaffold, either electronic or steric perturbations to the central piperidine ring led to a loss of selective M(1) allosteric agonism and afforded pan-[[ mAChR ]] antagonism, which was demonstrated to be mediated via the orthosteric site.",2203,1
2204,"Within the TPBP scaffold, either electronic or steric perturbations to the central << piperidine >> ring led to a loss of selective M(1) allosteric agonism and afforded pan-[[ mAChR ]] antagonism, which was demonstrated to be mediated via the orthosteric site.",2204,1
2205,"Additional SAR around a related M(1) allosteric agonist family (<< VU0357017 >>) identified similar, subtle 'molecular switches' that modulated modes of pharmacology from allosteric agonism to pan-[[ mAChR ]] orthosteric antagonism.",2205,1
2206,"2. The objective of this article is to examine the effects of single and repeated administrations of silymarin on pharmacokinetics of a << P-gp >> substrate, [[ risperidone ]], and its major metabolite, 9-hydroxyrisperidone, in rats.",2206,5
2207,"2. The objective of this article is to examine the effects of single and repeated administrations of silymarin on pharmacokinetics of a << P-gp >> substrate, risperidone, and its major metabolite, [[ 9-hydroxyrisperidone ]], in rats.",2207,5
2208,"On the other hand, peptides modified with << (2S,4R)-4-(naphthalene-2-ylmethyl)pyrrolidine-2-carboxylic acid >>, apart from their moderate antioxytocic activity, turned out to be weak antagonists of the pressor response to [[ arginine vasopressin ]].",2208,1
2209,"<< Liver X Receptor (LXR) α >> and LXR β are nuclear receptors activated by [[ oxysterols ]], oxidized derivatives of cholesterol.",2209,9
2210,"Liver X Receptor (LXR) α and << LXR β >> are nuclear receptors activated by [[ oxysterols ]], oxidized derivatives of cholesterol.",2210,9
2211,β-catenin regulates << GnRH >>-induced [[ FSHβ ]] gene expression.,2211,6
2212,"<< GnRH >> caused a sustained increase in nuclear [[ β-catenin ]] levels, which was significantly reduced by c-Jun N-terminal kinase (JNK) inhibition.",2212,6
2213,Small interfering RNA-mediated knockdown of β-catenin mRNA demonstrated that induction of << FSHβ >> mRNA by [[ GnRH ]] depended on β-catenin and that regulation of FSHβ by β-catenin occurred independently of the JNK-c-jun pathway.,2213,6
2214,"Furthermore, knockdown of Brms1L significantly attenuated << GnRH >>-induced [[ FSHβ ]] expression.",2214,6
2215,"Thus, our findings indicate that the expression of Brms1L depends on β-catenin activity and contributes to << FSHβ >> induction by [[ GnRH ]].",2215,6
2216,The herbicide << paraquat >> (PQ) is a [[ P-gp ]] substrate responsible for thousands of fatal intoxications worldwide that still lacks an effective antidote.,2216,5
2217,"The aim of the present work was to evaluate the effectiveness of such an antidote by testing whether << doxorubicin >> (DOX), a known [[ P-gp ]] inducer, could efficiently protect Caco-2 cells against PQ cytotoxicity, 6 h after the incubation with the herbicide, reflecting a real-life intoxication scenario.",2217,9
2218,"The aim of the present work was to evaluate the effectiveness of such an antidote by testing whether doxorubicin (<< DOX >>), a known [[ P-gp ]] inducer, could efficiently protect Caco-2 cells against PQ cytotoxicity, 6 h after the incubation with the herbicide, reflecting a real-life intoxication scenario.",2218,9
2219,"In conclusion, in this cellular model, << DOX >> effectively protects against PQ toxicity by inducing [[ P-gp ]] and through the interaction with the choline transporter, suggesting that compounds presenting this double feature of promoting the efflux and limiting the uptake of PQ could be used as effective antidotes to treat intoxications.",2219,9
2220,The selective << SYK >> inhibitor [[ P505-15 ]] (PRT062607) inhibits B cell signaling and function in vitro and in vivo and augments the activity of fludarabine in chronic lymphocytic leukemia.,2220,0
2221,The selective << SYK >> inhibitor P505-15 ([[ PRT062607 ]]) inhibits B cell signaling and function in vitro and in vivo and augments the activity of fludarabine in chronic lymphocytic leukemia.,2221,0
2222,"<< P505-15 >> (also known as PRT062607) is a novel, highly selective, and orally bioavailable small molecule [[ SYK ]] inhibitor (SYK IC(50) = 1 nM) with anti-SYK activity that is at least 80-fold greater than its affinity for other kinases.",2222,0
2223,"<< P505-15 >> (also known as PRT062607) is a novel, highly selective, and orally bioavailable small molecule SYK inhibitor ([[ SYK ]] IC(50) = 1 nM) with anti-SYK activity that is at least 80-fold greater than its affinity for other kinases.",2223,0
2224,"<< P505-15 >> (also known as PRT062607) is a novel, highly selective, and orally bioavailable small molecule SYK inhibitor (SYK IC(50) = 1 nM) with anti-[[ SYK ]] activity that is at least 80-fold greater than its affinity for other kinases.",2224,0
2225,"P505-15 (also known as << PRT062607 >>) is a novel, highly selective, and orally bioavailable small molecule [[ SYK ]] inhibitor (SYK IC(50) = 1 nM) with anti-SYK activity that is at least 80-fold greater than its affinity for other kinases.",2225,0
2226,"P505-15 (also known as << PRT062607 >>) is a novel, highly selective, and orally bioavailable small molecule SYK inhibitor ([[ SYK ]] IC(50) = 1 nM) with anti-SYK activity that is at least 80-fold greater than its affinity for other kinases.",2226,0
2227,"P505-15 (also known as << PRT062607 >>) is a novel, highly selective, and orally bioavailable small molecule SYK inhibitor (SYK IC(50) = 1 nM) with anti-[[ SYK ]] activity that is at least 80-fold greater than its affinity for other kinases.",2227,0
2228,<< P505-15 >> successfully inhibited SYK-mediated [[ B-cell receptor ]] signaling and decreased cell viability in NHL and CLL.,2228,8
2229,<< P505-15 >> successfully inhibited [[ SYK ]]-mediated B-cell receptor signaling and decreased cell viability in NHL and CLL.,2229,0
2230,"<< 17-Allylamino-17-demethoxygeldanamycin >> (17-AAG), an [[ Hsp90 ]] inhibitor, is currently under evaluation for its anticancer activity in clinical trials.",2230,0
2231,"17-Allylamino-17-demethoxygeldanamycin (<< 17-AAG >>), an [[ Hsp90 ]] inhibitor, is currently under evaluation for its anticancer activity in clinical trials.",2231,0
2232,"Although treatment with << 17-AAG >> reduced [[ AhR ]] levels and AhR-regulated gene expression in lung AD cells, AhR expression increased anticancer activity of 17-AAG.",2232,8
2233,"Although treatment with << 17-AAG >> reduced AhR levels and [[ AhR ]]-regulated gene expression in lung AD cells, AhR expression increased anticancer activity of 17-AAG.",2233,8
2234,"In addition, << 17-AAG >> treatment reduced cell viability, [[ CDK2 ]], CDK4, cyclin E, cyclin D1, and phosphorylated Rb levels in AhR-expressing lung AD cells.",2234,8
2235,"In addition, << 17-AAG >> treatment reduced cell viability, CDK2, [[ CDK4 ]], cyclin E, cyclin D1, and phosphorylated Rb levels in AhR-expressing lung AD cells.",2235,8
2236,"In addition, << 17-AAG >> treatment reduced cell viability, CDK2, CDK4, [[ cyclin E ]], cyclin D1, and phosphorylated Rb levels in AhR-expressing lung AD cells.",2236,8
2237,"In addition, << 17-AAG >> treatment reduced cell viability, CDK2, CDK4, cyclin E, [[ cyclin D1 ]], and phosphorylated Rb levels in AhR-expressing lung AD cells.",2237,8
2238,"In addition, << 17-AAG >> treatment reduced cell viability, CDK2, CDK4, cyclin E, cyclin D1, and [[ phosphorylated Rb ]] levels in AhR-expressing lung AD cells.",2238,8
2239,"<< Gemcitabine >> (dFdC, 2',2'-difluorodeoxycytidine) is metabolized by cytidine deaminase (CDA) and deoxycytidine kinase ([[ DCK ]]), but the contribution of genetic variation in these enzymes to the variability in systemic exposure and response observed in cancer patients is unclear.",2239,5
2240,"<< Gemcitabine >> (dFdC, 2',2'-difluorodeoxycytidine) is metabolized by [[ cytidine deaminase ]] (CDA) and deoxycytidine kinase (DCK), but the contribution of genetic variation in these enzymes to the variability in systemic exposure and response observed in cancer patients is unclear.",2240,5
2241,"<< Gemcitabine >> (dFdC, 2',2'-difluorodeoxycytidine) is metabolized by cytidine deaminase ([[ CDA ]]) and deoxycytidine kinase (DCK), but the contribution of genetic variation in these enzymes to the variability in systemic exposure and response observed in cancer patients is unclear.",2241,5
2242,"<< Gemcitabine >> (dFdC, 2',2'-difluorodeoxycytidine) is metabolized by cytidine deaminase (CDA) and [[ deoxycytidine kinase ]] (DCK), but the contribution of genetic variation in these enzymes to the variability in systemic exposure and response observed in cancer patients is unclear.",2242,5
2243,"Gemcitabine (<< dFdC >>, 2',2'-difluorodeoxycytidine) is metabolized by cytidine deaminase (CDA) and deoxycytidine kinase ([[ DCK ]]), but the contribution of genetic variation in these enzymes to the variability in systemic exposure and response observed in cancer patients is unclear.",2243,5
2244,"Gemcitabine (<< dFdC >>, 2',2'-difluorodeoxycytidine) is metabolized by [[ cytidine deaminase ]] (CDA) and deoxycytidine kinase (DCK), but the contribution of genetic variation in these enzymes to the variability in systemic exposure and response observed in cancer patients is unclear.",2244,5
2245,"Gemcitabine (<< dFdC >>, 2',2'-difluorodeoxycytidine) is metabolized by cytidine deaminase ([[ CDA ]]) and deoxycytidine kinase (DCK), but the contribution of genetic variation in these enzymes to the variability in systemic exposure and response observed in cancer patients is unclear.",2245,5
2246,"Gemcitabine (<< dFdC >>, 2',2'-difluorodeoxycytidine) is metabolized by cytidine deaminase (CDA) and [[ deoxycytidine kinase ]] (DCK), but the contribution of genetic variation in these enzymes to the variability in systemic exposure and response observed in cancer patients is unclear.",2246,5
2247,"Gemcitabine (dFdC, << 2',2'-difluorodeoxycytidine >>) is metabolized by cytidine deaminase (CDA) and deoxycytidine kinase ([[ DCK ]]), but the contribution of genetic variation in these enzymes to the variability in systemic exposure and response observed in cancer patients is unclear.",2247,5
2248,"Gemcitabine (dFdC, << 2',2'-difluorodeoxycytidine >>) is metabolized by [[ cytidine deaminase ]] (CDA) and deoxycytidine kinase (DCK), but the contribution of genetic variation in these enzymes to the variability in systemic exposure and response observed in cancer patients is unclear.",2248,5
2249,"Gemcitabine (dFdC, << 2',2'-difluorodeoxycytidine >>) is metabolized by cytidine deaminase ([[ CDA ]]) and deoxycytidine kinase (DCK), but the contribution of genetic variation in these enzymes to the variability in systemic exposure and response observed in cancer patients is unclear.",2249,5
2250,"Gemcitabine (dFdC, << 2',2'-difluorodeoxycytidine >>) is metabolized by cytidine deaminase (CDA) and [[ deoxycytidine kinase ]] (DCK), but the contribution of genetic variation in these enzymes to the variability in systemic exposure and response observed in cancer patients is unclear.",2250,5
2251,"Wild-type enzymes and variants of << CDA >> (Lys27Gln and Ala70Thr) and DCK (Ile24Val, Ala119Gly, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for cytarabine ([[ Ara-C ]]), dFdC, and its metabolite 2',2'-difluorodeoxyuridine (dFdU) as substrates.",2251,5
2252,"Wild-type enzymes and variants of CDA (<< Lys27Gln >> and Ala70Thr) and DCK (Ile24Val, Ala119Gly, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for cytarabine ([[ Ara-C ]]), dFdC, and its metabolite 2',2'-difluorodeoxyuridine (dFdU) as substrates.",2252,5
2253,"Wild-type enzymes and variants of CDA (Lys27Gln and << Ala70Thr >>) and DCK (Ile24Val, Ala119Gly, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for cytarabine ([[ Ara-C ]]), dFdC, and its metabolite 2',2'-difluorodeoxyuridine (dFdU) as substrates.",2253,5
2254,"Wild-type enzymes and variants of CDA (Lys27Gln and Ala70Thr) and << DCK >> (Ile24Val, Ala119Gly, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for cytarabine ([[ Ara-C ]]), dFdC, and its metabolite 2',2'-difluorodeoxyuridine (dFdU) as substrates.",2254,5
2255,"Wild-type enzymes and variants of CDA (Lys27Gln and Ala70Thr) and DCK (<< Ile24Val >>, Ala119Gly, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for cytarabine ([[ Ara-C ]]), dFdC, and its metabolite 2',2'-difluorodeoxyuridine (dFdU) as substrates.",2255,5
2256,"Wild-type enzymes and variants of CDA (Lys27Gln and Ala70Thr) and DCK (Ile24Val, << Ala119Gly >>, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for cytarabine ([[ Ara-C ]]), dFdC, and its metabolite 2',2'-difluorodeoxyuridine (dFdU) as substrates.",2256,5
2257,"Wild-type enzymes and variants of CDA (Lys27Gln and Ala70Thr) and DCK (Ile24Val, Ala119Gly, and << Pro122Ser >>) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for cytarabine ([[ Ara-C ]]), dFdC, and its metabolite 2',2'-difluorodeoxyuridine (dFdU) as substrates.",2257,5
2258,"Wild-type enzymes and variants of << CDA >> (Lys27Gln and Ala70Thr) and DCK (Ile24Val, Ala119Gly, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for cytarabine (Ara-C), [[ dFdC ]], and its metabolite 2',2'-difluorodeoxyuridine (dFdU) as substrates.",2258,5
2259,"Wild-type enzymes and variants of CDA (<< Lys27Gln >> and Ala70Thr) and DCK (Ile24Val, Ala119Gly, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for cytarabine (Ara-C), [[ dFdC ]], and its metabolite 2',2'-difluorodeoxyuridine (dFdU) as substrates.",2259,5
2260,"Wild-type enzymes and variants of CDA (Lys27Gln and << Ala70Thr >>) and DCK (Ile24Val, Ala119Gly, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for cytarabine (Ara-C), [[ dFdC ]], and its metabolite 2',2'-difluorodeoxyuridine (dFdU) as substrates.",2260,5
2261,"Wild-type enzymes and variants of CDA (Lys27Gln and Ala70Thr) and << DCK >> (Ile24Val, Ala119Gly, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for cytarabine (Ara-C), [[ dFdC ]], and its metabolite 2',2'-difluorodeoxyuridine (dFdU) as substrates.",2261,5
2262,"Wild-type enzymes and variants of CDA (Lys27Gln and Ala70Thr) and DCK (<< Ile24Val >>, Ala119Gly, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for cytarabine (Ara-C), [[ dFdC ]], and its metabolite 2',2'-difluorodeoxyuridine (dFdU) as substrates.",2262,5
2263,"Wild-type enzymes and variants of CDA (Lys27Gln and Ala70Thr) and DCK (Ile24Val, << Ala119Gly >>, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for cytarabine (Ara-C), [[ dFdC ]], and its metabolite 2',2'-difluorodeoxyuridine (dFdU) as substrates.",2263,5
2264,"Wild-type enzymes and variants of CDA (Lys27Gln and Ala70Thr) and DCK (Ile24Val, Ala119Gly, and << Pro122Ser >>) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for cytarabine (Ara-C), [[ dFdC ]], and its metabolite 2',2'-difluorodeoxyuridine (dFdU) as substrates.",2264,5
2265,"Wild-type enzymes and variants of << CDA >> (Lys27Gln and Ala70Thr) and DCK (Ile24Val, Ala119Gly, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for cytarabine (Ara-C), dFdC, and its metabolite [[ 2',2'-difluorodeoxyuridine ]] (dFdU) as substrates.",2265,5
2266,"Wild-type enzymes and variants of CDA (<< Lys27Gln >> and Ala70Thr) and DCK (Ile24Val, Ala119Gly, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for cytarabine (Ara-C), dFdC, and its metabolite [[ 2',2'-difluorodeoxyuridine ]] (dFdU) as substrates.",2266,5
2267,"Wild-type enzymes and variants of CDA (Lys27Gln and << Ala70Thr >>) and DCK (Ile24Val, Ala119Gly, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for cytarabine (Ara-C), dFdC, and its metabolite [[ 2',2'-difluorodeoxyuridine ]] (dFdU) as substrates.",2267,5
2268,"Wild-type enzymes and variants of CDA (Lys27Gln and Ala70Thr) and << DCK >> (Ile24Val, Ala119Gly, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for cytarabine (Ara-C), dFdC, and its metabolite [[ 2',2'-difluorodeoxyuridine ]] (dFdU) as substrates.",2268,5
2269,"Wild-type enzymes and variants of CDA (Lys27Gln and Ala70Thr) and DCK (<< Ile24Val >>, Ala119Gly, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for cytarabine (Ara-C), dFdC, and its metabolite [[ 2',2'-difluorodeoxyuridine ]] (dFdU) as substrates.",2269,5
2270,"Wild-type enzymes and variants of CDA (Lys27Gln and Ala70Thr) and DCK (Ile24Val, << Ala119Gly >>, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for cytarabine (Ara-C), dFdC, and its metabolite [[ 2',2'-difluorodeoxyuridine ]] (dFdU) as substrates.",2270,5
2271,"Wild-type enzymes and variants of CDA (Lys27Gln and Ala70Thr) and DCK (Ile24Val, Ala119Gly, and << Pro122Ser >>) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for cytarabine (Ara-C), dFdC, and its metabolite [[ 2',2'-difluorodeoxyuridine ]] (dFdU) as substrates.",2271,5
2272,"Wild-type enzymes and variants of << CDA >> (Lys27Gln and Ala70Thr) and DCK (Ile24Val, Ala119Gly, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for cytarabine (Ara-C), dFdC, and its metabolite 2',2'-difluorodeoxyuridine ([[ dFdU ]]) as substrates.",2272,5
2273,"Wild-type enzymes and variants of << CDA >> (Lys27Gln and Ala70Thr) and DCK (Ile24Val, Ala119Gly, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for [[ cytarabine ]] (Ara-C), dFdC, and its metabolite 2',2'-difluorodeoxyuridine (dFdU) as substrates.",2273,5
2274,"Wild-type enzymes and variants of CDA (<< Lys27Gln >> and Ala70Thr) and DCK (Ile24Val, Ala119Gly, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for [[ cytarabine ]] (Ara-C), dFdC, and its metabolite 2',2'-difluorodeoxyuridine (dFdU) as substrates.",2274,5
2275,"Wild-type enzymes and variants of CDA (Lys27Gln and << Ala70Thr >>) and DCK (Ile24Val, Ala119Gly, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for [[ cytarabine ]] (Ara-C), dFdC, and its metabolite 2',2'-difluorodeoxyuridine (dFdU) as substrates.",2275,5
2276,"Wild-type enzymes and variants of CDA (Lys27Gln and Ala70Thr) and << DCK >> (Ile24Val, Ala119Gly, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for [[ cytarabine ]] (Ara-C), dFdC, and its metabolite 2',2'-difluorodeoxyuridine (dFdU) as substrates.",2276,5
2277,"Wild-type enzymes and variants of CDA (Lys27Gln and Ala70Thr) and DCK (<< Ile24Val >>, Ala119Gly, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for [[ cytarabine ]] (Ara-C), dFdC, and its metabolite 2',2'-difluorodeoxyuridine (dFdU) as substrates.",2277,5
2278,"Wild-type enzymes and variants of CDA (Lys27Gln and Ala70Thr) and DCK (Ile24Val, << Ala119Gly >>, and Pro122Ser) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for [[ cytarabine ]] (Ara-C), dFdC, and its metabolite 2',2'-difluorodeoxyuridine (dFdU) as substrates.",2278,5
2279,"Wild-type enzymes and variants of CDA (Lys27Gln and Ala70Thr) and DCK (Ile24Val, Ala119Gly, and << Pro122Ser >>) were expressed in and purified from Escherichia coli, and enzyme kinetic parameters were estimated for [[ cytarabine ]] (Ara-C), dFdC, and its metabolite 2',2'-difluorodeoxyuridine (dFdU) as substrates.",2279,5
2280,"All three << CDA >> proteins showed similar K(m) and V(max) for [[ Ara-C ]] and dFdC deamination, except for CDA70Thr, which had a 2.5-fold lower K(m) and 6-fold lower V(max) for Ara-C deamination.",2280,5
2281,"All three << CDA >> proteins showed similar K(m) and V(max) for Ara-C and [[ dFdC ]] deamination, except for CDA70Thr, which had a 2.5-fold lower K(m) and 6-fold lower V(max) for Ara-C deamination.",2281,5
2282,"All three CDA proteins showed similar K(m) and V(max) for Ara-C and dFdC deamination, except for << CDA >>70Thr, which had a 2.5-fold lower K(m) and 6-fold lower V(max) for [[ Ara-C ]] deamination.",2282,5
2283,"All four << DCK >> proteins yielded comparable metabolic activity for [[ Ara-C ]] and dFdC monophosphorylation, except for DCK24Val, which demonstrated an approximately 2-fold increase (P < 0.05) in the intrinsic clearance of dFdC monophosphorylation due to a 40% decrease in K(m) (P < 0.05).",2283,5
2284,"All four << DCK >> proteins yielded comparable metabolic activity for Ara-C and [[ dFdC ]] monophosphorylation, except for DCK24Val, which demonstrated an approximately 2-fold increase (P < 0.05) in the intrinsic clearance of dFdC monophosphorylation due to a 40% decrease in K(m) (P < 0.05).",2284,5
2285,"All four DCK proteins yielded comparable metabolic activity for Ara-C and dFdC monophosphorylation, except for << DCK >>24Val, which demonstrated an approximately 2-fold increase (P < 0.05) in the intrinsic clearance of [[ dFdC ]] monophosphorylation due to a 40% decrease in K(m) (P < 0.05).",2285,5
2286,"In conclusion, the << Lys27Gln >> substitution does not significantly modulate CDA activity toward [[ dFdC ]], and therefore would not contribute to interindividual variability in response to gemcitabine.",2286,5
2287,"In conclusion, the Lys27Gln substitution does not significantly modulate << CDA >> activity toward [[ dFdC ]], and therefore would not contribute to interindividual variability in response to gemcitabine.",2287,5
2288,The higher in vitro catalytic efficiency of << DCK >>24Val toward [[ dFdC ]] monophosphorylation may be relevant to dFdC clinical response.,2288,5
2289,The higher in vitro catalytic efficiency of << DCK >>24Val toward dFdC monophosphorylation may be relevant to [[ dFdC ]] clinical response.,2289,5
2290,Discovery of << 4-phenyl-2-phenylaminopyridine >> based [[ TNIK ]] inhibitors.,2290,0
2291,A series of compounds based on a << 4-phenyl-2-phenylaminopyridine >> scaffold that are potent and selective inhibitors of [[ Traf2- and Nck-interacting kinase ]] (TNIK) activity are described.,2291,0
2292,A series of compounds based on a << 4-phenyl-2-phenylaminopyridine >> scaffold that are potent and selective inhibitors of Traf2- and Nck-interacting kinase ([[ TNIK ]]) activity are described.,2292,0
2293,<< Boron >>-based inhibitors of [[ acyl protein thioesterases 1 and 2 ]].,2293,0
2294,Here we present << boronic >> and borinic acid derivatives as a new class of potent and nontoxic [[ APT ]] inhibitors.,2294,0
2295,Here we present boronic and << borinic acid >> derivatives as a new class of potent and nontoxic [[ APT ]] inhibitors.,2295,0
2296,"Here, we report that << genistein >> at physiologically relevant concentrations (0.1-10 μM) significantly inhibited [[ thrombin ]]-induced increase in endothelial monolayer permeability.",2296,0
2297,<< Genistein >> also reduced the formation of stress fibers by [[ thrombin ]] and suppressed thrombin-induced phosphorylation of myosin light chain (MLC) on Ser(19)/Thr(18) in endothelial cells (ECs).,2297,0
2298,<< Genistein >> also reduced the formation of stress fibers by thrombin and suppressed [[ thrombin ]]-induced phosphorylation of myosin light chain (MLC) on Ser(19)/Thr(18) in endothelial cells (ECs).,2298,0
2299,<< Genistein >> also reduced the formation of stress fibers by thrombin and suppressed thrombin-induced phosphorylation of [[ myosin light chain ]] (MLC) on Ser(19)/Thr(18) in endothelial cells (ECs).,2299,0
2300,<< Genistein >> also reduced the formation of stress fibers by thrombin and suppressed thrombin-induced phosphorylation of myosin light chain ([[ MLC ]]) on Ser(19)/Thr(18) in endothelial cells (ECs).,2300,0
2301,"Furthermore, << thrombin >> diminished cAMP production in ECs, which were prevented by treatment with [[ genistein ]].",2301,0
2302,Evaluation of drug interactions of << GSK1292263 >> (a [[ GPR119 ]] agonist) with statins: from in vitro data to clinical study design.,2302,2
2303,"1. This work investigated the drug interaction potential of GSK1292263, a novel GPR119 agonist, with the << HMG-coA reductase >> inhibitors [[ simvastatin ]] and rosuvastatin.",2303,0
2304,"1. This work investigated the drug interaction potential of GSK1292263, a novel GPR119 agonist, with the << HMG-coA reductase >> inhibitors simvastatin and [[ rosuvastatin ]].",2304,0
2305,"1. This work investigated the drug interaction potential of << GSK1292263 >>, a novel [[ GPR119 ]] agonist, with the HMG-coA reductase inhibitors simvastatin and rosuvastatin.",2305,2
2306,"2. In vitro experiments assessed the inhibition of << transporters >> and CYP enzymes by [[ GSK1292263 ]], and a clinical drug interaction study investigated the effect of GSK1292263 (300 mg BID) on the pharmacokinetic profile of simvastatin (40 mg single dose) and rosuvastatin (10 mg single dose).",2306,0
2307,"2. In vitro experiments assessed the inhibition of transporters and << CYP >> enzymes by [[ GSK1292263 ]], and a clinical drug interaction study investigated the effect of GSK1292263 (300 mg BID) on the pharmacokinetic profile of simvastatin (40 mg single dose) and rosuvastatin (10 mg single dose).",2307,0
2308,"3. In vitro, << GSK1292263 >> demonstrated little/weak inhibition (IC50 values >30 μM) towards [[ CYPs ]] (CYP1A2, 2C9, 2C19, 2D6, 3A4), Pgp, OATP1B3, or OCT2.",2308,0
2309,"3. In vitro, << GSK1292263 >> demonstrated little/weak inhibition (IC50 values >30 μM) towards CYPs ([[ CYP1A2 ]], 2C9, 2C19, 2D6, 3A4), Pgp, OATP1B3, or OCT2.",2309,0
2310,"3. In vitro, << GSK1292263 >> demonstrated little/weak inhibition (IC50 values >30 μM) towards CYPs (CYP1A2, [[ 2C9 ]], 2C19, 2D6, 3A4), Pgp, OATP1B3, or OCT2.",2310,0
2311,"3. In vitro, << GSK1292263 >> demonstrated little/weak inhibition (IC50 values >30 μM) towards CYPs (CYP1A2, 2C9, [[ 2C19 ]], 2D6, 3A4), Pgp, OATP1B3, or OCT2.",2311,0
2312,"3. In vitro, << GSK1292263 >> demonstrated little/weak inhibition (IC50 values >30 μM) towards CYPs (CYP1A2, 2C9, 2C19, [[ 2D6 ]], 3A4), Pgp, OATP1B3, or OCT2.",2312,0
2313,"3. In vitro, << GSK1292263 >> demonstrated little/weak inhibition (IC50 values >30 μM) towards CYPs (CYP1A2, 2C9, 2C19, 2D6, [[ 3A4 ]]), Pgp, OATP1B3, or OCT2.",2313,0
2314,"3. In vitro, << GSK1292263 >> demonstrated little/weak inhibition (IC50 values >30 μM) towards CYPs (CYP1A2, 2C9, 2C19, 2D6, 3A4), [[ Pgp ]], OATP1B3, or OCT2.",2314,0
2315,"3. In vitro, << GSK1292263 >> demonstrated little/weak inhibition (IC50 values >30 μM) towards CYPs (CYP1A2, 2C9, 2C19, 2D6, 3A4), Pgp, [[ OATP1B3 ]], or OCT2.",2315,0
2316,"3. In vitro, << GSK1292263 >> demonstrated little/weak inhibition (IC50 values >30 μM) towards CYPs (CYP1A2, 2C9, 2C19, 2D6, 3A4), Pgp, OATP1B3, or [[ OCT2 ]].",2316,0
2317,"However, << GSK1292263 >> inhibited [[ BCRP ]] and OATP1B1, which are transporters involved in statin disposition.",2317,0
2318,"However, << GSK1292263 >> inhibited BCRP and [[ OATP1B1 ]], which are transporters involved in statin disposition.",2318,0
2319,"4. In the clinical study, small increases in the AUC(0-inf) of simvastatin [mean ratio (90% CI) of 1.34 (1.22, 1.48)] and rosuvastatin [mean ratio (90% CI) of 1.39 (1.30, 1.49)] were observed when co-administered with << GSK1292263 >>, which is consistent with an inhibitory effect on intestinal BCRP and [[ CYP3A4 ]].",2319,0
2320,"4. In the clinical study, small increases in the AUC(0-inf) of simvastatin [mean ratio (90% CI) of 1.34 (1.22, 1.48)] and rosuvastatin [mean ratio (90% CI) of 1.39 (1.30, 1.49)] were observed when co-administered with << GSK1292263 >>, which is consistent with an inhibitory effect on intestinal [[ BCRP ]] and CYP3A4.",2320,0
2321,This study provides a mechanistic understanding of the in vivo inhibition of << transporters >> and enzymes by [[ GSK1292263 ]].,2321,0
2322,The presence of << steroid >> hormones most probably causes the degradation of the [[ Tat2 ]] permease and impairment of tryptophan import.,2322,8
2323,Inhibition of Th1/Th17 responses via suppression of << STAT1 >> and STAT3 activation contributes to the amelioration of murine experimental colitis by a natural flavonoid glucoside [[ icariin ]].,2323,0
2324,Inhibition of Th1/Th17 responses via suppression of STAT1 and << STAT3 >> activation contributes to the amelioration of murine experimental colitis by a natural flavonoid glucoside [[ icariin ]].,2324,0
2325,Inhibition of Th1/Th17 responses via suppression of << STAT1 >> and STAT3 activation contributes to the amelioration of murine experimental colitis by a natural [[ flavonoid ]] glucoside icariin.,2325,0
2326,Inhibition of Th1/Th17 responses via suppression of STAT1 and << STAT3 >> activation contributes to the amelioration of murine experimental colitis by a natural [[ flavonoid ]] glucoside icariin.,2326,0
2327,"Further study showed that << icariin >> dose-dependently inhibited the proliferation and activation of T lymphocytes, and suppressed pro-inflammatory [[ cytokine ]] levels of activated T cells.",2327,8
2328,"Moreover, << icariin >> treatment inhibited the phosphorylations of [[ STAT1 ]] and STAT3 in CD4(+) T cells, which were the crucial transcription factors for Th1 and Th17 respectively.",2328,0
2329,"Moreover, << icariin >> treatment inhibited the phosphorylations of STAT1 and [[ STAT3 ]] in CD4(+) T cells, which were the crucial transcription factors for Th1 and Th17 respectively.",2329,0
2330,"Pharmacological inhibition of MTORC1 with << rapamycin >> abrogated the [[ insulin ]]-induced phosphorylation of EIF4EBP1, RPS6KB1 and its downstream effector, RPS6.",2330,3
2331,"Pharmacological inhibition of << MTORC1 >> with [[ rapamycin ]] abrogated the insulin-induced phosphorylation of EIF4EBP1, RPS6KB1 and its downstream effector, RPS6.",2331,0
2332,"Pharmacological inhibition of MTORC1 with << rapamycin >> abrogated the insulin-induced phosphorylation of [[ EIF4EBP1 ]], RPS6KB1 and its downstream effector, RPS6.",2332,0
2333,"Pharmacological inhibition of MTORC1 with << rapamycin >> abrogated the insulin-induced phosphorylation of EIF4EBP1, [[ RPS6KB1 ]] and its downstream effector, RPS6.",2333,0
2334,"Pharmacological inhibition of MTORC1 with << rapamycin >> abrogated the insulin-induced phosphorylation of EIF4EBP1, RPS6KB1 and its downstream effector, [[ RPS6 ]].",2334,0
2335,"Furthermore, << insulin >>-stimulated T-I cell proliferation and the expression of cell cycle regulatory proteins CDK4, CCND3 and PCNA were also blocked by [[ rapamycin ]].",2335,8
2336,"Furthermore, insulin-stimulated T-I cell proliferation and the expression of << cell cycle regulatory proteins >> CDK4, CCND3 and PCNA were also blocked by [[ rapamycin ]].",2336,8
2337,"Furthermore, insulin-stimulated T-I cell proliferation and the expression of cell cycle regulatory proteins << CDK4 >>, CCND3 and PCNA were also blocked by [[ rapamycin ]].",2337,8
2338,"Furthermore, insulin-stimulated T-I cell proliferation and the expression of cell cycle regulatory proteins CDK4, << CCND3 >> and PCNA were also blocked by [[ rapamycin ]].",2338,8
2339,"Furthermore, insulin-stimulated T-I cell proliferation and the expression of cell cycle regulatory proteins CDK4, CCND3 and << PCNA >> were also blocked by [[ rapamycin ]].",2339,8
2340,Synthesis and evaluation of << 8-oxoadenine >> derivatives as potent [[ Toll-like receptor 7 ]] agonists with high water solubility.,2340,2
2341,"We report the discovery of novel series of highly potent << TLR7 >> agonists based on 8-oxoadenines, 1 and 2 by introducing and optimizing various [[ tertiary amines ]] onto the N(9)-position of the adenine moiety.",2341,2
2342,"We report the discovery of novel series of highly potent << TLR7 >> agonists based on 8-oxoadenines, 1 and 2 by introducing and optimizing various tertiary amines onto the [[ N ]](9)-position of the adenine moiety.",2342,2
2343,"We report the discovery of novel series of highly potent << TLR7 >> agonists based on 8-oxoadenines, 1 and 2 by introducing and optimizing various tertiary amines onto the N(9)-position of the [[ adenine ]] moiety.",2343,2
2344,"We report the discovery of novel series of highly potent << TLR7 >> agonists based on [[ 8-oxoadenines ]], 1 and 2 by introducing and optimizing various tertiary amines onto the N(9)-position of the adenine moiety.",2344,2
2345,The introduction of the << amino >> group resulted in not only improved water solubility but also enhanced [[ TLR7 ]] agonistic activity.,2345,2
2346,Inhibitors based on a << benzo-fused spirocyclic oxazepine >> scaffold were discovered for stearoyl-coenzyme A (CoA) desaturase 1 ([[ SCD1 ]]) and subsequently optimized to potent compounds with favorable pharmacokinetic profiles and in vivo efficacy in reducing the desaturation index in a mouse model.,2346,0
2347,Inhibitors based on a << benzo-fused spirocyclic oxazepine >> scaffold were discovered for [[ stearoyl-coenzyme A (CoA) desaturase 1 ]] (SCD1) and subsequently optimized to potent compounds with favorable pharmacokinetic profiles and in vivo efficacy in reducing the desaturation index in a mouse model.,2347,0
2348,The porcine heart malate dehydrogenase (MDH) refolding assay revealed that compound 1l inhibited << human Hsp60 >> chaperone activity (IC(50): 6.80 ± 0.25 μM) and this inhibition activity was higher than that of [[ ETB ]] (IC(50): 10.9 ± 0.63 μM).,2348,0
2349,<< Apocynin >> and raisanberine alleviate intermittent hypoxia induced abnormal StAR and 3β-HSD and low testosterone by suppressing endoplasmic reticulum stress and activated [[ p66Shc ]] in rat testes.,2349,0
2350,Apocynin and << raisanberine >> alleviate intermittent hypoxia induced abnormal StAR and 3β-HSD and low testosterone by suppressing endoplasmic reticulum stress and activated [[ p66Shc ]] in rat testes.,2350,0
2351,Apocynin and << raisanberine >> alleviate intermittent hypoxia induced abnormal StAR and [[ 3β-HSD ]] and low testosterone by suppressing endoplasmic reticulum stress and activated p66Shc in rat testes.,2351,5
2352,"We hypothesized that hypoxia induced testicular damage is mediated by an activated NADPH oxidase (NOX), therefore, << APO >> (apocynin) an inhibitor of [[ NOX ]] and raisanberine (RS), a calcium influx inhibitor were tested if they could attenuate hypoxic toxicity to the testis.",2352,0
2353,"We hypothesized that hypoxia induced testicular damage is mediated by an activated NADPH oxidase (NOX), therefore, APO (<< apocynin >>) an inhibitor of [[ NOX ]] and raisanberine (RS), a calcium influx inhibitor were tested if they could attenuate hypoxic toxicity to the testis.",2353,0
2354,"<< APO >> and RS at least partially normalize hypoxia caused male hypogonadism by suppressing ER stress, and [[ p66Shc ]] in testes.",2354,0
2355,"Here we found that << arsenic trioxide >>, a frontline agent for acute promyelocytic leukemia, inhibits [[ ΔNp63 ]] but not TAp63 expression in time- and dose-dependent manners.",2355,8
2356,"In addition, we found that << arsenic trioxide >> decreases the stability of [[ ΔNp63 ]] protein via a proteasome-dependent pathway but has little effect on the level of ΔNp63 transcript.",2356,8
2357,"Furthermore, we found that << arsenic trioxide >> activates the [[ Pirh2 promoter ]] and consequently induces Pirh2 expression.",2357,9
2358,"Furthermore, we found that << arsenic trioxide >> activates the Pirh2 promoter and consequently induces [[ Pirh2 ]] expression.",2358,6
2359,"Consistent with this, we found that knockdown of Pirh2 inhibits, whereas ectopic expression of Pirh2 enhances, << arsenic >>-induced degradation of [[ ΔNp63 ]] protein.",2359,8
2360,"Together, these data suggest that << arsenic >> degrades [[ ΔNp63 ]] protein at least in part via Pirh2-dependent proteolysis and that inhibition of ΔNp63 expression facilitates tumor cells to arsenic-induced death.",2360,8
2361,"Together, these data suggest that << arsenic >> degrades ΔNp63 protein at least in part via Pirh2-dependent proteolysis and that inhibition of [[ ΔNp63 ]] expression facilitates tumor cells to arsenic-induced death.",2361,8
2362,"<< Jaceosidin >>, isolated from dietary mugwort (Artemisia princeps), induces G2/M cell cycle arrest by inactivating cdc25C-cdc2 via [[ ATM ]]-Chk1/2 activation.",2362,9
2363,"<< Jaceosidin >>, isolated from dietary mugwort (Artemisia princeps), induces G2/M cell cycle arrest by inactivating [[ cdc25C ]]-cdc2 via ATM-Chk1/2 activation.",2363,0
2364,"<< Jaceosidin >>, isolated from dietary mugwort (Artemisia princeps), induces G2/M cell cycle arrest by inactivating cdc25C-[[ cdc2 ]] via ATM-Chk1/2 activation.",2364,0
2365,Additional mechanistic studies revealed that << jaceosidin >> treatment resulted in an increase in phosphorylation of [[ Cdc25C ]] and ATM-Chk1/2.,2365,9
2366,Additional mechanistic studies revealed that << jaceosidin >> treatment resulted in an increase in phosphorylation of Cdc25C and [[ ATM ]]-Chk1/2.,2366,9
2367,"Moreover, jaceosidin treatment resulted in phosphorylation of ERK, and pretreatment with the << ERK >> inhibitor, [[ PD98059 ]], attenuated cell growth inhibition by jaceosidin.",2367,0
2368,"These data suggest that << jaceosidin >>, isolated from Japanese mugwort, modulates the ERK/ATM/Chk1/2 pathway, leading to inactivation of the [[ Cdc2 ]]-cyclin B1 complex, followed by G2/M cell cycle arrest in endometrial cancer cells.",2368,0
2369,"These data suggest that << jaceosidin >>, isolated from Japanese mugwort, modulates the ERK/ATM/Chk1/2 pathway, leading to inactivation of the Cdc2-[[ cyclin B1 ]] complex, followed by G2/M cell cycle arrest in endometrial cancer cells.",2369,0
2370,Electrical Stimuli Release ATP to Increase << GLUT4 >> Translocation and [[ Glucose ]] Uptake via PI3Kγ-Akt-AS160 in Skeletal Muscle Cells.,2370,5
2371,"Electrical stimulation, ATP, and insulin each increased fluorescent 2-NBD-Glucose (2-NBDG) uptake in primary myotubes, but only electrical stimulation and ATP-dependent 2-NBDG uptake were inhibited by << adenosine-phosphate phosphatase >> and by purinergic receptor blockade ([[ suramin ]]).",2371,0
2372,"Electrical stimulation, ATP, and insulin each increased fluorescent 2-NBD-Glucose (2-NBDG) uptake in primary myotubes, but only electrical stimulation and ATP-dependent 2-NBDG uptake were inhibited by adenosine-phosphate phosphatase and by << purinergic receptor >> blockade ([[ suramin ]]).",2372,0
2373,Electrical stimulation transiently elevated extracellular ATP and caused << Akt >> phosphorylation that was additive to insulin and inhibited by [[ suramin ]].,2373,0
2374,"Exogenous << ATP >> transiently activated [[ Akt ]] and, inhibiting phosphatidylinositol 3-kinase (PI3K) or Akt as well as dominant-negative Akt mutant, reduced ATP-dependent 2-NBDG uptake and Akt phosphorylation.",2374,9
2375,ATP-dependent 2-NBDG uptake was also inhibited by the G protein βγ subunit-interacting peptide βark-ct and by the << phosphatidylinositol 3-kinase-γ >> (PI3Kγ) inhibitor [[ AS605240 ]].,2375,0
2376,ATP-dependent 2-NBDG uptake was also inhibited by the G protein βγ subunit-interacting peptide βark-ct and by the phosphatidylinositol 3-kinase-γ (<< PI3Kγ >>) inhibitor [[ AS605240 ]].,2376,0
2377,"Structure-based design, synthesis and evaluation of novel << anthra[1,2-d]imidazole-6,11-dione >> derivatives as [[ telomerase ]] inhibitors and potential for cancer polypharmacology.",2377,0
2378,"A series of << anthra[1,2-d]imidazole-6,11-dione >> derivatives were synthesized and evaluated for [[ telomerase ]] inhibition, hTERT expression and suppression of cancer cell growth in vitro.",2378,0
2379,<< Trichostatin A >> inhibits transforming growth factor-β-induced reactive oxygen species accumulation and myofibroblast differentiation via enhanced [[ NF-E2-related factor 2 ]]-antioxidant response element signaling.,2379,6
2380,<< Trichostatin A >> inhibits transforming growth factor-β-induced reactive oxygen species accumulation and myofibroblast differentiation via enhanced NF-E2-related factor 2-[[ antioxidant response element ]] signaling.,2380,6
2381,<< Trichostatin A >> inhibits [[ transforming growth factor-β ]]-induced reactive oxygen species accumulation and myofibroblast differentiation via enhanced NF-E2-related factor 2-antioxidant response element signaling.,2381,0
2382,"Human immortalized corneal fibroblasts were treated with TGF-β in the presence of TSA, the NAD(P)H oxidase inhibitor diphenyleneiodonium (DPI), the antioxidant N-acetyl-cysteine (NAC), the << NF-E2-related factor 2 >>-antioxidant response element (Nrf2-ARE) activator [[ sulforaphane ]], or small interfering RNA.",2382,9
2383,"Human immortalized corneal fibroblasts were treated with TGF-β in the presence of TSA, the NAD(P)H oxidase inhibitor diphenyleneiodonium (DPI), the antioxidant N-acetyl-cysteine (NAC), the NF-E2-related factor 2-<< antioxidant response element >> (Nrf2-ARE) activator [[ sulforaphane ]], or small interfering RNA.",2383,9
2384,"Human immortalized corneal fibroblasts were treated with TGF-β in the presence of TSA, the NAD(P)H oxidase inhibitor diphenyleneiodonium (DPI), the antioxidant N-acetyl-cysteine (NAC), the NF-E2-related factor 2-antioxidant response element (<< Nrf2 >>-ARE) activator [[ sulforaphane ]], or small interfering RNA.",2384,9
2385,"Human immortalized corneal fibroblasts were treated with TGF-β in the presence of TSA, the NAD(P)H oxidase inhibitor diphenyleneiodonium (DPI), the antioxidant N-acetyl-cysteine (NAC), the NF-E2-related factor 2-antioxidant response element (Nrf2-<< ARE >>) activator [[ sulforaphane ]], or small interfering RNA.",2385,9
2386,"Human immortalized corneal fibroblasts were treated with TGF-β in the presence of TSA, the << NAD(P)H oxidase >> inhibitor [[ diphenyleneiodonium ]] (DPI), the antioxidant N-acetyl-cysteine (NAC), the NF-E2-related factor 2-antioxidant response element (Nrf2-ARE) activator sulforaphane, or small interfering RNA.",2386,0
2387,"Human immortalized corneal fibroblasts were treated with TGF-β in the presence of TSA, the << NAD(P)H oxidase >> inhibitor diphenyleneiodonium ([[ DPI ]]), the antioxidant N-acetyl-cysteine (NAC), the NF-E2-related factor 2-antioxidant response element (Nrf2-ARE) activator sulforaphane, or small interfering RNA.",2387,0
2388,Treatment with << TSA >> and the Nrf2-ARE activator resulted in increased inhibition of the [[ TGF-β ]]-induced myofibroblast differentiation as compared with treatment with DPI or NAC.,2388,0
2389,"Furthermore, << TSA >> also decreased cellular ROS and H(2)O(2) accumulation induced by [[ TGF-β ]], whereas it elevated intracellular GSH level and cellular total antioxidant capacity.",2389,0
2390,"In addition, << TSA >> induced Nrf2 nuclear translocation and up-regulated the expression of [[ Nrf2 ]]-ARE downstream antioxidant genes, whereas Nrf2 knockdown by RNA interference blocked the inhibition of TSA on myofibroblast differentiation.",2390,6
2391,"In addition, << TSA >> induced Nrf2 nuclear translocation and up-regulated the expression of Nrf2-[[ ARE ]] downstream antioxidant genes, whereas Nrf2 knockdown by RNA interference blocked the inhibition of TSA on myofibroblast differentiation.",2391,6
2392,"In conclusion, this study provides the first evidence implicating that << TSA >> inhibits TGF-β-induced ROS accumulation and myofibroblast differentiation via enhanced [[ Nrf2 ]]-ARE signaling.",2392,6
2393,"In conclusion, this study provides the first evidence implicating that << TSA >> inhibits TGF-β-induced ROS accumulation and myofibroblast differentiation via enhanced Nrf2-[[ ARE ]] signaling.",2393,6
2394,"In conclusion, this study provides the first evidence implicating that << TSA >> inhibits [[ TGF-β ]]-induced ROS accumulation and myofibroblast differentiation via enhanced Nrf2-ARE signaling.",2394,0
2395,"<< Cannabinoid receptor 1 >> (CB(1)) inverse agonists (e.g., [[ rimonabant ]]) have been reported to produce adverse effects including nausea, emesis, and anhedonia that limit their clinical applications.",2395,11
2396,"Cannabinoid receptor 1 (<< CB(1) >>) inverse agonists (e.g., [[ rimonabant ]]) have been reported to produce adverse effects including nausea, emesis, and anhedonia that limit their clinical applications.",2396,11
2397,"In the present studies, the CB(1) inverse agonist SR141716A (rimonabant) and the CB(1) neutral antagonist AM4113 were compared for their ability to modify CB(1) receptor-mediated discriminative stimulus effects in nonhuman primates trained to discriminate the novel << CB(1) >> full agonist [[ AM4054 ]].",2397,10
2398,"In the present studies, the << CB(1) >> inverse agonist [[ SR141716A ]] (rimonabant) and the CB(1) neutral antagonist AM4113 were compared for their ability to modify CB(1) receptor-mediated discriminative stimulus effects in nonhuman primates trained to discriminate the novel CB(1) full agonist AM4054.",2398,11
2399,"In the present studies, the << CB(1) >> inverse agonist SR141716A ([[ rimonabant ]]) and the CB(1) neutral antagonist AM4113 were compared for their ability to modify CB(1) receptor-mediated discriminative stimulus effects in nonhuman primates trained to discriminate the novel CB(1) full agonist AM4054.",2399,11
2400,"In the present studies, the CB(1) inverse agonist SR141716A (rimonabant) and the << CB(1) >> neutral antagonist [[ AM4113 ]] were compared for their ability to modify CB(1) receptor-mediated discriminative stimulus effects in nonhuman primates trained to discriminate the novel CB(1) full agonist AM4054.",2400,1
2401,"Results indicate that << AM4054 >> serves as an effective [[ CB(1) ]] discriminative stimulus, with an onset and time course of action comparable with that of the CB(1) agonist Δ(9)-tetrahydrocannabinol, and that the inverse agonist rimonabant and the neutral antagonist AM4113 produce dose-related rightward shifts in the AM4054 dose-effect curve, indicating that both drugs surmountably antagonize the discriminative stimulus effects of AM4054.",2401,9
2402,"Results indicate that AM4054 serves as an effective CB(1) discriminative stimulus, with an onset and time course of action comparable with that of the << CB(1) >> agonist [[ Δ(9)-tetrahydrocannabinol ]], and that the inverse agonist rimonabant and the neutral antagonist AM4113 produce dose-related rightward shifts in the AM4054 dose-effect curve, indicating that both drugs surmountably antagonize the discriminative stimulus effects of AM4054.",2402,2
2403,"Results indicate that AM4054 serves as an effective CB(1) discriminative stimulus, with an onset and time course of action comparable with that of the << CB(1) >> agonist Δ(9)-tetrahydrocannabinol, and that the inverse agonist rimonabant and the neutral antagonist AM4113 produce dose-related rightward shifts in the [[ AM4054 ]] dose-effect curve, indicating that both drugs surmountably antagonize the discriminative stimulus effects of AM4054.",2403,2
2404,"Results indicate that AM4054 serves as an effective CB(1) discriminative stimulus, with an onset and time course of action comparable with that of the << CB(1) >> agonist Δ(9)-tetrahydrocannabinol, and that the inverse agonist rimonabant and the neutral antagonist AM4113 produce dose-related rightward shifts in the AM4054 dose-effect curve, indicating that both drugs surmountably antagonize the discriminative stimulus effects of [[ AM4054 ]].",2404,2
2405,"Results indicate that AM4054 serves as an effective CB(1) discriminative stimulus, with an onset and time course of action comparable with that of the << CB(1) >> agonist Δ(9)-tetrahydrocannabinol, and that the inverse agonist [[ rimonabant ]] and the neutral antagonist AM4113 produce dose-related rightward shifts in the AM4054 dose-effect curve, indicating that both drugs surmountably antagonize the discriminative stimulus effects of AM4054.",2405,11
2406,"Results indicate that AM4054 serves as an effective CB(1) discriminative stimulus, with an onset and time course of action comparable with that of the << CB(1) >> agonist Δ(9)-tetrahydrocannabinol, and that the inverse agonist rimonabant and the neutral antagonist [[ AM4113 ]] produce dose-related rightward shifts in the AM4054 dose-effect curve, indicating that both drugs surmountably antagonize the discriminative stimulus effects of AM4054.",2406,1
2407,"<< FXa >> inhibitors, e.g. [[ rivaroxaban ]] and apixaban, are potent, oral direct inhibitors of prothrombinase-bound, clot-associated or free FXa.",2407,0
2408,"FXa inhibitors, e.g. << rivaroxaban >> and apixaban, are potent, oral direct inhibitors of [[ prothrombinase ]]-bound, clot-associated or free FXa.",2408,0
2409,"FXa inhibitors, e.g. << rivaroxaban >> and apixaban, are potent, oral direct inhibitors of prothrombinase-bound, clot-associated or free [[ FXa ]].",2409,0
2410,"<< FXa >> inhibitors, e.g. rivaroxaban and [[ apixaban ]], are potent, oral direct inhibitors of prothrombinase-bound, clot-associated or free FXa.",2410,0
2411,"FXa inhibitors, e.g. rivaroxaban and << apixaban >>, are potent, oral direct inhibitors of [[ prothrombinase ]]-bound, clot-associated or free FXa.",2411,0
2412,"FXa inhibitors, e.g. rivaroxaban and << apixaban >>, are potent, oral direct inhibitors of prothrombinase-bound, clot-associated or free [[ FXa ]].",2412,0
2413,"Although parenteral oral direct << thrombin >> inhibitors (DTIs), such as [[ argatroban ]] and bivalirudin, have been on the market for years, DTIs such as dabigatran are novel synthetic thrombin antagonists.",2413,0
2414,"Although parenteral oral direct thrombin inhibitors (DTIs), such as argatroban and bivalirudin, have been on the market for years, DTIs such as << dabigatran >> are novel synthetic [[ thrombin ]] antagonists.",2414,1
2415,"<< Dabigatran >> has an advantage over the indirect [[ thrombin ]] inhibitors, unfractionated heparin and low-molecular-weight heparin, in that it inhibits free and fibrin-bound thrombin.",2415,0
2416,"<< Dabigatran >> has an advantage over the indirect thrombin inhibitors, unfractionated heparin and low-molecular-weight heparin, in that it inhibits free and [[ fibrin ]]-bound thrombin.",2416,0
2417,"<< Dabigatran >> has an advantage over the indirect thrombin inhibitors, unfractionated heparin and low-molecular-weight heparin, in that it inhibits free and fibrin-bound [[ thrombin ]].",2417,0
2418,"The reversible binding of << dabigatran >> may provide safer and more predictable anticoagulant treatment than seen with irreversible, non-covalent [[ thrombin ]] inhibitors, e.g. hirudin.",2418,0
2419,<< Aldehyde dehydrogenase 1 >> (ALDH1A1) catalyzes the oxidation of toxic aldehydes to [[ carboxylic acids ]].,2419,4
2420,Aldehyde dehydrogenase 1 (<< ALDH1A1 >>) catalyzes the oxidation of toxic aldehydes to [[ carboxylic acids ]].,2420,4
2421,<< Aldehyde dehydrogenase 1 >> (ALDH1A1) catalyzes the oxidation of toxic [[ aldehydes ]] to carboxylic acids.,2421,5
2422,Aldehyde dehydrogenase 1 (<< ALDH1A1 >>) catalyzes the oxidation of toxic [[ aldehydes ]] to carboxylic acids.,2422,5
2423,Physiologic levels of << Mg(2+) >> ions decrease [[ ALDH1 ]] activity in part by increasing NADH binding affinity to the enzyme.,2423,0
2424,"As the << Mg(2+) >> ion concentration was increased, there was a consistent decrease of the enzyme catalytic turnover from 0.31 s(-1) (0 μM Mg(2+)) to 0.050 s(-1) (6000 μM Mg(2+)) and a distinct shift in steady-state conformational population from one that favors the [[ ALDH1 ]]-NADH complex with the shorter fluorescence lifetime (33% excess) in the absence of magnesium ion to one that favors the ALDH1-NADH complex with the longer fluorescence lifetime (13% excess) at 6000 μM Mg(2+).",2424,3
2425,This shift in conformational population at higher << Mg(2+) >> ion concentrations and to lower enzyme activity may be due to longer residence time of the NADH in the [[ ALDH1 ]] pocket.,2425,3
2426,"Interestingly, << Acrolein >> increased proteins' levels of [[ amyloid precursor protein ]] (APP), β-secretase (BACE-1) and the amyloid β-peptide transporter receptor for advanced glycation end products, and decreased A-disintegrin and metalloprotease (ADAM) 10 levels.",2426,6
2427,"Interestingly, << Acrolein >> increased proteins' levels of amyloid precursor protein (APP), [[ β-secretase ]] (BACE-1) and the amyloid β-peptide transporter receptor for advanced glycation end products, and decreased A-disintegrin and metalloprotease (ADAM) 10 levels.",2427,6
2428,"Interestingly, << Acrolein >> increased proteins' levels of amyloid precursor protein (APP), β-secretase ([[ BACE-1 ]]) and the amyloid β-peptide transporter receptor for advanced glycation end products, and decreased A-disintegrin and metalloprotease (ADAM) 10 levels.",2428,6
2429,"Interestingly, << Acrolein >> increased proteins' levels of amyloid precursor protein (APP), β-secretase (BACE-1) and the [[ amyloid β-peptide transporter ]] receptor for advanced glycation end products, and decreased A-disintegrin and metalloprotease (ADAM) 10 levels.",2429,6
2430,"Interestingly, << Acrolein >> increased proteins' levels of amyloid precursor protein (APP), β-secretase (BACE-1) and the amyloid β-peptide transporter [[ receptor for advanced glycation end products ]], and decreased A-disintegrin and metalloprotease (ADAM) 10 levels.",2430,6
2431,"Interestingly, << Acrolein >> increased proteins' levels of amyloid precursor protein (APP), β-secretase (BACE-1) and the amyloid β-peptide transporter receptor for advanced glycation end products, and decreased [[ A-disintegrin and metalloprotease (ADAM) 10 ]] levels.",2431,8
2432,"Moreover, << Acrolein >> resulted in activation of astrocytes, up-regulation of [[ BACE-1 ]] in cortex and down-regulation of ADAM-10 in hippocampus and cortex.",2432,6
2433,"Moreover, << Acrolein >> resulted in activation of astrocytes, up-regulation of BACE-1 in cortex and down-regulation of [[ ADAM-10 ]] in hippocampus and cortex.",2433,8
2434,Regulation of sexual reproduction by << estradiol >> involves the activation of [[ estrogen receptors ]] (ERs) in the hypothalamus.,2434,9
2435,Regulation of sexual reproduction by << estradiol >> involves the activation of estrogen receptors ([[ ERs ]]) in the hypothalamus.,2435,9
2436,"Using surface biotinylation, we observed that treatment of N-38 neurons with estradiol or with a membrane impermeant << estradiol >> elevated plasma membrane [[ ERα ]] protein levels, indicating that membrane signaling increased receptor insertion into the cell membrane.",2436,6
2437,"Using surface biotinylation, we observed that treatment of N-38 neurons with << estradiol >> or with a membrane impermeant estradiol elevated plasma membrane [[ ERα ]] protein levels, indicating that membrane signaling increased receptor insertion into the cell membrane.",2437,6
2438,"Insertion of << ERα >> was blocked by the ER antagonist [[ ICI 182,780 ]] or with the protein kinase C (PKC) pathway inhibitor bisindolylmaleimide (BIS).",2438,0
2439,"Insertion of << ERα >> was blocked by the ER antagonist ICI 182,780 or with the protein kinase C (PKC) pathway inhibitor [[ bisindolylmaleimide ]] (BIS).",2439,0
2440,"Insertion of ERα was blocked by the ER antagonist ICI 182,780 or with the << protein kinase C >> (PKC) pathway inhibitor [[ bisindolylmaleimide ]] (BIS).",2440,0
2441,"Insertion of ERα was blocked by the ER antagonist ICI 182,780 or with the protein kinase C (<< PKC >>) pathway inhibitor [[ bisindolylmaleimide ]] (BIS).",2441,0
2442,"Insertion of << ERα >> was blocked by the ER antagonist ICI 182,780 or with the protein kinase C (PKC) pathway inhibitor bisindolylmaleimide ([[ BIS ]]).",2442,0
2443,"Insertion of ERα was blocked by the ER antagonist ICI 182,780 or with the << protein kinase C >> (PKC) pathway inhibitor bisindolylmaleimide ([[ BIS ]]).",2443,0
2444,"Insertion of ERα was blocked by the ER antagonist ICI 182,780 or with the protein kinase C (<< PKC >>) pathway inhibitor bisindolylmaleimide ([[ BIS ]]).",2444,0
2445,"Insertion of ERα was blocked by the << ER >> antagonist [[ ICI 182,780 ]] or with the protein kinase C (PKC) pathway inhibitor bisindolylmaleimide (BIS).",2445,1
2446,These results indicate that membrane << ERα >> levels in N-38 neurons are dynamically autoregulated by [[ estradiol ]].,2446,6
2447,Reductions in striatal dopamine and << tyrosine hydroxylase >> content were also less pronounced with [[ EHT ]] treatment.,2447,6
2448,"The neuroinflammatory response to MPTP was markedly attenuated, and indices of oxidative stress and << JNK >> activation were significantly prevented with [[ EHT ]].",2448,0
2449,"In cultured primary microglia and astrocytes, << EHT >> had a direct anti-inflammatory effect demonstrated by repression of lipopolysaccharide-induced [[ NFκB ]] activation, iNOS induction, and nitric oxide production.",2449,0
2450,"In cultured primary microglia and astrocytes, << EHT >> had a direct anti-inflammatory effect demonstrated by repression of lipopolysaccharide-induced NFκB activation, [[ iNOS ]] induction, and nitric oxide production.",2450,0
2451,"Additionally, in SH-SY5Y cells, MPP(+)-induced demethylation of << phosphoprotein phosphatase 2A >> (PP2A), the master regulator of the cellular phosphoregulatory network, and cytotoxicity were ameliorated by [[ EHT ]].",2451,7
2452,"Additionally, in SH-SY5Y cells, MPP(+)-induced demethylation of phosphoprotein phosphatase 2A (<< PP2A >>), the master regulator of the cellular phosphoregulatory network, and cytotoxicity were ameliorated by [[ EHT ]].",2452,7
2453,"Additionally, in SH-SY5Y cells, << MPP(+) >>-induced demethylation of [[ phosphoprotein phosphatase 2A ]] (PP2A), the master regulator of the cellular phosphoregulatory network, and cytotoxicity were ameliorated by EHT.",2453,3
2454,"Additionally, in SH-SY5Y cells, << MPP(+) >>-induced demethylation of phosphoprotein phosphatase 2A ([[ PP2A ]]), the master regulator of the cellular phosphoregulatory network, and cytotoxicity were ameliorated by EHT.",2454,3
2455,"Substantial evidence shows that << H(2)S >> is involved in aging by inhibiting free-radical reactions, activating [[ SIRT1 ]], and probably interacting with the age-related gene Klotho.",2455,9
2456,Induction of << HO-1 >> through p38 MAPK/Nrf2 signaling pathway by [[ ethanol ]] extract of Inula helenium L. reduces inflammation in LPS-activated RAW 264.7 cells and CLP-induced septic mice.,2456,9
2457,Induction of HO-1 through << p38 >> MAPK/Nrf2 signaling pathway by [[ ethanol ]] extract of Inula helenium L. reduces inflammation in LPS-activated RAW 264.7 cells and CLP-induced septic mice.,2457,9
2458,Induction of HO-1 through p38 << MAPK >>/Nrf2 signaling pathway by [[ ethanol ]] extract of Inula helenium L. reduces inflammation in LPS-activated RAW 264.7 cells and CLP-induced septic mice.,2458,9
2459,"The induction of << HO-1 >> by EIH was inhibited by [[ SB203580 ]] but not by SP600125, PD98059, nor LY294002.",2459,0
2460,"We demonstrate that two << flavin mono-oxygenase >> family members, FMO1 and FMO3, oxidize trimethylamine (TMA), derived from gut flora metabolism of choline, to [[ TMAO ]].",2460,4
2461,"We demonstrate that two flavin mono-oxygenase family members, << FMO1 >> and FMO3, oxidize trimethylamine (TMA), derived from gut flora metabolism of choline, to [[ TMAO ]].",2461,4
2462,"We demonstrate that two flavin mono-oxygenase family members, FMO1 and << FMO3 >>, oxidize trimethylamine (TMA), derived from gut flora metabolism of choline, to [[ TMAO ]].",2462,4
2463,"We demonstrate that two << flavin mono-oxygenase >> family members, FMO1 and FMO3, oxidize [[ trimethylamine ]] (TMA), derived from gut flora metabolism of choline, to TMAO.",2463,5
2464,"We demonstrate that two flavin mono-oxygenase family members, << FMO1 >> and FMO3, oxidize [[ trimethylamine ]] (TMA), derived from gut flora metabolism of choline, to TMAO.",2464,5
2465,"We demonstrate that two flavin mono-oxygenase family members, FMO1 and << FMO3 >>, oxidize [[ trimethylamine ]] (TMA), derived from gut flora metabolism of choline, to TMAO.",2465,5
2466,"We demonstrate that two << flavin mono-oxygenase >> family members, FMO1 and FMO3, oxidize trimethylamine ([[ TMA ]]), derived from gut flora metabolism of choline, to TMAO.",2466,5
2467,"We demonstrate that two flavin mono-oxygenase family members, << FMO1 >> and FMO3, oxidize trimethylamine ([[ TMA ]]), derived from gut flora metabolism of choline, to TMAO.",2467,5
2468,"We demonstrate that two flavin mono-oxygenase family members, FMO1 and << FMO3 >>, oxidize trimethylamine ([[ TMA ]]), derived from gut flora metabolism of choline, to TMAO.",2468,5
2469,"We demonstrate that two << flavin mono-oxygenase >> family members, FMO1 and FMO3, oxidize trimethylamine (TMA), derived from gut flora metabolism of [[ choline ]], to TMAO.",2469,5
2470,"We demonstrate that two flavin mono-oxygenase family members, << FMO1 >> and FMO3, oxidize trimethylamine (TMA), derived from gut flora metabolism of [[ choline ]], to TMAO.",2470,5
2471,"We demonstrate that two flavin mono-oxygenase family members, FMO1 and << FMO3 >>, oxidize trimethylamine (TMA), derived from gut flora metabolism of [[ choline ]], to TMAO.",2471,5
2472,FMO3 overexpression in mice significantly increases plasma TMAO levels while silencing << FMO3 >> decreases [[ TMAO ]] levels.,2472,5
2473,<< FMO3 >> overexpression in mice significantly increases plasma [[ TMAO ]] levels while silencing FMO3 decreases TMAO levels.,2473,5
2474,"In mice, this reduction in << FMO3 >> expression is due primarily to downregulation by [[ androgens ]].",2474,8
2475,"FMO3 expression is induced by dietary bile acids by a mechanism that involves the << farnesoid X receptor >> (FXR), a [[ bile acid ]]-activated nuclear receptor.",2475,9
2476,"FMO3 expression is induced by dietary bile acids by a mechanism that involves the farnesoid X receptor (<< FXR >>), a [[ bile acid ]]-activated nuclear receptor.",2476,9
2477,"<< FMO3 >> expression is induced by dietary [[ bile acids ]] by a mechanism that involves the farnesoid X receptor (FXR), a bile acid-activated nuclear receptor.",2477,6
2478,"Analysis of natural genetic variation among inbred strains of mice indicates that << FMO3 >> and [[ TMAO ]] are significantly correlated, and TMAO levels explain 11% of the variation in atherosclerosis.",2478,4
2479,Synthesis of << quinoline >> derivatives: discovery of a potent and selective [[ phosphodiesterase 5 ]] inhibitor for the treatment of Alzheimer's disease.,2479,0
2480,Phosphodiesterase type 5 (<< PDE5 >>) mediates the degradation of [[ cGMP ]] in a variety of tissues including brain.,2480,5
2481,<< Phosphodiesterase type 5 >> (PDE5) mediates the degradation of [[ cGMP ]] in a variety of tissues including brain.,2481,5
2482,"Fragment-based design, synthesis, and biological evaluation of << N-substituted-5-(4-isopropylthiophenol)-2-hydroxynicotinamide >> derivatives as novel [[ Mcl-1 ]] inhibitors.",2482,0
2483,"We have previously reported a nanomolar inhibitor of antiapoptotic << Mcl-1 >> protein, [[ 3-thiomorpholin-8-oxo-8H-acenaphtho [1,2-b] pyrrole-9-carbonitrile ]] (S1).",2483,0
2484,"A novel potent compound, << N-benzyl-5-(4-isopropylthiophenol)-2-hydroxyl nicotinamide >> (12c), which binds [[ Mcl-1 ]] with an IC(50) value of 54 nM was obtained.",2484,0
2485,"<< Peginesatide >>, a polyethylene glycol (PEG)ylated peptide-based erythropoiesis-stimulating agent, stimulates the [[ erythropoietin receptor ]] dimer that governs erythropoiesis.",2485,9
2486,"Peginesatide, a << polyethylene glycol >> (PEG)ylated peptide-based erythropoiesis-stimulating agent, stimulates the [[ erythropoietin receptor ]] dimer that governs erythropoiesis.",2486,9
2487,"Peginesatide, a polyethylene glycol (<< PEG >>)ylated peptide-based erythropoiesis-stimulating agent, stimulates the [[ erythropoietin receptor ]] dimer that governs erythropoiesis.",2487,9
2488,"LPA1-induced cytoskeleton reorganization therefore makes a previously unrecognized but critically important contribution to the profibrotic activities of << LPA >> by driving MRTF-dependent [[ CTGF ]] expression, which, in turn, drives fibroblast proliferation.-Sakai, N., Chun, J., Duffield, J. S., Wada, T., Luster, A.",2488,6
2489,"<< Bile acids >> are signaling molecules that activate nuclear receptors, such as farnesoid X receptor, pregnane X receptor, [[ constitutive androstane receptor ]], and vitamin D receptor, and play a critical role in the regulation of lipid, glucose, energy, and drug metabolism.",2489,9
2490,"<< Bile acids >> are signaling molecules that activate nuclear receptors, such as farnesoid X receptor, pregnane X receptor, constitutive androstane receptor, and [[ vitamin D receptor ]], and play a critical role in the regulation of lipid, glucose, energy, and drug metabolism.",2490,9
2491,"<< Bile acids >> are signaling molecules that activate [[ nuclear receptors ]], such as farnesoid X receptor, pregnane X receptor, constitutive androstane receptor, and vitamin D receptor, and play a critical role in the regulation of lipid, glucose, energy, and drug metabolism.",2491,9
2492,"<< Bile acids >> are signaling molecules that activate nuclear receptors, such as [[ farnesoid X receptor ]], pregnane X receptor, constitutive androstane receptor, and vitamin D receptor, and play a critical role in the regulation of lipid, glucose, energy, and drug metabolism.",2492,9
2493,"<< Bile acids >> are signaling molecules that activate nuclear receptors, such as farnesoid X receptor, [[ pregnane X receptor ]], constitutive androstane receptor, and vitamin D receptor, and play a critical role in the regulation of lipid, glucose, energy, and drug metabolism.",2493,9
2494,"The peptide << YR-11 >> (YLEIEFSLKHR), obtained by direct substitution of cysteine with a serine residue in the template sequence, significantly (p<0.05) inhibited RANK-RANKL binding, and [[ RANKL ]] induced TRAP activity and formation of multinucleated osteoclasts without any cytotoxicity.",2494,0
2495,"The peptide << YR-11 >> (YLEIEFSLKHR), obtained by direct substitution of cysteine with a serine residue in the template sequence, significantly (p<0.05) inhibited RANK-RANKL binding, and RANKL induced [[ TRAP ]] activity and formation of multinucleated osteoclasts without any cytotoxicity.",2495,0
2496,"The peptide YR-11 (YLEIEFSLKHR), obtained by direct substitution of << cysteine >> with a serine residue in the template sequence, significantly (p<0.05) inhibited RANK-RANKL binding, and [[ RANKL ]] induced TRAP activity and formation of multinucleated osteoclasts without any cytotoxicity.",2496,0
2497,"The peptide YR-11 (YLEIEFSLKHR), obtained by direct substitution of << cysteine >> with a serine residue in the template sequence, significantly (p<0.05) inhibited RANK-RANKL binding, and RANKL induced [[ TRAP ]] activity and formation of multinucleated osteoclasts without any cytotoxicity.",2497,0
2498,"The peptide YR-11 (YLEIEFSLKHR), obtained by direct substitution of cysteine with a << serine >> residue in the template sequence, significantly (p<0.05) inhibited RANK-RANKL binding, and [[ RANKL ]] induced TRAP activity and formation of multinucleated osteoclasts without any cytotoxicity.",2498,0
2499,"The peptide YR-11 (YLEIEFSLKHR), obtained by direct substitution of cysteine with a << serine >> residue in the template sequence, significantly (p<0.05) inhibited RANK-RANKL binding, and RANKL induced [[ TRAP ]] activity and formation of multinucleated osteoclasts without any cytotoxicity.",2499,0
2500,Results confirmed that << YR-11 >> peptide inhibited pro-inflammatory cytokines in the sera and hind paw tissues of AIA rats through its suppressive effect on RANKL induced nuclear translocation of [[ NF-κB ]].,2500,8
2501,Results confirmed that << YR-11 >> peptide inhibited pro-inflammatory [[ cytokines ]] in the sera and hind paw tissues of AIA rats through its suppressive effect on RANKL induced nuclear translocation of NF-κB.,2501,0
2502,Results confirmed that << YR-11 >> peptide inhibited pro-inflammatory cytokines in the sera and hind paw tissues of AIA rats through its suppressive effect on [[ RANKL ]] induced nuclear translocation of NF-κB.,2502,0
2503,The activation of << Rac1 >> was induced by [[ silica ]] nanoparticles as well as BCG DNA and is suggested as the critical signaling event inducing both cytoskeleton changes as well as inflammatory cell activation.,2503,9
2504,Osteoblasts survive the << arsenic trioxide >> treatment by activation of [[ ATM ]]-mediated pathway.,2504,9
2505,"Additionally, these effects of << ATO >> on γ-H2AX, Chk1, Chk2, p53, and p21(waf1/cip1) were reduced by an [[ ATM ]] inhibitor.",2505,9
2506,"Additionally, these effects of << ATO >> on γ-H2AX, [[ Chk1 ]], Chk2, p53, and p21(waf1/cip1) were reduced by an ATM inhibitor.",2506,6
2507,"Additionally, these effects of << ATO >> on γ-H2AX, Chk1, [[ Chk2 ]], p53, and p21(waf1/cip1) were reduced by an ATM inhibitor.",2507,6
2508,"Additionally, these effects of << ATO >> on γ-H2AX, Chk1, Chk2, [[ p53 ]], and p21(waf1/cip1) were reduced by an ATM inhibitor.",2508,6
2509,"Additionally, these effects of << ATO >> on γ-H2AX, Chk1, Chk2, p53, and [[ p21 ]](waf1/cip1) were reduced by an ATM inhibitor.",2509,6
2510,"Additionally, these effects of << ATO >> on γ-H2AX, Chk1, Chk2, p53, and p21([[ waf1 ]]/cip1) were reduced by an ATM inhibitor.",2510,6
2511,"Additionally, these effects of << ATO >> on γ-H2AX, Chk1, Chk2, p53, and p21(waf1/[[ cip1 ]]) were reduced by an ATM inhibitor.",2511,6
2512,"Additionally, these effects of << ATO >> on γ-[[ H2AX ]], Chk1, Chk2, p53, and p21(waf1/cip1) were reduced by an ATM inhibitor.",2512,6
2513,"Furthermore, a mixture of << isoflavonoid >> parent compounds, and a mixture of isoflavonoid metabolites were found to have [[ PPARγ ]] activating abilities.",2513,9
2514,"Furthermore, a mixture of isoflavonoid parent compounds, and a mixture of << isoflavonoid >> metabolites were found to have [[ PPARγ ]] activating abilities.",2514,9
2515,"Both << fatty acids >>, but DHA to a lesser extent compared with EPA, selectively and dose-dependently reduced the percentage of [[ cytokine ]]-expressing Th cells in a peroxisome proliferator-activated receptor (PPAR)γ-dependent fashion, whereas the expression of the cell surface marker CD69 was unaltered on activated T cells.",2515,8
2516,"Both fatty acids, but << DHA >> to a lesser extent compared with EPA, selectively and dose-dependently reduced the percentage of [[ cytokine ]]-expressing Th cells in a peroxisome proliferator-activated receptor (PPAR)γ-dependent fashion, whereas the expression of the cell surface marker CD69 was unaltered on activated T cells.",2516,8
2517,"Both fatty acids, but DHA to a lesser extent compared with << EPA >>, selectively and dose-dependently reduced the percentage of [[ cytokine ]]-expressing Th cells in a peroxisome proliferator-activated receptor (PPAR)γ-dependent fashion, whereas the expression of the cell surface marker CD69 was unaltered on activated T cells.",2517,8
2518,"In monocytes, both << EPA >> and DHA increased [[ interleukin (IL)-10 ]] without affecting tumor necrosis factor (TNF)-α and IL-6.",2518,7
2519,"In monocytes, both EPA and << DHA >> increased [[ interleukin (IL)-10 ]] without affecting tumor necrosis factor (TNF)-α and IL-6.",2519,7
2520,"In the in vitro model we observed high permeability of << imperatorin >> and isoimperatorin with the [[ P-gp ]]-mediated efflux ratios of 0.53 and 0.06, as well as medium permeability of cnidilin with 0.82.",2520,5
2521,"In the in vitro model we observed high permeability of imperatorin and << isoimperatorin >> with the [[ P-gp ]]-mediated efflux ratios of 0.53 and 0.06, as well as medium permeability of cnidilin with 0.82.",2521,5
2522,"In the in vitro model we observed high permeability of imperatorin and isoimperatorin with the << P-gp >>-mediated efflux ratios of 0.53 and 0.06, as well as medium permeability of [[ cnidilin ]] with 0.82.",2522,5
2523,"Treatment with << adenosine dialdehyde >> (AdOx), an inhibitor of transmethylation-suppressive [[ adenosylhomocysteine (SAH) hydrolase ]] (SAHH), enhanced the level of SAH and effectively blocked the proliferation, migration, and invasion of cancer cells; the treatment also induced the differentiation of C6 glioma cells and suppressed the neovascular genesis of eggs in a dose-dependent manner.",2523,0
2524,"Treatment with << adenosine dialdehyde >> (AdOx), an inhibitor of transmethylation-suppressive adenosylhomocysteine (SAH) hydrolase ([[ SAHH ]]), enhanced the level of SAH and effectively blocked the proliferation, migration, and invasion of cancer cells; the treatment also induced the differentiation of C6 glioma cells and suppressed the neovascular genesis of eggs in a dose-dependent manner.",2524,0
2525,"Treatment with adenosine dialdehyde (<< AdOx >>), an inhibitor of transmethylation-suppressive [[ adenosylhomocysteine (SAH) hydrolase ]] (SAHH), enhanced the level of SAH and effectively blocked the proliferation, migration, and invasion of cancer cells; the treatment also induced the differentiation of C6 glioma cells and suppressed the neovascular genesis of eggs in a dose-dependent manner.",2525,0
2526,"Treatment with adenosine dialdehyde (<< AdOx >>), an inhibitor of transmethylation-suppressive adenosylhomocysteine (SAH) hydrolase ([[ SAHH ]]), enhanced the level of SAH and effectively blocked the proliferation, migration, and invasion of cancer cells; the treatment also induced the differentiation of C6 glioma cells and suppressed the neovascular genesis of eggs in a dose-dependent manner.",2526,0
2527,"Treatment with adenosine dialdehyde (AdOx), an inhibitor of transmethylation-suppressive << adenosylhomocysteine (SAH) hydrolase >> (SAHH), enhanced the level of [[ SAH ]] and effectively blocked the proliferation, migration, and invasion of cancer cells; the treatment also induced the differentiation of C6 glioma cells and suppressed the neovascular genesis of eggs in a dose-dependent manner.",2527,5
2528,"Treatment with adenosine dialdehyde (AdOx), an inhibitor of transmethylation-suppressive adenosylhomocysteine (SAH) hydrolase (<< SAHH >>), enhanced the level of [[ SAH ]] and effectively blocked the proliferation, migration, and invasion of cancer cells; the treatment also induced the differentiation of C6 glioma cells and suppressed the neovascular genesis of eggs in a dose-dependent manner.",2528,5
2529,"Through immunoblotting analysis, it was found that << AdOx >> was capable of indirectly diminishing the phosphorylation of oncogenic [[ Src ]] and its kinase activity.",2529,8
2530,"Through immunoblotting analysis, it was found that << AdOx >> was capable of indirectly diminishing the phosphorylation of oncogenic Src and its [[ kinase ]] activity.",2530,0
2531,"Interestingly, << AdOx >> disrupted actin cytoskeleton structures, leading to morphological changes, and suppressed the formation of a signaling complex composed of [[ Src ]] and p85/PI3K, which is linked to various tumorigenic responses.",2531,8
2532,"Interestingly, << AdOx >> disrupted actin cytoskeleton structures, leading to morphological changes, and suppressed the formation of a signaling complex composed of Src and [[ p85 ]]/PI3K, which is linked to various tumorigenic responses.",2532,8
2533,"Interestingly, << AdOx >> disrupted actin cytoskeleton structures, leading to morphological changes, and suppressed the formation of a signaling complex composed of Src and p85/[[ PI3K ]], which is linked to various tumorigenic responses.",2533,8
2534,"Interestingly, << AdOx >> disrupted [[ actin ]] cytoskeleton structures, leading to morphological changes, and suppressed the formation of a signaling complex composed of Src and p85/PI3K, which is linked to various tumorigenic responses.",2534,0
2535,"In agreement with these data, the exogenous treatment of << SAH >> or inhibition of SAHH by specific siRNA or another type of inhibitor, 3-deazaadenosine (DAZA), similarly resulted in antitumorigenic responses, suppressive activity on [[ Src ]], the alteration of actin cytoskeleton, and a change of the colocalization pattern between actin and Src.",2535,3
2536,"In agreement with these data, the exogenous treatment of SAH or inhibition of << SAHH >> by specific siRNA or another type of inhibitor, [[ 3-deazaadenosine ]] (DAZA), similarly resulted in antitumorigenic responses, suppressive activity on Src, the alteration of actin cytoskeleton, and a change of the colocalization pattern between actin and Src.",2536,0
2537,"In agreement with these data, the exogenous treatment of SAH or inhibition of << SAHH >> by specific siRNA or another type of inhibitor, 3-deazaadenosine ([[ DAZA ]]), similarly resulted in antitumorigenic responses, suppressive activity on Src, the alteration of actin cytoskeleton, and a change of the colocalization pattern between actin and Src.",2537,0
2538,Synthesis of derivatives of << methyl rosmarinate >> and their inhibitory activities against matrix metalloproteinase-1 ([[ MMP-1 ]]).,2538,0
2539,Synthesis of derivatives of << methyl rosmarinate >> and their inhibitory activities against [[ matrix metalloproteinase-1 ]] (MMP-1).,2539,0
2540,A series of << MMP-1 >> inhibitors have been identified based upon a [[ methyl rosmarinate ]] scaffold using structure-based drug design methods.,2540,0
2541,"All the compounds were evaluated for their anti-tumor activity against MCF-7, A549 and B16-F10 tumor cell lines as well as << cyclooxygenase-2 >> (COX-2)-derived [[ prostaglandin E2 ]] (PGE2) inhibitory activity of murine macrophage RAW 264.7 cell line.",2541,4
2542,"All the compounds were evaluated for their anti-tumor activity against MCF-7, A549 and B16-F10 tumor cell lines as well as cyclooxygenase-2 (<< COX-2 >>)-derived [[ prostaglandin E2 ]] (PGE2) inhibitory activity of murine macrophage RAW 264.7 cell line.",2542,4
2543,"All the compounds were evaluated for their anti-tumor activity against MCF-7, A549 and B16-F10 tumor cell lines as well as << cyclooxygenase-2 >> (COX-2)-derived prostaglandin E2 ([[ PGE2 ]]) inhibitory activity of murine macrophage RAW 264.7 cell line.",2543,4
2544,"All the compounds were evaluated for their anti-tumor activity against MCF-7, A549 and B16-F10 tumor cell lines as well as cyclooxygenase-2 (<< COX-2 >>)-derived prostaglandin E2 ([[ PGE2 ]]) inhibitory activity of murine macrophage RAW 264.7 cell line.",2544,4
2545,"Its head-space aroma displayed new volatile phytomolecules and also had higher levels of green volatiles from the << lipoxygenase >> (LOX)-pathway (one having as precursors the [[ polyunsaturated fatty acids ]] containing a cis-cis-1,4-pentadiene system).",2545,5
2546,"Its head-space aroma displayed new volatile phytomolecules and also had higher levels of green volatiles from the lipoxygenase (<< LOX >>)-pathway (one having as precursors the [[ polyunsaturated fatty acids ]] containing a cis-cis-1,4-pentadiene system).",2546,5
2547,"Its head-space aroma displayed new volatile phytomolecules and also had higher levels of green volatiles from the << lipoxygenase >> (LOX)-pathway (one having as precursors the polyunsaturated fatty acids containing a [[ cis-cis-1,4-pentadiene ]] system).",2547,5
2548,"Its head-space aroma displayed new volatile phytomolecules and also had higher levels of green volatiles from the lipoxygenase (<< LOX >>)-pathway (one having as precursors the polyunsaturated fatty acids containing a [[ cis-cis-1,4-pentadiene ]] system).",2548,5
2549,"In general, antiproliferative activity is greatly enhanced by low levels of the << glutathione synthase >> inhibitor [[ l-buthionine sulfoxime ]].",2549,0
2550,Cellular << zinc >> is controlled by [[ zinc-chelating proteins ]] and by zinc transporters.,2550,5
2551,Cellular << zinc >> is controlled by zinc-chelating proteins and by [[ zinc transporters ]].,2551,5
2552,"The recent identification of << zinc >> permeability of the lysosomal ion channel [[ TRPML1 ]] (transient receptor potential mucolipin 1), and the evidence of abnormal zinc levels in cells deficient in TRPML1, suggested a role for TRPML1 in zinc transport.",2552,5
2553,"The recent identification of << zinc >> permeability of the lysosomal ion channel TRPML1 ([[ transient receptor potential mucolipin 1 ]]), and the evidence of abnormal zinc levels in cells deficient in TRPML1, suggested a role for TRPML1 in zinc transport.",2553,5
2554,"The recent identification of zinc permeability of the lysosomal ion channel TRPML1 (transient receptor potential mucolipin 1), and the evidence of abnormal zinc levels in cells deficient in TRPML1, suggested a role for << TRPML1 >> in [[ zinc ]] transport.",2554,5
2555,These results underscore a role for << TRPML1 >> in [[ zinc ]] metabolism.,2555,5
2556,"Furthermore, they suggest that << TRPML1 >> works in concert with ZnT4 to regulate [[ zinc ]] translocation between the cytoplasm and lysosomes.",2556,5
2557,"Furthermore, they suggest that TRPML1 works in concert with << ZnT4 >> to regulate [[ zinc ]] translocation between the cytoplasm and lysosomes.",2557,5
2558,<< Serum amyloid A >> upsurge precedes standard biomarkers of hepatotoxicity in [[ ritodrine ]]-injected mice.,2558,6
2559,"Importantly, expression of the acute-phase reactant << serum amyloid A >> (SAA) significantly increased after [[ ritodrine ]] injection, with values indicating the largest fold-change.",2559,6
2560,"Importantly, expression of the acute-phase reactant serum amyloid A (<< SAA >>) significantly increased after [[ ritodrine ]] injection, with values indicating the largest fold-change.",2560,6
2561,"The increase in << SAA >> expression is specific to [[ ritodrine ]]-induced liver damage, because SAA expression was not induced by other hepatotoxic drugs such as acetaminophen, valproic acid, or metformin.",2561,6
2562,"Our in vitro studies showed that cyclic adenosine 3',5'-monophosphate (cAMP) accumulation was not a primary cause of the << ritodrine >>-induced [[ SAA ]] increase.",2562,6
2563,<< Ceftazidime >>-avibactam: a novel cephalosporin/[[ β-lactamase ]] inhibitor combination.,2563,0
2564,Ceftazidime-<< avibactam >>: a novel cephalosporin/[[ β-lactamase ]] inhibitor combination.,2564,0
2565,"Avibactam (formerly << NXL104 >>, AVE1330A) is a synthetic non-β-lactam, β-lactamase inhibitor that inhibits the activities of Ambler class A and C β-lactamases and some [[ Ambler class D ]] enzymes.",2565,0
2566,"Avibactam (formerly << NXL104 >>, AVE1330A) is a synthetic non-β-lactam, [[ β-lactamase ]] inhibitor that inhibits the activities of Ambler class A and C β-lactamases and some Ambler class D enzymes.",2566,0
2567,"<< Avibactam >> (formerly NXL104, AVE1330A) is a synthetic non-β-lactam, β-lactamase inhibitor that inhibits the activities of Ambler class A and C β-lactamases and some [[ Ambler class D ]] enzymes.",2567,0
2568,"<< Avibactam >> (formerly NXL104, AVE1330A) is a synthetic non-β-lactam, [[ β-lactamase ]] inhibitor that inhibits the activities of Ambler class A and C β-lactamases and some Ambler class D enzymes.",2568,0
2569,"Avibactam (formerly NXL104, << AVE1330A >>) is a synthetic non-β-lactam, β-lactamase inhibitor that inhibits the activities of Ambler class A and C β-lactamases and some [[ Ambler class D ]] enzymes.",2569,0
2570,"Avibactam (formerly NXL104, << AVE1330A >>) is a synthetic non-β-lactam, [[ β-lactamase ]] inhibitor that inhibits the activities of Ambler class A and C β-lactamases and some Ambler class D enzymes.",2570,0
2571,The addition of << avibactam >> greatly (4-1024-fold minimum inhibitory concentration [MIC] reduction) improves the activity of ceftazidime versus most species of Enterobacteriaceae depending on the presence or absence of [[ β-lactamase ]] enzyme(s).,2571,0
2572,The addition of avibactam greatly (4-1024-fold minimum inhibitory concentration [MIC] reduction) improves the activity of << ceftazidime >> versus most species of Enterobacteriaceae depending on the presence or absence of [[ β-lactamase ]] enzyme(s).,2572,0
2573,"Pharmacodynamic data suggest that << ceftazidime >>-avibactam is rapidly bactericidal versus [[ β-lactamase ]]-producing Gram-negative bacilli that are not inhibited by ceftazidime alone.Clinical trials to date have reported that ceftazidime-avibactam is as effective as standard carbapenem therapy in complicated intra-abdominal infection and complicated urinary tract infection, including infection caused by cephalosporin-resistant Gram-negative isolates.",2573,0
2574,"Pharmacodynamic data suggest that ceftazidime-<< avibactam >> is rapidly bactericidal versus [[ β-lactamase ]]-producing Gram-negative bacilli that are not inhibited by ceftazidime alone.Clinical trials to date have reported that ceftazidime-avibactam is as effective as standard carbapenem therapy in complicated intra-abdominal infection and complicated urinary tract infection, including infection caused by cephalosporin-resistant Gram-negative isolates.",2574,0
2575,"Ceftazidime-avibactam appears to be well tolerated in healthy subjects and hospitalized patients, with few serious drug-related treatment-emergent adverse events reported to date.In conclusion, << avibactam >> serves to broaden the spectrum of ceftazidime versus [[ ß-lactamase ]]-producing Gram-negative bacilli.",2575,0
2576,"Ceftazidime-avibactam appears to be well tolerated in healthy subjects and hospitalized patients, with few serious drug-related treatment-emergent adverse events reported to date.In conclusion, avibactam serves to broaden the spectrum of << ceftazidime >> versus [[ ß-lactamase ]]-producing Gram-negative bacilli.",2576,0
2577,"Moreover, treatment of high-fat-diet-fed apelin-knockout mice with a selective << cyclooxygenase-2 >> inhibitor, [[ celecoxib ]], improved vascular function, and also attenuated obesity.",2577,0
2578,<< Upamostat >> (Mesupron®) is a new small molecule [[ serine protease ]] inhibitor.,2578,0
2579,Upamostat (<< Mesupron >>®) is a new small molecule [[ serine protease ]] inhibitor.,2579,0
2580,"Interestingly, GPx1a was the most sensitive to selenium availability in non stressful conditions, whereas << GPx1b1 >> and GPx1b2 were highly induced by exposure to [[ selenium ]] levels that had some toxic effects on the cells.",2580,6
2581,"Interestingly, GPx1a was the most sensitive to selenium availability in non stressful conditions, whereas GPx1b1 and << GPx1b2 >> were highly induced by exposure to [[ selenium ]] levels that had some toxic effects on the cells.",2581,6
2582,"<< Mn >> exposure (20 mg/kg) increased [[ p38 ]](MAPK) and Akt phosphorylation, but decreased DARPP-32-Thr-34 phosphorylation.",2582,9
2583,"<< Mn >> exposure (20 mg/kg) increased p38([[ MAPK ]]) and Akt phosphorylation, but decreased DARPP-32-Thr-34 phosphorylation.",2583,9
2584,"<< Mn >> exposure (20 mg/kg) increased p38(MAPK) and [[ Akt ]] phosphorylation, but decreased DARPP-32-Thr-34 phosphorylation.",2584,9
2585,"<< Mn >> exposure (20 mg/kg) increased p38(MAPK) and Akt phosphorylation, but decreased [[ DARPP-32 ]]-Thr-34 phosphorylation.",2585,0
2586,<< Mn >> (10 and 20 mg/kg) increased [[ caspase ]] activity and F(2)-isoprostane production (a biological marker of lipid peroxidation).,2586,9
2587,"Notably, the antioxidant Trolox™ reversed the << Mn >> (20 mg/kg)-dependent augmentation in [[ p38 ]](MAPK) phosphorylation and reduced the Mn (20 mg/kg)-induced caspase activity and F(2)-isoprostane production.",2587,9
2588,"Notably, the antioxidant Trolox™ reversed the << Mn >> (20 mg/kg)-dependent augmentation in p38([[ MAPK ]]) phosphorylation and reduced the Mn (20 mg/kg)-induced caspase activity and F(2)-isoprostane production.",2588,9
2589,"Notably, the antioxidant Trolox™ reversed the Mn (20 mg/kg)-dependent augmentation in p38(MAPK) phosphorylation and reduced the << Mn >> (20 mg/kg)-induced [[ caspase ]] activity and F(2)-isoprostane production.",2589,9
2590,"Notably, the antioxidant << Trolox >>™ reversed the Mn (20 mg/kg)-dependent augmentation in [[ p38 ]](MAPK) phosphorylation and reduced the Mn (20 mg/kg)-induced caspase activity and F(2)-isoprostane production.",2590,0
2591,"Notably, the antioxidant << Trolox >>™ reversed the Mn (20 mg/kg)-dependent augmentation in p38([[ MAPK ]]) phosphorylation and reduced the Mn (20 mg/kg)-induced caspase activity and F(2)-isoprostane production.",2591,0
2592,"Notably, the antioxidant << Trolox >>™ reversed the Mn (20 mg/kg)-dependent augmentation in p38(MAPK) phosphorylation and reduced the Mn (20 mg/kg)-induced [[ caspase ]] activity and F(2)-isoprostane production.",2592,0
2593,"These findings are the first to show that long-term exposure to << Mn >> during a critical period of neurodevelopment causes motor coordination dysfunction with parallel increment in oxidative stress markers, [[ p38 ]](MAPK) phosphorylation and caspase activity in the striatum.",2593,9
2594,"These findings are the first to show that long-term exposure to << Mn >> during a critical period of neurodevelopment causes motor coordination dysfunction with parallel increment in oxidative stress markers, p38([[ MAPK ]]) phosphorylation and caspase activity in the striatum.",2594,9
2595,"These findings are the first to show that long-term exposure to << Mn >> during a critical period of neurodevelopment causes motor coordination dysfunction with parallel increment in oxidative stress markers, p38(MAPK) phosphorylation and [[ caspase ]] activity in the striatum.",2595,9
2596,"<< Nocapyrone H >> (1) reduced the pro-inflammatory factor such as nitric oxide (NO), prostaglandin E2 (PGE2) and [[ interleukin-1β ]] (IL-1β).",2596,8
2597,"<< Nocapyrone H >> (1) reduced the pro-inflammatory factor such as nitric oxide (NO), prostaglandin E2 (PGE2) and interleukin-1β ([[ IL-1β ]]).",2597,8
2598,"Investigating the enteroenteric recirculation of << apixaban >>, a [[ factor Xa ]] inhibitor: administration of activated charcoal to bile duct-cannulated rats and dogs receiving an intravenous dose and use of drug transporter knockout rats.",2598,0
2599,"The fecal elimination, IC, and systemic clearance of apixaban were increased upon AC administration in both BDC rats and dogs and were decreased in BDC rats dosed with << GF-120918 >>, a dual [[ BCRP ]] and P-gp inhibitor).",2599,0
2600,"The fecal elimination, IC, and systemic clearance of apixaban were increased upon AC administration in both BDC rats and dogs and were decreased in BDC rats dosed with << GF-120918 >>, a dual BCRP and [[ P-gp ]] inhibitor).",2600,0
2601,"<< BCRP >> appeared to play a more important role for absorption and intestinal and renal elimination of [[ apixaban ]] than P-gp in transporter-KO rats after oral and i.v. dosing, which led to a higher level of active renal excretion in rat than other species.",2601,5
2602,"BCRP appeared to play a more important role for absorption and intestinal and renal elimination of << apixaban >> than [[ P-gp ]] in transporter-KO rats after oral and i.v. dosing, which led to a higher level of active renal excretion in rat than other species.",2602,5
2603,"Cloning, Characterization, and << Sulfonamide >> and Thiol Inhibition Studies of an [[ α-Carbonic Anhydrase ]] from Trypanosoma cruzi, the Causative Agent of Chagas Disease.",2603,0
2604,"Cloning, Characterization, and Sulfonamide and << Thiol >> Inhibition Studies of an [[ α-Carbonic Anhydrase ]] from Trypanosoma cruzi, the Causative Agent of Chagas Disease.",2604,0
2605,"The enzyme (TcCA) has a very high catalytic activity for the << CO(2) >> hydration reaction, being similar kinetically to the human (h) isoform [[ hCA II ]], although it is devoid of the His64 proton shuttle.",2605,5
2606,"The enzyme (<< TcCA >>) has a very high catalytic activity for the [[ CO(2) ]] hydration reaction, being similar kinetically to the human (h) isoform hCA II, although it is devoid of the His64 proton shuttle.",2606,5
2607,"A large number of << aromatic/heterocyclic sulfonamides >> and some 5-mercapto-1,3,4-thiadiazoles were investigated as [[ TcCA ]] inhibitors.",2607,0
2608,"A large number of aromatic/heterocyclic sulfonamides and some << 5-mercapto-1,3,4-thiadiazoles >> were investigated as [[ TcCA ]] inhibitors.",2608,0
2609,"The mRNA level for << nestin >> (Nes, biomarker for stem Leydig cells) was significantly increased in the control testis on day 4 post-[[ EDS ]], but not in the DEHP treated testes, suggesting that these nestin positive stem cells were differentiated into progenitor Leydig cells in the DEHP-treated testes.",2609,6
2610,"The mRNA level for nestin (<< Nes >>, biomarker for stem Leydig cells) was significantly increased in the control testis on day 4 post-[[ EDS ]], but not in the DEHP treated testes, suggesting that these nestin positive stem cells were differentiated into progenitor Leydig cells in the DEHP-treated testes.",2610,6
2611,<< GnRH >> pulse frequency-dependent stimulation of FSHβ transcription is mediated via activation of PKA and [[ CREB ]].,2611,9
2612,<< GnRH >> pulse frequency-dependent stimulation of FSHβ transcription is mediated via activation of [[ PKA ]] and CREB.,2612,9
2613,<< GnRH >> pulse frequency-dependent stimulation of [[ FSHβ ]] transcription is mediated via activation of PKA and CREB.,2613,6
2614,"cAMP response element-binding protein (CREB) has been implicated in the regulation of FSHβ gene expression, but the molecular mechanisms by which pulsatile << GnRH >> regulates [[ CREB ]] activation remain poorly understood.",2614,9
2615,We hypothesized that << CREB >> is activated by a distinct signaling pathway in response to pulsatile [[ GnRH ]] in a frequency-dependent manner to dictate the FSHβ transcriptional response.,2615,9
2616,"<< GnRH >> stimulation of [[ CREB ]] phosphorylation (pCREB) in the gonadotrope-derived LβT2 cell line was attenuated by a protein kinase A (PKA) inhibitor, H89.",2616,9
2617,"<< GnRH >> stimulation of CREB phosphorylation ([[ pCREB ]]) in the gonadotrope-derived LβT2 cell line was attenuated by a protein kinase A (PKA) inhibitor, H89.",2617,9
2618,"GnRH stimulation of << CREB >> phosphorylation (pCREB) in the gonadotrope-derived LβT2 cell line was attenuated by a protein kinase A (PKA) inhibitor, [[ H89 ]].",2618,0
2619,"GnRH stimulation of CREB phosphorylation (<< pCREB >>) in the gonadotrope-derived LβT2 cell line was attenuated by a protein kinase A (PKA) inhibitor, [[ H89 ]].",2619,0
2620,"GnRH stimulation of CREB phosphorylation (pCREB) in the gonadotrope-derived LβT2 cell line was attenuated by a << protein kinase A >> (PKA) inhibitor, [[ H89 ]].",2620,0
2621,"GnRH stimulation of CREB phosphorylation (pCREB) in the gonadotrope-derived LβT2 cell line was attenuated by a protein kinase A (<< PKA >>) inhibitor, [[ H89 ]].",2621,0
2622,"A dominant negative PKA (DNPKA) reduced << GnRH >>-stimulated [[ pCREB ]] and markedly decreased GnRH stimulation of FSHβ mRNA and FSHβLUC activity, but had little effect on LHβLUC activity, indicating relative specificity of this pathway.",2622,9
2623,"A dominant negative PKA (DNPKA) reduced GnRH-stimulated pCREB and markedly decreased << GnRH >> stimulation of FSHβ mRNA and [[ FSHβ ]]LUC activity, but had little effect on LHβLUC activity, indicating relative specificity of this pathway.",2623,9
2624,"A dominant negative PKA (DNPKA) reduced GnRH-stimulated pCREB and markedly decreased << GnRH >> stimulation of [[ FSHβ ]] mRNA and FSHβLUC activity, but had little effect on LHβLUC activity, indicating relative specificity of this pathway.",2624,6
2625,"In perifusion studies, FSHβ mRNA levels and << FSHβ >>LUC activities were increased by pulsatile [[ GnRH ]], with significantly greater increases at low compared with high pulse frequencies.",2625,9
2626,"In perifusion studies, << FSHβ >> mRNA levels and FSHβLUC activities were increased by pulsatile [[ GnRH ]], with significantly greater increases at low compared with high pulse frequencies.",2626,6
2627,DNPKA markedly reduced these << GnRH >>-stimulated [[ FSHβ ]] responses at both low and high pulse frequencies.,2627,6
2628,"Correlating with << FSHβ >> activation, both PKA activity and levels of pCREB were increased to a greater extent by low compared with high [[ GnRH ]] pulse frequencies, and the induction of pCREB was also attenuated by overexpression of DNPKA at both low and high pulse frequencies.",2628,9
2629,"Correlating with FSHβ activation, both << PKA >> activity and levels of pCREB were increased to a greater extent by low compared with high [[ GnRH ]] pulse frequencies, and the induction of pCREB was also attenuated by overexpression of DNPKA at both low and high pulse frequencies.",2629,9
2630,"Correlating with FSHβ activation, both PKA activity and levels of pCREB were increased to a greater extent by low compared with high << GnRH >> pulse frequencies, and the induction of [[ pCREB ]] was also attenuated by overexpression of DNPKA at both low and high pulse frequencies.",2630,9
2631,"Correlating with FSHβ activation, both PKA activity and levels of << pCREB >> were increased to a greater extent by low compared with high [[ GnRH ]] pulse frequencies, and the induction of pCREB was also attenuated by overexpression of DNPKA at both low and high pulse frequencies.",2631,6
2632,"Taken together, these data indicate that a PKA-mediated signaling pathway mediates << GnRH >> activation of [[ CREB ]] at low-pulse frequencies, playing a significant role in the decoding of the hypothalamic GnRH signal to result in frequency-dependent FSHβ activation.",2632,9
2633,"Taken together, these data indicate that a PKA-mediated signaling pathway mediates GnRH activation of CREB at low-pulse frequencies, playing a significant role in the decoding of the hypothalamic << GnRH >> signal to result in frequency-dependent [[ FSHβ ]] activation.",2633,9
2634,<< Sophocarpine >> alleviates hepatocyte steatosis through activating [[ AMPK ]] signaling pathway.,2634,9
2635,"While << sophocarpine >> treatment resulted in: significant improvement of steatosis (>50% decrease), decrease of leptin expression (<0.57-fold) and increase of [[ adiponectin ]] expression (>1.48-fold).",2635,6
2636,"While << sophocarpine >> treatment resulted in: significant improvement of steatosis (>50% decrease), decrease of [[ leptin ]] expression (<0.57-fold) and increase of adiponectin expression (>1.48-fold).",2636,8
2637,"Moreover, compared with the model group, << sophocarpine >> could significantly increase P-AMPKα (>5.82-fold), AMPKα (>1.29-fold) and [[ ACC ]] (>3.27-fold) protein expressions, and reduce P-ACC (<0.30-fold) and HNF-4α (<0.20-fold) protein expression.",2637,6
2638,"Moreover, compared with the model group, << sophocarpine >> could significantly increase [[ P-AMPKα ]] (>5.82-fold), AMPKα (>1.29-fold) and ACC (>3.27-fold) protein expressions, and reduce P-ACC (<0.30-fold) and HNF-4α (<0.20-fold) protein expression.",2638,6
2639,"Moreover, compared with the model group, << sophocarpine >> could significantly increase P-AMPKα (>5.82-fold), [[ AMPKα ]] (>1.29-fold) and ACC (>3.27-fold) protein expressions, and reduce P-ACC (<0.30-fold) and HNF-4α (<0.20-fold) protein expression.",2639,6
2640,"Moreover, compared with the model group, << sophocarpine >> could significantly increase P-AMPKα (>5.82-fold), AMPKα (>1.29-fold) and ACC (>3.27-fold) protein expressions, and reduce [[ P-ACC ]] (<0.30-fold) and HNF-4α (<0.20-fold) protein expression.",2640,8
2641,"Moreover, compared with the model group, << sophocarpine >> could significantly increase P-AMPKα (>5.82-fold), AMPKα (>1.29-fold) and ACC (>3.27-fold) protein expressions, and reduce P-ACC (<0.30-fold) and [[ HNF-4α ]] (<0.20-fold) protein expression.",2641,8
2642,We concluded that << sophocarpine >> could alleviate hepatocyte steatosis and the potential mechanism might be the activated signaling pathway of [[ AMPK ]].,2642,9
2643,"To evaluate to what extent the regional differences in expression of << P-gp >> and P450 enzymes affect the absorption of a dual substrate, we investigated the transport of [[ darunavir ]] across different small intestinal segments (duodenum, proximal jejunum and ileum).",2643,5
2644,"To evaluate to what extent the regional differences in expression of P-gp and << P450 enzymes >> affect the absorption of a dual substrate, we investigated the transport of [[ darunavir ]] across different small intestinal segments (duodenum, proximal jejunum and ileum).",2644,5
2645,The involvement of P-gp in the absorption of darunavir was clearly shown by coperfusion of darunavir with the << P-gp >> inhibitor [[ zosuquidar ]].,2645,0
2646,The involvement of << P-gp >> in the absorption of [[ darunavir ]] was clearly shown by coperfusion of darunavir with the P-gp inhibitor zosuquidar.,2646,5
2647,Involvement of << P450 >> mediated metabolism in the absorption of [[ darunavir ]] could not be demonstrated in this rat model.,2647,5
2648,"Upon studying the drug-drug interaction of darunavir with ketoconazole, data were indicative for an inhibitory effect of << ketoconazole >> on [[ P-gp ]] as the main mechanism for the increased transport of darunavir across the small intestine.",2648,0
2649,"Upon studying the drug-drug interaction of darunavir with ketoconazole, data were indicative for an inhibitory effect of ketoconazole on << P-gp >> as the main mechanism for the increased transport of [[ darunavir ]] across the small intestine.",2649,5
2650,"In HaCaT cells, << buthanol >> and ethylacetate fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, clerosterol (CLS) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including [[ cyclooxygenase-2 ]] (COX-2), inducible nitric oxide synthase (iNOS), and tumor necrosis factor-α (TNF- α).",2650,8
2651,"In HaCaT cells, << buthanol >> and ethylacetate fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, clerosterol (CLS) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 ([[ COX-2 ]]), inducible nitric oxide synthase (iNOS), and tumor necrosis factor-α (TNF- α).",2651,8
2652,"In HaCaT cells, << buthanol >> and ethylacetate fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, clerosterol (CLS) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 (COX-2), [[ inducible nitric oxide synthase ]] (iNOS), and tumor necrosis factor-α (TNF- α).",2652,8
2653,"In HaCaT cells, << buthanol >> and ethylacetate fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, clerosterol (CLS) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 (COX-2), inducible nitric oxide synthase ([[ iNOS ]]), and tumor necrosis factor-α (TNF- α).",2653,8
2654,"In HaCaT cells, << buthanol >> and ethylacetate fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, clerosterol (CLS) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and [[ tumor necrosis factor-α ]] (TNF- α).",2654,8
2655,"In HaCaT cells, << buthanol >> and ethylacetate fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, clerosterol (CLS) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and tumor necrosis factor-α ([[ TNF- α ]]).",2655,8
2656,"In HaCaT cells, buthanol and << ethylacetate >> fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, clerosterol (CLS) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including [[ cyclooxygenase-2 ]] (COX-2), inducible nitric oxide synthase (iNOS), and tumor necrosis factor-α (TNF- α).",2656,8
2657,"In HaCaT cells, buthanol and << ethylacetate >> fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, clerosterol (CLS) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 ([[ COX-2 ]]), inducible nitric oxide synthase (iNOS), and tumor necrosis factor-α (TNF- α).",2657,8
2658,"In HaCaT cells, buthanol and << ethylacetate >> fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, clerosterol (CLS) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 (COX-2), [[ inducible nitric oxide synthase ]] (iNOS), and tumor necrosis factor-α (TNF- α).",2658,8
2659,"In HaCaT cells, buthanol and << ethylacetate >> fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, clerosterol (CLS) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 (COX-2), inducible nitric oxide synthase ([[ iNOS ]]), and tumor necrosis factor-α (TNF- α).",2659,8
2660,"In HaCaT cells, buthanol and << ethylacetate >> fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, clerosterol (CLS) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and [[ tumor necrosis factor-α ]] (TNF- α).",2660,8
2661,"In HaCaT cells, buthanol and << ethylacetate >> fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, clerosterol (CLS) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and tumor necrosis factor-α ([[ TNF- α ]]).",2661,8
2662,"In HaCaT cells, buthanol and ethylacetate fractions of 80% << methanol >> C. fragile extract (CFB or CFE) and a single compound, clerosterol (CLS) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including [[ cyclooxygenase-2 ]] (COX-2), inducible nitric oxide synthase (iNOS), and tumor necrosis factor-α (TNF- α).",2662,8
2663,"In HaCaT cells, buthanol and ethylacetate fractions of 80% << methanol >> C. fragile extract (CFB or CFE) and a single compound, clerosterol (CLS) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 ([[ COX-2 ]]), inducible nitric oxide synthase (iNOS), and tumor necrosis factor-α (TNF- α).",2663,8
2664,"In HaCaT cells, buthanol and ethylacetate fractions of 80% << methanol >> C. fragile extract (CFB or CFE) and a single compound, clerosterol (CLS) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 (COX-2), [[ inducible nitric oxide synthase ]] (iNOS), and tumor necrosis factor-α (TNF- α).",2664,8
2665,"In HaCaT cells, buthanol and ethylacetate fractions of 80% << methanol >> C. fragile extract (CFB or CFE) and a single compound, clerosterol (CLS) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 (COX-2), inducible nitric oxide synthase ([[ iNOS ]]), and tumor necrosis factor-α (TNF- α).",2665,8
2666,"In HaCaT cells, buthanol and ethylacetate fractions of 80% << methanol >> C. fragile extract (CFB or CFE) and a single compound, clerosterol (CLS) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and [[ tumor necrosis factor-α ]] (TNF- α).",2666,8
2667,"In HaCaT cells, buthanol and ethylacetate fractions of 80% << methanol >> C. fragile extract (CFB or CFE) and a single compound, clerosterol (CLS) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and tumor necrosis factor-α ([[ TNF- α ]]).",2667,8
2668,"In HaCaT cells, buthanol and ethylacetate fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, << clerosterol >> (CLS) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including [[ cyclooxygenase-2 ]] (COX-2), inducible nitric oxide synthase (iNOS), and tumor necrosis factor-α (TNF- α).",2668,8
2669,"In HaCaT cells, buthanol and ethylacetate fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, << clerosterol >> (CLS) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 ([[ COX-2 ]]), inducible nitric oxide synthase (iNOS), and tumor necrosis factor-α (TNF- α).",2669,8
2670,"In HaCaT cells, buthanol and ethylacetate fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, << clerosterol >> (CLS) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 (COX-2), [[ inducible nitric oxide synthase ]] (iNOS), and tumor necrosis factor-α (TNF- α).",2670,8
2671,"In HaCaT cells, buthanol and ethylacetate fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, << clerosterol >> (CLS) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 (COX-2), inducible nitric oxide synthase ([[ iNOS ]]), and tumor necrosis factor-α (TNF- α).",2671,8
2672,"In HaCaT cells, buthanol and ethylacetate fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, << clerosterol >> (CLS) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and [[ tumor necrosis factor-α ]] (TNF- α).",2672,8
2673,"In HaCaT cells, buthanol and ethylacetate fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, << clerosterol >> (CLS) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and tumor necrosis factor-α ([[ TNF- α ]]).",2673,8
2674,"In HaCaT cells, buthanol and ethylacetate fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, clerosterol (<< CLS >>) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including [[ cyclooxygenase-2 ]] (COX-2), inducible nitric oxide synthase (iNOS), and tumor necrosis factor-α (TNF- α).",2674,8
2675,"In HaCaT cells, buthanol and ethylacetate fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, clerosterol (<< CLS >>) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 ([[ COX-2 ]]), inducible nitric oxide synthase (iNOS), and tumor necrosis factor-α (TNF- α).",2675,8
2676,"In HaCaT cells, buthanol and ethylacetate fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, clerosterol (<< CLS >>) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 (COX-2), [[ inducible nitric oxide synthase ]] (iNOS), and tumor necrosis factor-α (TNF- α).",2676,8
2677,"In HaCaT cells, buthanol and ethylacetate fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, clerosterol (<< CLS >>) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 (COX-2), inducible nitric oxide synthase ([[ iNOS ]]), and tumor necrosis factor-α (TNF- α).",2677,8
2678,"In HaCaT cells, buthanol and ethylacetate fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, clerosterol (<< CLS >>) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and [[ tumor necrosis factor-α ]] (TNF- α).",2678,8
2679,"In HaCaT cells, buthanol and ethylacetate fractions of 80% methanol C. fragile extract (CFB or CFE) and a single compound, clerosterol (<< CLS >>) isolated from CFE attenuated UVB (60mJ/cm(2))-induced cytotoxicity and reduced expression of pro-inflammatory proteins including cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and tumor necrosis factor-α ([[ TNF- α ]]).",2679,8
2680,"In another experiment, topical application of CFB, CFE or << CLS >> prior to UVB irradiation (200mJ/cm(2)) on BALB/c mice, inhibited the UVB-elevated protein levels of [[ COX-2 ]], iNOS, and TNF-α.",2680,8
2681,"In another experiment, topical application of CFB, CFE or << CLS >> prior to UVB irradiation (200mJ/cm(2)) on BALB/c mice, inhibited the UVB-elevated protein levels of COX-2, [[ iNOS ]], and TNF-α.",2681,8
2682,"In another experiment, topical application of CFB, CFE or << CLS >> prior to UVB irradiation (200mJ/cm(2)) on BALB/c mice, inhibited the UVB-elevated protein levels of COX-2, iNOS, and [[ TNF-α ]].",2682,8
2683,"In overexpressing cell lines, << OATP1B1 >>- and OATP1B3-mediated estradiol-17β-glucuronide uptake and OATP2B1-mediated estrone-3-sulfate uptake were inhibited by most of the silymarin [[ flavonolignans ]] investigated.",2683,0
2684,"In overexpressing cell lines, OATP1B1- and << OATP1B3 >>-mediated estradiol-17β-glucuronide uptake and OATP2B1-mediated estrone-3-sulfate uptake were inhibited by most of the silymarin [[ flavonolignans ]] investigated.",2684,0
2685,"In overexpressing cell lines, OATP1B1- and OATP1B3-mediated estradiol-17β-glucuronide uptake and << OATP2B1 >>-mediated estrone-3-sulfate uptake were inhibited by most of the silymarin [[ flavonolignans ]] investigated.",2685,0
2686,"In overexpressing cell lines, << OATP1B1 >>- and OATP1B3-mediated [[ estradiol-17β-glucuronide ]] uptake and OATP2B1-mediated estrone-3-sulfate uptake were inhibited by most of the silymarin flavonolignans investigated.",2686,5
2687,"In overexpressing cell lines, OATP1B1- and << OATP1B3 >>-mediated [[ estradiol-17β-glucuronide ]] uptake and OATP2B1-mediated estrone-3-sulfate uptake were inhibited by most of the silymarin flavonolignans investigated.",2687,5
2688,"In overexpressing cell lines, OATP1B1- and OATP1B3-mediated estradiol-17β-glucuronide uptake and << OATP2B1 >>-mediated [[ estrone-3-sulfate ]] uptake were inhibited by most of the silymarin flavonolignans investigated.",2688,5
2689,"<< OATP1B1 >>-, OATP1B3-, and OATP2B1-mediated substrate transport was inhibited efficiently by silymarin (IC50 values of 1.3, 2.2 and 0.3 µM, respectively), [[ silybin A ]] (IC50 values of 9.7, 2.7 and 4.5 µM, respectively), silybin B (IC50 values of 8.5, 5.0 and 0.8 µM, respectively), and silychristin (IC50 values of 9.0, 36.4, and 3.6 µM, respectively).",2689,0
2690,"OATP1B1-, << OATP1B3 >>-, and OATP2B1-mediated substrate transport was inhibited efficiently by silymarin (IC50 values of 1.3, 2.2 and 0.3 µM, respectively), [[ silybin A ]] (IC50 values of 9.7, 2.7 and 4.5 µM, respectively), silybin B (IC50 values of 8.5, 5.0 and 0.8 µM, respectively), and silychristin (IC50 values of 9.0, 36.4, and 3.6 µM, respectively).",2690,0
2691,"OATP1B1-, OATP1B3-, and << OATP2B1 >>-mediated substrate transport was inhibited efficiently by silymarin (IC50 values of 1.3, 2.2 and 0.3 µM, respectively), [[ silybin A ]] (IC50 values of 9.7, 2.7 and 4.5 µM, respectively), silybin B (IC50 values of 8.5, 5.0 and 0.8 µM, respectively), and silychristin (IC50 values of 9.0, 36.4, and 3.6 µM, respectively).",2691,0
2692,"<< OATP1B1 >>-, OATP1B3-, and OATP2B1-mediated substrate transport was inhibited efficiently by silymarin (IC50 values of 1.3, 2.2 and 0.3 µM, respectively), silybin A (IC50 values of 9.7, 2.7 and 4.5 µM, respectively), [[ silybin B ]] (IC50 values of 8.5, 5.0 and 0.8 µM, respectively), and silychristin (IC50 values of 9.0, 36.4, and 3.6 µM, respectively).",2692,0
2693,"OATP1B1-, << OATP1B3 >>-, and OATP2B1-mediated substrate transport was inhibited efficiently by silymarin (IC50 values of 1.3, 2.2 and 0.3 µM, respectively), silybin A (IC50 values of 9.7, 2.7 and 4.5 µM, respectively), [[ silybin B ]] (IC50 values of 8.5, 5.0 and 0.8 µM, respectively), and silychristin (IC50 values of 9.0, 36.4, and 3.6 µM, respectively).",2693,0
2694,"OATP1B1-, OATP1B3-, and << OATP2B1 >>-mediated substrate transport was inhibited efficiently by silymarin (IC50 values of 1.3, 2.2 and 0.3 µM, respectively), silybin A (IC50 values of 9.7, 2.7 and 4.5 µM, respectively), [[ silybin B ]] (IC50 values of 8.5, 5.0 and 0.8 µM, respectively), and silychristin (IC50 values of 9.0, 36.4, and 3.6 µM, respectively).",2694,0
2695,"<< OATP1B1 >>-, OATP1B3-, and OATP2B1-mediated substrate transport was inhibited efficiently by silymarin (IC50 values of 1.3, 2.2 and 0.3 µM, respectively), silybin A (IC50 values of 9.7, 2.7 and 4.5 µM, respectively), silybin B (IC50 values of 8.5, 5.0 and 0.8 µM, respectively), and [[ silychristin ]] (IC50 values of 9.0, 36.4, and 3.6 µM, respectively).",2695,0
2696,"OATP1B1-, << OATP1B3 >>-, and OATP2B1-mediated substrate transport was inhibited efficiently by silymarin (IC50 values of 1.3, 2.2 and 0.3 µM, respectively), silybin A (IC50 values of 9.7, 2.7 and 4.5 µM, respectively), silybin B (IC50 values of 8.5, 5.0 and 0.8 µM, respectively), and [[ silychristin ]] (IC50 values of 9.0, 36.4, and 3.6 µM, respectively).",2696,0
2697,"OATP1B1-, OATP1B3-, and << OATP2B1 >>-mediated substrate transport was inhibited efficiently by silymarin (IC50 values of 1.3, 2.2 and 0.3 µM, respectively), silybin A (IC50 values of 9.7, 2.7 and 4.5 µM, respectively), silybin B (IC50 values of 8.5, 5.0 and 0.8 µM, respectively), and [[ silychristin ]] (IC50 values of 9.0, 36.4, and 3.6 µM, respectively).",2697,0
2698,"Furthermore, silymarin, << silybin A >>, and silybin B (100 µM) significantly inhibited [[ OATP ]]-mediated estradiol-17β-glucuronide and rosuvastatin uptake into human hepatocytes.",2698,0
2699,"Furthermore, silymarin, silybin A, and << silybin B >> (100 µM) significantly inhibited [[ OATP ]]-mediated estradiol-17β-glucuronide and rosuvastatin uptake into human hepatocytes.",2699,0
2700,"Furthermore, silymarin, silybin A, and silybin B (100 µM) significantly inhibited << OATP >>-mediated [[ estradiol-17β-glucuronide ]] and rosuvastatin uptake into human hepatocytes.",2700,5
2701,"Furthermore, silymarin, silybin A, and silybin B (100 µM) significantly inhibited << OATP >>-mediated estradiol-17β-glucuronide and [[ rosuvastatin ]] uptake into human hepatocytes.",2701,5
2702,Further investigation demonstrated that 8k reduced << H2O2 >>-induced activation of mitochondrial apoptosis by inhibiting the expression of [[ Bax ]] and elevating the expression of Bcl-2.,2702,6
2703,Further investigation demonstrated that 8k reduced << H2O2 >>-induced activation of mitochondrial apoptosis by inhibiting the expression of Bax and elevating the expression of [[ Bcl-2 ]].,2703,8
2704,"Three variables of cardiac vagal effects (the root mean square of successive differences [rMSSD] in the interbeat interval of the heart rate [IBI], heart-rate variability [HRV] caused by peak-valley respiratory sinus arrhythmia [pvRSA], and high-frequency power [HF]) and heart rate (HR) were obtained at seven time points during the clamps, characterised by increasing levels of << insulin >> (achieved by administering insulin plus [[ glucose ]], glucose only, glucose and GLP-1, and glucose and GLP-1 combined with arginine).",2704,6
2705,"Three variables of cardiac vagal effects (the root mean square of successive differences [rMSSD] in the interbeat interval of the heart rate [IBI], heart-rate variability [HRV] caused by peak-valley respiratory sinus arrhythmia [pvRSA], and high-frequency power [HF]) and heart rate (HR) were obtained at seven time points during the clamps, characterised by increasing levels of << insulin >> (achieved by administering insulin plus glucose, [[ glucose ]] only, glucose and GLP-1, and glucose and GLP-1 combined with arginine).",2705,6
2706,"Three variables of cardiac vagal effects (the root mean square of successive differences [rMSSD] in the interbeat interval of the heart rate [IBI], heart-rate variability [HRV] caused by peak-valley respiratory sinus arrhythmia [pvRSA], and high-frequency power [HF]) and heart rate (HR) were obtained at seven time points during the clamps, characterised by increasing levels of << insulin >> (achieved by administering insulin plus glucose, glucose only, [[ glucose ]] and GLP-1, and glucose and GLP-1 combined with arginine).",2706,6
2707,"Three variables of cardiac vagal effects (the root mean square of successive differences [rMSSD] in the interbeat interval of the heart rate [IBI], heart-rate variability [HRV] caused by peak-valley respiratory sinus arrhythmia [pvRSA], and high-frequency power [HF]) and heart rate (HR) were obtained at seven time points during the clamps, characterised by increasing levels of << insulin >> (achieved by administering insulin plus glucose, glucose only, glucose and GLP-1, and [[ glucose ]] and GLP-1 combined with arginine).",2707,6
2708,"Three variables of cardiac vagal effects (the root mean square of successive differences [rMSSD] in the interbeat interval of the heart rate [IBI], heart-rate variability [HRV] caused by peak-valley respiratory sinus arrhythmia [pvRSA], and high-frequency power [HF]) and heart rate (HR) were obtained at seven time points during the clamps, characterised by increasing levels of << insulin >> (achieved by administering insulin plus glucose, glucose only, glucose and GLP-1, and glucose and GLP-1 combined with [[ arginine ]]).",2708,6
2709,The << CRF(1) receptor >> antagonist [[ SSR125543 ]] prevents stress-induced cognitive deficit associated with hippocampal dysfunction: Comparison with paroxetine and D-cycloserine.,2709,1
2710,RATIONALE: The selective << CRF(1) (corticotropin releasing factor type 1) receptor >> antagonist [[ SSR125543 ]] has been previously shown to attenuate the long-term cognitive deficit produced by traumatic stress exposure.,2710,1
2711,"Effects of SSR125543 were compared to those of the 5-HT reuptake inhibitor, paroxetine (10 mg/kg/day), and the partial << N-methyl-D-aspartate (NMDA) receptor >> agonist, [[ D-cycloserine ]] (10 mg/kg/day), two compounds which have demonstrated clinical efficacy against PTSD.",2711,2
2712,CONCLUSIONS: These findings confirm that the << CRF(1) receptor >> antagonist [[ SSR125543 ]] is able to attenuate the behavioral effects of traumatic stress exposure and indicate that these effects are associated with a normalization of hippocampal neuronal excitability impaired by stress.,2712,1
2713,A series of << indazole arylsulfonamides >> were synthesized and examined as [[ human CCR4 ]] antagonists.,2713,1
2714,Repeated Low Dose Administration of the << Monoacylglycerol Lipase >> Inhibitor [[ JZL184 ]] Retains CB1 Receptor Mediated Antinociceptive and Gastroprotective Effects.,2714,0
2715,The monoacylglycerol lipase (<< MAGL >>) inhibitor [[ JZL184 ]] produces antinociceptive and anti-inflammatory effects.,2715,0
2716,The << monoacylglycerol lipase >> (MAGL) inhibitor [[ JZL184 ]] produces antinociceptive and anti-inflammatory effects.,2716,0
2717,"Mice given daily injections of high dose << JZL184 >> (≥16 mg/kg) for six days displayed decreased [[ CB(1) ]] receptor density and function in brain, as assessed in [(3)H]SR141716A binding and CP55,940-stimulated [(35)S]GTPγS binding assays, respectively.",2717,3
2718,Design and synthesis of << bicyclic pyrazinone and pyrimidinone amides >> as potent [[ TF ]]-FVIIa inhibitors.,2718,0
2719,Design and synthesis of << bicyclic pyrazinone and pyrimidinone amides >> as potent TF-[[ FVIIa ]] inhibitors.,2719,0
2720,<< Bicyclic pyrazinone and pyrimidinone amides >> were designed and synthesized as potent TF-[[ FVIIa ]] inhibitors.,2720,0
2721,<< Bicyclic pyrazinone and pyrimidinone amides >> were designed and synthesized as potent [[ TF ]]-FVIIa inhibitors.,2721,0
2722,"Fragment-based drug design and identification of << HJC0123 >>, a novel orally bioavailable [[ STAT3 ]] inhibitor for cancer therapy.",2722,0
2723,"The most potent compound 5 (<< HJC0123 >>) has demonstrated to inhibit STAT3 promoter activity, downregulate phosphorylation of STAT3, increase the expression of cleaved [[ caspase-3 ]], inhibit cell cycle progression and promote apoptosis in breast and pancreatic cancer cells with low micromolar to nanomolar IC50 values.",2723,6
2724,"The most potent compound 5 (<< HJC0123 >>) has demonstrated to inhibit [[ STAT3 promoter ]] activity, downregulate phosphorylation of STAT3, increase the expression of cleaved caspase-3, inhibit cell cycle progression and promote apoptosis in breast and pancreatic cancer cells with low micromolar to nanomolar IC50 values.",2724,0
2725,"The most potent compound 5 (<< HJC0123 >>) has demonstrated to inhibit STAT3 promoter activity, downregulate phosphorylation of [[ STAT3 ]], increase the expression of cleaved caspase-3, inhibit cell cycle progression and promote apoptosis in breast and pancreatic cancer cells with low micromolar to nanomolar IC50 values.",2725,0
2726,The effects of the << phosphodiesterase type 5 >> inhibitor [[ vardenafil ]] on cognitive performance in healthy adults: a behavioral- electroencephalography study.,2726,0
2727,"Therefore, we examined whether the << PDE5 >>-I [[ vardenafil ]] improves memory and executive functioning and affect electroencephalography (EEG) in healthy young adults.",2727,0
2728,"Statins are inhibitors of the enzyme << 3-hydroxy-3-methylglutaryl coenzyme A reductase >>, the rate-limiting step in [[ cholesterol ]] biosynthesis.",2728,4
2729,"We found that atorvastatin withdrawal decreased levels of nitric oxide and mitochondrial superoxide dismutase activity, whereas increased << NADPH oxidase >> activity and immunoreactivity for the protein nitration marker [[ 3-nitrotyrosine ]] in the cerebral cortex.",2729,9
2730,"Cardiac hypertrophy, structural remodeling, and expression of the genes associated with fatty acid metabolism were examined in rats treated with triiodothyronine (T3) alone (8 μg/100 g body weight (BW), i.p.) for 15 days or along with a << peroxisome proliferator-activated receptor alpha >> agonist [[ bezafibrate ]] (Bzf; 30 μg/100 g BW, oral) and were found to improve in the Bzf co-treated condition.",2730,2
2731,"Cardiac hypertrophy, structural remodeling, and expression of the genes associated with fatty acid metabolism were examined in rats treated with triiodothyronine (T3) alone (8 μg/100 g body weight (BW), i.p.) for 15 days or along with a << peroxisome proliferator-activated receptor alpha >> agonist bezafibrate ([[ Bzf ]]; 30 μg/100 g BW, oral) and were found to improve in the Bzf co-treated condition.",2731,2
2732,"Moreover, the effects of the << DRD3 >> agonist [[ 7-hydroxy-N,N-dipropyl-2-aminotetralin ]] (7-OH-DPAT)-induced locomotor hypoactivity were significantly increased when DRD3 proteins were abundant.",2732,2
2733,"Moreover, the effects of the DRD3 agonist << 7-hydroxy-N,N-dipropyl-2-aminotetralin >> (7-OH-DPAT)-induced locomotor hypoactivity were significantly increased when [[ DRD3 ]] proteins were abundant.",2733,2
2734,"Moreover, the effects of the << DRD3 >> agonist 7-hydroxy-N,N-dipropyl-2-aminotetralin ([[ 7-OH-DPAT ]])-induced locomotor hypoactivity were significantly increased when DRD3 proteins were abundant.",2734,2
2735,"Moreover, the effects of the DRD3 agonist 7-hydroxy-N,N-dipropyl-2-aminotetralin (<< 7-OH-DPAT >>)-induced locomotor hypoactivity were significantly increased when [[ DRD3 ]] proteins were abundant.",2735,2
2736,"Studies on an (S)-2-amino-3-(3-hydroxy-5-methyl-4-isoxazolyl)propionic acid << (AMPA) receptor >> antagonist [[ IKM-159 ]]: asymmetric synthesis, neuroactivity, and structural characterization.",2736,1
2737,<< IKM-159 >> was developed and identified as a member of a new class of heterotricyclic glutamate analogues that act as [[ AMPA receptor ]]-selective antagonists.,2737,1
2738,IKM-159 was developed and identified as a member of a new class of heterotricyclic << glutamate >> analogues that act as [[ AMPA receptor ]]-selective antagonists.,2738,1
2739,"<< (2R)-IKM-159 >> locks the [[ GluA2 ]] in an open form, consistent with a pharmacological action as competitive antagonist of AMPA receptors.",2739,0
2740,"<< (2R)-IKM-159 >> locks the GluA2 in an open form, consistent with a pharmacological action as competitive antagonist of [[ AMPA receptors ]].",2740,1
2741,"Coumarin 7-hydroxylation, catalyzed by << P450 2A13 >>, was strongly inhibited by 2'-methoxy-5,7-dihydroxyflavone, 2-ethynylnaphthalene, 2'-methoxyflavone, 2-naphththalene propargyl ether, acenaphthene, acenaphthylene, naphthalene, 1-acetylpyrene, [[ flavanone ]], chrysin, 3-ethynylphenanthrene, flavone, and 7-hydroxyflavone; these chemicals induced Type I spectral changes with low Ks values.",2741,0
2742,"Coumarin 7-hydroxylation, catalyzed by << P450 2A13 >>, was strongly inhibited by [[ 2'-methoxy-5,7-dihydroxyflavone ]], 2-ethynylnaphthalene, 2'-methoxyflavone, 2-naphththalene propargyl ether, acenaphthene, acenaphthylene, naphthalene, 1-acetylpyrene, flavanone, chrysin, 3-ethynylphenanthrene, flavone, and 7-hydroxyflavone; these chemicals induced Type I spectral changes with low Ks values.",2742,0
2743,"Coumarin 7-hydroxylation, catalyzed by << P450 2A13 >>, was strongly inhibited by 2'-methoxy-5,7-dihydroxyflavone, [[ 2-ethynylnaphthalene ]], 2'-methoxyflavone, 2-naphththalene propargyl ether, acenaphthene, acenaphthylene, naphthalene, 1-acetylpyrene, flavanone, chrysin, 3-ethynylphenanthrene, flavone, and 7-hydroxyflavone; these chemicals induced Type I spectral changes with low Ks values.",2743,0
2744,"Coumarin 7-hydroxylation, catalyzed by << P450 2A13 >>, was strongly inhibited by 2'-methoxy-5,7-dihydroxyflavone, 2-ethynylnaphthalene, [[ 2'-methoxyflavone ]], 2-naphththalene propargyl ether, acenaphthene, acenaphthylene, naphthalene, 1-acetylpyrene, flavanone, chrysin, 3-ethynylphenanthrene, flavone, and 7-hydroxyflavone; these chemicals induced Type I spectral changes with low Ks values.",2744,0
2745,"Coumarin 7-hydroxylation, catalyzed by << P450 2A13 >>, was strongly inhibited by 2'-methoxy-5,7-dihydroxyflavone, 2-ethynylnaphthalene, 2'-methoxyflavone, [[ 2-naphththalene propargyl ether ]], acenaphthene, acenaphthylene, naphthalene, 1-acetylpyrene, flavanone, chrysin, 3-ethynylphenanthrene, flavone, and 7-hydroxyflavone; these chemicals induced Type I spectral changes with low Ks values.",2745,0
2746,"Coumarin 7-hydroxylation, catalyzed by << P450 2A13 >>, was strongly inhibited by 2'-methoxy-5,7-dihydroxyflavone, 2-ethynylnaphthalene, 2'-methoxyflavone, 2-naphththalene propargyl ether, [[ acenaphthene ]], acenaphthylene, naphthalene, 1-acetylpyrene, flavanone, chrysin, 3-ethynylphenanthrene, flavone, and 7-hydroxyflavone; these chemicals induced Type I spectral changes with low Ks values.",2746,0
2747,"Coumarin 7-hydroxylation, catalyzed by << P450 2A13 >>, was strongly inhibited by 2'-methoxy-5,7-dihydroxyflavone, 2-ethynylnaphthalene, 2'-methoxyflavone, 2-naphththalene propargyl ether, acenaphthene, acenaphthylene, naphthalene, 1-acetylpyrene, flavanone, [[ chrysin ]], 3-ethynylphenanthrene, flavone, and 7-hydroxyflavone; these chemicals induced Type I spectral changes with low Ks values.",2747,0
2748,"Coumarin 7-hydroxylation, catalyzed by << P450 2A13 >>, was strongly inhibited by 2'-methoxy-5,7-dihydroxyflavone, 2-ethynylnaphthalene, 2'-methoxyflavone, 2-naphththalene propargyl ether, acenaphthene, [[ acenaphthylene ]], naphthalene, 1-acetylpyrene, flavanone, chrysin, 3-ethynylphenanthrene, flavone, and 7-hydroxyflavone; these chemicals induced Type I spectral changes with low Ks values.",2748,0
2749,"Coumarin 7-hydroxylation, catalyzed by << P450 2A13 >>, was strongly inhibited by 2'-methoxy-5,7-dihydroxyflavone, 2-ethynylnaphthalene, 2'-methoxyflavone, 2-naphththalene propargyl ether, acenaphthene, acenaphthylene, [[ naphthalene ]], 1-acetylpyrene, flavanone, chrysin, 3-ethynylphenanthrene, flavone, and 7-hydroxyflavone; these chemicals induced Type I spectral changes with low Ks values.",2749,0
2750,"Coumarin 7-hydroxylation, catalyzed by << P450 2A13 >>, was strongly inhibited by 2'-methoxy-5,7-dihydroxyflavone, 2-ethynylnaphthalene, 2'-methoxyflavone, 2-naphththalene propargyl ether, acenaphthene, acenaphthylene, naphthalene, [[ 1-acetylpyrene ]], flavanone, chrysin, 3-ethynylphenanthrene, flavone, and 7-hydroxyflavone; these chemicals induced Type I spectral changes with low Ks values.",2750,0
2751,"Coumarin 7-hydroxylation, catalyzed by << P450 2A13 >>, was strongly inhibited by 2'-methoxy-5,7-dihydroxyflavone, 2-ethynylnaphthalene, 2'-methoxyflavone, 2-naphththalene propargyl ether, acenaphthene, acenaphthylene, naphthalene, 1-acetylpyrene, flavanone, chrysin, [[ 3-ethynylphenanthrene ]], flavone, and 7-hydroxyflavone; these chemicals induced Type I spectral changes with low Ks values.",2751,0
2752,"Coumarin 7-hydroxylation, catalyzed by << P450 2A13 >>, was strongly inhibited by 2'-methoxy-5,7-dihydroxyflavone, 2-ethynylnaphthalene, 2'-methoxyflavone, 2-naphththalene propargyl ether, acenaphthene, acenaphthylene, naphthalene, 1-acetylpyrene, flavanone, chrysin, 3-ethynylphenanthrene, [[ flavone ]], and 7-hydroxyflavone; these chemicals induced Type I spectral changes with low Ks values.",2752,0
2753,"Coumarin 7-hydroxylation, catalyzed by << P450 2A13 >>, was strongly inhibited by 2'-methoxy-5,7-dihydroxyflavone, 2-ethynylnaphthalene, 2'-methoxyflavone, 2-naphththalene propargyl ether, acenaphthene, acenaphthylene, naphthalene, 1-acetylpyrene, flavanone, chrysin, 3-ethynylphenanthrene, flavone, and [[ 7-hydroxyflavone ]]; these chemicals induced Type I spectral changes with low Ks values.",2753,0
2754,"<< Coumarin >> 7-hydroxylation, catalyzed by [[ P450 2A13 ]], was strongly inhibited by 2'-methoxy-5,7-dihydroxyflavone, 2-ethynylnaphthalene, 2'-methoxyflavone, 2-naphththalene propargyl ether, acenaphthene, acenaphthylene, naphthalene, 1-acetylpyrene, flavanone, chrysin, 3-ethynylphenanthrene, flavone, and 7-hydroxyflavone; these chemicals induced Type I spectral changes with low Ks values.",2754,5
2755,"Full agonists to the << peroxisome proliferator-activated receptor (PPAR)γ >>, such as [[ Rosiglitazone ]], have been associated with a series of undesired side effects, such as weight gain, fluid retention, cardiac hypertrophy, and hepatotoxicity.",2755,10
2756,The << (R)-omeprazole >> hydroxylation index reflects [[ CYP2C19 ]] activity in healthy Japanese volunteers.,2756,5
2757,"PURPOSE: << Omeprazole >> has (R)- and (S)-enantiomers, which exhibit different pharmacokinetics (PK) among patients with [[ cytochrome P450 (CYP) 2C19 ]] genotype groups.",2757,5
2758,"Additionally, there was a significant difference in plasma concentrations of << (R)-5-hydroxyomeprazole >> among [[ CYP2C19 ]] genotype groups, whereas no significant differences were observed in that of (S)-5-hydroxyomeprazole.",2758,5
2759,"Additionally, there was a significant difference in plasma concentrations of (R)-5-hydroxyomeprazole among << CYP2C19 >> genotype groups, whereas no significant differences were observed in that of [[ (S)-5-hydroxyomeprazole ]].",2759,5
2760,"CONCLUSION: Our findings demonstrate that << (R)-omeprazole >> HI correlated better with [[ CYP2C19 ]] genotype groups than racemic-omeprazole HI, and these results may be useful for classification among patients in CYP2C19 genotype groups prior to omeprazole treatment.",2760,5
2761,"CONCLUSION: Our findings demonstrate that (R)-omeprazole HI correlated better with << CYP2C19 >> genotype groups than [[ racemic-omeprazole ]] HI, and these results may be useful for classification among patients in CYP2C19 genotype groups prior to omeprazole treatment.",2761,5
2762,"The pleiotropic effects of vitamin A are exerted mainly by one active metabolite, << all-trans retinoic acid >> (atRA), which regulates the expression of a battery of target genes through several families of [[ nuclear receptors ]] (RARs, RXRs and PPARβ/δ), polymorphic retinoic acid (RA) response elements and multiple coregulators.",2762,6
2763,"The pleiotropic effects of vitamin A are exerted mainly by one active metabolite, << all-trans retinoic acid >> (atRA), which regulates the expression of a battery of target genes through several families of nuclear receptors ([[ RARs ]], RXRs and PPARβ/δ), polymorphic retinoic acid (RA) response elements and multiple coregulators.",2763,6
2764,"The pleiotropic effects of vitamin A are exerted mainly by one active metabolite, << all-trans retinoic acid >> (atRA), which regulates the expression of a battery of target genes through several families of nuclear receptors (RARs, [[ RXRs ]] and PPARβ/δ), polymorphic retinoic acid (RA) response elements and multiple coregulators.",2764,6
2765,"The pleiotropic effects of vitamin A are exerted mainly by one active metabolite, << all-trans retinoic acid >> (atRA), which regulates the expression of a battery of target genes through several families of nuclear receptors (RARs, RXRs and PPARβ/δ), [[ polymorphic retinoic acid (RA) response elements ]] and multiple coregulators.",2765,6
2766,"The pleiotropic effects of vitamin A are exerted mainly by one active metabolite, all-trans retinoic acid (<< atRA >>), which regulates the expression of a battery of target genes through several families of [[ nuclear receptors ]] (RARs, RXRs and PPARβ/δ), polymorphic retinoic acid (RA) response elements and multiple coregulators.",2766,6
2767,"The pleiotropic effects of vitamin A are exerted mainly by one active metabolite, all-trans retinoic acid (<< atRA >>), which regulates the expression of a battery of target genes through several families of nuclear receptors ([[ RARs ]], RXRs and PPARβ/δ), polymorphic retinoic acid (RA) response elements and multiple coregulators.",2767,6
2768,"The pleiotropic effects of vitamin A are exerted mainly by one active metabolite, all-trans retinoic acid (<< atRA >>), which regulates the expression of a battery of target genes through several families of nuclear receptors (RARs, [[ RXRs ]] and PPARβ/δ), polymorphic retinoic acid (RA) response elements and multiple coregulators.",2768,6
2769,"The pleiotropic effects of vitamin A are exerted mainly by one active metabolite, all-trans retinoic acid (<< atRA >>), which regulates the expression of a battery of target genes through several families of nuclear receptors (RARs, RXRs and PPARβ/δ), [[ polymorphic retinoic acid (RA) response elements ]] and multiple coregulators.",2769,6
2770,"Interestingly, << miR-21 >> expression positively correlated with urine albumin [[ creatine ]] ratio (ACR), TIMP1, collagen IV (ColIV), and fibronectin (FN); while negatively correlated with creatine clearance ratio (Ccr) and MMP-9 protein.",2770,6
2771,"Interestingly, << miR-21 >> expression positively correlated with urine albumin creatine ratio (ACR), TIMP1, collagen IV (ColIV), and fibronectin (FN); while negatively correlated with [[ creatine ]] clearance ratio (Ccr) and MMP-9 protein.",2771,8
2772,"The << human cytosolic sulfotransferase hSULT2A1 >> catalyzes the sulfation of a broad range of xenobiotics, as well as endogenous [[ hydroxysteroids ]] and bile acids.",2772,5
2773,"The << human cytosolic sulfotransferase hSULT2A1 >> catalyzes the sulfation of a broad range of xenobiotics, as well as endogenous hydroxysteroids and [[ bile acids ]].",2773,5
2774,Studies on the kinetics of the << hSULT2A1 >>-catalyzed sulfation of [[ dehydroepiandrosterone ]] (DHEA) showed the effects of disulfide bond formation on the substrate inhibition characteristics of the enzyme.,2774,5
2775,Studies on the kinetics of the << hSULT2A1 >>-catalyzed sulfation of dehydroepiandrosterone ([[ DHEA ]]) showed the effects of disulfide bond formation on the substrate inhibition characteristics of the enzyme.,2775,5
2776,"Computational docking analysis was conducted to model the interaction of these antagonists with the human ERα and showed that they could tightly bind to the ERα in a manner similar to that of << ICI-182,780 >>, a pure [[ ER ]] antagonist.",2776,1
2777,"These results provide an example that attachment of a bulky side chain to the C-7α position of E2 can produce ER antagonists with << ER >> affinity comparable to that of [[ ICI-182,780 ]].",2777,1
2778,"Discovery of << 7-methoxy-6-[4-(4-methyl-1,3-thiazol-2-yl)-1H-imidazol-5-yl]-1,3-benzothiazole >> (TASP0382088): a potent and selective [[ transforming growth factor-β type I receptor ]] inhibitor as a topical drug for alopecia.",2778,0
2779,"Discovery of 7-methoxy-6-[4-(4-methyl-1,3-thiazol-2-yl)-1H-imidazol-5-yl]-1,3-benzothiazole (<< TASP0382088 >>): a potent and selective [[ transforming growth factor-β type I receptor ]] inhibitor as a topical drug for alopecia.",2779,0
2780,"<< 7-Methoxy-6-[4-(4-methyl-1,3-thiazol-2-yl)-1H-imidazol-5-yl]-1,3-benzothiazole >> 11 (TASP0382088) was synthesized and evaluated as transforming growth factor-β (TGF-β) type I receptor (also known as [[ activin receptor-like kinase 5 ]] or ALK5) inhibitor.",2780,0
2781,"<< 7-Methoxy-6-[4-(4-methyl-1,3-thiazol-2-yl)-1H-imidazol-5-yl]-1,3-benzothiazole >> 11 (TASP0382088) was synthesized and evaluated as transforming growth factor-β (TGF-β) type I receptor (also known as activin receptor-like kinase 5 or [[ ALK5 ]]) inhibitor.",2781,0
2782,"<< 7-Methoxy-6-[4-(4-methyl-1,3-thiazol-2-yl)-1H-imidazol-5-yl]-1,3-benzothiazole >> 11 (TASP0382088) was synthesized and evaluated as [[ transforming growth factor-β (TGF-β) type I receptor ]] (also known as activin receptor-like kinase 5 or ALK5) inhibitor.",2782,0
2783,"7-Methoxy-6-[4-(4-methyl-1,3-thiazol-2-yl)-1H-imidazol-5-yl]-1,3-benzothiazole 11 (<< TASP0382088 >>) was synthesized and evaluated as transforming growth factor-β (TGF-β) type I receptor (also known as [[ activin receptor-like kinase 5 ]] or ALK5) inhibitor.",2783,0
2784,"7-Methoxy-6-[4-(4-methyl-1,3-thiazol-2-yl)-1H-imidazol-5-yl]-1,3-benzothiazole 11 (<< TASP0382088 >>) was synthesized and evaluated as transforming growth factor-β (TGF-β) type I receptor (also known as activin receptor-like kinase 5 or [[ ALK5 ]]) inhibitor.",2784,0
2785,"7-Methoxy-6-[4-(4-methyl-1,3-thiazol-2-yl)-1H-imidazol-5-yl]-1,3-benzothiazole 11 (<< TASP0382088 >>) was synthesized and evaluated as [[ transforming growth factor-β (TGF-β) type I receptor ]] (also known as activin receptor-like kinase 5 or ALK5) inhibitor.",2785,0
2786,"In non-pre-treated cells, only << efflux transporters >> were down-regulated by [[ 7-ketosterols ]], showing a greater influence upon ABCG5 expression.",2786,3
2787,"Cell-pre-incubation with bradykinin induced changes in ABCG expression levels after 7-ketostigmasterol-incubation; however, the energetic metabolism inhibition reduced << NPC1L1 >> expression only in [[ 7-ketocholesterol ]]-incubated cells.",2787,8
2788,"In non-pre-treated cells, << HMG-CoA >> was up-regulated by both [[ 7-ketosterols ]].",2788,7
2789,"In lymphocytes, the NTPDase and << ADA >> activities were increased in all groups treated with [[ caffeic acid ]] when compared to control (P<0.05).",2789,9
2790,"In lymphocytes, the << NTPDase >> and ADA activities were increased in all groups treated with [[ caffeic acid ]] when compared to control (P<0.05).",2790,9
2791,"Currently, the most important insecticides are << neonicotinoids >>, which are metabolized in vitro by [[ AOX ]] on reduction of the nitroimino group and by CYPs via oxidation reactions.",2791,5
2792,"Currently, the most important insecticides are << neonicotinoids >>, which are metabolized in vitro by AOX on reduction of the nitroimino group and by [[ CYPs ]] via oxidation reactions.",2792,5
2793,"Currently, the most important insecticides are neonicotinoids, which are metabolized in vitro by << AOX >> on reduction of the [[ nitroimino ]] group and by CYPs via oxidation reactions.",2793,5
2794,The procedure was to reduce liver << AOX >> activity by providing [[ tungsten ]] or hydralazine in the drinking water or to use the AOX-deficient DBA/2 mouse strain.,2794,0
2795,The procedure was to reduce liver << AOX >> activity by providing tungsten or [[ hydralazine ]] in the drinking water or to use the AOX-deficient DBA/2 mouse strain.,2795,0
2796,Liver << AOX >> activity was reduced by 45% with [[ tungsten ]] and 61% with hydralazine and 81% in AOX-deficient mice relative to controls.,2796,0
2797,Liver << AOX >> activity was reduced by 45% with tungsten and 61% with [[ hydralazine ]] and 81% in AOX-deficient mice relative to controls.,2797,0
2798,"When mice were treated ip with the major neonicotinoid imidacloprid (IMI), metabolism by CYP oxidation reactions was not appreciably affected, whereas the << AOX >>-generated nitrosoguanidine metabolite was decreased by 30% with [[ tungsten ]] and 56% with hydralazine and 86% in the AOX-deficient mice.",2798,0
2799,"When mice were treated ip with the major neonicotinoid imidacloprid (IMI), metabolism by CYP oxidation reactions was not appreciably affected, whereas the << AOX >>-generated nitrosoguanidine metabolite was decreased by 30% with tungsten and 56% with [[ hydralazine ]] and 86% in the AOX-deficient mice.",2799,0
2800,"When mice were treated ip with the major neonicotinoid imidacloprid (IMI), metabolism by CYP oxidation reactions was not appreciably affected, whereas the << AOX >>-generated [[ nitrosoguanidine ]] metabolite was decreased by 30% with tungsten and 56% with hydralazine and 86% in the AOX-deficient mice.",2800,4
2801,"Thus, decreasing liver << AOX >> activity by three quite different procedures gave a corresponding decrease for in vivo reductive metabolites in the liver of [[ IMI ]]-treated mice.",2801,5
2802,"Possible << AOX >> involvement in [[ IMI ]] metabolism in insects was evaluated using AOX-expressing and AOX-deficient Drosophila, but no differences were found in IMI nitroreduction or sensitivity between the two strains.",2802,5
2803,"Possible AOX involvement in << IMI >> metabolism in insects was evaluated using [[ AOX ]]-expressing and AOX-deficient Drosophila, but no differences were found in IMI nitroreduction or sensitivity between the two strains.",2803,5
2804,This is the first study to establish the in vivo relevance of << AOX >> in [[ neonicotinoid ]] metabolism in mammals and one of the first for xenobiotics in general.,2804,5
2805,Recommended management may include use of << acetylcholinesterase >> inhibitors (e.g. [[ neostigmine ]]) and wound care on a case-by-case basis.,2805,0
2806,"Of the compounds active in the present assay system, the most potent compound 7, << platyphyllonol-5-O-β-d-xylopyranoside >>, significantly suppressed the induction of peroxisome proliferator activated receptor γ (PPARγ and [[ CCAAT/enhancer binding protein α ]] (C/EBPα) protein expression, and inhibited adipocyte differentiation induced by troglitazone, a PPARγ agonist.",2806,8
2807,"Of the compounds active in the present assay system, the most potent compound 7, << platyphyllonol-5-O-β-d-xylopyranoside >>, significantly suppressed the induction of peroxisome proliferator activated receptor γ (PPARγ and CCAAT/enhancer binding protein α ([[ C/EBPα ]]) protein expression, and inhibited adipocyte differentiation induced by troglitazone, a PPARγ agonist.",2807,8
2808,"Of the compounds active in the present assay system, the most potent compound 7, << platyphyllonol-5-O-β-d-xylopyranoside >>, significantly suppressed the induction of [[ peroxisome proliferator activated receptor γ ]] (PPARγ and CCAAT/enhancer binding protein α (C/EBPα) protein expression, and inhibited adipocyte differentiation induced by troglitazone, a PPARγ agonist.",2808,8
2809,"Of the compounds active in the present assay system, the most potent compound 7, << platyphyllonol-5-O-β-d-xylopyranoside >>, significantly suppressed the induction of peroxisome proliferator activated receptor γ ([[ PPARγ ]] and CCAAT/enhancer binding protein α (C/EBPα) protein expression, and inhibited adipocyte differentiation induced by troglitazone, a PPARγ agonist.",2809,8
2810,"Of the compounds active in the present assay system, the most potent compound 7, platyphyllonol-5-O-β-d-xylopyranoside, significantly suppressed the induction of peroxisome proliferator activated receptor γ (PPARγ and CCAAT/enhancer binding protein α (C/EBPα) protein expression, and inhibited adipocyte differentiation induced by << troglitazone >>, a [[ PPARγ ]] agonist.",2810,2
2811,<< Benzenesulfonamides >>: a unique class of [[ chemokine receptor type 4 ]] inhibitors.,2811,0
2812,"Based on our previously published work on CXCR4 antagonists, we have synthesized a series of << aryl sulfonamides >> that inhibit the [[ CXCR4 ]]/CXCL12 interaction.",2812,0
2813,"Based on our previously published work on CXCR4 antagonists, we have synthesized a series of << aryl sulfonamides >> that inhibit the CXCR4/[[ CXCL12 ]] interaction.",2813,0
2814,These data demonstrate that << benzenesulfonamides >> are a unique class of [[ CXCR4 ]] inhibitors with high potency.,2814,0
2815,Measurement of Transport Activities of << 3β-Hydroxy-Δ(5)-bile Acids >> in [[ Bile Salt Export Pump ]] and Multidrug Resistance-Associated Proteins Using LC-MS/MS.,2815,5
2816,Measurement of Transport Activities of << 3β-Hydroxy-Δ(5)-bile Acids >> in Bile Salt Export Pump and [[ Multidrug Resistance-Associated Proteins ]] Using LC-MS/MS.,2816,5
2817,"The analytical method was applied to measurements of transport activities in membrane vesicles obtained from human multidrug resistance-associated protein 2-, 3-, and << human bile salt export pump >>-expressing Sf9 cells for conjugated [[ 3β-hydroxy-Δ(5)-bile acids ]].",2817,5
2818,The present study demonstrated that << human multidrug resistance-associated protein 3 >> vesicles accepted conjugated [[ 3β-hydroxy-Δ(5)-bile acids ]] along with common bile acids such as glycocholic acid and taurolithocholic acid 3-sulfate.,2818,5
2819,The present study demonstrated that << human multidrug resistance-associated protein 3 >> vesicles accepted conjugated 3β-hydroxy-Δ(5)-bile acids along with common [[ bile acids ]] such as glycocholic acid and taurolithocholic acid 3-sulfate.,2819,5
2820,The present study demonstrated that << human multidrug resistance-associated protein 3 >> vesicles accepted conjugated 3β-hydroxy-Δ(5)-bile acids along with common bile acids such as [[ glycocholic acid ]] and taurolithocholic acid 3-sulfate.,2820,5
2821,The present study demonstrated that << human multidrug resistance-associated protein 3 >> vesicles accepted conjugated 3β-hydroxy-Δ(5)-bile acids along with common bile acids such as glycocholic acid and [[ taurolithocholic acid 3-sulfate ]].,2821,5
2822,"Synthesis and evaluation of << 3-(benzylthio)-5-(1H-indol-3-yl)-1,2,4-triazol-4-amines >> as [[ Bcl-2 ]] inhibitory anticancer agents.",2822,0
2823,"A series of substituted << 3-(benzylthio)-5-(1H-indol-3-yl)-4H-1,2,4-triazol-4-amines >> has been synthesised and tested in vitro as potential pro-apoptotic [[ Bcl-2 ]]-inhibitory anticancer agents.",2823,0
2824,"Active compounds, such as the << nitrobenzyl >> analogue 6c, were found to exhibit sub-micromolar IC50 values in [[ Bcl-2 ]] expressing human cancer cell lines.",2824,0
2825,"<< Glutathione-S-transferase >>, a phase II enzyme, was inhibited by both [[ arsenic ]] and nicotine but no such inhibition was noted in arsenic-treated animals pre-exposed to nicotine.",2825,0
2826,"<< Glutathione-S-transferase >>, a phase II enzyme, was inhibited by both arsenic and [[ nicotine ]] but no such inhibition was noted in arsenic-treated animals pre-exposed to nicotine.",2826,0
2827,"Upon << nicotine >> pre-exposure, brain [[ acetylcholinesterase ]] increased, while monoamine oxidase (MAO) decreased.",2827,7
2828,"Upon << nicotine >> pre-exposure, brain acetylcholinesterase increased, while [[ monoamine oxidase ]] (MAO) decreased.",2828,3
2829,"Upon << nicotine >> pre-exposure, brain acetylcholinesterase increased, while monoamine oxidase ([[ MAO ]]) decreased.",2829,3
2830,The toxic effects of << MAO >> significantly attenuated with [[ nicotine ]] pre-exposure.,2830,3
2831,"We developed a computational model of the hypothalamic-pituitary-gonadal (HPG) axis in female fathead minnows to predict dose-response and time-course (DRTC) behaviors for endocrine effects of the << aromatase >> inhibitor, [[ fadrozole ]] (FAD).",2831,0
2832,"We developed a computational model of the hypothalamic-pituitary-gonadal (HPG) axis in female fathead minnows to predict dose-response and time-course (DRTC) behaviors for endocrine effects of the << aromatase >> inhibitor, fadrozole ([[ FAD ]]).",2832,0
2833,"Although naturally occurring electrophilic plant compounds, such as mustard oil and << cinnamaldehyde >>, are [[ TRPA1 ]] agonists, it is unknown whether arthropod-produced electrophiles activate mammalian TRPA1.",2833,2
2834,We found that << pBQN >> activates [[ TRPA1 ]] starting at 10 nM and peaking at 300 nM; higher concentrations caused rapid activation followed by a fast decline.,2834,9
2835,"Interestingly, following pBQN desensitization, wild-type TRPA1 had dramatically reduced response to the nonelectrophile agonist << carvacrol >>, whereas the triple cysteine mutant [[ TRPA1 ]] retained its full response.",2835,10
2836,"Interestingly, following pBQN desensitization, wild-type << TRPA1 >> had dramatically reduced response to the nonelectrophile agonist [[ carvacrol ]], whereas the triple cysteine mutant TRPA1 retained its full response.",2836,2
2837,Synthesis and in-silico studies of some << diaryltriazole >> derivatives as potential [[ cyclooxygenase ]] inhibitors.,2837,0
2838,A highly potent inhibition of the << peroxidase >> catalytic reaction by [[ NO ]]/SNO was seen in assays employing the coupled Prx-Trx system.,2838,0
2839,A highly potent inhibition of the << peroxidase >> catalytic reaction by NO/[[ SNO ]] was seen in assays employing the coupled Prx-Trx system.,2839,0
2840,"In this setting, << S-nitrosocysteine >> (10 μm) effectively blocked the [[ Trx ]]-mediated regeneration of oxidized Prx1.",2840,0
2841,"In this setting, << S-nitrosocysteine >> (10 μm) effectively blocked the Trx-mediated regeneration of [[ oxidized Prx1 ]].",2841,0
2842,"CK significantly inhibited << DMN >>-induced increases in serum [[ alanine aminotransferase ]] (ALT) and aspartate aminotransferase (AST) activities, fibrosis score, and hepatic malondialdehyde and collagen content.",2842,9
2843,"CK significantly inhibited << DMN >>-induced increases in serum alanine aminotransferase ([[ ALT ]]) and aspartate aminotransferase (AST) activities, fibrosis score, and hepatic malondialdehyde and collagen content.",2843,9
2844,"CK significantly inhibited << DMN >>-induced increases in serum alanine aminotransferase (ALT) and [[ aspartate aminotransferase ]] (AST) activities, fibrosis score, and hepatic malondialdehyde and collagen content.",2844,9
2845,"CK significantly inhibited << DMN >>-induced increases in serum alanine aminotransferase (ALT) and aspartate aminotransferase ([[ AST ]]) activities, fibrosis score, and hepatic malondialdehyde and collagen content.",2845,9
2846,"CK significantly inhibited << DMN >>-induced increases in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, fibrosis score, and hepatic malondialdehyde and [[ collagen ]] content.",2846,6
2847,"Reverse transcription polymerase chain reaction (RT-PCR) and western blot analyses revealed that CK inhibited << DMN >>-induced increases in [[ matrix metalloproteinase-13 ]] (MMP-13), tissue inhibitor of metalloproteinase-1 (TIMP-1), and tumor necrosis factor-α (TNF-α) mRNA, and collagen type I and α-smooth muscle actin protein.",2847,6
2848,"Reverse transcription polymerase chain reaction (RT-PCR) and western blot analyses revealed that CK inhibited << DMN >>-induced increases in matrix metalloproteinase-13 ([[ MMP-13 ]]), tissue inhibitor of metalloproteinase-1 (TIMP-1), and tumor necrosis factor-α (TNF-α) mRNA, and collagen type I and α-smooth muscle actin protein.",2848,6
2849,"Reverse transcription polymerase chain reaction (RT-PCR) and western blot analyses revealed that CK inhibited << DMN >>-induced increases in matrix metalloproteinase-13 (MMP-13), [[ tissue inhibitor of metalloproteinase-1 ]] (TIMP-1), and tumor necrosis factor-α (TNF-α) mRNA, and collagen type I and α-smooth muscle actin protein.",2849,6
2850,"Reverse transcription polymerase chain reaction (RT-PCR) and western blot analyses revealed that CK inhibited << DMN >>-induced increases in matrix metalloproteinase-13 (MMP-13), tissue inhibitor of metalloproteinase-1 ([[ TIMP-1 ]]), and tumor necrosis factor-α (TNF-α) mRNA, and collagen type I and α-smooth muscle actin protein.",2850,6
2851,"Reverse transcription polymerase chain reaction (RT-PCR) and western blot analyses revealed that CK inhibited << DMN >>-induced increases in matrix metalloproteinase-13 (MMP-13), tissue inhibitor of metalloproteinase-1 (TIMP-1), and [[ tumor necrosis factor-α ]] (TNF-α) mRNA, and collagen type I and α-smooth muscle actin protein.",2851,6
2852,"Reverse transcription polymerase chain reaction (RT-PCR) and western blot analyses revealed that CK inhibited << DMN >>-induced increases in matrix metalloproteinase-13 (MMP-13), tissue inhibitor of metalloproteinase-1 (TIMP-1), and tumor necrosis factor-α ([[ TNF-α ]]) mRNA, and collagen type I and α-smooth muscle actin protein.",2852,6
2853,"Reverse transcription polymerase chain reaction (RT-PCR) and western blot analyses revealed that CK inhibited << DMN >>-induced increases in matrix metalloproteinase-13 (MMP-13), tissue inhibitor of metalloproteinase-1 (TIMP-1), and tumor necrosis factor-α (TNF-α) mRNA, and [[ collagen type I ]] and α-smooth muscle actin protein.",2853,6
2854,"Reverse transcription polymerase chain reaction (RT-PCR) and western blot analyses revealed that CK inhibited << DMN >>-induced increases in matrix metalloproteinase-13 (MMP-13), tissue inhibitor of metalloproteinase-1 (TIMP-1), and tumor necrosis factor-α (TNF-α) mRNA, and collagen type I and [[ α-smooth muscle actin ]] protein.",2854,6
2855,<< DMN >>-induced cyclooxygenase-2 (COX-2) expression and [[ nuclear factor-kappa B ]] (NF-κB) activation was reduced by CK treatment.,2855,9
2856,<< DMN >>-induced cyclooxygenase-2 (COX-2) expression and nuclear factor-kappa B ([[ NF-κB ]]) activation was reduced by CK treatment.,2856,9
2857,<< DMN >>-induced [[ cyclooxygenase-2 ]] (COX-2) expression and nuclear factor-kappa B (NF-κB) activation was reduced by CK treatment.,2857,6
2858,<< DMN >>-induced cyclooxygenase-2 ([[ COX-2 ]]) expression and nuclear factor-kappa B (NF-κB) activation was reduced by CK treatment.,2858,6
2859,Extrinsic apoptotic pathway markers such as Fas levels and << caspase-8 >> activity increased as a result of [[ CdTe ]]-QD exposure.,2859,9
2860,Extrinsic apoptotic pathway markers such as << Fas >> levels and caspase-8 activity increased as a result of [[ CdTe ]]-QD exposure.,2860,6
2861,"Our findings reveal that << CdTe >>-QDs cause oxidative stress, interfere with antioxidant defenses and activate protein [[ kinases ]], leading to apoptosis via both extrinsic and intrinsic pathways.",2861,9
2862,"<< Puerarin >> administration enhanced glutathione (GSH) activity, glial cell line-derived neurotrophic factor (GDNF) expression and [[ PI3K ]]/Akt pathway activation, which might ameliorate MPTP injection-induced progressive elevation of reactive oxygen species (ROS) formation in mice.",2862,9
2863,"<< Puerarin >> administration enhanced glutathione (GSH) activity, glial cell line-derived neurotrophic factor (GDNF) expression and PI3K/[[ Akt ]] pathway activation, which might ameliorate MPTP injection-induced progressive elevation of reactive oxygen species (ROS) formation in mice.",2863,9
2864,"<< Puerarin >> administration enhanced glutathione (GSH) activity, [[ glial cell line-derived neurotrophic factor ]] (GDNF) expression and PI3K/Akt pathway activation, which might ameliorate MPTP injection-induced progressive elevation of reactive oxygen species (ROS) formation in mice.",2864,6
2865,"<< Puerarin >> administration enhanced glutathione (GSH) activity, glial cell line-derived neurotrophic factor ([[ GDNF ]]) expression and PI3K/Akt pathway activation, which might ameliorate MPTP injection-induced progressive elevation of reactive oxygen species (ROS) formation in mice.",2865,6
2866,"In addition to the effect on ROS, << puerarin >> ameliorated MPTP-reduced lysosome-associated membrane protein type 2A ([[ Lamp 2A ]]) expression.",2866,8
2867,"In addition to the effect on ROS, puerarin ameliorated << MPTP >>-reduced [[ lysosome-associated membrane protein type 2A ]] (Lamp 2A) expression.",2867,8
2868,"In addition to the effect on ROS, puerarin ameliorated << MPTP >>-reduced lysosome-associated membrane protein type 2A ([[ Lamp 2A ]]) expression.",2868,8
2869,"Taken together, our data demonstrate that << puerarin >> attenuates MPTP-induced dopaminergic neuronal degeneration via modulating GDNF expression, PI3K/Akt pathway and GSH activation, which subsequently ameliorate MPTP-induced ROS formation and decrease of [[ Lamp 2A ]] expression.",2869,8
2870,"Taken together, our data demonstrate that puerarin attenuates MPTP-induced dopaminergic neuronal degeneration via modulating GDNF expression, PI3K/Akt pathway and GSH activation, which subsequently ameliorate << MPTP >>-induced ROS formation and decrease of [[ Lamp 2A ]] expression.",2870,8
2871,"Instead, radiolabeled << nucleosides >> resulting from [[ nuclease ]] hydrolysis were observed.",2871,4
2872,A series of N-substituted lobelane analogues was synthesized and evaluated for their [(3)H]dihydrotetrabenazine binding affinity at the << vesicular monoamine transporter >> and for their inhibition of vesicular [[ [(3)H]dopamine ]] uptake.,2872,5
2873,<< IPI-926 >> is both a substrate and inhibitor (IC50 = 1.9 µM) of [[ P-glycoprotein ]].,2873,0
2874,<< IPI-926 >> is both a substrate and inhibitor (IC50 = 1.9 µM) of [[ P-glycoprotein ]].,2874,5
2875,"Oral << lorcaserin >> (BELVIQ(®)), a selective serotonin [[ 5-HT2C ]] receptor agonist, is indicated in the US as an adjunct to diet and exercise in the chronic weight management of obese adults, or overweight adults with at least one weight-related comorbidity (e.g. dyslipidaemia, hypertension, type 2 diabetes).",2875,2
2876,"Oral lorcaserin (<< BELVIQ >>(®)), a selective serotonin [[ 5-HT2C ]] receptor agonist, is indicated in the US as an adjunct to diet and exercise in the chronic weight management of obese adults, or overweight adults with at least one weight-related comorbidity (e.g. dyslipidaemia, hypertension, type 2 diabetes).",2876,2
2877,"Design, Synthesis, Biological Evaluation, and Docking Studies of (S)-Phenylalanine Derivatives with a << 2-Cyanopyrrolidine >> Moiety as Potent [[ Dipeptidyl Peptidase 4 ]] Inhibitors.",2877,0
2878,"Design, Synthesis, Biological Evaluation, and Docking Studies of << (S)-Phenylalanine >> Derivatives with a 2-Cyanopyrrolidine Moiety as Potent [[ Dipeptidyl Peptidase 4 ]] Inhibitors.",2878,0
2879,"Biological evaluation revealed that most tested compounds were potent dipeptidyl peptidase 4 (DPP-4) inhibitors, among them, the << cyclopropyl-substituted phenylalanine >> derivative 11h displayed the most potent [[ DPP-4 ]] inhibitory activity with an IC50 value of 0.247 μM.",2879,0
2880,"<< TCPOBOP >>, a CAR ligand, modestly induced [[ mdr1a ]].fLUC in pxr(+/+) and pxr(-/-) strains, consistent with CAR's minor role in mdr1a regulation.",2880,6
2881,"<< Galangin >> decreased expression of pro-inflammatory [[ cytokines ]], such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, and IL-8.",2881,8
2882,"<< Galangin >> decreased expression of pro-inflammatory cytokines, such as [[ tumor necrosis factor (TNF)-α ]], interleukin (IL)-6, IL-1β, and IL-8.",2882,8
2883,"<< Galangin >> decreased expression of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, [[ interleukin ]] (IL)-6, IL-1β, and IL-8.",2883,8
2884,"<< Galangin >> decreased expression of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin [[ (IL)-6 ]], IL-1β, and IL-8.",2884,8
2885,"<< Galangin >> decreased expression of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, [[ IL-1β ]], and IL-8.",2885,8
2886,"<< Galangin >> decreased expression of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, and [[ IL-8 ]].",2886,8
2887,"The inhibitory effect of << galangin >> on theses pro-inflammatory [[ cytokines ]] was related with c-Jun N-terminal kinases, and p38 mitogen-activated protein kinase, nuclear factor-κB, and caspase-1.",2887,8
2888,"Furthermore, << galangin >> attenuated [[ IgE ]]-mediated passive cutaneous anaphylaxis and the expression of histamine receptor 1 at the inflamed tissue.",2888,3
2889,"Furthermore, << galangin >> attenuated IgE-mediated passive cutaneous anaphylaxis and the expression of [[ histamine receptor 1 ]] at the inflamed tissue.",2889,8
2890,Our results showed that << galangin >> down-regulates mast cell-derived allergic inflammatory reactions by blocking histamine release and expression of pro-inflammatory [[ cytokines ]].,2890,8
2891,<< Nobiletin >> attenuates metastasis via both [[ ERK ]] and PI3K/Akt pathways in HGF-treated liver cancer HepG2 cells.,2891,0
2892,<< Nobiletin >> attenuates metastasis via both ERK and [[ PI3K ]]/Akt pathways in HGF-treated liver cancer HepG2 cells.,2892,0
2893,<< Nobiletin >> attenuates metastasis via both ERK and PI3K/[[ Akt ]] pathways in HGF-treated liver cancer HepG2 cells.,2893,0
2894,"Among them, << nobiletin >> markedly inhibited [[ HGF ]]-induced the abilities of the adhesion, invasion, and migration by cell-matrix adhesion assay and transwell-chamber invasion/migration assay under non-cytotoxic concentrations.",2894,0
2895,Data also showed << nobiletin >> inhibited [[ HGF ]]-induced cell scattering and cytoskeleton changed such as filopodia and lamellipodia.,2895,0
2896,"Furthermore, << nobiletin >> could inhibit [[ HGF ]]-induced the membrane localization of phosphorylated c-Met, ERK2, and Akt, but not phosphorylated JNK1/2 and p38.",2896,0
2897,"Furthermore, << nobiletin >> could inhibit HGF-induced the membrane localization of phosphorylated [[ c-Met ]], ERK2, and Akt, but not phosphorylated JNK1/2 and p38.",2897,0
2898,"Furthermore, << nobiletin >> could inhibit HGF-induced the membrane localization of phosphorylated c-Met, [[ ERK2 ]], and Akt, but not phosphorylated JNK1/2 and p38.",2898,0
2899,"Furthermore, << nobiletin >> could inhibit HGF-induced the membrane localization of phosphorylated c-Met, ERK2, and [[ Akt ]], but not phosphorylated JNK1/2 and p38.",2899,0
2900,"Next, << nobiletin >> significantly decreased the levels of [[ phospho-ERK2 ]] and phospho-Akt in ERK2 or Akt siRNA-transfected cells concomitantly with a marked reduction on cell invasion and migration.",2900,8
2901,"Next, << nobiletin >> significantly decreased the levels of phospho-ERK2 and [[ phospho-Akt ]] in ERK2 or Akt siRNA-transfected cells concomitantly with a marked reduction on cell invasion and migration.",2901,8
2902,"Next, << nobiletin >> significantly decreased the levels of phospho-ERK2 and phospho-Akt in [[ ERK2 ]] or Akt siRNA-transfected cells concomitantly with a marked reduction on cell invasion and migration.",2902,8
2903,"Next, << nobiletin >> significantly decreased the levels of phospho-ERK2 and phospho-Akt in ERK2 or [[ Akt ]] siRNA-transfected cells concomitantly with a marked reduction on cell invasion and migration.",2903,8
2904,"In conclusion, << nobiletin >> attenuates [[ HGF ]]-induced HepG2 cells metastasis involving both ERK and PI3K/Akt pathways and are potentially useful as anti-metastatic agents for the treatment of hepatoma.",2904,0
2905,"In conclusion, << nobiletin >> attenuates HGF-induced HepG2 cells metastasis involving both [[ ERK ]] and PI3K/Akt pathways and are potentially useful as anti-metastatic agents for the treatment of hepatoma.",2905,0
2906,"In conclusion, << nobiletin >> attenuates HGF-induced HepG2 cells metastasis involving both ERK and [[ PI3K ]]/Akt pathways and are potentially useful as anti-metastatic agents for the treatment of hepatoma.",2906,0
2907,"In conclusion, << nobiletin >> attenuates HGF-induced HepG2 cells metastasis involving both ERK and PI3K/[[ Akt ]] pathways and are potentially useful as anti-metastatic agents for the treatment of hepatoma.",2907,0
2908,<< Cholesterol >> also increases [[ Amyloid β ]] (Aβ) deposition and tau pathology.,2908,3
2909,<< Cholesterol >> also increases Amyloid β ([[ Aβ ]]) deposition and tau pathology.,2909,3
2910,<< Cholesterol >> also increases Amyloid β (Aβ) deposition and [[ tau ]] pathology.,2910,3
2911,Excess of << cholesterol >> converted into 24OHC may up-regulate [[ ApoE ]] synthesis which is a scavenger for Aβ and Tau.,2911,6
2912,Excess of cholesterol converted into << 24OHC >> may up-regulate [[ ApoE ]] synthesis which is a scavenger for Aβ and Tau.,2912,6
2913,"In the current study, we extend these findings to show that the ability of astrocytes to buffer extracellular << glutamate >> is reduced when [[ CaMKII ]] is inhibited.",2913,5
2914,<< 3-Hydroxypyridin-2-thione >> as Novel Zinc Binding Group for Selective [[ Histone Deacetylase ]] Inhibition.,2914,0
2915,3-Hydroxypyridin-2-thione as Novel << Zinc >> Binding Group for Selective [[ Histone Deacetylase ]] Inhibition.,2915,0
2916,Small molecules bearing hydroxamic acid as the << zinc >> binding group (ZBG) have been the most effective [[ histone deacetylase ]] inhibitors (HDACi) to date.,2916,0
2917,Small molecules bearing hydroxamic acid as the << zinc >> binding group (ZBG) have been the most effective histone deacetylase inhibitors ([[ HDAC ]]i) to date.,2917,0
2918,We have identified << 3-hydroxypyridin-2-thione >> (3-HPT) as a novel ZBG that is compatible with [[ HDAC ]] inhibition.,2918,0
2919,We have identified 3-hydroxypyridin-2-thione (<< 3-HPT >>) as a novel ZBG that is compatible with [[ HDAC ]] inhibition.,2919,0
2920,"<< 3-HPT >> inhibits [[ HDAC 6 ]] and HDAC 8 with an IC50 of 681 and 3675 nM, respectively.",2920,0
2921,"<< 3-HPT >> inhibits HDAC 6 and [[ HDAC 8 ]] with an IC50 of 681 and 3675 nM, respectively.",2921,0
2922,Subsequent optimization led to several novel << 3HPT >>-based [[ HDAC ]]i that are selective for HDAC 6 and HDAC 8.,2922,0
2923,Subsequent optimization led to several novel << 3HPT >>-based HDACi that are selective for [[ HDAC 6 ]] and HDAC 8.,2923,0
2924,Subsequent optimization led to several novel << 3HPT >>-based HDACi that are selective for HDAC 6 and [[ HDAC 8 ]].,2924,0
2925,Maqui berry (Aristotelia chilensis) and the constituent << delphinidin glycoside >> inhibit [[ photoreceptor ]] cell death induced by visible light.,2925,9
2926,"These findings indicate that MBE and its << anthocyanidins >> suppress the light-induced photoreceptor cell death by inhibiting ROS production, suggesting that the inhibition of [[ phosphorylated-p38 ]] may be involved in the underlying mechanism.",2926,0
2927,"Moreover, << curcumin >> could also down-regulate the expression and activity of [[ matrix metalloproteinase-9 ]] (MMP-9).",2927,8
2928,"Moreover, << curcumin >> could also down-regulate the expression and activity of matrix metalloproteinase-9 ([[ MMP-9 ]]).",2928,8
2929,"Moreover, << curcumin >> could also down-regulate the expression and activity of [[ matrix metalloproteinase-9 ]] (MMP-9).",2929,0
2930,"Moreover, << curcumin >> could also down-regulate the expression and activity of matrix metalloproteinase-9 ([[ MMP-9 ]]).",2930,0
2931,"Treatment with << EVn-50 >> or VB1 resulted in arresting the MDA-MB-435 and SMMC-7721 cells at G2/M phase, which was further supported by observations of increased phosphorylation of [[ Histone 3 ]] at Ser10, phosphorylation of Cdk1 at Tyr15, expression of cyclin B1, and decreased expression of Cdc25c.",2931,9
2932,"Treatment with << EVn-50 >> or VB1 resulted in arresting the MDA-MB-435 and SMMC-7721 cells at G2/M phase, which was further supported by observations of increased phosphorylation of Histone 3 at Ser10, phosphorylation of [[ Cdk1 ]] at Tyr15, expression of cyclin B1, and decreased expression of Cdc25c.",2932,9
2933,"Treatment with EVn-50 or << VB1 >> resulted in arresting the MDA-MB-435 and SMMC-7721 cells at G2/M phase, which was further supported by observations of increased phosphorylation of [[ Histone 3 ]] at Ser10, phosphorylation of Cdk1 at Tyr15, expression of cyclin B1, and decreased expression of Cdc25c.",2933,9
2934,"Treatment with EVn-50 or << VB1 >> resulted in arresting the MDA-MB-435 and SMMC-7721 cells at G2/M phase, which was further supported by observations of increased phosphorylation of Histone 3 at Ser10, phosphorylation of [[ Cdk1 ]] at Tyr15, expression of cyclin B1, and decreased expression of Cdc25c.",2934,9
2935,"Treatment with << EVn-50 >> or VB1 resulted in arresting the MDA-MB-435 and SMMC-7721 cells at G2/M phase, which was further supported by observations of increased phosphorylation of Histone 3 at Ser10, phosphorylation of Cdk1 at Tyr15, expression of [[ cyclin B1 ]], and decreased expression of Cdc25c.",2935,6
2936,"Treatment with EVn-50 or << VB1 >> resulted in arresting the MDA-MB-435 and SMMC-7721 cells at G2/M phase, which was further supported by observations of increased phosphorylation of Histone 3 at Ser10, phosphorylation of Cdk1 at Tyr15, expression of [[ cyclin B1 ]], and decreased expression of Cdc25c.",2936,6
2937,"Treatment with << EVn-50 >> or VB1 resulted in arresting the MDA-MB-435 and SMMC-7721 cells at G2/M phase, which was further supported by observations of increased phosphorylation of Histone 3 at Ser10, phosphorylation of Cdk1 at Tyr15, expression of cyclin B1, and decreased expression of [[ Cdc25c ]].",2937,8
2938,"Treatment with EVn-50 or << VB1 >> resulted in arresting the MDA-MB-435 and SMMC-7721 cells at G2/M phase, which was further supported by observations of increased phosphorylation of Histone 3 at Ser10, phosphorylation of Cdk1 at Tyr15, expression of cyclin B1, and decreased expression of [[ Cdc25c ]].",2938,8
2939,<< Xanthohumol >> and 2-hydroxychalcone induced apoptosis by [[ Bcl-2 ]] downregulation.,2939,8
2940,Xanthohumol and << 2-hydroxychalcone >> induced apoptosis by [[ Bcl-2 ]] downregulation.,2940,8
2941,"Importantly, << 2-hydroxychalcone >> and xanthohumol exerted more potent inhibitory effects on the proliferation, [[ MMP-9 ]] expression and invasive phenotype of MDA-MB-231 than chalcone.",2941,8
2942,"Importantly, 2-hydroxychalcone and << xanthohumol >> exerted more potent inhibitory effects on the proliferation, [[ MMP-9 ]] expression and invasive phenotype of MDA-MB-231 than chalcone.",2942,8
2943,"<< 4-Hydroxypyridazin-3(2H)-one >> Derivatives as Novel [[ d-Amino Acid Oxidase ]] Inhibitors. d-Amino acid oxidase (DAAO) catalyzes the oxidation of d-amino acids including d-serine, a coagonist of the N-methyl-d-aspartate receptor.",2943,0
2944,"4-Hydroxypyridazin-3(2H)-one Derivatives as Novel d-Amino Acid Oxidase Inhibitors. d-Amino acid oxidase (DAAO) catalyzes the oxidation of d-amino acids including << d-serine >>, a coagonist of the [[ N-methyl-d-aspartate receptor ]].",2944,2
2945,"4-Hydroxypyridazin-3(2H)-one Derivatives as Novel d-Amino Acid Oxidase Inhibitors. << d-Amino acid oxidase >> (DAAO) catalyzes the oxidation of d-amino acids including [[ d-serine ]], a coagonist of the N-methyl-d-aspartate receptor.",2945,5
2946,"4-Hydroxypyridazin-3(2H)-one Derivatives as Novel d-Amino Acid Oxidase Inhibitors. d-Amino acid oxidase (<< DAAO >>) catalyzes the oxidation of d-amino acids including [[ d-serine ]], a coagonist of the N-methyl-d-aspartate receptor.",2946,5
2947,"4-Hydroxypyridazin-3(2H)-one Derivatives as Novel d-Amino Acid Oxidase Inhibitors. << d-Amino acid oxidase >> (DAAO) catalyzes the oxidation of [[ d-amino acids ]] including d-serine, a coagonist of the N-methyl-d-aspartate receptor.",2947,5
2948,"4-Hydroxypyridazin-3(2H)-one Derivatives as Novel d-Amino Acid Oxidase Inhibitors. d-Amino acid oxidase (<< DAAO >>) catalyzes the oxidation of [[ d-amino acids ]] including d-serine, a coagonist of the N-methyl-d-aspartate receptor.",2948,5
2949,We identified a series of << 4-hydroxypyridazin-3(2H)-one >> derivatives as novel [[ DAAO ]] inhibitors with high potency and substantial cell permeability using fragment-based drug design.,2949,0
2950,<< 3-Hydroxy-5-(2-phenylethyl)pyridine-2(1H)-one >> exhibited the predicted binding mode and demonstrated high inhibitory activity for [[ human DAAO ]] in enzyme- and cell-based assays.,2950,0
2951,"Fourteen of 17 << parabens >> exhibited [[ hERα ]] and/or hERβ agonistic activity at concentrations of ⩽1×10(-5)M, whereas none of the 17 parabens showed AR agonistic or antagonistic activity.",2951,2
2952,"Fourteen of 17 << parabens >> exhibited hERα and/or [[ hERβ ]] agonistic activity at concentrations of ⩽1×10(-5)M, whereas none of the 17 parabens showed AR agonistic or antagonistic activity.",2952,2
2953,"Among 12 parabens with linear alkyl chains ranging in length from C1 to C12, << heptylparaben >> (C7) and pentylparaben (C5) showed the most potent [[ ERα ]] and ERβ agonistic activity in the order of 10(-7)M and 10(-8)M, respectively, and the activities decreased in a stepwise manner as the alkyl chain was shortened to C1 or lengthened to C12.",2953,2
2954,"Among 12 parabens with linear alkyl chains ranging in length from C1 to C12, << heptylparaben >> (C7) and pentylparaben (C5) showed the most potent ERα and [[ ERβ ]] agonistic activity in the order of 10(-7)M and 10(-8)M, respectively, and the activities decreased in a stepwise manner as the alkyl chain was shortened to C1 or lengthened to C12.",2954,2
2955,"Among 12 parabens with linear alkyl chains ranging in length from C1 to C12, heptylparaben (C7) and << pentylparaben >> (C5) showed the most potent [[ ERα ]] and ERβ agonistic activity in the order of 10(-7)M and 10(-8)M, respectively, and the activities decreased in a stepwise manner as the alkyl chain was shortened to C1 or lengthened to C12.",2955,2
2956,"Among 12 parabens with linear alkyl chains ranging in length from C1 to C12, heptylparaben (C7) and << pentylparaben >> (C5) showed the most potent ERα and [[ ERβ ]] agonistic activity in the order of 10(-7)M and 10(-8)M, respectively, and the activities decreased in a stepwise manner as the alkyl chain was shortened to C1 or lengthened to C12.",2956,2
2957,"Among 12 << parabens >> with linear alkyl chains ranging in length from C1 to C12, heptylparaben (C7) and pentylparaben (C5) showed the most potent [[ ERα ]] and ERβ agonistic activity in the order of 10(-7)M and 10(-8)M, respectively, and the activities decreased in a stepwise manner as the alkyl chain was shortened to C1 or lengthened to C12.",2957,2
2958,"Among 12 << parabens >> with linear alkyl chains ranging in length from C1 to C12, heptylparaben (C7) and pentylparaben (C5) showed the most potent ERα and [[ ERβ ]] agonistic activity in the order of 10(-7)M and 10(-8)M, respectively, and the activities decreased in a stepwise manner as the alkyl chain was shortened to C1 or lengthened to C12.",2958,2
2959,"Among 12 parabens with linear << alkyl >> chains ranging in length from C1 to C12, heptylparaben (C7) and pentylparaben (C5) showed the most potent [[ ERα ]] and ERβ agonistic activity in the order of 10(-7)M and 10(-8)M, respectively, and the activities decreased in a stepwise manner as the alkyl chain was shortened to C1 or lengthened to C12.",2959,2
2960,"Among 12 parabens with linear << alkyl >> chains ranging in length from C1 to C12, heptylparaben (C7) and pentylparaben (C5) showed the most potent ERα and [[ ERβ ]] agonistic activity in the order of 10(-7)M and 10(-8)M, respectively, and the activities decreased in a stepwise manner as the alkyl chain was shortened to C1 or lengthened to C12.",2960,2
2961,Most << parabens >> showing estrogenic activity exhibited [[ ERβ ]]-agonistic activity at lower concentrations than those inducing ERα-agonistic activity.,2961,2
2962,Most << parabens >> showing estrogenic activity exhibited ERβ-agonistic activity at lower concentrations than those inducing [[ ERα ]]-agonistic activity.,2962,2
2963,"These results indicate that << parabens >> are selective agonists for [[ ERβ ]] over ERα; their interactions with ERα/β are dependent on the size and bulkiness of the alkyl groups; and they are metabolized by carboxylesterases, leading to attenuation of their estrogenic activity.",2963,2
2964,"These results indicate that << parabens >> are selective agonists for ERβ over [[ ERα ]]; their interactions with ERα/β are dependent on the size and bulkiness of the alkyl groups; and they are metabolized by carboxylesterases, leading to attenuation of their estrogenic activity.",2964,2
2965,"These results indicate that << parabens >> are selective agonists for ERβ over ERα; their interactions with ERα/β are dependent on the size and bulkiness of the alkyl groups; and they are metabolized by [[ carboxylesterases ]], leading to attenuation of their estrogenic activity.",2965,5
2966,Wattakaka volubilis << steroidal glycoside >> mixture (WVSM) and PPG (1-50μM) significantly inhibited the [[ COX-2 ]] and iNOS enzymes resulting in low levels of PGE2 and NO in LPS-induced RAW 264.7 macrophage cells.,2966,0
2967,Wattakaka volubilis << steroidal glycoside >> mixture (WVSM) and PPG (1-50μM) significantly inhibited the COX-2 and [[ iNOS ]] enzymes resulting in low levels of PGE2 and NO in LPS-induced RAW 264.7 macrophage cells.,2967,0
2968,Wattakaka volubilis steroidal glycoside mixture (WVSM) and << PPG >> (1-50μM) significantly inhibited the [[ COX-2 ]] and iNOS enzymes resulting in low levels of PGE2 and NO in LPS-induced RAW 264.7 macrophage cells.,2968,0
2969,Wattakaka volubilis steroidal glycoside mixture (WVSM) and << PPG >> (1-50μM) significantly inhibited the COX-2 and [[ iNOS ]] enzymes resulting in low levels of PGE2 and NO in LPS-induced RAW 264.7 macrophage cells.,2969,0
2970,<< Quercetin >> suppressed [[ CYP2E1 ]]-dependent ethanol hepatotoxicity via depleting heme pool and releasing CO.,2970,3
2971,"However, the precise mechanism by which << quercetin >> counteracts [[ CYP2E1 ]]-mediated ethanol hepatotoxicity through HO-1 system is still remained unclear.",2971,3
2972,"Our data showed that chronic << ethanol >> over-activated [[ CYP2E1 ]] but suppressed HO-1 with concurrent hepatic oxidative damage, which was partially normalized by quercetin (100mg/kg.bw.).",2972,9
2973,"Our data showed that chronic << ethanol >> over-activated CYP2E1 but suppressed [[ HO-1 ]] with concurrent hepatic oxidative damage, which was partially normalized by quercetin (100mg/kg.bw.).",2973,3
2974,<< Quercetin >> (100μM) induced [[ HO-1 ]] and depleted heme pool when incubated to human hepatocytes.,2974,7
2975,<< Ethanol >>-stimulated (100mM) [[ CYP2E1 ]] upregulation was suppressed by quercetin but further enhanced by HO-1 inhibition with resultant heme accumulation.,2975,7
2976,Ethanol-stimulated (100mM) << CYP2E1 >> upregulation was suppressed by [[ quercetin ]] but further enhanced by HO-1 inhibition with resultant heme accumulation.,2976,3
2977,<< Ethanol >>-stimulated (100mM) CYP2E1 upregulation was suppressed by quercetin but further enhanced by [[ HO-1 ]] inhibition with resultant heme accumulation.,2977,0
2978,Ethanol-stimulated (100mM) CYP2E1 upregulation was suppressed by quercetin but further enhanced by << HO-1 >> inhibition with resultant [[ heme ]] accumulation.,2978,5
2979,<< CO >> scavenging blocked the suppression of quercetin only on [[ CYP2E1 ]] activity.,2979,3
2980,"CO donor dose-dependently inactivated << CYP2E1 >> of [[ ethanol ]]-incubated microsome, which was mimicked by HO-1 substrate but abolished by CO scavenger.",2980,7
2981,"<< CO >> donor dose-dependently inactivated [[ CYP2E1 ]] of ethanol-incubated microsome, which was mimicked by HO-1 substrate but abolished by CO scavenger.",2981,3
2982,"CO donor dose-dependently inactivated << CYP2E1 >> of ethanol-incubated microsome, which was mimicked by HO-1 substrate but abolished by [[ CO ]] scavenger.",2982,3
2983,"Thus, CYP2E1-mediated ethanol hepatotoxicity was alleviated by << quercetin >> through [[ HO-1 ]] induction.",2983,7
2984,"Depleted heme pool and << CO >> releasing limited protein synthesis and inhibited enzymatic activity of [[ CYP2E1 ]], respectively.",2984,0
2985,Novel racemic << tetrahydrocurcuminoid dihydropyrimidinone >> analogues as potent [[ acetylcholinesterase ]] inhibitors.,2985,0
2986,Agonistic activity of << ICI 182 780 >> on activation of GSK 3β/[[ AKT ]] pathway in the rat uterus during the estrous cycle.,2986,9
2987,Agonistic activity of << ICI 182 780 >> on activation of [[ GSK 3β ]]/AKT pathway in the rat uterus during the estrous cycle.,2987,2
2988,"Both << ICI >> treatments, induced a significant decrease (p<0.01) in uterine [[ estrogen receptor alpha ]] (ERα) content, had no effect on uterine progesterone receptor (PR) protein expression and caused marked nuclear localization of cyclin D1, in both luminal and glandular uterine epithelium, as compared to vehicle-treated animals.",2988,8
2989,"Both << ICI >> treatments, induced a significant decrease (p<0.01) in uterine estrogen receptor alpha ([[ ERα ]]) content, had no effect on uterine progesterone receptor (PR) protein expression and caused marked nuclear localization of cyclin D1, in both luminal and glandular uterine epithelium, as compared to vehicle-treated animals.",2989,8
2990,"Furthermore, we detected that << ICI >> treatment induced [[ glycogen synthase kinase ]] (Gsk3-β) Ser 9 phosphorylation, which correlates with cyclin D1 nuclear localization.",2990,9
2991,"Furthermore, we detected that << ICI >> treatment induced glycogen synthase kinase ([[ Gsk3-β ]]) Ser 9 phosphorylation, which correlates with cyclin D1 nuclear localization.",2991,9
2992,"We observed that the administration of << ICI >> at 08:00h on proestrus day produced a 15% inhibition of luminal epithelial cell proliferation, reduced uterine wet weight by 21% and caused reduction of [[ Akt ]] phosphorylation at Ser 473 as compared to vehicle-treated animals, whereas ICI treatment at 00:00h on estrus day had no effect on these parameters.",2992,0
2993,"The overall results indicate that << ICI >> may exert agonistic and antagonistic effects on uterine cell proliferation through differential activation of the [[ Akt ]] pathway depending on the administration period during the estrous cycle, and indicates that the mechanism of cell proliferation during the physiological conditions of the estrous cycle, is under a different and more complex regulation than in the ovariectomized +E2 animal model.",2993,9
2994,<< Aminopropylindenes >> derived from Grundmann's ketone as a novel chemotype of [[ oxidosqualene cyclase ]] inhibitors.,2994,0
2995,Aminopropylindenes derived from << Grundmann's ketone >> as a novel chemotype of [[ oxidosqualene cyclase ]] inhibitors.,2995,0
2996,"A series of aminopropylindenes, designed as mimics of a cationic high energy intermediate in the oxidosqualene cyclase(1) (<< OSC >>)-mediated cyclization of 2,3-oxidosqualen to [[ lanosterol ]] was prepared from Grundmann's ketone.",2996,4
2997,"A series of aminopropylindenes, designed as mimics of a cationic high energy intermediate in the << oxidosqualene cyclase(1) >> (OSC)-mediated cyclization of 2,3-oxidosqualen to [[ lanosterol ]] was prepared from Grundmann's ketone.",2997,4
2998,"A series of aminopropylindenes, designed as mimics of a cationic high energy intermediate in the oxidosqualene cyclase(1) (<< OSC >>)-mediated cyclization of [[ 2,3-oxidosqualen ]] to lanosterol was prepared from Grundmann's ketone.",2998,5
2999,"A series of aminopropylindenes, designed as mimics of a cationic high energy intermediate in the << oxidosqualene cyclase(1) >> (OSC)-mediated cyclization of [[ 2,3-oxidosqualen ]] to lanosterol was prepared from Grundmann's ketone.",2999,5
3000,"A << N,N-dimethylaminopropyl >> derivative showed promising inhibition of [[ Trypanosoma cruzi OSC ]] in combination with low cytotoxicity, and showed significant reduction of cholesterol biosynthesis in a human cell line.",3000,0
3001,"A N,N-dimethylaminopropyl derivative showed promising inhibition of << Trypanosoma cruzi OSC >> in combination with low cytotoxicity, and showed significant reduction of [[ cholesterol ]] biosynthesis in a human cell line.",3001,4
3002,The << ATP >> required for potentiation of skeletal muscle contraction is released via [[ pannexin ]] hemichannels.,3002,5
3003,"During repetitive stimulation of skeletal muscle, extracellular << ATP >> levels raise, activating [[ purinergic receptors ]], increasing Ca(2+) influx, and enhancing contractile force, a response called potentiation.",3003,9
3004,"Consistent with two << glucose >> uptake pathways, induced uptake of 2-NBDG, a fluorescent glucose derivative, was decreased by inhibition of HCs or [[ glucose transporter ]] (GLUT4), and blocked by dual blockade.",3004,5
3005,"Consistent with two << glucose >> uptake pathways, induced uptake of 2-NBDG, a fluorescent glucose derivative, was decreased by inhibition of HCs or glucose transporter ([[ GLUT4 ]]), and blocked by dual blockade.",3005,5
3006,"Consistent with two glucose uptake pathways, induced uptake of << 2-NBDG >>, a fluorescent glucose derivative, was decreased by inhibition of HCs or [[ glucose transporter ]] (GLUT4), and blocked by dual blockade.",3006,5
3007,"Consistent with two glucose uptake pathways, induced uptake of << 2-NBDG >>, a fluorescent glucose derivative, was decreased by inhibition of HCs or glucose transporter ([[ GLUT4 ]]), and blocked by dual blockade.",3007,5
3008,"MRS2179, a P2Y1R blocker, prevented potentiation in EDL, but not soleus muscles, suggesting that in fast muscles << ATP >> activates [[ P2Y1 ]] but not P2X receptors.",3008,9
3009,"Opening of << Panx1 >> HCs during repetitive activation allows efflux of [[ ATP ]], influx of glucose and possibly Ca(2+) too, which are required for potentiation of contraction.",3009,5
3010,"Opening of << Panx1 >> HCs during repetitive activation allows efflux of ATP, influx of [[ glucose ]] and possibly Ca(2+) too, which are required for potentiation of contraction.",3010,5
3011,"Opening of << Panx1 >> HCs during repetitive activation allows efflux of ATP, influx of glucose and possibly [[ Ca(2+) ]] too, which are required for potentiation of contraction.",3011,5
3012,The rate limiting enzyme of beta-oxidation (<< ACOX1 >>) was significantly over-expressed in the liver with [[ tBHQ ]] treatment.,3012,6
3013,"These results indicate that << tBHQ >> suppresses body weight gain in mice, possibly at least related to the up-regulation of [[ ACOX1 ]] gene expression.",3013,6
3014,"When dual angiogenic growth factors (GFs), such as platelet-derived GF (PDGF) and vascular endothelial GF (VEGF), are encapsulated separately in the core and shell domains, respectively, the << VEGF >> release rate is much greater than that of PDGF, and the difference of the cumulative release percentage between the two GFs is about 30% on day 7 with LMW core [[ PLGA ]] and more than 45% with HMW core PLGA.",3014,6
3015,"When dual angiogenic growth factors (GFs), such as platelet-derived GF (PDGF) and vascular endothelial GF (VEGF), are encapsulated separately in the core and shell domains, respectively, the VEGF release rate is much greater than that of << PDGF >>, and the difference of the cumulative release percentage between the two GFs is about 30% on day 7 with LMW core [[ PLGA ]] and more than 45% with HMW core PLGA.",3015,6
3016,"When dual angiogenic growth factors (GFs), such as platelet-derived GF (PDGF) and vascular endothelial GF (VEGF), are encapsulated separately in the core and shell domains, respectively, the << VEGF >> release rate is much greater than that of PDGF, and the difference of the cumulative release percentage between the two GFs is about 30% on day 7 with LMW core PLGA and more than 45% with HMW core [[ PLGA ]].",3016,6
3017,"When dual angiogenic growth factors (GFs), such as platelet-derived GF (PDGF) and vascular endothelial GF (VEGF), are encapsulated separately in the core and shell domains, respectively, the VEGF release rate is much greater than that of << PDGF >>, and the difference of the cumulative release percentage between the two GFs is about 30% on day 7 with LMW core PLGA and more than 45% with HMW core [[ PLGA ]].",3017,6
3018,"Potency switch between CHK1 and << MK2 >>: Discovery of [[ imidazo[1,2-a]pyrazine ]]- and imidazo[1,2-c]pyrimidine-based kinase inhibitors.",3018,0
3019,"Potency switch between CHK1 and MK2: Discovery of << imidazo[1,2-a]pyrazine >>- and imidazo[1,2-c]pyrimidine-based [[ kinase ]] inhibitors.",3019,0
3020,"Potency switch between << CHK1 >> and MK2: Discovery of [[ imidazo[1,2-a]pyrazine ]]- and imidazo[1,2-c]pyrimidine-based kinase inhibitors.",3020,0
3021,"Potency switch between CHK1 and << MK2 >>: Discovery of imidazo[1,2-a]pyrazine- and [[ imidazo[1,2-c]pyrimidine ]]-based kinase inhibitors.",3021,0
3022,"Potency switch between CHK1 and MK2: Discovery of imidazo[1,2-a]pyrazine- and << imidazo[1,2-c]pyrimidine >>-based [[ kinase ]] inhibitors.",3022,0
3023,"Potency switch between << CHK1 >> and MK2: Discovery of imidazo[1,2-a]pyrazine- and [[ imidazo[1,2-c]pyrimidine ]]-based kinase inhibitors.",3023,0
3024,Discovery of << aryl ureas >> and aryl amides as potent and selective [[ histamine H3 receptor ]] antagonists for the treatment of obesity (Part I).,3024,1
3025,Discovery of aryl ureas and << aryl amides >> as potent and selective [[ histamine H3 receptor ]] antagonists for the treatment of obesity (Part I).,3025,1
3026,A series of structurally novel << aryl ureas >> was derived from optimization of the HTS lead as selective [[ histamine H3 receptor ]] (H3R) antagonists.,3026,1
3027,A series of structurally novel << aryl ureas >> was derived from optimization of the HTS lead as selective histamine H3 receptor ([[ H3R ]]) antagonists.,3027,1
3028,"In terms of the mechanisms, we found that fatty acid amide hydrolase (<< FAAH >>) which degrades [[ anandamide ]], was upregulated after nerve injury at both ages, so that this upregulation likely did not account for the age-dependent differences.",3028,5
3029,"In terms of the mechanisms, we found that << fatty acid amide hydrolase >> (FAAH) which degrades [[ anandamide ]], was upregulated after nerve injury at both ages, so that this upregulation likely did not account for the age-dependent differences.",3029,5
3030,"However, enzymes contributing to oxidative metabolism of << anandamide >>, namely [[ cyclooxygenase-1 ]] and Cyp2D6, were increased in the brain of aged mice, possibly enhancing the oxidative breakdown of anandamide.",3030,5
3031,"However, enzymes contributing to oxidative metabolism of << anandamide >>, namely cyclooxygenase-1 and [[ Cyp2D6 ]], were increased in the brain of aged mice, possibly enhancing the oxidative breakdown of anandamide.",3031,5
3032,"However, enzymes contributing to oxidative metabolism of anandamide, namely << cyclooxygenase-1 >> and Cyp2D6, were increased in the brain of aged mice, possibly enhancing the oxidative breakdown of [[ anandamide ]].",3032,5
3033,"However, enzymes contributing to oxidative metabolism of anandamide, namely cyclooxygenase-1 and << Cyp2D6 >>, were increased in the brain of aged mice, possibly enhancing the oxidative breakdown of [[ anandamide ]].",3033,5
3034,<< 24(S)-hydroxycholesterol >> is actively eliminated from neuronal cells by [[ ABCA1 ]].,3034,5
3035,"High << cholesterol >> turnover catalyzed by [[ cholesterol 24-hydroxylase ]] is essential for neural functions, especially learning.",3035,5
3036,"Because << 24(S)-hydroxycholesterol >> (24-OHC), produced by [[ 24-hydroxylase ]], induces apoptosis of neuronal cells, it is vital to eliminate it rapidly from cells.",3036,4
3037,"Because 24(S)-hydroxycholesterol (<< 24-OHC >>), produced by [[ 24-hydroxylase ]], induces apoptosis of neuronal cells, it is vital to eliminate it rapidly from cells.",3037,4
3038,"The expression of << ABCA1 >> and ABCG1 was induced by 24-OHC, as well as TO901317 and [[ retinoic acid ]], which are ligands of the nuclear receptors LXR/RXR.",3038,6
3039,"The expression of ABCA1 and << ABCG1 >> was induced by 24-OHC, as well as TO901317 and [[ retinoic acid ]], which are ligands of the nuclear receptors LXR/RXR.",3039,6
3040,"The expression of << ABCA1 >> and ABCG1 was induced by [[ 24-OHC ]], as well as TO901317 and retinoic acid, which are ligands of the nuclear receptors LXR/RXR.",3040,6
3041,"The expression of ABCA1 and << ABCG1 >> was induced by [[ 24-OHC ]], as well as TO901317 and retinoic acid, which are ligands of the nuclear receptors LXR/RXR.",3041,6
3042,"The expression of << ABCA1 >> and ABCG1 was induced by 24-OHC, as well as [[ TO901317 ]] and retinoic acid, which are ligands of the nuclear receptors LXR/RXR.",3042,6
3043,"The expression of ABCA1 and << ABCG1 >> was induced by 24-OHC, as well as [[ TO901317 ]] and retinoic acid, which are ligands of the nuclear receptors LXR/RXR.",3043,6
3044,"To confirm the role of each transporter, we analyzed HEK293 cells stably expressing << human ABCA1 >> or ABCG1; we clearly observed [[ 24-OHC ]] efflux in the presence of HDL, whereas efflux in the presence of apolipoprotein A-I was marginal.",3044,5
3045,"To confirm the role of each transporter, we analyzed HEK293 cells stably expressing human ABCA1 or << ABCG1 >>; we clearly observed [[ 24-OHC ]] efflux in the presence of HDL, whereas efflux in the presence of apolipoprotein A-I was marginal.",3045,5
3046,These results suggest that << ABCA1 >> actively eliminates [[ 24-OHC ]] in the presence of HDL as a lipid acceptor and protects neuronal cells.,3046,5
3047,The selective << CaMKIIα >> inhibitor [[ KN-62 ]] reversed the blockade produced by ionomycin and K(+)-depolarization.,3047,0
3048,The selective << CaMKIIα >> inhibitor KN-62 reversed the blockade produced by [[ ionomycin ]] and K(+)-depolarization.,3048,0
3049,"In K(+)-depolarized tissues, D3 receptors potentiated D1 receptor-induced stimulation of [(3)H]GABA release only when << CaMKIIα >> was blocked with [[ KN-62 ]].",3049,0
3050,"In the presence of this inhibitor, the selective << D3 >> agonist [[ PD 128,907 ]] reduced the ED50 for the D1 agonist SKF 38393 from 56 to 4 nM.",3050,2
3051,"In the presence of this inhibitor, the selective D3 agonist PD 128,907 reduced the ED50 for the << D1 >> agonist [[ SKF 38393 ]] from 56 to 4 nM.",3051,2
3052,The << Bcl2 >>/Bax ratio increased and Mfn2 expression decreased in MIN6 cells after [[ glucose ]] stimulation.,3052,6
3053,The Bcl2/<< Bax >> ratio increased and Mfn2 expression decreased in MIN6 cells after [[ glucose ]] stimulation.,3053,6
3054,The Bcl2/Bax ratio increased and << Mfn2 >> expression decreased in MIN6 cells after [[ glucose ]] stimulation.,3054,8
3055,"Additionally, treatment with << glucose >>/iron showed a higher [[ HO ]] activity.",3055,9
3056,"Additionally, treatment with glucose/<< iron >> showed a higher [[ HO ]] activity.",3056,9
3057,"Our study revealed that high << glucose >>/Fe concentrations in MIN6 cells induced an increase of the [[ Bcl2 ]]/Bax ratio, an indicator of increased cell apoptosis.",3057,6
3058,"Our study revealed that high << glucose >>/Fe concentrations in MIN6 cells induced an increase of the Bcl2/[[ Bax ]] ratio, an indicator of increased cell apoptosis.",3058,6
3059,"Our study revealed that high glucose/<< Fe >> concentrations in MIN6 cells induced an increase of the [[ Bcl2 ]]/Bax ratio, an indicator of increased cell apoptosis.",3059,6
3060,"Our study revealed that high glucose/<< Fe >> concentrations in MIN6 cells induced an increase of the Bcl2/[[ Bax ]] ratio, an indicator of increased cell apoptosis.",3060,6
3061,"This includes << nonribosomal peptide synthetases >> (NRPS) and polyketide synthases (PKS) required for the formation of the [[ benzopyranopyrrole ]] core unit, as well as a suite of tailoring enzymes (e.g., four halogenases, an O-methyltransferase, and an N-glycosyltransferase) necessary for further modifications of the core structure.",3061,4
3062,"This includes nonribosomal peptide synthetases (<< NRPS >>) and polyketide synthases (PKS) required for the formation of the [[ benzopyranopyrrole ]] core unit, as well as a suite of tailoring enzymes (e.g., four halogenases, an O-methyltransferase, and an N-glycosyltransferase) necessary for further modifications of the core structure.",3062,4
3063,"This includes nonribosomal peptide synthetases (NRPS) and << polyketide synthases >> (PKS) required for the formation of the [[ benzopyranopyrrole ]] core unit, as well as a suite of tailoring enzymes (e.g., four halogenases, an O-methyltransferase, and an N-glycosyltransferase) necessary for further modifications of the core structure.",3063,4
3064,"This includes nonribosomal peptide synthetases (NRPS) and polyketide synthases (<< PKS >>) required for the formation of the [[ benzopyranopyrrole ]] core unit, as well as a suite of tailoring enzymes (e.g., four halogenases, an O-methyltransferase, and an N-glycosyltransferase) necessary for further modifications of the core structure.",3064,4
3065,"This includes nonribosomal peptide synthetases (NRPS) and polyketide synthases (PKS) required for the formation of the << benzopyranopyrrole >> core unit, as well as a suite of tailoring enzymes (e.g., four [[ halogenases ]], an O-methyltransferase, and an N-glycosyltransferase) necessary for further modifications of the core structure.",3065,5
3066,"This includes nonribosomal peptide synthetases (NRPS) and polyketide synthases (PKS) required for the formation of the << benzopyranopyrrole >> core unit, as well as a suite of tailoring enzymes (e.g., four halogenases, an [[ O-methyltransferase ]], and an N-glycosyltransferase) necessary for further modifications of the core structure.",3066,5
3067,"This includes nonribosomal peptide synthetases (NRPS) and polyketide synthases (PKS) required for the formation of the << benzopyranopyrrole >> core unit, as well as a suite of tailoring enzymes (e.g., four halogenases, an O-methyltransferase, and an [[ N-glycosyltransferase ]]) necessary for further modifications of the core structure.",3067,5
3068,"Targeted disruption of the gene encoding the << N-glycosyltransferase >>, prlH, abolished [[ pyralomicin ]] production, and recombinant expression of PrlA confirms the activity of this enzyme as a sugar phosphate cyclase involved in the formation of the C7-cyclitol moiety.",3068,4
3069,"Targeted disruption of the gene encoding the N-glycosyltransferase, << prlH >>, abolished [[ pyralomicin ]] production, and recombinant expression of PrlA confirms the activity of this enzyme as a sugar phosphate cyclase involved in the formation of the C7-cyclitol moiety.",3069,4
3070,"Targeted disruption of the gene encoding the N-glycosyltransferase, prlH, abolished pyralomicin production, and recombinant expression of << PrlA >> confirms the activity of this enzyme as a sugar phosphate cyclase involved in the formation of the [[ C7 ]]-cyclitol moiety.",3070,4
3071,"Targeted disruption of the gene encoding the N-glycosyltransferase, prlH, abolished pyralomicin production, and recombinant expression of PrlA confirms the activity of this enzyme as a << sugar phosphate cyclase >> involved in the formation of the [[ C7 ]]-cyclitol moiety.",3071,4
3072,"Targeted disruption of the gene encoding the N-glycosyltransferase, prlH, abolished pyralomicin production, and recombinant expression of << PrlA >> confirms the activity of this enzyme as a sugar phosphate cyclase involved in the formation of the C7-[[ cyclitol ]] moiety.",3072,4
3073,"Targeted disruption of the gene encoding the N-glycosyltransferase, prlH, abolished pyralomicin production, and recombinant expression of PrlA confirms the activity of this enzyme as a << sugar phosphate cyclase >> involved in the formation of the C7-[[ cyclitol ]] moiety.",3073,4
3074,"To examine receptor mediation of estradiol effects, Ovx mice replaced for 2 days with either the << ERα >>-selective agonist [[ PPT ]] or the ERβ-selective agonist DPN were compared to Sham mice, and mice lacking either ERα (αERKO) or ERβ (βERKO) were compared to WT littermates.",3074,2
3075,"To examine receptor mediation of estradiol effects, Ovx mice replaced for 2 days with either the ERα-selective agonist PPT or the << ERβ >>-selective agonist [[ DPN ]] were compared to Sham mice, and mice lacking either ERα (αERKO) or ERβ (βERKO) were compared to WT littermates.",3075,2
3076,The << Intermediate-conductance Calcium-activated Potassium Channel KCa3.1 >> Regulates Vascular Smooth Muscle Cell Proliferation via Controlling [[ Calcium ]]-dependent Signaling.,3076,5
3077,"Reactive Metabolite Trapping Studies on << Imidazo- and 2-Methylimidazo[2,1-b]thiazole >>-based Inverse Agonists of the [[ Ghrelin Receptor ]].",3077,11
3078,"The current study examined the bioactivation potential of << ghrelin receptor >> inverse agonists, 1-(2-(2-chloro-4-(2H-1,2,3-triazol-2-yl)benzyl)-2,7-diazaspiro[3.5]nonan-7-yl)-2-(imidazo[2,1-b]thiazol-6-yl)ethanone (1) and [[ 1-(2-(2-chloro-4-(2H-1,2,3-triazol-2-yl)benzyl)-2,7-diazaspiro[3.5]nonan-7-yl)-2-(2-methylimidazo[2,1-b]thiazol-6-yl)ethanone ]] (2), containing a fused imidazo[2,1-b]thiazole motif in the core structure.",3078,11
3079,"The current study examined the bioactivation potential of << ghrelin receptor >> inverse agonists, 1-(2-(2-chloro-4-(2H-1,2,3-triazol-2-yl)benzyl)-2,7-diazaspiro[3.5]nonan-7-yl)-2-(imidazo[2,1-b]thiazol-6-yl)ethanone (1) and 1-(2-(2-chloro-4-(2H-1,2,3-triazol-2-yl)benzyl)-2,7-diazaspiro[3.5]nonan-7-yl)-2-(2-methylimidazo[2,1-b]thiazol-6-yl)ethanone (2), containing a fused [[ imidazo[2,1-b]thiazole ]] motif in the core structure.",3079,11
3080,"The current study examined the bioactivation potential of << ghrelin receptor >> inverse agonists, [[ 1-(2-(2-chloro-4-(2H-1,2,3-triazol-2-yl)benzyl)-2,7-diazaspiro[3.5]nonan-7-yl)-2-(imidazo[2,1-b]thiazol-6-yl)ethanone ]] (1) and 1-(2-(2-chloro-4-(2H-1,2,3-triazol-2-yl)benzyl)-2,7-diazaspiro[3.5]nonan-7-yl)-2-(2-methylimidazo[2,1-b]thiazol-6-yl)ethanone (2), containing a fused imidazo[2,1-b]thiazole motif in the core structure.",3080,11
3081,Processing of polysialylated NCAM was reproduced in a mouse model by << bleomycin >> administration leading to an activation of the inflammasome and secretion of [[ interleukin (IL)-1β ]].,3081,6
3082,<< 4-Hydroxytamoxifen >>-stimulated processing of [[ cyclin E ]] is mediated via G protein-coupled receptor 30 (GPR30) and accompanied by enhanced migration in MCF-7 breast cancer cells.,3082,6
3083,<< 17β-Estradiol >> (E2) has been recently shown to induce [[ cyclin E ]] processing in breast cancer cells.,3083,6
3084,"Collectively, our data indicate that << OHT >> contributes to the production of proteolyzed [[ cyclin E ]] via GPR30 with augmented migration in MCF-7 cells.",3084,6
3085,We have recently reported that a mono-hydroxylated metabolite of the synthetic << aminoalkylindole >> cannabinoid JHW-073 (3) exhibits neutral antagonist activity at [[ CB1Rs ]] and thus may serve as a promising lead for the development of novel alcohol abuse therapies.,3085,1
3086,We have recently reported that a mono-hydroxylated metabolite of the synthetic aminoalkylindole cannabinoid << JHW-073 >> (3) exhibits neutral antagonist activity at [[ CB1Rs ]] and thus may serve as a promising lead for the development of novel alcohol abuse therapies.,3086,1
3087,"In the current study, we show that systematic modification of an << aminoalkylindole >> scaffold identifies two new compounds with dual CB1R antagonist/[[ CB2R ]] agonist activity.",3087,2
3088,"In the current study, we show that systematic modification of an << aminoalkylindole >> scaffold identifies two new compounds with dual [[ CB1R ]] antagonist/CB2R agonist activity.",3088,1
3089,"Collectively, these initial findings suggest that design and systematic modification of << aminoalkylindoles >> such as 3 may lead to development of novel cannabinoid ligands with dual CB1R antagonist/[[ CB2R ]] agonist activity with potential for use as treatments of alcohol abuse.",3089,2
3090,"Collectively, these initial findings suggest that design and systematic modification of << aminoalkylindoles >> such as 3 may lead to development of novel cannabinoid ligands with dual [[ CB1R ]] antagonist/CB2R agonist activity with potential for use as treatments of alcohol abuse.",3090,1
3091,Enhanced beta cell function and anti-inflammatory effect after chronic treatment with the << dipeptidyl peptidase-4 >> inhibitor [[ vildagliptin ]] in an advanced-aged diet-induced obesity mouse model.,3091,0
3092,"METHODS: After 1 month of HFD alone, the mice were given the << DPP4 >> inhibitor [[ vildagliptin ]] for a further 11 months.",3092,0
3093,"The improved survival rates for obese mice chronically treated with << vildagliptin >> suggest that chronic [[ DPP4 ]] inhibition potentially results in additional quality-adjusted life-years for individuals with type 2 diabetes, which is the primary goal of any diabetes therapy.",3093,0
3094,Protein levels of the << glucose transporter >> (GLUT4) involved in [[ glucose ]] transport via these two pathways were also increased.,3094,5
3095,Protein levels of the glucose transporter (<< GLUT4 >>) involved in [[ glucose ]] transport via these two pathways were also increased.,3095,5
3096,<< Puerarin >> stimulates proliferation and differentiation and protects against cell death in human osteoblastic MG-63 cells via ER-dependent [[ MEK ]]/ERK and PI3K/Akt activation.,3096,9
3097,<< Puerarin >> stimulates proliferation and differentiation and protects against cell death in human osteoblastic MG-63 cells via ER-dependent MEK/[[ ERK ]] and PI3K/Akt activation.,3097,9
3098,<< Puerarin >> stimulates proliferation and differentiation and protects against cell death in human osteoblastic MG-63 cells via ER-dependent MEK/ERK and [[ PI3K ]]/Akt activation.,3098,9
3099,<< Puerarin >> stimulates proliferation and differentiation and protects against cell death in human osteoblastic MG-63 cells via ER-dependent MEK/ERK and PI3K/[[ Akt ]] activation.,3099,9
3100,Puerarin promotes proliferation by altering cell cycle distribution whereas << puerarin >>-mediated survival may be associated with up-regulation of [[ Bcl-xL ]] expression.,3100,6
3101,"Treatment with the << ER >> antagonist [[ ICI 182,780 ]] abolishes the above actions of puerarin on osteoblast-derived cells.",3101,1
3102,"Moreover, we also demonstrate that << puerarin >> functions at least partially through activation of [[ MEK ]]/ERK and PI3K/Akt signaling.",3102,9
3103,"Moreover, we also demonstrate that << puerarin >> functions at least partially through activation of MEK/[[ ERK ]] and PI3K/Akt signaling.",3103,9
3104,"Moreover, we also demonstrate that << puerarin >> functions at least partially through activation of MEK/ERK and [[ PI3K ]]/Akt signaling.",3104,6
3105,"Moreover, we also demonstrate that << puerarin >> functions at least partially through activation of MEK/ERK and PI3K/[[ Akt ]] signaling.",3105,6
3106,"RESULTS: Pretreatment of ucOC (30ng/ml) prevented LA-induced apoptosis in insulin-stimulated endothelial cells; effects were abolished by pretreatment with the << phosphatidylinositol 3-kinase >> (PI3-kinase) inhibitor, [[ wortmannin ]].",3106,0
3107,"RESULTS: Pretreatment of ucOC (30ng/ml) prevented LA-induced apoptosis in insulin-stimulated endothelial cells; effects were abolished by pretreatment with the phosphatidylinositol 3-kinase (<< PI3-kinase >>) inhibitor, [[ wortmannin ]].",3107,0
3108,"In addition, during acute exposure tests performed at the end of the chronic exposure, biofilms chronically exposed to 75 and 150μgL(-1) << oxyfluorfen >> showed a higher [[ CAT ]] activity than controls.",3108,9
3109,"The involvement of the various DA receptor subtypes in the motor effects of N/OFQ and NOP receptor antagonists was evaluated pharmacologically, using << D1 >>/D5 ([[ SCH23390 ]]), D2/D3 (raclopride, amisulpride) and D3 (S33084) receptor antagonists, and by using D2 receptor knockout mice.",3109,1
3110,"The involvement of the various DA receptor subtypes in the motor effects of N/OFQ and NOP receptor antagonists was evaluated pharmacologically, using D1/<< D5 >> ([[ SCH23390 ]]), D2/D3 (raclopride, amisulpride) and D3 (S33084) receptor antagonists, and by using D2 receptor knockout mice.",3110,1
3111,"The involvement of the various DA receptor subtypes in the motor effects of N/OFQ and NOP receptor antagonists was evaluated pharmacologically, using D1/D5 (SCH23390), << D2 >>/D3 ([[ raclopride ]], amisulpride) and D3 (S33084) receptor antagonists, and by using D2 receptor knockout mice.",3111,1
3112,"The involvement of the various DA receptor subtypes in the motor effects of N/OFQ and NOP receptor antagonists was evaluated pharmacologically, using D1/D5 (SCH23390), D2/<< D3 >> ([[ raclopride ]], amisulpride) and D3 (S33084) receptor antagonists, and by using D2 receptor knockout mice.",3112,1
3113,"The involvement of the various DA receptor subtypes in the motor effects of N/OFQ and NOP receptor antagonists was evaluated pharmacologically, using D1/D5 (SCH23390), << D2 >>/D3 (raclopride, [[ amisulpride ]]) and D3 (S33084) receptor antagonists, and by using D2 receptor knockout mice.",3113,1
3114,"The involvement of the various DA receptor subtypes in the motor effects of N/OFQ and NOP receptor antagonists was evaluated pharmacologically, using D1/D5 (SCH23390), D2/<< D3 >> (raclopride, [[ amisulpride ]]) and D3 (S33084) receptor antagonists, and by using D2 receptor knockout mice.",3114,1
3115,"The involvement of the various DA receptor subtypes in the motor effects of N/OFQ and NOP receptor antagonists was evaluated pharmacologically, using D1/D5 (SCH23390), D2/D3 (raclopride, amisulpride) and << D3 >> ([[ S33084 ]]) receptor antagonists, and by using D2 receptor knockout mice.",3115,1
3116,<< Haloperidol >> promotes mTORC1-dependent phosphorylation of [[ ribosomal protein S6 ]] via dopamine- and cAMP-regulated phosphoprotein of 32 kDa and inhibition of protein phosphatase-1.,3116,9
3117,<< Haloperidol >> promotes mTORC1-dependent phosphorylation of ribosomal protein S6 via dopamine- and cAMP-regulated phosphoprotein of 32 kDa and inhibition of [[ protein phosphatase-1 ]].,3117,0
3118,"This effect was prevented by << rapamycin >>, an inhibitor of the [[ mammalian target of rapamycin complex 1 ]] (mTORC1), or by PF470867, a selective inhibitor of the p70 ribosomal S6 kinase 1 (S6K1).",3118,0
3119,"This effect was prevented by << rapamycin >>, an inhibitor of the mammalian target of rapamycin complex 1 ([[ mTORC1 ]]), or by PF470867, a selective inhibitor of the p70 ribosomal S6 kinase 1 (S6K1).",3119,0
3120,"This effect was prevented by rapamycin, an inhibitor of the mammalian target of rapamycin complex 1 (mTORC1), or by << PF470867 >>, a selective inhibitor of the [[ p70 ribosomal S6 kinase 1 ]] (S6K1).",3120,0
3121,"This effect was prevented by rapamycin, an inhibitor of the mammalian target of rapamycin complex 1 (mTORC1), or by << PF470867 >>, a selective inhibitor of the p70 ribosomal S6 kinase 1 ([[ S6K1 ]]).",3121,0
3122,"In line with this observation, incubation of striatal slices with << okadaic acid >> and calyculin A, two inhibitors of [[ PP-1 ]], increased Ser240/244 phosphorylation.",3122,0
3123,"In line with this observation, incubation of striatal slices with okadaic acid and << calyculin A >>, two inhibitors of [[ PP-1 ]], increased Ser240/244 phosphorylation.",3123,0
3124,"These results show that << haloperidol >> promotes mTORC1- and S6K1-dependent phosphorylation of [[ rpS6 ]] at Ser240/244, in a subpopulation of striatal MSNs expressing D2Rs.",3124,9
3125,These compounds resulted from our efforts to merge the pharmacophores of selective << factor Xa >> inhibitor [[ rivaroxaban ]] with a mimic of the Arg-Gly-Asp (RGD) sequence of fibrinogen to obtain designed multiple ligands with potential antithrombotic activity.,3125,0
3126,"Resulting from this study, a structurally novel class of submicromolar fibrinogen << GPIIb/IIIa >> binding inhibitor bearing [[ 1,2,4-oxadiazol-5(4H)-one ]] moiety is also described.",3126,0
3127,"Rats intoxicated with << Cd >> for 30 days, significantly increased tissue malondialdehyde (MDA) levels and significantly decreased enzymatic antioxidants [[ superoxide dismutase ]], glutathione peroxidase and catalase in the frontal cortex tissue.",3127,3
3128,"Rats intoxicated with << Cd >> for 30 days, significantly increased tissue malondialdehyde (MDA) levels and significantly decreased enzymatic antioxidants superoxide dismutase, [[ glutathione peroxidase ]] and catalase in the frontal cortex tissue.",3128,3
3129,"Rats intoxicated with << Cd >> for 30 days, significantly increased tissue malondialdehyde (MDA) levels and significantly decreased enzymatic antioxidants superoxide dismutase, glutathione peroxidase and [[ catalase ]] in the frontal cortex tissue.",3129,3
3130,The << caspase-3 >> immunopositivity was increased in degenerating neurons of the [[ Cd ]] group.,3130,6
3131,"In contrast, TSH-induced differentiation of progenitor cells, in particular the expression of the << sodium iodide symporter >>, was significantly inhibited by [[ 17beta-oestradiol ]].In conclusion, oestrogen stimulated growth and simultaneously inhibited differentiation of thyroid nodules derived stem/progenitor cells.",3131,0
3132,"Drug-drug interactions are dependent on statins' pharmacokinetic profile: << simvastatin >>, lovastatin and atorvastatin are metabolized through [[ cytochrome P450 (CYP) 3A ]], while the metabolism of the other statins is independent of this CYP.",3132,5
3133,"Drug-drug interactions are dependent on statins' pharmacokinetic profile: simvastatin, << lovastatin >> and atorvastatin are metabolized through [[ cytochrome P450 (CYP) 3A ]], while the metabolism of the other statins is independent of this CYP.",3133,5
3134,"Drug-drug interactions are dependent on statins' pharmacokinetic profile: simvastatin, lovastatin and << atorvastatin >> are metabolized through [[ cytochrome P450 (CYP) 3A ]], while the metabolism of the other statins is independent of this CYP.",3134,5
3135,"All HIV PIs except nelfinavir are coadministered with a low dose of << ritonavir >>, a potent [[ CYP3A ]] inhibitor to improve their pharmacokinetic properties.",3135,0
3136,"The HCV-PIs << boceprevir >> and telaprevir are both, to different extents, inhibitors of [[ CYP3A ]].",3136,0
3137,"The HCV-PIs boceprevir and << telaprevir >> are both, to different extents, inhibitors of [[ CYP3A ]].",3137,0
3138,"Simvastatin and lovastatin metabolized through CYP3A have the highest potency for drug-drug interaction with potent << CYP3A >> inhibitors such as ritonavir- or cobicistat-boosted HIV-PI or the hepatitis C virus (HCV) PI, telaprevir or [[ boceprevir ]], and therefore their coadministration is contraindicated.",3138,0
3139,"Simvastatin and lovastatin metabolized through CYP3A have the highest potency for drug-drug interaction with potent << CYP3A >> inhibitors such as [[ ritonavir ]]- or cobicistat-boosted HIV-PI or the hepatitis C virus (HCV) PI, telaprevir or boceprevir, and therefore their coadministration is contraindicated.",3139,0
3140,"Simvastatin and lovastatin metabolized through CYP3A have the highest potency for drug-drug interaction with potent << CYP3A >> inhibitors such as ritonavir- or [[ cobicistat ]]-boosted HIV-PI or the hepatitis C virus (HCV) PI, telaprevir or boceprevir, and therefore their coadministration is contraindicated.",3140,0
3141,"Simvastatin and lovastatin metabolized through CYP3A have the highest potency for drug-drug interaction with potent << CYP3A >> inhibitors such as ritonavir- or cobicistat-boosted HIV-PI or the hepatitis C virus (HCV) PI, [[ telaprevir ]] or boceprevir, and therefore their coadministration is contraindicated.",3141,0
3142,"<< Simvastatin >> and lovastatin metabolized through [[ CYP3A ]] have the highest potency for drug-drug interaction with potent CYP3A inhibitors such as ritonavir- or cobicistat-boosted HIV-PI or the hepatitis C virus (HCV) PI, telaprevir or boceprevir, and therefore their coadministration is contraindicated.",3142,5
3143,"Simvastatin and << lovastatin >> metabolized through [[ CYP3A ]] have the highest potency for drug-drug interaction with potent CYP3A inhibitors such as ritonavir- or cobicistat-boosted HIV-PI or the hepatitis C virus (HCV) PI, telaprevir or boceprevir, and therefore their coadministration is contraindicated.",3143,5
3144,"<< Atorvastatin >> is also a [[ CYP3A ]] substrate, but less potent drug-drug interactions have been reported with CYP3A inhibitors.",3144,5
3145,"The synthesis, preclinical profile, and in vivo efficacy in rat xenograft models of the novel and selective << anaplastic lymphoma kinase >> inhibitor 15b ([[ LDK378 ]]) are described.",3145,0
3146,"In this initial report, preliminary structure-activity relationships (SARs) are described as well as the rational design strategy employed to overcome the development deficiencies of the first generation << ALK >> inhibitor 4 ([[ TAE684 ]]).",3146,0
3147,"Limitation of SRF was produced by the anticonvulsant BDZs (diazepam, clonazepam, nitrazepam and lorazepam) at low to mid nanomolar concentrations, by a convulsant BDZ which does not bind to high affinity BDZ receptors (Ro 5-4864) at high nanomolar concentrations and by a << BDZ receptor >> weak partial agonist ([[ Ro 15-1788 ]]) at micromolar concentrations.",3147,2
3148,"The limitation of SRF by diazepam was not prevented by inverse or partial agonists at the << BDZ receptor >>, including [[ Ro 15-1788 ]] and the beta CCs.",3148,2
3149,"The limitation of SRF by diazepam was not prevented by inverse or partial agonists at the << BDZ receptor >>, including Ro 15-1788 and the [[ beta CCs ]].",3149,2
3150,"The limitation of SRF by diazepam was not prevented by inverse or partial agonists at the << BDZ receptor >>, including [[ Ro 15-1788 ]] and the beta CCs.",3150,11
3151,"The limitation of SRF by diazepam was not prevented by inverse or partial agonists at the << BDZ receptor >>, including Ro 15-1788 and the [[ beta CCs ]].",3151,11
3152,"These findings suggest that limitation of SRF was produced by binding of BDZs, but not beta CCs, to voltage-dependent sodium channels and not to high affinity central BDZ receptors, and that << BDZs >> limit SRF by slowing recovery of [[ sodium channels ]] from inactivation.",3152,9
3153,"In addition to effects on cell proliferation, << DHT >> increased the percentage of [[ alkaline phosphatase ]] (ALP) positive cells in all three bone cell systems tested, and this effect was inhibited by antiandrogens.",3153,6
3154,"In addition to effects on cell proliferation, << DHT >> increased the percentage of alkaline phosphatase ([[ ALP ]]) positive cells in all three bone cell systems tested, and this effect was inhibited by antiandrogens.",3154,6
3155,"We conclude that << androgens >> can stimulate human and murine osteoblastic cell proliferation in vitro, and induce expression of the [[ osteoblast-line differentiation marker ]] ALP, presumably by an androgen receptor mediated mechanism.",3155,6
3156,"We conclude that << androgens >> can stimulate human and murine osteoblastic cell proliferation in vitro, and induce expression of the osteoblast-line differentiation marker [[ ALP ]], presumably by an androgen receptor mediated mechanism.",3156,6
3157,The effect of << histamine-H1 receptor >> antagonism with [[ terfenadine ]] on concentration-related AMP-induced bronchoconstriction in asthma.,3157,1
3158,"<< Ibrutinib >> (Imbruvica(R)) is a first-in-class, potent, orally administered, covalent inhibitor of Bruton's tyrosine kinase (BTK) that inhibits [[ B-cell antigen receptor ]] signalling downstream of BTK.",3158,8
3159,"Ibrutinib (<< Imbruvica(R) >>) is a first-in-class, potent, orally administered, covalent inhibitor of Bruton's tyrosine kinase (BTK) that inhibits [[ B-cell antigen receptor ]] signalling downstream of BTK.",3159,8
3160,"<< Ibrutinib >> (Imbruvica(R)) is a first-in-class, potent, orally administered, covalent inhibitor of Bruton's tyrosine kinase ([[ BTK ]]) that inhibits B-cell antigen receptor signalling downstream of BTK.",3160,0
3161,"<< Ibrutinib >> (Imbruvica(R)) is a first-in-class, potent, orally administered, covalent inhibitor of Bruton's tyrosine kinase (BTK) that inhibits B-cell antigen receptor signalling downstream of [[ BTK ]].",3161,0
3162,"<< Ibrutinib >> (Imbruvica(R)) is a first-in-class, potent, orally administered, covalent inhibitor of [[ Bruton's tyrosine kinase ]] (BTK) that inhibits B-cell antigen receptor signalling downstream of BTK.",3162,0
3163,"Ibrutinib (<< Imbruvica(R) >>) is a first-in-class, potent, orally administered, covalent inhibitor of Bruton's tyrosine kinase ([[ BTK ]]) that inhibits B-cell antigen receptor signalling downstream of BTK.",3163,0
3164,"Ibrutinib (<< Imbruvica(R) >>) is a first-in-class, potent, orally administered, covalent inhibitor of [[ Bruton's tyrosine kinase ]] (BTK) that inhibits B-cell antigen receptor signalling downstream of BTK.",3164,0
3165,"To study the mechanism underlying this phenomenon, the effects of the nonselective << beta-adrenoceptor >> antagonists [[ propranolol ]] [no intrinsic sympathomimetic activity (ISA)], alprenolol (weak ISA) and mepindolol (strong ISA) on lymphocyte beta 2-adrenoceptor density--assessed by (+/-)-[125I]-iodocyanopindolol (ICYP) binding--and plasma renin activity (PRA) were investigated in male healthy volunteers aged 23-35 years.",3165,1
3166,"To study the mechanism underlying this phenomenon, the effects of the nonselective << beta-adrenoceptor >> antagonists propranolol [no intrinsic sympathomimetic activity (ISA)], [[ alprenolol ]] (weak ISA) and mepindolol (strong ISA) on lymphocyte beta 2-adrenoceptor density--assessed by (+/-)-[125I]-iodocyanopindolol (ICYP) binding--and plasma renin activity (PRA) were investigated in male healthy volunteers aged 23-35 years.",3166,1
3167,"To study the mechanism underlying this phenomenon, the effects of the nonselective << beta-adrenoceptor >> antagonists propranolol [no intrinsic sympathomimetic activity (ISA)], alprenolol (weak ISA) and [[ mepindolol ]] (strong ISA) on lymphocyte beta 2-adrenoceptor density--assessed by (+/-)-[125I]-iodocyanopindolol (ICYP) binding--and plasma renin activity (PRA) were investigated in male healthy volunteers aged 23-35 years.",3167,1
3168,<< Propranolol >> treatment (4 X 40 mg/day) increased the density of [[ beta 2-adrenoceptors ]] by 25% after 2 days; concomitantly PRA and heart rate were reduced.,3168,6
3169,<< Mepindolol >> treatment (2 X 5 mg/day) caused a 30% decrease of [[ beta 2-adrenoceptor ]] density and PRA after 2 days; both parameters remained reduced during treatment.,3169,8
3170,Inhibition of << 5-lipoxygenase >> pathway of arachidonic acid metabolism in human neutrophils by sulfasalazine and [[ 5-aminosalicylic acid ]].,3170,0
3171,Inhibition of << 5-lipoxygenase >> pathway of arachidonic acid metabolism in human neutrophils by [[ sulfasalazine ]] and 5-aminosalicylic acid.,3171,0
3172,Inhibition of << 5-lipoxygenase >> pathway of [[ arachidonic acid ]] metabolism in human neutrophils by sulfasalazine and 5-aminosalicylic acid.,3172,5
3173,"Interference with << lipoxygenase >> enzymes, rather than a [[ steroid ]]-like inhibition of arachidonic acid release from intracellular phospholipids, seems to be the mode of action.",3173,0
3174,"Interference with << lipoxygenase >> enzymes, rather than a steroid-like inhibition of [[ arachidonic acid ]] release from intracellular phospholipids, seems to be the mode of action.",3174,5
3175,<< Bevantolol >>: a [[ beta-1 adrenoceptor ]] antagonist with unique additional actions.,3175,1
3176,UNLABELLED: << Bevantolol >> is a [[ beta-1 adrenoceptor ]] antagonist that has been shown to be as effective as other beta blockers for the treatment of angina pectoris and hypertension.,3176,1
3177,It is suggested that all the additional actions of << bevantolol >> can be attributed to a partial agonist action on [[ alpha-adrenoceptors ]].,3177,2
3178,"The apparent affinity of << benzodiazepine receptors >> for clonazepam in mice receiving alprazolam (0.05 mg/kg) was unchanged from that in untreated control mice, an observation suggesting that low doses of [[ alprazolam ]] increased receptor number.(ABSTRACT TRUNCATED AT 250 WORDS)",3178,9
3179,"When menadione was omitted from the diet, however, << 4HPR >>-dosed animals had elevated [[ prothrombin ]] times.",3179,6
3180,"In the high-dose << ROAc >> group, there was a twofold increase in [[ prothrombin ]] times but only after prolonged dosing.",3180,6
3181,"The order of effect was << 4HPR >> greater than ROAc greater than 13cisRA, with increases in [[ prothrombin ]] times correlating with increases in hemorrhagic deaths.",3181,6
3182,"The order of effect was 4HPR greater than << ROAc >> greater than 13cisRA, with increases in [[ prothrombin ]] times correlating with increases in hemorrhagic deaths.",3182,6
3183,"The order of effect was 4HPR greater than ROAc greater than << 13cisRA >>, with increases in [[ prothrombin ]] times correlating with increases in hemorrhagic deaths.",3183,6
3184,"<< 13cisRA >> and ROAc, but not 4HPR, caused a dose-dependent reduction in plasma [[ osteocalcin ]], an effect that correlated with retinoid-induced bone effects.",3184,8
3185,"13cisRA and << ROAc >>, but not 4HPR, caused a dose-dependent reduction in plasma [[ osteocalcin ]], an effect that correlated with retinoid-induced bone effects.",3185,8
3186,"13cisRA and ROAc, but not << 4HPR >>, caused a dose-dependent reduction in plasma [[ osteocalcin ]], an effect that correlated with retinoid-induced bone effects.",3186,8
3187,"In contrast, serum << alkaline phosphatase >> was elevated in animals dosed with [[ 13cisRA ]] or 4HPR but not in those dose with ROAc.",3187,6
3188,"In contrast, serum << alkaline phosphatase >> was elevated in animals dosed with 13cisRA or [[ 4HPR ]] but not in those dose with ROAc.",3188,6
3189,"However, in the presence of 100 mM << Na+ >>, which is required for opiate inhibition of [[ adenylate cyclase ]] activity, analysis of competition binding data revealed three sites: the first, consisting of 17.5% of total receptor population has a Kd = 0.38 +/- 0.18 nM; the second, 50.6% of the population, has a Kd = 6.8 +/- 2.2 nM; and the third, 31.9% of the population, has a Kd of 410 +/- 110 nM.",3189,0
3190,"Inhibition of the leukotriene synthetase of rat basophil leukemia cells by diethylcarbamazine, and synergism between << diethylcarbamazine >> and piriprost, a [[ 5-lipoxygenase ]] inhibitor.",3190,0
3191,"Inhibition of the leukotriene synthetase of rat basophil leukemia cells by diethylcarbamazine, and synergism between diethylcarbamazine and << piriprost >>, a [[ 5-lipoxygenase ]] inhibitor.",3191,0
3192,"Inhibition of the << leukotriene synthetase >> of rat basophil leukemia cells by [[ diethylcarbamazine ]], and synergism between diethylcarbamazine and piriprost, a 5-lipoxygenase inhibitor.",3192,0
3193,"Similar concentrations also inhibited the formation of << leukotriene C4 >> (LTC4) by [[ LTC synthetase ]], a detergent-solubilized cell free particulate enzyme from RBL cells which is capable of coupling LTA4 to glutathione.",3193,4
3194,"Similar concentrations also inhibited the formation of leukotriene C4 (<< LTC4 >>) by [[ LTC synthetase ]], a detergent-solubilized cell free particulate enzyme from RBL cells which is capable of coupling LTA4 to glutathione.",3194,4
3195,"Similar concentrations also inhibited the formation of leukotriene C4 (LTC4) by << LTC synthetase >>, a detergent-solubilized cell free particulate enzyme from RBL cells which is capable of coupling [[ LTA4 ]] to glutathione.",3195,5
3196,"The EC50 for inhibition of the << leukotriene C synthetase >> of RBL cells was directly proportional to the [[ LTA4 ]] concentration in the incubations, ranging from 1.5 mM at 10 microM LTA4 to over 40 mM at 500 microM LTA4.",3196,5
3197,Kinetic analysis revealed that the inhibition of the << leukotriene C synthetase >> reaction by [[ diethylcarbamazine ]] was competitive with respect to LTA4.,3197,0
3198,"In contrast to << diethylcarbamazine >>, piriprost (U-60,257; 6,9-deepoxy-6,9-(phenylimino)-delta 6,8-prostaglandin I1), which inhibits the formation of sulfidopeptide leuktrienes in RBL cells at the [[ 5-lipoxygenase ]] step (EC50 5 microM), did not inhibit the leukotriene synthetase of these cells.",3198,0
3199,"In contrast to << diethylcarbamazine >>, piriprost (U-60,257; 6,9-deepoxy-6,9-(phenylimino)-delta 6,8-prostaglandin I1), which inhibits the formation of sulfidopeptide leuktrienes in RBL cells at the 5-lipoxygenase step (EC50 5 microM), did not inhibit the [[ leukotriene synthetase ]] of these cells.",3199,0
3200,"In contrast to diethylcarbamazine, << piriprost >> (U-60,257; 6,9-deepoxy-6,9-(phenylimino)-delta 6,8-prostaglandin I1), which inhibits the formation of sulfidopeptide leuktrienes in RBL cells at the [[ 5-lipoxygenase ]] step (EC50 5 microM), did not inhibit the leukotriene synthetase of these cells.",3200,0
3201,"In contrast to diethylcarbamazine, piriprost (<< U-60,257 >>; 6,9-deepoxy-6,9-(phenylimino)-delta 6,8-prostaglandin I1), which inhibits the formation of sulfidopeptide leuktrienes in RBL cells at the [[ 5-lipoxygenase ]] step (EC50 5 microM), did not inhibit the leukotriene synthetase of these cells.",3201,0
3202,"In contrast to diethylcarbamazine, piriprost (U-60,257; << 6,9-deepoxy-6,9-(phenylimino)-delta 6,8-prostaglandin I1 >>), which inhibits the formation of sulfidopeptide leuktrienes in RBL cells at the [[ 5-lipoxygenase ]] step (EC50 5 microM), did not inhibit the leukotriene synthetase of these cells.",3202,0
3203,"In contrast to diethylcarbamazine, piriprost (U-60,257; 6,9-deepoxy-6,9-(phenylimino)-delta 6,8-prostaglandin I1), which inhibits the formation of << sulfidopeptide leuktrienes >> in RBL cells at the [[ 5-lipoxygenase ]] step (EC50 5 microM), did not inhibit the leukotriene synthetase of these cells.",3203,4
3204,These results are consistent with the interpretation that both piriprost and diethylcarbamazine inhibit leukotriene formation but that they act on sequential steps in the biosynthetic pathway in such a manner as to synergistically interfere with the availability or utilization of << LTA4 >> in the [[ leukotriene C synthetase ]] reaction.,3204,5
3205,The test procedure was verified with respect to intestinal << lactose >> hydrolysis by demonstrating a linear relationship between lactose/lactulose excretion and log jejunal mucosal [[ lactase ]] activity by in vitro assay (R2 = 0.95) in a further group of subjects.,3205,5
3206,The test procedure was verified with respect to intestinal lactose hydrolysis by demonstrating a linear relationship between << lactose >>/lactulose excretion and log jejunal mucosal [[ lactase ]] activity by in vitro assay (R2 = 0.95) in a further group of subjects.,3206,5
3207,The test procedure was verified with respect to intestinal lactose hydrolysis by demonstrating a linear relationship between lactose/<< lactulose >> excretion and log jejunal mucosal [[ lactase ]] activity by in vitro assay (R2 = 0.95) in a further group of subjects.,3207,5
3208,Differential << lactose >>/lactulose/L-rhamnose absorption provides a non-invasive and sensitive index of small intestinal integrity of value for the interpretation of prolonged or otherwise complicated enteritis and the distinction of primary secondary intestinal [[ lactase ]] deficiency.,3208,5
3209,Differential lactose/<< lactulose >>/L-rhamnose absorption provides a non-invasive and sensitive index of small intestinal integrity of value for the interpretation of prolonged or otherwise complicated enteritis and the distinction of primary secondary intestinal [[ lactase ]] deficiency.,3209,5
3210,Differential lactose/lactulose/<< L-rhamnose >> absorption provides a non-invasive and sensitive index of small intestinal integrity of value for the interpretation of prolonged or otherwise complicated enteritis and the distinction of primary secondary intestinal [[ lactase ]] deficiency.,3210,5
3211,The irreversible complex between << phenoxybenzamine >> and calmodulin may be useful for inhibiting certain [[ calmodulin ]]-dependent reactions and for studying the various biological functions of calmodulin.,3211,0
3212,<< Xanthines >> are classical antagonists for adenosine receptors for many of their pharmacological actions may be due to blockade of [[ adenosine receptors ]].,3212,0
3213,<< Xanthines >> are classical antagonists for [[ adenosine receptors ]] for many of their pharmacological actions may be due to blockade of adenosine receptors.,3213,1
3214,Inhibition of testicular << LDH-X >> from laboratory animals and man by [[ gossypol ]] and its isomers.,3214,0
3215,"The inhibitory effect of << (+)-, (-)-, (+/-)-gossypol >> and (+/-)-gossypol acetic acid upon testicular cytosolic [[ LDH-X ]] was measured in vitro.",3215,0
3216,"The inhibitory effect of (+)-, (-)-, (+/-)-gossypol and << (+/-)-gossypol acetic acid >> upon testicular cytosolic [[ LDH-X ]] was measured in vitro.",3216,0
3217,<< Gossypol acetic acid >> (0-100 mumol/l) inhibited [[ LDH-X ]] prepared from the testes of the mouse greater than rabbit greater than human greater than rat greater than hamster.,3217,0
3218,"<< Gossypol >> and its isomers were non-competitive inhibitors of [[ human and hamster LDH-X ]] with respect to the coenzyme NADH, competitive inhibitors of human LDH-X and noncompetitive-competitive inhibitors of hamster LDH-X with respect to the substrate alpha-ketobutyrate.",3218,0
3219,"Gossypol and its isomers were non-competitive inhibitors of human and hamster LDH-X with respect to the coenzyme << NADH >>, competitive inhibitors of [[ human LDH-X ]] and noncompetitive-competitive inhibitors of hamster LDH-X with respect to the substrate alpha-ketobutyrate.",3219,0
3220,"Gossypol and its isomers were non-competitive inhibitors of human and hamster LDH-X with respect to the coenzyme NADH, competitive inhibitors of human LDH-X and noncompetitive-competitive inhibitors of << hamster LDH-X >> with respect to the substrate [[ alpha-ketobutyrate ]].",3220,5
3221,Inactivation of << prostaglandin H synthase >> and prostacyclin synthase by [[ phenylbutazone ]].,3221,0
3222,Inactivation of prostaglandin H synthase and << prostacyclin synthase >> by [[ phenylbutazone ]].,3222,0
3223,Most reducing cofactors for the peroxidase protect << PHS >> and prostacyclin synthase from inactivation by [[ hydroperoxides ]].,3223,0
3224,Most reducing cofactors for the peroxidase protect PHS and << prostacyclin synthase >> from inactivation by [[ hydroperoxides ]].,3224,0
3225,Chromatographic analysis of the metabolism of 14C-labeled arachidonic acid in this system revealed that PB-dependent inactivation of << PHS >> is markedly increased in the presence of 100 microM [[ H2O2 ]].,3225,0
3226,Chromatographic analysis of the metabolism of << 14C-labeled arachidonic acid >> in this system revealed that PB-dependent inactivation of [[ PHS ]] is markedly increased in the presence of 100 microM H2O2.,3226,5
3227,"In plasma membranes prepared from these isolated brown fat cells by << borate >> extraction there was a similar enrichment of activity of [[ SSAO ]] and of the plasma membrane marker enzyme, phosphodiesterase I.",3227,9
3228,"Positive staining of mitochondria was achieved in the presence of the << MAO >> substrate, [[ tryptamine ]].",3228,5
3229,"Staining around the edges of the brown fat cells was observed with the << SSAO >> substrates, [[ tyramine ]] and benzylamine.",3229,5
3230,"Staining around the edges of the brown fat cells was observed with the << SSAO >> substrates, tyramine and [[ benzylamine ]].",3230,5
3231,"Staining was largely absent when substrate was omitted or after pretreatment with the irreversible << SSAO >> inhibitor, [[ hydralazine ]] and the slowly reversible inhibitor, semicarbazide.",3231,0
3232,"Staining was largely absent when substrate was omitted or after pretreatment with the irreversible << SSAO >> inhibitor, hydralazine and the slowly reversible inhibitor, [[ semicarbazide ]].",3232,0
3233,"This agent acts synergistically with many << penicillins >>, such as ampicillin, carbenicillin, and the like, and with cephalosporins, cefazolin, cefamandole, or cefoxitin to inhibit gram-negative bacilli, probably on the basis of binding to different proteins needed for the production of the [[ peptidoglycan ]] of the bacterial cell wall.",3233,6
3234,"This agent acts synergistically with many penicillins, such as << ampicillin >>, carbenicillin, and the like, and with cephalosporins, cefazolin, cefamandole, or cefoxitin to inhibit gram-negative bacilli, probably on the basis of binding to different proteins needed for the production of the [[ peptidoglycan ]] of the bacterial cell wall.",3234,6
3235,"This agent acts synergistically with many penicillins, such as ampicillin, << carbenicillin >>, and the like, and with cephalosporins, cefazolin, cefamandole, or cefoxitin to inhibit gram-negative bacilli, probably on the basis of binding to different proteins needed for the production of the [[ peptidoglycan ]] of the bacterial cell wall.",3235,6
3236,"This agent acts synergistically with many penicillins, such as ampicillin, carbenicillin, and the like, and with << cephalosporins >>, cefazolin, cefamandole, or cefoxitin to inhibit gram-negative bacilli, probably on the basis of binding to different proteins needed for the production of the [[ peptidoglycan ]] of the bacterial cell wall.",3236,6
3237,"This agent acts synergistically with many penicillins, such as ampicillin, carbenicillin, and the like, and with cephalosporins, << cefazolin >>, cefamandole, or cefoxitin to inhibit gram-negative bacilli, probably on the basis of binding to different proteins needed for the production of the [[ peptidoglycan ]] of the bacterial cell wall.",3237,6
3238,"This agent acts synergistically with many penicillins, such as ampicillin, carbenicillin, and the like, and with cephalosporins, cefazolin, << cefamandole >>, or cefoxitin to inhibit gram-negative bacilli, probably on the basis of binding to different proteins needed for the production of the [[ peptidoglycan ]] of the bacterial cell wall.",3238,6
3239,"This agent acts synergistically with many penicillins, such as ampicillin, carbenicillin, and the like, and with cephalosporins, cefazolin, cefamandole, or << cefoxitin >> to inhibit gram-negative bacilli, probably on the basis of binding to different proteins needed for the production of the [[ peptidoglycan ]] of the bacterial cell wall.",3239,6
3240,"Since both << TFP >> and W-7 are potent inhibitors of [[ calmodulin ]], we investigated the possibility that inhibition of calmodulin was responsible for the loss of receptors.",3240,0
3241,"Since both TFP and << W-7 >> are potent inhibitors of [[ calmodulin ]], we investigated the possibility that inhibition of calmodulin was responsible for the loss of receptors.",3241,0
3242,"Three lines of evidence suggest that calmodulin inhibition is not responsible for the inhibition of binding and endocytosis: 1) << Promethazine >>, a phenothiazine that is a poor inhibitor of calmodulin, is nearly as effective as TFP at inhibiting endocytosis; calmidazolium, a potent inhibitor of several [[ calmodulin ]] functions, did not cause a loss of binding; 2) the microinjection of calmodulin into cells did not reverse the effects of W-7; using pressure microinjection, we introduced up to a 100-fold excess of calmodulin over native levels into individual gerbil fibroma cells; using rhodamine-labeled alpha 2-macroglobulin, we saw that the W-7 induced inhibition of receptor-mediated endocytosis was the same in injected and uninjected cells; 3) we injected calcineurin, a calmodulin-binding protein, into cells (1-3 pg/cell) and observed no effect on the receptor-mediated endocytosis of rhodamine-labeled alpha 2-macroglobulin.",3242,0
3243,"Three lines of evidence suggest that calmodulin inhibition is not responsible for the inhibition of binding and endocytosis: 1) Promethazine, a << phenothiazine >> that is a poor inhibitor of calmodulin, is nearly as effective as TFP at inhibiting endocytosis; calmidazolium, a potent inhibitor of several [[ calmodulin ]] functions, did not cause a loss of binding; 2) the microinjection of calmodulin into cells did not reverse the effects of W-7; using pressure microinjection, we introduced up to a 100-fold excess of calmodulin over native levels into individual gerbil fibroma cells; using rhodamine-labeled alpha 2-macroglobulin, we saw that the W-7 induced inhibition of receptor-mediated endocytosis was the same in injected and uninjected cells; 3) we injected calcineurin, a calmodulin-binding protein, into cells (1-3 pg/cell) and observed no effect on the receptor-mediated endocytosis of rhodamine-labeled alpha 2-macroglobulin.",3243,0
3244,"Three lines of evidence suggest that calmodulin inhibition is not responsible for the inhibition of binding and endocytosis: 1) Promethazine, a phenothiazine that is a poor inhibitor of calmodulin, is nearly as effective as << TFP >> at inhibiting endocytosis; calmidazolium, a potent inhibitor of several [[ calmodulin ]] functions, did not cause a loss of binding; 2) the microinjection of calmodulin into cells did not reverse the effects of W-7; using pressure microinjection, we introduced up to a 100-fold excess of calmodulin over native levels into individual gerbil fibroma cells; using rhodamine-labeled alpha 2-macroglobulin, we saw that the W-7 induced inhibition of receptor-mediated endocytosis was the same in injected and uninjected cells; 3) we injected calcineurin, a calmodulin-binding protein, into cells (1-3 pg/cell) and observed no effect on the receptor-mediated endocytosis of rhodamine-labeled alpha 2-macroglobulin.",3244,0
3245,"From these results, it is proposed that << tyrosine hydroxylase >> activity determines p-HPAA concentrations by regulating [[ p-tyrosine ]] availability.",3245,5
3246,The binding of << FHA >>-HIS was inhibited on 35-79% of the platelets by the histamine H1 receptor antagonists [[ diphenhydramine ]] and clemastine.,3246,0
3247,The binding of << FHA >>-HIS was inhibited on 35-79% of the platelets by the histamine H1 receptor antagonists diphenhydramine and [[ clemastine ]].,3247,0
3248,The binding of FHA-HIS was inhibited on 35-79% of the platelets by the << histamine H1 receptor >> antagonists [[ diphenhydramine ]] and clemastine.,3248,1
3249,The binding of FHA-HIS was inhibited on 35-79% of the platelets by the << histamine H1 receptor >> antagonists diphenhydramine and [[ clemastine ]].,3249,1
3250,The histamine H2 receptor antagonist << cimetidine >> blocked the [[ FHA ]]-HIS binding on 14-37% of the platelets.,3250,0
3251,The << histamine H2 receptor >> antagonist [[ cimetidine ]] blocked the FHA-HIS binding on 14-37% of the platelets.,3251,1
3252,"<< Alanine:glyoxylate aminotransferase >> (AGT) in the liver catalyzes most of the [[ glyoxylate ]] transamination in mammalian tissues (E. V. Rowsell, K. Snell, J. A. Carnie, and K. V. Rowsell (1972) Biochem. J. 127, 155-165).",3252,5
3253,"Alanine:glyoxylate aminotransferase (<< AGT >>) in the liver catalyzes most of the [[ glyoxylate ]] transamination in mammalian tissues (E. V. Rowsell, K. Snell, J. A. Carnie, and K. V. Rowsell (1972) Biochem. J. 127, 155-165).",3253,5
3254,"The holo activity of combined peroxisomal and mitochondrial << AGT 1 >> with a low Km for [[ L-alanine ]] rapidly decreased after a lag time of about 2 days during feeding of the vitamin B6-deficient diet (by 50% in 5 days, by 86% in 14 days).",3254,5
3255,"The holo activity of AGT 2 with a high Km for << L-alanine >> decreased more slowly than [[ AGT 1 ]] (by 33% in 14 days, by 60% in 28 days).",3255,5
3256,"The holo activity of << AGT 2 >> with a high Km for [[ L-alanine ]] decreased more slowly than AGT 1 (by 33% in 14 days, by 60% in 28 days).",3256,5
3257,"<< Triclosan >> inhibited both [[ cyclooxygenase 1 ]] and cyclo-oxygenase 2 with IC-50 values of 43 microM and 227 microM, respectively.",3257,0
3258,"<< Triclosan >> inhibited both cyclooxygenase 1 and [[ cyclo-oxygenase 2 ]] with IC-50 values of 43 microM and 227 microM, respectively.",3258,0
3259,<< Triclosan >> also inhibited [[ 5-lipoxygenase ]] with an IC-50 of 43 microM.,3259,0
3260,The << 15-lipoxygenase >> was similarly inhibited by [[ triclosan ]] with an IC-50 of 61 microM.,3260,0
3261,"Hence, << triclosan >> has the ability to inhibit both the [[ cyclo-oxygenase ]] and lipoxygenase pathways of arachidonic acid metabolism with similar efficacy.",3261,0
3262,"Hence, << triclosan >> has the ability to inhibit both the cyclo-oxygenase and [[ lipoxygenase ]] pathways of arachidonic acid metabolism with similar efficacy.",3262,0
3263,"Hence, triclosan has the ability to inhibit both the << cyclo-oxygenase >> and lipoxygenase pathways of [[ arachidonic acid ]] metabolism with similar efficacy.",3263,5
3264,"Hence, triclosan has the ability to inhibit both the cyclo-oxygenase and << lipoxygenase >> pathways of [[ arachidonic acid ]] metabolism with similar efficacy.",3264,5
3265,"In cell culture experiments, it was found that << triclosan >> inhibited [[ IL-1 beta ]] induced prostaglandin E2 production by human gingival fibroblasts in a concentration dependent manner, and at relatively low concentrations.",3265,0
3266,"In cell culture experiments, it was found that triclosan inhibited << IL-1 beta >> induced [[ prostaglandin E2 ]] production by human gingival fibroblasts in a concentration dependent manner, and at relatively low concentrations.",3266,4
3267,Cells propagated in medium containing << N5-methyltetrahydrofolate >> and homocysteine showed a substantial increase in [[ MS ]] activity which paralleled the increase in the intracellular concentration of Me-Cbl and the Cbl bound to the enzyme.,3267,9
3268,Cells propagated in medium containing N5-methyltetrahydrofolate and << homocysteine >> showed a substantial increase in [[ MS ]] activity which paralleled the increase in the intracellular concentration of Me-Cbl and the Cbl bound to the enzyme.,3268,9
3269,<< Ergovaline >> binding and activation of [[ D2 dopamine receptors ]] in GH4ZR7 cells.,3269,9
3270,"Ergovaline inhibition of radioligand binding to the D2 dopamine receptor and << ergot alkaloid >> inhibition of [[ vasoactive intestinal peptide ]] (VIP)-stimulated cyclic AMP production in GH4ZR7 cells, stably transfected with a rat D2 dopamine receptor, were evaluated.",3270,0
3271,"Ergovaline inhibition of radioligand binding to the D2 dopamine receptor and << ergot alkaloid >> inhibition of vasoactive intestinal peptide ([[ VIP ]])-stimulated cyclic AMP production in GH4ZR7 cells, stably transfected with a rat D2 dopamine receptor, were evaluated.",3271,0
3272,"Ergovaline inhibition of radioligand binding to the D2 dopamine receptor and ergot alkaloid inhibition of << vasoactive intestinal peptide >> (VIP)-stimulated [[ cyclic AMP ]] production in GH4ZR7 cells, stably transfected with a rat D2 dopamine receptor, were evaluated.",3272,4
3273,"Ergovaline inhibition of radioligand binding to the D2 dopamine receptor and ergot alkaloid inhibition of vasoactive intestinal peptide (<< VIP >>)-stimulated [[ cyclic AMP ]] production in GH4ZR7 cells, stably transfected with a rat D2 dopamine receptor, were evaluated.",3273,4
3274,"<< Ergot alkaloids >> were also effective in inhibiting [[ VIP ]]-stimulated cyclic AMP production, with EC50 values for ergovaline, ergonovine, alpha-ergocryptine, ergotamine, and dopamine of 8 +/- 2, 47 +/- 2, 28 +/- 2, 2 +/- 1, and 8 +/- 1 nM, respectively.",3274,0
3275,"Ergot alkaloids were also effective in inhibiting << VIP >>-stimulated cyclic AMP production, with EC50 values for [[ ergovaline ]], ergonovine, alpha-ergocryptine, ergotamine, and dopamine of 8 +/- 2, 47 +/- 2, 28 +/- 2, 2 +/- 1, and 8 +/- 1 nM, respectively.",3275,0
3276,"Ergot alkaloids were also effective in inhibiting << VIP >>-stimulated cyclic AMP production, with EC50 values for ergovaline, [[ ergonovine ]], alpha-ergocryptine, ergotamine, and dopamine of 8 +/- 2, 47 +/- 2, 28 +/- 2, 2 +/- 1, and 8 +/- 1 nM, respectively.",3276,0
3277,"Ergot alkaloids were also effective in inhibiting << VIP >>-stimulated cyclic AMP production, with EC50 values for ergovaline, ergonovine, [[ alpha-ergocryptine ]], ergotamine, and dopamine of 8 +/- 2, 47 +/- 2, 28 +/- 2, 2 +/- 1, and 8 +/- 1 nM, respectively.",3277,0
3278,"Ergot alkaloids were also effective in inhibiting << VIP >>-stimulated cyclic AMP production, with EC50 values for ergovaline, ergonovine, alpha-ergocryptine, [[ ergotamine ]], and dopamine of 8 +/- 2, 47 +/- 2, 28 +/- 2, 2 +/- 1, and 8 +/- 1 nM, respectively.",3278,0
3279,"Ergot alkaloids were also effective in inhibiting << VIP >>-stimulated cyclic AMP production, with EC50 values for ergovaline, ergonovine, alpha-ergocryptine, ergotamine, and [[ dopamine ]] of 8 +/- 2, 47 +/- 2, 28 +/- 2, 2 +/- 1, and 8 +/- 1 nM, respectively.",3279,0
3280,"Ergot alkaloids were also effective in inhibiting << VIP >>-stimulated [[ cyclic AMP ]] production, with EC50 values for ergovaline, ergonovine, alpha-ergocryptine, ergotamine, and dopamine of 8 +/- 2, 47 +/- 2, 28 +/- 2, 2 +/- 1, and 8 +/- 1 nM, respectively.",3280,4
3281,"Inhibition of cyclic AMP production by ergovaline was blocked by the << dopamine receptor >> antagonist, [[ (-)-sulpiride ]] (IC50, 300 +/- 150 nM).",3281,1
3282,"These findings suggest that some of the deleterious effects of consumption of endophyte-infected tall fescue, which contains several << ergot alkaloids >> including ergovaline, may be due to [[ D2 dopamine receptor ]] activation.",3282,9
3283,"These findings suggest that some of the deleterious effects of consumption of endophyte-infected tall fescue, which contains several ergot alkaloids including << ergovaline >>, may be due to [[ D2 dopamine receptor ]] activation.",3283,9
3284,"Incubation of rat aortic membranes with the irreversible << alpha 1B-adrenoceptor >> antagonist, [[ chloroethylclonidine ]] (CEC: 10 microM) did not change the KD of [3H]-prazosin binding in comparison to untreated membranes, but reduced by 88% the total number of binding sites (Bmax).",3284,1
3285,"Incubation of rat aortic membranes with the irreversible << alpha 1B-adrenoceptor >> antagonist, chloroethylclonidine ([[ CEC ]]: 10 microM) did not change the KD of [3H]-prazosin binding in comparison to untreated membranes, but reduced by 88% the total number of binding sites (Bmax).",3285,1
3286,"Intraperitoneal administration of << (+/- )propranolol HCl >> (2.5-10 mg/kg), a nonselective [[ beta-adrenoceptor ]] antagonist, dose dependently attenuated the desipramine-induced enhancement of aggressive behavior without significantly affecting the basal aggressive responses.",3286,1
3287,"<< ICI118,551 HCl >> (1.25-5 mg/kg, IP), a selective [[ beta 2-adrenoceptor ]] antagonist, also blocked the desipramine-induced enhancement of aggressive behavior in a dose-dependent manner, whereas metoprolol tartrate (5-20 mg/kg, IP), a selective beta 1-adrenoceptor antagonist, did not affect it.",3287,1
3288,"ICI118,551 HCl (1.25-5 mg/kg, IP), a selective beta 2-adrenoceptor antagonist, also blocked the desipramine-induced enhancement of aggressive behavior in a dose-dependent manner, whereas << metoprolol tartrate >> (5-20 mg/kg, IP), a selective [[ beta 1-adrenoceptor ]] antagonist, did not affect it.",3288,1
3289,"Moreover, << clenbuterol HCl >> (0.1-0.5 mg/kg, IP), a lipophilic [[ beta 2-adrenoceptor ]] agonist, significantly increased the duration of basal aggressive behavior.",3289,2
3290,"Taken together with our previous finding that the desipramine-induced enhancement of aggressive behavior can be blocked by << yohimbine >>, an [[ alpha 2-adrenoceptor ]] antagonist, the present results indicate that not only alpha 2- but also beta 2-adrenoceptor stimulation plays important roles in modulation of aggressive behavior in long-term isolated mice.",3290,1
3291,"In beta-escin-skinned strips of chloroethylclonidine-pretreated smooth muscle, the enhancement of Ca2+ contraction produced by norepinephrine was significantly decreased, whereas the amplitude was the same as that produced by methoxamine or clonidine; this enhancement was inhibited by the selective << alpha 1A-adrenoceptor >> antagonist [[ WB 4101 ]] (100 nM).",3291,1
3292,"Furthermore, the phosphorylation of << myosin light chain >> produced by [[ norepinephrine ]] was greater than that produced by clonidine.",3292,9
3293,"Furthermore, the phosphorylation of << myosin light chain >> produced by norepinephrine was greater than that produced by [[ clonidine ]].",3293,9
3294,"The drug had a potent cytotoxic effect on RIN cells expressing << GLUT2 >>, but had no effect on cells lacking GLUT2 expression, as indicated by histological analysis and measurement of the blood [[ glucose ]] levels of treated animals.",3294,5
3295,"Consistent with these data, only << GLUT2 >>-expressing RIN or AtT-20ins cells transported [[ STZ ]] efficiently.",3295,5
3296,"We conclude that expression of << GLUT2 >> is required for efficient killing of neuroendocrine cells by [[ STZ ]], and this effect is related to specific recognition of the drug as a transported substrate by GLUT2 but not GLUT1.",3296,5
3297,"We conclude that expression of GLUT2 is required for efficient killing of neuroendocrine cells by << STZ >>, and this effect is related to specific recognition of the drug as a transported substrate by [[ GLUT2 ]] but not GLUT1.",3297,5
3298,Inhibitory effects of << lysine >> analogues on [[ t-PA ]] induced whole blood clot lysis.,3298,0
3299,The present study utilized blood from normal volunteers and 125I-fibrinogen in a dilute whole blood clot assay to determine the relative concentrations of << lysine >> analogues required for inhibition of clot lysis induced by exogenous [[ t-PA ]].,3299,0
3300,<< AMCA >> (0.06 mM) and EACA (0.6 mM) were effective in prolonging clot lysis if (1) whole blood clots were formed and then exposed to a lysine analogue and exogenous [[ t-PA ]] or if (2) whole blood clots were formed in the presence of exogenous t-PA and a lysine analogue.,3300,0
3301,<< AMCA >> (0.06 mM) and EACA (0.6 mM) were effective in prolonging clot lysis if (1) whole blood clots were formed and then exposed to a lysine analogue and exogenous t-PA or if (2) whole blood clots were formed in the presence of exogenous [[ t-PA ]] and a lysine analogue.,3301,0
3302,AMCA (0.06 mM) and << EACA >> (0.6 mM) were effective in prolonging clot lysis if (1) whole blood clots were formed and then exposed to a lysine analogue and exogenous [[ t-PA ]] or if (2) whole blood clots were formed in the presence of exogenous t-PA and a lysine analogue.,3302,0
3303,AMCA (0.06 mM) and << EACA >> (0.6 mM) were effective in prolonging clot lysis if (1) whole blood clots were formed and then exposed to a lysine analogue and exogenous t-PA or if (2) whole blood clots were formed in the presence of exogenous [[ t-PA ]] and a lysine analogue.,3303,0
3304,"However, their inhibitory effect was markedly reduced if clots were formed in the presence of << t-PA >> and then exposed to either of the [[ lysine ]] analogues.",3304,0
3305,"The data suggest that << lysine >> analogues, even at low concentrations, reduce the rate of [[ t-PA ]] induced whole blood clot lysis by several mechanisms.",3305,8
3306,<< Histamine >> enhances the depolarizing afterpotential of immunohistochemically identified vasopressin neurons in the rat supraoptic nucleus via [[ H1-receptor ]] activation.,3306,9
3307,"The enhancement of the depolarizing afterpotential by histamine was mimicked by the << histamine H1-receptor >> agonist [[ 2-thiazolylethylamine ]] and was reduced or blocked by the H1-receptor antagonist promethazine, but was not blocked or reduced in the presence of the histamine H2-receptor antagonist, cimetidine.",3307,2
3308,"The enhancement of the depolarizing afterpotential by histamine was mimicked by the histamine H1-receptor agonist 2-thiazolylethylamine and was reduced or blocked by the << H1-receptor >> antagonist [[ promethazine ]], but was not blocked or reduced in the presence of the histamine H2-receptor antagonist, cimetidine.",3308,1
3309,"The enhancement of the depolarizing afterpotential by histamine was mimicked by the histamine H1-receptor agonist 2-thiazolylethylamine and was reduced or blocked by the H1-receptor antagonist promethazine, but was not blocked or reduced in the presence of the << histamine H2-receptor >> antagonist, [[ cimetidine ]].",3309,1
3310,"In summary, these results show that the excitatory effect of << histamine >> on immunohistochemically identified vasopressin neurons in the supraoptic nucleus is due in part to the [[ H1-receptor ]]-mediated enhancement of the depolarizing afterpotential independent of any change in the afterhyperpolarizing potential or membrane potential.",3310,9
3311,"The goal of the present study was to compare the effects of three potent reference << renin >> inhibitors ([[ remikiren ]], CGP 38560A, and enalkiren) in sodium-depleted normotensive squirrel monkeys.",3311,0
3312,"The goal of the present study was to compare the effects of three potent reference << renin >> inhibitors (remikiren, [[ CGP 38560A ]], and enalkiren) in sodium-depleted normotensive squirrel monkeys.",3312,0
3313,"The goal of the present study was to compare the effects of three potent reference << renin >> inhibitors (remikiren, CGP 38560A, and [[ enalkiren ]]) in sodium-depleted normotensive squirrel monkeys.",3313,0
3314,"Finally, the three drugs were compared with the << angiotensin converting enzyme >> inhibitor [[ cilazapril ]].",3314,0
3315,"One possible explanation is that, in our model, << remikiren >> in contrast to CGP 38560A and enalkiren is able to inhibit [[ renin ]] in a functionally important extraplasmatic compartment.",3315,0
3316,"One possible explanation is that, in our model, remikiren in contrast to << CGP 38560A >> and enalkiren is able to inhibit [[ renin ]] in a functionally important extraplasmatic compartment.",3316,0
3317,"One possible explanation is that, in our model, remikiren in contrast to CGP 38560A and << enalkiren >> is able to inhibit [[ renin ]] in a functionally important extraplasmatic compartment.",3317,0
3318,Inhibition of << cytokine >>-primed eosinophil chemotaxis by [[ nedocromil sodium ]].,3318,0
3319,"RESULTS: << Nedocromil sodium >> inhibited the chemotactic response toward FMLP and NAF/IL-8 of [[ GM-CSF ]] primed eosinophils approximately 60% (inhibitory concentration of 50% [IC50] approximately 1 to 10 nmol/L), whereas these responses of IL-3 primed eosinophils was completely inhibited (IC50 approximately 1 nmol/L).",3319,8
3320,"RESULTS: << Nedocromil sodium >> inhibited the chemotactic response toward FMLP and NAF/IL-8 of GM-CSF primed eosinophils approximately 60% (inhibitory concentration of 50% [IC50] approximately 1 to 10 nmol/L), whereas these responses of [[ IL-3 ]] primed eosinophils was completely inhibited (IC50 approximately 1 nmol/L).",3320,0
3321,"RESULTS: << Nedocromil sodium >> inhibited the chemotactic response toward FMLP and [[ NAF ]]/IL-8 of GM-CSF primed eosinophils approximately 60% (inhibitory concentration of 50% [IC50] approximately 1 to 10 nmol/L), whereas these responses of IL-3 primed eosinophils was completely inhibited (IC50 approximately 1 nmol/L).",3321,0
3322,"RESULTS: << Nedocromil sodium >> inhibited the chemotactic response toward FMLP and NAF/[[ IL-8 ]] of GM-CSF primed eosinophils approximately 60% (inhibitory concentration of 50% [IC50] approximately 1 to 10 nmol/L), whereas these responses of IL-3 primed eosinophils was completely inhibited (IC50 approximately 1 nmol/L).",3322,0
3323,CONCLUSIONS: The chemotactic responses toward << C5a >> were inhibited by [[ nedocromil sodium ]] at higher concentrations than were required in the priming studies (IC50 approximately 10 to 100 nmol/L).,3323,0
3324,"Glutathione-independent prostaglandin D synthase [<< prostaglandin-H2 D-isomerase >>; (5Z,13E)-(15S)-9 alpha,11 alpha-epidioxy-15-hydroxyprosta-5,13-dienoate D-isomerase, EC 5.3.99.2] is an enzyme responsible for biosynthesis of [[ prostaglandin D2 ]] in the central nervous system.",3324,4
3325,"Glutathione-independent prostaglandin D synthase [prostaglandin-H2 D-isomerase; << (5Z,13E)-(15S)-9 alpha,11 alpha-epidioxy-15-hydroxyprosta-5,13-dienoate D-isomerase >>, EC 5.3.99.2] is an enzyme responsible for biosynthesis of [[ prostaglandin D2 ]] in the central nervous system.",3325,4
3326,"Glutathione-independent prostaglandin D synthase [prostaglandin-H2 D-isomerase; (5Z,13E)-(15S)-9 alpha,11 alpha-epidioxy-15-hydroxyprosta-5,13-dienoate D-isomerase, << EC 5.3.99.2 >>] is an enzyme responsible for biosynthesis of [[ prostaglandin D2 ]] in the central nervous system.",3326,4
3327,"Glutathione-independent << prostaglandin D synthase >> [prostaglandin-H2 D-isomerase; (5Z,13E)-(15S)-9 alpha,11 alpha-epidioxy-15-hydroxyprosta-5,13-dienoate D-isomerase, EC 5.3.99.2] is an enzyme responsible for biosynthesis of [[ prostaglandin D2 ]] in the central nervous system.",3327,4
3328,Kainate-evoked currents showed partial desensitization that was reduced on incubation with concanavalin A (conA) but not cyclothiazide and were attenuated by the non-<< N-methyl-D-aspartate (NMDA) receptor >> antagonist [[ CNQX ]] (6-cyano-7-nitro-quinoxalinedione).,3328,1
3329,Kainate-evoked currents showed partial desensitization that was reduced on incubation with concanavalin A (conA) but not cyclothiazide and were attenuated by the non-<< N-methyl-D-aspartate (NMDA) receptor >> antagonist CNQX ([[ 6-cyano-7-nitro-quinoxalinedione ]]).,3329,1
3330,"One group of experimental animals was treated with << 5-lipoxygenase >> (5-LO) inhibitor, [[ diethylcarbamazine ]] (DEC, Sigma, St. Louis, Missouri) (50 mg/kg, i.v.), immediately before blast.",3330,0
3331,"One group of experimental animals was treated with 5-lipoxygenase (<< 5-LO >>) inhibitor, [[ diethylcarbamazine ]] (DEC, Sigma, St. Louis, Missouri) (50 mg/kg, i.v.), immediately before blast.",3331,0
3332,"One group of experimental animals was treated with << 5-lipoxygenase >> (5-LO) inhibitor, diethylcarbamazine ([[ DEC ]], Sigma, St. Louis, Missouri) (50 mg/kg, i.v.), immediately before blast.",3332,0
3333,"One group of experimental animals was treated with 5-lipoxygenase (<< 5-LO >>) inhibitor, diethylcarbamazine ([[ DEC ]], Sigma, St. Louis, Missouri) (50 mg/kg, i.v.), immediately before blast.",3333,0
3334,"Although << DEC >> exerts local antioxidant activity with beneficial effects on lung tissue, this [[ 5-LO ]] inhibitor intensifies the blast overpressure caused hemodynamic insufficiency.",3334,0
3335,"<< Tamsulosin >>, the first prostate-selective [[ alpha 1A-adrenoceptor ]] antagonist.",3335,1
3336,"Expressions of << insulin >> and PC3, but not PC2, are coordinately regulated by [[ glucose ]], consistent with the important role of PC3 in regulating proinsulin processing.",3336,6
3337,"Expressions of insulin and << PC3 >>, but not PC2, are coordinately regulated by [[ glucose ]], consistent with the important role of PC3 in regulating proinsulin processing.",3337,6
3338,After 7 days of << DMI >> administration the number of [[ beta-adrenoceptors ]] was lower in frontal and occipital cortex and hippocampus.,3338,0
3339,The << DMI >> induced reduction in [[ beta-adrenoceptors ]] did not differ in OB and sham-operated control rats.,3339,0
3340,"<< DMI >> administration for up to 21 days produced a progressive reduction in the number of [[ 5-HT2A ]] receptors in frontal cortex, without significant alterations in occipital cortex.",3340,0
3341,The time course of the reduction in the number of << 5-HT2A >> receptors was similar to that of the [[ DMI ]]-induced behavioural changes whereas that for the reduction in beta-adrenoceptors was clearly different.,3341,0
3342,The time course of the reduction in the number of 5-HT2A receptors was similar to that of the << DMI >>-induced behavioural changes whereas that for the reduction in [[ beta-adrenoceptors ]] was clearly different.,3342,0
3343,The present results suggest that the action of << DMI >> in this animal model is unlikely to be directly related to a reduction in [[ beta-adrenoceptors ]] but may be related to a reduction in frontal cortical 5-HT2A receptors.,3343,8
3344,The present results suggest that the action of << DMI >> in this animal model is unlikely to be directly related to a reduction in beta-adrenoceptors but may be related to a reduction in frontal cortical [[ 5-HT2A ]] receptors.,3344,0
3345,Binding of << thalidomide >> to alpha1-acid glycoprotein may be involved in its inhibition of [[ tumor necrosis factor alpha ]] production.,3345,8
3346,The immunomodulatory activity of << thalidomide >> has been ascribed to the selective inhibition of [[ tumor necrosis factor alpha ]] from monocytes.,3346,0
3347,"We show that the binding of thalidomide photoaffinity label to authentic human AGP is competed with both << thalidomide >> and the nonradioactive photoaffinity label at concentrations comparable to those required for inhibition of production of [[ tumor necrosis factor alpha ]] from human monocytes, suggesting that AGP may be involved in the immunomodulatory activity of thalidomide.",3347,8
3348,"In conclusion, our data suggest that chronic << cocaine >> use is associated with modestly reduced levels of striatal DA and the [[ DA transporter ]] in some subjects and that these changes might contribute to the neurological and psychiatric effects of the drug.",3348,3
3349,It appears likely that the << histamine H2 receptor >> blocked by [[ cimetidine ]] obviated the pulmonary vasodilator effect of tolazoline therapy.,3349,0
3350,<< GYKI 52466 >> decreased the peak amplitude of hippocampal area CA1 [[ AMPA receptor ]]-mediated excitatory postsynaptic currents (e.p.s.cs) (IC50 10.8 +/- 0.8 microM) with no apparent effect on response kinetics.,3350,3
3351,<< Cyclothiazide >> prolonged the decay time constant of [[ AMPA receptor ]]-mediated e.p.s.cs (EC50 35.7 +/- 6.5 microM) with less pronounced effects in slowing e.p.s.c. onset kinetics and increasing e.p.s.c. amplitude.,3351,3
3352,Activation of cytoprotective << prostaglandin synthase-1 >> by [[ minoxidil ]] as a possible explanation for its hair growth-stimulating effect.,3352,9
3353,"We thus speculated that activation of << PGHS-1 >> might be a mechanism by which [[ minoxidil ]] (2,4-diamino-6-piperidinopyrimidine-3-oxyde) stimulates hair growth in vivo.",3353,9
3354,"We thus speculated that activation of << PGHS-1 >> might be a mechanism by which minoxidil ([[ 2,4-diamino-6-piperidinopyrimidine-3-oxyde ]]) stimulates hair growth in vivo.",3354,9
3355,"We demonstrate here that << minoxidil >> is a potent activator of purified [[ PGHS-1 ]] (AC50 = 80 microM), as assayed by oxygen consumption and PGE2 production.",3355,9
3356,"This study was designed to determine the gastroprotective properties of << cinitapride >> (CNT), a novel prokinetic benzamide derivative agonist of [[ 5-HT4 ]] and 5-HT1 receptors and 5-HT2 antagonist, on mucosal injury produced by 50% (v/v) ethanol.",3356,2
3357,"This study was designed to determine the gastroprotective properties of << cinitapride >> (CNT), a novel prokinetic benzamide derivative agonist of 5-HT4 and [[ 5-HT1 ]] receptors and 5-HT2 antagonist, on mucosal injury produced by 50% (v/v) ethanol.",3357,2
3358,"This study was designed to determine the gastroprotective properties of cinitapride (CNT), a novel prokinetic << benzamide >> derivative agonist of [[ 5-HT4 ]] and 5-HT1 receptors and 5-HT2 antagonist, on mucosal injury produced by 50% (v/v) ethanol.",3358,2
3359,"This study was designed to determine the gastroprotective properties of cinitapride (CNT), a novel prokinetic << benzamide >> derivative agonist of 5-HT4 and [[ 5-HT1 ]] receptors and 5-HT2 antagonist, on mucosal injury produced by 50% (v/v) ethanol.",3359,2
3360,"This study was designed to determine the gastroprotective properties of cinitapride (<< CNT >>), a novel prokinetic benzamide derivative agonist of [[ 5-HT4 ]] and 5-HT1 receptors and 5-HT2 antagonist, on mucosal injury produced by 50% (v/v) ethanol.",3360,2
3361,"This study was designed to determine the gastroprotective properties of cinitapride (<< CNT >>), a novel prokinetic benzamide derivative agonist of 5-HT4 and [[ 5-HT1 ]] receptors and 5-HT2 antagonist, on mucosal injury produced by 50% (v/v) ethanol.",3361,2
3362,"This study was designed to determine the gastroprotective properties of << cinitapride >> (CNT), a novel prokinetic benzamide derivative agonist of 5-HT4 and 5-HT1 receptors and [[ 5-HT2 ]] antagonist, on mucosal injury produced by 50% (v/v) ethanol.",3362,1
3363,"This study was designed to determine the gastroprotective properties of cinitapride (CNT), a novel prokinetic << benzamide >> derivative agonist of 5-HT4 and 5-HT1 receptors and [[ 5-HT2 ]] antagonist, on mucosal injury produced by 50% (v/v) ethanol.",3363,1
3364,"This study was designed to determine the gastroprotective properties of cinitapride (<< CNT >>), a novel prokinetic benzamide derivative agonist of 5-HT4 and 5-HT1 receptors and [[ 5-HT2 ]] antagonist, on mucosal injury produced by 50% (v/v) ethanol.",3364,1
3365,"We have identified << adenosine deaminase >>, an enzyme involved in [[ purine ]] metabolism whose deficiency is associated with severe combined immunodeficiency, as a Grb3-3 binding protein that is not able to bind to Grb2.",3365,5
3366,<< Alendronate >> inhibition of [[ protein-tyrosine-phosphatase-meg1 ]].,3366,0
3367,Here we report that << alendronate >> is a potent inhibitor of the [[ protein-tyrosine-phosphatase-meg1 ]] (PTPmeg1).,3367,0
3368,Here we report that << alendronate >> is a potent inhibitor of the protein-tyrosine-phosphatase-meg1 ([[ PTPmeg1 ]]).,3368,0
3369,"With either substrate, << alendronate >> was a slow binding inhibitor of [[ PTPmeg1 ]].",3369,0
3370,"Among the other << bisphosphonates >> studied, alendronate was more potent and selective for [[ PTPmeg1 ]].",3370,0
3371,"Among the other bisphosphonates studied, << alendronate >> was more potent and selective for [[ PTPmeg1 ]].",3371,0
3372,"The hydrolysis of fluorescein diphosphate by PTP epsilon and PTPmeg1 was sensitive to alendronate, with IC50 values of less than 1 microM; << PTPsigma >>, however, under the same conditions, was inhibited by only 50% with 141 microM [[ alendronate ]].",3372,0
3373,"The hydrolysis of fluorescein << diphosphate >> by [[ PTP epsilon ]] and PTPmeg1 was sensitive to alendronate, with IC50 values of less than 1 microM; PTPsigma, however, under the same conditions, was inhibited by only 50% with 141 microM alendronate.",3373,5
3374,"The hydrolysis of fluorescein << diphosphate >> by PTP epsilon and [[ PTPmeg1 ]] was sensitive to alendronate, with IC50 values of less than 1 microM; PTPsigma, however, under the same conditions, was inhibited by only 50% with 141 microM alendronate.",3374,5
3375,"<< Alendronate >> inhibited [[ PTPmeg1 ]] with an IC50 value of 23 microM, PTPsigma with an IC50 value of 2 microM, and did not inhibit PTP epsilon at concentrations up to 1 mM.",3375,0
3376,"<< Alendronate >> inhibited PTPmeg1 with an IC50 value of 23 microM, [[ PTPsigma ]] with an IC50 value of 2 microM, and did not inhibit PTP epsilon at concentrations up to 1 mM.",3376,0
3377,"The << alendronate >> inhibition of these three [[ PTPs ]] and two substrates is consistent with the formation of a ternary complex comprised of enzyme, substrate, and inhibitor.",3377,0
3378,"<< PTP >> inhibition by [[ hisphosphonates ]] or vanadate was diminished by the metal chelating agent EDTA, or by the reducing agent dithiothreitol, suggesting that a metal ion and the oxidation of a cysteine residue are required for full inhibition.",3378,0
3379,"<< PTP >> inhibition by hisphosphonates or [[ vanadate ]] was diminished by the metal chelating agent EDTA, or by the reducing agent dithiothreitol, suggesting that a metal ion and the oxidation of a cysteine residue are required for full inhibition.",3379,0
3380,These observations show substrate- and enzyme-specific << PTP >> inhibition by [[ alendronate ]] and support the possibility that a certain PTP(s) may be the molecular target for alendronate action.,3380,0
3381,"16,16-dimethyl-PGE2 and two putative << EP1 >> antagonists, [[ AH6809 ]] and SC-19220, did not show any significant binding to this receptor.",3381,1
3382,"16,16-dimethyl-PGE2 and two putative << EP1 >> antagonists, AH6809 and [[ SC-19220 ]], did not show any significant binding to this receptor.",3382,1
3383,"<< M&B-28767 >>, a putative [[ EP3 ]] agonist, and misoprostol, a putative EP2/EP3 agonist, also bound to this receptor with Ki values of 120 nM.",3383,2
3384,"M&B-28767, a putative EP3 agonist, and << misoprostol >>, a putative [[ EP2 ]]/EP3 agonist, also bound to this receptor with Ki values of 120 nM.",3384,2
3385,"M&B-28767, a putative EP3 agonist, and << misoprostol >>, a putative EP2/[[ EP3 ]] agonist, also bound to this receptor with Ki values of 120 nM.",3385,2
3386,Blockage of the << HERG human cardiac K+ channel >> by the gastrointestinal prokinetic agent [[ cisapride ]].,3386,0
3387,We tested the hypothesis that << cisapride >> blocks [[ HERG ]].,3387,0
3388,"Under voltage-clamp conditions, << cisapride >> block of [[ HERG ]] is dose dependent with a half-maximal inhibitory concentration of 6.5 nM at 22 degrees C (n = 25 cells).",3388,0
3389,Block of << HERG >> with [[ cisapride ]] after channel activation was voltage dependent.,3389,0
3390,"At -20 mV, 10 nM << cisapride >> reduced [[ HERG ]] tail-current amplitude by 5%, whereas, at + 20 mV, the tail-current amplitude was reduced by 45% (n = 4 cells).",3390,8
3391,We conclude that << cisapride >> is a potent blocker of [[ HERG ]] channels expressed in HEK293 cells.,3391,0
3392,"Intravenous (I.V.) cocaine (0.03-3 mg/kg) produced dose-dependent, rapid, and brief increases in blood pressure (BP) in conscious rats pretreated with the << dopamine receptor >> antagonist, [[ SCH 23390 ]].",3392,1
3393,"Monoamine uptake inhibitors structurally analogous to cocaine (cocaethylene, CFT, betaCIT, CPT, (+)-cocaine, norcocaine, and benztropine) also produced this rapid pressor response, whereas structurally unrelated uptake inhibitors with diverse << monoamine transporter >> selectivities ([[ BTCP ]], indatraline, GBR 12935, mazindol, nomifensine, and zimeldine) either did not produce a rapid pressor response or produced only a small pressor response.",3393,0
3394,"Monoamine uptake inhibitors structurally analogous to cocaine (cocaethylene, CFT, betaCIT, CPT, (+)-cocaine, norcocaine, and benztropine) also produced this rapid pressor response, whereas structurally unrelated uptake inhibitors with diverse << monoamine transporter >> selectivities (BTCP, [[ indatraline ]], GBR 12935, mazindol, nomifensine, and zimeldine) either did not produce a rapid pressor response or produced only a small pressor response.",3394,0
3395,"Monoamine uptake inhibitors structurally analogous to cocaine (cocaethylene, CFT, betaCIT, CPT, (+)-cocaine, norcocaine, and benztropine) also produced this rapid pressor response, whereas structurally unrelated uptake inhibitors with diverse << monoamine transporter >> selectivities (BTCP, indatraline, [[ GBR 12935 ]], mazindol, nomifensine, and zimeldine) either did not produce a rapid pressor response or produced only a small pressor response.",3395,0
3396,"Monoamine uptake inhibitors structurally analogous to cocaine (cocaethylene, CFT, betaCIT, CPT, (+)-cocaine, norcocaine, and benztropine) also produced this rapid pressor response, whereas structurally unrelated uptake inhibitors with diverse << monoamine transporter >> selectivities (BTCP, indatraline, GBR 12935, [[ mazindol ]], nomifensine, and zimeldine) either did not produce a rapid pressor response or produced only a small pressor response.",3396,0
3397,"Monoamine uptake inhibitors structurally analogous to cocaine (cocaethylene, CFT, betaCIT, CPT, (+)-cocaine, norcocaine, and benztropine) also produced this rapid pressor response, whereas structurally unrelated uptake inhibitors with diverse << monoamine transporter >> selectivities (BTCP, indatraline, GBR 12935, mazindol, [[ nomifensine ]], and zimeldine) either did not produce a rapid pressor response or produced only a small pressor response.",3397,0
3398,"Monoamine uptake inhibitors structurally analogous to cocaine (cocaethylene, CFT, betaCIT, CPT, (+)-cocaine, norcocaine, and benztropine) also produced this rapid pressor response, whereas structurally unrelated uptake inhibitors with diverse << monoamine transporter >> selectivities (BTCP, indatraline, GBR 12935, mazindol, nomifensine, and [[ zimeldine ]]) either did not produce a rapid pressor response or produced only a small pressor response.",3398,0
3399,"At nonconvulsant doses, the << sodium channel >> blockers [[ acetylprocainamide ]], dibucaine, dyclonine, prilocaine, proparacaine, quinidine, and tetracaine produced a small pressor response or no increase in BP.",3399,0
3400,"At nonconvulsant doses, the << sodium channel >> blockers acetylprocainamide, [[ dibucaine ]], dyclonine, prilocaine, proparacaine, quinidine, and tetracaine produced a small pressor response or no increase in BP.",3400,0
3401,"At nonconvulsant doses, the << sodium channel >> blockers acetylprocainamide, dibucaine, [[ dyclonine ]], prilocaine, proparacaine, quinidine, and tetracaine produced a small pressor response or no increase in BP.",3401,0
3402,"At nonconvulsant doses, the << sodium channel >> blockers acetylprocainamide, dibucaine, dyclonine, [[ prilocaine ]], proparacaine, quinidine, and tetracaine produced a small pressor response or no increase in BP.",3402,0
3403,"At nonconvulsant doses, the << sodium channel >> blockers acetylprocainamide, dibucaine, dyclonine, prilocaine, [[ proparacaine ]], quinidine, and tetracaine produced a small pressor response or no increase in BP.",3403,0
3404,"At nonconvulsant doses, the << sodium channel >> blockers acetylprocainamide, dibucaine, dyclonine, prilocaine, proparacaine, [[ quinidine ]], and tetracaine produced a small pressor response or no increase in BP.",3404,0
3405,"At nonconvulsant doses, the << sodium channel >> blockers acetylprocainamide, dibucaine, dyclonine, prilocaine, proparacaine, quinidine, and [[ tetracaine ]] produced a small pressor response or no increase in BP.",3405,0
3406,The << sodium channel >>-blocking action of [[ cocaine ]] per se does not appear to be involved in the rapid pressor response to cocaine.,3406,0
3407,"Characterization of binding sites of a new << neurotensin receptor >> antagonist, [[ [3H]SR 142948A ]], in the rat brain.",3407,1
3408,"The present study describes the characterization of the binding properties and autoradiographic distribution of a new nonpeptide antagonist of << neurotensin receptors >>, [[ [3H]SR 142948A ]] (2-[[5-(2,6-dimethoxyphenyl)-1-(4-(N-(3-dimethylaminopropyl)-N-methyl carbamoyl)-2-isopropylphenyl)-1H-pyrazole-3-carbonyl]-amino]-ad amantane-2-carboxylic acid, hydrochloride), in the rat brain.",3408,1
3409,"The present study describes the characterization of the binding properties and autoradiographic distribution of a new nonpeptide antagonist of << neurotensin receptors >>, [3H]SR 142948A ([[ 2-[[5-(2,6-dimethoxyphenyl)-1-(4-(N-(3-dimethylaminopropyl)-N-methyl carbamoyl)-2-isopropylphenyl)-1H-pyrazole-3-carbonyl]-amino]-ad amantane-2-carboxylic acid, hydrochloride ]]), in the rat brain.",3409,1
3410,"Saturation and competition studies in the presence or absence of the << histamine H1 receptor >> antagonist, [[ levocabastine ]], revealed that [3H]SR 142948A bound with similar affinities to both the levocabastine-insensitive neurotensin NT1 receptors (20% of the total binding population) and the recently cloned levocabastine-sensitive neurotensin NT2 receptors (80% of the receptors) (Kd = 6.8 and 4.8 nM, respectively).",3410,1
3411,"In conclusion, these findings indicate that << [3H]SR 142948A >> is a new potent antagonist radioligand which recognizes with high affinity both [[ neurotensin NT1 ]] and NT2 receptors and represents thus an excellent tool to study neurotensin receptors in the rat brain.",3411,1
3412,"In conclusion, these findings indicate that << [3H]SR 142948A >> is a new potent antagonist radioligand which recognizes with high affinity both neurotensin NT1 and [[ NT2 receptors ]] and represents thus an excellent tool to study neurotensin receptors in the rat brain.",3412,1
3413,Isoform-specific inhibition of << L-type calcium channels >> by [[ dihydropyridines ]] is independent of isoform-specific gating properties.,3413,0
3414,"<< Dihydropyridines >> (DHPs) block [[ L-type Ca2+ channels ]] more potently at depolarized membrane potentials, consistent with high affinity binding to the inactivated state.",3414,0
3415,"Dihydropyridines (<< DHPs >>) block [[ L-type Ca2+ channels ]] more potently at depolarized membrane potentials, consistent with high affinity binding to the inactivated state.",3415,0
3416,"<< Nisoldipine >> (a DHP antagonist) blocks the [[ smooth muscle channel ]] more potently than the cardiac one, a phenomenon observed not only in native channels but also in expressed channels.",3416,0
3417,"Nisoldipine (a << DHP >> antagonist) blocks the [[ smooth muscle channel ]] more potently than the cardiac one, a phenomenon observed not only in native channels but also in expressed channels.",3417,0
3418,We thus conclude that the more potent << nisoldipine >> inhibition of smooth muscle versus [[ cardiac L-type Ca2+ channels ]] is not attributable to differences in channel inactivation or activation.,3418,0
3419,"<< Methylenetetrahydrofolate reductase >> deficiency impairs [[ methyltetrahydrofolate ]] synthesis, defects in cytosolic reduction of hydroxocobalamin (CblC/D) impair the synthesis of both methyl- and adenosyl cobalamin and deficiencies of methionine synthase (CblE/G) are associated with defective methyl cobalamin synthesis.",3419,4
3420,"Methylenetetrahydrofolate reductase deficiency impairs methyltetrahydrofolate synthesis, defects in cytosolic reduction of hydroxocobalamin (CblC/D) impair the synthesis of both methyl- and adenosyl cobalamin and deficiencies of << methionine synthase >> (CblE/G) are associated with defective [[ methyl cobalamin ]] synthesis.",3420,4
3421,Increased << Cat3 >>-mediated cationic [[ amino acid ]] transport functionally compensates in Cat1 knockout cell lines.,3421,5
3422,"The majority of << L-Arg >> transport is mediated by [[ System y+ ]], although several other carriers have been kinetically defined.",3422,5
3423,"<< System y+ >> cationic [[ amino acid ]] transport is mediated by proteins encoded by a family of genes, Cat1, Cat2, and Cat3.",3423,5
3424,"System y+ cationic << amino acid >> transport is mediated by proteins encoded by a family of genes, [[ Cat1 ]], Cat2, and Cat3.",3424,5
3425,"System y+ cationic << amino acid >> transport is mediated by proteins encoded by a family of genes, Cat1, [[ Cat2 ]], and Cat3.",3425,5
3426,"System y+ cationic << amino acid >> transport is mediated by proteins encoded by a family of genes, Cat1, Cat2, and [[ Cat3 ]].",3426,5
3427,"However, the apparent affinity for << lysine >> transport was 2.4 times lower in Cat1(-/-) cells when compared with wild type cells, a property characteristic of [[ Cat3 ]]-mediated transport.",3427,5
3428,These results suggest that << Cat3 >> compensates for the loss of functional Cat1 in cells derived from Cat1 knockout mice and mediates the majority of high affinity [[ arginine ]] transport.,3428,5
3429,"Effect of << lintitript >>, a new [[ CCK-A receptor ]] antagonist, on gastric emptying of a solid-liquid meal in humans.",3429,1
3430,"We studied the role of endogenous CCK in the emptying of a solid/liquid meal administering the new, highly specific and potent << CCK-A receptor >> antagonist [[ lintitript ]].",3430,1
3431,<< Lintitript >> markedly increased postprandial plasma [[ CCK ]] release (P<0.001) while distinctly reducing postprandial PP levels (P<0.01) as compared to placebo.,3431,6
3432,<< Lintitript >> markedly increased postprandial plasma CCK release (P<0.001) while distinctly reducing postprandial [[ PP ]] levels (P<0.01) as compared to placebo.,3432,8
3433,The study demonstrates for the first time the marked gastrokinetic properties of the new << CCK-A receptor >> antagonist [[ lintitript ]] in humans.,3433,1
3434,"Concanavalin A (Con A)-induced << IFN-gamma >>, GM-CSF, and IL-3 mRNAs are dose-dependently inhibited by the nonselective betaAR agonist [[ isoproterenol ]] and by the selective beta2AR agonist fenoterol.",3434,8
3435,"Concanavalin A (Con A)-induced IFN-gamma, << GM-CSF >>, and IL-3 mRNAs are dose-dependently inhibited by the nonselective betaAR agonist [[ isoproterenol ]] and by the selective beta2AR agonist fenoterol.",3435,8
3436,"Concanavalin A (Con A)-induced IFN-gamma, GM-CSF, and << IL-3 >> mRNAs are dose-dependently inhibited by the nonselective betaAR agonist [[ isoproterenol ]] and by the selective beta2AR agonist fenoterol.",3436,8
3437,"Concanavalin A (Con A)-induced << IFN-gamma >>, GM-CSF, and IL-3 mRNAs are dose-dependently inhibited by the nonselective betaAR agonist isoproterenol and by the selective beta2AR agonist [[ fenoterol ]].",3437,8
3438,"Concanavalin A (Con A)-induced IFN-gamma, << GM-CSF >>, and IL-3 mRNAs are dose-dependently inhibited by the nonselective betaAR agonist isoproterenol and by the selective beta2AR agonist [[ fenoterol ]].",3438,8
3439,"Concanavalin A (Con A)-induced IFN-gamma, GM-CSF, and << IL-3 >> mRNAs are dose-dependently inhibited by the nonselective betaAR agonist isoproterenol and by the selective beta2AR agonist [[ fenoterol ]].",3439,8
3440,"Concanavalin A (Con A)-induced IFN-gamma, GM-CSF, and IL-3 mRNAs are dose-dependently inhibited by the nonselective << betaAR >> agonist [[ isoproterenol ]] and by the selective beta2AR agonist fenoterol.",3440,2
3441,"Concanavalin A (Con A)-induced IFN-gamma, GM-CSF, and IL-3 mRNAs are dose-dependently inhibited by the nonselective betaAR agonist isoproterenol and by the selective << beta2AR >> agonist [[ fenoterol ]].",3441,2
3442,"The observed inhibition on << IFN-gamma >>, GM-CSF, and IL-3 mRNA was blocked by the selective beta2AR antagonist [[ ICI 118,551 ]] (10(-6) M) and by timolol (10(-6) M), a nonselective antagonist.",3442,6
3443,"The observed inhibition on IFN-gamma, << GM-CSF >>, and IL-3 mRNA was blocked by the selective beta2AR antagonist [[ ICI 118,551 ]] (10(-6) M) and by timolol (10(-6) M), a nonselective antagonist.",3443,6
3444,"The observed inhibition on IFN-gamma, GM-CSF, and << IL-3 >> mRNA was blocked by the selective beta2AR antagonist [[ ICI 118,551 ]] (10(-6) M) and by timolol (10(-6) M), a nonselective antagonist.",3444,6
3445,"The observed inhibition on << IFN-gamma >>, GM-CSF, and IL-3 mRNA was blocked by the selective beta2AR antagonist ICI 118,551 (10(-6) M) and by [[ timolol ]] (10(-6) M), a nonselective antagonist.",3445,6
3446,"The observed inhibition on IFN-gamma, << GM-CSF >>, and IL-3 mRNA was blocked by the selective beta2AR antagonist ICI 118,551 (10(-6) M) and by [[ timolol ]] (10(-6) M), a nonselective antagonist.",3446,6
3447,"The observed inhibition on IFN-gamma, GM-CSF, and << IL-3 >> mRNA was blocked by the selective beta2AR antagonist ICI 118,551 (10(-6) M) and by [[ timolol ]] (10(-6) M), a nonselective antagonist.",3447,6
3448,"The observed inhibition on IFN-gamma, GM-CSF, and IL-3 mRNA was blocked by the selective << beta2AR >> antagonist [[ ICI 118,551 ]] (10(-6) M) and by timolol (10(-6) M), a nonselective antagonist.",3448,1
3449,"The observed inhibition on IFN-gamma, GM-CSF, and IL-3 mRNA was blocked by the selective << beta2AR >> antagonist ICI 118,551 (10(-6) M) and by [[ timolol ]] (10(-6) M), a nonselective antagonist.",3449,1
3450,The selective << beta1AR >> antagonist [[ atenolol ]] (0.3 x 10(-6) M) did not have any effect.,3450,1
3451,Secretion of << GM-CSF >> protein in the presence of increasing concentrations of [[ isoproterenol ]] followed a similar pattern as observed for GM-CSF mRNA.,3451,6
3452,Secretion of GM-CSF protein in the presence of increasing concentrations of << isoproterenol >> followed a similar pattern as observed for [[ GM-CSF ]] mRNA.,3452,6
3453,"Although beta3AR mRNA was detectable in Con A-activated T lymphocytes, we could not demonstrate a functional activity in the regulation of cytokine expression: the << beta3AR >> agonist [[ BRL 37344 ]] had no effect on the accumulation of the studied cytokine mRNAs, and did not significantly affect cellular cAMP levels.",3453,2
3454,"All three compounds displayed antagonistic properties against << oxytocin >> in vitro, with [[ carbetocin ]] being the strongest inhibitor (pA2 = 8.21) and carbetocin metabolite II (pA2 = 8.01) being stronger than carbetocin metabolite I (pA2 = 7.81).",3454,0
3455,"All three compounds displayed antagonistic properties against << oxytocin >> in vitro, with carbetocin being the strongest inhibitor (pA2 = 8.21) and [[ carbetocin ]] metabolite II (pA2 = 8.01) being stronger than carbetocin metabolite I (pA2 = 7.81).",3455,0
3456,"All three compounds displayed antagonistic properties against << oxytocin >> in vitro, with carbetocin being the strongest inhibitor (pA2 = 8.21) and carbetocin metabolite II (pA2 = 8.01) being stronger than [[ carbetocin ]] metabolite I (pA2 = 7.81).",3456,0
3457,These results indicate that << carbetocin >> is a partial agonist/antagonist to the [[ oxytocin receptor ]] while the two metabolites carbetocin metabolite I and carbetocin metabolite II are pure antagonists.,3457,2
3458,These results indicate that << carbetocin >> is a partial agonist/antagonist to the [[ oxytocin receptor ]] while the two metabolites carbetocin metabolite I and carbetocin metabolite II are pure antagonists.,3458,1
3459,These results indicate that carbetocin is a partial agonist/antagonist to the << oxytocin receptor >> while the two metabolites [[ carbetocin ]] metabolite I and carbetocin metabolite II are pure antagonists.,3459,1
3460,These results indicate that carbetocin is a partial agonist/antagonist to the << oxytocin receptor >> while the two metabolites carbetocin metabolite I and [[ carbetocin ]] metabolite II are pure antagonists.,3460,1
3461,Crystallographic analysis of the << human phenylalanine hydroxylase catalytic domain >> with bound [[ catechol ]] inhibitors at 2.0 A resolution.,3461,0
3462,"The << aromatic amino acid hydroxylases >> represent a superfamily of structurally and functionally closely related enzymes, one of those functions being reversible inhibition by [[ catechol ]] derivatives.",3462,0
3463,"Here we present the crystal structure of the dimeric catalytic domain (residues 117-424) of << human phenylalanine hydroxylase >> (hPheOH), cocrystallized with various potent and well-known [[ catechol ]] inhibitors and refined at a resolution of 2.0 A.",3463,0
3464,"Here we present the crystal structure of the dimeric catalytic domain (residues 117-424) of human phenylalanine hydroxylase (<< hPheOH >>), cocrystallized with various potent and well-known [[ catechol ]] inhibitors and refined at a resolution of 2.0 A.",3464,0
3465,"Crystallographic comparison with the structurally related << rat tyrosine hydroxylase >> binary complex with the oxidized cofactor 7,8-dihydrobiopterin revealed overlapping binding sites for the catechols and the cofactor, compatible with a competitive type of inhibition of the [[ catechols ]] versus BH4.",3465,0
3466,"All GCs including the antagonistic compound << RU486 >> efficiently reduced [[ NF-kappaB ]]-mediated transactivation to comparable extents, suggesting that ligand-induced nuclear localization of the GR is sufficient for transrepression.",3466,3
3467,The ATP-sensitive potassium (KATP) channels in pancreatic beta cells are critical in the regulation of << glucose >>-induced [[ insulin ]] secretion.,3467,6
3468,"These results suggest that SUR1 binds 8-azido-ATP strongly at NBF1 and that MgADP, either by direct binding to NBF2 or by hydrolysis of bound << MgATP >> at [[ NBF2 ]], stabilizes prebound 8-azido-ATP binding at NBF1.",3468,5