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+0,"At 4 hours, losartan blocked 43% of the << Ang II >>-induced systolic blood pressure increase; [[ valsartan ]], 51%; and irbesartan, 88% (P<0.01 between drugs).",0,8
+1,"At 4 hours, losartan blocked 43% of the << Ang II >>-induced systolic blood pressure increase; valsartan, 51%; and [[ irbesartan ]], 88% (P<0.01 between drugs).",1,8
+2,This study thus demonstrates that the first administration of the recommended starting dose of << irbesartan >> induces a greater and longer lasting [[ Ang II receptor ]] blockade than that of valsartan and losartan in normotensive subjects.,2,0
+3,This study thus demonstrates that the first administration of the recommended starting dose of irbesartan induces a greater and longer lasting << Ang II receptor >> blockade than that of [[ valsartan ]] and losartan in normotensive subjects.,3,0
+4,This study thus demonstrates that the first administration of the recommended starting dose of irbesartan induces a greater and longer lasting << Ang II receptor >> blockade than that of valsartan and [[ losartan ]] in normotensive subjects.,4,0
+5,"In humans, prolonged administration of the << beta 2-adrenoceptor >> agonist [[ terbutaline ]] leads to a desensitization of beta 2-adrenoceptor-mediated cardiovascular responses, which can be blunted by concomitant administration of the antianaphylactic drug ketotifen.",5,2
+6,"In a double-blind, placebo-controlled, randomized design, nine healthy male volunteers received disodium cromoglycate (4 x 200 mg/day, p.o.) or placebo for 3 weeks with terbutaline (3 x 5 mg/day, p.o.) administered concomitantly during the last 2 weeks. beta 2-Adrenoceptor cardiovascular function was assessed by the increase in heart rate and reduction of diastolic blood pressure induced by an incremental intravenous infusion of the unselective << beta-adrenoceptor >> agonist [[ isoprenaline ]]; beta 1-adrenoceptor cardiovascular function was assessed by exercise-induced tachycardia.",6,2
+7,"OBJECTIVES: This study examined the effect of a small-molecule, direct << thrombin >> inhibitor, [[ argatroban ]], on reperfusion induced by tissue plasminogen activator (TPA) in patients with acute myocardial infarction (AMI).",7,0
+8,In vitro and in vivo studies have shown that << argatroban >> has advantages over heparin for the inhibition of clot-bound [[ thrombin ]] and for the enhancement of thrombolysis with TPA.,8,0
+9,The functional inhibitory characteristics of the << angiotensin II type 1 receptor >> blockers (ARB) candesartan; [[ irbesartan ]]; and losartan and its active metabolite EXP 3174 (EXP) were studied in rabbit aortic strips and rat portal vein preparations in vitro.,9,0
+10,The functional inhibitory characteristics of the << angiotensin II type 1 receptor >> blockers (ARB) [[ candesartan ]]; irbesartan; and losartan and its active metabolite EXP 3174 (EXP) were studied in rabbit aortic strips and rat portal vein preparations in vitro.,10,0
+11,The functional inhibitory characteristics of the << angiotensin II type 1 receptor >> blockers (ARB) candesartan; irbesartan; and [[ losartan ]] and its active metabolite EXP 3174 (EXP) were studied in rabbit aortic strips and rat portal vein preparations in vitro.,11,0
+12,The functional inhibitory characteristics of the << angiotensin II type 1 receptor >> blockers (ARB) candesartan; irbesartan; and losartan and its active metabolite [[ EXP 3174 ]] (EXP) were studied in rabbit aortic strips and rat portal vein preparations in vitro.,12,0
+13,The functional inhibitory characteristics of the << angiotensin II type 1 receptor >> blockers (ARB) candesartan; irbesartan; and losartan and its active metabolite EXP 3174 ([[ EXP ]]) were studied in rabbit aortic strips and rat portal vein preparations in vitro.,13,0
+14,"In both vascular preparations, << candesartan >> caused a marked decrease in the maximal contractile response of the [[ angiotensin II ]] (Ang II) concentration-response curve.",14,8
+15,"In both vascular preparations, << candesartan >> caused a marked decrease in the maximal contractile response of the angiotensin II ([[ Ang II ]]) concentration-response curve.",15,8
+16,"In addition, when << candesartan >> was given to conscious rats, the inhibitory effect on [[ Ang II ]]-induced blood pressure responses persisted during the 24-hour period despite nondetectable plasma concentrations of candesartan at 24 hours.",16,8
+17,"At clinically relevant concentrations, << candesartan >> is an insurmountable and long-lasting antagonist of the vascular contractile responses to [[ Ang II ]].",17,8
+18,Dose-dependent inhibition of platelet << cyclooxygenase-1 >> and monocyte cyclooxygenase-2 by [[ meloxicam ]] in healthy subjects.,18,0
+19,Dose-dependent inhibition of platelet cyclooxygenase-1 and monocyte << cyclooxygenase-2 >> by [[ meloxicam ]] in healthy subjects.,19,0
+20,Concentration-response curves for the inhibition of monocyte << COX-2 >> and platelet COX-1 were obtained in vitro after the incubation of [[ meloxicam ]] with whole blood samples.,20,0
+21,Concentration-response curves for the inhibition of monocyte COX-2 and platelet << COX-1 >> were obtained in vitro after the incubation of [[ meloxicam ]] with whole blood samples.,21,0
+22,"Before dosing and 24 h after the seventh dose of each regimen, heparinized whole blood samples were incubated with lipopolysaccharide (10 microgram/ml) for 24 h at 37 degrees C, and << prostaglandin E2 >> was measured in plasma as an index of monocyte [[ COX-2 ]] activity.",22,4
+23,The production of << thromboxane B2 >> in whole blood allowed to clot at 37 degrees C for 60 min was assessed as an index of platelet [[ COX-1 ]] activity.,23,4
+24,"In contrast, the administration of 7.5 and 15 mg of << meloxicam >> caused dose-dependent reductions in monocyte [[ COX-2 ]] activity by 51% and 70%, respectively, and in platelet COX-1 activity by 25% and 35%, respectively.",24,0
+25,"In contrast, the administration of 7.5 and 15 mg of << meloxicam >> caused dose-dependent reductions in monocyte COX-2 activity by 51% and 70%, respectively, and in platelet [[ COX-1 ]] activity by 25% and 35%, respectively.",25,0
+26,"Although the IC50 value of << meloxicam >> for inhibition of [[ COX-1 ]] was 10-fold higher than the IC50 value of COX-2 in vitro, this biochemical selectivity was inadequate to clearly separate the effects of meloxicam on the two isozymes after oral dosing as a function of the daily dose and interindividual variation in steady-state plasma levels.",26,0
+27,"Although the IC50 value of << meloxicam >> for inhibition of COX-1 was 10-fold higher than the IC50 value of [[ COX-2 ]] in vitro, this biochemical selectivity was inadequate to clearly separate the effects of meloxicam on the two isozymes after oral dosing as a function of the daily dose and interindividual variation in steady-state plasma levels.",27,0
+28,"In distinction, the preferential << beta 1-AR >> antagonist, [[ betaxolol ]], and the preferential beta 2-AR antagonist, ICI118,551, did not increase basal levels of DA, NAD, or 5-HT.",28,1
+29,"In distinction, the preferential beta 1-AR antagonist, betaxolol, and the preferential << beta 2-AR >> antagonist, [[ ICI118,551 ]], did not increase basal levels of DA, NAD, or 5-HT.",29,1
+30,"The selective << 5-HT1A >> receptor antagonist, [[ WAY100,635 ]], slightly attenuated the (-)-pindolol-induced increase in DA and NAD levels, while the selective 5-HT1B antagonist, SB224,289, was ineffective.",30,1
+31,"The selective 5-HT1A receptor antagonist, WAY100,635, slightly attenuated the (-)-pindolol-induced increase in DA and NAD levels, while the selective << 5-HT1B >> antagonist, [[ SB224,289 ]], was ineffective.",31,1
+32,UNLABELLED: << Entacapone >> is a potent and specific peripheral [[ catechol-O-methyltransferase ]] (COMT) inhibitor.,32,0
+33,UNLABELLED: << Entacapone >> is a potent and specific peripheral catechol-O-methyltransferase ([[ COMT ]]) inhibitor.,33,0
+34,<< 5-hydroxytryptamine >> evokes [[ endothelial nitric oxide synthase ]] activation in bovine aortic endothelial cell cultures.,34,9
+35,Activation of << endothelial nitric oxide synthase >> (eNOS) results in the production of [[ nitric oxide ]] (NO) that mediates the vasorelaxing properties of endothelial cells.,35,4
+36,Activation of endothelial nitric oxide synthase (<< eNOS >>) results in the production of [[ nitric oxide ]] (NO) that mediates the vasorelaxing properties of endothelial cells.,36,4
+37,Activation of << endothelial nitric oxide synthase >> (eNOS) results in the production of nitric oxide ([[ NO ]]) that mediates the vasorelaxing properties of endothelial cells.,37,4
+38,Activation of endothelial nitric oxide synthase (<< eNOS >>) results in the production of nitric oxide ([[ NO ]]) that mediates the vasorelaxing properties of endothelial cells.,38,4
+39,"Here, we tested the hypothesis that 5-HT receptors mediate << eNOS >> activation by measuring agonist-stimulated [[ [3H]L-citrulline ]] ([3H]L-Cit) formation in BAEC cultures.",39,4
+40,"Here, we tested the hypothesis that 5-HT receptors mediate << eNOS >> activation by measuring agonist-stimulated [3H]L-citrulline ([[ [3H]L-Cit ]]) formation in BAEC cultures.",40,4
+41,"We found that << 5-HT >> stimulated the conversion of [3H]L-arginine ([3H]L-Arg) to [3H]L-Cit, indicating [[ eNOS ]] activation.",41,9
+42,"We found that 5-HT stimulated the conversion of [3H]L-arginine ([3H]L-Arg) to << [3H]L-Cit >>, indicating [[ eNOS ]] activation.",42,4
+43,"We found that 5-HT stimulated the conversion of << [3H]L-arginine >> ([3H]L-Arg) to [3H]L-Cit, indicating [[ eNOS ]] activation.",43,5
+44,"We found that 5-HT stimulated the conversion of [3H]L-arginine (<< [3H]L-Arg >>) to [3H]L-Cit, indicating [[ eNOS ]] activation.",44,5
+45,"The high affinity << 5-HT1B >> receptor agonist, [[ 5-nonyloxytryptamine ]] (5-NOT)-stimulated [3H]L-Cit turnover responses were concentration-(0.01 nM to 100 microM) and time-dependent.",45,2
+46,"These responses were effectively blocked by the 5-HT1B receptor antagonist, isamoltane, the 5-HT1B/5-HT2 receptor antagonist, methiothepin, and the << eNOS >> selective antagonists (0.01-10 microM): [[ L-Nomega -monomethyl-L-arginine ]] (L-NMMA) and L-N omega-iminoethyl-L-ornithine (L-NIO).",46,1
+47,"These responses were effectively blocked by the 5-HT1B receptor antagonist, isamoltane, the << 5-HT1B >>/5-HT2 receptor antagonist, [[ methiothepin ]], and the eNOS selective antagonists (0.01-10 microM): L-Nomega -monomethyl-L-arginine (L-NMMA) and L-N omega-iminoethyl-L-ornithine (L-NIO).",47,1
+48,"These responses were effectively blocked by the 5-HT1B receptor antagonist, isamoltane, the 5-HT1B/<< 5-HT2 receptor >> antagonist, [[ methiothepin ]], and the eNOS selective antagonists (0.01-10 microM): L-Nomega -monomethyl-L-arginine (L-NMMA) and L-N omega-iminoethyl-L-ornithine (L-NIO).",48,1
+49,"These responses were effectively blocked by the 5-HT1B receptor antagonist, isamoltane, the 5-HT1B/5-HT2 receptor antagonist, methiothepin, and the << eNOS >> selective antagonists (0.01-10 microM): L-Nomega -monomethyl-L-arginine ([[ L-NMMA ]]) and L-N omega-iminoethyl-L-ornithine (L-NIO).",49,1
+50,"These responses were effectively blocked by the 5-HT1B receptor antagonist, isamoltane, the 5-HT1B/5-HT2 receptor antagonist, methiothepin, and the << eNOS >> selective antagonists (0.01-10 microM): L-Nomega -monomethyl-L-arginine (L-NMMA) and [[ L-N omega-iminoethyl-L-ornithine ]] (L-NIO).",50,1
+51,"These responses were effectively blocked by the 5-HT1B receptor antagonist, isamoltane, the 5-HT1B/5-HT2 receptor antagonist, methiothepin, and the << eNOS >> selective antagonists (0.01-10 microM): L-Nomega -monomethyl-L-arginine (L-NMMA) and L-N omega-iminoethyl-L-ornithine ([[ L-NIO ]]).",51,1
+52,"These findings lend evidence of a 5-HT1B receptor/eNOS pathway, accounting in part for the activation of << eNOS >> by [[ 5-HT ]].",52,9
+53,<< Caffeine >> inhibits the checkpoint [[ kinase ]] ATM.,53,0
+54,<< Caffeine >> inhibits the checkpoint kinase [[ ATM ]].,54,0
+55,We report that the radiation-induced activation of the kinase Cds1 [4] (also known as Chk2 [5]) is inhibited by caffeine in vivo and that << ATM >> kinase activity is directly inhibited by [[ caffeine ]] in vitro.,55,0
+56,We report that the radiation-induced activation of the kinase Cds1 [4] (also known as Chk2 [5]) is inhibited by caffeine in vivo and that ATM << kinase >> activity is directly inhibited by [[ caffeine ]] in vitro.,56,0
+57,We report that the radiation-induced activation of the << kinase >> Cds1 [4] (also known as Chk2 [5]) is inhibited by [[ caffeine ]] in vivo and that ATM kinase activity is directly inhibited by caffeine in vitro.,57,0
+58,We report that the radiation-induced activation of the kinase << Cds1 >> [4] (also known as Chk2 [5]) is inhibited by [[ caffeine ]] in vivo and that ATM kinase activity is directly inhibited by caffeine in vitro.,58,0
+59,We report that the radiation-induced activation of the kinase Cds1 [4] (also known as << Chk2 >> [5]) is inhibited by [[ caffeine ]] in vivo and that ATM kinase activity is directly inhibited by caffeine in vitro.,59,0
+60,Inhibition of << ATM >> provides a molecular explanation of the attenuation of DNA-damage checkpoint responses and for the increased radiosensitivity of [[ caffeine ]]-treated cells [6] [7] [8].,60,0
+61,"The turnover of << SERT >> was determined from the rate of recovery of binding after administration of [[ RTI-76 ]], an irreversible inhibitor of ligand binding.",61,0
+62,"In preliminary studies, in vitro incubation of rat cerebral cortex with << RTI-76 >> produced a wash and temperature resistant inhibition of [[ SERT ]] binding densities (Bmax).",62,0
+63,Citalopram protected against the << RTI-76 >>-induced inhibition of [[ SERT ]] binding.,63,0
+64,The decrease and recovery of << [3H]-5-HT >> uptake correlated highly (r = 0.93) with the recovery of [[ SERT ]] binding.,64,5
+65,"<< Losartan >> was the first, but by no means remained the only, [[ AT1 ]] receptor antagonist.",65,1
+66,"Among the current << AT1 >> receptor antagonists, the rank order of the relative binding affinities (highest affinity = 1) is: candesartan 1, telmisartan 10, E3174 (the active metabolite of [[ losartan ]]) 10, tasosartan 20, losartan 50, eprosartan 100 and the prodrug candesartan cilexetil 280.",66,1
+67,"Among the current << AT1 >> receptor antagonists, the rank order of the relative binding affinities (highest affinity = 1) is: candesartan 1, telmisartan 10, E3174 (the active metabolite of losartan) 10, [[ tasosartan ]] 20, losartan 50, eprosartan 100 and the prodrug candesartan cilexetil 280.",67,1
+68,"Among the current << AT1 >> receptor antagonists, the rank order of the relative binding affinities (highest affinity = 1) is: [[ candesartan ]] 1, telmisartan 10, E3174 (the active metabolite of losartan) 10, tasosartan 20, losartan 50, eprosartan 100 and the prodrug candesartan cilexetil 280.",68,1
+69,"Among the current << AT1 >> receptor antagonists, the rank order of the relative binding affinities (highest affinity = 1) is: candesartan 1, [[ telmisartan ]] 10, E3174 (the active metabolite of losartan) 10, tasosartan 20, losartan 50, eprosartan 100 and the prodrug candesartan cilexetil 280.",69,1
+70,"Among the current << AT1 >> receptor antagonists, the rank order of the relative binding affinities (highest affinity = 1) is: candesartan 1, telmisartan 10, [[ E3174 ]] (the active metabolite of losartan) 10, tasosartan 20, losartan 50, eprosartan 100 and the prodrug candesartan cilexetil 280.",70,1
+71,"Among the current << AT1 >> receptor antagonists, the rank order of the relative binding affinities (highest affinity = 1) is: candesartan 1, telmisartan 10, E3174 (the active metabolite of losartan) 10, tasosartan 20, [[ losartan ]] 50, eprosartan 100 and the prodrug candesartan cilexetil 280.",71,1
+72,"Among the current << AT1 >> receptor antagonists, the rank order of the relative binding affinities (highest affinity = 1) is: candesartan 1, telmisartan 10, E3174 (the active metabolite of losartan) 10, tasosartan 20, losartan 50, [[ eprosartan ]] 100 and the prodrug candesartan cilexetil 280.",72,1
+73,"Among the current << AT1 >> receptor antagonists, the rank order of the relative binding affinities (highest affinity = 1) is: candesartan 1, telmisartan 10, E3174 (the active metabolite of losartan) 10, tasosartan 20, losartan 50, eprosartan 100 and the prodrug [[ candesartan cilexetil ]] 280.",73,1
+74,"The mode of (functional) << AT1 >> receptor antagonism has been characterized as surmountable/noncompetitive (losartan, tasosartan, eprosartan) or insurmountable/noncompetitive (candesartan, [[ saprisartan ]], zolasartan, irbesartan, valsartan, telmisartan, E3174).",74,1
+75,"The mode of (functional) << AT1 >> receptor antagonism has been characterized as surmountable/noncompetitive (losartan, tasosartan, eprosartan) or insurmountable/noncompetitive (candesartan, saprisartan, [[ zolasartan ]], irbesartan, valsartan, telmisartan, E3174).",75,1
+76,"The mode of (functional) << AT1 >> receptor antagonism has been characterized as surmountable/noncompetitive (losartan, tasosartan, eprosartan) or insurmountable/noncompetitive (candesartan, saprisartan, zolasartan, [[ irbesartan ]], valsartan, telmisartan, E3174).",76,1
+77,"The mode of (functional) << AT1 >> receptor antagonism has been characterized as surmountable/noncompetitive (losartan, tasosartan, eprosartan) or insurmountable/noncompetitive (candesartan, saprisartan, zolasartan, irbesartan, [[ valsartan ]], telmisartan, E3174).",77,1
+78,"The mode of (functional) << AT1 >> receptor antagonism has been characterized as surmountable/noncompetitive (losartan, tasosartan, eprosartan) or insurmountable/noncompetitive (candesartan, saprisartan, zolasartan, irbesartan, valsartan, [[ telmisartan ]], E3174).",78,1
+79,"The mode of (functional) << AT1 >> receptor antagonism has been characterized as surmountable/noncompetitive (losartan, tasosartan, eprosartan) or insurmountable/noncompetitive (candesartan, saprisartan, zolasartan, irbesartan, valsartan, telmisartan, [[ E3174 ]]).",79,1
+80,"The mode of (functional) << AT1 >> receptor antagonism has been characterized as surmountable/noncompetitive ([[ losartan ]], tasosartan, eprosartan) or insurmountable/noncompetitive (candesartan, saprisartan, zolasartan, irbesartan, valsartan, telmisartan, E3174).",80,1
+81,"The mode of (functional) << AT1 >> receptor antagonism has been characterized as surmountable/noncompetitive (losartan, [[ tasosartan ]], eprosartan) or insurmountable/noncompetitive (candesartan, saprisartan, zolasartan, irbesartan, valsartan, telmisartan, E3174).",81,1
+82,"The mode of (functional) << AT1 >> receptor antagonism has been characterized as surmountable/noncompetitive (losartan, tasosartan, [[ eprosartan ]]) or insurmountable/noncompetitive (candesartan, saprisartan, zolasartan, irbesartan, valsartan, telmisartan, E3174).",82,1
+83,"The mode of (functional) << AT1 >> receptor antagonism has been characterized as surmountable/noncompetitive (losartan, tasosartan, eprosartan) or insurmountable/noncompetitive ([[ candesartan ]], saprisartan, zolasartan, irbesartan, valsartan, telmisartan, E3174).",83,1
+84,<< Quinone oxidoreductases >> are flavoproteins that catalyze two-electron reduction and detoxification of [[ quinones ]].,84,5
+85,"A role of cytosolic << NQO1 >> in protection of cells from oxidative stress, cytotoxicity, and mutagenicity of [[ quinones ]] was established.",85,5
+86,"The << mNQO >> activity showed significantly higher affinity for NADH than NADPH as electron donors and catalyzed reduction of [[ 2,6-dichlorophenolindophenol ]] and menadione.",86,5
+87,"The << mNQO >> activity showed significantly higher affinity for NADH than NADPH as electron donors and catalyzed reduction of 2,6-dichlorophenolindophenol and [[ menadione ]].",87,5
+88,"The mNQO activity was insensitive to << dicoumarol >>, a potent inhibitor of cytosolic [[ NQO1 ]].",88,0
+89,The << mu-opioid receptor >>-selective agonist [[ lofentanil ]] potently and competitively displaced [3H]nociceptin at rat brain receptors (IC(50) 62 nM).,89,2
+90,<< Lofentanil >> exhibited full agonism for enhancement of [35S]GTPgammaS binding to human recombinant [[ ORL1 ]] receptors (EC(50) 50 nM).,90,10
+91,The related piperidines ohmefentanyl and << sufentanil >> and the nonselective opioid receptor agonist etorphine were less potent [[ nociceptin receptor ]] agonists.,91,2
+92,The related piperidines ohmefentanyl and sufentanil and the nonselective << opioid receptor >> agonist [[ etorphine ]] were less potent nociceptin receptor agonists.,92,2
+93,The related piperidines ohmefentanyl and sufentanil and the nonselective opioid receptor agonist << etorphine >> were less potent [[ nociceptin receptor ]] agonists.,93,2
+94,The related << piperidines >> ohmefentanyl and sufentanil and the nonselective opioid receptor agonist etorphine were less potent [[ nociceptin receptor ]] agonists.,94,2
+95,The related piperidines << ohmefentanyl >> and sufentanil and the nonselective opioid receptor agonist etorphine were less potent [[ nociceptin receptor ]] agonists.,95,2
+96,The kappa(1)+kappa(3)-opioid receptor agonist/mu-opioid receptor antagonist << naloxone benzoylhydrazone >> was a pure antagonist at both rat brain and human [[ ORL1 ]] receptors.,96,1
+97,The kappa(1)+kappa(3)-opioid receptor agonist/<< mu-opioid receptor >> antagonist [[ naloxone benzoylhydrazone ]] was a pure antagonist at both rat brain and human ORL1 receptors.,97,1
+98,"The nonselective << opioid receptor >> partial agonist [[ buprenorphine ]] and the nonselective opioid receptor antagonist (-)-quadazocine exhibited pure antagonism at rat brain receptors, but displayed partial agonism at human ORL1 receptors.",98,2
+99,"The nonselective opioid receptor partial agonist buprenorphine and the nonselective opioid receptor antagonist << (-)-quadazocine >> exhibited pure antagonism at rat brain receptors, but displayed partial agonism at [[ human ORL1 ]] receptors.",99,2
+100,"The nonselective opioid receptor partial agonist buprenorphine and the nonselective << opioid receptor >> antagonist [[ (-)-quadazocine ]] exhibited pure antagonism at rat brain receptors, but displayed partial agonism at human ORL1 receptors.",100,1
+101,"<< Thymidylate synthase >> and thymidine kinase are key enzymes involved in the de novo and salvage pathways for [[ pyrimidine nucleotide ]] synthesis, respectively.",101,4
+102,"Thymidylate synthase and << thymidine kinase >> are key enzymes involved in the de novo and salvage pathways for [[ pyrimidine nucleotide ]] synthesis, respectively.",102,4
+103,"<< Thymidylate synthase >> is inhibited by [[ 5-fluorodeoxyuridine monophosphate ]], forming an inactive ternary complex with intracellular folate.",103,0
+104,"Thirty-week administration of << UFT >> with or without leucovorin markedly suppressed both colorectal carcinogenesis and tumor growth, resulted in the increase of [[ thymidylate synthase ]] inhibition and the decrease of thymidine kinase activity in the tumor cells.",104,0
+105,"Thirty-week administration of << UFT >> with or without leucovorin markedly suppressed both colorectal carcinogenesis and tumor growth, resulted in the increase of thymidylate synthase inhibition and the decrease of [[ thymidine kinase ]] activity in the tumor cells.",105,0
+106,"Thirty-week administration of UFT with or without << leucovorin >> markedly suppressed both colorectal carcinogenesis and tumor growth, resulted in the increase of [[ thymidylate synthase ]] inhibition and the decrease of thymidine kinase activity in the tumor cells.",106,0
+107,"Thirty-week administration of UFT with or without << leucovorin >> markedly suppressed both colorectal carcinogenesis and tumor growth, resulted in the increase of thymidylate synthase inhibition and the decrease of [[ thymidine kinase ]] activity in the tumor cells.",107,0
+108,"Ornithine decarboxylase (<< ODC >>) catalyses the first step in the synthesis of the polyamines putrescine, [[ spermidine ]] and spermine.",108,4
+109,"<< Ornithine decarboxylase >> (ODC) catalyses the first step in the synthesis of the polyamines putrescine, [[ spermidine ]] and spermine.",109,4
+110,"Ornithine decarboxylase (<< ODC >>) catalyses the first step in the synthesis of the polyamines putrescine, spermidine and [[ spermine ]].",110,4
+111,"<< Ornithine decarboxylase >> (ODC) catalyses the first step in the synthesis of the polyamines putrescine, spermidine and [[ spermine ]].",111,4
+112,"Ornithine decarboxylase (<< ODC >>) catalyses the first step in the synthesis of the polyamines [[ putrescine ]], spermidine and spermine.",112,4
+113,"<< Ornithine decarboxylase >> (ODC) catalyses the first step in the synthesis of the polyamines [[ putrescine ]], spermidine and spermine.",113,4
+114,In << alpha(2A)-adrenoceptor >> transfected cells the rank order of agonist potency was [[ A-54741 ]] (mean pEC(50)=8.96)>dexmedetomidine (8.88)>UK-14304 (8.42)>B-HT 920 (7.05)>noradrenaline (6.92).,114,2
+115,In << alpha(2A)-adrenoceptor >> transfected cells the rank order of agonist potency was A-54741 (mean pEC(50)=8.96)>[[ dexmedetomidine ]] (8.88)>UK-14304 (8.42)>B-HT 920 (7.05)>noradrenaline (6.92).,115,2
+116,In << alpha(2A)-adrenoceptor >> transfected cells the rank order of agonist potency was A-54741 (mean pEC(50)=8.96)>dexmedetomidine (8.88)>[[ UK-14304 ]] (8.42)>B-HT 920 (7.05)>noradrenaline (6.92).,116,2
+117,In << alpha(2A)-adrenoceptor >> transfected cells the rank order of agonist potency was A-54741 (mean pEC(50)=8.96)>dexmedetomidine (8.88)>UK-14304 (8.42)>[[ B-HT 920 ]] (7.05)>noradrenaline (6.92).,117,2
+118,In << alpha(2A)-adrenoceptor >> transfected cells the rank order of agonist potency was A-54741 (mean pEC(50)=8.96)>dexmedetomidine (8.88)>UK-14304 (8.42)>B-HT 920 (7.05)>[[ noradrenaline ]] (6.92).,118,2
+119,"<< Glucocorticoid receptors >> were activated by [[ dexamethasone ]] as assessed using a glucocorticoid-responsive reporter plasmid, pTAT3-CAT.",119,9
+120,"The << glucocorticoid receptor >> antagonist [[ RU-486 ]] (mifepristone) significantly counteracted the effect of dexamethasone on glucocorticoid receptor activation, indicating that the dexamethasone effect is specific and is mediated through the glucocorticoid receptor.",120,1
+121,"The << glucocorticoid receptor >> antagonist RU-486 ([[ mifepristone ]]) significantly counteracted the effect of dexamethasone on glucocorticoid receptor activation, indicating that the dexamethasone effect is specific and is mediated through the glucocorticoid receptor.",121,1
+122,RESULTS: << Quetiapine >> was an effective antipsychotic and improved the extrapyramidal symptoms and [[ prolactin ]] level elevation noted at baseline.,122,6
+123,"In a physiological K(+) gradient, << TWIK-2 >> is half inhibited by 0.1 mm [[ Ba(2+) ]], quinine, and quinidine.",123,0
+124,"In a physiological K(+) gradient, << TWIK-2 >> is half inhibited by 0.1 mm Ba(2+), [[ quinine ]], and quinidine.",124,0
+125,"In a physiological K(+) gradient, << TWIK-2 >> is half inhibited by 0.1 mm Ba(2+), quinine, and [[ quinidine ]].",125,0
+126,"Initial in vitro studies utilizing HEP-G2 liver cells revealed that addition of << eicosapentaenoic acid >> (EPA) blocked [[ Delta-5-desaturase ]] activity, the terminal enzymatic step in AA synthesis.",126,0
+127,"Initial in vitro studies utilizing HEP-G2 liver cells revealed that addition of eicosapentaenoic acid (<< EPA >>) blocked [[ Delta-5-desaturase ]] activity, the terminal enzymatic step in AA synthesis.",127,0
+128,"BACKGROUND: This study examines the effects of << nicorandil >>, a [[ K(+) channel ]] opener, on transmural dispersion of repolarization (TDR) and induction of torsade de pointes (TdP) under conditions mimicking the LQT1, LQT2, and LQT3 forms of the congenital long-QT syndrome (LQTS).",128,9
+129,"Isoproterenol (50 to 100 nmol/L) was used to mimic an increase in beta-adrenergic tone, << d-sotalol >> (100 micromol/L) to block [[ I(Kr) ]] (LQT2 model), and ATX-II (20 nmol/L) to augment late I(Na) (LQT3 model).",129,0
+130,"Isoproterenol (50 to 100 nmol/L) was used to mimic an increase in beta-adrenergic tone, << d-sotalol >> (100 micromol/L) to block I(Kr) (LQT2 model), and [[ ATX-II ]] (20 nmol/L) to augment late I(Na) (LQT3 model).",130,0
+131,"<< Isoproterenol >> (50 to 100 nmol/L) was used to mimic an increase in beta-adrenergic tone, d-sotalol (100 micromol/L) to block [[ I(Kr) ]] (LQT2 model), and ATX-II (20 nmol/L) to augment late I(Na) (LQT3 model).",131,0
+132,"<< Isoproterenol >> (50 to 100 nmol/L) was used to mimic an increase in beta-adrenergic tone, d-sotalol (100 micromol/L) to block I(Kr) (LQT2 model), and [[ ATX-II ]] (20 nmol/L) to augment late I(Na) (LQT3 model).",132,0
+133,"<< Peroxisome proliferator-activated receptor alpha >> (PPARalpha) activators, [[ bezafibrate ]] and Wy-14,643, increase uncoupling protein-3 mRNA levels without modifying the mitochondrial membrane potential in primary culture of rat preadipocytes.",133,9
+134,"Peroxisome proliferator-activated receptor alpha (<< PPARalpha >>) activators, [[ bezafibrate ]] and Wy-14,643, increase uncoupling protein-3 mRNA levels without modifying the mitochondrial membrane potential in primary culture of rat preadipocytes.",134,9
+135,"<< Peroxisome proliferator-activated receptor alpha >> (PPARalpha) activators, bezafibrate and [[ Wy-14,643 ]], increase uncoupling protein-3 mRNA levels without modifying the mitochondrial membrane potential in primary culture of rat preadipocytes.",135,9
+136,"Peroxisome proliferator-activated receptor alpha (<< PPARalpha >>) activators, bezafibrate and [[ Wy-14,643 ]], increase uncoupling protein-3 mRNA levels without modifying the mitochondrial membrane potential in primary culture of rat preadipocytes.",136,9
+137,"Peroxisome proliferator-activated receptor alpha (PPARalpha) activators, << bezafibrate >> and Wy-14,643, increase [[ uncoupling protein-3 ]] mRNA levels without modifying the mitochondrial membrane potential in primary culture of rat preadipocytes.",137,6
+138,"Peroxisome proliferator-activated receptor alpha (PPARalpha) activators, bezafibrate and << Wy-14,643 >>, increase [[ uncoupling protein-3 ]] mRNA levels without modifying the mitochondrial membrane potential in primary culture of rat preadipocytes.",138,6
+139,"<< Uncoupling proteins >> (UCPs) are inner mitochondrial membrane transporters which act as pores for [[ H(+) ]] ions, dissipating the electrochemical gradient that develops during mitochondrial respiration at the expense of ATP synthesis.",139,5
+140,"Uncoupling proteins (<< UCPs >>) are inner mitochondrial membrane transporters which act as pores for [[ H(+) ]] ions, dissipating the electrochemical gradient that develops during mitochondrial respiration at the expense of ATP synthesis.",140,5
+141,"Thus, << bezafibrate >> treatment resulted in an 8-fold induction in [[ UCP-3 ]] mRNA levels in preadipocytes compared with the 3.5-fold induction observed in adipocytes.",141,6
+142,"The induction in << UCP-3 >> expression was not accompanied by changes in the mitochondrial membrane potential of rat primary preadipocytes after [[ bezafibrate ]] or Wy-14,643 treatment.",142,6
+143,"The induction in << UCP-3 >> expression was not accompanied by changes in the mitochondrial membrane potential of rat primary preadipocytes after bezafibrate or [[ Wy-14,643 ]] treatment.",143,6
+144,"Since it has been proposed that UCP-3 could be involved in the regulation of the use of fatty acids as fuel substrates, the << UCP-3 >> induction achieved after [[ bezafibrate ]] and Wy-14, 643 treatment may indicate a higher oxidation of fatty acids, limiting their availability to be stored as triglycerides.",144,6
+145,"Since it has been proposed that UCP-3 could be involved in the regulation of the use of fatty acids as fuel substrates, the << UCP-3 >> induction achieved after bezafibrate and [[ Wy-14, 643 ]] treatment may indicate a higher oxidation of fatty acids, limiting their availability to be stored as triglycerides.",145,6
+146,<< Schisandrin B >> protects against menadione-induced hepatotoxicity by enhancing [[ DT-diaphorase ]] activity.,146,9
+147,"Pretreating mice with schisandrin B (Sch B), a dibenzocyclooctadiene derivative isolated from the fruit of Schisandra chinensis, at a daily dose of 1 mmol/kg for 3 days protected against << menadione >>-induced hepatic oxidative damage in mice, as evidenced by decreases in plasma [[ alanine aminotransferase ]] activity (78%) and hepatic malondialdehyde level (70%), when compared with the menadione intoxicated control.",147,0
+148,Hepatocytes isolated from << Sch B >> pretreated (a daily dose of 1 mmol/kg for 3 days) rats showed a significant increase (25%) in [[ DTD ]] activity.,148,9
+149,The ensemble of results suggests that the ability of << Sch B >> pretreatment to enhance hepatocellular [[ DTD ]] activity may at least in part be attributed to the protection against menadione hepatotoxicity.,149,9
+150,"The group treated with << pyridostigmine >> alone showed decreased plasma [[ butyrylcholinesterase ]] (BChE) activity (87% of control), whereas pyridostigmine plus exercise significantly decreased the BChE activity (79% of control), indicating an interactive effect of the combination.",150,0
+151,"The group treated with << pyridostigmine >> alone showed decreased plasma butyrylcholinesterase ([[ BChE ]]) activity (87% of control), whereas pyridostigmine plus exercise significantly decreased the BChE activity (79% of control), indicating an interactive effect of the combination.",151,0
+152,"The group treated with pyridostigmine alone showed decreased plasma butyrylcholinesterase (BChE) activity (87% of control), whereas << pyridostigmine >> plus exercise significantly decreased the [[ BChE ]] activity (79% of control), indicating an interactive effect of the combination.",152,0
+153,"However, << AChE >> activity in triceps muscle decreased significantly (78% of control) in the group treated with [[ pyridostigmine ]] plus exercise.",153,0
+154,"<< Creatine phosphokinase >> activity in plasma increased slightly (compared to control, [[ pyridostigmine ]] or exercise group) in mice treated with pyridostigmine plus exercise, which may be indicative of perturbation in the integrity of the skeletal muscle due to combination.",154,9
+155,"<< Creatine phosphokinase >> activity in plasma increased slightly (compared to control, pyridostigmine or exercise group) in mice treated with [[ pyridostigmine ]] plus exercise, which may be indicative of perturbation in the integrity of the skeletal muscle due to combination.",155,9
+156,"RESULT(S): Buserelin acetate, a GnRH agonist (0.1-10 ng/mL), had no significant effect on MCP-1 expression, whereas << danazol >> (10(-7)-10(-5) M), a testosterone analog, and dexamethasone, an anti-inflammatory glucocorticoid hormone (10(-12)-10(-6)M), showed a direct and a dose-dependent inhibitory effect on [[ MCP-1 ]] expression.",156,0
+157,"RESULT(S): Buserelin acetate, a GnRH agonist (0.1-10 ng/mL), had no significant effect on MCP-1 expression, whereas danazol (10(-7)-10(-5) M), a << testosterone >> analog, and dexamethasone, an anti-inflammatory glucocorticoid hormone (10(-12)-10(-6)M), showed a direct and a dose-dependent inhibitory effect on [[ MCP-1 ]] expression.",157,0
+158,"RESULT(S): Buserelin acetate, a GnRH agonist (0.1-10 ng/mL), had no significant effect on MCP-1 expression, whereas danazol (10(-7)-10(-5) M), a testosterone analog, and << dexamethasone >>, an anti-inflammatory glucocorticoid hormone (10(-12)-10(-6)M), showed a direct and a dose-dependent inhibitory effect on [[ MCP-1 ]] expression.",158,0
+159,"RESULT(S): << Buserelin acetate >>, a [[ GnRH ]] agonist (0.1-10 ng/mL), had no significant effect on MCP-1 expression, whereas danazol (10(-7)-10(-5) M), a testosterone analog, and dexamethasone, an anti-inflammatory glucocorticoid hormone (10(-12)-10(-6)M), showed a direct and a dose-dependent inhibitory effect on MCP-1 expression.",159,2
+160,"The present studies were undertaken to compare two compounds, a vitamin D(3) analogue (<< CB1093 >>) with minimal calcaemic effects, and clenbuterol, a long-acting beta(2)-adrenoceptor agonist, both of which induce [[ NGF ]] synthesis in vivo.",160,6
+161,"The present studies were undertaken to compare two compounds, a vitamin D(3) analogue (CB1093) with minimal calcaemic effects, and << clenbuterol >>, a long-acting beta(2)-adrenoceptor agonist, both of which induce [[ NGF ]] synthesis in vivo.",161,6
+162,"The present studies were undertaken to compare two compounds, a << vitamin D(3) >> analogue (CB1093) with minimal calcaemic effects, and clenbuterol, a long-acting beta(2)-adrenoceptor agonist, both of which induce [[ NGF ]] synthesis in vivo.",162,8
+163,"The present studies were undertaken to compare two compounds, a vitamin D(3) analogue (CB1093) with minimal calcaemic effects, and << clenbuterol >>, a long-acting [[ beta(2)-adrenoceptor ]] agonist, both of which induce NGF synthesis in vivo.",163,2
+164,<< Clenbuterol >> caused significant increases in both [[ NGF ]] mRNA and protein in 3T3 cells; with maxima at 10 nM and at 8-12 h exposure.,164,6
+165,Mobility shift assays on whole cell extracts showed that << clenbuterol >> increased AP1 binding in 3T3 cells prior to increasing [[ NGF ]] synthesis.,165,6
+166,"Clenbuterol was without effect on NGF mRNA levels in L929 cells, whereas << CB1093 >> caused significant increases in both [[ NGF ]] mRNA and protein levels in both 3T3 and L929 cells.",166,6
+167,This study demonstrates that << CB1093 >> and clenbuterol stimulate [[ NGF ]] levels in vitro and that AP-1 binding could be a commonality between the mechanism of NGF induction of these two compounds.,167,6
+168,This study demonstrates that << CB1093 >> and clenbuterol stimulate NGF levels in vitro and that AP-1 binding could be a commonality between the mechanism of [[ NGF ]] induction of these two compounds.,168,6
+169,This study demonstrates that CB1093 and << clenbuterol >> stimulate [[ NGF ]] levels in vitro and that AP-1 binding could be a commonality between the mechanism of NGF induction of these two compounds.,169,6
+170,This study demonstrates that CB1093 and << clenbuterol >> stimulate NGF levels in vitro and that AP-1 binding could be a commonality between the mechanism of [[ NGF ]] induction of these two compounds.,170,6
+171,Protective effect of << halothane >> anesthesia on retinal light damage: inhibition of metabolic [[ rhodopsin ]] regeneration.,171,8
+172,RESULTS: << Halothane >> anesthesia reversibly inhibited metabolic [[ rhodopsin ]] regeneration and thus prevented rhodopsin from absorbing high numbers of photons during light exposure.,172,8
+173,RESULTS: << Halothane >> anesthesia reversibly inhibited metabolic rhodopsin regeneration and thus prevented [[ rhodopsin ]] from absorbing high numbers of photons during light exposure.,173,8
+174,"CONCLUSIONS: After the initial bleach, << halothane >> impeded photon absorption by rhodopsin by inhibiting metabolic [[ rhodopsin ]] regeneration.",174,8
+175,"METHODS: Different classes of antidepressants [imipramine (tricyclic), maprotiline (noradrenline reuptake inhibitor), venlafaxine (mixed serotonin and noradrenaline reuptake inhibitors), fluvoxamine and sertraline (selective serotonin reuptake inhibitor)] were tested in the same randomised experimental session, alone and in combination with 5-HT1A and 5-HT1B receptor agonists [<< buspirone >> (partial [[ 5-HT1A ]] agonist), anpirtoline (5-HT1B agonist)] in the mouse forced swimming test.",175,2
+176,"METHODS: Different classes of antidepressants [imipramine (tricyclic), maprotiline (noradrenline reuptake inhibitor), venlafaxine (mixed serotonin and noradrenaline reuptake inhibitors), fluvoxamine and sertraline (selective serotonin reuptake inhibitor)] were tested in the same randomised experimental session, alone and in combination with 5-HT1A and 5-HT1B receptor agonists [buspirone (partial 5-HT1A agonist), << anpirtoline >> ([[ 5-HT1B ]] agonist)] in the mouse forced swimming test.",176,2
+177,"<< Pemetrexed disodium >> (Alimta, LY231514) is a novel, multitargeted antifolate that inhibits thymidylate synthase, [[ dihydrofolate reductase ]], and glycinamide ribonucleotide formyl transferase.",177,0
+178,"<< Pemetrexed disodium >> (Alimta, LY231514) is a novel, multitargeted antifolate that inhibits thymidylate synthase, dihydrofolate reductase, and [[ glycinamide ribonucleotide formyl transferase ]].",178,0
+179,"<< Pemetrexed disodium >> (Alimta, LY231514) is a novel, multitargeted antifolate that inhibits [[ thymidylate synthase ]], dihydrofolate reductase, and glycinamide ribonucleotide formyl transferase.",179,0
+180,"Pemetrexed disodium (<< Alimta >>, LY231514) is a novel, multitargeted antifolate that inhibits thymidylate synthase, [[ dihydrofolate reductase ]], and glycinamide ribonucleotide formyl transferase.",180,0
+181,"Pemetrexed disodium (<< Alimta >>, LY231514) is a novel, multitargeted antifolate that inhibits thymidylate synthase, dihydrofolate reductase, and [[ glycinamide ribonucleotide formyl transferase ]].",181,0
+182,"Pemetrexed disodium (<< Alimta >>, LY231514) is a novel, multitargeted antifolate that inhibits [[ thymidylate synthase ]], dihydrofolate reductase, and glycinamide ribonucleotide formyl transferase.",182,0
+183,"Pemetrexed disodium (Alimta, << LY231514 >>) is a novel, multitargeted antifolate that inhibits thymidylate synthase, [[ dihydrofolate reductase ]], and glycinamide ribonucleotide formyl transferase.",183,0
+184,"Pemetrexed disodium (Alimta, << LY231514 >>) is a novel, multitargeted antifolate that inhibits thymidylate synthase, dihydrofolate reductase, and [[ glycinamide ribonucleotide formyl transferase ]].",184,0
+185,"Pemetrexed disodium (Alimta, << LY231514 >>) is a novel, multitargeted antifolate that inhibits [[ thymidylate synthase ]], dihydrofolate reductase, and glycinamide ribonucleotide formyl transferase.",185,0
+186,"To mechanistically evaluate this regional selectivity, we assessed << cyclo-oxygenase-2 >> (COX-2) expression in the uninvolved mucosa and demonstrated a 3- to 4-fold excess in the distal relative to the proximal bowel in both MIN mice and [[ AOM ]]-treated rats.",186,6
+187,"To mechanistically evaluate this regional selectivity, we assessed cyclo-oxygenase-2 (<< COX-2 >>) expression in the uninvolved mucosa and demonstrated a 3- to 4-fold excess in the distal relative to the proximal bowel in both MIN mice and [[ AOM ]]-treated rats.",187,6
+188,"<< Diacylglycerol kinase >> (DGK) catalyzes the conversion of diacylglycerol to [[ phosphatidic acid ]], making it an attractive candidate for a signal transduction component.",188,4
+189,"Diacylglycerol kinase (<< DGK >>) catalyzes the conversion of diacylglycerol to [[ phosphatidic acid ]], making it an attractive candidate for a signal transduction component.",189,4
+190,"<< Diacylglycerol kinase >> (DGK) catalyzes the conversion of [[ diacylglycerol ]] to phosphatidic acid, making it an attractive candidate for a signal transduction component.",190,5
+191,"Diacylglycerol kinase (<< DGK >>) catalyzes the conversion of [[ diacylglycerol ]] to phosphatidic acid, making it an attractive candidate for a signal transduction component.",191,5
+192,"We took advantage of the previous observations that << phosphatidylserine >> inhibits [[ DGK-delta ]] (reviewed by Sakane, F., Imai, S., Kai, M., Wada, I., and Kanoh, H. (1996) J. Biol. Chem. 271, 8394-8401), and constitutively active RhoA inhibits DGK-theta (reviewed by Houssa, B., de Widt, J., Kranenburg, O., Moolenaar, W. H., and van Blitterswijk, W. J. (1999) J. Biol. Chem. 274, 6820-6822) to identify the activity induced by alpha-thrombin.",192,0
+193,<< Nordihydroguaiaretic acid >> (NDGA) has been shown to inhibit both 5-lipoxygenase and [[ ornithine decarboxylase ]] and is active against several cancer cell lines and at least one mouse tumor model.,193,0
+194,<< Nordihydroguaiaretic acid >> (NDGA) has been shown to inhibit both [[ 5-lipoxygenase ]] and ornithine decarboxylase and is active against several cancer cell lines and at least one mouse tumor model.,194,0
+195,Nordihydroguaiaretic acid (<< NDGA >>) has been shown to inhibit both 5-lipoxygenase and [[ ornithine decarboxylase ]] and is active against several cancer cell lines and at least one mouse tumor model.,195,0
+196,Nordihydroguaiaretic acid (<< NDGA >>) has been shown to inhibit both [[ 5-lipoxygenase ]] and ornithine decarboxylase and is active against several cancer cell lines and at least one mouse tumor model.,196,0
+197,<< Carbonic anhydrase >> (CA) is a zinc enzyme that catalyses the reversible hydration reaction of [[ CO2 ]] and plays a major role in the acid-base balance.,197,12
+198,Carbonic anhydrase (<< CA >>) is a zinc enzyme that catalyses the reversible hydration reaction of [[ CO2 ]] and plays a major role in the acid-base balance.,198,12
+199,The temporal profile of butyrylcholinesterase (BuChE) and in vitro << pralidoxime >>-reactivated [[ BuChE ]] was studied in a cohort of 25 organophosphate-poisoned patients to examine their relationship to the development of intermediate syndrome and to understand reasons for lack of efficacy of oxime treatment.,199,9
+200,Reactivation potentials of << BuChE >> (the difference between [[ oxime ]]-reactivated and -unreactivated enzyme activity) declined significantly with time after organophosphate ingestion.,200,9
+201,Reactivation potentials of << BuChE >> (the difference between oxime-reactivated and -unreactivated enzyme activity) declined significantly with time after [[ organophosphate ]] ingestion.,201,3
+202,Patients who received << oxime >> prior to hospitalization had a higher rate of intermediate syndrome and lower levels of [[ BuChE ]] at admission than those who had not.,202,8
+203,"The segments were contracted with the << alpha(2)-adrenoceptor >> agonists [[ brimonidine ]], apraclonidine, and oxymetazoline.",203,2
+204,"The segments were contracted with the << alpha(2)-adrenoceptor >> agonists brimonidine, [[ apraclonidine ]], and oxymetazoline.",204,2
+205,"The segments were contracted with the << alpha(2)-adrenoceptor >> agonists brimonidine, apraclonidine, and [[ oxymetazoline ]].",205,2
+206,"The following alpha(2)-adrenoceptor antagonists were applied: << BRL44408 >> ([[ alpha(2A) ]]-selective), ARC239 (alpha(2B)- and alpha(2C)-selective), and prazosin (alpha(2B)- and alpha(2C)-selective).",206,1
+207,"The following alpha(2)-adrenoceptor antagonists were applied: BRL44408 (alpha(2A)-selective), << ARC239 >> ([[ alpha(2B) ]]- and alpha(2C)-selective), and prazosin (alpha(2B)- and alpha(2C)-selective).",207,1
+208,"The following alpha(2)-adrenoceptor antagonists were applied: BRL44408 (alpha(2A)-selective), << ARC239 >> (alpha(2B)- and [[ alpha(2C) ]]-selective), and prazosin (alpha(2B)- and alpha(2C)-selective).",208,1
+209,"The following alpha(2)-adrenoceptor antagonists were applied: BRL44408 (alpha(2A)-selective), ARC239 (alpha(2B)- and alpha(2C)-selective), and << prazosin >> ([[ alpha(2B) ]]- and alpha(2C)-selective).",209,1
+210,"The following alpha(2)-adrenoceptor antagonists were applied: BRL44408 (alpha(2A)-selective), ARC239 (alpha(2B)- and alpha(2C)-selective), and << prazosin >> (alpha(2B)- and [[ alpha(2C) ]]-selective).",210,1
+211,"RESULTS: The << alpha(2)-adrenoceptor >> agonists induced vasoconstriction in the porcine ciliary artery with the following potency order (EC(50)) expressed in nanomolar: [[ brimonidine ]] 2.11, oxymetazoline 5.26, and apraclonidine 13.0.",211,2
+212,"RESULTS: The << alpha(2)-adrenoceptor >> agonists induced vasoconstriction in the porcine ciliary artery with the following potency order (EC(50)) expressed in nanomolar: brimonidine 2.11, [[ oxymetazoline ]] 5.26, and apraclonidine 13.0.",212,2
+213,"RESULTS: The << alpha(2)-adrenoceptor >> agonists induced vasoconstriction in the porcine ciliary artery with the following potency order (EC(50)) expressed in nanomolar: brimonidine 2.11, oxymetazoline 5.26, and [[ apraclonidine ]] 13.0.",213,2
+214,"Schild analyses for the antagonists against brimonidine yielded regression lines with slopes of unity and functional antagonist potencies (pK(B)) for << BRL44408 >> (7.8), ARC 239 (5.8) and for prazosin (6.0) suggesting the presence of functional [[ alpha(2A)-adrenoceptors ]].",214,1
+215,"Schild analyses for the antagonists against brimonidine yielded regression lines with slopes of unity and functional antagonist potencies (pK(B)) for BRL44408 (7.8), << ARC 239 >> (5.8) and for prazosin (6.0) suggesting the presence of functional [[ alpha(2A)-adrenoceptors ]].",215,1
+216,"Schild analyses for the antagonists against brimonidine yielded regression lines with slopes of unity and functional antagonist potencies (pK(B)) for BRL44408 (7.8), ARC 239 (5.8) and for << prazosin >> (6.0) suggesting the presence of functional [[ alpha(2A)-adrenoceptors ]].",216,1
+217,"CONCLUSIONS: The << alpha(2)-adrenoceptor >> agonists [[ brimonidine ]], apraclonidine, and oxymetazoline are potent vasoconstrictors in the porcine ciliary artery.",217,2
+218,"CONCLUSIONS: The << alpha(2)-adrenoceptor >> agonists brimonidine, [[ apraclonidine ]], and oxymetazoline are potent vasoconstrictors in the porcine ciliary artery.",218,2
+219,"CONCLUSIONS: The << alpha(2)-adrenoceptor >> agonists brimonidine, apraclonidine, and [[ oxymetazoline ]] are potent vasoconstrictors in the porcine ciliary artery.",219,2
+220,"<< Pemetrexed disodium >> (ALIMTA) is a novel antimetabolite that inhibits at least three folate-dependent enzymes, [[ thymidylate synthase ]], dihydrofolate reductase, and glycinamide ribonucleotide formyltransferase.",220,0
+221,"<< Pemetrexed disodium >> (ALIMTA) is a novel antimetabolite that inhibits at least three folate-dependent enzymes, thymidylate synthase, [[ dihydrofolate reductase ]], and glycinamide ribonucleotide formyltransferase.",221,0
+222,"<< Pemetrexed disodium >> (ALIMTA) is a novel antimetabolite that inhibits at least three folate-dependent enzymes, thymidylate synthase, dihydrofolate reductase, and [[ glycinamide ribonucleotide formyltransferase ]].",222,0
+223,"Pemetrexed disodium (<< ALIMTA >>) is a novel antimetabolite that inhibits at least three folate-dependent enzymes, [[ thymidylate synthase ]], dihydrofolate reductase, and glycinamide ribonucleotide formyltransferase.",223,0
+224,"Pemetrexed disodium (<< ALIMTA >>) is a novel antimetabolite that inhibits at least three folate-dependent enzymes, thymidylate synthase, [[ dihydrofolate reductase ]], and glycinamide ribonucleotide formyltransferase.",224,0
+225,"Pemetrexed disodium (<< ALIMTA >>) is a novel antimetabolite that inhibits at least three folate-dependent enzymes, thymidylate synthase, dihydrofolate reductase, and [[ glycinamide ribonucleotide formyltransferase ]].",225,0
+226,"<< DHFS >> is present exclusively in the mitochondria, making this compartment the sole site of synthesis of [[ dihydrofolate ]] in the plant cell.",226,4
+227,UNLABELLED: << Rabeprazole >> is an inhibitor of the [[ gastric proton pump ]].,227,0
+228,CONCLUSION: << Rabeprazole >> is a well tolerated [[ proton pump ]] inhibitor.,228,0
+229,<< Angiotensin II >> suppression in humans by the orally active renin inhibitor [[ Aliskiren ]] (SPP100): comparison with enalapril.,229,8
+230,<< Angiotensin II >> suppression in humans by the orally active renin inhibitor Aliskiren ([[ SPP100 ]]): comparison with enalapril.,230,8
+231,Angiotensin II suppression in humans by the orally active << renin >> inhibitor [[ Aliskiren ]] (SPP100): comparison with enalapril.,231,0
+232,Angiotensin II suppression in humans by the orally active << renin >> inhibitor Aliskiren ([[ SPP100 ]]): comparison with enalapril.,232,0
+233,"We tested the new orally active nonpeptidic << renin >> inhibitor [[ SPP100 ]] (Aliskiren, an octanamide with a 50% inhibitory concentration [IC50] in the low nanomolar range) in 18 healthy volunteers on a constant 100 mmol/d sodium diet using a double-blind, 3-way crossover protocol.",233,0
+234,"We tested the new orally active nonpeptidic << renin >> inhibitor SPP100 ([[ Aliskiren ]], an octanamide with a 50% inhibitory concentration [IC50] in the low nanomolar range) in 18 healthy volunteers on a constant 100 mmol/d sodium diet using a double-blind, 3-way crossover protocol.",234,0
+235,"We tested the new orally active nonpeptidic << renin >> inhibitor SPP100 (Aliskiren, an [[ octanamide ]] with a 50% inhibitory concentration [IC50] in the low nanomolar range) in 18 healthy volunteers on a constant 100 mmol/d sodium diet using a double-blind, 3-way crossover protocol.",235,0
+236,"There was a dose-dependent decrease in plasma renin activity, << Ang I >>, and Ang II following single doses of [[ Aliskiren ]] starting with 40 mg.",236,8
+237,"There was a dose-dependent decrease in plasma renin activity, Ang I, and << Ang II >> following single doses of [[ Aliskiren ]] starting with 40 mg.",237,8
+238,"There was a dose-dependent decrease in plasma << renin >> activity, Ang I, and Ang II following single doses of [[ Aliskiren ]] starting with 40 mg.",238,0
+239,"Inhibition was still marked and significant after repeated dosing with maximal decreases in << Ang II >> levels by 89% and 75% on Days 1 and 8, respectively, when the highest dose of [[ Aliskiren ]] was compared with placebo.",239,8
+240,"At the same time, mean plasma active << renin >> was increased 16- and 34-fold at the highest dose of [[ Aliskiren ]].",240,9
+241,"In conclusion, the renin inhibitor << Aliskiren >> dose-dependently decreases [[ Ang II ]] levels in humans following oral administration.",241,8
+242,"In conclusion, the << renin >> inhibitor [[ Aliskiren ]] dose-dependently decreases Ang II levels in humans following oral administration.",242,0
+243,<< Aliskiren >> has the potential to become the first orally active [[ renin ]] inhibitor that provides a true alternative to ACE-inhibitors and Ang II receptor antagonists in therapy for hypertension and other cardiovascular and renal diseases.,243,0
+244,<< Aliskiren >> has the potential to become the first orally active renin inhibitor that provides a true alternative to [[ ACE ]]-inhibitors and Ang II receptor antagonists in therapy for hypertension and other cardiovascular and renal diseases.,244,0
+245,<< Aliskiren >> has the potential to become the first orally active renin inhibitor that provides a true alternative to ACE-inhibitors and [[ Ang II receptor ]] antagonists in therapy for hypertension and other cardiovascular and renal diseases.,245,1
+246,"The earliest known << AChE >> inhibitors, namely, [[ physostigmine ]] and tacrine, performed poorly in clinical trials (e.g., poor oral activity, brain penetration, and hepatotoxic liability).",246,0
+247,"The earliest known << AChE >> inhibitors, namely, physostigmine and [[ tacrine ]], performed poorly in clinical trials (e.g., poor oral activity, brain penetration, and hepatotoxic liability).",247,0
+248,<< Donepezil hydrochloride >> inaugurates a new class of [[ AChE ]] inhibitors with longer and more selective action and with manageable adverse effects.,248,0
+249,"<< Thalidomide >>--removed from widespread clinical use by 1962 because of severe teratogenicity--has anti-angiogenic and immunomodulatory effects, including the inhibition of [[ TNF alpha ]].",249,0
+250,"As a prodrug << leflunomide >> is completely converted to its active metabolite A 77 1726 (M1) which blocks the [[ dihydroorotate dehydrogenase ]], a key enzyme of the pyrimidine de novo synthesis.",250,0
+251,"As a prodrug leflunomide is completely converted to its active metabolite << A 77 1726 >> (M1) which blocks the [[ dihydroorotate dehydrogenase ]], a key enzyme of the pyrimidine de novo synthesis.",251,0
+252,"A recent study showed that << anastrozole >>, an [[ aromatase ]] inhibitor, is as effective or even superior to tamoxifen when used as a first-line therapy.",252,0
+253,"<< Fulvestrant >>, the first agent in this new class, not only induces the degradation of the [[ estrogen receptor ]] but also is an estrogen antagonist; further, its lack of agonist activity provides a better safety profile.",253,3
+254,"<< Lovastatin >>, a specific inhibitor of [[ HMG-CoA reductase ]], induces a pronounced apoptotic response in a specific subset of tumor types, including HNSCC and CC.",254,0
+255,"Chronic treatment with the NET inhibitor, << desipramine >> (DMI), reduced [[ NET ]] levels in both control and Dbh -/- mice, demonstrating that NE is not required for the regulation of NET by antidepressant drugs.",255,8
+256,"Chronic treatment with the << NET >> inhibitor, [[ desipramine ]] (DMI), reduced NET levels in both control and Dbh -/- mice, demonstrating that NE is not required for the regulation of NET by antidepressant drugs.",256,0
+257,"Probes were perfused with artificial cerebrospinal fluid containing nicotine, the specific << alpha(4)beta(2*) nAChR >> agonist [[ metanicotine ]], or nicotine plus nAChR antagonists and norepinephrine measured in the microdialysates.",257,2
+258,"Probes were perfused with artificial cerebrospinal fluid containing nicotine, the specific << alpha(4)beta(2*) nAChR >> agonist metanicotine, or [[ nicotine ]] plus nAChR antagonists and norepinephrine measured in the microdialysates.",258,2
+259,<< Cilostazol >> decreases levels of serum triglycerides and causes some increase in [[ HDL ]]-cholesterol levels.,259,6
+260,<< Cilostazol >> undergoes intensive and finally complete hepatic metabolism via the [[ cytochrome P450 ]] systems.,260,5
+261,"We changed the residues to alanine using site-directed mutagenesis technique, expressed the mutants in a baculovirus/Sf9 cell system, and analyzed the kinetic characteristics of inhibition of the mutant enzymes by << milrinone >> and cilostazol, specific inhibitors of [[ PDE3 ]].",261,0
+262,"We changed the residues to alanine using site-directed mutagenesis technique, expressed the mutants in a baculovirus/Sf9 cell system, and analyzed the kinetic characteristics of inhibition of the mutant enzymes by milrinone and << cilostazol >>, specific inhibitors of [[ PDE3 ]].",262,0
+263,"Mutants << Y751A >>, D950A, and F1004A had reduced sensitivity to [[ milrinone ]] (K(i) changed from 0.66 microM for the recombinant PDE3A to 7.5 to 156 microM for the mutants), and diminished sensitivity to cilostazol (K(i) of the mutants were 18- to 371-fold higher than that of the recombinant PDE3A).",263,0
+264,"Mutants Y751A, << D950A >>, and F1004A had reduced sensitivity to [[ milrinone ]] (K(i) changed from 0.66 microM for the recombinant PDE3A to 7.5 to 156 microM for the mutants), and diminished sensitivity to cilostazol (K(i) of the mutants were 18- to 371-fold higher than that of the recombinant PDE3A).",264,0
+265,"Mutants Y751A, D950A, and << F1004A >> had reduced sensitivity to [[ milrinone ]] (K(i) changed from 0.66 microM for the recombinant PDE3A to 7.5 to 156 microM for the mutants), and diminished sensitivity to cilostazol (K(i) of the mutants were 18- to 371-fold higher than that of the recombinant PDE3A).",265,0
+266,"Mutants Y751A, D950A, and F1004A had reduced sensitivity to << milrinone >> (K(i) changed from 0.66 microM for the recombinant [[ PDE3A ]] to 7.5 to 156 microM for the mutants), and diminished sensitivity to cilostazol (K(i) of the mutants were 18- to 371-fold higher than that of the recombinant PDE3A).",266,0
+267,"Mutants Y751A, D950A, and F1004A had reduced sensitivity to milrinone (K(i) changed from 0.66 microM for the recombinant PDE3A to 7.5 to 156 microM for the mutants), and diminished sensitivity to << cilostazol >> (K(i) of the mutants were 18- to 371-fold higher than that of the recombinant [[ PDE3A ]]).",267,0
+268,"In contrast, the mutants T844A, F972A and Q975A showed increased K(i) for << cilostazol >> but no difference for milrinone from the recombinant [[ PDE3A ]].",268,0
+269,"In contrast, the mutants << T844A >>, F972A and Q975A showed increased K(i) for [[ cilostazol ]] but no difference for milrinone from the recombinant PDE3A.",269,0
+270,"In contrast, the mutants T844A, << F972A >> and Q975A showed increased K(i) for [[ cilostazol ]] but no difference for milrinone from the recombinant PDE3A.",270,0
+271,"In contrast, the mutants T844A, F972A and << Q975A >> showed increased K(i) for [[ cilostazol ]] but no difference for milrinone from the recombinant PDE3A.",271,0
+272,"In contrast, the mutants T844A, F972A and Q975A showed increased K(i) for cilostazol but no difference for << milrinone >> from the recombinant [[ PDE3A ]].",272,0
+273,"In contrast, the mutants << T844A >>, F972A and Q975A showed increased K(i) for cilostazol but no difference for [[ milrinone ]] from the recombinant PDE3A.",273,0
+274,"In contrast, the mutants T844A, << F972A >> and Q975A showed increased K(i) for cilostazol but no difference for [[ milrinone ]] from the recombinant PDE3A.",274,0
+275,"In contrast, the mutants T844A, F972A and << Q975A >> showed increased K(i) for cilostazol but no difference for [[ milrinone ]] from the recombinant PDE3A.",275,0
+276,"Molecular models show that the << PDE3 >> inhibitors [[ cilostazol ]] and milrinone share some of common residues but interact with distinct residues at the active site, suggesting that selective inhibitors can be designed with flexible size against PDE3 active site.",276,0
+277,"Molecular models show that the << PDE3 >> inhibitors cilostazol and [[ milrinone ]] share some of common residues but interact with distinct residues at the active site, suggesting that selective inhibitors can be designed with flexible size against PDE3 active site.",277,0
+278,"Our study implies that highly conserved residuals Y751, D950 and F1004 in the << PDE >> families are key residues for binding of both substrate and inhibitors, and nonconserved T844 may be responsible for the [[ cilostazol ]] selectivity of PDE3A.",278,0
+279,"Our study implies that highly conserved residuals Y751, D950 and F1004 in the PDE families are key residues for binding of both substrate and inhibitors, and nonconserved T844 may be responsible for the << cilostazol >> selectivity of [[ PDE3A ]].",279,0
+280,"The bacterial enzyme << maltodextrin phosphorylase >> (MalP) catalyses the phosphorolysis of an alpha-1,4-glycosidic bond in maltodextrins, removing the non-reducing glucosyl residues of linear oligosaccharides as [[ glucose-1-phosphate ]] (Glc1P).",280,4
+281,"The bacterial enzyme maltodextrin phosphorylase (<< MalP >>) catalyses the phosphorolysis of an alpha-1,4-glycosidic bond in maltodextrins, removing the non-reducing glucosyl residues of linear oligosaccharides as [[ glucose-1-phosphate ]] (Glc1P).",281,4
+282,"The bacterial enzyme << maltodextrin phosphorylase >> (MalP) catalyses the phosphorolysis of an alpha-1,4-glycosidic bond in maltodextrins, removing the non-reducing glucosyl residues of linear oligosaccharides as glucose-1-phosphate ([[ Glc1P ]]).",282,4
+283,"The bacterial enzyme maltodextrin phosphorylase (<< MalP >>) catalyses the phosphorolysis of an alpha-1,4-glycosidic bond in maltodextrins, removing the non-reducing glucosyl residues of linear oligosaccharides as glucose-1-phosphate ([[ Glc1P ]]).",283,4
+284,OBJECTIVE: << Fondaparinux sodium >> is the first in a new class of synthetic [[ factor Xa ]] inhibitors that binds reversibly with high affinity to antithrombin III.,284,0
+285,"It is caused by a deficiency of << propionyl-CoA carboxylase >> (PCC, EC 6.4.1.3), a biotin-dependent enzyme that catalyzes the carboxylation of [[ propionyl-CoA ]] to D-methylmalonyl-CoA.",285,5
+286,"It is caused by a deficiency of propionyl-CoA carboxylase (<< PCC >>, EC 6.4.1.3), a biotin-dependent enzyme that catalyzes the carboxylation of [[ propionyl-CoA ]] to D-methylmalonyl-CoA.",286,5
+287,"It is caused by a deficiency of propionyl-CoA carboxylase (PCC, << EC 6.4.1.3 >>), a biotin-dependent enzyme that catalyzes the carboxylation of [[ propionyl-CoA ]] to D-methylmalonyl-CoA.",287,5
+288,"It is caused by a deficiency of << propionyl-CoA carboxylase >> (PCC, EC 6.4.1.3), a biotin-dependent enzyme that catalyzes the carboxylation of propionyl-CoA to [[ D-methylmalonyl-CoA ]].",288,5
+289,"It is caused by a deficiency of propionyl-CoA carboxylase (<< PCC >>, EC 6.4.1.3), a biotin-dependent enzyme that catalyzes the carboxylation of propionyl-CoA to [[ D-methylmalonyl-CoA ]].",289,5
+290,"It is caused by a deficiency of propionyl-CoA carboxylase (PCC, << EC 6.4.1.3 >>), a biotin-dependent enzyme that catalyzes the carboxylation of propionyl-CoA to [[ D-methylmalonyl-CoA ]].",290,5
+291,"Although only << clozapine >> and ziprasidone are directly acting 5-HT(1A) agonists, WAY100635, a selective 5-HT(1A) antagonist, partially attenuates these atypical APD-induced increases in cortical DA release that may be due to combined [[ 5-HT(2A) ]] and D(2) blockade.",291,0
+292,"Although only << clozapine >> and ziprasidone are directly acting 5-HT(1A) agonists, WAY100635, a selective 5-HT(1A) antagonist, partially attenuates these atypical APD-induced increases in cortical DA release that may be due to combined 5-HT(2A) and [[ D(2) ]] blockade.",292,0
+293,"Although only clozapine and << ziprasidone >> are directly acting 5-HT(1A) agonists, WAY100635, a selective 5-HT(1A) antagonist, partially attenuates these atypical APD-induced increases in cortical DA release that may be due to combined [[ 5-HT(2A) ]] and D(2) blockade.",293,0
+294,"Although only clozapine and << ziprasidone >> are directly acting 5-HT(1A) agonists, WAY100635, a selective 5-HT(1A) antagonist, partially attenuates these atypical APD-induced increases in cortical DA release that may be due to combined 5-HT(2A) and [[ D(2) ]] blockade.",294,0
+295,"Although only clozapine and ziprasidone are directly acting 5-HT(1A) agonists, << WAY100635 >>, a selective 5-HT(1A) antagonist, partially attenuates these atypical APD-induced increases in cortical DA release that may be due to combined [[ 5-HT(2A) ]] and D(2) blockade.",295,0
+296,"Although only clozapine and ziprasidone are directly acting 5-HT(1A) agonists, << WAY100635 >>, a selective 5-HT(1A) antagonist, partially attenuates these atypical APD-induced increases in cortical DA release that may be due to combined 5-HT(2A) and [[ D(2) ]] blockade.",296,0
+297,"Although only << clozapine >> and ziprasidone are directly acting [[ 5-HT(1A) ]] agonists, WAY100635, a selective 5-HT(1A) antagonist, partially attenuates these atypical APD-induced increases in cortical DA release that may be due to combined 5-HT(2A) and D(2) blockade.",297,2
+298,"Although only clozapine and << ziprasidone >> are directly acting [[ 5-HT(1A) ]] agonists, WAY100635, a selective 5-HT(1A) antagonist, partially attenuates these atypical APD-induced increases in cortical DA release that may be due to combined 5-HT(2A) and D(2) blockade.",298,2
+299,"Although only clozapine and ziprasidone are directly acting 5-HT(1A) agonists, << WAY100635 >>, a selective [[ 5-HT(1A) ]] antagonist, partially attenuates these atypical APD-induced increases in cortical DA release that may be due to combined 5-HT(2A) and D(2) blockade.",299,1
+300,"However, << 5-HT(1A) >> agonism may be important only for [[ quetiapine ]]-induced ACh release.",300,2
+301,BACKGROUND: The novel antiepileptic drug << retigabine >> is the first selective M-current potassium channel opener for [[ KCNQ2/3 ]] and KCNQ3/5 channels.,301,9
+302,BACKGROUND: The novel antiepileptic drug << retigabine >> is the first selective M-current potassium channel opener for KCNQ2/3 and [[ KCNQ3/5 ]] channels.,302,9
+303,BACKGROUND: The novel antiepileptic drug << retigabine >> is the first selective [[ M-current potassium channel ]] opener for KCNQ2/3 and KCNQ3/5 channels.,303,9
+304,"OBJECTIVE: Because of these physiological effects and the widespread use of the selective << COX-2 >> inhibitor, [[ celecoxib ]], we wanted to determine if inhibition of COX-2 would affect incisional skin wound healing.",304,0
+305,"METHODS: Using a cutaneous full-thickness, sutured, incisional wound model in hairless SKH-1 mice, we evaluated the role of COX-2 in the wound healing process by comparing the effects of a nonselective << COX >> inhibitor, [[ diclofenac ]], with a selective COX-2 inhibitor, SC-791.",305,0
+306,"<< Histamine H1-receptor >> antagonists, [[ promethazine ]] and homochlorcyclizine, increase the steady-state plasma concentrations of haloperidol and reduced haloperidol.",306,1
+307,"<< Histamine H1-receptor >> antagonists, promethazine and [[ homochlorcyclizine ]], increase the steady-state plasma concentrations of haloperidol and reduced haloperidol.",307,1
+308,"The effects of histamine H1-receptor antagonists, << promethazine >> and homochlorcyclizine, both of which are inhibitors of [[ CYP2D6 ]], on the steady-state plasma concentrations (Css) of haloperidol and reduced haloperidol were studied in 23 schizophrenic inpatients receiving haloperidol, 12 to 36 mg/d, for 2 to 29 weeks.",308,0
+309,"The effects of histamine H1-receptor antagonists, promethazine and << homochlorcyclizine >>, both of which are inhibitors of [[ CYP2D6 ]], on the steady-state plasma concentrations (Css) of haloperidol and reduced haloperidol were studied in 23 schizophrenic inpatients receiving haloperidol, 12 to 36 mg/d, for 2 to 29 weeks.",309,0
+310,"The effects of << histamine H1-receptor >> antagonists, [[ promethazine ]] and homochlorcyclizine, both of which are inhibitors of CYP2D6, on the steady-state plasma concentrations (Css) of haloperidol and reduced haloperidol were studied in 23 schizophrenic inpatients receiving haloperidol, 12 to 36 mg/d, for 2 to 29 weeks.",310,1
+311,"The effects of << histamine H1-receptor >> antagonists, promethazine and [[ homochlorcyclizine ]], both of which are inhibitors of CYP2D6, on the steady-state plasma concentrations (Css) of haloperidol and reduced haloperidol were studied in 23 schizophrenic inpatients receiving haloperidol, 12 to 36 mg/d, for 2 to 29 weeks.",311,1
+312,"Thus, the current study suggests that coadministration of clinical doses of << promethazine >> and homochlorcyclizine increases the Css of haloperidol and reduced haloperidol via the inhibitory effects on the [[ CYP2D6 ]]-catalyzed metabolism of haloperidol and reduced haloperidol.",312,0
+313,"Thus, the current study suggests that coadministration of clinical doses of promethazine and << homochlorcyclizine >> increases the Css of haloperidol and reduced haloperidol via the inhibitory effects on the [[ CYP2D6 ]]-catalyzed metabolism of haloperidol and reduced haloperidol.",313,0
+314,"Thus, the current study suggests that coadministration of clinical doses of promethazine and homochlorcyclizine increases the Css of haloperidol and reduced haloperidol via the inhibitory effects on the << CYP2D6 >>-catalyzed metabolism of haloperidol and reduced [[ haloperidol ]].",314,5
+315,"Thus, the current study suggests that coadministration of clinical doses of promethazine and homochlorcyclizine increases the Css of haloperidol and reduced haloperidol via the inhibitory effects on the << CYP2D6 >>-catalyzed metabolism of [[ haloperidol ]] and reduced haloperidol.",315,5
+316,"The four lysine residues located in the SMG loop, Lys-260, Lys-263, Lys-265, and Lys-268, also play an important role in mediating the sensitivity of << OTCase >> to [[ ornithine ]] and to arginase and appear to be involved in transducing and enhancing the signal given by ornithine for the closure of the catalytic domain.",316,0
+317,"Inhibition of binding of both << plasminogen >> and plasmin to gp330 by [[ benzamidine ]] was similar, although EACA inhibited the binding of plasmin to gp330 slightly more than the binding of plasminogen to gp330.",317,0
+318,"Inhibition of binding of both plasminogen and << plasmin >> to gp330 by [[ benzamidine ]] was similar, although EACA inhibited the binding of plasmin to gp330 slightly more than the binding of plasminogen to gp330.",318,0
+319,"Inhibition of binding of both plasminogen and plasmin to gp330 by benzamidine was similar, although << EACA >> inhibited the binding of [[ plasmin ]] to gp330 slightly more than the binding of plasminogen to gp330.",319,0
+320,"Inhibition of binding of both plasminogen and plasmin to gp330 by benzamidine was similar, although << EACA >> inhibited the binding of plasmin to gp330 slightly more than the binding of [[ plasminogen ]] to gp330.",320,0
+321,"Involvement of alpha(1)-adrenoceptors was established as mydriatic responses were inhibited by systemic administration of nonselective << alpha-adrenoceptor >> antagonists, [[ phentolamine ]] (0.3-3 mg/kg) and phenoxybenzamine (0.03-0.3 mg/kg), as well as by the selective alpha(1)-adrenoceptor antagonist, prazosin (0.3 mg/kg).",321,1
+322,"Involvement of alpha(1)-adrenoceptors was established as mydriatic responses were inhibited by systemic administration of nonselective << alpha-adrenoceptor >> antagonists, phentolamine (0.3-3 mg/kg) and [[ phenoxybenzamine ]] (0.03-0.3 mg/kg), as well as by the selective alpha(1)-adrenoceptor antagonist, prazosin (0.3 mg/kg).",322,1
+323,"Involvement of alpha(1)-adrenoceptors was established as mydriatic responses were inhibited by systemic administration of nonselective alpha-adrenoceptor antagonists, phentolamine (0.3-3 mg/kg) and phenoxybenzamine (0.03-0.3 mg/kg), as well as by the selective << alpha(1)-adrenoceptor >> antagonist, [[ prazosin ]] (0.3 mg/kg).",323,1
+324,"The << alpha(2)-adrenoceptor >> antagonist, [[ rauwolscine ]] (0.5 mg/kg), was without antagonistic effects.",324,1
+325,"<< alpha(1A)-Adrenoceptor >> selective antagonists, [[ 2-([2,6-dimethoxyphenoxyethyl]aminomethyl)-1,4-benzodioxane ]] (WB-4101; 0.1-1 mg/kg) and 5-methylurapidil (0.1-1 mg/kg), the alpha(1B)-adrenoceptor selective antagonist, 4-amino-2-[4-[1-(benzyloxycarbonyl)-2(S)- [[(1,1-dimethylethyl)amino]carbonyl]-piperazinyl]-6,7-dimethoxyquinazoline (L-765314; 0.3-1 mg/kg), as well as the alpha(1D)-adrenoceptor selective antagonist, 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione (BMY-7378; 1 mg/kg), were used to delineate the adrenoceptor subtypes involved.",325,1
+326,"<< alpha(1A)-Adrenoceptor >> selective antagonists, 2-([2,6-dimethoxyphenoxyethyl]aminomethyl)-1,4-benzodioxane ([[ WB-4101 ]]; 0.1-1 mg/kg) and 5-methylurapidil (0.1-1 mg/kg), the alpha(1B)-adrenoceptor selective antagonist, 4-amino-2-[4-[1-(benzyloxycarbonyl)-2(S)- [[(1,1-dimethylethyl)amino]carbonyl]-piperazinyl]-6,7-dimethoxyquinazoline (L-765314; 0.3-1 mg/kg), as well as the alpha(1D)-adrenoceptor selective antagonist, 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione (BMY-7378; 1 mg/kg), were used to delineate the adrenoceptor subtypes involved.",326,1
+327,"<< alpha(1A)-Adrenoceptor >> selective antagonists, 2-([2,6-dimethoxyphenoxyethyl]aminomethyl)-1,4-benzodioxane (WB-4101; 0.1-1 mg/kg) and [[ 5-methylurapidil ]] (0.1-1 mg/kg), the alpha(1B)-adrenoceptor selective antagonist, 4-amino-2-[4-[1-(benzyloxycarbonyl)-2(S)- [[(1,1-dimethylethyl)amino]carbonyl]-piperazinyl]-6,7-dimethoxyquinazoline (L-765314; 0.3-1 mg/kg), as well as the alpha(1D)-adrenoceptor selective antagonist, 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione (BMY-7378; 1 mg/kg), were used to delineate the adrenoceptor subtypes involved.",327,1
+328,"alpha(1A)-Adrenoceptor selective antagonists, 2-([2,6-dimethoxyphenoxyethyl]aminomethyl)-1,4-benzodioxane (WB-4101; 0.1-1 mg/kg) and 5-methylurapidil (0.1-1 mg/kg), the << alpha(1B)-adrenoceptor >> selective antagonist, [[ 4-amino-2-[4-[1-(benzyloxycarbonyl)-2(S)- [[(1,1-dimethylethyl)amino]carbonyl]-piperazinyl]-6,7-dimethoxyquinazoline ]] (L-765314; 0.3-1 mg/kg), as well as the alpha(1D)-adrenoceptor selective antagonist, 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione (BMY-7378; 1 mg/kg), were used to delineate the adrenoceptor subtypes involved.",328,1
+329,"alpha(1A)-Adrenoceptor selective antagonists, 2-([2,6-dimethoxyphenoxyethyl]aminomethyl)-1,4-benzodioxane (WB-4101; 0.1-1 mg/kg) and 5-methylurapidil (0.1-1 mg/kg), the << alpha(1B)-adrenoceptor >> selective antagonist, 4-amino-2-[4-[1-(benzyloxycarbonyl)-2(S)- [[(1,1-dimethylethyl)amino]carbonyl]-piperazinyl]-6,7-dimethoxyquinazoline ([[ L-765314 ]]; 0.3-1 mg/kg), as well as the alpha(1D)-adrenoceptor selective antagonist, 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione (BMY-7378; 1 mg/kg), were used to delineate the adrenoceptor subtypes involved.",329,1
+330,"alpha(1A)-Adrenoceptor selective antagonists, 2-([2,6-dimethoxyphenoxyethyl]aminomethyl)-1,4-benzodioxane (WB-4101; 0.1-1 mg/kg) and 5-methylurapidil (0.1-1 mg/kg), the alpha(1B)-adrenoceptor selective antagonist, 4-amino-2-[4-[1-(benzyloxycarbonyl)-2(S)- [[(1,1-dimethylethyl)amino]carbonyl]-piperazinyl]-6,7-dimethoxyquinazoline (L-765314; 0.3-1 mg/kg), as well as the << alpha(1D)-adrenoceptor >> selective antagonist, [[ 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione ]] (BMY-7378; 1 mg/kg), were used to delineate the adrenoceptor subtypes involved.",330,1
+331,"alpha(1A)-Adrenoceptor selective antagonists, 2-([2,6-dimethoxyphenoxyethyl]aminomethyl)-1,4-benzodioxane (WB-4101; 0.1-1 mg/kg) and 5-methylurapidil (0.1-1 mg/kg), the alpha(1B)-adrenoceptor selective antagonist, 4-amino-2-[4-[1-(benzyloxycarbonyl)-2(S)- [[(1,1-dimethylethyl)amino]carbonyl]-piperazinyl]-6,7-dimethoxyquinazoline (L-765314; 0.3-1 mg/kg), as well as the << alpha(1D)-adrenoceptor >> selective antagonist, 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione ([[ BMY-7378 ]]; 1 mg/kg), were used to delineate the adrenoceptor subtypes involved.",331,1
+332,"To further investigate this positive correlation and its possible therapeutic implications, a selective << COX-2 >> inhibitor, [[ etodolac ]], was tested on three variants of HT-29 colon cancer cell lines, HT-29/Inv1, HT-29/Inv2 and HT-29/Inv3, with graded increases of in vitro Matrigel invasive potential and COX-2 expression levels.",332,0
+333,"However, other << alpha(1)-adrenoceptor >> antagonists ([[ tamsulosin ]], WB4101 and corynanthine) did not inhibit the binding at a range of concentrations that generally exhibit alpha(1)-adrenoceptor antagonism, and noradrenaline, rauwolscine and propranolol were without effect on the [(3)H]prazosin binding.",333,1
+334,"However, other << alpha(1)-adrenoceptor >> antagonists (tamsulosin, [[ WB4101 ]] and corynanthine) did not inhibit the binding at a range of concentrations that generally exhibit alpha(1)-adrenoceptor antagonism, and noradrenaline, rauwolscine and propranolol were without effect on the [(3)H]prazosin binding.",334,1
+335,"However, other << alpha(1)-adrenoceptor >> antagonists (tamsulosin, WB4101 and [[ corynanthine ]]) did not inhibit the binding at a range of concentrations that generally exhibit alpha(1)-adrenoceptor antagonism, and noradrenaline, rauwolscine and propranolol were without effect on the [(3)H]prazosin binding.",335,1
+336,"The potency of MrIA was greater for inhibition of uptake by << hNET >> of [[ [3H]norepinephrine ]] (Ki 1.89 microM) than [3H]dopamine (Ki 4.33 microM), and the human dopamine transporter and serotonin transporter were not inhibited by MrIA (to 7 microM).",336,5
+337,"The potency of MrIA was greater for inhibition of uptake by << hNET >> of [3H]norepinephrine (Ki 1.89 microM) than [[ [3H]dopamine ]] (Ki 4.33 microM), and the human dopamine transporter and serotonin transporter were not inhibited by MrIA (to 7 microM).",337,5
+338,A comparison of the results with previous data for desipramine and cocaine inhibition of << norepinephrine >> uptake by the mutant [[ hNETs ]] reveals that MrIA binding to hNET occurs at a site that is distinct from but overlaps with the binding sites for tricyclic antidepressants and cocaine.,338,5
+339,"A cDNA encoding the complete amino acid sequence of aminoacylase 1 (N-acylamino acid aminohydrolase, << ACY-1 >>) [EC 3.5.1.14], a dimeric metalloprotein having two Zn2+ in the molecule, which catalyzes the deacylation of [[ N-acylated L-amino acids ]] except L-aspartic acid, has been isolated from porcine kidney lambda gt10 cDNA library and sequenced.",339,5
+340,"A cDNA encoding the complete amino acid sequence of aminoacylase 1 (N-acylamino acid aminohydrolase, ACY-1) [<< EC 3.5.1.14 >>], a dimeric metalloprotein having two Zn2+ in the molecule, which catalyzes the deacylation of [[ N-acylated L-amino acids ]] except L-aspartic acid, has been isolated from porcine kidney lambda gt10 cDNA library and sequenced.",340,5
+341,"A cDNA encoding the complete amino acid sequence of aminoacylase 1 (N-acylamino acid aminohydrolase, ACY-1) [EC 3.5.1.14], a dimeric << metalloprotein >> having two Zn2+ in the molecule, which catalyzes the deacylation of [[ N-acylated L-amino acids ]] except L-aspartic acid, has been isolated from porcine kidney lambda gt10 cDNA library and sequenced.",341,5
+342,"A cDNA encoding the complete amino acid sequence of << aminoacylase 1 >> (N-acylamino acid aminohydrolase, ACY-1) [EC 3.5.1.14], a dimeric metalloprotein having two Zn2+ in the molecule, which catalyzes the deacylation of [[ N-acylated L-amino acids ]] except L-aspartic acid, has been isolated from porcine kidney lambda gt10 cDNA library and sequenced.",342,5
+343,"A cDNA encoding the complete amino acid sequence of aminoacylase 1 (<< N-acylamino acid aminohydrolase >>, ACY-1) [EC 3.5.1.14], a dimeric metalloprotein having two Zn2+ in the molecule, which catalyzes the deacylation of [[ N-acylated L-amino acids ]] except L-aspartic acid, has been isolated from porcine kidney lambda gt10 cDNA library and sequenced.",343,5
+344,"Patients stable on warfarin therapy and concurrently taking a << cyclooxygenase-2 >> (COX-2) inhibitor comparator (traditional nonsteroidal antiinflammatory medications, [[ salsalate ]], or acetaminophen) randomly received celecoxib 200 mg/day or rofecoxib 25 mg/day for three weeks.",344,0
+345,"Patients stable on warfarin therapy and concurrently taking a cyclooxygenase-2 (<< COX-2 >>) inhibitor comparator (traditional nonsteroidal antiinflammatory medications, [[ salsalate ]], or acetaminophen) randomly received celecoxib 200 mg/day or rofecoxib 25 mg/day for three weeks.",345,0
+346,"Patients stable on warfarin therapy and concurrently taking a << cyclooxygenase-2 >> (COX-2) inhibitor comparator (traditional nonsteroidal antiinflammatory medications, salsalate, or [[ acetaminophen ]]) randomly received celecoxib 200 mg/day or rofecoxib 25 mg/day for three weeks.",346,0
+347,"Patients stable on warfarin therapy and concurrently taking a cyclooxygenase-2 (<< COX-2 >>) inhibitor comparator (traditional nonsteroidal antiinflammatory medications, salsalate, or [[ acetaminophen ]]) randomly received celecoxib 200 mg/day or rofecoxib 25 mg/day for three weeks.",347,0
+348,"Patients stable on warfarin therapy and concurrently taking a << cyclooxygenase-2 >> (COX-2) inhibitor comparator (traditional nonsteroidal antiinflammatory medications, salsalate, or acetaminophen) randomly received [[ celecoxib ]] 200 mg/day or rofecoxib 25 mg/day for three weeks.",348,0
+349,"Patients stable on warfarin therapy and concurrently taking a cyclooxygenase-2 (<< COX-2 >>) inhibitor comparator (traditional nonsteroidal antiinflammatory medications, salsalate, or acetaminophen) randomly received [[ celecoxib ]] 200 mg/day or rofecoxib 25 mg/day for three weeks.",349,0
+350,"Patients stable on warfarin therapy and concurrently taking a << cyclooxygenase-2 >> (COX-2) inhibitor comparator (traditional nonsteroidal antiinflammatory medications, salsalate, or acetaminophen) randomly received celecoxib 200 mg/day or [[ rofecoxib ]] 25 mg/day for three weeks.",350,0
+351,"Patients stable on warfarin therapy and concurrently taking a cyclooxygenase-2 (<< COX-2 >>) inhibitor comparator (traditional nonsteroidal antiinflammatory medications, salsalate, or acetaminophen) randomly received celecoxib 200 mg/day or [[ rofecoxib ]] 25 mg/day for three weeks.",351,0
+352,<< AT1 >> antagonism by [[ eprosartan ]] lowers heart rate variability and baroreflex gain.,352,1
+353,We sought to assess the effects of the << angiotensin type 1 (AT1) receptor >> blocker [[ eprosartan ]] on HRV and BRG.,353,0
+354,"RESULTS: << Eprosartan >> tended to lower mean AP, it slightly increased heart rate (HR) (p<0.05), and markedly increased circulating [[ Ang-II ]] levels (p<0.01).",354,6
+355,CONCLUSIONS: << AT1 >> antagonism by [[ eprosartan ]] lowers heart rate variability and baroreflex gain.,355,1
+356,The antinociceptive activity of the << alpha 2-adrenoceptor >> agonist [[ clonidine ]] was also increased in mice treated with alpha N-acetyl beta-endorphin-(1-31).,356,2
+357,"<< Loperamide >>, an opiate agonist of high specificity for mu-receptors, was recently reported to suppress [[ ACTH ]] and cortisol levels in normal subjects, but not in patients with proven ACTH-dependent Cushing's disease.",357,8
+358,"In seven normal subjects, basal << ACTH >> plasma levels were significantly suppressed 3 h after [[ loperamide ]] administration (16 mg, orally) from 5 +/- 1 to 2 +/- 0 pmol/L (P less than 0.0001).",358,8
+359,"After the combined pituitary stimulation test (100 micrograms << human CRH >>, 100 micrograms GnRH, 100 micrograms GH-releasing hormone, and 200 micrograms TRH), the ACTH peak (maximum increase at 30 min) was significantly blunted by [[ loperamide ]] from 9 +/- 1 to 4 +/- 1 pmol/L (P less than 0.001) and the area under the curve of ACTH from 0-120 min was reduced from 35 +/- 5 to 23 +/- 4 pmol/L.2 h (P less than 0.05).",359,3
+360,"After the combined pituitary stimulation test (100 micrograms human CRH, 100 micrograms << GnRH >>, 100 micrograms GH-releasing hormone, and 200 micrograms TRH), the ACTH peak (maximum increase at 30 min) was significantly blunted by [[ loperamide ]] from 9 +/- 1 to 4 +/- 1 pmol/L (P less than 0.001) and the area under the curve of ACTH from 0-120 min was reduced from 35 +/- 5 to 23 +/- 4 pmol/L.2 h (P less than 0.05).",360,3
+361,"After the combined pituitary stimulation test (100 micrograms human CRH, 100 micrograms GnRH, 100 micrograms << GH-releasing hormone >>, and 200 micrograms TRH), the ACTH peak (maximum increase at 30 min) was significantly blunted by [[ loperamide ]] from 9 +/- 1 to 4 +/- 1 pmol/L (P less than 0.001) and the area under the curve of ACTH from 0-120 min was reduced from 35 +/- 5 to 23 +/- 4 pmol/L.2 h (P less than 0.05).",361,3
+362,"After the combined pituitary stimulation test (100 micrograms human CRH, 100 micrograms GnRH, 100 micrograms GH-releasing hormone, and 200 micrograms << TRH >>), the ACTH peak (maximum increase at 30 min) was significantly blunted by [[ loperamide ]] from 9 +/- 1 to 4 +/- 1 pmol/L (P less than 0.001) and the area under the curve of ACTH from 0-120 min was reduced from 35 +/- 5 to 23 +/- 4 pmol/L.2 h (P less than 0.05).",362,3
+363,"After the combined pituitary stimulation test (100 micrograms human CRH, 100 micrograms GnRH, 100 micrograms GH-releasing hormone, and 200 micrograms TRH), the << ACTH >> peak (maximum increase at 30 min) was significantly blunted by [[ loperamide ]] from 9 +/- 1 to 4 +/- 1 pmol/L (P less than 0.001) and the area under the curve of ACTH from 0-120 min was reduced from 35 +/- 5 to 23 +/- 4 pmol/L.2 h (P less than 0.05).",363,3
+364,"After the combined pituitary stimulation test (100 micrograms human CRH, 100 micrograms GnRH, 100 micrograms GH-releasing hormone, and 200 micrograms TRH), the ACTH peak (maximum increase at 30 min) was significantly blunted by << loperamide >> from 9 +/- 1 to 4 +/- 1 pmol/L (P less than 0.001) and the area under the curve of [[ ACTH ]] from 0-120 min was reduced from 35 +/- 5 to 23 +/- 4 pmol/L.2 h (P less than 0.05).",364,3
+365,"In summary, << loperamide >> is able to reduce basal and [[ CRH ]]-induced ACTH and cortisol levels in normal subjects, but not in patients with Cushing's disease or secondary adrenal failure of hypothalamic origin.",365,8
+366,"In summary, << loperamide >> is able to reduce basal and CRH-induced [[ ACTH ]] and cortisol levels in normal subjects, but not in patients with Cushing's disease or secondary adrenal failure of hypothalamic origin.",366,8
+367,"We also examined the effects of << WEB 2086 >>, a [[ platelet-activating factor (PAF) receptor ]] antagonist, in parallel.",367,1
+368,The unique role of the enzyme << 5-lipoxygenase >> (5-LO) in the production of [[ leukotrienes ]] (LTs) makes it a likely target for biochemical manipulation.,368,4
+369,The unique role of the enzyme 5-lipoxygenase (<< 5-LO >>) in the production of [[ leukotrienes ]] (LTs) makes it a likely target for biochemical manipulation.,369,4
+370,The unique role of the enzyme << 5-lipoxygenase >> (5-LO) in the production of leukotrienes ([[ LTs ]]) makes it a likely target for biochemical manipulation.,370,4
+371,The unique role of the enzyme 5-lipoxygenase (<< 5-LO >>) in the production of leukotrienes ([[ LTs ]]) makes it a likely target for biochemical manipulation.,371,4
+372,"The compounds identified as 5-LO inhibitors can be divided into antioxidants, substrate-analogous, and a large miscellaneous group of inhibitors, where << hydroxamic acids >> are potent and more selective inhibitors of [[ 5-LO ]].",372,0
+373,"The << benzothiophene hydroxyurea >>, zileuton, is the first selective [[ 5-LO ]] inhibitor evaluated for the treatment of patients with IBD.",373,0
+374,"The benzothiophene hydroxyurea, << zileuton >>, is the first selective [[ 5-LO ]] inhibitor evaluated for the treatment of patients with IBD.",374,0
+375,"Ribonucleotide reductase (<< RR >>) is responsible for the de novo conversion of the ribonucleoside diphosphates to [[ deoxyribonucleoside diphosphates ]], which are essential for DNA synthesis and repair.",375,4
+376,"<< Ribonucleotide reductase >> (RR) is responsible for the de novo conversion of the ribonucleoside diphosphates to [[ deoxyribonucleoside diphosphates ]], which are essential for DNA synthesis and repair.",376,4
+377,"Ribonucleotide reductase (<< RR >>) is responsible for the de novo conversion of the [[ ribonucleoside diphosphates ]] to deoxyribonucleoside diphosphates, which are essential for DNA synthesis and repair.",377,5
+378,"<< Ribonucleotide reductase >> (RR) is responsible for the de novo conversion of the [[ ribonucleoside diphosphates ]] to deoxyribonucleoside diphosphates, which are essential for DNA synthesis and repair.",378,5
+379,"In PC3 cells, << hydroxyurea >> inhibited [[ hRRM2 ]] and resulted in increased sensitivity to UV irradiation.",379,0
+380,"In addition, << minocycline >> treatment significantly reduced the specific [[ caspase-3 ]] activity after SCI as compared to that of vehicle control.",380,0
+381,"Furthermore, RT-PCR analyses revealed that << minocycline >> treatment increased expression of [[ interleukin-10 ]] mRNA but decreased tumor necrosis factor-alpha expression.",381,6
+382,"Furthermore, RT-PCR analyses revealed that << minocycline >> treatment increased expression of interleukin-10 mRNA but decreased [[ tumor necrosis factor-alpha ]] expression.",382,8
+383,RESULTS: The density of << AR >> in liver tissue in [[ NP ]] group was higher than that in control group (P < 0.05).,383,6
+384,"CONCLUSION: << Nandrolone phenylpropionate >> up-regulated the density of [[ AR ]] in liver tissue, whereas it had no significant effects on the density of AR in testis and ovary tissues.",384,6
+385,"Rats received a concomitant treatment with the selective beta(1)-adrenoceptor antagonist, bisoprolol (50 mg/kg/day p.o.) or were chronically pretreated with the selective << beta(2)-adrenoceptor >> agonist [[ salbutamol ]] (40 microg/kg/h) for 1 week to induce beta(2)-adrenoceptor desensitization.",385,2
+386,"Rats received a concomitant treatment with the selective << beta(1)-adrenoceptor >> antagonist, [[ bisoprolol ]] (50 mg/kg/day p.o.) or were chronically pretreated with the selective beta(2)-adrenoceptor agonist salbutamol (40 microg/kg/h) for 1 week to induce beta(2)-adrenoceptor desensitization.",386,1
+387,The pretreatment with << salbutamol >> induced a 59% down-regulation of left ventricular [[ beta(2)-adrenoceptors ]] compared to control.,387,3
+388,"TRPM8 (<< CMR1 >>) is a Ca(2+)-permeable channel, which can be activated by low temperatures, menthol, [[ eucalyptol ]] and icilin.",388,9
+389,"TRPM8 (CMR1) is a << Ca(2+)-permeable channel >>, which can be activated by low temperatures, menthol, [[ eucalyptol ]] and icilin.",389,9
+390,"<< TRPM8 >> (CMR1) is a Ca(2+)-permeable channel, which can be activated by low temperatures, menthol, [[ eucalyptol ]] and icilin.",390,9
+391,"TRPM8 (<< CMR1 >>) is a Ca(2+)-permeable channel, which can be activated by low temperatures, [[ menthol ]], eucalyptol and icilin.",391,9
+392,"TRPM8 (CMR1) is a << Ca(2+)-permeable channel >>, which can be activated by low temperatures, [[ menthol ]], eucalyptol and icilin.",392,9
+393,"<< TRPM8 >> (CMR1) is a Ca(2+)-permeable channel, which can be activated by low temperatures, [[ menthol ]], eucalyptol and icilin.",393,9
+394,"TRPM8 (<< CMR1 >>) is a Ca(2+)-permeable channel, which can be activated by low temperatures, menthol, eucalyptol and [[ icilin ]].",394,9
+395,"TRPM8 (CMR1) is a << Ca(2+)-permeable channel >>, which can be activated by low temperatures, menthol, eucalyptol and [[ icilin ]].",395,9
+396,"<< TRPM8 >> (CMR1) is a Ca(2+)-permeable channel, which can be activated by low temperatures, menthol, eucalyptol and [[ icilin ]].",396,9
+397,"Known VR1 antagonists (BCTC, thio-BCTC and capsazepine) were also able to block the response of << TRPM8 >> to [[ menthol ]] (IC(50): 0.8+/-1.0, 3.5+/-1.1 and 18+/-1.1 microM, respectively).",397,9
+398,"Known VR1 antagonists (<< BCTC >>, thio-BCTC and capsazepine) were also able to block the response of [[ TRPM8 ]] to menthol (IC(50): 0.8+/-1.0, 3.5+/-1.1 and 18+/-1.1 microM, respectively).",398,0
+399,"Known VR1 antagonists (BCTC, << thio-BCTC >> and capsazepine) were also able to block the response of [[ TRPM8 ]] to menthol (IC(50): 0.8+/-1.0, 3.5+/-1.1 and 18+/-1.1 microM, respectively).",399,0
+400,"Known VR1 antagonists (BCTC, thio-BCTC and << capsazepine >>) were also able to block the response of [[ TRPM8 ]] to menthol (IC(50): 0.8+/-1.0, 3.5+/-1.1 and 18+/-1.1 microM, respectively).",400,0
+401,"Known << VR1 >> antagonists ([[ BCTC ]], thio-BCTC and capsazepine) were also able to block the response of TRPM8 to menthol (IC(50): 0.8+/-1.0, 3.5+/-1.1 and 18+/-1.1 microM, respectively).",401,1
+402,"Known << VR1 >> antagonists (BCTC, [[ thio-BCTC ]] and capsazepine) were also able to block the response of TRPM8 to menthol (IC(50): 0.8+/-1.0, 3.5+/-1.1 and 18+/-1.1 microM, respectively).",402,1
+403,"Known << VR1 >> antagonists (BCTC, thio-BCTC and [[ capsazepine ]]) were also able to block the response of TRPM8 to menthol (IC(50): 0.8+/-1.0, 3.5+/-1.1 and 18+/-1.1 microM, respectively).",403,1
+404,The Ca(2+) response of << hVR1 >>-transfected HEK293 cells to the endogenous VR1 agonist [[ N-arachidonoyl-dopamine ]] was potentiated by low pH.,404,9
+405,The Ca(2+) response of hVR1-transfected HEK293 cells to the endogenous << VR1 >> agonist [[ N-arachidonoyl-dopamine ]] was potentiated by low pH.,405,2
+406,"In contrast, << menthol >>- and icilin-activated [[ TRPM8 ]] currents were suppressed by low pH.",406,9
+407,"In contrast, menthol- and << icilin >>-activated [[ TRPM8 ]] currents were suppressed by low pH.",407,9
+408,"Inhibitory effects of the << monoamine oxidase >> inhibitor [[ tranylcypromine ]] on the cytochrome P450 enzymes CYP2C19, CYP2C9, and CYP2D6.",408,0
+409,"The inhibitory effects of << tranylcypromine >>, a nonselective irreversible inhibitor of [[ monoamine oxidase ]] (MAO), on three cytochrome P450 (CYP) enzymes, namely CYP2C9, CYP2C19, and CYP2D6, have been evaluated in vitro.",409,0
+410,"The inhibitory effects of << tranylcypromine >>, a nonselective irreversible inhibitor of monoamine oxidase ([[ MAO ]]), on three cytochrome P450 (CYP) enzymes, namely CYP2C9, CYP2C19, and CYP2D6, have been evaluated in vitro.",410,0
+411,The results demonstrated that << tranylcypromine >> is a competitive inhibitor of [[ CYP2C19 ]] (Ki = 32 microM) and CYP2D6 (Ki = 367 microM) and a noncompetitive inhibitor of CYP2C9 (Ki = 56 microM).,411,0
+412,The results demonstrated that << tranylcypromine >> is a competitive inhibitor of CYP2C19 (Ki = 32 microM) and [[ CYP2D6 ]] (Ki = 367 microM) and a noncompetitive inhibitor of CYP2C9 (Ki = 56 microM).,412,0
+413,The results demonstrated that << tranylcypromine >> is a competitive inhibitor of CYP2C19 (Ki = 32 microM) and CYP2D6 (Ki = 367 microM) and a noncompetitive inhibitor of [[ CYP2C9 ]] (Ki = 56 microM).,413,0
+414,"Studies in rats, mice and monkeys show that GC-1 lowers cholesterol with 600- to 1400-fold more potency and approximately two- to threefold more efficacy than << atorvastatin >>, a compound that blocks [[ HMG-CoA reductase ]].",414,0
+415,"Although highly homologous to other class III RTKs, Flt3 is resistant to the << phenylaminopyrimidine >> STI571 (Gleevec, Imatinib), a potent inhibitor of other [[ RTKs ]] in the family, such as the PDGFbeta-receptor or c-Kit.",415,0
+416,"Although highly homologous to other class III RTKs, Flt3 is resistant to the << phenylaminopyrimidine >> STI571 (Gleevec, Imatinib), a potent inhibitor of other RTKs in the family, such as the [[ PDGFbeta-receptor ]] or c-Kit.",416,0
+417,"Although highly homologous to other class III RTKs, Flt3 is resistant to the << phenylaminopyrimidine >> STI571 (Gleevec, Imatinib), a potent inhibitor of other RTKs in the family, such as the PDGFbeta-receptor or [[ c-Kit ]].",417,0
+418,"Although highly homologous to other class III RTKs, Flt3 is resistant to the phenylaminopyrimidine << STI571 >> (Gleevec, Imatinib), a potent inhibitor of other [[ RTKs ]] in the family, such as the PDGFbeta-receptor or c-Kit.",418,0
+419,"Although highly homologous to other class III RTKs, Flt3 is resistant to the phenylaminopyrimidine << STI571 >> (Gleevec, Imatinib), a potent inhibitor of other RTKs in the family, such as the [[ PDGFbeta-receptor ]] or c-Kit.",419,0
+420,"Although highly homologous to other class III RTKs, Flt3 is resistant to the phenylaminopyrimidine << STI571 >> (Gleevec, Imatinib), a potent inhibitor of other RTKs in the family, such as the PDGFbeta-receptor or [[ c-Kit ]].",420,0
+421,"Although highly homologous to other class III RTKs, Flt3 is resistant to the phenylaminopyrimidine STI571 (<< Gleevec >>, Imatinib), a potent inhibitor of other [[ RTKs ]] in the family, such as the PDGFbeta-receptor or c-Kit.",421,0
+422,"Although highly homologous to other class III RTKs, Flt3 is resistant to the phenylaminopyrimidine STI571 (<< Gleevec >>, Imatinib), a potent inhibitor of other RTKs in the family, such as the [[ PDGFbeta-receptor ]] or c-Kit.",422,0
+423,"Although highly homologous to other class III RTKs, Flt3 is resistant to the phenylaminopyrimidine STI571 (<< Gleevec >>, Imatinib), a potent inhibitor of other RTKs in the family, such as the PDGFbeta-receptor or [[ c-Kit ]].",423,0
+424,"Although highly homologous to other class III RTKs, Flt3 is resistant to the phenylaminopyrimidine STI571 (Gleevec, << Imatinib >>), a potent inhibitor of other [[ RTKs ]] in the family, such as the PDGFbeta-receptor or c-Kit.",424,0
+425,"Although highly homologous to other class III RTKs, Flt3 is resistant to the phenylaminopyrimidine STI571 (Gleevec, << Imatinib >>), a potent inhibitor of other RTKs in the family, such as the [[ PDGFbeta-receptor ]] or c-Kit.",425,0
+426,"Although highly homologous to other class III RTKs, Flt3 is resistant to the phenylaminopyrimidine STI571 (Gleevec, << Imatinib >>), a potent inhibitor of other RTKs in the family, such as the PDGFbeta-receptor or [[ c-Kit ]].",426,0
+427,STI571 binding to Flt3 is prevented by the phenylalanine 691 side-chain in the ATP binding center and mutating this site to threonine renders the corresponding << Flt3 >> mutant sensitive to [[ STI571 ]].,427,0
+428,"Compounds of several other structural families, including the << quinoxaline >> AG1296, the bis(1H-2-indolyl)-1-methanone D-65476, the indolinones SU5416 and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of [[ Flt3 ]] kinase.",428,0
+429,"Compounds of several other structural families, including the << quinoxaline >> AG1296, the bis(1H-2-indolyl)-1-methanone D-65476, the indolinones SU5416 and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of Flt3 [[ kinase ]].",429,0
+430,"Compounds of several other structural families, including the quinoxaline << AG1296 >>, the bis(1H-2-indolyl)-1-methanone D-65476, the indolinones SU5416 and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of [[ Flt3 ]] kinase.",430,0
+431,"Compounds of several other structural families, including the quinoxaline << AG1296 >>, the bis(1H-2-indolyl)-1-methanone D-65476, the indolinones SU5416 and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of Flt3 [[ kinase ]].",431,0
+432,"Compounds of several other structural families, including the quinoxaline AG1296, the << bis(1H-2-indolyl)-1-methanone >> D-65476, the indolinones SU5416 and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of [[ Flt3 ]] kinase.",432,0
+433,"Compounds of several other structural families, including the quinoxaline AG1296, the << bis(1H-2-indolyl)-1-methanone >> D-65476, the indolinones SU5416 and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of Flt3 [[ kinase ]].",433,0
+434,"Compounds of several other structural families, including the quinoxaline AG1296, the bis(1H-2-indolyl)-1-methanone << D-65476 >>, the indolinones SU5416 and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of [[ Flt3 ]] kinase.",434,0
+435,"Compounds of several other structural families, including the quinoxaline AG1296, the bis(1H-2-indolyl)-1-methanone << D-65476 >>, the indolinones SU5416 and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of Flt3 [[ kinase ]].",435,0
+436,"Compounds of several other structural families, including the quinoxaline AG1296, the bis(1H-2-indolyl)-1-methanone D-65476, the << indolinones >> SU5416 and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of [[ Flt3 ]] kinase.",436,0
+437,"Compounds of several other structural families, including the quinoxaline AG1296, the bis(1H-2-indolyl)-1-methanone D-65476, the << indolinones >> SU5416 and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of Flt3 [[ kinase ]].",437,0
+438,"Compounds of several other structural families, including the quinoxaline AG1296, the bis(1H-2-indolyl)-1-methanone D-65476, the indolinones << SU5416 >> and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of [[ Flt3 ]] kinase.",438,0
+439,"Compounds of several other structural families, including the quinoxaline AG1296, the bis(1H-2-indolyl)-1-methanone D-65476, the indolinones << SU5416 >> and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of Flt3 [[ kinase ]].",439,0
+440,"Compounds of several other structural families, including the quinoxaline AG1296, the bis(1H-2-indolyl)-1-methanone D-65476, the indolinones SU5416 and << SU11248 >>, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of [[ Flt3 ]] kinase.",440,0
+441,"Compounds of several other structural families, including the quinoxaline AG1296, the bis(1H-2-indolyl)-1-methanone D-65476, the indolinones SU5416 and << SU11248 >>, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of Flt3 [[ kinase ]].",441,0
+442,"Compounds of several other structural families, including the quinoxaline AG1296, the bis(1H-2-indolyl)-1-methanone D-65476, the indolinones SU5416 and SU11248, the << indolocarbazoles >> PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of [[ Flt3 ]] kinase.",442,0
+443,"Compounds of several other structural families, including the quinoxaline AG1296, the bis(1H-2-indolyl)-1-methanone D-65476, the indolinones SU5416 and SU11248, the << indolocarbazoles >> PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of Flt3 [[ kinase ]].",443,0
+444,"Compounds of several other structural families, including the quinoxaline AG1296, the bis(1H-2-indolyl)-1-methanone D-65476, the indolinones SU5416 and SU11248, the indolocarbazoles << PKC412 >> and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of [[ Flt3 ]] kinase.",444,0
+445,"Compounds of several other structural families, including the quinoxaline AG1296, the bis(1H-2-indolyl)-1-methanone D-65476, the indolinones SU5416 and SU11248, the indolocarbazoles << PKC412 >> and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of Flt3 [[ kinase ]].",445,0
+446,"Compounds of several other structural families, including the quinoxaline AG1296, the bis(1H-2-indolyl)-1-methanone D-65476, the indolinones SU5416 and SU11248, the indolocarbazoles PKC412 and << CEP-701 >>, and the piperazonyl quinazoline CT53518, are potent inhibitors of [[ Flt3 ]] kinase.",446,0
+447,"Compounds of several other structural families, including the quinoxaline AG1296, the bis(1H-2-indolyl)-1-methanone D-65476, the indolinones SU5416 and SU11248, the indolocarbazoles PKC412 and << CEP-701 >>, and the piperazonyl quinazoline CT53518, are potent inhibitors of Flt3 [[ kinase ]].",447,0
+448,"Compounds of several other structural families, including the quinoxaline AG1296, the bis(1H-2-indolyl)-1-methanone D-65476, the indolinones SU5416 and SU11248, the indolocarbazoles PKC412 and CEP-701, and the << piperazonyl quinazoline >> CT53518, are potent inhibitors of [[ Flt3 ]] kinase.",448,0
+449,"Compounds of several other structural families, including the quinoxaline AG1296, the bis(1H-2-indolyl)-1-methanone D-65476, the indolinones SU5416 and SU11248, the indolocarbazoles PKC412 and CEP-701, and the << piperazonyl quinazoline >> CT53518, are potent inhibitors of Flt3 [[ kinase ]].",449,0
+450,"Compounds of several other structural families, including the quinoxaline AG1296, the bis(1H-2-indolyl)-1-methanone D-65476, the indolinones SU5416 and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline << CT53518 >>, are potent inhibitors of [[ Flt3 ]] kinase.",450,0
+451,"Compounds of several other structural families, including the quinoxaline AG1296, the bis(1H-2-indolyl)-1-methanone D-65476, the indolinones SU5416 and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline << CT53518 >>, are potent inhibitors of Flt3 [[ kinase ]].",451,0
+452,"Novel mechanism of action for << hydralazine >>: induction of hypoxia-inducible factor-1alpha, [[ vascular endothelial growth factor ]], and angiogenesis by inhibition of prolyl hydroxylases.",452,6
+453,"Novel mechanism of action for << hydralazine >>: induction of [[ hypoxia-inducible factor-1alpha ]], vascular endothelial growth factor, and angiogenesis by inhibition of prolyl hydroxylases.",453,7
+454,"Novel mechanism of action for << hydralazine >>: induction of hypoxia-inducible factor-1alpha, vascular endothelial growth factor, and angiogenesis by inhibition of [[ prolyl hydroxylases ]].",454,0
+455,"<< Hydralazine >> induced rapid and transient expression of HIF-1alpha and downstream targets of HIF ([[ endothelin-1 ]], adrenomedullin, haem oxygenase 1, and vascular endothelial growth factor [VEGF]) in endothelial and smooth muscle cells and induced endothelial cell-specific proliferation.",455,6
+456,"<< Hydralazine >> induced rapid and transient expression of HIF-1alpha and downstream targets of HIF (endothelin-1, [[ adrenomedullin ]], haem oxygenase 1, and vascular endothelial growth factor [VEGF]) in endothelial and smooth muscle cells and induced endothelial cell-specific proliferation.",456,6
+457,"<< Hydralazine >> induced rapid and transient expression of HIF-1alpha and downstream targets of HIF (endothelin-1, adrenomedullin, [[ haem oxygenase 1 ]], and vascular endothelial growth factor [VEGF]) in endothelial and smooth muscle cells and induced endothelial cell-specific proliferation.",457,6
+458,"<< Hydralazine >> induced rapid and transient expression of HIF-1alpha and downstream targets of HIF (endothelin-1, adrenomedullin, haem oxygenase 1, and [[ vascular endothelial growth factor ]] [VEGF]) in endothelial and smooth muscle cells and induced endothelial cell-specific proliferation.",458,6
+459,"<< Hydralazine >> induced rapid and transient expression of HIF-1alpha and downstream targets of HIF (endothelin-1, adrenomedullin, haem oxygenase 1, and vascular endothelial growth factor [[[ VEGF ]]]) in endothelial and smooth muscle cells and induced endothelial cell-specific proliferation.",459,6
+460,"<< Hydralazine >> induced rapid and transient expression of [[ HIF-1alpha ]] and downstream targets of HIF (endothelin-1, adrenomedullin, haem oxygenase 1, and vascular endothelial growth factor [VEGF]) in endothelial and smooth muscle cells and induced endothelial cell-specific proliferation.",460,7
+461,"<< Hydralazine >> induced rapid and transient expression of HIF-1alpha and downstream targets of [[ HIF ]] (endothelin-1, adrenomedullin, haem oxygenase 1, and vascular endothelial growth factor [VEGF]) in endothelial and smooth muscle cells and induced endothelial cell-specific proliferation.",461,7
+462,"<< Hydralazine >> dose-dependently inhibited PHD activity and induced nonhydroxylated [[ HIF-1alpha ]], evidence for HIF stabilization specifically by inhibition of PHD enzyme activity.",462,7
+463,"<< Hydralazine >> dose-dependently inhibited [[ PHD ]] activity and induced nonhydroxylated HIF-1alpha, evidence for HIF stabilization specifically by inhibition of PHD enzyme activity.",463,0
+464,"<< Hydralazine >> dose-dependently inhibited PHD activity and induced nonhydroxylated HIF-1alpha, evidence for HIF stabilization specifically by inhibition of [[ PHD ]] enzyme activity.",464,0
+465,"In vivo, << hydralazine >> induced HIF-1alpha and VEGF protein in tissue extracts and elevated plasma [[ VEGF ]] levels.",465,6
+466,"In vivo, << hydralazine >> induced HIF-1alpha and [[ VEGF ]] protein in tissue extracts and elevated plasma VEGF levels.",466,6
+467,"In vivo, << hydralazine >> induced [[ HIF-1alpha ]] and VEGF protein in tissue extracts and elevated plasma VEGF levels.",467,7
+468,"Thus, << hydralazine >> activates the [[ HIF ]] pathway through inhibition of PHD activity and initiates a pro-angiogenic phenotype.",468,9
+469,"Thus, << hydralazine >> activates the HIF pathway through inhibition of [[ PHD ]] activity and initiates a pro-angiogenic phenotype.",469,0
+470,"RESULTS: Aspirin, diclofenac, indomethacin, ketoprofen, meclofenamic acid, and piroxicam had little selectivity toward COX isozymes, whereas << NS398 >>, carprofen, tolfenamic acid, nimesulide, and etodolac had more than 5 times greater preference for inhibiting [[ COX-2 ]] than COX-1.",470,0
+471,"RESULTS: Aspirin, diclofenac, indomethacin, ketoprofen, meclofenamic acid, and piroxicam had little selectivity toward COX isozymes, whereas << NS398 >>, carprofen, tolfenamic acid, nimesulide, and etodolac had more than 5 times greater preference for inhibiting COX-2 than [[ COX-1 ]].",471,0
+472,"RESULTS: Aspirin, diclofenac, indomethacin, ketoprofen, meclofenamic acid, and piroxicam had little selectivity toward COX isozymes, whereas NS398, << carprofen >>, tolfenamic acid, nimesulide, and etodolac had more than 5 times greater preference for inhibiting [[ COX-2 ]] than COX-1.",472,0
+473,"RESULTS: Aspirin, diclofenac, indomethacin, ketoprofen, meclofenamic acid, and piroxicam had little selectivity toward COX isozymes, whereas NS398, << carprofen >>, tolfenamic acid, nimesulide, and etodolac had more than 5 times greater preference for inhibiting COX-2 than [[ COX-1 ]].",473,0
+474,"RESULTS: Aspirin, diclofenac, indomethacin, ketoprofen, meclofenamic acid, and piroxicam had little selectivity toward COX isozymes, whereas NS398, carprofen, << tolfenamic acid >>, nimesulide, and etodolac had more than 5 times greater preference for inhibiting [[ COX-2 ]] than COX-1.",474,0
+475,"RESULTS: Aspirin, diclofenac, indomethacin, ketoprofen, meclofenamic acid, and piroxicam had little selectivity toward COX isozymes, whereas NS398, carprofen, << tolfenamic acid >>, nimesulide, and etodolac had more than 5 times greater preference for inhibiting COX-2 than [[ COX-1 ]].",475,0
+476,"RESULTS: Aspirin, diclofenac, indomethacin, ketoprofen, meclofenamic acid, and piroxicam had little selectivity toward COX isozymes, whereas NS398, carprofen, tolfenamic acid, << nimesulide >>, and etodolac had more than 5 times greater preference for inhibiting [[ COX-2 ]] than COX-1.",476,0
+477,"RESULTS: Aspirin, diclofenac, indomethacin, ketoprofen, meclofenamic acid, and piroxicam had little selectivity toward COX isozymes, whereas NS398, carprofen, tolfenamic acid, << nimesulide >>, and etodolac had more than 5 times greater preference for inhibiting COX-2 than [[ COX-1 ]].",477,0
+478,"RESULTS: Aspirin, diclofenac, indomethacin, ketoprofen, meclofenamic acid, and piroxicam had little selectivity toward COX isozymes, whereas NS398, carprofen, tolfenamic acid, nimesulide, and << etodolac >> had more than 5 times greater preference for inhibiting [[ COX-2 ]] than COX-1.",478,0
+479,"RESULTS: Aspirin, diclofenac, indomethacin, ketoprofen, meclofenamic acid, and piroxicam had little selectivity toward COX isozymes, whereas NS398, carprofen, tolfenamic acid, nimesulide, and << etodolac >> had more than 5 times greater preference for inhibiting COX-2 than [[ COX-1 ]].",479,0
+480,"CONCLUSIONS AND CLINICAL RELEVANCE: << Canine COX-2 >> was selectively inhibited by [[ etodolac ]], nimesulide, and NS398; tolfenamic acid and carprofen also appeared to be preferential COX-2 inhibitors in dogs.",480,0
+481,"CONCLUSIONS AND CLINICAL RELEVANCE: << Canine COX-2 >> was selectively inhibited by etodolac, [[ nimesulide ]], and NS398; tolfenamic acid and carprofen also appeared to be preferential COX-2 inhibitors in dogs.",481,0
+482,"CONCLUSIONS AND CLINICAL RELEVANCE: << Canine COX-2 >> was selectively inhibited by etodolac, nimesulide, and [[ NS398 ]]; tolfenamic acid and carprofen also appeared to be preferential COX-2 inhibitors in dogs.",482,0
+483,"CONCLUSIONS AND CLINICAL RELEVANCE: Canine COX-2 was selectively inhibited by etodolac, nimesulide, and NS398; << tolfenamic acid >> and carprofen also appeared to be preferential [[ COX-2 ]] inhibitors in dogs.",483,0
+484,"CONCLUSIONS AND CLINICAL RELEVANCE: Canine COX-2 was selectively inhibited by etodolac, nimesulide, and NS398; tolfenamic acid and << carprofen >> also appeared to be preferential [[ COX-2 ]] inhibitors in dogs.",484,0
+485,"<< Acarbose >> served as inhibitor of an interfering [[ acid alpha-glucosidase ]] present in neutrophils, which allowed the lysosomal enzyme implicated in Pompe disease to be selectively analyzed.",485,0
+486,"After 12 months of treatment, << carvedilol >> significantly improved all end points (plasma concentration of [[ B-type natriuretic peptide ]] [BNP] from 175 (35 to 209) to 106 (52 to 160) pg/ml, mean (95% confidence interval) p <0.01; New York Heart Association functional class from 2.37 (2.13 to 2.61) to 1.56 (1.21 to 1.91), p <0.01; exercise capacity estimated with the Specific Activity Scale from 4.75 (4.50 to 5.00) to 5.68 (5.22 to 6.14) METs, p <0.02), whereas conventional therapy did not (plasma BNP concentration from 150 (114 to 186) to 174 (100 to 248) pg/ml; New York Heart Association functional class from 2.29 (2.08 to 2.50) to 2.11 (1.73 to 2.49); exercise capacity from 4.57 (4.34 to 4.80) to 4.72 (4.41 to 5.03) METs).",486,8
+487,"After 12 months of treatment, << carvedilol >> significantly improved all end points (plasma concentration of B-type natriuretic peptide [[[ BNP ]]] from 175 (35 to 209) to 106 (52 to 160) pg/ml, mean (95% confidence interval) p <0.01; New York Heart Association functional class from 2.37 (2.13 to 2.61) to 1.56 (1.21 to 1.91), p <0.01; exercise capacity estimated with the Specific Activity Scale from 4.75 (4.50 to 5.00) to 5.68 (5.22 to 6.14) METs, p <0.02), whereas conventional therapy did not (plasma BNP concentration from 150 (114 to 186) to 174 (100 to 248) pg/ml; New York Heart Association functional class from 2.29 (2.08 to 2.50) to 2.11 (1.73 to 2.49); exercise capacity from 4.57 (4.34 to 4.80) to 4.72 (4.41 to 5.03) METs).",487,8
+488,Univariate regression analyses showed that only the use of << carvedilol >> was correlated with the decrease in [[ plasma BNP ]] concentration (p <0.03).,488,8
+489,<< Terbinafine >>: mode of action and properties of the [[ squalene epoxidase ]] inhibition.,489,0
+490,<< Terbinafine >> (Lamisil) has primarily fungicidal action against many fungi as a result of its specific mechanism of [[ squalene epoxidase ]] inhibition.,490,0
+491,Terbinafine (<< Lamisil >>) has primarily fungicidal action against many fungi as a result of its specific mechanism of [[ squalene epoxidase ]] inhibition.,491,0
+492,<< Terbinafine >> is a potent non-competitive inhibitor of [[ squalene epoxidase ]] from Candida (Ki = 30 nM).,492,0
+493,"In contrast, inhibition of << rat liver squalene epoxidase >> only occurs at higher drug concentrations (Ki = 77 microM), and is competitive with [[ squalene ]].",493,0
+494,Each statin induced apoA-I expression (mRNA and protein) dose-dependently: the rank order of the << apoA-I >> induction [[ pitavastatin ]] (3 microM)>simvastatin (10 microM)>atorvastatin (30 microM).,494,6
+495,Each statin induced apoA-I expression (mRNA and protein) dose-dependently: the rank order of the << apoA-I >> induction pitavastatin (3 microM)>[[ simvastatin ]] (10 microM)>atorvastatin (30 microM).,495,6
+496,Each statin induced apoA-I expression (mRNA and protein) dose-dependently: the rank order of the << apoA-I >> induction pitavastatin (3 microM)>simvastatin (10 microM)>[[ atorvastatin ]] (30 microM).,496,6
+497,"The induction of << apoA-I >> by statins disappeared with addition of [[ mevalonate ]], which indicates that the effect is HMG-CoA reductase inhibition-dependent.",497,8
+498,"Based on HMG-CoA reductase inhibition, pitavastatin-induced << apoA-I >> more efficiently than [[ simvastatin ]] and atorvastatin.",498,6
+499,"Based on HMG-CoA reductase inhibition, pitavastatin-induced << apoA-I >> more efficiently than simvastatin and [[ atorvastatin ]].",499,6
+500,"Based on HMG-CoA reductase inhibition, << pitavastatin >>-induced [[ apoA-I ]] more efficiently than simvastatin and atorvastatin.",500,6
+501,Further study revealed that << pitavastatin >> increased [[ ABCA1 ]] mRNA in HMG-CoA reductase-dependent manner and that Rho and Rho kinase inhibitor (C3T and Y27632) increased apoA-I production in the HepG2 cells.,501,6
+502,Further study revealed that pitavastatin increased ABCA1 mRNA in HMG-CoA reductase-dependent manner and that Rho and Rho kinase inhibitor (C3T and << Y27632 >>) increased [[ apoA-I ]] production in the HepG2 cells.,502,6
+503,Further study revealed that pitavastatin increased ABCA1 mRNA in HMG-CoA reductase-dependent manner and that << Rho >> and Rho kinase inhibitor (C3T and [[ Y27632 ]]) increased apoA-I production in the HepG2 cells.,503,0
+504,Further study revealed that pitavastatin increased ABCA1 mRNA in HMG-CoA reductase-dependent manner and that Rho and << Rho kinase >> inhibitor (C3T and [[ Y27632 ]]) increased apoA-I production in the HepG2 cells.,504,0
+505,These results suggest that << pitavastatin >> efficiently increases [[ apoA-I ]] in the culture medium of HepG2 cells by promoting apoA-I production through inhibition of HMG-CoA reductase and suppression of Rho activity and by protecting apoA-I from catabolism through ABCA1 induction and lipidation of apoA-I.,505,6
+506,These results suggest that << pitavastatin >> efficiently increases apoA-I in the culture medium of HepG2 cells by promoting [[ apoA-I ]] production through inhibition of HMG-CoA reductase and suppression of Rho activity and by protecting apoA-I from catabolism through ABCA1 induction and lipidation of apoA-I.,506,6
+507,These results suggest that << pitavastatin >> efficiently increases apoA-I in the culture medium of HepG2 cells by promoting apoA-I production through inhibition of HMG-CoA reductase and suppression of Rho activity and by protecting apoA-I from catabolism through [[ ABCA1 ]] induction and lipidation of apoA-I.,507,6
+508,These results suggest that << pitavastatin >> efficiently increases apoA-I in the culture medium of HepG2 cells by promoting apoA-I production through inhibition of HMG-CoA reductase and suppression of Rho activity and by protecting apoA-I from catabolism through ABCA1 induction and lipidation of [[ apoA-I ]].,508,6
+509,These results suggest that << pitavastatin >> efficiently increases apoA-I in the culture medium of HepG2 cells by promoting apoA-I production through inhibition of [[ HMG-CoA reductase ]] and suppression of Rho activity and by protecting apoA-I from catabolism through ABCA1 induction and lipidation of apoA-I.,509,0
+510,These results suggest that << pitavastatin >> efficiently increases apoA-I in the culture medium of HepG2 cells by promoting apoA-I production through inhibition of HMG-CoA reductase and suppression of [[ Rho ]] activity and by protecting apoA-I from catabolism through ABCA1 induction and lipidation of apoA-I.,510,0
+511,"MATERIALS AND METHODS: Seeking to improve efficacy against otherwise intractable end-stage pancreatic islet tumors, two << receptor tyrosine kinase >> inhibitors, [[ imatinib ]] and SU11248, were used to disrupt PDGFR-mediated pericyte support of tumor endothelial cells in concert with maximum-tolerated dose (MTD) or metronomic chemotherapy and/or VEGFR inhibition.",511,0
+512,"MATERIALS AND METHODS: Seeking to improve efficacy against otherwise intractable end-stage pancreatic islet tumors, two receptor tyrosine kinase inhibitors, << imatinib >> and SU11248, were used to disrupt [[ PDGFR ]]-mediated pericyte support of tumor endothelial cells in concert with maximum-tolerated dose (MTD) or metronomic chemotherapy and/or VEGFR inhibition.",512,0
+513,"MATERIALS AND METHODS: Seeking to improve efficacy against otherwise intractable end-stage pancreatic islet tumors, two receptor tyrosine kinase inhibitors, << imatinib >> and SU11248, were used to disrupt PDGFR-mediated pericyte support of tumor endothelial cells in concert with maximum-tolerated dose (MTD) or metronomic chemotherapy and/or [[ VEGFR ]] inhibition.",513,0
+514,"MATERIALS AND METHODS: Seeking to improve efficacy against otherwise intractable end-stage pancreatic islet tumors, two << receptor tyrosine kinase >> inhibitors, imatinib and [[ SU11248 ]], were used to disrupt PDGFR-mediated pericyte support of tumor endothelial cells in concert with maximum-tolerated dose (MTD) or metronomic chemotherapy and/or VEGFR inhibition.",514,0
+515,"MATERIALS AND METHODS: Seeking to improve efficacy against otherwise intractable end-stage pancreatic islet tumors, two receptor tyrosine kinase inhibitors, imatinib and << SU11248 >>, were used to disrupt [[ PDGFR ]]-mediated pericyte support of tumor endothelial cells in concert with maximum-tolerated dose (MTD) or metronomic chemotherapy and/or VEGFR inhibition.",515,0
+516,"MATERIALS AND METHODS: Seeking to improve efficacy against otherwise intractable end-stage pancreatic islet tumors, two receptor tyrosine kinase inhibitors, imatinib and << SU11248 >>, were used to disrupt PDGFR-mediated pericyte support of tumor endothelial cells in concert with maximum-tolerated dose (MTD) or metronomic chemotherapy and/or [[ VEGFR ]] inhibition.",516,0
+517,"RESULTS: << Imatinib >>, despite equivocal efficacy as monotherapy, reduced pericyte coverage of tumor vessels and enhanced efficacy in combination with metronomic chemotherapy or [[ VEGFR ]] inhibition.",517,0
+518,The objective of the present study was to compare the anti-inflammatory effects of the preferential COX-2 inhibitor etodolac with the non-selective << COX >> inhibitor [[ phenylbutazone ]] in horses with lipopolysaccharide (LPS)-induced synovitis.,518,0
+519,"In addition, both drugs significantly reduced PGE2 levels (P<0.05) 6-h following LPS injection, whereas the probable << COX-1 >> prostanoid TXB2 was significantly reduced by [[ phenylbutazone ]] (P<0.05), but not etodolac.",519,8
+520,Effect of << bosentan >> ([[ ETA ]]/ETB receptor antagonist) on metabolic changes during stress and diabetes.,520,1
+521,Effect of << bosentan >> (ETA/[[ ETB ]] receptor antagonist) on metabolic changes during stress and diabetes.,521,1
+522,"To test this, we studied the possible effect of the << endothelin receptor >> antagonist, [[ bosentan ]] (50 and 100 mg kg(-1)) on serum glucose and insulin levels as well as on liver glycogen contents in normoglycemic stressed animals.",522,1
+523,"Pre-irradiation administration of RP-1 enhanced levels of << GSH >> induced increase in [[ complex I ]] (upto 16 h), complex I/III (4 h) complex II/III activity (upto 24 h; p < 0.01) and inhibited the radiation-induced decrease in MMP significantly (24 h; p < 0.01).",523,9
+524,"Pre-irradiation administration of RP-1 enhanced levels of << GSH >> induced increase in complex I (upto 16 h), [[ complex I/III ]] (4 h) complex II/III activity (upto 24 h; p < 0.01) and inhibited the radiation-induced decrease in MMP significantly (24 h; p < 0.01).",524,9
+525,"Pre-irradiation administration of RP-1 enhanced levels of << GSH >> induced increase in complex I (upto 16 h), complex I/III (4 h) [[ complex II/III ]] activity (upto 24 h; p < 0.01) and inhibited the radiation-induced decrease in MMP significantly (24 h; p < 0.01).",525,9
+526,"Moreover, << minocycline >> efficiently suppressed the release of [[ cytochrome c ]] from mitochondria of the liver tissues from Jo2-challenged mice.",526,8
+527,"Our results suggest that easing of Fas-triggered fulminant hepatitis by << minocycline >> may involve a mitochondrial apoptotic pathway, probably through preventing [[ cytochrome c ]] release and thereby blocking downstream caspase activation.",527,8
+528,"Our results suggest that easing of Fas-triggered fulminant hepatitis by << minocycline >> may involve a mitochondrial apoptotic pathway, probably through preventing cytochrome c release and thereby blocking downstream [[ caspase ]] activation.",528,0
+529,Cystathionine-gamma-lyase (<< CSE >>) and cystathionine-beta-synthase (CBS) utilize L-cysteine as substrate to form [[ H2S ]].,529,4
+530,Cystathionine-gamma-lyase (CSE) and << cystathionine-beta-synthase >> (CBS) utilize L-cysteine as substrate to form [[ H2S ]].,530,4
+531,Cystathionine-gamma-lyase (CSE) and cystathionine-beta-synthase (<< CBS >>) utilize L-cysteine as substrate to form [[ H2S ]].,531,4
+532,<< Cystathionine-gamma-lyase >> (CSE) and cystathionine-beta-synthase (CBS) utilize L-cysteine as substrate to form [[ H2S ]].,532,4
+533,Cystathionine-gamma-lyase (<< CSE >>) and cystathionine-beta-synthase (CBS) utilize [[ L-cysteine ]] as substrate to form H2S.,533,5
+534,Cystathionine-gamma-lyase (CSE) and << cystathionine-beta-synthase >> (CBS) utilize [[ L-cysteine ]] as substrate to form H2S.,534,5
+535,Cystathionine-gamma-lyase (CSE) and cystathionine-beta-synthase (<< CBS >>) utilize [[ L-cysteine ]] as substrate to form H2S.,535,5
+536,<< Cystathionine-gamma-lyase >> (CSE) and cystathionine-beta-synthase (CBS) utilize [[ L-cysteine ]] as substrate to form H2S.,536,5
+537,"Of these two enzymes, << cystathionine-gamma-lyase >> (CSE) is believed to be the key enzyme that forms [[ H2S ]] in the cardiovascular system.",537,4
+538,"Of these two enzymes, cystathionine-gamma-lyase (<< CSE >>) is believed to be the key enzyme that forms [[ H2S ]] in the cardiovascular system.",538,4
+539,"Also, prophylactic, as well as therapeutic, treatment with the CSE inhibitor, DL-propargylglycine (PAG), significantly reduced the severity of caerulein-induced pancreatitis and associated lung injury, as determined by 1) hyperamylasemia [plasma amylase (U/L) (control, 1204+/-59); prophylactic treatment: placebo, 10635+/-305; PAG, 7904+/-495; therapeutic treatment: placebo, 10427+/-470; PAG, 7811+/-428; P<0.05 PAG c.f. placebo; n=24 animals in each group]; 2) neutrophil sequestration in the pancreas [pancreatic << myeloperoxidase oxidase >> (MPO) activity (fold increase over control) (prophylactic treatment: placebo, 5.78+/-0.63; [[ PAG ]], 2.97+/-0.39; therapeutic treatment: placebo, 5.48+/-0.52; PAG, 3.03+/-0.47; P<0.05 PAG c.f. placebo; n=24 animals in each group)]; 3) pancreatic acinar cell injury/necrosis; 4) lung MPO activity (fold increase over control) [prophylactic treatment: placebo, 1.99+/-0.16; PAG, 1.34+/-0.14; therapeutic treatment: placebo, 2.03+/-0.12; PAG, 1.41+/-0.97; P<0.05 PAG c.f. placebo; n=24 animals in each group]; and 5) histological evidence of lung injury.",539,9
+540,"Also, prophylactic, as well as therapeutic, treatment with the CSE inhibitor, DL-propargylglycine (PAG), significantly reduced the severity of caerulein-induced pancreatitis and associated lung injury, as determined by 1) hyperamylasemia [plasma amylase (U/L) (control, 1204+/-59); prophylactic treatment: placebo, 10635+/-305; PAG, 7904+/-495; therapeutic treatment: placebo, 10427+/-470; PAG, 7811+/-428; P<0.05 PAG c.f. placebo; n=24 animals in each group]; 2) neutrophil sequestration in the pancreas [pancreatic myeloperoxidase oxidase (<< MPO >>) activity (fold increase over control) (prophylactic treatment: placebo, 5.78+/-0.63; [[ PAG ]], 2.97+/-0.39; therapeutic treatment: placebo, 5.48+/-0.52; PAG, 3.03+/-0.47; P<0.05 PAG c.f. placebo; n=24 animals in each group)]; 3) pancreatic acinar cell injury/necrosis; 4) lung MPO activity (fold increase over control) [prophylactic treatment: placebo, 1.99+/-0.16; PAG, 1.34+/-0.14; therapeutic treatment: placebo, 2.03+/-0.12; PAG, 1.41+/-0.97; P<0.05 PAG c.f. placebo; n=24 animals in each group]; and 5) histological evidence of lung injury.",540,9
+541,"Also, prophylactic, as well as therapeutic, treatment with the << CSE >> inhibitor, [[ DL-propargylglycine ]] (PAG), significantly reduced the severity of caerulein-induced pancreatitis and associated lung injury, as determined by 1) hyperamylasemia [plasma amylase (U/L) (control, 1204+/-59); prophylactic treatment: placebo, 10635+/-305; PAG, 7904+/-495; therapeutic treatment: placebo, 10427+/-470; PAG, 7811+/-428; P<0.05 PAG c.f. placebo; n=24 animals in each group]; 2) neutrophil sequestration in the pancreas [pancreatic myeloperoxidase oxidase (MPO) activity (fold increase over control) (prophylactic treatment: placebo, 5.78+/-0.63; PAG, 2.97+/-0.39; therapeutic treatment: placebo, 5.48+/-0.52; PAG, 3.03+/-0.47; P<0.05 PAG c.f. placebo; n=24 animals in each group)]; 3) pancreatic acinar cell injury/necrosis; 4) lung MPO activity (fold increase over control) [prophylactic treatment: placebo, 1.99+/-0.16; PAG, 1.34+/-0.14; therapeutic treatment: placebo, 2.03+/-0.12; PAG, 1.41+/-0.97; P<0.05 PAG c.f. placebo; n=24 animals in each group]; and 5) histological evidence of lung injury.",541,0
+542,"Also, prophylactic, as well as therapeutic, treatment with the << CSE >> inhibitor, DL-propargylglycine ([[ PAG ]]), significantly reduced the severity of caerulein-induced pancreatitis and associated lung injury, as determined by 1) hyperamylasemia [plasma amylase (U/L) (control, 1204+/-59); prophylactic treatment: placebo, 10635+/-305; PAG, 7904+/-495; therapeutic treatment: placebo, 10427+/-470; PAG, 7811+/-428; P<0.05 PAG c.f. placebo; n=24 animals in each group]; 2) neutrophil sequestration in the pancreas [pancreatic myeloperoxidase oxidase (MPO) activity (fold increase over control) (prophylactic treatment: placebo, 5.78+/-0.63; PAG, 2.97+/-0.39; therapeutic treatment: placebo, 5.48+/-0.52; PAG, 3.03+/-0.47; P<0.05 PAG c.f. placebo; n=24 animals in each group)]; 3) pancreatic acinar cell injury/necrosis; 4) lung MPO activity (fold increase over control) [prophylactic treatment: placebo, 1.99+/-0.16; PAG, 1.34+/-0.14; therapeutic treatment: placebo, 2.03+/-0.12; PAG, 1.41+/-0.97; P<0.05 PAG c.f. placebo; n=24 animals in each group]; and 5) histological evidence of lung injury.",542,0
+543,"ABCG5 and ABCG8 themselves are regulated by cholesterol via liver X receptors (<< LXRs >>), which are also activated by oxysterols and some derivatives of plant [[ sterols ]].",543,9
+544,<< NPC1L1 >> could recently be identified as a major sterol transporter for the intestinal uptake of [[ cholesterol ]] as well as plant sterols.,544,5
+545,NPC1L1 could recently be identified as a major << sterol transporter >> for the intestinal uptake of [[ cholesterol ]] as well as plant sterols.,545,5
+546,<< NPC1L1 >> could recently be identified as a major sterol transporter for the intestinal uptake of cholesterol as well as plant [[ sterols ]].,546,5
+547,NPC1L1 could recently be identified as a major << sterol transporter >> for the intestinal uptake of cholesterol as well as plant [[ sterols ]].,547,5
+548,<< Bupropion >> has an antidepressant effect through blocking the [[ dopamine transporter ]].,548,0
+549,"In vitro studies demonstrated that the retinoid X receptor (RXR) retinoid, << bexarotene >>, at biologically relevant concentrations of 10(-6) M to 10(-8) M, upregulated both the [[ p55 ]] and p75 subunits of the IL-2R and enhanced 5- to 10-fold the susceptibility of T-cell leukemia cells to denileukin diftitox.",549,6
+550,"In vitro studies demonstrated that the retinoid X receptor (RXR) retinoid, << bexarotene >>, at biologically relevant concentrations of 10(-6) M to 10(-8) M, upregulated both the p55 and [[ p75 ]] subunits of the IL-2R and enhanced 5- to 10-fold the susceptibility of T-cell leukemia cells to denileukin diftitox.",550,6
+551,"In vitro studies demonstrated that the retinoid X receptor (RXR) retinoid, << bexarotene >>, at biologically relevant concentrations of 10(-6) M to 10(-8) M, upregulated both the p55 and p75 subunits of the [[ IL-2R ]] and enhanced 5- to 10-fold the susceptibility of T-cell leukemia cells to denileukin diftitox.",551,7
+552,Our results demonstrate that the combination of denileukin diftitox and bexarotene is well tolerated and that even low doses (150 mg/day) of << bexarotene >> are capable of in vivo upregulation of [[ CD25 ]] expression on circulating leukemia cells.,552,6
+553,"<< PSMA >> acts as a glutamate carboxypeptidase (GCPII) on small molecule substrates, including [[ folate ]], the anticancer drug methotrexate, and the neuropeptide N-acetyl-l-aspartyl-l-glutamate.",553,5
+554,"PSMA acts as a << glutamate carboxypeptidase >> (GCPII) on small molecule substrates, including [[ folate ]], the anticancer drug methotrexate, and the neuropeptide N-acetyl-l-aspartyl-l-glutamate.",554,5
+555,"PSMA acts as a glutamate carboxypeptidase (<< GCPII >>) on small molecule substrates, including [[ folate ]], the anticancer drug methotrexate, and the neuropeptide N-acetyl-l-aspartyl-l-glutamate.",555,5
+556,"<< PSMA >> acts as a glutamate carboxypeptidase (GCPII) on small molecule substrates, including folate, the anticancer drug [[ methotrexate ]], and the neuropeptide N-acetyl-l-aspartyl-l-glutamate.",556,5
+557,"PSMA acts as a << glutamate carboxypeptidase >> (GCPII) on small molecule substrates, including folate, the anticancer drug [[ methotrexate ]], and the neuropeptide N-acetyl-l-aspartyl-l-glutamate.",557,5
+558,"PSMA acts as a glutamate carboxypeptidase (<< GCPII >>) on small molecule substrates, including folate, the anticancer drug [[ methotrexate ]], and the neuropeptide N-acetyl-l-aspartyl-l-glutamate.",558,5
+559,"<< PSMA >> acts as a glutamate carboxypeptidase (GCPII) on small molecule substrates, including folate, the anticancer drug methotrexate, and the neuropeptide [[ N-acetyl-l-aspartyl-l-glutamate ]].",559,5
+560,"PSMA acts as a << glutamate carboxypeptidase >> (GCPII) on small molecule substrates, including folate, the anticancer drug methotrexate, and the neuropeptide [[ N-acetyl-l-aspartyl-l-glutamate ]].",560,5
+561,Elucidation of the << PSMA >> structure combined with docking studies and a proposed catalytic mechanism provides insight into the recognition of inhibitors and the natural substrate [[ N-acetyl-l-aspartyl-l-glutamate ]].,561,5
+562,"A number of selective << 5-HT3 >> antagonists have been developed including ondansetron, granisetron, tropisetron renzapride and [[ zacopride ]].",562,1
+563,"A number of selective << 5-HT3 >> antagonists have been developed including [[ ondansetron ]], granisetron, tropisetron renzapride and zacopride.",563,1
+564,"A number of selective << 5-HT3 >> antagonists have been developed including ondansetron, [[ granisetron ]], tropisetron renzapride and zacopride.",564,1
+565,"A number of selective << 5-HT3 >> antagonists have been developed including ondansetron, granisetron, [[ tropisetron ]] renzapride and zacopride.",565,1
+566,"A number of selective << 5-HT3 >> antagonists have been developed including ondansetron, granisetron, tropisetron [[ renzapride ]] and zacopride.",566,1
+567,"While the substituted << benzamide >> prokinetics (for example, metoclopramide, cisapride) also block [[ 5-HT3 ]] receptors in high concentrations, their prokinetic action is believed to be on the basis of their agonist effects on the putative 5-HT4 receptor.",567,0
+568,"While the substituted benzamide prokinetics (for example, << metoclopramide >>, cisapride) also block [[ 5-HT3 ]] receptors in high concentrations, their prokinetic action is believed to be on the basis of their agonist effects on the putative 5-HT4 receptor.",568,0
+569,"While the substituted benzamide prokinetics (for example, metoclopramide, << cisapride >>) also block [[ 5-HT3 ]] receptors in high concentrations, their prokinetic action is believed to be on the basis of their agonist effects on the putative 5-HT4 receptor.",569,0
+570,"While the substituted << benzamide >> prokinetics (for example, metoclopramide, cisapride) also block 5-HT3 receptors in high concentrations, their prokinetic action is believed to be on the basis of their agonist effects on the putative [[ 5-HT4 ]] receptor.",570,2
+571,"While the substituted benzamide prokinetics (for example, << metoclopramide >>, cisapride) also block 5-HT3 receptors in high concentrations, their prokinetic action is believed to be on the basis of their agonist effects on the putative [[ 5-HT4 ]] receptor.",571,2
+572,"While the substituted benzamide prokinetics (for example, metoclopramide, << cisapride >>) also block 5-HT3 receptors in high concentrations, their prokinetic action is believed to be on the basis of their agonist effects on the putative [[ 5-HT4 ]] receptor.",572,2
+573,"Some 5-HT3 antagonists have << 5-HT4 >> agonist activity (for example, [[ renzapride ]], zacopride) and others do not (for example, ondansetron, granisetron), while tropisetron in high concentrations is a 5-HT4 antagonist.",573,2
+574,"Some 5-HT3 antagonists have << 5-HT4 >> agonist activity (for example, renzapride, [[ zacopride ]]) and others do not (for example, ondansetron, granisetron), while tropisetron in high concentrations is a 5-HT4 antagonist.",574,2
+575,"Some << 5-HT3 >> antagonists have 5-HT4 agonist activity (for example, [[ renzapride ]], zacopride) and others do not (for example, ondansetron, granisetron), while tropisetron in high concentrations is a 5-HT4 antagonist.",575,1
+576,"Some << 5-HT3 >> antagonists have 5-HT4 agonist activity (for example, renzapride, [[ zacopride ]]) and others do not (for example, ondansetron, granisetron), while tropisetron in high concentrations is a 5-HT4 antagonist.",576,1
+577,"Some 5-HT3 antagonists have 5-HT4 agonist activity (for example, renzapride, zacopride) and others do not (for example, ondansetron, granisetron), while << tropisetron >> in high concentrations is a [[ 5-HT4 ]] antagonist.",577,1
+578,"We present our studies to demonstrate that HM74A, but not HM74, binds << niacin >> at high affinities and effectively mediates [[ Gi ]] signaling events in human embryonic kidney HEK293 cells as well as in 3T3L1 adipocytes expressing HM74A.",578,6
+579,"When cultured in YPD medium containing 15% glucose under aerobic conditions, the << KGD1 >> (alpha-ketoglutarate dehydrogenase) gene disrupted mutant produced a lower level of [[ succinate ]] than the wild-type strain, while the SDH1 (succinate dehydrogenase) gene-disrupted mutant produced an increased level of succinate.",579,4
+580,"When cultured in YPD medium containing 15% glucose under aerobic conditions, the KGD1 (<< alpha-ketoglutarate dehydrogenase >>) gene disrupted mutant produced a lower level of [[ succinate ]] than the wild-type strain, while the SDH1 (succinate dehydrogenase) gene-disrupted mutant produced an increased level of succinate.",580,4
+581,"When cultured in YPD medium containing 15% glucose under aerobic conditions, the KGD1 (alpha-ketoglutarate dehydrogenase) gene disrupted mutant produced a lower level of succinate than the wild-type strain, while the << SDH1 >> (succinate dehydrogenase) gene-disrupted mutant produced an increased level of [[ succinate ]].",581,4
+582,"When cultured in YPD medium containing 15% glucose under aerobic conditions, the KGD1 (alpha-ketoglutarate dehydrogenase) gene disrupted mutant produced a lower level of succinate than the wild-type strain, while the SDH1 (<< succinate dehydrogenase >>) gene-disrupted mutant produced an increased level of [[ succinate ]].",582,4
+583,"On the other hand, the << FUM1 >> (fumarase) gene disrupted mutant produced significantly higher levels of [[ fumarate ]] but did not form malate at all.",583,4
+584,"On the other hand, the FUM1 (<< fumarase >>) gene disrupted mutant produced significantly higher levels of [[ fumarate ]] but did not form malate at all.",584,4
+585,"When the growth condition was shifted from aerobic to anaerobic, the increased level of << succinate >> in [[ SDH1 ]] disruptants was no longer observed, whereas the decreased level of succinate in the KGD1 diruptant was still observed.",585,4
+586,"When the growth condition was shifted from aerobic to anaerobic, the increased level of succinate in SDH1 disruptants was no longer observed, whereas the decreased level of << succinate >> in the [[ KGD1 ]] diruptant was still observed.",586,4
+587,A double mutant of the two << fumarate reductase >> isozyme genes (OSM1 and FRDS) showed a [[ succinate ]] productivity of 50% as compared to the parent when cells were incubated in glucose-buffered solution.,587,4
+588,A double mutant of the two fumarate reductase isozyme genes (<< OSM1 >> and FRDS) showed a [[ succinate ]] productivity of 50% as compared to the parent when cells were incubated in glucose-buffered solution.,588,4
+589,A double mutant of the two fumarate reductase isozyme genes (OSM1 and << FRDS >>) showed a [[ succinate ]] productivity of 50% as compared to the parent when cells were incubated in glucose-buffered solution.,589,4
+590,<< Vitamin E >> and probucol significantly suppressed an increase in plasma total-cholesterol (total-C) and [[ low-density lipoprotein ]] cholesterol compared to HC-control group.,590,8
+591,Vitamin E and << probucol >> significantly suppressed an increase in plasma total-cholesterol (total-C) and [[ low-density lipoprotein ]] cholesterol compared to HC-control group.,591,8
+592,"However, plasma high-density lipoprotein-cholesterol (HDL-C) and HDL-C/total-C ratio levels and plasma << paraoxonase >> activity were only significantly higher in [[ vitamin E ]] group after 8 weeks.",592,9
+593,"However, plasma << high-density lipoprotein >>-cholesterol (HDL-C) and HDL-C/total-C ratio levels and plasma paraoxonase activity were only significantly higher in [[ vitamin E ]] group after 8 weeks.",593,6
+594,"However, plasma high-density lipoprotein-cholesterol (<< HDL >>-C) and HDL-C/total-C ratio levels and plasma paraoxonase activity were only significantly higher in [[ vitamin E ]] group after 8 weeks.",594,6
+595,"However, plasma high-density lipoprotein-cholesterol (HDL-C) and << HDL >>-C/total-C ratio levels and plasma paraoxonase activity were only significantly higher in [[ vitamin E ]] group after 8 weeks.",595,6
+596,"Hepatic ACAT activity was significantly lower in both vitamin E and probucol groups than in HC-control group, while << HMG-CoA reductase >> activity was the highest only in the [[ probucol ]] group.",596,9
+597,"Hepatic << ACAT >> activity was significantly lower in both [[ vitamin E ]] and probucol groups than in HC-control group, while HMG-CoA reductase activity was the highest only in the probucol group.",597,0
+598,"Hepatic << ACAT >> activity was significantly lower in both vitamin E and [[ probucol ]] groups than in HC-control group, while HMG-CoA reductase activity was the highest only in the probucol group.",598,0
+599,Hepatic mRNA expressions of << apo B-100 >> and apo C-III were significantly lower in [[ probucol ]] group than in other groups.,599,8
+600,Hepatic mRNA expressions of apo B-100 and << apo C-III >> were significantly lower in [[ probucol ]] group than in other groups.,600,8
+601,"Vitamin E supplementation was found to alter the plasma HDL-C-related factors; meanwhile, << probucol >> supplementation was very effective in enhancing cholesterol metabolism, except for a negative effect that reduced plasma [[ HDL ]]-C concentration.",601,8
+602,"The aim of this study was to determine if macaque represents a suitable species for the pre-clinical evaluation of novel << CCR5 >> antagonists, such as [[ maraviroc ]] (UK-427,857).",602,1
+603,"The aim of this study was to determine if macaque represents a suitable species for the pre-clinical evaluation of novel << CCR5 >> antagonists, such as maraviroc ([[ UK-427,857 ]]).",603,1
+604,"<< Maraviroc >> inhibited binding of [125I]-MIP-1beta to CCR5 from macaque and human with similar potency (IC50 = 17.50 +/- 1.24 nM and 7.18 +/- 0.93 nM, respectively) and antagonised MIP-1beta induced intracellular calcium release mediated through [[ CCR5 ]] from macaque and human with similar potency (IC50 = 17.50 +/- 3.30 nM and 12.07 +/- 1.89, respectively).",604,1
+605,"However, as with the human receptor, << maraviroc >> was shown to be a high affinity, potent functional antagonist of [[ macaque CCR5 ]] thereby indicating that the macaque should be a suitable species in which to evaluate the pharmacology, safety and potential mechanism-related toxicology of novel CCR5 antagonists.",605,1
+606,"However, as with the human receptor, << maraviroc >> was shown to be a high affinity, potent functional antagonist of macaque CCR5 thereby indicating that the macaque should be a suitable species in which to evaluate the pharmacology, safety and potential mechanism-related toxicology of novel [[ CCR5 ]] antagonists.",606,1
+607,"Hence, re-expression of the p75NTR appears to partially reverse de-differentiation of prostate cancer cells by up-regulating the expression of << CRABPI >> for localized sequestration of [[ retinoids ]] that are available to newly up-regulated RAR-beta, RXR-alpha, and RXR-beta.",607,6
+608,"Its special profile of actions, especially the rise in << HDL >>-cholesterol levels induced by [[ nicotinic acid ]], is unique among the currently available pharmacological tools to treat lipid disorders.",608,6
+609,<< Valproic acid >> selectively inhibits conversion of arachidonic acid to arachidonoyl-CoA by [[ brain microsomal long-chain fatty acyl-CoA synthetases ]]: relevance to bipolar disorder.,609,0
+610,Valproic acid selectively inhibits conversion of arachidonic acid to << arachidonoyl-CoA >> by [[ brain microsomal long-chain fatty acyl-CoA synthetases ]]: relevance to bipolar disorder.,610,4
+611,Valproic acid selectively inhibits conversion of << arachidonic acid >> to arachidonoyl-CoA by [[ brain microsomal long-chain fatty acyl-CoA synthetases ]]: relevance to bipolar disorder.,611,5
+612,"RATIONALE: Several drugs used to treat bipolar disorder (<< lithium >> and carbamazepine), when administered chronically to rats, reduce the turnover of arachidonic acid, but not docosahexaenoic acid, in brain phospholipids by decreasing the activity of an arachidonic acid-selective [[ phospholipase A(2) ]].",612,0
+613,"RATIONALE: Several drugs used to treat bipolar disorder (lithium and << carbamazepine >>), when administered chronically to rats, reduce the turnover of arachidonic acid, but not docosahexaenoic acid, in brain phospholipids by decreasing the activity of an arachidonic acid-selective [[ phospholipase A(2) ]].",613,0
+614,"MATERIALS AND METHODS/RESULTS: By isolating rat brain microsomal long-chain fatty acyl-CoA synthetases (Acsl), we show in vitro that << valproic acid >> is a non-competitive inhibitor of [[ Acsl ]], as it reduces the maximal velocity of the reaction without changing the affinity of the substrate for the enzyme.",614,0
+615,"CONCLUSIONS: This study shows that << valproic acid >> acts as a non-competitive inhibitor of [[ brain microsomal Acsl ]], and that inhibition is substrate-selective.",615,0
+616,"On the other hand, holocarboxylase synthetase (<< HCS >>) mRNA levels were markedly low in the deficient animals, and increased upon [[ biotin ]] injection.",616,6
+617,"On the other hand, << holocarboxylase synthetase >> (HCS) mRNA levels were markedly low in the deficient animals, and increased upon [[ biotin ]] injection.",617,6
+618,Involvement of << COX-1 >> and up-regulated prostaglandin E synthases in phosphatidylserine liposome-induced [[ prostaglandin E2 ]] production by microglia.,618,4
+619,Involvement of COX-1 and up-regulated << prostaglandin E synthases >> in phosphatidylserine liposome-induced [[ prostaglandin E2 ]] production by microglia.,619,4
+620,"Furthermore, PS liposome-induced PGE2 production was significantly suppressed by << indomethacin >>, a preferential [[ COX-1 ]] inhibitor, but not by NS-398, a selective COX-2 inhibitor.",620,0
+621,"Furthermore, PS liposome-induced PGE2 production was significantly suppressed by indomethacin, a preferential COX-1 inhibitor, but not by << NS-398 >>, a selective [[ COX-2 ]] inhibitor.",621,0
+622,"These observations strongly suggest that the up-regulation of terminal << PGESs >> that are preferentially coupled with COX-1, especially mPGES-2, plays the pivotal role in PS liposome-induced [[ PGE2 ]] production by microglia.",622,4
+623,"These observations strongly suggest that the up-regulation of terminal PGESs that are preferentially coupled with << COX-1 >>, especially mPGES-2, plays the pivotal role in PS liposome-induced [[ PGE2 ]] production by microglia.",623,4
+624,"These observations strongly suggest that the up-regulation of terminal PGESs that are preferentially coupled with COX-1, especially << mPGES-2 >>, plays the pivotal role in PS liposome-induced [[ PGE2 ]] production by microglia.",624,4
+625,"Significant advances in the treatment of clear-cell RCC have been derived from agents that target these pathways, including the multiple-<< kinase >> inhibitors (MKIs) [[ sorafenib ]], sunitinib, and AG013736, which target multiple VEGFRs as well as PDGFR-beta.",625,0
+626,"Significant advances in the treatment of clear-cell RCC have been derived from agents that target these pathways, including the multiple-kinase inhibitors (MKIs) << sorafenib >>, sunitinib, and AG013736, which target multiple [[ VEGFRs ]] as well as PDGFR-beta.",626,0
+627,"Significant advances in the treatment of clear-cell RCC have been derived from agents that target these pathways, including the multiple-kinase inhibitors (MKIs) << sorafenib >>, sunitinib, and AG013736, which target multiple VEGFRs as well as [[ PDGFR-beta ]].",627,0
+628,"Significant advances in the treatment of clear-cell RCC have been derived from agents that target these pathways, including the multiple-<< kinase >> inhibitors (MKIs) sorafenib, [[ sunitinib ]], and AG013736, which target multiple VEGFRs as well as PDGFR-beta.",628,0
+629,"Significant advances in the treatment of clear-cell RCC have been derived from agents that target these pathways, including the multiple-kinase inhibitors (MKIs) sorafenib, << sunitinib >>, and AG013736, which target multiple [[ VEGFRs ]] as well as PDGFR-beta.",629,0
+630,"Significant advances in the treatment of clear-cell RCC have been derived from agents that target these pathways, including the multiple-kinase inhibitors (MKIs) sorafenib, << sunitinib >>, and AG013736, which target multiple VEGFRs as well as [[ PDGFR-beta ]].",630,0
+631,"Significant advances in the treatment of clear-cell RCC have been derived from agents that target these pathways, including the multiple-<< kinase >> inhibitors (MKIs) sorafenib, sunitinib, and [[ AG013736 ]], which target multiple VEGFRs as well as PDGFR-beta.",631,0
+632,"Significant advances in the treatment of clear-cell RCC have been derived from agents that target these pathways, including the multiple-kinase inhibitors (MKIs) sorafenib, sunitinib, and << AG013736 >>, which target multiple [[ VEGFRs ]] as well as PDGFR-beta.",632,0
+633,"Significant advances in the treatment of clear-cell RCC have been derived from agents that target these pathways, including the multiple-kinase inhibitors (MKIs) sorafenib, sunitinib, and << AG013736 >>, which target multiple VEGFRs as well as [[ PDGFR-beta ]].",633,0
+634,"<< Sorafenib >> has the added advantage of inhibiting multiple different [[ Raf ]] isoforms, which enables it to target TGF-alpha/EGFR signaling and may also enhance its inhibition of VEGFR and PDGFR-beta.",634,0
+635,"<< Sorafenib >> has the added advantage of inhibiting multiple different Raf isoforms, which enables it to target [[ TGF-alpha ]]/EGFR signaling and may also enhance its inhibition of VEGFR and PDGFR-beta.",635,0
+636,"<< Sorafenib >> has the added advantage of inhibiting multiple different Raf isoforms, which enables it to target TGF-alpha/[[ EGFR ]] signaling and may also enhance its inhibition of VEGFR and PDGFR-beta.",636,0
+637,"<< Sorafenib >> has the added advantage of inhibiting multiple different Raf isoforms, which enables it to target TGF-alpha/EGFR signaling and may also enhance its inhibition of [[ VEGFR ]] and PDGFR-beta.",637,0
+638,"<< Sorafenib >> has the added advantage of inhibiting multiple different Raf isoforms, which enables it to target TGF-alpha/EGFR signaling and may also enhance its inhibition of VEGFR and [[ PDGFR-beta ]].",638,0
+639,"Low << TS >> expression levels, cytoplasmic expression pattern and C SNP arose as variables associated to longer progression-free survival (PFS) in patients treated with [[ 5FU ]].",639,8
+640,"Therefore, in the present studies, animals were rendered tolerant to the << delta-opioid receptor >>-selective agonist [D-Pen2,D-Pen5]enkephalin ([[ DPDPE ]]), and receptor binding activities were measured.",640,2
+641,"Therefore, in the present studies, animals were rendered tolerant to the << delta-opioid receptor >>-selective agonist [[ [D-Pen2,D-Pen5]enkephalin ]] (DPDPE), and receptor binding activities were measured.",641,2
+642,Our conclusion is that chronic << DPDPE >> treatment preferentially reduces [[ delta-opioid receptor ]] binding activity.,642,0
+643,"Complementary experiments using the 5-HT3-dependent Bezold-Jarisch reflex confirmed that << amoxapine >> really acts in vivo as a [[ 5-HT3 ]] antagonist (IC50 = 50 micrograms/kg i.v.), whereas amitriptyline is essentially inactive on 5-HT3 receptors.",643,1
+644,"Competitive radioligand binding assays were performed using cells expressing either the << human serotonin (5-HT) transporter >> (hSERT) or norepinephrine (NE) transporter (hNET) with K(i) values for [[ DVS ]] of 40.2 +/- 1.6 and 558.4 +/- 121.6 nM, respectively.",644,0
+645,"Competitive radioligand binding assays were performed using cells expressing either the human serotonin (5-HT) transporter (<< hSERT >>) or norepinephrine (NE) transporter (hNET) with K(i) values for [[ DVS ]] of 40.2 +/- 1.6 and 558.4 +/- 121.6 nM, respectively.",645,0
+646,"Competitive radioligand binding assays were performed using cells expressing either the human serotonin (5-HT) transporter (hSERT) or << norepinephrine (NE) transporter >> (hNET) with K(i) values for [[ DVS ]] of 40.2 +/- 1.6 and 558.4 +/- 121.6 nM, respectively.",646,0
+647,"Competitive radioligand binding assays were performed using cells expressing either the human serotonin (5-HT) transporter (hSERT) or norepinephrine (NE) transporter (<< hNET >>) with K(i) values for [[ DVS ]] of 40.2 +/- 1.6 and 558.4 +/- 121.6 nM, respectively.",647,0
+648,"Inhibition of << [3H]5-HT >> or [3H]NE uptake by DVS for the [[ hSERT ]] or hNET produced IC50 values of 47.3 +/- 19.4 and 531.3 +/- 113.0 nM, respectively.",648,5
+649,"Inhibition of [3H]5-HT or << [3H]NE >> uptake by DVS for the hSERT or [[ hNET ]] produced IC50 values of 47.3 +/- 19.4 and 531.3 +/- 113.0 nM, respectively.",649,5
+650,"To mimic chronic selective serotonin reuptake inhibitor treatment and to block the inhibitory 5-HT(1A) autoreceptors, a << 5-HT(1A) >> antagonist, [[ N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-2-pyridinylcyclo hexanecarboxamide maleate salt ]] (WAY-100635) (0.3 mg/kg s.c.), was administered with DVS (30 mg/kg orally).",650,1
+651,"To mimic chronic selective serotonin reuptake inhibitor treatment and to block the inhibitory 5-HT(1A) autoreceptors, a << 5-HT(1A) >> antagonist, N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-2-pyridinylcyclo hexanecarboxamide maleate salt ([[ WAY-100635 ]]) (0.3 mg/kg s.c.), was administered with DVS (30 mg/kg orally).",651,1
+652,"The tissue RA level is maintained through a cascade of metabolic reactions where << retinal dehydrogenases >> (RALDHs) catalyze the terminal reaction of [[ RA ]] biosynthesis from retinal, a rate-limiting step.",652,4
+653,"The tissue RA level is maintained through a cascade of metabolic reactions where retinal dehydrogenases (<< RALDHs >>) catalyze the terminal reaction of [[ RA ]] biosynthesis from retinal, a rate-limiting step.",653,4
+654,"The tissue RA level is maintained through a cascade of metabolic reactions where << retinal dehydrogenases >> (RALDHs) catalyze the terminal reaction of RA biosynthesis from [[ retinal ]], a rate-limiting step.",654,5
+655,"The tissue RA level is maintained through a cascade of metabolic reactions where retinal dehydrogenases (<< RALDHs >>) catalyze the terminal reaction of RA biosynthesis from [[ retinal ]], a rate-limiting step.",655,5
+656,"Further, << cholesterol >> metabolites, predominantly the oxysterols, the natural ligands for liver X receptor (LXR), induced these genes via upregulation of [[ sterol regulatory element binding protein-1c ]] (SREBP-1c) that bound to the regulatory regions of these genes.",656,6
+657,"Further, << cholesterol >> metabolites, predominantly the oxysterols, the natural ligands for liver X receptor (LXR), induced these genes via upregulation of sterol regulatory element binding protein-1c ([[ SREBP-1c ]]) that bound to the regulatory regions of these genes.",657,6
+658,"Further, cholesterol metabolites, predominantly the << oxysterols >>, the natural ligands for liver X receptor (LXR), induced these genes via upregulation of [[ sterol regulatory element binding protein-1c ]] (SREBP-1c) that bound to the regulatory regions of these genes.",658,6
+659,"Further, cholesterol metabolites, predominantly the << oxysterols >>, the natural ligands for liver X receptor (LXR), induced these genes via upregulation of sterol regulatory element binding protein-1c ([[ SREBP-1c ]]) that bound to the regulatory regions of these genes.",659,6
+660,"Hypermethlyation of << RELN and GAD67 promoters >> can be induced by treating mice with [[ methionine ]], and these mice display brain and behavioral abnormalities similar to +/rl.",660,7
+661,Functional and bioenergetic consequences of << AT1 >> antagonist [[ olmesartan medoxomil ]] in hearts with postinfarction LV remodeling.,661,1
+662,"Thus, severe LV dysfunction and accompanying abnormal myocardial bioenergetic phenotype were prevented by the << AT1 >> antagonist [[ olmesartan medoxomil ]].",662,1
+663,"We evaluated << imatinib >>, a [[ tyrosine kinase ]] inhibitor currently used to treat chronic myelogenous leukemia and gastrointestinal stromal tumors, as a potential drug for systemic treatment of MTC, in 2 MTC-derived cell lines expressing multiple endocrine neoplasia-associated mutant RET receptors.",663,0
+664,RESULTS: << Imatinib >> inhibited [[ RET ]] Y1062 phosphorylation in a dose-dependent manner after 1.5 hours of exposure.,664,0
+665,RESULTS: << Imatinib >> inhibited RET [[ Y1062 ]] phosphorylation in a dose-dependent manner after 1.5 hours of exposure.,665,0
+666,CONCLUSIONS: << Imatinib >> inhibits RET-mediated MTC cell growth affecting [[ RET ]] protein levels in vitro in a dose-dependent manner.,666,8
+667,CONCLUSIONS: << Imatinib >> inhibits [[ RET ]]-mediated MTC cell growth affecting RET protein levels in vitro in a dose-dependent manner.,667,0
+668,"The concentration of << imatinib >> necessary to inhibit [[ RET ]] in vitro, however, makes it impossible to conclude that imatinib monotherapy will be a good option for systemic therapy of MTC.",668,0
+669,"In eukaryotes, the most prominent Mo-enzymes are (1) << sulfite oxidase >>, which catalyzes the final step in the degradation of [[ sulfur ]]-containing amino acids and is involved in detoxifying excess sulfite, (2) xanthine dehydrogenase, which is involved in purine catabolism and reactive oxygen production, (3) aldehyde oxidase, which oxidizes a variety of aldehydes and is essential for the biosynthesis of the phytohormone abscisic acid, and in autotrophic organisms also (4) nitrate reductase, which catalyzes the key step in inorganic nitrogen assimilation.",669,5
+670,"<< Retinoid >> is a collective term for compounds which bind to and activate retinoic acid receptors (RARalpha, beta, gamma and RXRalpha, beta, gamma), members of [[ nuclear hormone receptor ]] superfamily.",670,9
+671,"<< Retinoid >> is a collective term for compounds which bind to and activate [[ retinoic acid receptors ]] (RARalpha, beta, gamma and RXRalpha, beta, gamma), members of nuclear hormone receptor superfamily.",671,9
+672,"The cholesterol-lowering drug << simvastatin >> inhibits [[ LFA-1 ]] signaling by binding to an allosteric site on CD11a (LFA-1 alpha chain), which leads to immunomodulation.",672,8
+673,<< Simvastatin >> abolished these anti-[[ CD11a ]] mAb-induced increases in lymphocytic cholinergic activity in a manner independent of its cholesterol-lowering activity.,673,8
+674,"<< Menthol >>, popularly known for its cooling effect, activates [[ TRPM8 ]]--a cold-activated thermoTRP ion channel.",674,9
+675,"<< Menthol >>, popularly known for its cooling effect, activates TRPM8--a cold-activated [[ thermoTRP ion channel ]].",675,9
+676,"However, human physiological studies demonstrate a paradoxical role of menthol in modulation of warm sensation, and here, we show that << menthol >> also activates heat-activated [[ TRPV3 ]].",676,9
+677,"We further show that << menthol >> inhibits [[ TRPA1 ]], potentially explaining the use of menthol as an analgesic.",677,0
+678,"Similar to << menthol >>, both camphor and cinnamaldehyde (initially reported to be specific activators of [[ TRPV3 ]] and TRPA1, respectively) also modulate other thermoTRPs.",678,9
+679,"Similar to << menthol >>, both camphor and cinnamaldehyde (initially reported to be specific activators of TRPV3 and [[ TRPA1 ]], respectively) also modulate other thermoTRPs.",679,9
+680,"Similar to menthol, both << camphor >> and cinnamaldehyde (initially reported to be specific activators of [[ TRPV3 ]] and TRPA1, respectively) also modulate other thermoTRPs.",680,9
+681,"Similar to menthol, both << camphor >> and cinnamaldehyde (initially reported to be specific activators of TRPV3 and [[ TRPA1 ]], respectively) also modulate other thermoTRPs.",681,9
+682,"Similar to menthol, both camphor and << cinnamaldehyde >> (initially reported to be specific activators of [[ TRPV3 ]] and TRPA1, respectively) also modulate other thermoTRPs.",682,9
+683,"Similar to menthol, both camphor and << cinnamaldehyde >> (initially reported to be specific activators of TRPV3 and [[ TRPA1 ]], respectively) also modulate other thermoTRPs.",683,9
+684,The glutamate-aspartate transporter << GLAST >> mediates [[ glutamate ]] uptake at inner hair cell afferent synapses in the mammalian cochlea.,684,5
+685,The << glutamate-aspartate transporter >> GLAST mediates [[ glutamate ]] uptake at inner hair cell afferent synapses in the mammalian cochlea.,685,5
+686,"Focal application of the transporter substrate D-aspartate elicited inward currents in IPCs, which were larger in the presence of anions that permeate the transporter-associated << anion channel >> and blocked by the transporter antagonist [[ D,L-threo-beta-benzyloxyaspartate ]].",686,1
+687,"These currents were produced by << glutamate-aspartate transporters >> (GLAST) (excitatory amino acid transporter 1) because they were weakly inhibited by [[ dihydrokainate ]], an antagonist of glutamate transporter-1 (excitatory amino acid transporter 2) and were absent from IPCs in GLAST-/- cochleas.",687,0
+688,"These currents were produced by glutamate-aspartate transporters (<< GLAST >>) (excitatory amino acid transporter 1) because they were weakly inhibited by [[ dihydrokainate ]], an antagonist of glutamate transporter-1 (excitatory amino acid transporter 2) and were absent from IPCs in GLAST-/- cochleas.",688,0
+689,"These currents were produced by glutamate-aspartate transporters (GLAST) (<< excitatory amino acid transporter 1 >>) because they were weakly inhibited by [[ dihydrokainate ]], an antagonist of glutamate transporter-1 (excitatory amino acid transporter 2) and were absent from IPCs in GLAST-/- cochleas.",689,0
+690,"These currents were produced by glutamate-aspartate transporters (GLAST) (excitatory amino acid transporter 1) because they were weakly inhibited by << dihydrokainate >>, an antagonist of [[ glutamate transporter-1 ]] (excitatory amino acid transporter 2) and were absent from IPCs in GLAST-/- cochleas.",690,1
+691,"These currents were produced by glutamate-aspartate transporters (GLAST) (excitatory amino acid transporter 1) because they were weakly inhibited by << dihydrokainate >>, an antagonist of glutamate transporter-1 ([[ excitatory amino acid transporter 2 ]]) and were absent from IPCs in GLAST-/- cochleas.",691,1
+692,"Furthermore, D-aspartate-induced currents in outside-out patches from IPCs exhibited larger steady-state currents than responses elicited by << L-glutamate >>, a prominent feature of [[ GLAST ]], and examination of cochlea from GLAST-Discosoma red (DsRed) promoter reporter mice revealed that DsRed expression was restricted to IPCs and other supporting cells surrounding IHCs.",692,5
+693,Overexpression of << proline oxidase >> induces [[ proline ]]-dependent and mitochondria-mediated apoptosis.,693,5
+694,"<< Proline oxidase >> (POX), a mitochondrial inner-membrane protein, catalyzes the rate-limiting oxidation of proline to [[ pyrroline- 5-carboxylate ]] (P5C).",694,4
+695,"Proline oxidase (<< POX >>), a mitochondrial inner-membrane protein, catalyzes the rate-limiting oxidation of proline to [[ pyrroline- 5-carboxylate ]] (P5C).",695,4
+696,"<< Proline oxidase >> (POX), a mitochondrial inner-membrane protein, catalyzes the rate-limiting oxidation of proline to pyrroline- 5-carboxylate ([[ P5C ]]).",696,4
+697,"Proline oxidase (<< POX >>), a mitochondrial inner-membrane protein, catalyzes the rate-limiting oxidation of proline to pyrroline- 5-carboxylate ([[ P5C ]]).",697,4
+698,"<< Proline oxidase >> (POX), a mitochondrial inner-membrane protein, catalyzes the rate-limiting oxidation of [[ proline ]] to pyrroline- 5-carboxylate (P5C).",698,5
+699,"Proline oxidase (<< POX >>), a mitochondrial inner-membrane protein, catalyzes the rate-limiting oxidation of [[ proline ]] to pyrroline- 5-carboxylate (P5C).",699,5
+700,"To further investigate the molecular basis of POX-induced apoptosis, we utilized the DLD-1.POX cells to show that cells overproducing << POX >> exhibit an [[ L-proline ]]-dependent apoptotic response.",700,5
+701,"The apoptotic effect is specific for L-proline, detectable at 0.2 mM, maximal at 1 mM, and occurs during 48-72 h following the addition of << L-proline >> to cells with maximally induced [[ POX ]].",701,5
+702,"We conclude that in the presence of << proline >>, high [[ POX ]] activity is sufficient to induce mitochondria-mediated apoptosis.",702,5
+703,"The exception was << bupropion >>, a dual [[ norepinephrine transporter ]]/dopamine transporter blocker, which tended to increase spontaneous locomotor activity.",703,0
+704,"The exception was << bupropion >>, a dual norepinephrine transporter/[[ dopamine transporter ]] blocker, which tended to increase spontaneous locomotor activity.",704,0
+705,Coadministration of reboxetine and the << dopamine transporter >> blocker [[ GBR 12909 ]] also increased spontaneous locomotor activity.,705,0
+706,"<< Tamoxifen >> blocks the action of estrogen by binding to the ER, and possesses both [[ ER ]]-agonist and antagonist properties.",706,2
+707,"<< Tamoxifen >> blocks the action of estrogen by binding to the ER, and possesses both [[ ER ]]-agonist and antagonist properties.",707,1
+708,<< Fulvestrant >> is a novel ER antagonist that destroys the [[ ER ]] and its signaling pathway and is not associated with tamoxifen-like agonist effects.,708,0
+709,<< Fulvestrant >> is a novel [[ ER ]] antagonist that destroys the ER and its signaling pathway and is not associated with tamoxifen-like agonist effects.,709,1
+710,"<< Phosphodiesterase-5 >> (PDE5) contains a catalytic domain (C domain) that hydrolyzes [[ cGMP ]] and a regulatory domain (R domain) that contains two mammalian cGMP-binding phosphodiesterase, Anabaena adenylyl cyclases, Escherichia coli FhlAs (GAFs) (A and B) and a phosphorylation site for cyclic nucleotide-dependent protein kinases (cNPKs).",710,5
+711,"Phosphodiesterase-5 (<< PDE5 >>) contains a catalytic domain (C domain) that hydrolyzes [[ cGMP ]] and a regulatory domain (R domain) that contains two mammalian cGMP-binding phosphodiesterase, Anabaena adenylyl cyclases, Escherichia coli FhlAs (GAFs) (A and B) and a phosphorylation site for cyclic nucleotide-dependent protein kinases (cNPKs).",711,5
+712,Binding of << cGMP >> to GAF-A increases [[ cNPK ]] phosphorylation of PDE5 and improves catalytic site affinity for cGMP or inhibitors.,712,6
+713,Binding of << cGMP >> to GAF-A increases cNPK phosphorylation of [[ PDE5 ]] and improves catalytic site affinity for cGMP or inhibitors.,713,6
+714,K(m) values of the mutants for << cGMP >> were similar to that of full-length [[ PDE5 ]].,714,5
+715,<< Telmisartan >> downregulates angiotensin II type 1 receptor through activation of [[ peroxisome proliferator-activated receptor gamma ]].,715,9
+716,<< Telmisartan >> downregulates [[ angiotensin II type 1 receptor ]] through activation of peroxisome proliferator-activated receptor gamma.,716,3
+717,"OBJECTIVE: << Telmisartan >>, an angiotensin II type 1 receptor (AT1R) antagonist, was found to have a unique property: it is a partial agonist of [[ peroxisome proliferator-activated receptor gamma ]] (PPARgamma).",717,2
+718,"OBJECTIVE: << Telmisartan >>, an angiotensin II type 1 receptor (AT1R) antagonist, was found to have a unique property: it is a partial agonist of peroxisome proliferator-activated receptor gamma ([[ PPARgamma ]]).",718,2
+719,"OBJECTIVE: << Telmisartan >>, an [[ angiotensin II type 1 receptor ]] (AT1R) antagonist, was found to have a unique property: it is a partial agonist of peroxisome proliferator-activated receptor gamma (PPARgamma).",719,1
+720,"OBJECTIVE: << Telmisartan >>, an angiotensin II type 1 receptor ([[ AT1R ]]) antagonist, was found to have a unique property: it is a partial agonist of peroxisome proliferator-activated receptor gamma (PPARgamma).",720,1
+721,RESULTS: << Telmisartan >> decreased the expression of [[ AT1R ]] at the mRNA and protein levels in a dose- and time-dependent manner.,721,8
+722,Decreased AT1R promoter activity with unchanged mRNA stability suggested that << telmisartan >> suppressed [[ AT1R ]] gene expression at the transcriptional level.,722,8
+723,"However, the expression of AT1R was not suppressed by other << AT1R >> antagonists such as [[ candesartan ]] or olmesartan.",723,1
+724,"However, the expression of AT1R was not suppressed by other << AT1R >> antagonists such as candesartan or [[ olmesartan ]].",724,1
+725,"Since the suppression of << AT1R >> expression was prevented by pretreatment with [[ GW9662 ]], a PPARgamma antagonist, PPARgamma should have participated in the process.",725,6
+726,"Since the suppression of AT1R expression was prevented by pretreatment with << GW9662 >>, a [[ PPARgamma ]] antagonist, PPARgamma should have participated in the process.",726,1
+727,The deletion and mutation analysis of the << AT1R >> gene promoter indicated that a GC box located in the proximal promoter region is responsible for the [[ telmisartan ]]-induced downregulation.,727,8
+728,The deletion and mutation analysis of the AT1R gene promoter indicated that a << GC box >> located in the proximal promoter region is responsible for the [[ telmisartan ]]-induced downregulation.,728,8
+729,CONCLUSION: Our data provides a novel insight into an effect of telmisartan: << telmisartan >> inhibits AT1R gene expression through [[ PPARgamma ]] activation.,729,9
+730,CONCLUSION: Our data provides a novel insight into an effect of telmisartan: << telmisartan >> inhibits [[ AT1R ]] gene expression through PPARgamma activation.,730,8
+731,"Upon differentiation, osteoclasts express << vesicular glutamate transporter 1 >> (VGLUT1), which is essential for vesicular storage and subsequent exocytosis of [[ glutamate ]] in neurons.",731,5
+732,"Upon differentiation, osteoclasts express vesicular glutamate transporter 1 (<< VGLUT1 >>), which is essential for vesicular storage and subsequent exocytosis of [[ glutamate ]] in neurons.",732,5
+733,<< VGLUT1 >> is localized in transcytotic vesicles and accumulates [[ L-glutamate ]].,733,5
+734,"Synthesis, << dihydrofolate reductase >> inhibition, antitumor testing, and molecular modeling study of some new [[ 4(3H)-quinazolinone ]] analogs.",734,0
+735,"In order to produce potent new leads for anticancer drugs, a new series of quinazoline analogs was designed to resemble << methotrexate >> (MTX, 1) structure features and fitted with functional groups believed to enhance inhibition of [[ mammalian DHFR ]] activity.",735,0
+736,"In order to produce potent new leads for anticancer drugs, a new series of quinazoline analogs was designed to resemble methotrexate (<< MTX >>, 1) structure features and fitted with functional groups believed to enhance inhibition of [[ mammalian DHFR ]] activity.",736,0
+737,"In order to produce potent new leads for anticancer drugs, a new series of << quinazoline >> analogs was designed to resemble methotrexate (MTX, 1) structure features and fitted with functional groups believed to enhance inhibition of [[ mammalian DHFR ]] activity.",737,0
+738,"A significant positive correlation was found between dietary intake of total SFAs and total MUFAs and expression of PBMC D6D and D5D genes, but a significant negative correlation between dietary intake of << linoleic acid >> (LA) and alpha-linolenic acid (LNA) and the expression of PBMC [[ D6D ]] and D5D genes.",738,8
+739,"A significant positive correlation was found between dietary intake of total SFAs and total MUFAs and expression of PBMC D6D and D5D genes, but a significant negative correlation between dietary intake of << linoleic acid >> (LA) and alpha-linolenic acid (LNA) and the expression of PBMC D6D and [[ D5D ]] genes.",739,8
+740,"A significant positive correlation was found between dietary intake of total SFAs and total MUFAs and expression of PBMC D6D and D5D genes, but a significant negative correlation between dietary intake of linoleic acid (<< LA >>) and alpha-linolenic acid (LNA) and the expression of PBMC [[ D6D ]] and D5D genes.",740,8
+741,"A significant positive correlation was found between dietary intake of total SFAs and total MUFAs and expression of PBMC D6D and D5D genes, but a significant negative correlation between dietary intake of linoleic acid (<< LA >>) and alpha-linolenic acid (LNA) and the expression of PBMC D6D and [[ D5D ]] genes.",741,8
+742,"A significant positive correlation was found between dietary intake of total SFAs and total MUFAs and expression of PBMC D6D and D5D genes, but a significant negative correlation between dietary intake of linoleic acid (LA) and << alpha-linolenic acid >> (LNA) and the expression of PBMC [[ D6D ]] and D5D genes.",742,8
+743,"A significant positive correlation was found between dietary intake of total SFAs and total MUFAs and expression of PBMC D6D and D5D genes, but a significant negative correlation between dietary intake of linoleic acid (LA) and << alpha-linolenic acid >> (LNA) and the expression of PBMC D6D and [[ D5D ]] genes.",743,8
+744,"A significant positive correlation was found between dietary intake of total SFAs and total MUFAs and expression of PBMC D6D and D5D genes, but a significant negative correlation between dietary intake of linoleic acid (LA) and alpha-linolenic acid (<< LNA >>) and the expression of PBMC [[ D6D ]] and D5D genes.",744,8
+745,"A significant positive correlation was found between dietary intake of total SFAs and total MUFAs and expression of PBMC D6D and D5D genes, but a significant negative correlation between dietary intake of linoleic acid (LA) and alpha-linolenic acid (<< LNA >>) and the expression of PBMC D6D and [[ D5D ]] genes.",745,8
+746,"CONCLUSION: Intake of high << SFAs >> and MUFAs appears to increase expression of PBMC [[ D6D ]] and D5D genes, whilst high EFAs intake appears to decrease expression of PBMC D6D and D5D genes.",746,6
+747,"CONCLUSION: Intake of high << SFAs >> and MUFAs appears to increase expression of PBMC D6D and [[ D5D ]] genes, whilst high EFAs intake appears to decrease expression of PBMC D6D and D5D genes.",747,6
+748,"CONCLUSION: Intake of high SFAs and << MUFAs >> appears to increase expression of PBMC [[ D6D ]] and D5D genes, whilst high EFAs intake appears to decrease expression of PBMC D6D and D5D genes.",748,6
+749,"CONCLUSION: Intake of high SFAs and << MUFAs >> appears to increase expression of PBMC D6D and [[ D5D ]] genes, whilst high EFAs intake appears to decrease expression of PBMC D6D and D5D genes.",749,6
+750,"CONCLUSION: Intake of high SFAs and MUFAs appears to increase expression of PBMC D6D and D5D genes, whilst high << EFAs >> intake appears to decrease expression of PBMC [[ D6D ]] and D5D genes.",750,8
+751,"CONCLUSION: Intake of high SFAs and MUFAs appears to increase expression of PBMC D6D and D5D genes, whilst high << EFAs >> intake appears to decrease expression of PBMC D6D and [[ D5D ]] genes.",751,8
+752,<< Decitabine >> inhibits [[ DNA methyltransferase ]] and has shown therapeutic effects in patients with hematologic malignancies.,752,0
+753,"Our data suggest that << l-arginine >> is taken up by Sertoli cells and peritubular cells, principally via system y(+)L ([[ SLC3A2 ]]/SLC7A6) and system y(+) (SLC7A1 and SLC7A2), with system B(0+) making a minor contribution.",753,5
+754,KIEs were measured on the arsenolysis of << 5'-methylthioadenosine >> (MTA) catalyzed by [[ MTAP ]] and were corrected for the forward commitment to catalysis.,754,5
+755,KIEs were measured on the arsenolysis of 5'-methylthioadenosine (<< MTA >>) catalyzed by [[ MTAP ]] and were corrected for the forward commitment to catalysis.,755,5
+756,"During embryogenesis, lratb is expressed in mostly non-overlapping domains opposite to << retinal dehydrogenase 2 >> (raldh2), the key enzyme for [[ retinoic acid ]] synthesis.",756,4
+757,"During embryogenesis, lratb is expressed in mostly non-overlapping domains opposite to retinal dehydrogenase 2 (<< raldh2 >>), the key enzyme for [[ retinoic acid ]] synthesis.",757,4
+758,"Blocking << retinyl ester >> formation by a targeted knock down of [[ Lratb ]] results in significantly increased retinoic acid levels, which lead to severe embryonic patterning defects.",758,4
+759,"<< ADP >> initiates platelet aggregation by 'simultaneous activation of two [[ G protein-coupled receptors ]], P2Y1 and P2Y12.",759,9
+760,"<< ADP >> initiates platelet aggregation by 'simultaneous activation of two G protein-coupled receptors, [[ P2Y1 ]] and P2Y12.",760,9
+761,"<< ADP >> initiates platelet aggregation by 'simultaneous activation of two G protein-coupled receptors, P2Y1 and [[ P2Y12 ]].",761,9
+762,"Our results imply that << P2Y12 >> has the potential to be inhibited by [[ ADP ]]/ATP analogs, and it suggests that P2Y12 acts as a target of new drugs that inhibit platelet aggregation.",762,0
+763,"Our results imply that << P2Y12 >> has the potential to be inhibited by ADP/[[ ATP ]] analogs, and it suggests that P2Y12 acts as a target of new drugs that inhibit platelet aggregation.",763,0
+764,"<< Cd >> decreased [[ ERalpha ]] expression, but not ERbeta.",764,8
+765,"<< Cd >> also increased ERK1/2, [[ Akt ]] and PDGFRalpha phosphorylation while ICI blocked it.",765,9
+766,"<< Cd >> also increased ERK1/2, Akt and [[ PDGFRalpha ]] phosphorylation while ICI blocked it.",766,9
+767,"<< Cd >> rapidly increased [[ c-jun ]], c-fos and PDGFA expression.",767,6
+768,"<< Cd >> rapidly increased c-jun, [[ c-fos ]] and PDGFA expression.",768,6
+769,"<< Cd >> rapidly increased c-jun, c-fos and [[ PDGFA ]] expression.",769,6
+770,"In conclusion, our results indicate that << Cd >> increases BC cell proliferation in vitro by stimulating [[ Akt ]], ERK1/2 and PDGFRalpha kinases activity likely by activating c-fos, c-jun and PDGFA by an ERalpha-dependent mechanism.",770,9
+771,"In conclusion, our results indicate that << Cd >> increases BC cell proliferation in vitro by stimulating Akt, ERK1/2 and [[ PDGFRalpha ]] kinases activity likely by activating c-fos, c-jun and PDGFA by an ERalpha-dependent mechanism.",771,9
+772,"In conclusion, our results indicate that << Cd >> increases BC cell proliferation in vitro by stimulating Akt, ERK1/2 and PDGFRalpha [[ kinases ]] activity likely by activating c-fos, c-jun and PDGFA by an ERalpha-dependent mechanism.",772,9
+773,"In conclusion, our results indicate that << Cd >> increases BC cell proliferation in vitro by stimulating Akt, ERK1/2 and PDGFRalpha kinases activity likely by activating [[ c-fos ]], c-jun and PDGFA by an ERalpha-dependent mechanism.",773,9
+774,"In conclusion, our results indicate that << Cd >> increases BC cell proliferation in vitro by stimulating Akt, ERK1/2 and PDGFRalpha kinases activity likely by activating c-fos, [[ c-jun ]] and PDGFA by an ERalpha-dependent mechanism.",774,9
+775,"In conclusion, our results indicate that << Cd >> increases BC cell proliferation in vitro by stimulating Akt, ERK1/2 and PDGFRalpha kinases activity likely by activating c-fos, c-jun and [[ PDGFA ]] by an ERalpha-dependent mechanism.",775,9
+776,Gonadotropin-releasing hormone functionally antagonizes << testosterone >> activation of the [[ human androgen receptor ]] in prostate cells through focal adhesion complexes involving Hic-5.,776,9
+777,<< Gonadotropin-releasing hormone >> functionally antagonizes testosterone activation of the [[ human androgen receptor ]] in prostate cells through focal adhesion complexes involving Hic-5.,777,1
+778,<< GnRH >>-induced [[ Pyk2 ]] activation opposed the association of Hic-5 with androgen receptor as overexpression of a dominant negative Pyk2 enhanced the GnRH-induced nuclear translocation of a green fluorescent protein-tagged human androgen receptor.,778,9
+779,<< GnRH >>-induced Pyk2 activation opposed the association of [[ Hic-5 ]] with androgen receptor as overexpression of a dominant negative Pyk2 enhanced the GnRH-induced nuclear translocation of a green fluorescent protein-tagged human androgen receptor.,779,3
+780,<< GnRH >>-induced Pyk2 activation opposed the association of Hic-5 with [[ androgen receptor ]] as overexpression of a dominant negative Pyk2 enhanced the GnRH-induced nuclear translocation of a green fluorescent protein-tagged human androgen receptor.,780,3
+781,<< GnRH >>-induced [[ c-Src ]] activation resulted in the phosphorylation of expressed Hic-5 and promoted its association with the human androgen receptor.,781,9
+782,"In contrast to << testosterone >>, GnRH-induced nuclear translocation did not transcriptionally activate the [[ androgen receptor ]].",782,9
+783,The discovery that << METH >> and AMPH activate the [[ rTAAR1 ]] motivated us to study the effect of these drugs on the mouse TAAR1 (mTAAR1) and a human-rat chimera (hrChTAAR1).,783,9
+784,The discovery that METH and << AMPH >> activate the [[ rTAAR1 ]] motivated us to study the effect of these drugs on the mouse TAAR1 (mTAAR1) and a human-rat chimera (hrChTAAR1).,784,9
+785,"Furthermore, because S-(+)-isomers of << METH >> and AMPH are reported to be more potent and efficacious in vivo than R-(-), we determined the enantiomeric selectivity of all three species of [[ TAAR1 ]].",785,9
+786,"Furthermore, because S-(+)-isomers of METH and << AMPH >> are reported to be more potent and efficacious in vivo than R-(-), we determined the enantiomeric selectivity of all three species of [[ TAAR1 ]].",786,9
+787,"EC50 values for << S-(+)-METH >> were 0.89, 0.92, and 4.44 microM for [[ rTAAR1 ]], mTAAR1, and h-rChTAAR1, respectively.",787,9
+788,"EC50 values for << S-(+)-METH >> were 0.89, 0.92, and 4.44 microM for rTAAR1, [[ mTAAR1 ]], and h-rChTAAR1, respectively.",788,9
+789,"EC50 values for << S-(+)-METH >> were 0.89, 0.92, and 4.44 microM for rTAAR1, mTAAR1, and [[ h-rChTAAR1 ]], respectively.",789,9
+790,"<< PEA >> was a potent and full agonist at each species of [[ TAAR1 ]], whereas TYR was a full agonist for the rodent TAAR1s but was a partial agonist at h-rChTAAR1.",790,10
+791,"PEA was a potent and full agonist at each species of TAAR1, whereas << TYR >> was a full agonist for the [[ rodent TAAR1s ]] but was a partial agonist at h-rChTAAR1.",791,10
+792,"PEA was a potent and full agonist at each species of TAAR1, whereas << TYR >> was a full agonist for the rodent TAAR1s but was a partial agonist at [[ h-rChTAAR1 ]].",792,2
+793,"Interestingly, both isomers of << METH >> were full agonists at [[ mTAAR1 ]] and h-rChTAAR1, whereas both were partial agonists at rTAAR1.",793,10
+794,"Interestingly, both isomers of << METH >> were full agonists at mTAAR1 and [[ h-rChTAAR1 ]], whereas both were partial agonists at rTAAR1.",794,10
+795,"Interestingly, both isomers of << METH >> were full agonists at mTAAR1 and h-rChTAAR1, whereas both were partial agonists at [[ rTAAR1 ]].",795,2
+796,"Finally, we showed that << chlorate >> activated endocrine cell development by inducing [[ neurogenin 3 ]] (Neurog3) expression in early endocrine progenitor cells.",796,6
+797,"Finally, we showed that << chlorate >> activated endocrine cell development by inducing neurogenin 3 ([[ Neurog3 ]]) expression in early endocrine progenitor cells.",797,6
+798,"DNA cloning, characterization, and inhibition studies of the << human secretory isoform VI >>, a new target for [[ sulfonamide ]] and sulfamate inhibitors.",798,0
+799,"DNA cloning, characterization, and inhibition studies of the << human secretory isoform VI >>, a new target for sulfonamide and [[ sulfamate ]] inhibitors.",799,0
+800,"The kinetic parameters for the << CO2 >> hydration reaction proved [[ hCA VI ]] to possess a kcat of 3.4 x 10(5) s-1 and kcat/KM of 4.9 x 10(7) M-1 s-1 (at pH 7.5 and 20 degrees C). hCA VI has a significant catalytic activity for the physiological reaction on the same order of magnitude as the ubiquitous isoform CA I or the transmembrane, tumor-associated isozyme CA IX.",800,12
+801,"Some clinically used compounds, such as acetazolamide, methazolamide, ethoxzolamide, << dichlorophenamide >>, dorzolamide, brinzolamide, topiramate, sulpiride, and indisulam, or the orphan drug benzolamide, showed effective [[ hCA VI ]] inhibitory activity, with inhibition constants of 0.8-79 nM.",801,0
+802,"Some clinically used compounds, such as << acetazolamide >>, methazolamide, ethoxzolamide, dichlorophenamide, dorzolamide, brinzolamide, topiramate, sulpiride, and indisulam, or the orphan drug benzolamide, showed effective [[ hCA VI ]] inhibitory activity, with inhibition constants of 0.8-79 nM.",802,0
+803,"Some clinically used compounds, such as acetazolamide, << methazolamide >>, ethoxzolamide, dichlorophenamide, dorzolamide, brinzolamide, topiramate, sulpiride, and indisulam, or the orphan drug benzolamide, showed effective [[ hCA VI ]] inhibitory activity, with inhibition constants of 0.8-79 nM.",803,0
+804,"Some clinically used compounds, such as acetazolamide, methazolamide, << ethoxzolamide >>, dichlorophenamide, dorzolamide, brinzolamide, topiramate, sulpiride, and indisulam, or the orphan drug benzolamide, showed effective [[ hCA VI ]] inhibitory activity, with inhibition constants of 0.8-79 nM.",804,0
+805,"Some clinically used compounds, such as acetazolamide, methazolamide, ethoxzolamide, dichlorophenamide, << dorzolamide >>, brinzolamide, topiramate, sulpiride, and indisulam, or the orphan drug benzolamide, showed effective [[ hCA VI ]] inhibitory activity, with inhibition constants of 0.8-79 nM.",805,0
+806,"Some clinically used compounds, such as acetazolamide, methazolamide, ethoxzolamide, dichlorophenamide, dorzolamide, << brinzolamide >>, topiramate, sulpiride, and indisulam, or the orphan drug benzolamide, showed effective [[ hCA VI ]] inhibitory activity, with inhibition constants of 0.8-79 nM.",806,0
+807,"Some clinically used compounds, such as acetazolamide, methazolamide, ethoxzolamide, dichlorophenamide, dorzolamide, brinzolamide, << topiramate >>, sulpiride, and indisulam, or the orphan drug benzolamide, showed effective [[ hCA VI ]] inhibitory activity, with inhibition constants of 0.8-79 nM.",807,0
+808,"Some clinically used compounds, such as acetazolamide, methazolamide, ethoxzolamide, dichlorophenamide, dorzolamide, brinzolamide, topiramate, << sulpiride >>, and indisulam, or the orphan drug benzolamide, showed effective [[ hCA VI ]] inhibitory activity, with inhibition constants of 0.8-79 nM.",808,0
+809,"Some clinically used compounds, such as acetazolamide, methazolamide, ethoxzolamide, dichlorophenamide, dorzolamide, brinzolamide, topiramate, sulpiride, and << indisulam >>, or the orphan drug benzolamide, showed effective [[ hCA VI ]] inhibitory activity, with inhibition constants of 0.8-79 nM.",809,0
+810,"Some clinically used compounds, such as acetazolamide, methazolamide, ethoxzolamide, dichlorophenamide, dorzolamide, brinzolamide, topiramate, sulpiride, and indisulam, or the orphan drug << benzolamide >>, showed effective [[ hCA VI ]] inhibitory activity, with inhibition constants of 0.8-79 nM.",810,0
+811,"The best inhibitors were << brinzolamide >> and sulpiride (KI values of 0.8-0.9 nM), the latter compound being also a [[ CA VI ]]-selective inhibitor.",811,0
+812,"The best inhibitors were brinzolamide and << sulpiride >> (KI values of 0.8-0.9 nM), the latter compound being also a [[ CA VI ]]-selective inhibitor.",812,0
+813,The metallic taste reported as a side effect after the treatment with systemic << sulfonamides >> may be due to the inhibition of the [[ salivary CA VI ]].,813,0
+814,"Some of the compounds investigated in this study might be used as additives in toothpastes for reducing the acidification produced by the relevant << CO2 >> hydrase activity of enamel [[ CA VI ]], which leads to the formation of protons and bicarbonate and may have a role in cariogenesis.",814,12
+815,"Some of the compounds investigated in this study might be used as additives in toothpastes for reducing the acidification produced by the relevant CO2 hydrase activity of enamel << CA VI >>, which leads to the formation of protons and [[ bicarbonate ]] and may have a role in cariogenesis.",815,12
+816,Transmembrane isoforms of << adenylate cyclases >> (AC) integrate a wide variety of extracellular signals from neurotransmitters to morphogens and can also regulate [[ cAMP ]] production in response to calcium entry.,816,4
+817,Transmembrane isoforms of adenylate cyclases (<< AC >>) integrate a wide variety of extracellular signals from neurotransmitters to morphogens and can also regulate [[ cAMP ]] production in response to calcium entry.,817,4
+818,<< Pirfenidone >> inhibits [[ TGF-beta ]] expression in malignant glioma cells.,818,8
+819,"Here, we report that the antifibrotic drug << 5-methyl-1-phenyl-2-(1H)-pyridone >> (pirfenidone, PFD) elicits growth-inhibitory effects and reduces [[ TGF-beta2 ]] protein levels in human glioma cell lines.",819,8
+820,"Here, we report that the antifibrotic drug 5-methyl-1-phenyl-2-(1H)-pyridone (<< pirfenidone >>, PFD) elicits growth-inhibitory effects and reduces [[ TGF-beta2 ]] protein levels in human glioma cell lines.",820,8
+821,"Here, we report that the antifibrotic drug 5-methyl-1-phenyl-2-(1H)-pyridone (pirfenidone, << PFD >>) elicits growth-inhibitory effects and reduces [[ TGF-beta2 ]] protein levels in human glioma cell lines.",821,8
+822,This reduction in << TGF-beta2 >> is biologically relevant since [[ PFD ]] treatment reduces the growth inhibition of TGF-beta-sensitive CCL-64 cells mediated by conditioned media of glioma cells.,822,8
+823,This reduction in TGF-beta2 is biologically relevant since << PFD >> treatment reduces the growth inhibition of [[ TGF-beta ]]-sensitive CCL-64 cells mediated by conditioned media of glioma cells.,823,8
+824,<< PFD >> leads to a reduction of [[ TGF-beta2 ]] mRNA levels and of the mature TGF-beta2 protein due to decreased expression and direct inhibition of the TGF-beta pro-protein convertase furin.,824,8
+825,<< PFD >> leads to a reduction of TGF-beta2 mRNA levels and of the mature [[ TGF-beta2 ]] protein due to decreased expression and direct inhibition of the TGF-beta pro-protein convertase furin.,825,8
+826,<< PFD >> leads to a reduction of TGF-beta2 mRNA levels and of the mature TGF-beta2 protein due to decreased expression and direct inhibition of the [[ TGF-beta ]] pro-protein convertase furin.,826,8
+827,<< PFD >> leads to a reduction of TGF-beta2 mRNA levels and of the mature TGF-beta2 protein due to decreased expression and direct inhibition of the TGF-beta [[ pro-protein convertase ]] furin.,827,8
+828,<< PFD >> leads to a reduction of TGF-beta2 mRNA levels and of the mature TGF-beta2 protein due to decreased expression and direct inhibition of the TGF-beta pro-protein convertase [[ furin ]].,828,8
+829,<< PFD >> leads to a reduction of TGF-beta2 mRNA levels and of the mature TGF-beta2 protein due to decreased expression and direct inhibition of the [[ TGF-beta ]] pro-protein convertase furin.,829,0
+830,<< PFD >> leads to a reduction of TGF-beta2 mRNA levels and of the mature TGF-beta2 protein due to decreased expression and direct inhibition of the TGF-beta [[ pro-protein convertase ]] furin.,830,0
+831,<< PFD >> leads to a reduction of TGF-beta2 mRNA levels and of the mature TGF-beta2 protein due to decreased expression and direct inhibition of the TGF-beta pro-protein convertase [[ furin ]].,831,0
+832,"In addition, << PFD >> reduces the protein levels of the [[ matrix metalloproteinase (MMP)-11 ]], a TGF-beta target gene and furin substrate involved in carcinogenesis.",832,8
+833,"In addition, << PFD >> reduces the protein levels of the matrix metalloproteinase (MMP)-11, a [[ TGF-beta ]] target gene and furin substrate involved in carcinogenesis.",833,0
+834,UNLABELLED: << Bile acid-coenzyme A:amino acid N-acyltransferase >> (BAAT) is the sole enzyme responsible for conjugation of primary and secondary bile acids to [[ taurine ]] and glycine.,834,4
+835,UNLABELLED: Bile acid-coenzyme A:amino acid N-acyltransferase (<< BAAT >>) is the sole enzyme responsible for conjugation of primary and secondary bile acids to [[ taurine ]] and glycine.,835,4
+836,UNLABELLED: << Bile acid-coenzyme A:amino acid N-acyltransferase >> (BAAT) is the sole enzyme responsible for conjugation of primary and secondary bile acids to taurine and [[ glycine ]].,836,4
+837,UNLABELLED: Bile acid-coenzyme A:amino acid N-acyltransferase (<< BAAT >>) is the sole enzyme responsible for conjugation of primary and secondary bile acids to taurine and [[ glycine ]].,837,4
+838,UNLABELLED: << Bile acid-coenzyme A:amino acid N-acyltransferase >> (BAAT) is the sole enzyme responsible for conjugation of primary and secondary [[ bile acids ]] to taurine and glycine.,838,5
+839,UNLABELLED: Bile acid-coenzyme A:amino acid N-acyltransferase (<< BAAT >>) is the sole enzyme responsible for conjugation of primary and secondary [[ bile acids ]] to taurine and glycine.,839,5
+840,The absence or presence of a cytosolic pool of << BAAT >> has important implications for the intracellular transport of unconjugated/deconjugated [[ bile salts ]].,840,5
+841,"The recombinant strains of the flavinogenic yeast Candida famata, which contain the DNA fragment consisting of the FMN1 gene (encoding the << riboflavin kinase >>, enzyme that converts riboflavin to [[ flavinmononucleotide ]]) driven by the strong promoters (the regulated RIB1 or constitutive TEF1 promoter) were isolated.",841,4
+842,"The recombinant strains of the flavinogenic yeast Candida famata, which contain the DNA fragment consisting of the FMN1 gene (encoding the << riboflavin kinase >>, enzyme that converts [[ riboflavin ]] to flavinmononucleotide) driven by the strong promoters (the regulated RIB1 or constitutive TEF1 promoter) were isolated.",842,5
+843,Mechanism of the irreversible inactivation of << mouse ornithine decarboxylase >> by [[ alpha-difluoromethylornithine ]].,843,0
+844,"<< Mouse ornithine decarboxylase >> (ODC) was expressed in Escherichia coli and the purified recombinant enzyme used for determination of the binding site for pyridoxal 5'-phosphate and of the residues modified in the inactivation of the enzyme by the enzyme-activated irreversible inhibitor, [[ alpha-difluoromethylornithine ]] (DFMO).",844,0
+845,"Mouse ornithine decarboxylase (<< ODC >>) was expressed in Escherichia coli and the purified recombinant enzyme used for determination of the binding site for pyridoxal 5'-phosphate and of the residues modified in the inactivation of the enzyme by the enzyme-activated irreversible inhibitor, [[ alpha-difluoromethylornithine ]] (DFMO).",845,0
+846,"<< Mouse ornithine decarboxylase >> (ODC) was expressed in Escherichia coli and the purified recombinant enzyme used for determination of the binding site for pyridoxal 5'-phosphate and of the residues modified in the inactivation of the enzyme by the enzyme-activated irreversible inhibitor, alpha-difluoromethylornithine ([[ DFMO ]]).",846,0
+847,"Mouse ornithine decarboxylase (<< ODC >>) was expressed in Escherichia coli and the purified recombinant enzyme used for determination of the binding site for pyridoxal 5'-phosphate and of the residues modified in the inactivation of the enzyme by the enzyme-activated irreversible inhibitor, alpha-difluoromethylornithine ([[ DFMO ]]).",847,0
+848,"Na+-Dependent transmembrane transport of small neutral << amino acids >>, such as glutamine and alanine, is mediated, among others, by the [[ neutral amino acid transporters ]] of the solute carrier 1 [SLC1, alanine serine cysteine transporter 1 (ASCT1), and ASCT2] and SLC38 families [sodium-coupled neutral amino acid transporter 1 (SNAT1), SNAT2, and SNAT4].",848,5
+849,"Na+-Dependent transmembrane transport of small neutral << amino acids >>, such as glutamine and alanine, is mediated, among others, by the neutral amino acid transporters of the [[ solute carrier 1 ]] [SLC1, alanine serine cysteine transporter 1 (ASCT1), and ASCT2] and SLC38 families [sodium-coupled neutral amino acid transporter 1 (SNAT1), SNAT2, and SNAT4].",849,5
+850,"Na+-Dependent transmembrane transport of small neutral << amino acids >>, such as glutamine and alanine, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [[[ SLC1 ]], alanine serine cysteine transporter 1 (ASCT1), and ASCT2] and SLC38 families [sodium-coupled neutral amino acid transporter 1 (SNAT1), SNAT2, and SNAT4].",850,5
+851,"Na+-Dependent transmembrane transport of small neutral << amino acids >>, such as glutamine and alanine, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [SLC1, [[ alanine serine cysteine transporter 1 ]] (ASCT1), and ASCT2] and SLC38 families [sodium-coupled neutral amino acid transporter 1 (SNAT1), SNAT2, and SNAT4].",851,5
+852,"Na+-Dependent transmembrane transport of small neutral << amino acids >>, such as glutamine and alanine, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [SLC1, alanine serine cysteine transporter 1 ([[ ASCT1 ]]), and ASCT2] and SLC38 families [sodium-coupled neutral amino acid transporter 1 (SNAT1), SNAT2, and SNAT4].",852,5
+853,"Na+-Dependent transmembrane transport of small neutral << amino acids >>, such as glutamine and alanine, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [SLC1, alanine serine cysteine transporter 1 (ASCT1), and [[ ASCT2 ]]] and SLC38 families [sodium-coupled neutral amino acid transporter 1 (SNAT1), SNAT2, and SNAT4].",853,5
+854,"Na+-Dependent transmembrane transport of small neutral << amino acids >>, such as glutamine and alanine, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [SLC1, alanine serine cysteine transporter 1 (ASCT1), and ASCT2] and [[ SLC38 ]] families [sodium-coupled neutral amino acid transporter 1 (SNAT1), SNAT2, and SNAT4].",854,5
+855,"Na+-Dependent transmembrane transport of small neutral << amino acids >>, such as glutamine and alanine, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [SLC1, alanine serine cysteine transporter 1 (ASCT1), and ASCT2] and SLC38 families [[[ sodium-coupled neutral amino acid transporter 1 ]] (SNAT1), SNAT2, and SNAT4].",855,5
+856,"Na+-Dependent transmembrane transport of small neutral << amino acids >>, such as glutamine and alanine, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [SLC1, alanine serine cysteine transporter 1 (ASCT1), and ASCT2] and SLC38 families [sodium-coupled neutral amino acid transporter 1 ([[ SNAT1 ]]), SNAT2, and SNAT4].",856,5
+857,"Na+-Dependent transmembrane transport of small neutral << amino acids >>, such as glutamine and alanine, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [SLC1, alanine serine cysteine transporter 1 (ASCT1), and ASCT2] and SLC38 families [sodium-coupled neutral amino acid transporter 1 (SNAT1), [[ SNAT2 ]], and SNAT4].",857,5
+858,"Na+-Dependent transmembrane transport of small neutral << amino acids >>, such as glutamine and alanine, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [SLC1, alanine serine cysteine transporter 1 (ASCT1), and ASCT2] and SLC38 families [sodium-coupled neutral amino acid transporter 1 (SNAT1), SNAT2, and [[ SNAT4 ]]].",858,5
+859,"Na+-Dependent transmembrane transport of small neutral amino acids, such as << glutamine >> and alanine, is mediated, among others, by the [[ neutral amino acid transporters ]] of the solute carrier 1 [SLC1, alanine serine cysteine transporter 1 (ASCT1), and ASCT2] and SLC38 families [sodium-coupled neutral amino acid transporter 1 (SNAT1), SNAT2, and SNAT4].",859,5
+860,"Na+-Dependent transmembrane transport of small neutral amino acids, such as << glutamine >> and alanine, is mediated, among others, by the neutral amino acid transporters of the [[ solute carrier 1 ]] [SLC1, alanine serine cysteine transporter 1 (ASCT1), and ASCT2] and SLC38 families [sodium-coupled neutral amino acid transporter 1 (SNAT1), SNAT2, and SNAT4].",860,5
+861,"Na+-Dependent transmembrane transport of small neutral amino acids, such as << glutamine >> and alanine, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [[[ SLC1 ]], alanine serine cysteine transporter 1 (ASCT1), and ASCT2] and SLC38 families [sodium-coupled neutral amino acid transporter 1 (SNAT1), SNAT2, and SNAT4].",861,5
+862,"Na+-Dependent transmembrane transport of small neutral amino acids, such as << glutamine >> and alanine, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [SLC1, [[ alanine serine cysteine transporter 1 ]] (ASCT1), and ASCT2] and SLC38 families [sodium-coupled neutral amino acid transporter 1 (SNAT1), SNAT2, and SNAT4].",862,5
+863,"Na+-Dependent transmembrane transport of small neutral amino acids, such as << glutamine >> and alanine, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [SLC1, alanine serine cysteine transporter 1 ([[ ASCT1 ]]), and ASCT2] and SLC38 families [sodium-coupled neutral amino acid transporter 1 (SNAT1), SNAT2, and SNAT4].",863,5
+864,"Na+-Dependent transmembrane transport of small neutral amino acids, such as << glutamine >> and alanine, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [SLC1, alanine serine cysteine transporter 1 (ASCT1), and [[ ASCT2 ]]] and SLC38 families [sodium-coupled neutral amino acid transporter 1 (SNAT1), SNAT2, and SNAT4].",864,5
+865,"Na+-Dependent transmembrane transport of small neutral amino acids, such as << glutamine >> and alanine, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [SLC1, alanine serine cysteine transporter 1 (ASCT1), and ASCT2] and [[ SLC38 ]] families [sodium-coupled neutral amino acid transporter 1 (SNAT1), SNAT2, and SNAT4].",865,5
+866,"Na+-Dependent transmembrane transport of small neutral amino acids, such as << glutamine >> and alanine, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [SLC1, alanine serine cysteine transporter 1 (ASCT1), and ASCT2] and SLC38 families [[[ sodium-coupled neutral amino acid transporter 1 ]] (SNAT1), SNAT2, and SNAT4].",866,5
+867,"Na+-Dependent transmembrane transport of small neutral amino acids, such as << glutamine >> and alanine, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [SLC1, alanine serine cysteine transporter 1 (ASCT1), and ASCT2] and SLC38 families [sodium-coupled neutral amino acid transporter 1 ([[ SNAT1 ]]), SNAT2, and SNAT4].",867,5
+868,"Na+-Dependent transmembrane transport of small neutral amino acids, such as << glutamine >> and alanine, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [SLC1, alanine serine cysteine transporter 1 (ASCT1), and ASCT2] and SLC38 families [sodium-coupled neutral amino acid transporter 1 (SNAT1), [[ SNAT2 ]], and SNAT4].",868,5
+869,"Na+-Dependent transmembrane transport of small neutral amino acids, such as << glutamine >> and alanine, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [SLC1, alanine serine cysteine transporter 1 (ASCT1), and ASCT2] and SLC38 families [sodium-coupled neutral amino acid transporter 1 (SNAT1), SNAT2, and [[ SNAT4 ]]].",869,5
+870,"Na+-Dependent transmembrane transport of small neutral amino acids, such as glutamine and << alanine >>, is mediated, among others, by the [[ neutral amino acid transporters ]] of the solute carrier 1 [SLC1, alanine serine cysteine transporter 1 (ASCT1), and ASCT2] and SLC38 families [sodium-coupled neutral amino acid transporter 1 (SNAT1), SNAT2, and SNAT4].",870,5
+871,"Na+-Dependent transmembrane transport of small neutral amino acids, such as glutamine and << alanine >>, is mediated, among others, by the neutral amino acid transporters of the [[ solute carrier 1 ]] [SLC1, alanine serine cysteine transporter 1 (ASCT1), and ASCT2] and SLC38 families [sodium-coupled neutral amino acid transporter 1 (SNAT1), SNAT2, and SNAT4].",871,5
+872,"Na+-Dependent transmembrane transport of small neutral amino acids, such as glutamine and << alanine >>, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [[[ SLC1 ]], alanine serine cysteine transporter 1 (ASCT1), and ASCT2] and SLC38 families [sodium-coupled neutral amino acid transporter 1 (SNAT1), SNAT2, and SNAT4].",872,5
+873,"Na+-Dependent transmembrane transport of small neutral amino acids, such as glutamine and << alanine >>, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [SLC1, [[ alanine serine cysteine transporter 1 ]] (ASCT1), and ASCT2] and SLC38 families [sodium-coupled neutral amino acid transporter 1 (SNAT1), SNAT2, and SNAT4].",873,5
+874,"Na+-Dependent transmembrane transport of small neutral amino acids, such as glutamine and << alanine >>, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [SLC1, alanine serine cysteine transporter 1 ([[ ASCT1 ]]), and ASCT2] and SLC38 families [sodium-coupled neutral amino acid transporter 1 (SNAT1), SNAT2, and SNAT4].",874,5
+875,"Na+-Dependent transmembrane transport of small neutral amino acids, such as glutamine and << alanine >>, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [SLC1, alanine serine cysteine transporter 1 (ASCT1), and [[ ASCT2 ]]] and SLC38 families [sodium-coupled neutral amino acid transporter 1 (SNAT1), SNAT2, and SNAT4].",875,5
+876,"Na+-Dependent transmembrane transport of small neutral amino acids, such as glutamine and << alanine >>, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [SLC1, alanine serine cysteine transporter 1 (ASCT1), and ASCT2] and SLC38 families [[[ sodium-coupled neutral amino acid transporter 1 ]] (SNAT1), SNAT2, and SNAT4].",876,5
+877,"Na+-Dependent transmembrane transport of small neutral amino acids, such as glutamine and << alanine >>, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [SLC1, alanine serine cysteine transporter 1 (ASCT1), and ASCT2] and SLC38 families [sodium-coupled neutral amino acid transporter 1 ([[ SNAT1 ]]), SNAT2, and SNAT4].",877,5
+878,"Na+-Dependent transmembrane transport of small neutral amino acids, such as glutamine and << alanine >>, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [SLC1, alanine serine cysteine transporter 1 (ASCT1), and ASCT2] and SLC38 families [sodium-coupled neutral amino acid transporter 1 (SNAT1), [[ SNAT2 ]], and SNAT4].",878,5
+879,"Na+-Dependent transmembrane transport of small neutral amino acids, such as glutamine and << alanine >>, is mediated, among others, by the neutral amino acid transporters of the solute carrier 1 [SLC1, alanine serine cysteine transporter 1 (ASCT1), and ASCT2] and SLC38 families [sodium-coupled neutral amino acid transporter 1 (SNAT1), SNAT2, and [[ SNAT4 ]]].",879,5
+880,"Here, we describe a new photolabile << alanine >> derivative based on protection of alanine with the 4-methoxy-7-nitroindolinyl (MNI) caging group, which we use for pre-steady-state kinetic analysis of alanine transport by [[ ASCT2 ]], SNAT1, and SNAT2.",880,5
+881,"Here, we describe a new photolabile << alanine >> derivative based on protection of alanine with the 4-methoxy-7-nitroindolinyl (MNI) caging group, which we use for pre-steady-state kinetic analysis of alanine transport by ASCT2, [[ SNAT1 ]], and SNAT2.",881,5
+882,"Here, we describe a new photolabile << alanine >> derivative based on protection of alanine with the 4-methoxy-7-nitroindolinyl (MNI) caging group, which we use for pre-steady-state kinetic analysis of alanine transport by ASCT2, SNAT1, and [[ SNAT2 ]].",882,5
+883,"Here, we describe a new photolabile alanine derivative based on protection of << alanine >> with the 4-methoxy-7-nitroindolinyl (MNI) caging group, which we use for pre-steady-state kinetic analysis of alanine transport by [[ ASCT2 ]], SNAT1, and SNAT2.",883,5
+884,"Here, we describe a new photolabile alanine derivative based on protection of << alanine >> with the 4-methoxy-7-nitroindolinyl (MNI) caging group, which we use for pre-steady-state kinetic analysis of alanine transport by ASCT2, [[ SNAT1 ]], and SNAT2.",884,5
+885,"Here, we describe a new photolabile alanine derivative based on protection of << alanine >> with the 4-methoxy-7-nitroindolinyl (MNI) caging group, which we use for pre-steady-state kinetic analysis of alanine transport by ASCT2, SNAT1, and [[ SNAT2 ]].",885,5
+886,"Here, we describe a new photolabile alanine derivative based on protection of alanine with the << 4-methoxy-7-nitroindolinyl >> (MNI) caging group, which we use for pre-steady-state kinetic analysis of alanine transport by [[ ASCT2 ]], SNAT1, and SNAT2.",886,5
+887,"Here, we describe a new photolabile alanine derivative based on protection of alanine with the << 4-methoxy-7-nitroindolinyl >> (MNI) caging group, which we use for pre-steady-state kinetic analysis of alanine transport by ASCT2, [[ SNAT1 ]], and SNAT2.",887,5
+888,"Here, we describe a new photolabile alanine derivative based on protection of alanine with the << 4-methoxy-7-nitroindolinyl >> (MNI) caging group, which we use for pre-steady-state kinetic analysis of alanine transport by ASCT2, SNAT1, and [[ SNAT2 ]].",888,5
+889,"Here, we describe a new photolabile alanine derivative based on protection of alanine with the 4-methoxy-7-nitroindolinyl (<< MNI >>) caging group, which we use for pre-steady-state kinetic analysis of alanine transport by [[ ASCT2 ]], SNAT1, and SNAT2.",889,5
+890,"Here, we describe a new photolabile alanine derivative based on protection of alanine with the 4-methoxy-7-nitroindolinyl (<< MNI >>) caging group, which we use for pre-steady-state kinetic analysis of alanine transport by ASCT2, [[ SNAT1 ]], and SNAT2.",890,5
+891,"Here, we describe a new photolabile alanine derivative based on protection of alanine with the 4-methoxy-7-nitroindolinyl (<< MNI >>) caging group, which we use for pre-steady-state kinetic analysis of alanine transport by ASCT2, SNAT1, and [[ SNAT2 ]].",891,5
+892,Stimulated << P-selectin >> and integrin alpha(IIb)beta(3) expression were also higher in the upper tertile both before and after [[ aspirin ]].,892,6
+893,Stimulated P-selectin and << integrin alpha(IIb)beta(3) >> expression were also higher in the upper tertile both before and after [[ aspirin ]].,893,6
+894,"At least 4 h of estrogen pre-treatment was required to elicit protection, an effect that was blocked by the << ER >> antagonist, [[ ICI 182,780 ]].",894,1
+895,"Moreover, ERalpha mediated the protection afforded by estrogen since only the ERalpha agonist, HPTE, but not the << ERbeta >> agonist, [[ DPN ]], protected against dopamine cell loss.",895,2
+896,Differential activation of << cAMP response element binding protein >> in discrete nucleus accumbens subregions during early and late [[ cocaine ]] sensitization.,896,9
+897,The present study examined the differential << cocaine >>-induced activation of the cyclic adenosine monophosphate (cAMP) response element binding protein ([[ CREB ]]) throughout discrete zones of analysis of the nucleus accumbens (NAc) in rats.,897,9
+898,The present study examined the differential << cocaine >>-induced activation of the [[ cyclic adenosine monophosphate (cAMP) response element binding protein ]] (CREB) throughout discrete zones of analysis of the nucleus accumbens (NAc) in rats.,898,9
+899,"Using immunohistochemistry, the authors analyzed changes in << CREB >> phosphorylation in the NAc after 5 days of [[ cocaine ]], a short or long drug-free period, and a subsequent challenge injection.",899,9
+900,"Repeated << cocaine >> resulted in [[ CREB ]] phosphorylation in all analyzed subregions of the NAc excluding the most ventrolateral region of the shell 2 weeks after cessation of repeated cocaine, but rats challenged after 2 drug-free days yielded a more localized activation of CREB in the 3 most dorsomedial zones of the shell.",900,9
+901,"Repeated cocaine resulted in CREB phosphorylation in all analyzed subregions of the NAc excluding the most ventrolateral region of the shell 2 weeks after cessation of repeated << cocaine >>, but rats challenged after 2 drug-free days yielded a more localized activation of [[ CREB ]] in the 3 most dorsomedial zones of the shell.",901,9
+902,The temporal and anatomical determinants of << cocaine >>-induced [[ CREB ]] activity may indicate functional differences among NAc shell subregions and suggest the involvement of CREB in early and late cocaine effects.,902,9
+903,"The carboxylation of glutamic acid residues to << gamma-carboxyglutamic acid >> (Gla) by the [[ vitamin K-dependent gamma-glutamyl carboxylase ]] (gamma-carboxylase) is an essential posttranslational modification required for the biological activity of a number of proteins, including proteins involved in blood coagulation and its regulation.",903,4
+904,"The carboxylation of glutamic acid residues to << gamma-carboxyglutamic acid >> (Gla) by the vitamin K-dependent gamma-glutamyl carboxylase ([[ gamma-carboxylase ]]) is an essential posttranslational modification required for the biological activity of a number of proteins, including proteins involved in blood coagulation and its regulation.",904,4
+905,"The carboxylation of glutamic acid residues to gamma-carboxyglutamic acid (<< Gla >>) by the [[ vitamin K-dependent gamma-glutamyl carboxylase ]] (gamma-carboxylase) is an essential posttranslational modification required for the biological activity of a number of proteins, including proteins involved in blood coagulation and its regulation.",905,4
+906,"The carboxylation of glutamic acid residues to gamma-carboxyglutamic acid (<< Gla >>) by the vitamin K-dependent gamma-glutamyl carboxylase ([[ gamma-carboxylase ]]) is an essential posttranslational modification required for the biological activity of a number of proteins, including proteins involved in blood coagulation and its regulation.",906,4
+907,"The carboxylation of << glutamic acid >> residues to gamma-carboxyglutamic acid (Gla) by the [[ vitamin K-dependent gamma-glutamyl carboxylase ]] (gamma-carboxylase) is an essential posttranslational modification required for the biological activity of a number of proteins, including proteins involved in blood coagulation and its regulation.",907,5
+908,"The carboxylation of << glutamic acid >> residues to gamma-carboxyglutamic acid (Gla) by the vitamin K-dependent gamma-glutamyl carboxylase ([[ gamma-carboxylase ]]) is an essential posttranslational modification required for the biological activity of a number of proteins, including proteins involved in blood coagulation and its regulation.",908,5
+909,"We posed the following questions: (1) Do cholangiocytes express H3R? (2) Does in vivo administration of << (R)-(alpha)-(-)-methylhistamine dihydrobromide >> (RAMH) ([[ H3R ]] agonist), thioperamide maleate (H3R antagonist) or histamine, in the absence/presence of thioperamide maleate, to bile duct ligated (BDL) rats regulate cholangiocyte proliferation? and (3) Does RAMH inhibit cholangiocyte proliferation by downregulation of cAMP-dependent phosphorylation of protein kinase A (PKA)/extracellular signal-regulated kinase 1/2 (ERK1/2)/ets-like gene-1 (Elk-1)? The expression of H3R was evaluated in liver sections by immunohistochemistry and immunofluorescence, and by real-time PCR in cholangiocyte RNA from normal and BDL rats.",909,2
+910,"We posed the following questions: (1) Do cholangiocytes express H3R? (2) Does in vivo administration of (R)-(alpha)-(-)-methylhistamine dihydrobromide (<< RAMH >>) ([[ H3R ]] agonist), thioperamide maleate (H3R antagonist) or histamine, in the absence/presence of thioperamide maleate, to bile duct ligated (BDL) rats regulate cholangiocyte proliferation? and (3) Does RAMH inhibit cholangiocyte proliferation by downregulation of cAMP-dependent phosphorylation of protein kinase A (PKA)/extracellular signal-regulated kinase 1/2 (ERK1/2)/ets-like gene-1 (Elk-1)? The expression of H3R was evaluated in liver sections by immunohistochemistry and immunofluorescence, and by real-time PCR in cholangiocyte RNA from normal and BDL rats.",910,2
+911,"We posed the following questions: (1) Do cholangiocytes express H3R? (2) Does in vivo administration of (R)-(alpha)-(-)-methylhistamine dihydrobromide (RAMH) (H3R agonist), << thioperamide maleate >> ([[ H3R ]] antagonist) or histamine, in the absence/presence of thioperamide maleate, to bile duct ligated (BDL) rats regulate cholangiocyte proliferation? and (3) Does RAMH inhibit cholangiocyte proliferation by downregulation of cAMP-dependent phosphorylation of protein kinase A (PKA)/extracellular signal-regulated kinase 1/2 (ERK1/2)/ets-like gene-1 (Elk-1)? The expression of H3R was evaluated in liver sections by immunohistochemistry and immunofluorescence, and by real-time PCR in cholangiocyte RNA from normal and BDL rats.",911,1
+912,<< RAMH >> inhibition of cholangiocyte growth was associated with decreased cAMP levels and [[ PKA ]]/ERK1/2/Elk-1 phosphorylation.,912,0
+913,<< RAMH >> inhibition of cholangiocyte growth was associated with decreased cAMP levels and PKA/[[ ERK1/2 ]]/Elk-1 phosphorylation.,913,0
+914,<< RAMH >> inhibition of cholangiocyte growth was associated with decreased cAMP levels and PKA/ERK1/2/[[ Elk-1 ]] phosphorylation.,914,0
+915,<< Proline dehydrogenase >> (PRODH) and Delta(1)-pyrroline-5-carboxylate dehydrogenase (P5CDH) catalyze the two-step oxidation of proline to [[ glutamate ]].,915,4
+916,Proline dehydrogenase (<< PRODH >>) and Delta(1)-pyrroline-5-carboxylate dehydrogenase (P5CDH) catalyze the two-step oxidation of proline to [[ glutamate ]].,916,4
+917,Proline dehydrogenase (PRODH) and << Delta(1)-pyrroline-5-carboxylate dehydrogenase >> (P5CDH) catalyze the two-step oxidation of proline to [[ glutamate ]].,917,4
+918,Proline dehydrogenase (PRODH) and Delta(1)-pyrroline-5-carboxylate dehydrogenase (<< P5CDH >>) catalyze the two-step oxidation of proline to [[ glutamate ]].,918,4
+919,<< Proline dehydrogenase >> (PRODH) and Delta(1)-pyrroline-5-carboxylate dehydrogenase (P5CDH) catalyze the two-step oxidation of [[ proline ]] to glutamate.,919,5
+920,Proline dehydrogenase (<< PRODH >>) and Delta(1)-pyrroline-5-carboxylate dehydrogenase (P5CDH) catalyze the two-step oxidation of [[ proline ]] to glutamate.,920,5
+921,Proline dehydrogenase (PRODH) and << Delta(1)-pyrroline-5-carboxylate dehydrogenase >> (P5CDH) catalyze the two-step oxidation of [[ proline ]] to glutamate.,921,5
+922,Proline dehydrogenase (PRODH) and Delta(1)-pyrroline-5-carboxylate dehydrogenase (<< P5CDH >>) catalyze the two-step oxidation of [[ proline ]] to glutamate.,922,5
+923,"Finally, we demonstrate that << T. thermophilus PRODH >> reacts with O(2) producing [[ superoxide ]].",923,4
+924,"Finally, we demonstrate that << T. thermophilus PRODH >> reacts with [[ O(2) ]] producing superoxide.",924,5
+925,"This is significant because << superoxide >> production underlies the role of [[ human PRODH ]] in p53-mediated apoptosis, implying commonalities between eukaryotic and bacterial monofunctional PRODHs.",925,4
+926,"The << phosphodiesterase (PDE) 4 >> is the predominant [[ cyclic AMP ]] degrading enzyme in a variety of inflammatory cells including eosinophils, neutrophils, macrophages, T cells and monocytes.",926,5
+927,"Consequently, << PDE4 >> inhibitors including [[ cilomilast ]] and AWD 12-281 have been tested in several models of allergic and irritant skin inflammation.",927,0
+928,"Consequently, << PDE4 >> inhibitors including cilomilast and [[ AWD 12-281 ]] have been tested in several models of allergic and irritant skin inflammation.",928,0
+929,"Results of early clinical trials with both topically (<< cipamfylline >>, CP80,633) and systemically (CC-10004) active [[ PDE4 ]] inhibitors demonstrated efficacy in atopic dermatitis and in the case of CC-10004, also in psoriasis.",929,0
+930,"Results of early clinical trials with both topically (cipamfylline, << CP80,633 >>) and systemically (CC-10004) active [[ PDE4 ]] inhibitors demonstrated efficacy in atopic dermatitis and in the case of CC-10004, also in psoriasis.",930,0
+931,"Although considerable functional diversity exists, most << C2 domains >> are activated by [[ Ca2+ ]] binding and then dock to a specific cellular membrane.",931,9
+932,<< Bile acid coenzyme A:amino acid N-acyltransferase >> (BAT) is responsible for the amidation of [[ bile acids ]] with the amino acids glycine and taurine.,932,5
+933,Bile acid coenzyme A:amino acid N-acyltransferase (<< BAT >>) is responsible for the amidation of [[ bile acids ]] with the amino acids glycine and taurine.,933,5
+934,"Because of their low asparagine synthetase (<< ASNS >>) expression and [[ asparagine ]] biosynthesis, acute lymphoblastic leukemia (ALL) cells are exquisitely sensitive to asparagine depletion.",934,4
+935,"Because of their low << asparagine synthetase >> (ASNS) expression and [[ asparagine ]] biosynthesis, acute lymphoblastic leukemia (ALL) cells are exquisitely sensitive to asparagine depletion.",935,4
+936,"<< Asparagine >> secretion by MSCs was directly related to their [[ ASNS ]] expression levels, suggesting a mechanism - increased concentrations of asparagine in the leukemic cell microenvironment - for the protective effects we observed.",936,4
+937,"<< MK-801 >> ((+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate), a noncompetitive [[ NMDA receptor ]] antagonist, partially prevented the decrease in cell viability and the energy impairment.",937,1
+938,"MK-801 (<< (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate >>), a noncompetitive [[ NMDA receptor ]] antagonist, partially prevented the decrease in cell viability and the energy impairment.",938,1
+939,The use of << Delta 6 desaturase >> (D6D) twice in the conversion of alpha-linolenic acid (ALA; 18:3n-3) to docosahexaenoic acid (DHA; 22:6n-3) suggests that this enzyme may play a key regulatory role in the synthesis and accumulation of [[ DHA ]] from ALA.,939,4
+940,The use of Delta 6 desaturase (<< D6D >>) twice in the conversion of alpha-linolenic acid (ALA; 18:3n-3) to docosahexaenoic acid (DHA; 22:6n-3) suggests that this enzyme may play a key regulatory role in the synthesis and accumulation of DHA from [[ ALA ]].,940,4
+941,The use of << Delta 6 desaturase >> (D6D) twice in the conversion of alpha-linolenic acid (ALA; 18:3n-3) to [[ docosahexaenoic acid ]] (DHA; 22:6n-3) suggests that this enzyme may play a key regulatory role in the synthesis and accumulation of DHA from ALA.,941,4
+942,The use of Delta 6 desaturase (<< D6D >>) twice in the conversion of alpha-linolenic acid (ALA; 18:3n-3) to [[ docosahexaenoic acid ]] (DHA; 22:6n-3) suggests that this enzyme may play a key regulatory role in the synthesis and accumulation of DHA from ALA.,942,4
+943,The use of << Delta 6 desaturase >> (D6D) twice in the conversion of alpha-linolenic acid (ALA; 18:3n-3) to docosahexaenoic acid ([[ DHA ]]; 22:6n-3) suggests that this enzyme may play a key regulatory role in the synthesis and accumulation of DHA from ALA.,943,4
+944,The use of Delta 6 desaturase (<< D6D >>) twice in the conversion of alpha-linolenic acid (ALA; 18:3n-3) to docosahexaenoic acid ([[ DHA ]]; 22:6n-3) suggests that this enzyme may play a key regulatory role in the synthesis and accumulation of DHA from ALA.,944,4
+945,The use of Delta 6 desaturase (<< D6D >>) twice in the conversion of alpha-linolenic acid (ALA; 18:3n-3) to docosahexaenoic acid (DHA; 22:6n-3) suggests that this enzyme may play a key regulatory role in the synthesis and accumulation of [[ DHA ]] from ALA.,945,5
+946,The use of << Delta 6 desaturase >> (D6D) twice in the conversion of alpha-linolenic acid (ALA; 18:3n-3) to docosahexaenoic acid (DHA; 22:6n-3) suggests that this enzyme may play a key regulatory role in the synthesis and accumulation of DHA from [[ ALA ]].,946,5
+947,The use of << Delta 6 desaturase >> (D6D) twice in the conversion of [[ alpha-linolenic acid ]] (ALA; 18:3n-3) to docosahexaenoic acid (DHA; 22:6n-3) suggests that this enzyme may play a key regulatory role in the synthesis and accumulation of DHA from ALA.,947,5
+948,The use of Delta 6 desaturase (<< D6D >>) twice in the conversion of [[ alpha-linolenic acid ]] (ALA; 18:3n-3) to docosahexaenoic acid (DHA; 22:6n-3) suggests that this enzyme may play a key regulatory role in the synthesis and accumulation of DHA from ALA.,948,5
+949,The use of << Delta 6 desaturase >> (D6D) twice in the conversion of alpha-linolenic acid ([[ ALA ]]; 18:3n-3) to docosahexaenoic acid (DHA; 22:6n-3) suggests that this enzyme may play a key regulatory role in the synthesis and accumulation of DHA from ALA.,949,5
+950,The use of Delta 6 desaturase (<< D6D >>) twice in the conversion of alpha-linolenic acid ([[ ALA ]]; 18:3n-3) to docosahexaenoic acid (DHA; 22:6n-3) suggests that this enzyme may play a key regulatory role in the synthesis and accumulation of DHA from ALA.,950,5
+951,"The accumulation of the post-<< D6D >> products of 22:5n-3, 24:6n-3 and [[ DHA ]], in cell phospholipids was saturated at concentrations of >18 microM ALA.",951,4
+952,The parallel pattern of accumulation of 24:6n-3 and DHA in response to increasing concentrations of ALA suggests that the competition between 24:5n-3 and ALA for << D6D >> may contribute to the limited accumulation of [[ DHA ]] in cell membranes.,952,4
+953,The parallel pattern of accumulation of 24:6n-3 and DHA in response to increasing concentrations of ALA suggests that the competition between 24:5n-3 and << ALA >> for [[ D6D ]] may contribute to the limited accumulation of DHA in cell membranes.,953,5
+954,<< Dopamine D1 receptor >> agonist and D2 receptor antagonist effects of the natural product [[ (-)-stepholidine ]]: molecular modeling and dynamics simulations.,954,2
+955,Dopamine D1 receptor agonist and << D2 receptor >> antagonist effects of the natural product [[ (-)-stepholidine ]]: molecular modeling and dynamics simulations.,955,1
+956,"<< (-)-Stepholidine >> (SPD), an active ingredient of the Chinese herb Stephania, is the first compound found to have dual function as a [[ dopamine receptor D1 ]] agonist and D2 antagonist.",956,2
+957,"(-)-Stepholidine (<< SPD >>), an active ingredient of the Chinese herb Stephania, is the first compound found to have dual function as a [[ dopamine receptor D1 ]] agonist and D2 antagonist.",957,2
+958,"<< (-)-Stepholidine >> (SPD), an active ingredient of the Chinese herb Stephania, is the first compound found to have dual function as a dopamine receptor D1 agonist and [[ D2 ]] antagonist.",958,1
+959,"(-)-Stepholidine (<< SPD >>), an active ingredient of the Chinese herb Stephania, is the first compound found to have dual function as a dopamine receptor D1 agonist and [[ D2 ]] antagonist.",959,1
+960,"The Ki for << mycophenolic acid >> inhibition of the [[ L263F ]] variant was comparable with the wild-type, and the variant Km for inosine 5'-monophosphate and nicotinamide adenine dinucleotide did not change significantly.",960,0
+961,"<< L-BOAA >> causes loss of GSH and inhibition of [[ mitochondrial complex I ]] in lumbosacral cord of male mice through oxidation of thiol groups, while female mice are resistant.",961,0
+962,Female mice express higher levels of glutaredoxin in certain CNS regions and downregulation of glutaredoxin using antisense oligonucleotides sensitizes them to << L-BOAA >> toxicity seen as [[ mitochondrial complex I ]] loss.,962,3
+963,"Ovariectomy downregulates glutaredoxin and renders female mice vulnerable to << L-BOAA >> toxicity as evidenced by activation of [[ AP1 ]], loss of GSH and complex I activity indicating the important role of glutaredoxin in neuroprotection.",963,9
+964,"Ovariectomy downregulates glutaredoxin and renders female mice vulnerable to << L-BOAA >> toxicity as evidenced by activation of AP1, loss of GSH and [[ complex I ]] activity indicating the important role of glutaredoxin in neuroprotection.",964,9
+965,<< Estrogen >> protects against mitochondrial dysfunction caused by excitotoxicity by maintaining cellular redox status through higher constitutive expression of [[ glutaredoxin ]] in the CNS.,965,6
+966,"The mechanisms that specify the vesicular phenotype of inhibitory interneurons in vertebrates are poorly understood because the two main inhibitory transmitters, << glycine >> and GABA, share the same [[ vesicular inhibitory amino acid transporter ]] (VIAAT) and are both present in neurons during postnatal development.",966,5
+967,"The mechanisms that specify the vesicular phenotype of inhibitory interneurons in vertebrates are poorly understood because the two main inhibitory transmitters, << glycine >> and GABA, share the same vesicular inhibitory amino acid transporter ([[ VIAAT ]]) and are both present in neurons during postnatal development.",967,5
+968,"The mechanisms that specify the vesicular phenotype of inhibitory interneurons in vertebrates are poorly understood because the two main inhibitory transmitters, glycine and << GABA >>, share the same [[ vesicular inhibitory amino acid transporter ]] (VIAAT) and are both present in neurons during postnatal development.",968,5
+969,"The mechanisms that specify the vesicular phenotype of inhibitory interneurons in vertebrates are poorly understood because the two main inhibitory transmitters, glycine and << GABA >>, share the same vesicular inhibitory amino acid transporter ([[ VIAAT ]]) and are both present in neurons during postnatal development.",969,5
+970,We have expressed << VIAAT >> and the plasmalemmal transporters for glycine and [[ GABA ]] in a neuroendocrine cell line and measured the quantal release of glycine and GABA using a novel double-sniffer patch-clamp technique.,970,5
+971,We have expressed VIAAT and the << plasmalemmal transporters >> for glycine and [[ GABA ]] in a neuroendocrine cell line and measured the quantal release of glycine and GABA using a novel double-sniffer patch-clamp technique.,971,5
+972,We have expressed << VIAAT >> and the plasmalemmal transporters for [[ glycine ]] and GABA in a neuroendocrine cell line and measured the quantal release of glycine and GABA using a novel double-sniffer patch-clamp technique.,972,5
+973,We have expressed VIAAT and the << plasmalemmal transporters >> for [[ glycine ]] and GABA in a neuroendocrine cell line and measured the quantal release of glycine and GABA using a novel double-sniffer patch-clamp technique.,973,5
+974,We found that << glycine >> is released from vesicles when [[ VIAAT ]] is coexpressed with either the neuronal transporter GlyT2 or the glial transporter GlyT1.,974,5
+975,"However, GlyT2 was more effective than GlyT1, probably because GlyT2 is unable to operate in the reverse mode, which gives it an advantage in maintaining the high cytosolic << glycine >> concentration required for efficient vesicular loading by [[ VIAAT ]].",975,5
+976,The vesicular inhibitory phenotype was gradually altered from glycinergic to GABAergic through mixed events when << GABA >> is introduced into the secretory cell and competes for uptake by [[ VIAAT ]].,976,5
+977,"Interestingly, the VIAAT ortholog from Caenorhabditis elegans (UNC-47), a species lacking glycine transmission, also supports << glycine >> exocytosis in the presence of [[ GlyT2 ]], and a point mutation of UNC-47 that abolishes GABA transmission in the worm confers glycine specificity.",977,5
+978,"Together, these results suggest that an increased cytosolic availability of << glycine >> in [[ VIAAT ]]-containing terminals was crucial for the emergence of glycinergic transmission in vertebrates.",978,5
+979,<< Na+ >>/Cl- dipole couples agonist binding to [[ kainate receptor ]] activation.,979,9
+980,Na+/<< Cl- >> dipole couples agonist binding to [[ kainate receptor ]] activation.,980,9
+981,<< Kainate-selective ionotropic glutamate receptors >> (GluRs) require external Na+ and Cl- as well as the neurotransmitter [[ L-glutamate ]] for activation.,981,9
+982,Kainate-selective ionotropic glutamate receptors (<< GluRs >>) require external Na+ and Cl- as well as the neurotransmitter [[ L-glutamate ]] for activation.,982,9
+983,<< Kainate-selective ionotropic glutamate receptors >> (GluRs) require external [[ Na+ ]] and Cl- as well as the neurotransmitter L-glutamate for activation.,983,9
+984,Kainate-selective ionotropic glutamate receptors (<< GluRs >>) require external [[ Na+ ]] and Cl- as well as the neurotransmitter L-glutamate for activation.,984,9
+985,<< Kainate-selective ionotropic glutamate receptors >> (GluRs) require external Na+ and [[ Cl- ]] as well as the neurotransmitter L-glutamate for activation.,985,9
+986,Kainate-selective ionotropic glutamate receptors (<< GluRs >>) require external Na+ and [[ Cl- ]] as well as the neurotransmitter L-glutamate for activation.,986,9
+987,"Additionally, << Na+ >> and Cl- ions coactivate [[ GluR6 ]] receptors by establishing a dipole, accounting for their common effect on KARs.",987,9
+988,"Additionally, Na+ and << Cl- >> ions coactivate [[ GluR6 ]] receptors by establishing a dipole, accounting for their common effect on KARs.",988,9
+989,"Phenserine. << Phenserine >>, a derivative of physostigmine, was first described as an inhibitor of acetylcholinesterase ([[ AChE ]]) and was shown to improve cognition in various experimental paradigms in rodents and dogs.",989,0
+990,"Phenserine. << Phenserine >>, a derivative of physostigmine, was first described as an inhibitor of [[ acetylcholinesterase ]] (AChE) and was shown to improve cognition in various experimental paradigms in rodents and dogs.",990,0
+991,"Phenserine. Phenserine, a derivative of << physostigmine >>, was first described as an inhibitor of acetylcholinesterase ([[ AChE ]]) and was shown to improve cognition in various experimental paradigms in rodents and dogs.",991,0
+992,"Phenserine. Phenserine, a derivative of << physostigmine >>, was first described as an inhibitor of [[ acetylcholinesterase ]] (AChE) and was shown to improve cognition in various experimental paradigms in rodents and dogs.",992,0
+993,"<< Phenserine >> deserves attention for an additional quality of action: in addition to inhibiting AChE, it modulates the amount of beta-amyloid precursor protein (APP) in neuronal cell culture by reducing [[ APP ]] translation.",993,8
+994,"<< Phenserine >> deserves attention for an additional quality of action: in addition to inhibiting [[ AChE ]], it modulates the amount of beta-amyloid precursor protein (APP) in neuronal cell culture by reducing APP translation.",994,0
+995,"<< Phenserine >> apparently reduces translational efficiency of [[ APP ]] mRNA into protein, a process that may involve an interaction with iron and/or an iron-responsive element.",995,8
+996,"As a consequence, << phenserine >> reduces [[ beta-amyloid ]] peptide (Abeta) formation in vitro and in vivo.",996,8
+997,"As a consequence, << phenserine >> reduces beta-amyloid peptide ([[ Abeta ]]) formation in vitro and in vivo.",997,8
+998,"Phenserine is also unique because of differing actions of its enantiomers: << (-)-phenserine >> is the active enantiomer for inhibition of [[ AChE ]], whereas (+)-phenserine ('posiphen') has weak activity as an AChE inhibitor and can be dosed much higher.",998,0
+999,"Phenserine is also unique because of differing actions of its enantiomers: (-)-phenserine is the active enantiomer for inhibition of AChE, whereas << (+)-phenserine >> ('posiphen') has weak activity as an [[ AChE ]] inhibitor and can be dosed much higher.",999,0
+1000,"Phenserine is also unique because of differing actions of its enantiomers: (-)-phenserine is the active enantiomer for inhibition of AChE, whereas (+)-phenserine ('<< posiphen >>') has weak activity as an [[ AChE ]] inhibitor and can be dosed much higher.",1000,0
+1001,"BACKGROUND AND PURPOSE: << AMP-activated protein kinase >> (AMPK) is activated by metformin, phenformin, and the AMP mimetic, 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside ([[ AICAR ]]).",1001,9
+1002,"BACKGROUND AND PURPOSE: AMP-activated protein kinase (<< AMPK >>) is activated by metformin, phenformin, and the AMP mimetic, 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside ([[ AICAR ]]).",1002,9
+1003,"BACKGROUND AND PURPOSE: << AMP-activated protein kinase >> (AMPK) is activated by [[ metformin ]], phenformin, and the AMP mimetic, 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR).",1003,9
+1004,"BACKGROUND AND PURPOSE: AMP-activated protein kinase (<< AMPK >>) is activated by [[ metformin ]], phenformin, and the AMP mimetic, 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR).",1004,9
+1005,"BACKGROUND AND PURPOSE: << AMP-activated protein kinase >> (AMPK) is activated by metformin, [[ phenformin ]], and the AMP mimetic, 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR).",1005,9
+1006,"BACKGROUND AND PURPOSE: AMP-activated protein kinase (<< AMPK >>) is activated by metformin, [[ phenformin ]], and the AMP mimetic, 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR).",1006,9
+1007,"BACKGROUND AND PURPOSE: << AMP-activated protein kinase >> (AMPK) is activated by metformin, phenformin, and the AMP mimetic, [[ 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside ]] (AICAR).",1007,9
+1008,"BACKGROUND AND PURPOSE: AMP-activated protein kinase (<< AMPK >>) is activated by metformin, phenformin, and the AMP mimetic, [[ 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside ]] (AICAR).",1008,9
+1009,"KEY RESULTS: << Phenformin >>, AICAR and metformin increased [[ AMPK (alpha1) ]] activity and decreased I(amiloride).",1009,9
+1010,"KEY RESULTS: Phenformin, << AICAR >> and metformin increased [[ AMPK (alpha1) ]] activity and decreased I(amiloride).",1010,9
+1011,"KEY RESULTS: Phenformin, AICAR and << metformin >> increased [[ AMPK (alpha1) ]] activity and decreased I(amiloride).",1011,9
+1012,The << AMPK >> inhibitor Compound C prevented the action of metformin and AICAR but not [[ phenformin ]].,1012,9
+1013,"Additional pharmacological effects evoked by << AICAR >> and phenformin on I(ouabain), with potential secondary effects on apical Na+ conductance, ENaC activity and monolayer resistance, have important consequences for their use as pharmacological activators of [[ AMPK ]] in cell systems where Na+K+ATPase is an important component.",1013,9
+1014,"Additional pharmacological effects evoked by AICAR and << phenformin >> on I(ouabain), with potential secondary effects on apical Na+ conductance, ENaC activity and monolayer resistance, have important consequences for their use as pharmacological activators of [[ AMPK ]] in cell systems where Na+K+ATPase is an important component.",1014,9
+1015,"Additional pharmacological effects evoked by AICAR and phenformin on I(<< ouabain >>), with potential secondary effects on apical Na+ conductance, ENaC activity and monolayer resistance, have important consequences for their use as pharmacological activators of [[ AMPK ]] in cell systems where Na+K+ATPase is an important component.",1015,9
+1016,"Neuroprotective effect of << nimesulide >>, a preferential [[ COX-2 ]] inhibitor, against pentylenetetrazol (PTZ)-induced chemical kindling and associated biochemical parameters in mice.",1016,0
+1017,"Brain cyclooxygenases (<< COX >>), the rate-limiting enzyme in [[ prostaglandin ]] synthesis, is rapidly and transiently induced by convulsions in hippocampal and cortical neurons.",1017,4
+1018,"Brain << cyclooxygenases >> (COX), the rate-limiting enzyme in [[ prostaglandin ]] synthesis, is rapidly and transiently induced by convulsions in hippocampal and cortical neurons.",1018,4
+1019,Previous studies have explored the protective effect of naproxen (non-selective COX-inhibitor) or << rofecoxib >> (selective [[ COX-2 ]] inhibitor) against chemical kindling in mice.,1019,0
+1020,Previous studies have explored the protective effect of << naproxen >> (non-selective [[ COX ]]-inhibitor) or rofecoxib (selective COX-2 inhibitor) against chemical kindling in mice.,1020,0
+1021,"With this background, the present study was designed to explore the possible effect of << nimesulide >> (a preferential [[ COX-2 ]] inhibitor) against pentylenetetrazol (PTZ)-induced kindling epilepsy in mice.",1021,0
+1022,"Compared with normal control group, << PTZ >>-kindled mice had significantly higher levels of malondialdehyde, nitrite, [[ myeloperoxidase ]] but had lower levels of reduced glutathione in the whole brain homogenate.",1022,6
+1023,"These results suggested that << nimesulide >>, a preferential [[ COX-2 ]] inhibitor offered neuroprotection against PTZ-induced kindling in mice.",1023,0
+1024,"While vitamin C is essential for PHD activity in vitro, N-acetyl-L-cysteine had no effect, and << gallic acid >> or n-propyl gallate efficiently inhibited the activity of all three [[ PHDs ]], demonstrating different functions of these antioxidants.",1024,0
+1025,"While vitamin C is essential for PHD activity in vitro, N-acetyl-L-cysteine had no effect, and gallic acid or << n-propyl gallate >> efficiently inhibited the activity of all three [[ PHDs ]], demonstrating different functions of these antioxidants.",1025,0
+1026,"<< LTC4 synthase >> (LTC4S), the pivotal enzyme for the biosynthesis of [[ LTC4 ]] (ref. 10), is an 18-kDa integral nuclear membrane protein that belongs to a superfamily of membrane-associated proteins in eicosanoid and glutathione metabolism that includes 5-lipoxygenase-activating protein, microsomal glutathione S-transferases (MGSTs), and microsomal prostaglandin E synthase 1 (ref. 13).",1026,4
+1027,"LTC4 synthase (<< LTC4S >>), the pivotal enzyme for the biosynthesis of [[ LTC4 ]] (ref. 10), is an 18-kDa integral nuclear membrane protein that belongs to a superfamily of membrane-associated proteins in eicosanoid and glutathione metabolism that includes 5-lipoxygenase-activating protein, microsomal glutathione S-transferases (MGSTs), and microsomal prostaglandin E synthase 1 (ref. 13).",1027,4
+1028,"LTC4 synthase (LTC4S), the pivotal enzyme for the biosynthesis of LTC4 (ref. 10), is an 18-kDa integral nuclear membrane protein that belongs to a superfamily of membrane-associated proteins in << eicosanoid >> and glutathione metabolism that includes 5-lipoxygenase-activating protein, [[ microsomal glutathione S-transferases ]] (MGSTs), and microsomal prostaglandin E synthase 1 (ref. 13).",1028,5
+1029,"LTC4 synthase (LTC4S), the pivotal enzyme for the biosynthesis of LTC4 (ref. 10), is an 18-kDa integral nuclear membrane protein that belongs to a superfamily of membrane-associated proteins in << eicosanoid >> and glutathione metabolism that includes 5-lipoxygenase-activating protein, microsomal glutathione S-transferases ([[ MGSTs ]]), and microsomal prostaglandin E synthase 1 (ref. 13).",1029,5
+1030,"LTC4 synthase (LTC4S), the pivotal enzyme for the biosynthesis of LTC4 (ref. 10), is an 18-kDa integral nuclear membrane protein that belongs to a superfamily of membrane-associated proteins in << eicosanoid >> and glutathione metabolism that includes 5-lipoxygenase-activating protein, microsomal glutathione S-transferases (MGSTs), and [[ microsomal prostaglandin E synthase 1 ]] (ref. 13).",1030,5
+1031,"LTC4 synthase (LTC4S), the pivotal enzyme for the biosynthesis of LTC4 (ref. 10), is an 18-kDa integral nuclear membrane protein that belongs to a superfamily of membrane-associated proteins in eicosanoid and << glutathione >> metabolism that includes 5-lipoxygenase-activating protein, [[ microsomal glutathione S-transferases ]] (MGSTs), and microsomal prostaglandin E synthase 1 (ref. 13).",1031,5
+1032,"LTC4 synthase (LTC4S), the pivotal enzyme for the biosynthesis of LTC4 (ref. 10), is an 18-kDa integral nuclear membrane protein that belongs to a superfamily of membrane-associated proteins in eicosanoid and << glutathione >> metabolism that includes 5-lipoxygenase-activating protein, microsomal glutathione S-transferases ([[ MGSTs ]]), and microsomal prostaglandin E synthase 1 (ref. 13).",1032,5
+1033,"LTC4 synthase (LTC4S), the pivotal enzyme for the biosynthesis of LTC4 (ref. 10), is an 18-kDa integral nuclear membrane protein that belongs to a superfamily of membrane-associated proteins in eicosanoid and << glutathione >> metabolism that includes 5-lipoxygenase-activating protein, microsomal glutathione S-transferases (MGSTs), and [[ microsomal prostaglandin E synthase 1 ]] (ref. 13).",1033,5
+1034,<< Phenelzine >> causes an increase in brain ornithine that is prevented by prior [[ monoamine oxidase ]] inhibition.,1034,0
+1035,"<< Phenelzine >> (PLZ), a nonselective irreversible inhibitor of monoamine oxidase (MAO), also inhibits GABA-transaminase ([[ GABA-T ]]), markedly increasing brain GABA levels.",1035,0
+1036,"<< Phenelzine >> (PLZ), a nonselective irreversible inhibitor of [[ monoamine oxidase ]] (MAO), also inhibits GABA-transaminase (GABA-T), markedly increasing brain GABA levels.",1036,0
+1037,"<< Phenelzine >> (PLZ), a nonselective irreversible inhibitor of monoamine oxidase ([[ MAO ]]), also inhibits GABA-transaminase (GABA-T), markedly increasing brain GABA levels.",1037,0
+1038,"<< Phenelzine >> (PLZ), a nonselective irreversible inhibitor of monoamine oxidase (MAO), also inhibits [[ GABA-transaminase ]] (GABA-T), markedly increasing brain GABA levels.",1038,0
+1039,"Phenelzine (<< PLZ >>), a nonselective irreversible inhibitor of monoamine oxidase (MAO), also inhibits GABA-transaminase ([[ GABA-T ]]), markedly increasing brain GABA levels.",1039,0
+1040,"Phenelzine (<< PLZ >>), a nonselective irreversible inhibitor of [[ monoamine oxidase ]] (MAO), also inhibits GABA-transaminase (GABA-T), markedly increasing brain GABA levels.",1040,0
+1041,"Phenelzine (<< PLZ >>), a nonselective irreversible inhibitor of monoamine oxidase ([[ MAO ]]), also inhibits GABA-transaminase (GABA-T), markedly increasing brain GABA levels.",1041,0
+1042,"Phenelzine (<< PLZ >>), a nonselective irreversible inhibitor of monoamine oxidase (MAO), also inhibits [[ GABA-transaminase ]] (GABA-T), markedly increasing brain GABA levels.",1042,0
+1043,"<< PLZ >> is also a substrate for [[ MAO ]], and studies suggest that a metabolite formed by the action of this enzyme on PLZ may be responsible for the increase in GABA observed.",1043,5
+1044,"To determine whether a metabolite formed by the action of MAO on PLZ may be responsible for the elevation in brain ORN observed, animals were pretreated with vehicle or the << MAO >> inhibitor [[ tranylcypromine ]] (TCP) before vehicle or PLZ (15 mg/kg), and brains collected 3 h later.",1044,0
+1045,"To determine whether a metabolite formed by the action of MAO on PLZ may be responsible for the elevation in brain ORN observed, animals were pretreated with vehicle or the << MAO >> inhibitor tranylcypromine ([[ TCP ]]) before vehicle or PLZ (15 mg/kg), and brains collected 3 h later.",1045,0
+1046,"Pretreatment with TCP completely abolished the PLZ-induced increase in brain ORN, suggesting, as with GABA, that a metabolite of << PLZ >> formed by the action of [[ MAO ]] is responsible for the elevation of brain ORN observed.",1046,5
+1047,Nitric oxide (<< NO >>) is an important vasorelaxant produced along with L-citrulline from L-arginine in a reaction catalyzed by [[ endothelial nitric oxide synthase ]] (eNOS).,1047,4
+1048,Nitric oxide (<< NO >>) is an important vasorelaxant produced along with L-citrulline from L-arginine in a reaction catalyzed by endothelial nitric oxide synthase ([[ eNOS ]]).,1048,4
+1049,<< Nitric oxide >> (NO) is an important vasorelaxant produced along with L-citrulline from L-arginine in a reaction catalyzed by [[ endothelial nitric oxide synthase ]] (eNOS).,1049,4
+1050,<< Nitric oxide >> (NO) is an important vasorelaxant produced along with L-citrulline from L-arginine in a reaction catalyzed by endothelial nitric oxide synthase ([[ eNOS ]]).,1050,4
+1051,Nitric oxide (NO) is an important vasorelaxant produced along with << L-citrulline >> from L-arginine in a reaction catalyzed by [[ endothelial nitric oxide synthase ]] (eNOS).,1051,4
+1052,Nitric oxide (NO) is an important vasorelaxant produced along with << L-citrulline >> from L-arginine in a reaction catalyzed by endothelial nitric oxide synthase ([[ eNOS ]]).,1052,4
+1053,Nitric oxide (NO) is an important vasorelaxant produced along with L-citrulline from << L-arginine >> in a reaction catalyzed by [[ endothelial nitric oxide synthase ]] (eNOS).,1053,5
+1054,Nitric oxide (NO) is an important vasorelaxant produced along with L-citrulline from << L-arginine >> in a reaction catalyzed by endothelial nitric oxide synthase ([[ eNOS ]]).,1054,5
+1055,"As further support, << alpha-methyl-DL-aspartate >>, an inhibitor of [[ argininosuccinate synthase ]] (AS), a component of the citrulline-NO cycle, inhibited NO production in a dose-dependent manner.",1055,0
+1056,"As further support, << alpha-methyl-DL-aspartate >>, an inhibitor of argininosuccinate synthase ([[ AS ]]), a component of the citrulline-NO cycle, inhibited NO production in a dose-dependent manner.",1056,0
+1057,"Caution is necessary only when it is coadministered with drugs metabolised by << CYP2D6 >>, such as [[ metoprolol ]], or administered to the elderly or patients with severe hepatic or renal impairment.",1057,5
+1058,"Inhibition of platelet aggregation by AZD6140, a reversible oral << P2Y12 >> receptor antagonist, compared with [[ clopidogrel ]] in patients with acute coronary syndromes.",1058,1
+1059,"Inhibition of platelet aggregation by << AZD6140 >>, a reversible oral [[ P2Y12 ]] receptor antagonist, compared with clopidogrel in patients with acute coronary syndromes.",1059,1
+1060,<< AZD6140 >> is a reversible oral [[ P2Y(12) ]] receptor antagonist that has been studied in ACS patients in comparison with clopidogrel (DISPERSE-2 study).,1060,1
+1061,AZD6140 is a reversible oral << P2Y(12) >> receptor antagonist that has been studied in ACS patients in comparison with [[ clopidogrel ]] (DISPERSE-2 study).,1061,1
+1062,<< Oxybutynin >> (1) is a non-selective [[ muscarinic receptor ]] antagonist that is used clinically for the treatment of urinary incontinence.,1062,1
+1063,"Degradation of submandibular gland << AQP5 >> by parasympathetic denervation of chorda tympani and its recovery by [[ cevimeline ]], an M3 muscarinic receptor agonist.",1063,6
+1064,"Degradation of submandibular gland AQP5 by parasympathetic denervation of chorda tympani and its recovery by << cevimeline >>, an [[ M3 muscarinic receptor ]] agonist.",1064,2
+1065,"Administration of << cevimeline hydrochloride >>, an M3 muscarinic receptor agonist (10 mg/kg for 7 days po), but not pilocarpine (0.3 mg/kg for 7 days po), recovered the [[ AQP5 ]] protein level reduced by CTD and increased the AQP1 protein level above the control one.",1065,6
+1066,"Administration of << cevimeline hydrochloride >>, an M3 muscarinic receptor agonist (10 mg/kg for 7 days po), but not pilocarpine (0.3 mg/kg for 7 days po), recovered the AQP5 protein level reduced by CTD and increased the [[ AQP1 ]] protein level above the control one.",1066,6
+1067,"Administration of << cevimeline hydrochloride >>, an [[ M3 muscarinic receptor ]] agonist (10 mg/kg for 7 days po), but not pilocarpine (0.3 mg/kg for 7 days po), recovered the AQP5 protein level reduced by CTD and increased the AQP1 protein level above the control one.",1067,2
+1068,"Administration of << chloroquine >> (50 mg/kg for 7 days po), a denaturant of lysosomes, increased the [[ AQP5 ]] protein level reduced by CTD.",1068,6
+1069,"Differential pharmacokinetics and pharmacodynamics of methylphenidate enantiomers: does chirality matter? d,l-threo-methylphenidate (MPH) is an effective first-line treatment for the symptoms associated with attention-deficit/hyperactivity disorder. << threo-methylphenidate >> inhibits the [[ dopamine transporter ]] and the norepinephrine transporter, resulting in elevations of these monoamines after impulse release.",1069,0
+1070,"Differential pharmacokinetics and pharmacodynamics of methylphenidate enantiomers: does chirality matter? d,l-threo-methylphenidate (MPH) is an effective first-line treatment for the symptoms associated with attention-deficit/hyperactivity disorder. << threo-methylphenidate >> inhibits the dopamine transporter and the [[ norepinephrine transporter ]], resulting in elevations of these monoamines after impulse release.",1070,0
+1071,"Differential pharmacokinetics and pharmacodynamics of methylphenidate enantiomers: does chirality matter? d,l-threo-methylphenidate (MPH) is an effective first-line treatment for the symptoms associated with attention-deficit/hyperactivity disorder. threo-methylphenidate inhibits the << dopamine transporter >> and the norepinephrine transporter, resulting in elevations of these [[ monoamines ]] after impulse release.",1071,5
+1072,"Differential pharmacokinetics and pharmacodynamics of methylphenidate enantiomers: does chirality matter? d,l-threo-methylphenidate (MPH) is an effective first-line treatment for the symptoms associated with attention-deficit/hyperactivity disorder. threo-methylphenidate inhibits the dopamine transporter and the << norepinephrine transporter >>, resulting in elevations of these [[ monoamines ]] after impulse release.",1072,5
+1073,The direct inhibition of << stathmin >> by [[ CCNU ]] is likely a contributing factor.,1073,0
+1074,The principal aim of the study was to find << amiodarone >> analogues that retained [[ human ether-a-go-go-related protein (hERG) channel ]] inhibition but with reduced cytotoxicity.,1074,0
+1075,"CONCLUSIONS AND IMPLICATIONS: << Amiodarone >> analogues with better [[ hERG ]] channel inhibition and cytotoxicity profiles than the parent compound have been identified, demonstrating that cytotoxicity and hERG channel interaction are mechanistically distinct and separable properties of the compounds.",1075,0
+1076,"In addition to OT and to a lesser extent AVP (pitressin), a number of OT and AVP analogues; such as << carbetocin >> ([[ OT ]] agonist) dDAVP (desmopressin, V(2) agonist), terlipressin (V(1a) agonist), felypressin (V(1a) agonist) and atosiban (Tractocile OT antagonist) are also in clinical use.",1076,2
+1077,"In addition to OT and to a lesser extent AVP (pitressin), a number of OT and AVP analogues; such as carbetocin (OT agonist) dDAVP (<< desmopressin >>, [[ V(2) ]] agonist), terlipressin (V(1a) agonist), felypressin (V(1a) agonist) and atosiban (Tractocile OT antagonist) are also in clinical use.",1077,2
+1078,"In addition to OT and to a lesser extent AVP (pitressin), a number of OT and AVP analogues; such as carbetocin (OT agonist) dDAVP (desmopressin, V(2) agonist), << terlipressin >> ([[ V(1a) ]] agonist), felypressin (V(1a) agonist) and atosiban (Tractocile OT antagonist) are also in clinical use.",1078,2
+1079,"In addition to OT and to a lesser extent AVP (pitressin), a number of OT and AVP analogues; such as carbetocin (OT agonist) dDAVP (desmopressin, V(2) agonist), terlipressin (V(1a) agonist), << felypressin >> ([[ V(1a) ]] agonist) and atosiban (Tractocile OT antagonist) are also in clinical use.",1079,2
+1080,"In addition to OT and to a lesser extent AVP (pitressin), a number of OT and AVP analogues; such as carbetocin (OT agonist) dDAVP (desmopressin, V(2) agonist), terlipressin (V(1a) agonist), felypressin (V(1a) agonist) and << atosiban >> (Tractocile [[ OT ]] antagonist) are also in clinical use.",1080,1
+1081,"In addition to OT and to a lesser extent AVP (pitressin), a number of OT and AVP analogues; such as carbetocin (OT agonist) dDAVP (desmopressin, V(2) agonist), terlipressin (V(1a) agonist), felypressin (V(1a) agonist) and atosiban (<< Tractocile >> [[ OT ]] antagonist) are also in clinical use.",1081,1
+1082,"While a number of orally active non-peptide << V(2) >> antagonists (Vaptans); notably, [[ Tolvaptan ]], Lixivaptan and Satavaptan, are currently in Phase III clinical trials; to date, only the mixed V(2)/V(1a), antagonist Conivaptan (Vaprisol), has been approved by the US FDA for clinical use (by i.v. administration), for the treatment of euvolemic and hypervolemic hyponatremia in hospitalized patients.",1082,1
+1083,"While a number of orally active non-peptide << V(2) >> antagonists (Vaptans); notably, Tolvaptan, [[ Lixivaptan ]] and Satavaptan, are currently in Phase III clinical trials; to date, only the mixed V(2)/V(1a), antagonist Conivaptan (Vaprisol), has been approved by the US FDA for clinical use (by i.v. administration), for the treatment of euvolemic and hypervolemic hyponatremia in hospitalized patients.",1083,1
+1084,"While a number of orally active non-peptide << V(2) >> antagonists (Vaptans); notably, Tolvaptan, Lixivaptan and [[ Satavaptan ]], are currently in Phase III clinical trials; to date, only the mixed V(2)/V(1a), antagonist Conivaptan (Vaprisol), has been approved by the US FDA for clinical use (by i.v. administration), for the treatment of euvolemic and hypervolemic hyponatremia in hospitalized patients.",1084,1
+1085,"While a number of orally active non-peptide V(2) antagonists (Vaptans); notably, Tolvaptan, Lixivaptan and Satavaptan, are currently in Phase III clinical trials; to date, only the mixed << V(2) >>/V(1a), antagonist [[ Conivaptan ]] (Vaprisol), has been approved by the US FDA for clinical use (by i.v. administration), for the treatment of euvolemic and hypervolemic hyponatremia in hospitalized patients.",1085,1
+1086,"While a number of orally active non-peptide V(2) antagonists (Vaptans); notably, Tolvaptan, Lixivaptan and Satavaptan, are currently in Phase III clinical trials; to date, only the mixed V(2)/<< V(1a) >>, antagonist [[ Conivaptan ]] (Vaprisol), has been approved by the US FDA for clinical use (by i.v. administration), for the treatment of euvolemic and hypervolemic hyponatremia in hospitalized patients.",1086,1
+1087,"While a number of orally active non-peptide V(2) antagonists (Vaptans); notably, Tolvaptan, Lixivaptan and Satavaptan, are currently in Phase III clinical trials; to date, only the mixed << V(2) >>/V(1a), antagonist Conivaptan ([[ Vaprisol ]]), has been approved by the US FDA for clinical use (by i.v. administration), for the treatment of euvolemic and hypervolemic hyponatremia in hospitalized patients.",1087,1
+1088,"While a number of orally active non-peptide V(2) antagonists (Vaptans); notably, Tolvaptan, Lixivaptan and Satavaptan, are currently in Phase III clinical trials; to date, only the mixed V(2)/<< V(1a) >>, antagonist Conivaptan ([[ Vaprisol ]]), has been approved by the US FDA for clinical use (by i.v. administration), for the treatment of euvolemic and hypervolemic hyponatremia in hospitalized patients.",1088,1
+1089,"Absorbable drugs (<< fibric acids >>, nicotinic acid, probucol, HMG-CoA reductase inhibitors) reduce [[ plasma very-low-density lipoproteins ]] (VLDL) and/or low-density lipoproteins (LDL) by a variety of mechanisms.",1089,8
+1090,"Absorbable drugs (<< fibric acids >>, nicotinic acid, probucol, HMG-CoA reductase inhibitors) reduce plasma very-low-density lipoproteins ([[ VLDL ]]) and/or low-density lipoproteins (LDL) by a variety of mechanisms.",1090,8
+1091,"Absorbable drugs (<< fibric acids >>, nicotinic acid, probucol, HMG-CoA reductase inhibitors) reduce plasma very-low-density lipoproteins (VLDL) and/or [[ low-density lipoproteins ]] (LDL) by a variety of mechanisms.",1091,8
+1092,"Absorbable drugs (<< fibric acids >>, nicotinic acid, probucol, HMG-CoA reductase inhibitors) reduce plasma very-low-density lipoproteins (VLDL) and/or low-density lipoproteins ([[ LDL ]]) by a variety of mechanisms.",1092,8
+1093,"Absorbable drugs (fibric acids, << nicotinic acid >>, probucol, HMG-CoA reductase inhibitors) reduce [[ plasma very-low-density lipoproteins ]] (VLDL) and/or low-density lipoproteins (LDL) by a variety of mechanisms.",1093,8
+1094,"Absorbable drugs (fibric acids, << nicotinic acid >>, probucol, HMG-CoA reductase inhibitors) reduce plasma very-low-density lipoproteins ([[ VLDL ]]) and/or low-density lipoproteins (LDL) by a variety of mechanisms.",1094,8
+1095,"Absorbable drugs (fibric acids, << nicotinic acid >>, probucol, HMG-CoA reductase inhibitors) reduce plasma very-low-density lipoproteins (VLDL) and/or [[ low-density lipoproteins ]] (LDL) by a variety of mechanisms.",1095,8
+1096,"Absorbable drugs (fibric acids, << nicotinic acid >>, probucol, HMG-CoA reductase inhibitors) reduce plasma very-low-density lipoproteins (VLDL) and/or low-density lipoproteins ([[ LDL ]]) by a variety of mechanisms.",1096,8
+1097,"Absorbable drugs (fibric acids, nicotinic acid, << probucol >>, HMG-CoA reductase inhibitors) reduce [[ plasma very-low-density lipoproteins ]] (VLDL) and/or low-density lipoproteins (LDL) by a variety of mechanisms.",1097,8
+1098,"Absorbable drugs (fibric acids, nicotinic acid, << probucol >>, HMG-CoA reductase inhibitors) reduce plasma very-low-density lipoproteins ([[ VLDL ]]) and/or low-density lipoproteins (LDL) by a variety of mechanisms.",1098,8
+1099,"Absorbable drugs (fibric acids, nicotinic acid, << probucol >>, HMG-CoA reductase inhibitors) reduce plasma very-low-density lipoproteins (VLDL) and/or [[ low-density lipoproteins ]] (LDL) by a variety of mechanisms.",1099,8
+1100,"Absorbable drugs (fibric acids, nicotinic acid, << probucol >>, HMG-CoA reductase inhibitors) reduce plasma very-low-density lipoproteins (VLDL) and/or low-density lipoproteins ([[ LDL ]]) by a variety of mechanisms.",1100,8
+1101,"<< Fibric acids >>, in particular, act by stimulating the catabolism of [[ VLDL ]] and also, as a consequence, improving LDL delipidation, thus favoring receptor uptake.",1101,8
+1102,"Probucol acts by a newly described mechanism, i.e. accelerating reverse transport of << cholesteryl esters >> from [[ high-density lipoproteins ]] to lower-density lipoproteins.",1102,5
+1103,"Probucol acts by a newly described mechanism, i.e. accelerating reverse transport of << cholesteryl esters >> from high-density lipoproteins to [[ lower-density lipoproteins ]].",1103,5
+1104,<< Lapatinib >>: a dual inhibitor of [[ human epidermal growth factor receptor ]] tyrosine kinases.,1104,0
+1105,<< Lapatinib >>: a dual inhibitor of human epidermal growth factor receptor [[ tyrosine kinases ]].,1105,0
+1106,"BACKGROUND: << Lapatinib >>, the first dual inhibitor of epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 ([[ HER2 ]]) tyrosine kinases, was approved by the US Food and Drug Administration (FDA) in 2007.",1106,0
+1107,"BACKGROUND: << Lapatinib >>, the first dual inhibitor of epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2) [[ tyrosine kinases ]], was approved by the US Food and Drug Administration (FDA) in 2007.",1107,0
+1108,"BACKGROUND: << Lapatinib >>, the first dual inhibitor of [[ epidermal growth factor receptor ]] (EGFR) and human epidermal growth factor receptor 2 (HER2) tyrosine kinases, was approved by the US Food and Drug Administration (FDA) in 2007.",1108,0
+1109,"BACKGROUND: << Lapatinib >>, the first dual inhibitor of epidermal growth factor receptor ([[ EGFR ]]) and human epidermal growth factor receptor 2 (HER2) tyrosine kinases, was approved by the US Food and Drug Administration (FDA) in 2007.",1109,0
+1110,"BACKGROUND: << Lapatinib >>, the first dual inhibitor of epidermal growth factor receptor (EGFR) and [[ human epidermal growth factor receptor 2 ]] (HER2) tyrosine kinases, was approved by the US Food and Drug Administration (FDA) in 2007.",1110,0
+1111,"<< Lapatinib >> is metabolized primarily by the [[ cytochrome P450 3A4 ]] isozyme, with 1 metabolite remaining active against EGFR but not HER2.",1111,5
+1112,CONCLUSIONS: << Lapatinib >> is a dual inhibitor of the [[ EGFR ]] and HER2 tyrosine kinases.,1112,0
+1113,CONCLUSIONS: << Lapatinib >> is a dual inhibitor of the EGFR and [[ HER2 ]] tyrosine kinases.,1113,0
+1114,CONCLUSIONS: << Lapatinib >> is a dual inhibitor of the EGFR and HER2 [[ tyrosine kinases ]].,1114,0
+1115,Phenelzine is a more potent << monoamine oxidase >> inhibitor than is [[ N2-acetylphenelzine ]].,1115,0
+1116,<< Phenelzine >> is a more potent [[ monoamine oxidase ]] inhibitor than is N2-acetylphenelzine.,1116,0
+1117,Acetylation of << phenelzine >> at the N2 position presumably interferes with the inhibition of the [[ transaminase ]] enzymes for gamma-aminobutyric acid and alanine.,1117,0
+1118,Acetylation of phenelzine at the << N2 >> position presumably interferes with the inhibition of the [[ transaminase ]] enzymes for gamma-aminobutyric acid and alanine.,1118,0
+1119,Acetylation of phenelzine at the N2 position presumably interferes with the inhibition of the << transaminase >> enzymes for [[ gamma-aminobutyric acid ]] and alanine.,1119,0
+1120,Acetylation of phenelzine at the N2 position presumably interferes with the inhibition of the << transaminase >> enzymes for gamma-aminobutyric acid and [[ alanine ]].,1120,0
+1121,All neurotrophic effects were blocked by the unselective D2/D3 receptor antagonist sulpiride (5 microm) and by the selective << D3 receptor >> antagonist [[ SB-277011-A ]] at a low dose (50 nm).,1121,1
+1122,"<< Quinpirole >> and 7-OH-DPAT also increased the phosphorylation of [[ extracellular signal-regulated kinase ]] (ERK) within minutes, an effect blocked by pretreatment with SB-277011-A.",1122,9
+1123,"<< Quinpirole >> and 7-OH-DPAT also increased the phosphorylation of extracellular signal-regulated kinase ([[ ERK ]]) within minutes, an effect blocked by pretreatment with SB-277011-A.",1123,9
+1124,"Quinpirole and << 7-OH-DPAT >> also increased the phosphorylation of [[ extracellular signal-regulated kinase ]] (ERK) within minutes, an effect blocked by pretreatment with SB-277011-A.",1124,9
+1125,"Quinpirole and << 7-OH-DPAT >> also increased the phosphorylation of extracellular signal-regulated kinase ([[ ERK ]]) within minutes, an effect blocked by pretreatment with SB-277011-A.",1125,9
+1126,"Quinpirole and 7-OH-DPAT also increased the phosphorylation of << extracellular signal-regulated kinase >> (ERK) within minutes, an effect blocked by pretreatment with [[ SB-277011-A ]].",1126,0
+1127,"Quinpirole and 7-OH-DPAT also increased the phosphorylation of extracellular signal-regulated kinase (<< ERK >>) within minutes, an effect blocked by pretreatment with [[ SB-277011-A ]].",1127,0
+1128,"This study identified four clinically approved antihypertensive drugs (<< efonidipine >>, felodipine, isradipine, and nitrendipine) as potent [[ T-channel ]] blockers (IC(50) < 3 microM).",1128,0
+1129,"This study identified four clinically approved antihypertensive drugs (efonidipine, << felodipine >>, isradipine, and nitrendipine) as potent [[ T-channel ]] blockers (IC(50) < 3 microM).",1129,0
+1130,"This study identified four clinically approved antihypertensive drugs (efonidipine, felodipine, << isradipine >>, and nitrendipine) as potent [[ T-channel ]] blockers (IC(50) < 3 microM).",1130,0
+1131,"This study identified four clinically approved antihypertensive drugs (efonidipine, felodipine, isradipine, and << nitrendipine >>) as potent [[ T-channel ]] blockers (IC(50) < 3 microM).",1131,0
+1132,"We found compounds that inhibited << Panx1 >> currents with a rank order of potency: [[ carbenoxolone ]] > disodium 4,4'-diisothiocyanatostilbene-2,2'-disulfonate (DIDS) approximately disodium 4-acetamido-4'-isothiocyanato-stilben-2,2'-disulfonate approximately 5-nitro-2-(3-phenylpropylamino)benzoic acid > indanyloxyacetic acid 94 >> probenecid >> flufenamic acid = niflumic acid.",1132,0
+1133,"We found compounds that inhibited << Panx1 >> currents with a rank order of potency: carbenoxolone > [[ disodium 4,4'-diisothiocyanatostilbene-2,2'-disulfonate ]] (DIDS) approximately disodium 4-acetamido-4'-isothiocyanato-stilben-2,2'-disulfonate approximately 5-nitro-2-(3-phenylpropylamino)benzoic acid > indanyloxyacetic acid 94 >> probenecid >> flufenamic acid = niflumic acid.",1133,0
+1134,"We found compounds that inhibited << Panx1 >> currents with a rank order of potency: carbenoxolone > disodium 4,4'-diisothiocyanatostilbene-2,2'-disulfonate ([[ DIDS ]]) approximately disodium 4-acetamido-4'-isothiocyanato-stilben-2,2'-disulfonate approximately 5-nitro-2-(3-phenylpropylamino)benzoic acid > indanyloxyacetic acid 94 >> probenecid >> flufenamic acid = niflumic acid.",1134,0
+1135,"We found compounds that inhibited << Panx1 >> currents with a rank order of potency: carbenoxolone > disodium 4,4'-diisothiocyanatostilbene-2,2'-disulfonate (DIDS) approximately [[ disodium 4-acetamido-4'-isothiocyanato-stilben-2,2'-disulfonate ]] approximately 5-nitro-2-(3-phenylpropylamino)benzoic acid > indanyloxyacetic acid 94 >> probenecid >> flufenamic acid = niflumic acid.",1135,0
+1136,"We found compounds that inhibited << Panx1 >> currents with a rank order of potency: carbenoxolone > disodium 4,4'-diisothiocyanatostilbene-2,2'-disulfonate (DIDS) approximately disodium 4-acetamido-4'-isothiocyanato-stilben-2,2'-disulfonate approximately [[ 5-nitro-2-(3-phenylpropylamino)benzoic acid ]] > indanyloxyacetic acid 94 >> probenecid >> flufenamic acid = niflumic acid.",1136,0
+1137,"We found compounds that inhibited << Panx1 >> currents with a rank order of potency: carbenoxolone > disodium 4,4'-diisothiocyanatostilbene-2,2'-disulfonate (DIDS) approximately disodium 4-acetamido-4'-isothiocyanato-stilben-2,2'-disulfonate approximately 5-nitro-2-(3-phenylpropylamino)benzoic acid > [[ indanyloxyacetic acid 94 ]] >> probenecid >> flufenamic acid = niflumic acid.",1137,0
+1138,"We found compounds that inhibited << Panx1 >> currents with a rank order of potency: carbenoxolone > disodium 4,4'-diisothiocyanatostilbene-2,2'-disulfonate (DIDS) approximately disodium 4-acetamido-4'-isothiocyanato-stilben-2,2'-disulfonate approximately 5-nitro-2-(3-phenylpropylamino)benzoic acid > indanyloxyacetic acid 94 >> [[ probenecid ]] >> flufenamic acid = niflumic acid.",1138,0
+1139,"We found compounds that inhibited << Panx1 >> currents with a rank order of potency: carbenoxolone > disodium 4,4'-diisothiocyanatostilbene-2,2'-disulfonate (DIDS) approximately disodium 4-acetamido-4'-isothiocyanato-stilben-2,2'-disulfonate approximately 5-nitro-2-(3-phenylpropylamino)benzoic acid > indanyloxyacetic acid 94 >> probenecid >> [[ flufenamic acid ]] = niflumic acid.",1139,0
+1140,"We found compounds that inhibited << Panx1 >> currents with a rank order of potency: carbenoxolone > disodium 4,4'-diisothiocyanatostilbene-2,2'-disulfonate (DIDS) approximately disodium 4-acetamido-4'-isothiocyanato-stilben-2,2'-disulfonate approximately 5-nitro-2-(3-phenylpropylamino)benzoic acid > indanyloxyacetic acid 94 >> probenecid >> flufenamic acid = [[ niflumic acid ]].",1140,0
+1141,"Triphosphate nucleotides (ATP, GTP, and << UTP >>) rapidly and reversibly inhibited [[ Panx1 ]] currents via mechanism(s) independent of purine receptors.",1141,0
+1142,"<< Triphosphate nucleotides >> (ATP, GTP, and UTP) rapidly and reversibly inhibited [[ Panx1 ]] currents via mechanism(s) independent of purine receptors.",1142,0
+1143,"Triphosphate nucleotides (<< ATP >>, GTP, and UTP) rapidly and reversibly inhibited [[ Panx1 ]] currents via mechanism(s) independent of purine receptors.",1143,0
+1144,"Triphosphate nucleotides (ATP, << GTP >>, and UTP) rapidly and reversibly inhibited [[ Panx1 ]] currents via mechanism(s) independent of purine receptors.",1144,0
+1145,"When Panx1 was coexpressed with purinergic P2X(7) receptor (P2X(7)R), << DIDS >> was found to act as a [[ P2X(7)R ]] antagonist to inhibit ATP-evoked currents, but none of the other compounds inhibited P2X(7)R currents.",1145,1
+1146,"We investigated the effect of << captopril >>, an [[ ACE ]] inhibitor, on MMP-2 and MMP-9 in monocrotaline-induced right ventricular hypertrophy.",1146,0
+1147,<< MMP-2 >> and MMP-9 expressions and activities in right ventricles increased significantly in [[ monocrotaline ]]-injected rats and captopril inhibited them.,1147,9
+1148,MMP-2 and << MMP-9 >> expressions and activities in right ventricles increased significantly in [[ monocrotaline ]]-injected rats and captopril inhibited them.,1148,9
+1149,<< MMP-2 >> and MMP-9 expressions and activities in right ventricles increased significantly in [[ monocrotaline ]]-injected rats and captopril inhibited them.,1149,6
+1150,MMP-2 and << MMP-9 >> expressions and activities in right ventricles increased significantly in [[ monocrotaline ]]-injected rats and captopril inhibited them.,1150,6
+1151,<< MMP-2 >> and MMP-9 expressions and activities in right ventricles increased significantly in monocrotaline-injected rats and [[ captopril ]] inhibited them.,1151,8
+1152,MMP-2 and << MMP-9 >> expressions and activities in right ventricles increased significantly in monocrotaline-injected rats and [[ captopril ]] inhibited them.,1152,8
+1153,<< MMP-2 >> and MMP-9 expressions and activities in right ventricles increased significantly in monocrotaline-injected rats and [[ captopril ]] inhibited them.,1153,0
+1154,MMP-2 and << MMP-9 >> expressions and activities in right ventricles increased significantly in monocrotaline-injected rats and [[ captopril ]] inhibited them.,1154,0
+1155,These findings indicate that captopril attenuates the development of << monocrotaline >>-induced right ventricular hypertrophy in association with inhibition of [[ MMP-2 ]] and MMP-9 in rats.,1155,9
+1156,These findings indicate that captopril attenuates the development of << monocrotaline >>-induced right ventricular hypertrophy in association with inhibition of MMP-2 and [[ MMP-9 ]] in rats.,1156,9
+1157,These findings indicate that << captopril >> attenuates the development of monocrotaline-induced right ventricular hypertrophy in association with inhibition of [[ MMP-2 ]] and MMP-9 in rats.,1157,0
+1158,These findings indicate that << captopril >> attenuates the development of monocrotaline-induced right ventricular hypertrophy in association with inhibition of MMP-2 and [[ MMP-9 ]] in rats.,1158,0
+1159,"<< Thiazide >> and high ceiling diuretics were recently shown to inhibit all mammalian isoforms of carbonic anhydrase ([[ CA ]], EC 4.2.1.1) with a very different profile as compared to classical inhibitors, such as acetazolamide, methazolamide, and ethoxzolamide.",1159,0
+1160,"<< Thiazide >> and high ceiling diuretics were recently shown to inhibit all mammalian isoforms of carbonic anhydrase (CA, [[ EC 4.2.1.1 ]]) with a very different profile as compared to classical inhibitors, such as acetazolamide, methazolamide, and ethoxzolamide.",1160,0
+1161,"<< Thiazide >> and high ceiling diuretics were recently shown to inhibit all mammalian isoforms of [[ carbonic anhydrase ]] (CA, EC 4.2.1.1) with a very different profile as compared to classical inhibitors, such as acetazolamide, methazolamide, and ethoxzolamide.",1161,0
+1162,"Thiazide and high ceiling diuretics were recently shown to inhibit all mammalian isoforms of carbonic anhydrase (<< CA >>, EC 4.2.1.1) with a very different profile as compared to classical inhibitors, such as [[ acetazolamide ]], methazolamide, and ethoxzolamide.",1162,0
+1163,"Thiazide and high ceiling diuretics were recently shown to inhibit all mammalian isoforms of carbonic anhydrase (CA, << EC 4.2.1.1 >>) with a very different profile as compared to classical inhibitors, such as [[ acetazolamide ]], methazolamide, and ethoxzolamide.",1163,0
+1164,"Thiazide and high ceiling diuretics were recently shown to inhibit all mammalian isoforms of << carbonic anhydrase >> (CA, EC 4.2.1.1) with a very different profile as compared to classical inhibitors, such as [[ acetazolamide ]], methazolamide, and ethoxzolamide.",1164,0
+1165,"Thiazide and high ceiling diuretics were recently shown to inhibit all mammalian isoforms of carbonic anhydrase (<< CA >>, EC 4.2.1.1) with a very different profile as compared to classical inhibitors, such as acetazolamide, [[ methazolamide ]], and ethoxzolamide.",1165,0
+1166,"Thiazide and high ceiling diuretics were recently shown to inhibit all mammalian isoforms of carbonic anhydrase (CA, << EC 4.2.1.1 >>) with a very different profile as compared to classical inhibitors, such as acetazolamide, [[ methazolamide ]], and ethoxzolamide.",1166,0
+1167,"Thiazide and high ceiling diuretics were recently shown to inhibit all mammalian isoforms of << carbonic anhydrase >> (CA, EC 4.2.1.1) with a very different profile as compared to classical inhibitors, such as acetazolamide, [[ methazolamide ]], and ethoxzolamide.",1167,0
+1168,"Thiazide and high ceiling diuretics were recently shown to inhibit all mammalian isoforms of carbonic anhydrase (<< CA >>, EC 4.2.1.1) with a very different profile as compared to classical inhibitors, such as acetazolamide, methazolamide, and [[ ethoxzolamide ]].",1168,0
+1169,"Thiazide and high ceiling diuretics were recently shown to inhibit all mammalian isoforms of carbonic anhydrase (CA, << EC 4.2.1.1 >>) with a very different profile as compared to classical inhibitors, such as acetazolamide, methazolamide, and [[ ethoxzolamide ]].",1169,0
+1170,"Thiazide and high ceiling diuretics were recently shown to inhibit all mammalian isoforms of << carbonic anhydrase >> (CA, EC 4.2.1.1) with a very different profile as compared to classical inhibitors, such as acetazolamide, methazolamide, and [[ ethoxzolamide ]].",1170,0
+1171,"Some of these structurally related compounds have a very different behavior against the widespread isozyme CA II, with << chlorthalidone >>, trichloromethiazide, and furosemide being efficient inhibitors against [[ CA II ]] (K(I)s of 65-138 nM), whereas indapamide is a much weaker one (K(I) of 2520 nM).",1171,0
+1172,"Some of these structurally related compounds have a very different behavior against the widespread isozyme CA II, with chlorthalidone, << trichloromethiazide >>, and furosemide being efficient inhibitors against [[ CA II ]] (K(I)s of 65-138 nM), whereas indapamide is a much weaker one (K(I) of 2520 nM).",1172,0
+1173,"Some of these structurally related compounds have a very different behavior against the widespread isozyme CA II, with chlorthalidone, trichloromethiazide, and << furosemide >> being efficient inhibitors against [[ CA II ]] (K(I)s of 65-138 nM), whereas indapamide is a much weaker one (K(I) of 2520 nM).",1173,0
+1174,"Some of these structurally related compounds have a very different behavior against the widespread isozyme CA II, with chlorthalidone, trichloromethiazide, and furosemide being efficient inhibitors against << CA II >> (K(I)s of 65-138 nM), whereas [[ indapamide ]] is a much weaker one (K(I) of 2520 nM).",1174,0
+1175,"<< Sergliflozin etabonate >>, a selective [[ SGLT2 ]] inhibitor, improves glycemic control in streptozotocin-induced diabetic rats and Zucker fatty rats.",1175,0
+1176,The low-affinity << sodium glucose cotransporter >> (SGLT2) is responsible for most of the [[ glucose ]] reabsorption in the kidney and has been highlighted as a novel therapeutic target for the treatment of diabetes.,1176,5
+1177,The low-affinity sodium glucose cotransporter (<< SGLT2 >>) is responsible for most of the [[ glucose ]] reabsorption in the kidney and has been highlighted as a novel therapeutic target for the treatment of diabetes.,1177,5
+1178,"We discovered << sergliflozin etabonate >>, a novel selective [[ SGLT2 ]] inhibitor, and found that selective inhibition of SGLT2 increased urinary glucose excretion and consequently decreased plasma glucose levels.",1178,0
+1179,"We discovered << sergliflozin etabonate >>, a novel selective SGLT2 inhibitor, and found that selective inhibition of [[ SGLT2 ]] increased urinary glucose excretion and consequently decreased plasma glucose levels.",1179,0
+1180,"In this report, we examined the antihyperglycemic effects of sergliflozin etabonate in normal and diabetic rats in comparison with those of a sulfonylurea (gliclazide) and an << alpha-glucosidase >> inhibitor ([[ voglibose ]]).",1180,0
+1181,"Chronic treatment with << sergliflozin etabonate >> reduced the levels of [[ glycated hemoglobin ]] and fasting plasma glucose, and improved the glycemic response after glucose loading in Zucker fatty rats.",1181,8
+1182,"Although the D1-like receptor, by itself, had no effect on VSMC proliferation, stimulation with << fenoldopam >>, a D1-like receptor agonist, inhibited the stimulatory effect of [[ insulin ]].",1182,8
+1183,"Although the D1-like receptor, by itself, had no effect on VSMC proliferation, stimulation with << fenoldopam >>, a [[ D1-like receptor ]] agonist, inhibited the stimulatory effect of insulin.",1183,2
+1184,"The inhibitory effect of << fenoldopam >> on [[ insulin ]]-mediated VSMC proliferation was receptor specific, because its effect could be blocked by SCH23390, a D1-like receptor antagonist.",1184,8
+1185,"The inhibitory effect of fenoldopam on insulin-mediated VSMC proliferation was receptor specific, because its effect could be blocked by << SCH23390 >>, a [[ D1-like receptor ]] antagonist.",1185,1
+1186,"<< Fenoldopam >> also inhibited [[ insulin receptor ]] mRNA and protein expression, which was time dependent and concentration dependent.",1186,8
+1187,"A PKC or MAP kinase inhibitor blocked the inhibitory effect of << fenoldopam >> on [[ insulin receptor ]] expression, indicating that PKC and MAP kinase were involved in the signaling pathway.",1187,8
+1188,The progress of the enzymatic reaction of the hydrolysis of << acetylthiocholine >> at pH 8 in the presence of [[ AChE ]] and the inhibitor studied is determined by measuring at 230 nm the peak area of the reaction product thiocholine (TCh).,1188,5
+1189,The mechanism of << OP >> poisoning involves inhibition of [[ acetylcholinesterase ]] (AChE) leading to inactivation of the enzyme which has an important role in neurotransmission.,1189,0
+1190,The mechanism of << OP >> poisoning involves inhibition of acetylcholinesterase ([[ AChE ]]) leading to inactivation of the enzyme which has an important role in neurotransmission.,1190,0
+1191,They act by reactivation of << AChE >> inhibited by [[ OP ]].,1191,0
+1192,"Presently, a combination of an antimuscarinic agent, e.g. atropine, << AChE >> reactivator such as one of the recommended pyridinium oximes (pralidoxime, [[ trimedoxime ]], obidoxime and HI-6) and diazepam are used for the treatment of OP poisoning in humans.",1192,9
+1193,"Presently, a combination of an antimuscarinic agent, e.g. atropine, << AChE >> reactivator such as one of the recommended pyridinium oximes (pralidoxime, trimedoxime, [[ obidoxime ]] and HI-6) and diazepam are used for the treatment of OP poisoning in humans.",1193,9
+1194,"Presently, a combination of an antimuscarinic agent, e.g. atropine, << AChE >> reactivator such as one of the recommended pyridinium oximes (pralidoxime, trimedoxime, obidoxime and [[ HI-6 ]]) and diazepam are used for the treatment of OP poisoning in humans.",1194,9
+1195,"Presently, a combination of an antimuscarinic agent, e.g. atropine, << AChE >> reactivator such as one of the recommended pyridinium oximes (pralidoxime, trimedoxime, obidoxime and HI-6) and [[ diazepam ]] are used for the treatment of OP poisoning in humans.",1195,9
+1196,"Presently, a combination of an antimuscarinic agent, e.g. << atropine >>, [[ AChE ]] reactivator such as one of the recommended pyridinium oximes (pralidoxime, trimedoxime, obidoxime and HI-6) and diazepam are used for the treatment of OP poisoning in humans.",1196,9
+1197,"Presently, a combination of an antimuscarinic agent, e.g. atropine, << AChE >> reactivator such as one of the recommended [[ pyridinium oximes ]] (pralidoxime, trimedoxime, obidoxime and HI-6) and diazepam are used for the treatment of OP poisoning in humans.",1197,9
+1198,"Presently, a combination of an antimuscarinic agent, e.g. atropine, << AChE >> reactivator such as one of the recommended pyridinium oximes ([[ pralidoxime ]], trimedoxime, obidoxime and HI-6) and diazepam are used for the treatment of OP poisoning in humans.",1198,9
+1199,"Presently, a combination of an antimuscarinic agent, e.g. atropine, << AChE >> reactivator such as one of the recommended pyridinium oximes (pralidoxime, trimedoxime, obidoxime and HI-6) and diazepam are used for the treatment of [[ OP ]] poisoning in humans.",1199,0
+1200,"<< Palonosetron >> is a second-generation serotonin 5-HT3 receptor antagonist, with a distinct pharmacological profile that differs from first-generation [[ 5-HT3 receptor ]] antagonists.",1200,1
+1201,"<< Palonosetron >> is a second-generation [[ serotonin 5-HT3 receptor ]] antagonist, with a distinct pharmacological profile that differs from first-generation 5-HT3 receptor antagonists.",1201,1
+1202,Oral << palonosetron >> is likely to be a useful addition to oral formulations of other [[ 5-HT3 recepto ]]r antagonists in preventing CINV in patients receiving MEC.,1202,1
+1203,"Luteinizing hormone-releasing hormone (LHRH) agonists, such as << buserelin >>, goserelin, leuprorelin and triptorelin, stimulate the pituitary's [[ gonadotrophin-releasing hormone (GnRH) receptor ]], ultimately leading to its de-sensitization and subsequent reduction of LH and testosterone levels.",1203,9
+1204,"Luteinizing hormone-releasing hormone (LHRH) agonists, such as buserelin, << goserelin >>, leuprorelin and triptorelin, stimulate the pituitary's [[ gonadotrophin-releasing hormone (GnRH) receptor ]], ultimately leading to its de-sensitization and subsequent reduction of LH and testosterone levels.",1204,9
+1205,"Luteinizing hormone-releasing hormone (LHRH) agonists, such as buserelin, goserelin, << leuprorelin >> and triptorelin, stimulate the pituitary's [[ gonadotrophin-releasing hormone (GnRH) receptor ]], ultimately leading to its de-sensitization and subsequent reduction of LH and testosterone levels.",1205,9
+1206,"Luteinizing hormone-releasing hormone (LHRH) agonists, such as buserelin, goserelin, leuprorelin and << triptorelin >>, stimulate the pituitary's [[ gonadotrophin-releasing hormone (GnRH) receptor ]], ultimately leading to its de-sensitization and subsequent reduction of LH and testosterone levels.",1206,9
+1207,"Luteinizing hormone-releasing hormone (LHRH) agonists, such as << buserelin >>, goserelin, leuprorelin and triptorelin, stimulate the pituitary's gonadotrophin-releasing hormone (GnRH) receptor, ultimately leading to its de-sensitization and subsequent reduction of [[ LH ]] and testosterone levels.",1207,8
+1208,"Luteinizing hormone-releasing hormone (LHRH) agonists, such as buserelin, << goserelin >>, leuprorelin and triptorelin, stimulate the pituitary's gonadotrophin-releasing hormone (GnRH) receptor, ultimately leading to its de-sensitization and subsequent reduction of [[ LH ]] and testosterone levels.",1208,8
+1209,"Luteinizing hormone-releasing hormone (LHRH) agonists, such as buserelin, goserelin, << leuprorelin >> and triptorelin, stimulate the pituitary's gonadotrophin-releasing hormone (GnRH) receptor, ultimately leading to its de-sensitization and subsequent reduction of [[ LH ]] and testosterone levels.",1209,8
+1210,"Luteinizing hormone-releasing hormone (LHRH) agonists, such as buserelin, goserelin, leuprorelin and << triptorelin >>, stimulate the pituitary's gonadotrophin-releasing hormone (GnRH) receptor, ultimately leading to its de-sensitization and subsequent reduction of [[ LH ]] and testosterone levels.",1210,8
+1211,"<< Luteinizing hormone-releasing hormone >> (LHRH) agonists, such as [[ buserelin ]], goserelin, leuprorelin and triptorelin, stimulate the pituitary's gonadotrophin-releasing hormone (GnRH) receptor, ultimately leading to its de-sensitization and subsequent reduction of LH and testosterone levels.",1211,2
+1212,"Luteinizing hormone-releasing hormone (<< LHRH >>) agonists, such as [[ buserelin ]], goserelin, leuprorelin and triptorelin, stimulate the pituitary's gonadotrophin-releasing hormone (GnRH) receptor, ultimately leading to its de-sensitization and subsequent reduction of LH and testosterone levels.",1212,2
+1213,"<< Luteinizing hormone-releasing hormone >> (LHRH) agonists, such as buserelin, [[ goserelin ]], leuprorelin and triptorelin, stimulate the pituitary's gonadotrophin-releasing hormone (GnRH) receptor, ultimately leading to its de-sensitization and subsequent reduction of LH and testosterone levels.",1213,2
+1214,"Luteinizing hormone-releasing hormone (<< LHRH >>) agonists, such as buserelin, [[ goserelin ]], leuprorelin and triptorelin, stimulate the pituitary's gonadotrophin-releasing hormone (GnRH) receptor, ultimately leading to its de-sensitization and subsequent reduction of LH and testosterone levels.",1214,2
+1215,"<< Luteinizing hormone-releasing hormone >> (LHRH) agonists, such as buserelin, goserelin, [[ leuprorelin ]] and triptorelin, stimulate the pituitary's gonadotrophin-releasing hormone (GnRH) receptor, ultimately leading to its de-sensitization and subsequent reduction of LH and testosterone levels.",1215,2
+1216,"Luteinizing hormone-releasing hormone (<< LHRH >>) agonists, such as buserelin, goserelin, [[ leuprorelin ]] and triptorelin, stimulate the pituitary's gonadotrophin-releasing hormone (GnRH) receptor, ultimately leading to its de-sensitization and subsequent reduction of LH and testosterone levels.",1216,2
+1217,"<< Luteinizing hormone-releasing hormone >> (LHRH) agonists, such as buserelin, goserelin, leuprorelin and [[ triptorelin ]], stimulate the pituitary's gonadotrophin-releasing hormone (GnRH) receptor, ultimately leading to its de-sensitization and subsequent reduction of LH and testosterone levels.",1217,2
+1218,"Luteinizing hormone-releasing hormone (<< LHRH >>) agonists, such as buserelin, goserelin, leuprorelin and [[ triptorelin ]], stimulate the pituitary's gonadotrophin-releasing hormone (GnRH) receptor, ultimately leading to its de-sensitization and subsequent reduction of LH and testosterone levels.",1218,2
+1219,"Two pure << GnRH >> antagonists have been developed, [[ abarelix ]] and degarelix, that are devoid of any agonist effect on the GnRH receptor and consequently do not result in testosterone flare.",1219,1
+1220,"Two pure << GnRH >> antagonists have been developed, abarelix and [[ degarelix ]], that are devoid of any agonist effect on the GnRH receptor and consequently do not result in testosterone flare.",1220,1
+1221,"<< Abarelix >> was the first [[ GnRH ]] antagonist to be developed and was approved by the USA Food and Drug Administration in 2004 for the initiation of hormonal castration in advanced or metastasizing hormone-dependent prostate carcinoma, when rapid androgen suppression is necessary.",1221,1
+1222,"<< Fulvestrant >>, a pure [[ estrogen receptor ]] downregulator, is a new addition to the antiestrogen therapeutic armamentarium since its FDA approval in 2002.",1222,3
+1223,The concentration of << estramustine phosphate >> required to inhibit the assembly or to induce the disassembly of [[ chick brain MAP2 ]]:tubulin microtubules is markedly dependent upon the microtubule protein concentration.,1223,9
+1224,The concentration of << estramustine phosphate >> required to inhibit the assembly or to induce the disassembly of chick brain MAP2:[[ tubulin ]] microtubules is markedly dependent upon the microtubule protein concentration.,1224,9
+1225,The concentration of << estramustine phosphate >> required to inhibit the assembly or to induce the disassembly of [[ chick brain MAP2 ]]:tubulin microtubules is markedly dependent upon the microtubule protein concentration.,1225,0
+1226,The concentration of << estramustine phosphate >> required to inhibit the assembly or to induce the disassembly of chick brain MAP2:[[ tubulin ]] microtubules is markedly dependent upon the microtubule protein concentration.,1226,0
+1227,It is proposed that two molecules of << estramustine phosphate >> interact with each of the three tubulin-binding sites of MAP2 and inhibit the [[ MAP2 ]]:tubulin interaction by neutralising two highly conserved basic residues.,1227,0
+1228,It is proposed that two molecules of << estramustine phosphate >> interact with each of the three tubulin-binding sites of MAP2 and inhibit the MAP2:[[ tubulin ]] interaction by neutralising two highly conserved basic residues.,1228,0
+1229,"Activity of << XL184 >> (Cabozantinib), an oral [[ tyrosine kinase ]] inhibitor, in patients with medullary thyroid cancer.",1229,0
+1230,"Activity of XL184 (<< Cabozantinib >>), an oral [[ tyrosine kinase ]] inhibitor, in patients with medullary thyroid cancer.",1230,0
+1231,"PURPOSE: XL184 (<< cabozantinib >>) is a potent inhibitor of MET, vascular endothelial growth factor receptor 2 ([[ VEGFR2 ]]), and RET, with robust antiangiogenic, antitumor, and anti-invasive effects in preclinical models.",1231,0
+1232,"PURPOSE: XL184 (<< cabozantinib >>) is a potent inhibitor of MET, vascular endothelial growth factor receptor 2 (VEGFR2), and [[ RET ]], with robust antiangiogenic, antitumor, and anti-invasive effects in preclinical models.",1232,0
+1233,"PURPOSE: XL184 (<< cabozantinib >>) is a potent inhibitor of [[ MET ]], vascular endothelial growth factor receptor 2 (VEGFR2), and RET, with robust antiangiogenic, antitumor, and anti-invasive effects in preclinical models.",1233,0
+1234,"PURPOSE: XL184 (<< cabozantinib >>) is a potent inhibitor of MET, [[ vascular endothelial growth factor receptor 2 ]] (VEGFR2), and RET, with robust antiangiogenic, antitumor, and anti-invasive effects in preclinical models.",1234,0
+1235,"PURPOSE: << XL184 >> (cabozantinib) is a potent inhibitor of MET, vascular endothelial growth factor receptor 2 ([[ VEGFR2 ]]), and RET, with robust antiangiogenic, antitumor, and anti-invasive effects in preclinical models.",1235,0
+1236,"PURPOSE: << XL184 >> (cabozantinib) is a potent inhibitor of MET, vascular endothelial growth factor receptor 2 (VEGFR2), and [[ RET ]], with robust antiangiogenic, antitumor, and anti-invasive effects in preclinical models.",1236,0
+1237,"PURPOSE: << XL184 >> (cabozantinib) is a potent inhibitor of [[ MET ]], vascular endothelial growth factor receptor 2 (VEGFR2), and RET, with robust antiangiogenic, antitumor, and anti-invasive effects in preclinical models.",1237,0
+1238,"PURPOSE: << XL184 >> (cabozantinib) is a potent inhibitor of MET, [[ vascular endothelial growth factor receptor 2 ]] (VEGFR2), and RET, with robust antiangiogenic, antitumor, and anti-invasive effects in preclinical models.",1238,0
+1239,"Further, we used this model to test the efficacy of << GDC-0941 >>, a [[ PI3K ]] inhibitor, in clinical development, and showed that the tumors respond to PI3K inhibition.",1239,0
+1240,"Further, we used this model to test the efficacy of << GDC-0941 >>, a PI3K inhibitor, in clinical development, and showed that the tumors respond to [[ PI3K ]] inhibition.",1240,0
+1241,"Inhibitory effect of synthetic << progestins >>, 4-MA and cyanoketone on [[ human placental 3 beta-hydroxysteroid dehydrogenase/5----4-ene-isomerase ]] activity.",1241,0
+1242,"Inhibitory effect of synthetic progestins, << 4-MA >> and cyanoketone on [[ human placental 3 beta-hydroxysteroid dehydrogenase/5----4-ene-isomerase ]] activity.",1242,0
+1243,"Inhibitory effect of synthetic progestins, 4-MA and << cyanoketone >> on [[ human placental 3 beta-hydroxysteroid dehydrogenase/5----4-ene-isomerase ]] activity.",1243,0
+1244,"<< Human placental 3 beta-hydroxysteroid dehydrogenase/5----4-ene isomerase >> (3 beta-HSD) purified from human placenta transforms C-21 (pregnenolone and 17 alpha-hydroxy pregnenolone) as well as C-19 (dehydroepiandrosterone and androst-5-ene-3 beta, 17 beta-diol) steroids into the corresponding [[ 3-keto-4-ene-steroids ]] and is thus involved in the biosynthesis of all classes of hormonal steroids.",1244,4
+1245,"Human placental 3 beta-hydroxysteroid dehydrogenase/5----4-ene isomerase (<< 3 beta-HSD >>) purified from human placenta transforms C-21 (pregnenolone and 17 alpha-hydroxy pregnenolone) as well as C-19 (dehydroepiandrosterone and androst-5-ene-3 beta, 17 beta-diol) steroids into the corresponding [[ 3-keto-4-ene-steroids ]] and is thus involved in the biosynthesis of all classes of hormonal steroids.",1245,4
+1246,"<< Human placental 3 beta-hydroxysteroid dehydrogenase/5----4-ene isomerase >> (3 beta-HSD) purified from human placenta transforms C-21 ([[ pregnenolone ]] and 17 alpha-hydroxy pregnenolone) as well as C-19 (dehydroepiandrosterone and androst-5-ene-3 beta, 17 beta-diol) steroids into the corresponding 3-keto-4-ene-steroids and is thus involved in the biosynthesis of all classes of hormonal steroids.",1246,5
+1247,"Human placental 3 beta-hydroxysteroid dehydrogenase/5----4-ene isomerase (<< 3 beta-HSD >>) purified from human placenta transforms C-21 ([[ pregnenolone ]] and 17 alpha-hydroxy pregnenolone) as well as C-19 (dehydroepiandrosterone and androst-5-ene-3 beta, 17 beta-diol) steroids into the corresponding 3-keto-4-ene-steroids and is thus involved in the biosynthesis of all classes of hormonal steroids.",1247,5
+1248,"<< Human placental 3 beta-hydroxysteroid dehydrogenase/5----4-ene isomerase >> (3 beta-HSD) purified from human placenta transforms C-21 (pregnenolone and [[ 17 alpha-hydroxy pregnenolone ]]) as well as C-19 (dehydroepiandrosterone and androst-5-ene-3 beta, 17 beta-diol) steroids into the corresponding 3-keto-4-ene-steroids and is thus involved in the biosynthesis of all classes of hormonal steroids.",1248,5
+1249,"Human placental 3 beta-hydroxysteroid dehydrogenase/5----4-ene isomerase (<< 3 beta-HSD >>) purified from human placenta transforms C-21 (pregnenolone and [[ 17 alpha-hydroxy pregnenolone ]]) as well as C-19 (dehydroepiandrosterone and androst-5-ene-3 beta, 17 beta-diol) steroids into the corresponding 3-keto-4-ene-steroids and is thus involved in the biosynthesis of all classes of hormonal steroids.",1249,5
+1250,"<< Human placental 3 beta-hydroxysteroid dehydrogenase/5----4-ene isomerase >> (3 beta-HSD) purified from human placenta transforms C-21 (pregnenolone and 17 alpha-hydroxy pregnenolone) as well as C-19 ([[ dehydroepiandrosterone ]] and androst-5-ene-3 beta, 17 beta-diol) steroids into the corresponding 3-keto-4-ene-steroids and is thus involved in the biosynthesis of all classes of hormonal steroids.",1250,5
+1251,"Human placental 3 beta-hydroxysteroid dehydrogenase/5----4-ene isomerase (<< 3 beta-HSD >>) purified from human placenta transforms C-21 (pregnenolone and 17 alpha-hydroxy pregnenolone) as well as C-19 ([[ dehydroepiandrosterone ]] and androst-5-ene-3 beta, 17 beta-diol) steroids into the corresponding 3-keto-4-ene-steroids and is thus involved in the biosynthesis of all classes of hormonal steroids.",1251,5
+1252,"<< Human placental 3 beta-hydroxysteroid dehydrogenase/5----4-ene isomerase >> (3 beta-HSD) purified from human placenta transforms C-21 (pregnenolone and 17 alpha-hydroxy pregnenolone) as well as C-19 (dehydroepiandrosterone and [[ androst-5-ene-3 beta, 17 beta-diol ]]) steroids into the corresponding 3-keto-4-ene-steroids and is thus involved in the biosynthesis of all classes of hormonal steroids.",1252,5
+1253,"Human placental 3 beta-hydroxysteroid dehydrogenase/5----4-ene isomerase (<< 3 beta-HSD >>) purified from human placenta transforms C-21 (pregnenolone and 17 alpha-hydroxy pregnenolone) as well as C-19 (dehydroepiandrosterone and [[ androst-5-ene-3 beta, 17 beta-diol ]]) steroids into the corresponding 3-keto-4-ene-steroids and is thus involved in the biosynthesis of all classes of hormonal steroids.",1253,5
+1254,"<< Trilostane >>, epostane and cyanoketone are potent inhibitors of [[ 3 beta-HSD ]] with Ki values of approximately 50 nM.",1254,0
+1255,"Trilostane, << epostane >> and cyanoketone are potent inhibitors of [[ 3 beta-HSD ]] with Ki values of approximately 50 nM.",1255,0
+1256,"Trilostane, epostane and << cyanoketone >> are potent inhibitors of [[ 3 beta-HSD ]] with Ki values of approximately 50 nM.",1256,0
+1257,"<< 4-MA >>, a well known [[ 5 alpha-reductase ]] inhibitor, is also a potent inhibitor of 3 beta-HSD with a Ki value of 56 nM.",1257,0
+1258,"<< 4-MA >>, a well known 5 alpha-reductase inhibitor, is also a potent inhibitor of [[ 3 beta-HSD ]] with a Ki value of 56 nM.",1258,0
+1259,"<< Cyproterone acetate >>, a progestin used in the treatment of hirsutism, acne and prostate cancer as well as norgestrel and norethindrone that are widely used as oral contraceptives also inhibit [[ 3 beta-HSD ]] activity at Ki values of 1.5, 1.7 and 2.5 microM, respectively.",1259,0
+1260,"Cyproterone acetate, a << progestin >> used in the treatment of hirsutism, acne and prostate cancer as well as norgestrel and norethindrone that are widely used as oral contraceptives also inhibit [[ 3 beta-HSD ]] activity at Ki values of 1.5, 1.7 and 2.5 microM, respectively.",1260,0
+1261,"Cyproterone acetate, a progestin used in the treatment of hirsutism, acne and prostate cancer as well as << norgestrel >> and norethindrone that are widely used as oral contraceptives also inhibit [[ 3 beta-HSD ]] activity at Ki values of 1.5, 1.7 and 2.5 microM, respectively.",1261,0
+1262,"Cyproterone acetate, a progestin used in the treatment of hirsutism, acne and prostate cancer as well as norgestrel and << norethindrone >> that are widely used as oral contraceptives also inhibit [[ 3 beta-HSD ]] activity at Ki values of 1.5, 1.7 and 2.5 microM, respectively.",1262,0
+1263,"However, chronic treatment of cLH rats with << MPEP >> did not reverse learned helplessness, indicating that the enhanced [[ mGlu5 receptor ]] function is not the only player in the behavioral phenotype of this genetic model of depression.",1263,9
+1264,"Rescue of this impaired extinction consolidation/retrieval was achieved with d-cycloserine (N-methly-d-aspartate partial agonist) or << MS-275 >> ([[ histone deacetylase ]] (HDAC) inhibitor), applied after extinction training.",1264,0
+1265,"Rescue of this impaired extinction consolidation/retrieval was achieved with d-cycloserine (N-methly-d-aspartate partial agonist) or << MS-275 >> (histone deacetylase ([[ HDAC ]]) inhibitor), applied after extinction training.",1265,0
+1266,"Rescue of both impaired extinction acquisition and deficient extinction consolidation/retrieval was achieved with prior extinction training administration of valproic acid (a GABAergic enhancer and HDAC inhibitor) or AMN082 [metabotropic glutamate receptor 7 (mGlu7) agonist], while << MS-275 >> or PEPA ([[ AMPA receptor ]] potentiator) failed to affect extinction acquisition in S1 mice.",1266,9
+1267,"Rescue of both impaired extinction acquisition and deficient extinction consolidation/retrieval was achieved with prior extinction training administration of valproic acid (a GABAergic enhancer and HDAC inhibitor) or AMN082 [metabotropic glutamate receptor 7 (mGlu7) agonist], while MS-275 or << PEPA >> ([[ AMPA receptor ]] potentiator) failed to affect extinction acquisition in S1 mice.",1267,9
+1268,"Rescue of both impaired extinction acquisition and deficient extinction consolidation/retrieval was achieved with prior extinction training administration of << valproic acid >> (a GABAergic enhancer and [[ HDAC ]] inhibitor) or AMN082 [metabotropic glutamate receptor 7 (mGlu7) agonist], while MS-275 or PEPA (AMPA receptor potentiator) failed to affect extinction acquisition in S1 mice.",1268,0
+1269,"Rescue of both impaired extinction acquisition and deficient extinction consolidation/retrieval was achieved with prior extinction training administration of valproic acid (a GABAergic enhancer and HDAC inhibitor) or << AMN082 >> [[[ metabotropic glutamate receptor 7 ]] (mGlu7) agonist], while MS-275 or PEPA (AMPA receptor potentiator) failed to affect extinction acquisition in S1 mice.",1269,2
+1270,"Rescue of both impaired extinction acquisition and deficient extinction consolidation/retrieval was achieved with prior extinction training administration of valproic acid (a GABAergic enhancer and HDAC inhibitor) or << AMN082 >> [metabotropic glutamate receptor 7 ([[ mGlu7 ]]) agonist], while MS-275 or PEPA (AMPA receptor potentiator) failed to affect extinction acquisition in S1 mice.",1270,2
+1271,Electroencephalographic recordings during substance consumption showed reduced alpha activity and << P300 >> latencies in the [[ nicotine ]] group compared to the control group.,1271,8
+1272,These findings suggest that oral consumption of << nicotine >> enhances the efficacy of [[ nicotinic acetylcholine receptors ]].,1272,6
+1273,Toxicity profile of small-molecule << IAP >> antagonist [[ GDC-0152 ]] is linked to TNF-α pharmacology.,1273,1
+1274,<< GDC-0152 >> is a small-molecule drug that triggers tumor cell apoptosis by selectively antagonizing [[ IAPs ]].,1274,1
+1275,"<< GDC-0152 >> induces [[ NF-κB ]] transcriptional activity leading to expression of several chemokines and cytokines, of which tumor necrosis factor alpha (TNF-α) is the most important for single-agent tumor activity.",1275,9
+1276,"The << PARP >> inhibitor [[ PJ34 ]] modifies proliferation, NIS expression and epigenetic marks in thyroid cancer cell lines.",1276,0
+1277,"Since PARP-1 is supposed to be part of a multimeric repressor of sodium iodide symporter (NIS) expression, in this study the effect of the << PARP >> inhibitor [[ PJ34 ]] on several properties of thyroid cancer cell lines was investigated.",1277,0
+1278,"In TPC1, BCPAP, FRO, WRO cell lines << PJ34 >> induced a strong increase in [[ NIS ]] mRNA levels.",1278,6
+1279,"Accordingly, in transfection experiments performed in TPC1 cells, treatment with << PJ34 >> increased [[ NIS promoter ]] activity without affecting PARP-1 binding to the promoter sequence.",1279,9
+1280,"We also investigated the epigenetic status of NIS promoter after << PJ34 >> treatment in TPC1 cell line: in addition to an increase of [[ histone modification activation marks ]] (H3K9K14ac, H3K4me3), surprisingly we observed also an increase of H3K27me3, a classical repressive mark.",1280,6
+1281,"We also investigated the epigenetic status of NIS promoter after << PJ34 >> treatment in TPC1 cell line: in addition to an increase of histone modification activation marks ([[ H3K9K14ac ]], H3K4me3), surprisingly we observed also an increase of H3K27me3, a classical repressive mark.",1281,6
+1282,"We also investigated the epigenetic status of NIS promoter after << PJ34 >> treatment in TPC1 cell line: in addition to an increase of histone modification activation marks (H3K9K14ac, [[ H3K4me3 ]]), surprisingly we observed also an increase of H3K27me3, a classical repressive mark.",1282,6
+1283,"Both << apo-lycopenoic acids >> also decreased CSE-induced ROS production, 8-OHdG formation and reduced the increase in [[ NOX-4 ]] and COX-2 expressions caused by CSE.",1283,8
+1284,"Both << apo-lycopenoic acids >> also decreased CSE-induced ROS production, 8-OHdG formation and reduced the increase in NOX-4 and [[ COX-2 ]] expressions caused by CSE.",1284,8
+1285,"Recent studies, however, have demonstrated a promising potential treatment option with the help of the serum enzyme << butyrylcholinesterase >> (BChE), which is capable of breaking down naturally occurring [[ (-)-cocaine ]] before the drug can influence the reward centers of the brain or affect other areas of the body.",1285,5
+1286,"Recent studies, however, have demonstrated a promising potential treatment option with the help of the serum enzyme butyrylcholinesterase (<< BChE >>), which is capable of breaking down naturally occurring [[ (-)-cocaine ]] before the drug can influence the reward centers of the brain or affect other areas of the body.",1286,5
+1287,This prompted the design of variants of << BChE >> which exhibit significantly improved catalytic activity against [[ (-)-cocaine ]].,1287,5
+1288,"Here, in expressing << cocaine >>-hydrolyzing mutants of [[ BChE ]] in Nicotiana benthamiana using the MagnICON virus-assisted transient expression system, and in reporting their initial biochemical analysis, we provide proof-of-principle that plants can express engineered BChE proteins with desired properties.",1288,5
+1289,"We examined in cats the 1) ulcerogenic effects of selective << COX-1 >> ([[ SC-560 ]], ketorolac) and COX-2 (celecoxib, meloxicam) inhibitors on the gastrointestinal mucosa, 2) effect of feeding and cimetidine on the expression of COX isoforms and prostaglandin E(2) (PGE(2)) level in the duodenum, and 3) localization of COX isoforms in the duodenum.",1289,0
+1290,"We examined in cats the 1) ulcerogenic effects of selective << COX-1 >> (SC-560, [[ ketorolac ]]) and COX-2 (celecoxib, meloxicam) inhibitors on the gastrointestinal mucosa, 2) effect of feeding and cimetidine on the expression of COX isoforms and prostaglandin E(2) (PGE(2)) level in the duodenum, and 3) localization of COX isoforms in the duodenum.",1290,0
+1291,"We examined in cats the 1) ulcerogenic effects of selective COX-1 (SC-560, ketorolac) and << COX-2 >> ([[ celecoxib ]], meloxicam) inhibitors on the gastrointestinal mucosa, 2) effect of feeding and cimetidine on the expression of COX isoforms and prostaglandin E(2) (PGE(2)) level in the duodenum, and 3) localization of COX isoforms in the duodenum.",1291,0
+1292,"We examined in cats the 1) ulcerogenic effects of selective COX-1 (SC-560, ketorolac) and << COX-2 >> (celecoxib, [[ meloxicam ]]) inhibitors on the gastrointestinal mucosa, 2) effect of feeding and cimetidine on the expression of COX isoforms and prostaglandin E(2) (PGE(2)) level in the duodenum, and 3) localization of COX isoforms in the duodenum.",1292,0
+1293,"Second, feeding increased both the expression of << COX >> isoforms and PGE(2) level in the duodenum, and the effects were markedly inhibited by pretreatment with [[ cimetidine ]].",1293,8
+1294,Reversal of inhibition by << D2 >> agonist quinpirole was produced by serotonin (50 µM) and by [[ neurotensin ]] (5-10 nM).,1294,9
+1295,Reversal of inhibition by << D2 >> agonist quinpirole was produced by [[ serotonin ]] (50 µM) and by neurotensin (5-10 nM).,1295,9
+1296,Reversal of inhibition by << D2 >> agonist [[ quinpirole ]] was produced by serotonin (50 µM) and by neurotensin (5-10 nM).,1296,2
+1297,"Serotonin-induced or neurotensin-induced reversal was blocked by β-ARK1 inhibitor, dynasore, or << cPKC >> antagonist [[ 5,6,7,13-tetrahydro-13-methyl-5-oxo-12H-indolo[2,3-a]pyrrolo[3,4c]carbazole-12-propanenitrile ]] (Gö6976).",1297,1
+1298,"Serotonin-induced or neurotensin-induced reversal was blocked by β-ARK1 inhibitor, dynasore, or << cPKC >> antagonist 5,6,7,13-tetrahydro-13-methyl-5-oxo-12H-indolo[2,3-a]pyrrolo[3,4c]carbazole-12-propanenitrile ([[ Gö6976 ]]).",1298,1
+1299,"<< RSV >> targets and activates the [[ NAD(+)-dependent protein deacetylase SIRT1 ]]; in turn, SIRT1 induces an intracellular antioxidative mechanism by inducing mitochondrial superoxide dismutase (SOD2).",1299,9
+1300,"<< RSV >> targets and activates the NAD(+)-dependent protein deacetylase SIRT1; in turn, [[ SIRT1 ]] induces an intracellular antioxidative mechanism by inducing mitochondrial superoxide dismutase (SOD2).",1300,9
+1301,"<< RSV >> targets and activates the NAD(+)-dependent protein deacetylase SIRT1; in turn, SIRT1 induces an intracellular antioxidative mechanism by inducing [[ mitochondrial superoxide dismutase ]] (SOD2).",1301,6
+1302,"<< RSV >> targets and activates the NAD(+)-dependent protein deacetylase SIRT1; in turn, SIRT1 induces an intracellular antioxidative mechanism by inducing mitochondrial superoxide dismutase ([[ SOD2 ]]).",1302,6
+1303,"However, << 4'G-RSV >>, but not 3G-RSV, induced [[ SIRT1 ]]-dependent histone H3 deacetylation and SOD2 expression in mouse C2C12 skeletal myoblasts; as with RSV, SIRT1 knockdown blunted these effects.",1303,9
+1304,"However, << 4'G-RSV >>, but not 3G-RSV, induced SIRT1-dependent histone H3 deacetylation and [[ SOD2 ]] expression in mouse C2C12 skeletal myoblasts; as with RSV, SIRT1 knockdown blunted these effects.",1304,6
+1305,Hydrophobic amino acids in the hinge region of the 5A apolipoprotein mimetic peptide are essential for promoting << cholesterol >> efflux by the [[ ABCA1 ]] transporter.,1305,5
+1306,The bihelical << apolipoprotein mimetic peptide 5A >> effluxes [[ cholesterol ]] from cells and reduces inflammation and atherosclerosis in animal models.,1306,5
+1307,"Compared with active peptides containing F or W, peptides containing E in either of these two positions were more than 10-fold less effective in effluxing << cholesterol >> by the [[ ABCA1 ]] transporter.",1307,5
+1308,These results provide a rationale for future design of therapeutic apolipoprotein mimetic peptides and provide new insights into the interaction of hydrophobic residues on apolipoproteins with phospholipids in the lipid microdomain created by the << ABCA1 >> transporter during the [[ cholesterol ]] efflux process.,1308,5
+1309,Efficacy of the << GluK1 >>/AMPA receptor antagonist [[ LY293558 ]] against seizures and neuropathology in a soman-exposure model without pretreatment and its pharmacokinetics after intramuscular administration.,1309,1
+1310,Efficacy of the GluK1/<< AMPA receptor >> antagonist [[ LY293558 ]] against seizures and neuropathology in a soman-exposure model without pretreatment and its pharmacokinetics after intramuscular administration.,1310,1
+1311,"To determine if control of seizures and survival are still possible without pretreatment or immediate pharmacologic intervention, we studied the anticonvulsant efficacy of the << GluK1 >> (GluR5)/α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist [[ (3S,4aR,6R,8aR)-6-[2-(1(2)H-tetrazole-5-yl)ethyl]decahydroisoquinoline-3-carboxylic acid ]] (LY293558) in rats that did not receive any treatment until 20 minutes after exposure to the nerve agent soman.",1311,1
+1312,"To determine if control of seizures and survival are still possible without pretreatment or immediate pharmacologic intervention, we studied the anticonvulsant efficacy of the GluK1 (<< GluR5 >>)/α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist [[ (3S,4aR,6R,8aR)-6-[2-(1(2)H-tetrazole-5-yl)ethyl]decahydroisoquinoline-3-carboxylic acid ]] (LY293558) in rats that did not receive any treatment until 20 minutes after exposure to the nerve agent soman.",1312,1
+1313,"To determine if control of seizures and survival are still possible without pretreatment or immediate pharmacologic intervention, we studied the anticonvulsant efficacy of the GluK1 (GluR5)/<< α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor >> antagonist [[ (3S,4aR,6R,8aR)-6-[2-(1(2)H-tetrazole-5-yl)ethyl]decahydroisoquinoline-3-carboxylic acid ]] (LY293558) in rats that did not receive any treatment until 20 minutes after exposure to the nerve agent soman.",1313,1
+1314,"To determine if control of seizures and survival are still possible without pretreatment or immediate pharmacologic intervention, we studied the anticonvulsant efficacy of the << GluK1 >> (GluR5)/α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist (3S,4aR,6R,8aR)-6-[2-(1(2)H-tetrazole-5-yl)ethyl]decahydroisoquinoline-3-carboxylic acid ([[ LY293558 ]]) in rats that did not receive any treatment until 20 minutes after exposure to the nerve agent soman.",1314,1
+1315,"To determine if control of seizures and survival are still possible without pretreatment or immediate pharmacologic intervention, we studied the anticonvulsant efficacy of the GluK1 (<< GluR5 >>)/α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist (3S,4aR,6R,8aR)-6-[2-(1(2)H-tetrazole-5-yl)ethyl]decahydroisoquinoline-3-carboxylic acid ([[ LY293558 ]]) in rats that did not receive any treatment until 20 minutes after exposure to the nerve agent soman.",1315,1
+1316,"To determine if control of seizures and survival are still possible without pretreatment or immediate pharmacologic intervention, we studied the anticonvulsant efficacy of the GluK1 (GluR5)/<< α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor >> antagonist (3S,4aR,6R,8aR)-6-[2-(1(2)H-tetrazole-5-yl)ethyl]decahydroisoquinoline-3-carboxylic acid ([[ LY293558 ]]) in rats that did not receive any treatment until 20 minutes after exposure to the nerve agent soman.",1316,1
+1317,"Although acetylcholinesterase (<< AChE >>) is primarily a hydrolytic enzyme, metabolising the neurotransmitter [[ acetylcholine ]] in cholinergic synapses, it also has some non-catalytic functions in the brain which are far less well characterised.",1317,5
+1318,"Although << acetylcholinesterase >> (AChE) is primarily a hydrolytic enzyme, metabolising the neurotransmitter [[ acetylcholine ]] in cholinergic synapses, it also has some non-catalytic functions in the brain which are far less well characterised.",1318,5
+1319,"Cellular release of << AChE >> by SH-SY5Y is significantly enhanced by the muscarinic acetylcholine receptor (mAChR) agonists [[ carbachol ]] or muscarine, with the effect of carbachol blocked by the mAChR antagonist atropine.",1319,6
+1320,"Cellular release of << AChE >> by SH-SY5Y is significantly enhanced by the muscarinic acetylcholine receptor (mAChR) agonists carbachol or [[ muscarine ]], with the effect of carbachol blocked by the mAChR antagonist atropine.",1320,6
+1321,"Cellular release of << AChE >> by SH-SY5Y is significantly enhanced by the muscarinic acetylcholine receptor (mAChR) agonists carbachol or muscarine, with the effect of [[ carbachol ]] blocked by the mAChR antagonist atropine.",1321,6
+1322,"Cellular release of << AChE >> by SH-SY5Y is significantly enhanced by the muscarinic acetylcholine receptor (mAChR) agonists carbachol or muscarine, with the effect of carbachol blocked by the mAChR antagonist [[ atropine ]].",1322,8
+1323,"Cellular release of AChE by SH-SY5Y is significantly enhanced by the << muscarinic acetylcholine receptor >> (mAChR) agonists [[ carbachol ]] or muscarine, with the effect of carbachol blocked by the mAChR antagonist atropine.",1323,2
+1324,"Cellular release of AChE by SH-SY5Y is significantly enhanced by the muscarinic acetylcholine receptor (<< mAChR >>) agonists [[ carbachol ]] or muscarine, with the effect of carbachol blocked by the mAChR antagonist atropine.",1324,2
+1325,"Cellular release of AChE by SH-SY5Y is significantly enhanced by the << muscarinic acetylcholine receptor >> (mAChR) agonists carbachol or [[ muscarine ]], with the effect of carbachol blocked by the mAChR antagonist atropine.",1325,2
+1326,"Cellular release of AChE by SH-SY5Y is significantly enhanced by the muscarinic acetylcholine receptor (<< mAChR >>) agonists carbachol or [[ muscarine ]], with the effect of carbachol blocked by the mAChR antagonist atropine.",1326,2
+1327,"Cellular release of AChE by SH-SY5Y is significantly enhanced by the muscarinic acetylcholine receptor (mAChR) agonists carbachol or muscarine, with the effect of carbachol blocked by the << mAChR >> antagonist [[ atropine ]].",1327,1
+1328,<< L-BMAA >> induced ER stress and enhanced [[ caspase 12 ]] cleavage in human neuroblastoma SH-SY5Y cells at low nonexcitotoxic concentrations.,1328,6
+1329,"Nevertheless, low << L-BMAA >> concentrations (≥ 0.1mM, 48 h) increased protein ubiquitination, [[ 20S proteasomal ]] and caspase 12 activity, expression of the endoplasmic reticulum (ER) stress marker CHOP, and enhanced phosphorylation of elf2α in SH-SY5Y cells.",1329,9
+1330,"Nevertheless, low << L-BMAA >> concentrations (≥ 0.1mM, 48 h) increased protein ubiquitination, 20S proteasomal and [[ caspase 12 ]] activity, expression of the endoplasmic reticulum (ER) stress marker CHOP, and enhanced phosphorylation of elf2α in SH-SY5Y cells.",1330,9
+1331,"Nevertheless, low << L-BMAA >> concentrations (≥ 0.1mM, 48 h) increased protein ubiquitination, 20S proteasomal and caspase 12 activity, expression of the endoplasmic reticulum (ER) stress marker CHOP, and enhanced phosphorylation of [[ elf2α ]] in SH-SY5Y cells.",1331,9
+1332,"Nevertheless, low << L-BMAA >> concentrations (≥ 0.1mM, 48 h) increased protein ubiquitination, 20S proteasomal and caspase 12 activity, expression of the endoplasmic reticulum (ER) stress marker [[ CHOP ]], and enhanced phosphorylation of elf2α in SH-SY5Y cells.",1332,6
+1333,<< Ribavirin >>-induced intracellular GTP depletion activates transcription elongation in [[ coagulation factor VII ]] gene expression.,1333,6
+1334,"It was reported previously that << FVII >> gene (F7) expression was up-regulated by [[ ribavirin ]] treatment in hepatitis C virus-infected haemophilia patients; however, its precise mechanism is still unknown.",1334,6
+1335,"It was reported previously that FVII gene (<< F7 >>) expression was up-regulated by [[ ribavirin ]] treatment in hepatitis C virus-infected haemophilia patients; however, its precise mechanism is still unknown.",1335,6
+1336,"In the present study, we investigated the molecular mechanism of << ribavirin >>-induced up-regulation of [[ F7 ]] expression in HepG2 (human hepatoma cell line).",1336,6
+1337,"We found that intracellular GTP depletion by ribavirin as well as other IMPDH (inosine-5'-monophosphate dehydrogenase) inhibitors, such as << mycophenolic acid >> and 6-mercaptopurine, up-regulated [[ F7 ]] expression.",1337,6
+1338,"We found that intracellular GTP depletion by ribavirin as well as other IMPDH (inosine-5'-monophosphate dehydrogenase) inhibitors, such as mycophenolic acid and << 6-mercaptopurine >>, up-regulated [[ F7 ]] expression.",1338,6
+1339,<< Ribavirin >> unregulated [[ ELL ]] (eleven-nineteen lysine-rich leukaemia) 3 mRNA expression before F7 up-regulation.,1339,6
+1340,<< Ribavirin >> unregulated ELL ([[ eleven-nineteen lysine-rich leukaemia) 3 ]] mRNA expression before F7 up-regulation.,1340,6
+1341,<< Ribavirin >> unregulated ELL (eleven-nineteen lysine-rich leukaemia) 3 mRNA expression before [[ F7 ]] up-regulation.,1341,6
+1342,"We observed that << ribavirin >> enhanced [[ ELL3 ]] recruitment to F7, whereas knockdown of ELL3 diminished ribavirin-induced FVII mRNA up-regulation.",1342,6
+1343,"We observed that << ribavirin >> enhanced ELL3 recruitment to [[ F7 ]], whereas knockdown of ELL3 diminished ribavirin-induced FVII mRNA up-regulation.",1343,6
+1344,"We observed that ribavirin enhanced ELL3 recruitment to F7, whereas knockdown of ELL3 diminished << ribavirin >>-induced [[ FVII ]] mRNA up-regulation.",1344,6
+1345,<< Ribavirin >> also enhanced recruitment of [[ CDK9 ]] (cyclin-dependent kinase 9) and AFF4 to F7.,1345,6
+1346,<< Ribavirin >> also enhanced recruitment of CDK9 ([[ cyclin-dependent kinase 9 ]]) and AFF4 to F7.,1346,6
+1347,<< Ribavirin >> also enhanced recruitment of CDK9 (cyclin-dependent kinase 9) and [[ AFF4 ]] to F7.,1347,6
+1348,<< Ribavirin >> also enhanced recruitment of CDK9 (cyclin-dependent kinase 9) and AFF4 to [[ F7 ]].,1348,6
+1349,"These data suggest that << ribavirin >>-induced intracellular GTP depletion recruits a super elongation complex containing [[ P-TEFb ]], AFF4 and ELL3, to F7, and modulates FVII mRNA transcription elongation.",1349,6
+1350,"These data suggest that << ribavirin >>-induced intracellular GTP depletion recruits a super elongation complex containing P-TEFb, [[ AFF4 ]] and ELL3, to F7, and modulates FVII mRNA transcription elongation.",1350,6
+1351,"These data suggest that << ribavirin >>-induced intracellular GTP depletion recruits a super elongation complex containing P-TEFb, AFF4 and [[ ELL3 ]], to F7, and modulates FVII mRNA transcription elongation.",1351,6
+1352,"These data suggest that << ribavirin >>-induced intracellular GTP depletion recruits a super elongation complex containing P-TEFb, AFF4 and ELL3, to [[ F7 ]], and modulates FVII mRNA transcription elongation.",1352,6
+1353,"Collectively, we have elucidated a basal mechanism for << ribavirin >>-induced [[ FVII ]] mRNA up-regulation by acceleration of transcription elongation, which may be crucial in understanding its pleiotropic functions in vivo.",1353,6
+1354,"The potentiation of heteromeric << KARs >> by mGlu1 activation was attenuated by GDPβS, blocked by an inhibitor of phospholipase C or the calcium chelator [[ 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid ]] (BAPTA), prolonged by the phosphatase inhibitor okadaic acid, but unaffected by the tyrosine kinase inhibitor lavendustin A.",1354,0
+1355,"The potentiation of heteromeric KARs by << mGlu1 >> activation was attenuated by GDPβS, blocked by an inhibitor of phospholipase C or the calcium chelator [[ 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid ]] (BAPTA), prolonged by the phosphatase inhibitor okadaic acid, but unaffected by the tyrosine kinase inhibitor lavendustin A.",1355,0
+1356,"The potentiation of heteromeric << KARs >> by mGlu1 activation was attenuated by GDPβS, blocked by an inhibitor of phospholipase C or the calcium chelator 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid ([[ BAPTA ]]), prolonged by the phosphatase inhibitor okadaic acid, but unaffected by the tyrosine kinase inhibitor lavendustin A.",1356,0
+1357,"The potentiation of heteromeric KARs by << mGlu1 >> activation was attenuated by GDPβS, blocked by an inhibitor of phospholipase C or the calcium chelator 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid ([[ BAPTA ]]), prolonged by the phosphatase inhibitor okadaic acid, but unaffected by the tyrosine kinase inhibitor lavendustin A.",1357,0
+1358,"The potentiation of heteromeric KARs by mGlu1 activation was attenuated by GDPβS, blocked by an inhibitor of phospholipase C or the calcium chelator 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), prolonged by the << phosphatase >> inhibitor [[ okadaic acid ]], but unaffected by the tyrosine kinase inhibitor lavendustin A.",1358,0
+1359,"The potentiation of heteromeric << KARs >> by mGlu1 activation was attenuated by GDPβS, blocked by an inhibitor of phospholipase C or the calcium chelator 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), prolonged by the phosphatase inhibitor [[ okadaic acid ]], but unaffected by the tyrosine kinase inhibitor lavendustin A.",1359,0
+1360,"The potentiation of heteromeric KARs by << mGlu1 >> activation was attenuated by GDPβS, blocked by an inhibitor of phospholipase C or the calcium chelator 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), prolonged by the phosphatase inhibitor [[ okadaic acid ]], but unaffected by the tyrosine kinase inhibitor lavendustin A.",1360,0
+1361,"The potentiation of heteromeric KARs by mGlu1 activation was attenuated by GDPβS, blocked by an inhibitor of phospholipase C or the calcium chelator 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), prolonged by the phosphatase inhibitor okadaic acid, but unaffected by the << tyrosine kinase >> inhibitor [[ lavendustin A ]].",1361,0
+1362,"The potentiation of heteromeric << KARs >> by mGlu1 activation was attenuated by GDPβS, blocked by an inhibitor of phospholipase C or the calcium chelator 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), prolonged by the phosphatase inhibitor okadaic acid, but unaffected by the tyrosine kinase inhibitor [[ lavendustin A ]].",1362,0
+1363,"The potentiation of heteromeric KARs by << mGlu1 >> activation was attenuated by GDPβS, blocked by an inhibitor of phospholipase C or the calcium chelator 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), prolonged by the phosphatase inhibitor okadaic acid, but unaffected by the tyrosine kinase inhibitor [[ lavendustin A ]].",1363,0
+1364,"Protein kinase C (PKC) inhibition reduced the potentiation by mGlu1 of GluK2/GluK5, and conversely, direct activation of << PKC >> by [[ phorbol 12-myristate,13-acetate ]] potentiated GluK2/GluK5.",1364,9
+1365,"Protein kinase C (PKC) inhibition reduced the potentiation by mGlu1 of GluK2/GluK5, and conversely, direct activation of PKC by << phorbol 12-myristate,13-acetate >> potentiated [[ GluK2 ]]/GluK5.",1365,9
+1366,"Protein kinase C (PKC) inhibition reduced the potentiation by mGlu1 of GluK2/GluK5, and conversely, direct activation of PKC by << phorbol 12-myristate,13-acetate >> potentiated GluK2/[[ GluK5 ]].",1366,9
+1367,"<< Fingolimod >> (FTY720), a novel drug approved for the treatment of relapsing-remitting multiple sclerosis, activates different [[ sphingosine-1-phosphate receptor ]] (S1PR) subtypes.",1367,9
+1368,"<< Fingolimod >> (FTY720), a novel drug approved for the treatment of relapsing-remitting multiple sclerosis, activates different sphingosine-1-phosphate receptor ([[ S1PR ]]) subtypes.",1368,9
+1369,"Fingolimod (<< FTY720 >>), a novel drug approved for the treatment of relapsing-remitting multiple sclerosis, activates different [[ sphingosine-1-phosphate receptor ]] (S1PR) subtypes.",1369,9
+1370,"Fingolimod (<< FTY720 >>), a novel drug approved for the treatment of relapsing-remitting multiple sclerosis, activates different sphingosine-1-phosphate receptor ([[ S1PR ]]) subtypes.",1370,9
+1371,"Neuroprotection was attenuated by pertussis toxin, and inhibited by the selective << type-1 S1PR >> (S1P1R) antagonist, [[ W146 ]], and by inhibitors of the mitogen associated protein kinase (MAPK) and the phosphatidylinositol-3-kinase (PtdIns-3-K) pathways.",1371,1
+1372,"Neuroprotection was attenuated by pertussis toxin, and inhibited by the selective type-1 S1PR (<< S1P1R >>) antagonist, [[ W146 ]], and by inhibitors of the mitogen associated protein kinase (MAPK) and the phosphatidylinositol-3-kinase (PtdIns-3-K) pathways.",1372,1
+1373,"Pharmacokinetics and metabolism of << [(14)C]anagliptin >>, a novel [[ dipeptidyl peptidase-4 ]] inhibitor, in humans.",1373,0
+1374,"1. The disposition of << anagliptin >>, an orally active, highly selective [[ dipeptidyl peptidase-4 ]] inhibitor, was investigated after a single oral dose of 100 mg/1.92 MBq [(14)C]anagliptin to six healthy men.",1374,0
+1375,"Renal clearance of unbound anagliptin and unbound M1 far exceeded glomerular filtration rate, indicating active renal elimination: that might reflect the fact that << anagliptin >> may be a substrate of [[ OAT1 ]], OAT3, MDR1 and MRP2, and M1 a substrate of OAT3, BCRP, MRP2 and MRP4.",1375,5
+1376,"Renal clearance of unbound anagliptin and unbound M1 far exceeded glomerular filtration rate, indicating active renal elimination: that might reflect the fact that << anagliptin >> may be a substrate of OAT1, [[ OAT3 ]], MDR1 and MRP2, and M1 a substrate of OAT3, BCRP, MRP2 and MRP4.",1376,5
+1377,"Renal clearance of unbound anagliptin and unbound M1 far exceeded glomerular filtration rate, indicating active renal elimination: that might reflect the fact that << anagliptin >> may be a substrate of OAT1, OAT3, [[ MDR1 ]] and MRP2, and M1 a substrate of OAT3, BCRP, MRP2 and MRP4.",1377,5
+1378,"Renal clearance of unbound anagliptin and unbound M1 far exceeded glomerular filtration rate, indicating active renal elimination: that might reflect the fact that << anagliptin >> may be a substrate of OAT1, OAT3, MDR1 and [[ MRP2 ]], and M1 a substrate of OAT3, BCRP, MRP2 and MRP4.",1378,5
+1379,Antiretroviral << protease >> inhibitors [[ lopinavir ]] (LPV) and ritonavir (RTV) are reported BSEP inhibitors.,1379,0
+1380,Antiretroviral protease inhibitors << lopinavir >> (LPV) and ritonavir (RTV) are reported [[ BSEP ]] inhibitors.,1380,0
+1381,Antiretroviral << protease >> inhibitors lopinavir ([[ LPV ]]) and ritonavir (RTV) are reported BSEP inhibitors.,1381,0
+1382,Antiretroviral protease inhibitors lopinavir (<< LPV >>) and ritonavir (RTV) are reported [[ BSEP ]] inhibitors.,1382,0
+1383,Antiretroviral << protease >> inhibitors lopinavir (LPV) and [[ ritonavir ]] (RTV) are reported BSEP inhibitors.,1383,0
+1384,Antiretroviral protease inhibitors lopinavir (LPV) and << ritonavir >> (RTV) are reported [[ BSEP ]] inhibitors.,1384,0
+1385,Antiretroviral << protease >> inhibitors lopinavir (LPV) and ritonavir ([[ RTV ]]) are reported BSEP inhibitors.,1385,0
+1386,Antiretroviral protease inhibitors lopinavir (LPV) and ritonavir (<< RTV >>) are reported [[ BSEP ]] inhibitors.,1386,0
+1387,<< GHRP-6 >> is a [[ growth hormone ]] secretagogue that also enhances tissue viability in different organs.,1387,6
+1388,"The altered activities of key enzymes such as << glucose-6-phosphatase >> and fructose-1,6-bisphosphatase of [[ carbohydrate ]] metabolism significantly (p<0.05) increased whereas hexokinase, pyruvate kinase, glucose-6-phosphate dehydrogenase and glycogen content significantly (p<0.05) decreased in the liver of diabetic rats and also increased activities of aspartate transaminase (AST), alanine transaminase (ALT) and alkaline phosphatase (ALP).",1388,4
+1389,"The altered activities of key enzymes such as glucose-6-phosphatase and << fructose-1,6-bisphosphatase >> of [[ carbohydrate ]] metabolism significantly (p<0.05) increased whereas hexokinase, pyruvate kinase, glucose-6-phosphate dehydrogenase and glycogen content significantly (p<0.05) decreased in the liver of diabetic rats and also increased activities of aspartate transaminase (AST), alanine transaminase (ALT) and alkaline phosphatase (ALP).",1389,4
+1390,<< Ibandronate >> increases the expression of the pro-apoptotic gene [[ FAS ]] by epigenetic mechanisms in tumor cells.,1390,6
+1391,"Further we found stimulation of FAS-expression as a result of epigenetic DNA demethylation that was due to down-regulation of << DNMT1 >>, which was rescued by re-isoprenylation by both [[ geranylgeranyl-pyrophosphate ]] and farnesylpyrophosphate.",1391,7
+1392,"Further we found stimulation of FAS-expression as a result of epigenetic DNA demethylation that was due to down-regulation of << DNMT1 >>, which was rescued by re-isoprenylation by both geranylgeranyl-pyrophosphate and [[ farnesylpyrophosphate ]].",1392,7
+1393,Data suggest that << bisphosphonates >> via modulation of the activity of small-GTPases induce apoptosis in neoplastic cells by DNA-CpG-demethylation and stimulation of [[ FAS ]]-expression.,1393,6
+1394,"The AhR target gene << CYP1A1 >> mRNA expression was induced by [[ TCDD ]], but was not affected by the AR CAG length.",1394,6
+1395,"TCDD had no effect on AR activity in PC-3 cells, whereas the shortest << AR >> variant was induced by [[ TCDD ]] in PNT1A cells.",1395,9
+1396,"Systemic injection to mice of siRNA lipoplexes, rather than of cationic liposome, triggered a production of several cytokines in mice and replacement of plasmid by << polyglutamate >> reduced the elevation of all assayed [[ cytokines ]].",1396,3
+1397,"We found that << helenalin >> markedly induced endoplasmic reticulum (ER) stress-related genes, such as [[ regulated in development and DNA damage responses (REDD) 1 ]], activating transcription factor-4 (ATF4) and/or the CCAAT enhancer-binding protein-homologous protein (CHOP).",1397,6
+1398,"We found that << helenalin >> markedly induced endoplasmic reticulum (ER) stress-related genes, such as regulated in development and DNA damage responses (REDD) 1, [[ activating transcription factor-4 ]] (ATF4) and/or the CCAAT enhancer-binding protein-homologous protein (CHOP).",1398,6
+1399,"We found that << helenalin >> markedly induced endoplasmic reticulum (ER) stress-related genes, such as regulated in development and DNA damage responses (REDD) 1, activating transcription factor-4 ([[ ATF4 ]]) and/or the CCAAT enhancer-binding protein-homologous protein (CHOP).",1399,6
+1400,"We found that << helenalin >> markedly induced endoplasmic reticulum (ER) stress-related genes, such as regulated in development and DNA damage responses (REDD) 1, activating transcription factor-4 (ATF4) and/or the [[ CCAAT enhancer-binding protein-homologous protein ]] (CHOP).",1400,6
+1401,"We found that << helenalin >> markedly induced endoplasmic reticulum (ER) stress-related genes, such as regulated in development and DNA damage responses (REDD) 1, activating transcription factor-4 (ATF4) and/or the CCAAT enhancer-binding protein-homologous protein ([[ CHOP ]]).",1401,6
+1402,Contributions of << rat Ctr1 >> to the uptake and toxicity of [[ copper ]] and platinum anticancer drugs in dorsal root ganglion neurons.,1402,5
+1403,Contributions of << rat Ctr1 >> to the uptake and toxicity of copper and [[ platinum ]] anticancer drugs in dorsal root ganglion neurons.,1403,5
+1404,"Heterologous expression of << rCtr1 >> in HEK293 cells (HEK/rCtr1 cells) increased the uptake and cytotoxicity of [[ copper ]], oxaliplatin, cisplatin and carboplatin, in comparison to isogenic vector-transfected control cells.",1404,5
+1405,"Heterologous expression of rCtr1 in HEK293 cells (HEK/<< rCtr1 >> cells) increased the uptake and cytotoxicity of [[ copper ]], oxaliplatin, cisplatin and carboplatin, in comparison to isogenic vector-transfected control cells.",1405,5
+1406,"Heterologous expression of << rCtr1 >> in HEK293 cells (HEK/rCtr1 cells) increased the uptake and cytotoxicity of copper, [[ oxaliplatin ]], cisplatin and carboplatin, in comparison to isogenic vector-transfected control cells.",1406,5
+1407,"Heterologous expression of rCtr1 in HEK293 cells (HEK/<< rCtr1 >> cells) increased the uptake and cytotoxicity of copper, [[ oxaliplatin ]], cisplatin and carboplatin, in comparison to isogenic vector-transfected control cells.",1407,5
+1408,"Heterologous expression of << rCtr1 >> in HEK293 cells (HEK/rCtr1 cells) increased the uptake and cytotoxicity of copper, oxaliplatin, [[ cisplatin ]] and carboplatin, in comparison to isogenic vector-transfected control cells.",1408,5
+1409,"Heterologous expression of rCtr1 in HEK293 cells (HEK/<< rCtr1 >> cells) increased the uptake and cytotoxicity of copper, oxaliplatin, [[ cisplatin ]] and carboplatin, in comparison to isogenic vector-transfected control cells.",1409,5
+1410,"Heterologous expression of << rCtr1 >> in HEK293 cells (HEK/rCtr1 cells) increased the uptake and cytotoxicity of copper, oxaliplatin, cisplatin and [[ carboplatin ]], in comparison to isogenic vector-transfected control cells.",1410,5
+1411,"Heterologous expression of rCtr1 in HEK293 cells (HEK/<< rCtr1 >> cells) increased the uptake and cytotoxicity of copper, oxaliplatin, cisplatin and [[ carboplatin ]], in comparison to isogenic vector-transfected control cells.",1411,5
+1412,"Cultured rat DRG neurons endogenously expressed << rCtr1 >> protein on their neuronal cell body plasma membranes and cytoplasm, and displayed substantial capacity for taking up [[ copper ]], but were resistant to copper toxicity.",1412,5
+1413,"The uptake of << copper >> by both cultured rat DRG neurons and HEK/[[ rCtr1 ]] cells was saturable and inhibited by cold temperature, silver and zinc, consistent with it being mediated by rCtr1.",1413,5
+1414,"In conclusion, << rCtr1 >> can transport copper and [[ platinum ]] drugs, and sensitizes cells to their cytotoxicities.",1414,5
+1415,"In conclusion, << rCtr1 >> can transport [[ copper ]] and platinum drugs, and sensitizes cells to their cytotoxicities.",1415,5
+1416,"DRG neurons display substantial capacity for accumulating << copper >> via a transport process mediated by [[ rCtr1 ]], but appear able to resist copper toxicity and use alternative mechanisms to take up oxaliplatin.",1416,5
+1417,"DRG neurons display substantial capacity for accumulating copper via a transport process mediated by << rCtr1 >>, but appear able to resist copper toxicity and use alternative mechanisms to take up [[ oxaliplatin ]].",1417,5
+1418,"Examination of phosphorylation in << retinoblastoma (Rb) protein >>, we found an inhibitory effect by [[ glucosamine ]] at 20 and 50 mM.",1418,0
+1419,"<< Glucosamine >> at 50 mM was demonstrated to elevate both the mRNA and protein expression of [[ p53 ]] and heme oxygenase-1 (HO-1), but also caused a reduction in p21 protein expression.",1419,6
+1420,"<< Glucosamine >> at 50 mM was demonstrated to elevate both the mRNA and protein expression of p53 and [[ heme oxygenase-1 ]] (HO-1), but also caused a reduction in p21 protein expression.",1420,6
+1421,"<< Glucosamine >> at 50 mM was demonstrated to elevate both the mRNA and protein expression of p53 and heme oxygenase-1 (HO-1), but also caused a reduction in [[ p21 ]] protein expression.",1421,8
+1422,"In addition, << glucosamine >> attenuated p21 protein stability via the proteasomal proteolytic pathway, as well as inducing [[ p21 ]] nuclear accumulation.",1422,6
+1423,"In addition, << glucosamine >> attenuated [[ p21 ]] protein stability via the proteasomal proteolytic pathway, as well as inducing p21 nuclear accumulation.",1423,8
+1424,"Altogether, our results suggest that a high dose of << glucosamine >> may inhibit cell proliferation through apoptosis and disturb cell cycle progression with a halt at G(0)/G(1) phase, and that this occurs, at least in part, by a reduction in Rb phosphorylation together with modulation of p21, p53 and HO-1 expression, and nuclear [[ p21 ]] accumulation.",1424,6
+1425,"Altogether, our results suggest that a high dose of << glucosamine >> may inhibit cell proliferation through apoptosis and disturb cell cycle progression with a halt at G(0)/G(1) phase, and that this occurs, at least in part, by a reduction in [[ Rb ]] phosphorylation together with modulation of p21, p53 and HO-1 expression, and nuclear p21 accumulation.",1425,0
+1426,Characterization of substituted << phenylpropylamides >> as highly selective agonists at the [[ melatonin MT2 receptor ]].,1426,2
+1427,We show that the expression of PIM-1 is induced in response to << estradiol >> in MCF-7 cells and that the induction is mediated by [[ ERα ]]-regulated enhancers located distally upstream from the gene.,1427,9
+1428,We show that the expression of << PIM-1 >> is induced in response to [[ estradiol ]] in MCF-7 cells and that the induction is mediated by ERα-regulated enhancers located distally upstream from the gene.,1428,6
+1429,"In this work, the metabolism of four frequently prescribed inhaled GCs, << triamcinolone acetonide >>, flunisolide, budesonide, and fluticasone propionate, by the [[ CYP3A ]] family of enzymes was studied to identify differences in their rates of clearance and to identify their metabolites.",1429,5
+1430,"In this work, the metabolism of four frequently prescribed inhaled GCs, triamcinolone acetonide, << flunisolide >>, budesonide, and fluticasone propionate, by the [[ CYP3A ]] family of enzymes was studied to identify differences in their rates of clearance and to identify their metabolites.",1430,5
+1431,"In this work, the metabolism of four frequently prescribed inhaled GCs, triamcinolone acetonide, flunisolide, << budesonide >>, and fluticasone propionate, by the [[ CYP3A ]] family of enzymes was studied to identify differences in their rates of clearance and to identify their metabolites.",1431,5
+1432,"In this work, the metabolism of four frequently prescribed inhaled GCs, triamcinolone acetonide, flunisolide, budesonide, and << fluticasone propionate >>, by the [[ CYP3A ]] family of enzymes was studied to identify differences in their rates of clearance and to identify their metabolites.",1432,5
+1433,"<< CYP3A5 >>, which is particularly relevant to GC metabolism in the lungs, was also shown to efficiently metabolize [[ triamcinolone acetonide ]], budesonide, and fluticasone propionate.",1433,5
+1434,"<< CYP3A5 >>, which is particularly relevant to GC metabolism in the lungs, was also shown to efficiently metabolize triamcinolone acetonide, [[ budesonide ]], and fluticasone propionate.",1434,5
+1435,"<< CYP3A5 >>, which is particularly relevant to GC metabolism in the lungs, was also shown to efficiently metabolize triamcinolone acetonide, budesonide, and [[ fluticasone propionate ]].",1435,5
+1436,"In contrast, << flunisolide >> was only metabolized via [[ CYP3A4 ]], with no significant turnover by CYP3A5 or CYP3A7.",1436,5
+1437,"Distinct roles of << methamphetamine >> in modulating spatial memory consolidation, retrieval, reconsolidation and the accompanying changes of [[ ERK ]] and CREB activation in hippocampus and prefrontal cortex.",1437,9
+1438,"Distinct roles of << methamphetamine >> in modulating spatial memory consolidation, retrieval, reconsolidation and the accompanying changes of ERK and [[ CREB ]] activation in hippocampus and prefrontal cortex.",1438,9
+1439,"In contrast, activation of both << ERK >> and CREB in the PFC was found following memory retrieval but not other processes in [[ METH ]]-treated mouse groups.",1439,9
+1440,"In contrast, activation of both ERK and << CREB >> in the PFC was found following memory retrieval but not other processes in [[ METH ]]-treated mouse groups.",1440,9
+1441,"Moreover, activation of the << ERK >> and CREB signaling pathway in the hippocampus might be involved in [[ METH ]]-induced spatial memory changes.",1441,9
+1442,"Moreover, activation of the ERK and << CREB >> signaling pathway in the hippocampus might be involved in [[ METH ]]-induced spatial memory changes.",1442,9
+1443,"A reporter construct driven by 4 kb of the << chicken ras-dva >> 5'-flanking region, containing six putative pituitary-specific transcription factor-1 (Pit-1) binding sites and two potential glucocorticoid receptor (GR) binding sites, was highly activated in embryonic pituitary cells and up-regulated by [[ corticosterone ]].",1443,6
+1444,"A reporter construct driven by 4 kb of the chicken ras-dva 5'-flanking region, containing six putative << pituitary-specific transcription factor-1 (Pit-1) binding sites >> and two potential glucocorticoid receptor (GR) binding sites, was highly activated in embryonic pituitary cells and up-regulated by [[ corticosterone ]].",1444,6
+1445,"A reporter construct driven by 4 kb of the chicken ras-dva 5'-flanking region, containing six putative pituitary-specific transcription factor-1 (Pit-1) binding sites and two potential << glucocorticoid receptor (GR) binding sites >>, was highly activated in embryonic pituitary cells and up-regulated by [[ corticosterone ]].",1445,6
+1446,"However, mutating putative << GR binding sites >> did not substantially reduce induction of ras-dva promoter activity by [[ corticosterone ]], suggesting additional DNA elements within the 5'-flanking region are responsible for glucocorticoid regulation.",1446,6
+1447,"However, mutating putative GR binding sites did not substantially reduce induction of << ras-dva promoter >> activity by [[ corticosterone ]], suggesting additional DNA elements within the 5'-flanking region are responsible for glucocorticoid regulation.",1447,6
+1448,"To investigate the role of mGluR8 in modulating the synaptic responses of retinal ganglion cells, we used a recently identified positive allosteric modulator of mGluR8, AZ12216052 (AZ) and the << mGluR8 >>-specific orthosteric agonist [[ (S)-3,4-dicarboxyphenylglycine ]] (DCPG).",1448,2
+1449,"To investigate the role of mGluR8 in modulating the synaptic responses of retinal ganglion cells, we used a recently identified positive allosteric modulator of mGluR8, AZ12216052 (AZ) and the << mGluR8 >>-specific orthosteric agonist (S)-3,4-dicarboxyphenylglycine ([[ DCPG ]]).",1449,2
+1450,"UCCB01-125, a dimeric inhibitor of PSD-95, reduces inflammatory pain without disrupting cognitive or motor performance: comparison with the << NMDA receptor >> antagonist [[ MK-801 ]].",1450,1
+1451,"Here, we compared the effects of a dimeric << PSD-95 >> inhibitor, [[ UCCB01-125 ]], and the NMDAR antagonist, MK-801, on mechanical hypersensitivity in the complete Freund's adjuvant (CFA) model of inflammatory pain.",1451,0
+1452,"Here, we compared the effects of a dimeric PSD-95 inhibitor, UCCB01-125, and the << NMDAR >> antagonist, [[ MK-801 ]], on mechanical hypersensitivity in the complete Freund's adjuvant (CFA) model of inflammatory pain.",1452,1
+1453,"The treatment also prevented the high << cholesterol >> diet-induced increase in serum [[ creatine kinase ]], total and isoforms, markers of neurological, cardiac and muscular damage.",1453,6
+1454,"GIP potentiates << glucose >>-stimulated [[ insulin ]] secretion and induces energy accumulation into adipose tissue, resulting in obesity.",1454,6
+1455,"Diet, physical exercise and << Orlistat >> administration increase serum [[ Anti-Müllerian Hormone ]] (AMH) levels in women with polycystic ovary syndrome (PCOS).",1455,6
+1456,"Diet, physical exercise and << Orlistat >> administration increase serum Anti-Müllerian Hormone ([[ AMH ]]) levels in women with polycystic ovary syndrome (PCOS).",1456,6
+1457,"We concluded that in overweight and obese women with PCOS << Orlistat >> administration, combined with diet and physical exercise, for 24 weeks, resulted in significant weight loss, improvement of hyperandrogenism and insulin sensitivity, and increased serum [[ AMH ]] levels.",1457,6
+1458,"Moreover, << 1,25(OH)(2)D(3) >> decreased expression of [[ Oat1 ]] and Oat3 in rat kidney.",1458,8
+1459,"Moreover, << 1,25(OH)(2)D(3) >> decreased expression of Oat1 and [[ Oat3 ]] in rat kidney.",1459,8
+1460,"The mechanism of interaction between JBP485 and 1,25(OH)(2)D(3) could be explained at least in part by inhibitory effect of << 1,25(OH)(2)D(3) >> on expression of [[ Oats ]] in rat kidney.",1460,8
+1461,"<< ISO >> is able to induce apoptosis through mitochondrial dysfunction and inhibition of [[ PI3K ]]/Akt signaling pathway in HepG2 cells, however, the effects of ISO on MAPK signaling pathways remain unknown.",1461,0
+1462,"<< ISO >> is able to induce apoptosis through mitochondrial dysfunction and inhibition of PI3K/[[ Akt ]] signaling pathway in HepG2 cells, however, the effects of ISO on MAPK signaling pathways remain unknown.",1462,0
+1463,<< ISO >> significantly inhibited the levels of ERK1/2 kinase and increased the expression of [[ JNK ]] and p38 kinases.,1463,6
+1464,<< ISO >> significantly inhibited the levels of ERK1/2 kinase and increased the expression of JNK and [[ p38 ]] kinases.,1464,6
+1465,<< ISO >> significantly inhibited the levels of ERK1/2 kinase and increased the expression of JNK and p38 [[ kinases ]].,1465,6
+1466,"Furthermore, << U0126 >> (an ERK1/2 inhibitor) significantly enhanced the ISO-induced the [[ Bax ]]/Bcl-2 ratio, the release of cytochrome c to the cytosol fraction, and the levels of cleaved caspase-3.",1466,6
+1467,"Furthermore, << U0126 >> (an ERK1/2 inhibitor) significantly enhanced the ISO-induced the Bax/[[ Bcl-2 ]] ratio, the release of cytochrome c to the cytosol fraction, and the levels of cleaved caspase-3.",1467,6
+1468,"Furthermore, U0126 (an ERK1/2 inhibitor) significantly enhanced the << ISO >>-induced the [[ Bax ]]/Bcl-2 ratio, the release of cytochrome c to the cytosol fraction, and the levels of cleaved caspase-3.",1468,6
+1469,"Furthermore, U0126 (an ERK1/2 inhibitor) significantly enhanced the << ISO >>-induced the Bax/[[ Bcl-2 ]] ratio, the release of cytochrome c to the cytosol fraction, and the levels of cleaved caspase-3.",1469,6
+1470,While SP600125 (a << JNK >> inhibitor) and SB203580 (a p38 inhibitor) markedly prevented the expression of these proteins induced by [[ ISO ]].,1470,6
+1471,While SP600125 (a JNK inhibitor) and SB203580 (a << p38 >> inhibitor) markedly prevented the expression of these proteins induced by [[ ISO ]].,1471,6
+1472,While << SP600125 >> (a [[ JNK ]] inhibitor) and SB203580 (a p38 inhibitor) markedly prevented the expression of these proteins induced by ISO.,1472,0
+1473,While SP600125 (a JNK inhibitor) and << SB203580 >> (a [[ p38 ]] inhibitor) markedly prevented the expression of these proteins induced by ISO.,1473,0
+1474,"<< NAC >> also suppressed the p-[[ JNK ]] and p-p38, but failed to reverse the effects of ISO.",1474,0
+1475,"<< NAC >> also suppressed the p-JNK and [[ p-p38 ]], but failed to reverse the effects of ISO.",1475,0
+1476,"These results demonstrated for the first time that << ISO >> induces apoptosis in HepG2 cells through inactivating ERK1/2 kinase and activating [[ JNK ]] and p38 kinases, and ROS stimulated by ISO is able to activate the MAPK singaling pathway as the upstream signaling molecules.",1476,9
+1477,"These results demonstrated for the first time that << ISO >> induces apoptosis in HepG2 cells through inactivating ERK1/2 kinase and activating JNK and [[ p38 ]] kinases, and ROS stimulated by ISO is able to activate the MAPK singaling pathway as the upstream signaling molecules.",1477,9
+1478,"These results demonstrated for the first time that << ISO >> induces apoptosis in HepG2 cells through inactivating ERK1/2 kinase and activating JNK and p38 [[ kinases ]], and ROS stimulated by ISO is able to activate the MAPK singaling pathway as the upstream signaling molecules.",1478,9
+1479,"These results demonstrated for the first time that ISO induces apoptosis in HepG2 cells through inactivating ERK1/2 kinase and activating JNK and p38 kinases, and ROS stimulated by << ISO >> is able to activate the [[ MAPK ]] singaling pathway as the upstream signaling molecules.",1479,9
+1480,"Treatment with IMG and hyperoside resulted in significantly prolonged aPTT and PT and inhibition of the activities of thrombin and FXa, and << IMG >> or hyperoside inhibited production of [[ thrombin ]] and FXa in HUVECs.",1480,6
+1481,"Treatment with IMG and hyperoside resulted in significantly prolonged aPTT and PT and inhibition of the activities of thrombin and FXa, and << IMG >> or hyperoside inhibited production of thrombin and [[ FXa ]] in HUVECs.",1481,8
+1482,"Treatment with IMG and hyperoside resulted in significantly prolonged aPTT and PT and inhibition of the activities of thrombin and FXa, and IMG or << hyperoside >> inhibited production of [[ thrombin ]] and FXa in HUVECs.",1482,8
+1483,"Treatment with IMG and hyperoside resulted in significantly prolonged aPTT and PT and inhibition of the activities of thrombin and FXa, and IMG or << hyperoside >> inhibited production of thrombin and [[ FXa ]] in HUVECs.",1483,8
+1484,"Treatment with << IMG >> and hyperoside resulted in significantly prolonged aPTT and PT and inhibition of the activities of [[ thrombin ]] and FXa, and IMG or hyperoside inhibited production of thrombin and FXa in HUVECs.",1484,0
+1485,"Treatment with << IMG >> and hyperoside resulted in significantly prolonged aPTT and PT and inhibition of the activities of thrombin and [[ FXa ]], and IMG or hyperoside inhibited production of thrombin and FXa in HUVECs.",1485,0
+1486,"Treatment with IMG and << hyperoside >> resulted in significantly prolonged aPTT and PT and inhibition of the activities of [[ thrombin ]] and FXa, and IMG or hyperoside inhibited production of thrombin and FXa in HUVECs.",1486,0
+1487,"Treatment with IMG and << hyperoside >> resulted in significantly prolonged aPTT and PT and inhibition of the activities of thrombin and [[ FXa ]], and IMG or hyperoside inhibited production of thrombin and FXa in HUVECs.",1487,0
+1488,"In addition, treatment with << IMG >> and hyperoside resulted in inhibition of TNF-α-induced production of [[ PAI-1 ]], and treatment with IMG resulted in significant reduction of the PAI-1 to t-PA ratio.",1488,8
+1489,"In addition, treatment with IMG and << hyperoside >> resulted in inhibition of TNF-α-induced production of [[ PAI-1 ]], and treatment with IMG resulted in significant reduction of the PAI-1 to t-PA ratio.",1489,8
+1490,"In addition, treatment with IMG and hyperoside resulted in inhibition of TNF-α-induced production of PAI-1, and treatment with << IMG >> resulted in significant reduction of the [[ PAI-1 ]] to t-PA ratio.",1490,8
+1491,"In addition, treatment with IMG and hyperoside resulted in inhibition of TNF-α-induced production of PAI-1, and treatment with << IMG >> resulted in significant reduction of the PAI-1 to [[ t-PA ]] ratio.",1491,8
+1492,"In addition, treatment with << IMG >> and hyperoside resulted in inhibition of [[ TNF-α ]]-induced production of PAI-1, and treatment with IMG resulted in significant reduction of the PAI-1 to t-PA ratio.",1492,0
+1493,"In addition, treatment with IMG and << hyperoside >> resulted in inhibition of [[ TNF-α ]]-induced production of PAI-1, and treatment with IMG resulted in significant reduction of the PAI-1 to t-PA ratio.",1493,0
+1494,Optimization of << 5-hydroxytryptamines >> as dual function inhibitors targeting [[ phospholipase A2 ]] and leukotriene A4 hydrolase.,1494,0
+1495,Optimization of << 5-hydroxytryptamines >> as dual function inhibitors targeting phospholipase A2 and [[ leukotriene A4 hydrolase ]].,1495,0
+1496,Dual function inhibitors targeting phospholipase A(2) (<< PLA(2) >>) and leukotriene A(4) hydrolase (LTA(4)H) may balance the [[ arachidonic acid ]] (AA) metabolic network and be used as new anti-inflammatory drugs.,1496,4
+1497,Dual function inhibitors targeting phospholipase A(2) (PLA(2)) and << leukotriene A(4) hydrolase >> (LTA(4)H) may balance the [[ arachidonic acid ]] (AA) metabolic network and be used as new anti-inflammatory drugs.,1497,4
+1498,Dual function inhibitors targeting phospholipase A(2) (PLA(2)) and leukotriene A(4) hydrolase (<< LTA(4)H >>) may balance the [[ arachidonic acid ]] (AA) metabolic network and be used as new anti-inflammatory drugs.,1498,4
+1499,Dual function inhibitors targeting << phospholipase A(2) >> (PLA(2)) and leukotriene A(4) hydrolase (LTA(4)H) may balance the [[ arachidonic acid ]] (AA) metabolic network and be used as new anti-inflammatory drugs.,1499,4
+1500,"In previous study, we discovered multi-target drugs towards the AA metabolic network, among which a dual-target inhibitor (<< JMC08-4 >>) for human nonpancreatic secretory phospholipase A(2) (hnps-PLA(2)) and [[ human leukotriene A(4) hydrolase ]] (LTA(4)H-h) was found.",1500,0
+1501,"In previous study, we discovered multi-target drugs towards the AA metabolic network, among which a dual-target inhibitor (<< JMC08-4 >>) for human nonpancreatic secretory phospholipase A(2) (hnps-PLA(2)) and human leukotriene A(4) hydrolase ([[ LTA(4)H-h ]]) was found.",1501,0
+1502,"In previous study, we discovered multi-target drugs towards the AA metabolic network, among which a dual-target inhibitor (<< JMC08-4 >>) for [[ human nonpancreatic secretory phospholipase A(2) ]] (hnps-PLA(2)) and human leukotriene A(4) hydrolase (LTA(4)H-h) was found.",1502,0
+1503,"In previous study, we discovered multi-target drugs towards the AA metabolic network, among which a dual-target inhibitor (<< JMC08-4 >>) for human nonpancreatic secretory phospholipase A(2) ([[ hnps-PLA(2) ]]) and human leukotriene A(4) hydrolase (LTA(4)H-h) was found.",1503,0
+1504,"Whereas the addition of << apomorphine >> in the low micromolar range produced an irreversible activation of the channel, application of higher concentrations caused a reversible voltage-dependent inhibition of heterologously expressed [[ TRPA1 ]] channels, resulting from a reduction of single-channel open times.",1504,0
+1505,"In addition, we provide evidence that << apomorphine >> also acts on endogenous TRPA1 in cultured dorsal root ganglion neurons from rats and in the enterochromaffin model cell line QGP-1, from which serotonin is released upon activation of [[ TRPA1 ]].",1505,9
+1506,"Our study shows that human TRPA1 is a target for << apomorphine >>, suggesting that an activation of [[ TRPA1 ]] might contribute to adverse side effects such as nausea and painful injections, which can occur during treatment with apomorphine.",1506,9
+1507,"Our study shows that human TRPA1 is a target for apomorphine, suggesting that an activation of << TRPA1 >> might contribute to adverse side effects such as nausea and painful injections, which can occur during treatment with [[ apomorphine ]].",1507,9
+1508,<< Human stearoyl-CoA desaturase 1 >> (SCD-1) gene expression is negatively regulated by [[ thyroid hormone ]] without direct binding of thyroid hormone receptor to the gene promoter.,1508,8
+1509,Human stearoyl-CoA desaturase 1 (<< SCD-1 >>) gene expression is negatively regulated by [[ thyroid hormone ]] without direct binding of thyroid hormone receptor to the gene promoter.,1509,8
+1510,Dietary << carbohydrates >> increase [[ SCD-1 ]] gene expression in liver by sterol response element binding protein (SREBP)-1c-dependent and SREBP-1c -independent pathways.,1510,6
+1511,Previous report demonstrated that << thyroid hormone >> (TH) negatively regulates [[ mouse SCD-1 gene promoter ]] before SREBP-1c was revealed.,1511,8
+1512,"Exposure of H9c2 cells to high << glucose >> reduced AMPK activity, inhibited [[ Jun NH2-terminal kinase 1 ]] (JNK1)-B-cell lymphoma 2 (Bcl-2) signaling, and promoted Beclin1 binding to Bcl-2.",1512,8
+1513,"Exposure of H9c2 cells to high << glucose >> reduced AMPK activity, inhibited Jun NH2-terminal kinase 1 ([[ JNK1 ]])-B-cell lymphoma 2 (Bcl-2) signaling, and promoted Beclin1 binding to Bcl-2.",1513,8
+1514,"Exposure of H9c2 cells to high << glucose >> reduced AMPK activity, inhibited Jun NH2-terminal kinase 1 (JNK1)-[[ B-cell lymphoma 2 ]] (Bcl-2) signaling, and promoted Beclin1 binding to Bcl-2.",1514,8
+1515,"Exposure of H9c2 cells to high << glucose >> reduced AMPK activity, inhibited Jun NH2-terminal kinase 1 (JNK1)-B-cell lymphoma 2 ([[ Bcl-2 ]]) signaling, and promoted Beclin1 binding to Bcl-2.",1515,8
+1516,"Exposure of H9c2 cells to high << glucose >> reduced [[ AMPK ]] activity, inhibited Jun NH2-terminal kinase 1 (JNK1)-B-cell lymphoma 2 (Bcl-2) signaling, and promoted Beclin1 binding to Bcl-2.",1516,0
+1517,"Finally, chronic administration of << metformin >> in diabetic mice restored cardiac autophagy by activating [[ JNK1 ]]-Bcl-2 pathways and dissociating Beclin1 and Bcl-2.",1517,9
+1518,"Finally, chronic administration of << metformin >> in diabetic mice restored cardiac autophagy by activating JNK1-[[ Bcl-2 ]] pathways and dissociating Beclin1 and Bcl-2.",1518,9
+1519,<< Metformin >>-mediated downregulation of [[ p38 ]] mitogen-activated protein kinase-dependent excision repair cross-complementing 1 decreases DNA repair capacity and sensitizes human lung cancer cells to paclitaxel.,1519,3
+1520,<< Metformin >>-mediated downregulation of p38 [[ mitogen-activated protein kinase ]]-dependent excision repair cross-complementing 1 decreases DNA repair capacity and sensitizes human lung cancer cells to paclitaxel.,1520,3
+1521,"In this current study, << paclitaxel >> was found to increase phosphorylation of [[ mitogen-activated protein kinase ]] (MAPK) kinase 3/6 (MKK3/6)-p38 MAPK as well as protein and mRNA levels of ERCC1 in H1650 and H1703 cells.",1521,9
+1522,"In this current study, << paclitaxel >> was found to increase phosphorylation of mitogen-activated protein kinase (MAPK) kinase 3/6 (MKK3/6)-[[ p38 ]] MAPK as well as protein and mRNA levels of ERCC1 in H1650 and H1703 cells.",1522,9
+1523,"In this current study, << paclitaxel >> was found to increase phosphorylation of mitogen-activated protein kinase (MAPK) kinase 3/6 (MKK3/6)-p38 [[ MAPK ]] as well as protein and mRNA levels of ERCC1 in H1650 and H1703 cells.",1523,9
+1524,"In this current study, << paclitaxel >> was found to increase phosphorylation of mitogen-activated protein kinase (MAPK) kinase 3/6 (MKK3/6)-p38 MAPK as well as protein and mRNA levels of [[ ERCC1 ]] in H1650 and H1703 cells.",1524,6
+1525,"Moreover, << paclitaxel >>-induced [[ ERCC1 ]] protein and mRNA levels significantly decreased via the downregulation of p38 activity by either a p38 MAPK inhibitor SB202190 or p38 knockdown with specific small interfering RNA (siRNA).",1525,6
+1526,"Moreover, paclitaxel-induced ERCC1 protein and mRNA levels significantly decreased via the downregulation of << p38 >> activity by either a p38 MAPK inhibitor [[ SB202190 ]] or p38 knockdown with specific small interfering RNA (siRNA).",1526,0
+1527,"Moreover, paclitaxel-induced ERCC1 protein and mRNA levels significantly decreased via the downregulation of p38 activity by either a << p38 >> MAPK inhibitor [[ SB202190 ]] or p38 knockdown with specific small interfering RNA (siRNA).",1527,0
+1528,"Moreover, paclitaxel-induced ERCC1 protein and mRNA levels significantly decreased via the downregulation of p38 activity by either a p38 << MAPK >> inhibitor [[ SB202190 ]] or p38 knockdown with specific small interfering RNA (siRNA).",1528,0
+1529,"Furthermore, metformin was able to not only decrease the << paclitaxel >>-induced [[ p38 ]] MAPK-mediated ERCC1 expression, but also augment the cytotoxic effect induced by paclitaxel.",1529,9
+1530,"Furthermore, metformin was able to not only decrease the << paclitaxel >>-induced p38 [[ MAPK ]]-mediated ERCC1 expression, but also augment the cytotoxic effect induced by paclitaxel.",1530,9
+1531,"Furthermore, metformin was able to not only decrease the << paclitaxel >>-induced p38 MAPK-mediated [[ ERCC1 ]] expression, but also augment the cytotoxic effect induced by paclitaxel.",1531,6
+1532,"Furthermore, << metformin >> was able to not only decrease the paclitaxel-induced p38 MAPK-mediated [[ ERCC1 ]] expression, but also augment the cytotoxic effect induced by paclitaxel.",1532,8
+1533,"Furthermore, << metformin >> was able to not only decrease the paclitaxel-induced [[ p38 ]] MAPK-mediated ERCC1 expression, but also augment the cytotoxic effect induced by paclitaxel.",1533,0
+1534,"Furthermore, << metformin >> was able to not only decrease the paclitaxel-induced p38 [[ MAPK ]]-mediated ERCC1 expression, but also augment the cytotoxic effect induced by paclitaxel.",1534,0
+1535,"Finally, expression of constitutive activate MKK6 or HA-p38 MAPK vectors in lung cancer cells was able to abrogate << ERCC1 >> downregulation by [[ metformin ]] and paclitaxel as well as cell viability and DNA repair capacity.",1535,8
+1536,"Finally, expression of constitutive activate MKK6 or HA-p38 MAPK vectors in lung cancer cells was able to abrogate << ERCC1 >> downregulation by metformin and [[ paclitaxel ]] as well as cell viability and DNA repair capacity.",1536,8
+1537,"Overall, our results suggest that inhibition of the << p38 >> MAPK signaling by [[ metformin ]] coupled with paclitaxel therapy in human NSCLC cells may be a clinically useful combination, which however will require further validation.",1537,0
+1538,"Overall, our results suggest that inhibition of the p38 << MAPK >> signaling by [[ metformin ]] coupled with paclitaxel therapy in human NSCLC cells may be a clinically useful combination, which however will require further validation.",1538,0
+1539,<< Orlistat >> has been the most used anti-obesity drug and the mechanism of its action is to reduce lipid absorption by inhibiting gastrointestinal [[ lipases ]].,1539,0
+1540,"This study was designed to test the hypothesis that << orlistat >> inhibits [[ CESs ]] with higher potency toward CES1 than CES2, a carboxylesterase with little lipase activity.",1540,0
+1541,"This study was designed to test the hypothesis that << orlistat >> inhibits CESs with higher potency toward [[ CES1 ]] than CES2, a carboxylesterase with little lipase activity.",1541,0
+1542,"This study was designed to test the hypothesis that << orlistat >> inhibits CESs with higher potency toward CES1 than [[ CES2 ]], a carboxylesterase with little lipase activity.",1542,0
+1543,"This study was designed to test the hypothesis that << orlistat >> inhibits CESs with higher potency toward CES1 than CES2, a [[ carboxylesterase ]] with little lipase activity.",1543,0
+1544,"This study was designed to test the hypothesis that << orlistat >> inhibits CESs with higher potency toward CES1 than CES2, a carboxylesterase with little [[ lipase ]] activity.",1544,0
+1545,"Contrary to the hypothesis, orlistat at 1 nM inhibited << CES2 >> activity by 75% but no inhibition on CES1, placing CES2 one of the most sensitive targets of [[ orlistat ]].",1545,0
+1546,"Contrary to the hypothesis, orlistat at 1 nM inhibited CES2 activity by 75% but no inhibition on CES1, placing << CES2 >> one of the most sensitive targets of [[ orlistat ]].",1546,0
+1547,Inhibition of this << carboxylesterase >> probably presents a major source for altered therapeutic activity of these medicines if co-administered with [[ orlistat ]].,1547,0
+1548,"Regulation of multiple << adenylyl cyclases >> (AC) provides unique inputs to mediate the synthesis of [[ cAMP ]], a ubiquitous second messenger that controls many aspects of cellular function.",1548,4
+1549,"Regulation of multiple adenylyl cyclases (<< AC >>) provides unique inputs to mediate the synthesis of [[ cAMP ]], a ubiquitous second messenger that controls many aspects of cellular function.",1549,4
+1550,"On stimulation by G(s), the activities of << ACs >> can be further selectively modulated by other pathways to ensure precise control of intracellular [[ cAMP ]] responses to specific stimuli.",1550,4
+1551,"We identified one compound, << E235 >> (N-(1-benzyl-piperidin-4-yl)-2-(4-fluoro-phenyl)-benzo[d]imidazo[2,1-b]thiazole-7-carboxamide), that activated the ISR and dose-dependently increased levels of [[ ATF4 ]] in transformed cells.",1551,6
+1552,"We identified one compound, E235 << (N-(1-benzyl-piperidin-4-yl)-2-(4-fluoro-phenyl)-benzo[d]imidazo[2,1-b]thiazole-7-carboxamide) >>, that activated the ISR and dose-dependently increased levels of [[ ATF4 ]] in transformed cells.",1552,6
+1553,"<< E235 >> also activated DNA damage response signaling, resulting in increased levels of Ser15-[[ phosphorylated p53 ]], γ-H2AX, and phosphorylated checkpoint kinase 2 (Chk2), although E235 does not appear to cause physical DNA damage.",1553,6
+1554,"<< E235 >> also activated DNA damage response signaling, resulting in increased levels of Ser15-phosphorylated p53, [[ γ-H2AX ]], and phosphorylated checkpoint kinase 2 (Chk2), although E235 does not appear to cause physical DNA damage.",1554,6
+1555,"<< E235 >> also activated DNA damage response signaling, resulting in increased levels of Ser15-phosphorylated p53, γ-H2AX, and [[ phosphorylated checkpoint kinase 2 ]] (Chk2), although E235 does not appear to cause physical DNA damage.",1555,6
+1556,"<< E235 >> also activated DNA damage response signaling, resulting in increased levels of Ser15-phosphorylated p53, γ-H2AX, and phosphorylated checkpoint kinase 2 ([[ Chk2 ]]), although E235 does not appear to cause physical DNA damage.",1556,6
+1557,Cell culture studies demonstrated that << PKAA >> is capable of delivering anti-TNF (tumor necrosis factor)-α siRNA to lipopolysaccharide (LPS)-stimulated macrophages and significantly inhibits the expression of [[ TNF-α ]].,1557,8
+1558,<< PKAA >>/anti-TNF-α siRNA nanocomplexes significantly reduced the [[ ALT ]] (alanine transaminase) and the hepatic cellular damages in APAP-intoxicated mice.,1558,8
+1559,<< PKAA >>/anti-TNF-α siRNA nanocomplexes significantly reduced the ALT ([[ alanine transaminase ]]) and the hepatic cellular damages in APAP-intoxicated mice.,1559,8
+1560,Wogonin inhibits << H2O2 >>-induced vascular permeability through suppressing the phosphorylation of [[ caveolin-1 ]].,1560,9
+1561,<< Wogonin >> inhibits H2O2-induced vascular permeability through suppressing the phosphorylation of [[ caveolin-1 ]].,1561,0
+1562,"We found that wogonin can suppress the << H2O2 >>-stimulated [[ actin ]] remodeling and albumin uptake of HUVECs, as well as transendothelial cell migration of the human breast carcinoma cell MDA-MB-231.",1562,6
+1563,"We found that wogonin can suppress the << H2O2 >>-stimulated actin remodeling and [[ albumin ]] uptake of HUVECs, as well as transendothelial cell migration of the human breast carcinoma cell MDA-MB-231.",1563,6
+1564,"We found that << wogonin >> can suppress the H2O2-stimulated [[ actin ]] remodeling and albumin uptake of HUVECs, as well as transendothelial cell migration of the human breast carcinoma cell MDA-MB-231.",1564,8
+1565,"We found that << wogonin >> can suppress the H2O2-stimulated actin remodeling and [[ albumin ]] uptake of HUVECs, as well as transendothelial cell migration of the human breast carcinoma cell MDA-MB-231.",1565,8
+1566,The mechanism revealed that wogonin inhibited << H2O2 >>-induced phosphorylation of [[ caveolin-1 ]] (cav-1) associating with the suppression of stabilization of VE-cadherin and β-catenin.,1566,9
+1567,The mechanism revealed that wogonin inhibited << H2O2 >>-induced phosphorylation of caveolin-1 ([[ cav-1 ]]) associating with the suppression of stabilization of VE-cadherin and β-catenin.,1567,9
+1568,The mechanism revealed that << wogonin >> inhibited H2O2-induced phosphorylation of caveolin-1 (cav-1) associating with the suppression of stabilization of [[ VE-cadherin ]] and β-catenin.,1568,8
+1569,The mechanism revealed that << wogonin >> inhibited H2O2-induced phosphorylation of caveolin-1 (cav-1) associating with the suppression of stabilization of VE-cadherin and [[ β-catenin ]].,1569,8
+1570,The mechanism revealed that << wogonin >> inhibited H2O2-induced phosphorylation of [[ caveolin-1 ]] (cav-1) associating with the suppression of stabilization of VE-cadherin and β-catenin.,1570,0
+1571,The mechanism revealed that << wogonin >> inhibited H2O2-induced phosphorylation of caveolin-1 ([[ cav-1 ]]) associating with the suppression of stabilization of VE-cadherin and β-catenin.,1571,0
+1572,"Moreover, wogonin repressed << anisomycin >>-induced phosphorylation of [[ p38 ]], cav-1 and vascular permeability.",1572,9
+1573,"Moreover, wogonin repressed << anisomycin >>-induced phosphorylation of p38, [[ cav-1 ]] and vascular permeability.",1573,9
+1574,"Moreover, << wogonin >> repressed anisomycin-induced phosphorylation of [[ p38 ]], cav-1 and vascular permeability.",1574,0
+1575,"Moreover, << wogonin >> repressed anisomycin-induced phosphorylation of p38, [[ cav-1 ]] and vascular permeability.",1575,0
+1576,"These results suggested that wogonin could inhibit << H2O2 >>-induced vascular permeability by downregulating the phosphorylation of [[ cav-1 ]], and that it might have a therapeutic potential for the diseases associated with the development of both oxidant and vascular permeability.",1576,9
+1577,"These results suggested that << wogonin >> could inhibit H2O2-induced vascular permeability by downregulating the phosphorylation of [[ cav-1 ]], and that it might have a therapeutic potential for the diseases associated with the development of both oxidant and vascular permeability.",1577,0
+1578,"In an attempt to further improve overall profiles of the oxadiazine series of GSMs, in particular the hERG activity, conformational modifications of the core structure resulted in the identification of fused << oxadiazepines >> such as 7i which had an improved [[ hERG ]] inhibition profile and was a highly efficacious GSM in vitro and in vivo in rats.",1578,0
+1579,"Both CE and E(2) alone increased DNA synthesis and reduced apoptosis with activation of MAPK, Akt, and p70S6K and up-regulation of antiapoptotic factors << survivin >>, Bcl-2, and X-linked inhibitor of apoptosis protein, These effects could be completely blocked by [[ BZA ]].",1579,8
+1580,"Both CE and E(2) alone increased DNA synthesis and reduced apoptosis with activation of MAPK, Akt, and p70S6K and up-regulation of antiapoptotic factors survivin, << Bcl-2 >>, and X-linked inhibitor of apoptosis protein, These effects could be completely blocked by [[ BZA ]].",1580,8
+1581,"Both CE and E(2) alone increased DNA synthesis and reduced apoptosis with activation of MAPK, Akt, and p70S6K and up-regulation of antiapoptotic factors survivin, Bcl-2, and << X-linked inhibitor of apoptosis protein >>, These effects could be completely blocked by [[ BZA ]].",1581,8
+1582,"Both CE and E(2) alone increased DNA synthesis and reduced apoptosis with activation of << MAPK >>, Akt, and p70S6K and up-regulation of antiapoptotic factors survivin, Bcl-2, and X-linked inhibitor of apoptosis protein, These effects could be completely blocked by [[ BZA ]].",1582,0
+1583,"Both CE and E(2) alone increased DNA synthesis and reduced apoptosis with activation of MAPK, << Akt >>, and p70S6K and up-regulation of antiapoptotic factors survivin, Bcl-2, and X-linked inhibitor of apoptosis protein, These effects could be completely blocked by [[ BZA ]].",1583,0
+1584,"Both CE and E(2) alone increased DNA synthesis and reduced apoptosis with activation of MAPK, Akt, and << p70S6K >> and up-regulation of antiapoptotic factors survivin, Bcl-2, and X-linked inhibitor of apoptosis protein, These effects could be completely blocked by [[ BZA ]].",1584,0
+1585,"We used << nutlin-3 >>, a well-known disruptor of [[ p53 ]]-Mdm2 interaction, to validate the specificity of the assay.",1585,0
+1586,"We used << nutlin-3 >>, a well-known disruptor of p53-[[ Mdm2 ]] interaction, to validate the specificity of the assay.",1586,0
+1587,"The reduction of BiFC signal mediated by << nutlin-3 >> was correlated with an increase in [[ Puma ]] transactivation, PARP cleavage, and cell death.",1587,9
+1588,"The reduction of BiFC signal mediated by << nutlin-3 >> was correlated with an increase in Puma transactivation, [[ PARP ]] cleavage, and cell death.",1588,6
+1589,"<< Sal >> toxicity coincided with reduced [[ pAkt ]] level and its downstream effectors: pCREB, pGSK-3β, Bcl-2 and neurotrophins GDNF, BDNF suggesting repressed PI3K/Akt signaling.",1589,8
+1590,"<< Sal >> toxicity coincided with reduced pAkt level and its downstream effectors: [[ pCREB ]], pGSK-3β, Bcl-2 and neurotrophins GDNF, BDNF suggesting repressed PI3K/Akt signaling.",1590,8
+1591,"<< Sal >> toxicity coincided with reduced pAkt level and its downstream effectors: pCREB, [[ pGSK-3β ]], Bcl-2 and neurotrophins GDNF, BDNF suggesting repressed PI3K/Akt signaling.",1591,8
+1592,"<< Sal >> toxicity coincided with reduced pAkt level and its downstream effectors: pCREB, pGSK-3β, [[ Bcl-2 ]] and neurotrophins GDNF, BDNF suggesting repressed PI3K/Akt signaling.",1592,8
+1593,"<< Sal >> toxicity coincided with reduced pAkt level and its downstream effectors: pCREB, pGSK-3β, Bcl-2 and [[ neurotrophins ]] GDNF, BDNF suggesting repressed PI3K/Akt signaling.",1593,8
+1594,"<< Sal >> toxicity coincided with reduced pAkt level and its downstream effectors: pCREB, pGSK-3β, Bcl-2 and neurotrophins [[ GDNF ]], BDNF suggesting repressed PI3K/Akt signaling.",1594,8
+1595,"<< Sal >> toxicity coincided with reduced pAkt level and its downstream effectors: pCREB, pGSK-3β, Bcl-2 and neurotrophins GDNF, [[ BDNF ]] suggesting repressed PI3K/Akt signaling.",1595,8
+1596,"<< Sal >> toxicity coincided with reduced pAkt level and its downstream effectors: pCREB, pGSK-3β, Bcl-2 and neurotrophins GDNF, BDNF suggesting repressed [[ PI3K ]]/Akt signaling.",1596,8
+1597,"<< Sal >> toxicity coincided with reduced pAkt level and its downstream effectors: pCREB, pGSK-3β, Bcl-2 and neurotrophins GDNF, BDNF suggesting repressed PI3K/[[ Akt ]] signaling.",1597,8
+1598,This was confirmed on adding << LY294002 >> the [[ PI3K ]] inhibitor which abolished the protection.,1598,0
+1599,"<< Isoproterenol >> induced myocardial infarcted rats showed a significant increase in the levels of cardiac diagnostic markers, heart mitochondrial lipid peroxidation, calcium, and a significant decrease in the activities/levels of heart mitochondrial [[ glutathione peroxidase ]], glutathione reductase, reduced glutathione, isocitrate, succinate, malate, α-ketoglutarate and NADH-dehydrogenases, cytochrome-C-oxidase and adenosine triphosphate.",1599,8
+1600,"<< Isoproterenol >> induced myocardial infarcted rats showed a significant increase in the levels of cardiac diagnostic markers, heart mitochondrial lipid peroxidation, calcium, and a significant decrease in the activities/levels of heart mitochondrial glutathione peroxidase, [[ glutathione reductase ]], reduced glutathione, isocitrate, succinate, malate, α-ketoglutarate and NADH-dehydrogenases, cytochrome-C-oxidase and adenosine triphosphate.",1600,8
+1601,"<< Isoproterenol >> induced myocardial infarcted rats showed a significant increase in the levels of cardiac diagnostic markers, heart mitochondrial lipid peroxidation, calcium, and a significant decrease in the activities/levels of heart mitochondrial glutathione peroxidase, glutathione reductase, reduced glutathione, isocitrate, succinate, malate, α-ketoglutarate and [[ NADH-dehydrogenases ]], cytochrome-C-oxidase and adenosine triphosphate.",1601,8
+1602,"<< Isoproterenol >> induced myocardial infarcted rats showed a significant increase in the levels of cardiac diagnostic markers, heart mitochondrial lipid peroxidation, calcium, and a significant decrease in the activities/levels of heart mitochondrial glutathione peroxidase, glutathione reductase, reduced glutathione, isocitrate, succinate, malate, α-ketoglutarate and NADH-dehydrogenases, [[ cytochrome-C-oxidase ]] and adenosine triphosphate.",1602,8
+1603,"<< Isoproterenol >> induced myocardial infarcted rats showed a significant increase in the levels of cardiac diagnostic markers, heart mitochondrial lipid peroxidation, calcium, and a significant decrease in the activities/levels of heart mitochondrial [[ glutathione peroxidase ]], glutathione reductase, reduced glutathione, isocitrate, succinate, malate, α-ketoglutarate and NADH-dehydrogenases, cytochrome-C-oxidase and adenosine triphosphate.",1603,0
+1604,"<< Isoproterenol >> induced myocardial infarcted rats showed a significant increase in the levels of cardiac diagnostic markers, heart mitochondrial lipid peroxidation, calcium, and a significant decrease in the activities/levels of heart mitochondrial glutathione peroxidase, [[ glutathione reductase ]], reduced glutathione, isocitrate, succinate, malate, α-ketoglutarate and NADH-dehydrogenases, cytochrome-C-oxidase and adenosine triphosphate.",1604,0
+1605,"<< Isoproterenol >> induced myocardial infarcted rats showed a significant increase in the levels of cardiac diagnostic markers, heart mitochondrial lipid peroxidation, calcium, and a significant decrease in the activities/levels of heart mitochondrial glutathione peroxidase, glutathione reductase, reduced glutathione, isocitrate, succinate, malate, α-ketoglutarate and [[ NADH-dehydrogenases ]], cytochrome-C-oxidase and adenosine triphosphate.",1605,0
+1606,"<< Isoproterenol >> induced myocardial infarcted rats showed a significant increase in the levels of cardiac diagnostic markers, heart mitochondrial lipid peroxidation, calcium, and a significant decrease in the activities/levels of heart mitochondrial glutathione peroxidase, glutathione reductase, reduced glutathione, isocitrate, succinate, malate, α-ketoglutarate and NADH-dehydrogenases, [[ cytochrome-C-oxidase ]] and adenosine triphosphate.",1606,0
+1607,"Increased urinary excretion of << albumin >>, hemopexin, transferrin and VDBP correlates with chronic sensitization to [[ gentamicin ]] nephrotoxicity in rats.",1607,6
+1608,"Increased urinary excretion of albumin, << hemopexin >>, transferrin and VDBP correlates with chronic sensitization to [[ gentamicin ]] nephrotoxicity in rats.",1608,6
+1609,"Increased urinary excretion of albumin, hemopexin, << transferrin >> and VDBP correlates with chronic sensitization to [[ gentamicin ]] nephrotoxicity in rats.",1609,6
+1610,"Increased urinary excretion of albumin, hemopexin, transferrin and << VDBP >> correlates with chronic sensitization to [[ gentamicin ]] nephrotoxicity in rats.",1610,6
+1611,"Design and synthesis of novel << 2-methyl-4,5-substitutedbenzo[f]-3,3a,4,5-tetrahydro-pyrazolo[1,5-d][1,4]oxazepin-8(7H)-one >> derivatives as [[ telomerase ]] inhibitors.",1611,0
+1612,<< DPEP >> induced dose-dependent reduction of the protein levels of [[ inducible nitric oxide synthase ]] (iNOS) and cyclooxygenase-2 (COX-2) and concomitant reduction in the production of NO and prostaglandin E(2) (PGE(2)).,1612,8
+1613,<< DPEP >> induced dose-dependent reduction of the protein levels of inducible nitric oxide synthase ([[ iNOS ]]) and cyclooxygenase-2 (COX-2) and concomitant reduction in the production of NO and prostaglandin E(2) (PGE(2)).,1613,8
+1614,<< DPEP >> induced dose-dependent reduction of the protein levels of inducible nitric oxide synthase (iNOS) and [[ cyclooxygenase-2 ]] (COX-2) and concomitant reduction in the production of NO and prostaglandin E(2) (PGE(2)).,1614,8
+1615,<< DPEP >> induced dose-dependent reduction of the protein levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 ([[ COX-2 ]]) and concomitant reduction in the production of NO and prostaglandin E(2) (PGE(2)).,1615,8
+1616,"Additionally, << DPEP >> suppressed the production of inflammatory [[ cytokines ]], including tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6.",1616,8
+1617,"Additionally, << DPEP >> suppressed the production of inflammatory cytokines, including [[ tumor necrosis factor-α ]] (TNF-α), interleukin (IL)-1β, and IL-6.",1617,8
+1618,"Additionally, << DPEP >> suppressed the production of inflammatory cytokines, including tumor necrosis factor-α ([[ TNF-α ]]), interleukin (IL)-1β, and IL-6.",1618,8
+1619,"Additionally, << DPEP >> suppressed the production of inflammatory cytokines, including tumor necrosis factor-α (TNF-α), [[ interleukin (IL)-1β ]], and IL-6.",1619,8
+1620,"Additionally, << DPEP >> suppressed the production of inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and [[ IL-6 ]].",1620,8
+1621,"<< DPEP >> inhibited LPS-induced phosphorylation of [[ ERK ]], JNK, and p38.",1621,0
+1622,"<< DPEP >> inhibited LPS-induced phosphorylation of ERK, [[ JNK ]], and p38.",1622,0
+1623,"<< DPEP >> inhibited LPS-induced phosphorylation of ERK, JNK, and [[ p38 ]].",1623,0
+1624,"Furthermore, << DPEP >> inhibited the LPS-induced phosphorylation of inhibitor κB (IκB)-α and NF-κB [[ p50 ]].",1624,0
+1625,"Furthermore, << DPEP >> inhibited the LPS-induced phosphorylation of [[ inhibitor κB (IκB)-α ]] and NF-κB p50.",1625,0
+1626,"Furthermore, << DPEP >> inhibited the LPS-induced phosphorylation of inhibitor κB (IκB)-α and [[ NF-κB ]] p50.",1626,0
+1627,"Taken together, the results of this study demonstrate that << DPEP >> inhibits LPS-stimulated inflammation by blocking the [[ NF-κB ]] and MAPK pathways in macrophages.",1627,0
+1628,"Taken together, the results of this study demonstrate that << DPEP >> inhibits LPS-stimulated inflammation by blocking the NF-κB and [[ MAPK ]] pathways in macrophages.",1628,0
+1629,"This leads to decreased expression of << glutamate aspartate transporter >>, which in turn reduces [[ glutamate ]] transport.",1629,5
+1630,<< Tetrahydropyrroloquinolinone >> type dual inhibitors of [[ aromatase ]]/aldosterone synthase as a novel strategy for breast cancer patients with elevated cardiovascular risks.,1630,0
+1631,<< Tetrahydropyrroloquinolinone >> type dual inhibitors of aromatase/[[ aldosterone synthase ]] as a novel strategy for breast cancer patients with elevated cardiovascular risks.,1631,0
+1632,"Furthermore, << MDZ >> caused mechanism-based inactivation of [[ cytochrome P450 3A ]]-dependent TRZ 1'-hydroxylation in mouse, rat and human intestinal microsomes with similar potencies.",1632,0
+1633,"Furthermore, MDZ caused mechanism-based inactivation of << cytochrome P450 3A >>-dependent [[ TRZ ]] 1'-hydroxylation in mouse, rat and human intestinal microsomes with similar potencies.",1633,5
+1634,<< Tamoxifen >> represses miR-200 microRNAs and promotes epithelial-to-mesenchymal transition by up-regulating [[ c-Myc ]] in endometrial carcinoma cell lines.,1634,7
+1635,<< Tamoxifen >> represses [[ miR-200 ]] microRNAs and promotes epithelial-to-mesenchymal transition by up-regulating c-Myc in endometrial carcinoma cell lines.,1635,8
+1636,"When treated with TAM, ECC-1 and Ishikawa cells were characterized by higher invasiveness and motility and underwent EMT. << miR-200 >>, a miRNA family with tumor suppressive functions in a wide range of cancers, was found reduced in response to [[ TAM ]] treatment.",1636,8
+1637,"Consistent with zinc finger E-box binding homeobox 2, which was confirmed as a direct target of miR-200b in endometrial cancer cell lines, some other key factors of EMT such as << Snail >> and N-cadherin increased, whereas E-cadherin decreased in the [[ TAM ]]-treated cells, contributing to TAM-induced EMT in these endometrial cancer cells.",1637,6
+1638,"Consistent with zinc finger E-box binding homeobox 2, which was confirmed as a direct target of miR-200b in endometrial cancer cell lines, some other key factors of EMT such as Snail and << N-cadherin >> increased, whereas E-cadherin decreased in the [[ TAM ]]-treated cells, contributing to TAM-induced EMT in these endometrial cancer cells.",1638,6
+1639,"Consistent with zinc finger E-box binding homeobox 2, which was confirmed as a direct target of miR-200b in endometrial cancer cell lines, some other key factors of EMT such as Snail and N-cadherin increased, whereas << E-cadherin >> decreased in the [[ TAM ]]-treated cells, contributing to TAM-induced EMT in these endometrial cancer cells.",1639,8
+1640,"In addition, we showed that c-Myc directly binds to and represses the promoter of miR-200 miRNAs, and its up-regulation in << TAM >>-treated endometrial cancer cells leads to the down-regulation of [[ miR-200 ]] and eventually to EMT.",1640,8
+1641,"Collectively, our data suggest that << TAM >> can repress the miR-200 family and induce EMT via the up-regulation of [[ c-Myc ]] in endometrial cancer cells.",1641,7
+1642,"Collectively, our data suggest that << TAM >> can repress the [[ miR-200 ]] family and induce EMT via the up-regulation of c-Myc in endometrial cancer cells.",1642,8
+1643,"Here, we show that oral administration of << resveratrol >>, which leads to activation of an [[ NAD(+)-dependent protein deacetylase SIRT1 ]], suppresses cardiac hypertrophy and fibrosis and restores cardiac diastolic function in dystrophin-deficient mdx mice.",1643,9
+1644,"The pro-hypertrophic co-activator p300 protein but not p300 mRNA was up-regulated in the mdx heart, and << resveratrol >> administration down-regulated the [[ p300 ]] protein level.",1644,8
+1645,"In cultured cardiomyocytes, cardiomyocyte hypertrophy induced by the α(1)-agonist phenylephrine was inhibited by the overexpression of SIRT1 as well as << resveratrol >>, both of which down-regulated [[ p300 ]] protein levels but not p300 mRNA levels.",1645,8
+1646,Synthesis and dual biological effects of << hydroxycinnamoyl phenylalanyl >>/prolyl hydroxamic acid derivatives as [[ tyrosinase ]] inhibitor and antioxidant.,1646,0
+1647,Synthesis and dual biological effects of hydroxycinnamoyl phenylalanyl/<< prolyl hydroxamic acid >> derivatives as [[ tyrosinase ]] inhibitor and antioxidant.,1647,0
+1648,"We previously reported that caffeoyl-amino acidyl-hydroxamic acid (<< CA-Xaa-NHOH >>) acted as both a good antioxidant and [[ tyrosinase ]] inhibitor, in particular when caffeic acid was conjugated with proline or amino acids having aromatic ring like phenylalanine.",1648,0
+1649,"We previously reported that << caffeoyl-amino acidyl-hydroxamic acid >> (CA-Xaa-NHOH) acted as both a good antioxidant and [[ tyrosinase ]] inhibitor, in particular when caffeic acid was conjugated with proline or amino acids having aromatic ring like phenylalanine.",1649,0
+1650,"In addition, derivatives of << caffeic acid >> and sinapic acid efficiently inhibited [[ tyrosinase ]] activity and reduced melanin content in melanocytes Mel-Ab cell.",1650,0
+1651,"In addition, derivatives of caffeic acid and << sinapic acid >> efficiently inhibited [[ tyrosinase ]] activity and reduced melanin content in melanocytes Mel-Ab cell.",1651,0
+1652,<< Ruxolitinib >> is a small-molecule inhibitor of [[ JAK1 ]] and JAK2 and recently became the first drug approved by the United States Food and Drug Administration for the treatment of symptomatic intermediate- or high-risk myelofibrosis.,1652,0
+1653,<< Ruxolitinib >> is a small-molecule inhibitor of JAK1 and [[ JAK2 ]] and recently became the first drug approved by the United States Food and Drug Administration for the treatment of symptomatic intermediate- or high-risk myelofibrosis.,1653,0
+1654,<< Pb >> and BaP treatments significantly increased active [[ caspase-3 ]] levels in a time-dependent manner.,1654,6
+1655,Pb and << BaP >> treatments significantly increased active [[ caspase-3 ]] levels in a time-dependent manner.,1655,6
+1656,<< TAA >> increased the number and area of [[ glutathione S-transferase placental form ]] (GST-P)(+) liver cell foci and the numbers of proliferating and apoptotic cells in randomly selected areas in liver sections.,1656,6
+1657,<< TAA >> increased the number and area of glutathione S-transferase placental form ([[ GST-P ]])(+) liver cell foci and the numbers of proliferating and apoptotic cells in randomly selected areas in liver sections.,1657,6
+1658,"<< TAA >> also increased the numbers of ED2(+), [[ cyclooxygenase-2 ]](+), and heme oxygenase-1(+) liver cells, as well as the number of CD3(+) lymphocytes.",1658,8
+1659,"<< TAA >> also increased the numbers of ED2(+), cyclooxygenase-2(+), and [[ heme oxygenase-1 ]](+) liver cells, as well as the number of CD3(+) lymphocytes.",1659,8
+1660,"<< TAA >> also increased the numbers of ED2(+), cyclooxygenase-2(+), and heme oxygenase-1(+) liver cells, as well as the number of [[ CD3 ]](+) lymphocytes.",1660,8
+1661,<< ICA-105574 >> interacts with a common binding site to elicit opposite effects on inactivation gating of [[ EAG ]] and ERG potassium channels.,1661,9
+1662,<< ICA-105574 >> interacts with a common binding site to elicit opposite effects on inactivation gating of EAG and [[ ERG ]] potassium channels.,1662,9
+1663,<< ICA-105574 >> interacts with a common binding site to elicit opposite effects on inactivation gating of EAG and ERG [[ potassium channels ]].,1663,9
+1664,"Although << ICA >> greatly attenuates [[ ERG ]] inactivation by shifting its voltage dependence to more positive potentials, it enhances the rate and extent of EAG inactivation without altering its voltage dependence.",1664,9
+1665,"Although << ICA >> greatly attenuates ERG inactivation by shifting its voltage dependence to more positive potentials, it enhances the rate and extent of [[ EAG ]] inactivation without altering its voltage dependence.",1665,0
+1666,<< ICA >> is a mixed agonist of mutant [[ EAG ]] and EAG/ERG chimera channels that inactivate by a combination of slow and fast mechanisms.,1666,2
+1667,<< ICA >> is a mixed agonist of mutant EAG and [[ EAG ]]/ERG chimera channels that inactivate by a combination of slow and fast mechanisms.,1667,2
+1668,<< ICA >> is a mixed agonist of mutant EAG and EAG/[[ ERG ]] chimera channels that inactivate by a combination of slow and fast mechanisms.,1668,2
+1669,PNU-282987 on the other hand displayed an increase in anxiety-like behavior at a higher dose (10 mg/kg) that was significantly reduced by the << serotonin 5-HT1a receptor >> antagonist [[ WAY-100135 ]].,1669,1
+1670,However the << α7 receptor >> antagonist [[ methyllycaconitine ]] was unable to reverse these anxiety-like effects seen with PNU-282987.,1670,1
+1671,<< Carnitine palmitoyltransferase 2 >> and carnitine/acylcarnitine translocase are involved in the mitochondrial synthesis and export of [[ acylcarnitines ]].,1671,4
+1672,Carnitine palmitoyltransferase 2 and << carnitine/acylcarnitine translocase >> are involved in the mitochondrial synthesis and export of [[ acylcarnitines ]].,1672,4
+1673,"This shows that << CPT2 >> and CACT are crucial for mitochondrial [[ acylcarnitine ]] formation and export to the extracellular fluids in mFAOD.-Violante, S., IJlst, L., te Brinke, H., Tavares de Almeida, I., Wanders, R.",1673,4
+1674,"This shows that CPT2 and << CACT >> are crucial for mitochondrial [[ acylcarnitine ]] formation and export to the extracellular fluids in mFAOD.-Violante, S., IJlst, L., te Brinke, H., Tavares de Almeida, I., Wanders, R.",1674,4
+1675,<< Carnitine palmitoyltransferase 2 >> and carnitine/acylcarnitine translocase are involved in the mitochondrial synthesis and export of [[ acylcarnitines ]].,1675,4
+1676,Carnitine palmitoyltransferase 2 and << carnitine/acylcarnitine translocase >> are involved in the mitochondrial synthesis and export of [[ acylcarnitines ]].,1676,4
+1677,"As a result of this study, << microgrewiapine A >> (1) was found to be a selective cytotoxic agent for colon cancer cells over normal colon cells and to exhibit [[ nicotinic receptor ]] antagonistic activity for both the hα3β4 and hα4β2 receptor subtypes.",1677,1
+1678,PURPOSE: To characterise further the previously observed cytochrome P450 3A4 (CYP3A4) interaction of the dual << orexin receptor >> antagonist [[ almorexant ]].,1678,1
+1679,"Commercially-available << 5-HT2C >> agonists ([[ CP 809101 ]], Ro 60-0175, WAY 161503, mCPP, and 1-methylpsilocin), novel 4-phenyl-2-N,N-dimethyl-aminotetralin (PAT)-type 5-HT2C agonists (with 5-HT2A/2B antagonist activity), and antagonists selective for 5-HT2A (M100907), 5-HT2C (SB-242084), and 5-HT2B/2C (SB-206553) receptors attenuated the DOI-elicited-HTR.",1679,2
+1680,"Commercially-available << 5-HT2C >> agonists (CP 809101, [[ Ro 60-0175 ]], WAY 161503, mCPP, and 1-methylpsilocin), novel 4-phenyl-2-N,N-dimethyl-aminotetralin (PAT)-type 5-HT2C agonists (with 5-HT2A/2B antagonist activity), and antagonists selective for 5-HT2A (M100907), 5-HT2C (SB-242084), and 5-HT2B/2C (SB-206553) receptors attenuated the DOI-elicited-HTR.",1680,2
+1681,"Commercially-available << 5-HT2C >> agonists (CP 809101, Ro 60-0175, [[ WAY 161503 ]], mCPP, and 1-methylpsilocin), novel 4-phenyl-2-N,N-dimethyl-aminotetralin (PAT)-type 5-HT2C agonists (with 5-HT2A/2B antagonist activity), and antagonists selective for 5-HT2A (M100907), 5-HT2C (SB-242084), and 5-HT2B/2C (SB-206553) receptors attenuated the DOI-elicited-HTR.",1681,2
+1682,"Commercially-available << 5-HT2C >> agonists (CP 809101, Ro 60-0175, WAY 161503, [[ mCPP ]], and 1-methylpsilocin), novel 4-phenyl-2-N,N-dimethyl-aminotetralin (PAT)-type 5-HT2C agonists (with 5-HT2A/2B antagonist activity), and antagonists selective for 5-HT2A (M100907), 5-HT2C (SB-242084), and 5-HT2B/2C (SB-206553) receptors attenuated the DOI-elicited-HTR.",1682,2
+1683,"Commercially-available << 5-HT2C >> agonists (CP 809101, Ro 60-0175, WAY 161503, mCPP, and [[ 1-methylpsilocin ]]), novel 4-phenyl-2-N,N-dimethyl-aminotetralin (PAT)-type 5-HT2C agonists (with 5-HT2A/2B antagonist activity), and antagonists selective for 5-HT2A (M100907), 5-HT2C (SB-242084), and 5-HT2B/2C (SB-206553) receptors attenuated the DOI-elicited-HTR.",1683,2
+1684,"Commercially-available 5-HT2C agonists (CP 809101, Ro 60-0175, WAY 161503, mCPP, and 1-methylpsilocin), novel << 4-phenyl-2-N,N-dimethyl-aminotetralin >> (PAT)-type [[ 5-HT2C ]] agonists (with 5-HT2A/2B antagonist activity), and antagonists selective for 5-HT2A (M100907), 5-HT2C (SB-242084), and 5-HT2B/2C (SB-206553) receptors attenuated the DOI-elicited-HTR.",1684,2
+1685,"Commercially-available 5-HT2C agonists (CP 809101, Ro 60-0175, WAY 161503, mCPP, and 1-methylpsilocin), novel 4-phenyl-2-N,N-dimethyl-aminotetralin (<< PAT >>)-type [[ 5-HT2C ]] agonists (with 5-HT2A/2B antagonist activity), and antagonists selective for 5-HT2A (M100907), 5-HT2C (SB-242084), and 5-HT2B/2C (SB-206553) receptors attenuated the DOI-elicited-HTR.",1685,2
+1686,"Commercially-available 5-HT2C agonists (CP 809101, Ro 60-0175, WAY 161503, mCPP, and 1-methylpsilocin), novel 4-phenyl-2-N,N-dimethyl-aminotetralin (PAT)-type 5-HT2C agonists (with 5-HT2A/2B antagonist activity), and antagonists selective for << 5-HT2A >> ([[ M100907 ]]), 5-HT2C (SB-242084), and 5-HT2B/2C (SB-206553) receptors attenuated the DOI-elicited-HTR.",1686,1
+1687,"Commercially-available 5-HT2C agonists (CP 809101, Ro 60-0175, WAY 161503, mCPP, and 1-methylpsilocin), novel 4-phenyl-2-N,N-dimethyl-aminotetralin (PAT)-type 5-HT2C agonists (with 5-HT2A/2B antagonist activity), and antagonists selective for 5-HT2A (M100907), << 5-HT2C >> ([[ SB-242084 ]]), and 5-HT2B/2C (SB-206553) receptors attenuated the DOI-elicited-HTR.",1687,1
+1688,In vitro molecular pharmacology studies showed that 5-HT2C agonists potent for attenuating the DOI-elicited-HTR also reduced the efficacy of << DOI >> to activate [[ mouse 5-HT2C ]] receptor-mediated PLC signaling in HEK cells.,1688,9
+1689,"<< Methadone >> N-demethylation in vitro is catalyzed by hepatic cytochrome P4502B6 (CYP2B6) and CYP3A4, but clinical disposition is often attributed to [[ CYP3A4 ]].",1689,5
+1690,"<< Methadone >> N-demethylation in vitro is catalyzed by hepatic [[ cytochrome P4502B6 ]] (CYP2B6) and CYP3A4, but clinical disposition is often attributed to CYP3A4.",1690,5
+1691,"<< Methadone >> N-demethylation in vitro is catalyzed by hepatic cytochrome P4502B6 ([[ CYP2B6 ]]) and CYP3A4, but clinical disposition is often attributed to CYP3A4.",1691,5
+1692,"<< Methadone >> N-demethylation in vitro is catalyzed by hepatic cytochrome P4502B6 (CYP2B6) and [[ CYP3A4 ]], but clinical disposition is often attributed to CYP3A4.",1692,5
+1693,"Methadone << N >>-demethylation in vitro is catalyzed by hepatic cytochrome P4502B6 (CYP2B6) and CYP3A4, but clinical disposition is often attributed to [[ CYP3A4 ]].",1693,5
+1694,"Methadone << N >>-demethylation in vitro is catalyzed by hepatic [[ cytochrome P4502B6 ]] (CYP2B6) and CYP3A4, but clinical disposition is often attributed to CYP3A4.",1694,5
+1695,"Methadone << N >>-demethylation in vitro is catalyzed by hepatic cytochrome P4502B6 ([[ CYP2B6 ]]) and CYP3A4, but clinical disposition is often attributed to CYP3A4.",1695,5
+1696,"Methadone << N >>-demethylation in vitro is catalyzed by hepatic cytochrome P4502B6 (CYP2B6) and [[ CYP3A4 ]], but clinical disposition is often attributed to CYP3A4.",1696,5
+1697,"This investigation tested the hypothesis that CYP2B6 is a prominent CYP isoform responsible for clinical methadone N-demethylation and clearance, using the in vivo mechanism-based << CYP2B6 >> inhibitor [[ ticlopidine ]], given orally for 4 days.",1697,0
+1698,"This investigation tested the hypothesis that << CYP2B6 >> is a prominent CYP isoform responsible for clinical [[ methadone ]] N-demethylation and clearance, using the in vivo mechanism-based CYP2B6 inhibitor ticlopidine, given orally for 4 days.",1698,5
+1699,"This investigation tested the hypothesis that CYP2B6 is a prominent << CYP >> isoform responsible for clinical [[ methadone ]] N-demethylation and clearance, using the in vivo mechanism-based CYP2B6 inhibitor ticlopidine, given orally for 4 days.",1699,5
+1700,"This investigation tested the hypothesis that << CYP2B6 >> is a prominent CYP isoform responsible for clinical methadone [[ N ]]-demethylation and clearance, using the in vivo mechanism-based CYP2B6 inhibitor ticlopidine, given orally for 4 days.",1700,5
+1701,"This investigation tested the hypothesis that CYP2B6 is a prominent << CYP >> isoform responsible for clinical methadone [[ N ]]-demethylation and clearance, using the in vivo mechanism-based CYP2B6 inhibitor ticlopidine, given orally for 4 days.",1701,5
+1702,"CYP2B6 inhibition reduces methadone N-demethylation and clearance, and alters methadone concentrations, demonstrating an important role for << CYP2B6 >> in clinical [[ methadone ]] disposition.",1702,5
+1703,"We found that treatment of both differentiated dopaminergic-like SH-SY5Y cells and rat midbrain slices with the dopamine D2 receptor (D2R) agonist, << quinpirole >>, triggered an increase in the expression of [[ GDNF ]] that was temporally preceded by an increase in the levels of zinc-finger protein 268 (Zif268), a DNA-binding transcription factor encoded by an immediate-early gene.",1703,6
+1704,"We found that treatment of both differentiated dopaminergic-like SH-SY5Y cells and rat midbrain slices with the dopamine D2 receptor (D2R) agonist, << quinpirole >>, triggered an increase in the expression of GDNF that was temporally preceded by an increase in the levels of [[ zinc-finger protein 268 ]] (Zif268), a DNA-binding transcription factor encoded by an immediate-early gene.",1704,6
+1705,"We found that treatment of both differentiated dopaminergic-like SH-SY5Y cells and rat midbrain slices with the dopamine D2 receptor (D2R) agonist, << quinpirole >>, triggered an increase in the expression of GDNF that was temporally preceded by an increase in the levels of zinc-finger protein 268 ([[ Zif268 ]]), a DNA-binding transcription factor encoded by an immediate-early gene.",1705,6
+1706,"We found that treatment of both differentiated dopaminergic-like SH-SY5Y cells and rat midbrain slices with the << dopamine D2 receptor >> (D2R) agonist, [[ quinpirole ]], triggered an increase in the expression of GDNF that was temporally preceded by an increase in the levels of zinc-finger protein 268 (Zif268), a DNA-binding transcription factor encoded by an immediate-early gene.",1706,2
+1707,"We found that treatment of both differentiated dopaminergic-like SH-SY5Y cells and rat midbrain slices with the dopamine D2 receptor (<< D2R >>) agonist, [[ quinpirole ]], triggered an increase in the expression of GDNF that was temporally preceded by an increase in the levels of zinc-finger protein 268 (Zif268), a DNA-binding transcription factor encoded by an immediate-early gene.",1707,2
+1708,"Moreover, the D2R inhibitor << raclopride >> blocked the increase of both [[ GDNF ]] and Zif268 expression following potassium-evoked dopamine release in SH-SY5Y cells.",1708,8
+1709,"Moreover, the D2R inhibitor << raclopride >> blocked the increase of both GDNF and [[ Zif268 ]] expression following potassium-evoked dopamine release in SH-SY5Y cells.",1709,8
+1710,"Moreover, the << D2R >> inhibitor [[ raclopride ]] blocked the increase of both GDNF and Zif268 expression following potassium-evoked dopamine release in SH-SY5Y cells.",1710,0
+1711,"Synthesis and biological evaluation of << 1,3,4-thiadiazole >> analogues as novel [[ AChE ]] and BuChE inhibitors.",1711,0
+1712,"Synthesis and biological evaluation of << 1,3,4-thiadiazole >> analogues as novel AChE and [[ BuChE ]] inhibitors.",1712,0
+1713,"In this paper a series of new << 1,3,4-thiadiazole >> derivatives has been designed, synthesized and evaluated as the [[ acetyl- and butyrylcholinesterase ]] inhibitors.",1713,0
+1714,"<< LY294002 >>, a specific PI3K/AKT inhibitor, selectively activated the [[ p38 ]] MAPK kinase pathway and enhanced c-Jun phosphorylation, but did not activate JNK.",1714,9
+1715,"<< LY294002 >>, a specific PI3K/AKT inhibitor, selectively activated the p38 [[ MAPK ]] kinase pathway and enhanced c-Jun phosphorylation, but did not activate JNK.",1715,9
+1716,"<< LY294002 >>, a specific PI3K/AKT inhibitor, selectively activated the p38 MAPK [[ kinase ]] pathway and enhanced c-Jun phosphorylation, but did not activate JNK.",1716,9
+1717,"<< LY294002 >>, a specific PI3K/AKT inhibitor, selectively activated the p38 MAPK kinase pathway and enhanced [[ c-Jun ]] phosphorylation, but did not activate JNK.",1717,9
+1718,"<< LY294002 >>, a specific [[ PI3K ]]/AKT inhibitor, selectively activated the p38 MAPK kinase pathway and enhanced c-Jun phosphorylation, but did not activate JNK.",1718,0
+1719,"<< LY294002 >>, a specific PI3K/[[ AKT ]] inhibitor, selectively activated the p38 MAPK kinase pathway and enhanced c-Jun phosphorylation, but did not activate JNK.",1719,0
+1720,The pharmacological inhibitors << SB203580 >> ([[ p38 ]] inhibitor) and SP600125 (a JNK inhibitor) protected primary cultures of rat CGCs from LY294002-induced apoptosis.,1720,0
+1721,The pharmacological inhibitors SB203580 (p38 inhibitor) and << SP600125 >> (a [[ JNK ]] inhibitor) protected primary cultures of rat CGCs from LY294002-induced apoptosis.,1721,0
+1722,"Today, we used << cobalt chloride >>, a hypoxia mimetic that inhibits proteasomal [[ HIF-1 ]] degradation and generates reactive oxygen species (ROS).",1722,6
+1723,"An autophagic signaling was evidenced by an increase of Beclin-1, ATG 5-12, and LC3-II expression whereas the << p53 >>(mut) presence decreased with [[ CoCl2 ]] time exposure.",1723,8
+1724,Cellular responses to DNA damage induced by << etoposide >> or doxorubicin include down-regulation of endogenous supervillin coincident with increases in [[ p53 ]].,1724,6
+1725,Cellular responses to DNA damage induced by etoposide or << doxorubicin >> include down-regulation of endogenous supervillin coincident with increases in [[ p53 ]].,1725,6
+1726,Cellular responses to DNA damage induced by << etoposide >> or doxorubicin include down-regulation of endogenous [[ supervillin ]] coincident with increases in p53.,1726,8
+1727,Cellular responses to DNA damage induced by etoposide or << doxorubicin >> include down-regulation of endogenous [[ supervillin ]] coincident with increases in p53.,1727,8
+1728,Novel << acylethanolamide >> derivatives that modulate body weight through enhancement of hypothalamic pro-opiomelanocortin ([[ POMC ]]) and/or decreased neuropeptide Y (NPY).,1728,7
+1729,Novel << acylethanolamide >> derivatives that modulate body weight through enhancement of hypothalamic [[ pro-opiomelanocortin ]] (POMC) and/or decreased neuropeptide Y (NPY).,1729,7
+1730,Novel << acylethanolamide >> derivatives that modulate body weight through enhancement of hypothalamic pro-opiomelanocortin (POMC) and/or decreased [[ neuropeptide Y ]] (NPY).,1730,3
+1731,Novel << acylethanolamide >> derivatives that modulate body weight through enhancement of hypothalamic pro-opiomelanocortin (POMC) and/or decreased neuropeptide Y ([[ NPY ]]).,1731,3
+1732,"<< Dexamethasone >> suppressed [[ IL-11 ]] gene transcription enhanced by PTH(1-34) without affecting ΔFosB expression or Smad1 phosphorylation, and dexamethasone-GC receptor complex was bound to JunD, which forms heterodimers with ΔFosB.",1732,8
+1733,Number and area of preneoplastic foci positive for << glutathione S-transferase placental form >> (GST-P) were consistently higher in these groups than the sum of individual values in the groups treated with [[ HEP ]] or HCB alone.,1733,6
+1734,Number and area of preneoplastic foci positive for glutathione S-transferase placental form (<< GST-P >>) were consistently higher in these groups than the sum of individual values in the groups treated with [[ HEP ]] or HCB alone.,1734,6
+1735,Number and area of preneoplastic foci positive for << glutathione S-transferase placental form >> (GST-P) were consistently higher in these groups than the sum of individual values in the groups treated with HEP or [[ HCB ]] alone.,1735,6
+1736,Number and area of preneoplastic foci positive for glutathione S-transferase placental form (<< GST-P >>) were consistently higher in these groups than the sum of individual values in the groups treated with HEP or [[ HCB ]] alone.,1736,6
+1737,"On the basis of these findings, we conclude that << HEP >> and HCB have additive and synergistic effects on the development of [[ GST-P ]]-positive foci and that higher risks are associated with a combination of residual organochlorine pesticides in foods than with individual residual organochlorine pesticides.",1737,6
+1738,"On the basis of these findings, we conclude that HEP and << HCB >> have additive and synergistic effects on the development of [[ GST-P ]]-positive foci and that higher risks are associated with a combination of residual organochlorine pesticides in foods than with individual residual organochlorine pesticides.",1738,6
+1739,The food contaminant << deoxynivalenol >> activates the [[ mitogen activated protein kinases ]] in the intestine: interest of ex vivo models as an alternative to in vivo experiments.,1739,9
+1740,Taken together these results indicate that in vivo or ex vivo exposure of intestinal tissue to << DON >> lead to similar intestinal lesions and activation of [[ MAPK ]].,1740,9
+1741,<< Paeoniflorin >> protects human EA.hy926 endothelial cells against gamma-radiation induced oxidative injury by activating the [[ NF-E2-related factor 2 ]]/heme oxygenase-1 pathway.,1741,9
+1742,<< Paeoniflorin >> protects human EA.hy926 endothelial cells against gamma-radiation induced oxidative injury by activating the NF-E2-related factor 2/[[ heme oxygenase-1 ]] pathway.,1742,9
+1743,"In particular, we showed that << Paeoniflorin >> significantly reduced the formation of intracellular reactive oxygen species (ROS), the level of malondialdehyde (MDA) and lactate dehydrogenase (LDH) leakage, and enhanced production of the endogenous antioxidants, glutathione (GSH) and [[ superoxide dismutase ]] (SOD) in EA.hy926 cells.",1743,6
+1744,"In particular, we showed that << Paeoniflorin >> significantly reduced the formation of intracellular reactive oxygen species (ROS), the level of malondialdehyde (MDA) and lactate dehydrogenase (LDH) leakage, and enhanced production of the endogenous antioxidants, glutathione (GSH) and superoxide dismutase ([[ SOD ]]) in EA.hy926 cells.",1744,6
+1745,"In particular, we showed that << Paeoniflorin >> significantly reduced the formation of intracellular reactive oxygen species (ROS), the level of malondialdehyde (MDA) and [[ lactate dehydrogenase ]] (LDH) leakage, and enhanced production of the endogenous antioxidants, glutathione (GSH) and superoxide dismutase (SOD) in EA.hy926 cells.",1745,8
+1746,"In particular, we showed that << Paeoniflorin >> significantly reduced the formation of intracellular reactive oxygen species (ROS), the level of malondialdehyde (MDA) and lactate dehydrogenase ([[ LDH ]]) leakage, and enhanced production of the endogenous antioxidants, glutathione (GSH) and superoxide dismutase (SOD) in EA.hy926 cells.",1746,8
+1747,Treatment of these cells with << Paeoniflorin >> significantly induced [[ HO-1 ]] expression.,1747,6
+1748,The << Paeoniflorin >>-induced [[ HO-1 ]] expression was abrogated by Nrf2 siRNA.,1748,6
+1749,"Furthermore, inhibition of << HO-1 >> with zinc protoporphyrin IX (ZNPP) significantly reversed the protective effect of [[ Paeoniflorin ]] against radiation-induced damage in EA.hy926 cells.",1749,9
+1750,"Furthermore, inhibition of << HO-1 >> with [[ zinc protoporphyrin IX ]] (ZNPP) significantly reversed the protective effect of Paeoniflorin against radiation-induced damage in EA.hy926 cells.",1750,0
+1751,"Furthermore, inhibition of << HO-1 >> with zinc protoporphyrin IX ([[ ZNPP ]]) significantly reversed the protective effect of Paeoniflorin against radiation-induced damage in EA.hy926 cells.",1751,0
+1752,Our findings confirmed that << Paeoniflorin >> protected EA.hy926 cells against radiation-induced injury through the [[ Nrf2 ]]/HO-1 pathway.,1752,9
+1753,Our findings confirmed that << Paeoniflorin >> protected EA.hy926 cells against radiation-induced injury through the Nrf2/[[ HO-1 ]] pathway.,1753,9
+1754,"<< Palonosetron >>, a second-generation [[ 5-HT3 ]] receptor antagonist with a different half-life, a different binding capacity and a different mechanism of action than the first-generation 5-HT3 receptor antagonists appears to be the most effective agent in its class.",1754,1
+1755,"<< Aprepitant >>, the first and only agent clinically available in the [[ NK1 receptor ]] antagonist drug class has been used effectively as an additive agent to the 5-HT3 receptor antagonists and dexamethasone to control CINV.",1755,1
+1756,<< Rolapitant >> and netupitant are other [[ NK1 receptor ]] antagonists that are currently in phase III clinical trials.,1756,1
+1757,Rolapitant and << netupitant >> are other [[ NK1 receptor ]] antagonists that are currently in phase III clinical trials.,1757,1
+1758,Moderate inhibitory effect of << LDL >>-C oxidation by [[ phytosteryl phenolates ]] was observed.,1758,8
+1759,"Aqueous << ethanol >> (80%) extract of lentil hulls exhibited high antioxidant and anti-inflammatory activities preferentially inhibiting [[ 15-LOX ]] (IC(50), 55 μg/ml), with moderate COX-1 (IC(50), 66 μg/ml) and COX-2 (IC(50), 119 μg/ml) inhibitory effects on the COX pathway, whereas faba bean hull extracts exerted relatively mild LOX inhibitory activity.",1759,0
+1760,"Aqueous << ethanol >> (80%) extract of lentil hulls exhibited high antioxidant and anti-inflammatory activities preferentially inhibiting 15-LOX (IC(50), 55 μg/ml), with moderate [[ COX-1 ]] (IC(50), 66 μg/ml) and COX-2 (IC(50), 119 μg/ml) inhibitory effects on the COX pathway, whereas faba bean hull extracts exerted relatively mild LOX inhibitory activity.",1760,0
+1761,"Aqueous << ethanol >> (80%) extract of lentil hulls exhibited high antioxidant and anti-inflammatory activities preferentially inhibiting 15-LOX (IC(50), 55 μg/ml), with moderate COX-1 (IC(50), 66 μg/ml) and [[ COX-2 ]] (IC(50), 119 μg/ml) inhibitory effects on the COX pathway, whereas faba bean hull extracts exerted relatively mild LOX inhibitory activity.",1761,0
+1762,"Aqueous << ethanol >> (80%) extract of lentil hulls exhibited high antioxidant and anti-inflammatory activities preferentially inhibiting 15-LOX (IC(50), 55 μg/ml), with moderate COX-1 (IC(50), 66 μg/ml) and COX-2 (IC(50), 119 μg/ml) inhibitory effects on the [[ COX ]] pathway, whereas faba bean hull extracts exerted relatively mild LOX inhibitory activity.",1762,0
+1763,"Aqueous << ethanol >> (80%) extract of lentil hulls exhibited high antioxidant and anti-inflammatory activities preferentially inhibiting 15-LOX (IC(50), 55 μg/ml), with moderate COX-1 (IC(50), 66 μg/ml) and COX-2 (IC(50), 119 μg/ml) inhibitory effects on the COX pathway, whereas faba bean hull extracts exerted relatively mild [[ LOX ]] inhibitory activity.",1763,0
+1764,"<< Histidine decarboxylase >> (HDC) catalyses the formation of histamine, a bioactive [[ amine ]].",1764,4
+1765,"Histidine decarboxylase (<< HDC >>) catalyses the formation of histamine, a bioactive [[ amine ]].",1765,4
+1766,"<< Histidine decarboxylase >> (HDC) catalyses the formation of [[ histamine ]], a bioactive amine.",1766,4
+1767,"Histidine decarboxylase (<< HDC >>) catalyses the formation of [[ histamine ]], a bioactive amine.",1767,4
+1768,"We searched for inhibitors of << HDC >> from the [[ ethyl acetate ]] extract of the petal of Filipendula ulmaria, also called meadowsweet.",1768,0
+1769,Discovery of a novel series of << quinolone >> [[ α7 nicotinic acetylcholine receptor ]] agonists.,1769,2
+1770,High throughput screening led to the identification of a novel series of << quinolone >> α7 nicotinic acetylcholine receptor ([[ nAChR ]]) agonists.,1770,2
+1771,High throughput screening led to the identification of a novel series of << quinolone >> [[ α7 nicotinic acetylcholine receptor ]] (nAChR) agonists.,1771,2
+1772,<< Amino acid >> derived quinazolines as [[ Rock ]]/PKA inhibitors.,1772,0
+1773,<< Amino acid >> derived quinazolines as Rock/[[ PKA ]] inhibitors.,1773,0
+1774,Amino acid derived << quinazolines >> as [[ Rock ]]/PKA inhibitors.,1774,0
+1775,Amino acid derived << quinazolines >> as Rock/[[ PKA ]] inhibitors.,1775,0
+1776,SAR and lead optimization studies for << Rock >> inhibitors based on [[ amino acid ]]-derived quinazolines are described.,1776,0
+1777,SAR and lead optimization studies for << Rock >> inhibitors based on amino acid-derived [[ quinazolines ]] are described.,1777,0
+1778,"This is distinct from << Rock >> inhibitors based on non-[[ amino acid ]] derived quinazolinones, where high selectivity against PKA could be obtained.(22) The inhibitors presented here in some cases possessed sub-nanomolar inhibition of Rock, nanomolar potency in ppMLC cell based assays, low to fair cytochrome P-450 inhibition, and good human microsomal stability.",1778,0
+1779,"This is distinct from Rock inhibitors based on non-<< amino acid >> derived quinazolinones, where high selectivity against [[ PKA ]] could be obtained.(22) The inhibitors presented here in some cases possessed sub-nanomolar inhibition of Rock, nanomolar potency in ppMLC cell based assays, low to fair cytochrome P-450 inhibition, and good human microsomal stability.",1779,0
+1780,"This is distinct from << Rock >> inhibitors based on non-amino acid derived [[ quinazolinones ]], where high selectivity against PKA could be obtained.(22) The inhibitors presented here in some cases possessed sub-nanomolar inhibition of Rock, nanomolar potency in ppMLC cell based assays, low to fair cytochrome P-450 inhibition, and good human microsomal stability.",1780,0
+1781,"This is distinct from Rock inhibitors based on non-amino acid derived << quinazolinones >>, where high selectivity against [[ PKA ]] could be obtained.(22) The inhibitors presented here in some cases possessed sub-nanomolar inhibition of Rock, nanomolar potency in ppMLC cell based assays, low to fair cytochrome P-450 inhibition, and good human microsomal stability.",1781,0
+1782,"The << cyclooxygenase-2 >> inhibitor, [[ diflunisal ]], is used in the clinic for its anti-inflammatory activity.",1782,0
+1783,"Although there was no change in the levels of insulin receptor (IR), Akt (protein kinase B) and glucose transporter-4 (GLUT4) messenger RNA, << BPA >> significantly decreased the IR, [[ Akt ]] and GLUT4 protein levels (both plasma membrane and cytosolic fraction) of the gastrocnemius muscle.",1783,8
+1784,"Although there was no change in the levels of insulin receptor (IR), Akt (protein kinase B) and glucose transporter-4 (GLUT4) messenger RNA, << BPA >> significantly decreased the IR, Akt and [[ GLUT4 ]] protein levels (both plasma membrane and cytosolic fraction) of the gastrocnemius muscle.",1784,8
+1785,"Although there was no change in the levels of insulin receptor (IR), Akt (protein kinase B) and glucose transporter-4 (GLUT4) messenger RNA, << BPA >> significantly decreased the [[ IR ]], Akt and GLUT4 protein levels (both plasma membrane and cytosolic fraction) of the gastrocnemius muscle.",1785,8
+1786,"In conclusion, << BPA >> has adverse effects on phosphorylation of Akt, [[ GLUT4 ]] translocation and (14)C-glucose oxidation.",1786,8
+1787,"In conclusion, << BPA >> has adverse effects on phosphorylation of [[ Akt ]], GLUT4 translocation and (14)C-glucose oxidation.",1787,0
+1788,"The obtained results showed that << Cd >> increased lipid peroxidation and abnormal sperm count and decreased plasma testosterone, [[ lactate dehydrogenase ]], acid phosphatase, alkaline phosphatase and testicular steroidogenic enzymes: 3β-hydroxysteroid dehydrogenase (HSD), 17β-HSD activities as well as epididymal sperm counts and motility, while RUT and Se treatment reversed this change to control values.",1788,0
+1789,"The obtained results showed that << Cd >> increased lipid peroxidation and abnormal sperm count and decreased plasma testosterone, lactate dehydrogenase, [[ acid phosphatase ]], alkaline phosphatase and testicular steroidogenic enzymes: 3β-hydroxysteroid dehydrogenase (HSD), 17β-HSD activities as well as epididymal sperm counts and motility, while RUT and Se treatment reversed this change to control values.",1789,0
+1790,"The obtained results showed that << Cd >> increased lipid peroxidation and abnormal sperm count and decreased plasma testosterone, lactate dehydrogenase, acid phosphatase, [[ alkaline phosphatase ]] and testicular steroidogenic enzymes: 3β-hydroxysteroid dehydrogenase (HSD), 17β-HSD activities as well as epididymal sperm counts and motility, while RUT and Se treatment reversed this change to control values.",1790,0
+1791,"The obtained results showed that << Cd >> increased lipid peroxidation and abnormal sperm count and decreased plasma testosterone, lactate dehydrogenase, acid phosphatase, alkaline phosphatase and [[ testicular steroidogenic enzymes ]]: 3β-hydroxysteroid dehydrogenase (HSD), 17β-HSD activities as well as epididymal sperm counts and motility, while RUT and Se treatment reversed this change to control values.",1791,0
+1792,"The obtained results showed that << Cd >> increased lipid peroxidation and abnormal sperm count and decreased plasma testosterone, lactate dehydrogenase, acid phosphatase, alkaline phosphatase and testicular steroidogenic enzymes: [[ 3β-hydroxysteroid dehydrogenase ]] (HSD), 17β-HSD activities as well as epididymal sperm counts and motility, while RUT and Se treatment reversed this change to control values.",1792,0
+1793,"The obtained results showed that << Cd >> increased lipid peroxidation and abnormal sperm count and decreased plasma testosterone, lactate dehydrogenase, acid phosphatase, alkaline phosphatase and testicular steroidogenic enzymes: 3β-hydroxysteroid dehydrogenase ([[ HSD ]]), 17β-HSD activities as well as epididymal sperm counts and motility, while RUT and Se treatment reversed this change to control values.",1793,0
+1794,"The obtained results showed that << Cd >> increased lipid peroxidation and abnormal sperm count and decreased plasma testosterone, lactate dehydrogenase, acid phosphatase, alkaline phosphatase and testicular steroidogenic enzymes: 3β-hydroxysteroid dehydrogenase (HSD), [[ 17β-HSD ]] activities as well as epididymal sperm counts and motility, while RUT and Se treatment reversed this change to control values.",1794,0
+1795,"Acute intoxication with << Cd >> was also followed by significantly decreased activity of the antioxidant defence system (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GR), glutathione (GSH), and glutathione-S-transferase ([[ GST ]])).",1795,0
+1796,"Acute intoxication with << Cd >> was also followed by significantly decreased activity of the antioxidant defence system ([[ superoxide dismutase ]] (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GR), glutathione (GSH), and glutathione-S-transferase (GST)).",1796,0
+1797,"Acute intoxication with << Cd >> was also followed by significantly decreased activity of the antioxidant defence system (superoxide dismutase ([[ SOD ]]), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GR), glutathione (GSH), and glutathione-S-transferase (GST)).",1797,0
+1798,"Acute intoxication with << Cd >> was also followed by significantly decreased activity of the antioxidant defence system (superoxide dismutase (SOD), [[ catalase ]] (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GR), glutathione (GSH), and glutathione-S-transferase (GST)).",1798,0
+1799,"Acute intoxication with << Cd >> was also followed by significantly decreased activity of the antioxidant defence system (superoxide dismutase (SOD), catalase ([[ CAT ]]), glutathione peroxidase (GSH-Px), glutathione reductase (GR), glutathione (GSH), and glutathione-S-transferase (GST)).",1799,0
+1800,"Acute intoxication with << Cd >> was also followed by significantly decreased activity of the antioxidant defence system (superoxide dismutase (SOD), catalase (CAT), [[ glutathione peroxidase ]] (GSH-Px), glutathione reductase (GR), glutathione (GSH), and glutathione-S-transferase (GST)).",1800,0
+1801,"Acute intoxication with << Cd >> was also followed by significantly decreased activity of the antioxidant defence system (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase ([[ GSH-Px ]]), glutathione reductase (GR), glutathione (GSH), and glutathione-S-transferase (GST)).",1801,0
+1802,"Acute intoxication with << Cd >> was also followed by significantly decreased activity of the antioxidant defence system (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), [[ glutathione reductase ]] (GR), glutathione (GSH), and glutathione-S-transferase (GST)).",1802,0
+1803,"Acute intoxication with << Cd >> was also followed by significantly decreased activity of the antioxidant defence system (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase ([[ GR ]]), glutathione (GSH), and glutathione-S-transferase (GST)).",1803,0
+1804,"Acute intoxication with << Cd >> was also followed by significantly decreased activity of the antioxidant defence system (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GR), glutathione (GSH), and [[ glutathione-S-transferase ]] (GST)).",1804,0
+1805,"The << tyrosine hydroxylase >> inhibitor [[ α-methyltyrosine ]] (300µM, 24h) completely abolished MeHg-induced DA release.",1805,0
+1806,"MeHg significantly increased DA precursor accumulation in cells treated with 3-hydroxybenzylhydrazine (10µM), revealing that << MeHg >> increases [[ tyrosine hydroxylase ]] activity.",1806,9
+1807,"The solubility-driven structural modification of (pyridin-3-yl) benzoxazinyl-oxazolidinones is described, which resulted in the development of a new series of << benzoxazinyl-oxazolidinone >> analogues with high antibacterial activity against Gram-positive pathogens, including that against linezolid-resistant strains and low [[ hERG ]] inhibition.",1807,0
+1808,Secondary point mutations in the Fms-like tyrosine kinase 3 (FLT3) tyrosine kinase domain (KD) are common causes of acquired clinical resistance to the << FLT3 >> inhibitors [[ AC220 ]] (quizartinib) and sorafenib.,1808,0
+1809,Secondary point mutations in the Fms-like tyrosine kinase 3 (FLT3) tyrosine kinase domain (KD) are common causes of acquired clinical resistance to the << FLT3 >> inhibitors AC220 ([[ quizartinib ]]) and sorafenib.,1809,0
+1810,Secondary point mutations in the Fms-like tyrosine kinase 3 (FLT3) tyrosine kinase domain (KD) are common causes of acquired clinical resistance to the << FLT3 >> inhibitors AC220 (quizartinib) and [[ sorafenib ]].,1810,0
+1811,"<< Ponatinib >> (AP24534) is a [[ multikinase ]] inhibitor with in vitro and clinical activity in tyrosine kinase inhibitor (TKI)-resistant chronic myeloid leukemia, irrespective of BCR-ABL KD mutation.",1811,0
+1812,"Ponatinib (<< AP24534 >>) is a [[ multikinase ]] inhibitor with in vitro and clinical activity in tyrosine kinase inhibitor (TKI)-resistant chronic myeloid leukemia, irrespective of BCR-ABL KD mutation.",1812,0
+1813,"However, the involvement of the caspase-dependent pathway in the process of cell death induced by either BSC 3g or 3n is discarded since cell death could not be prevented by pretreatment with the pan<< caspase >> inhibitor [[ z-VAD-fmk ]].",1813,0
+1814,"Moreover, since reduced levels of << p21CIP1 >> and Chk2 proteins but no change in p53 levels could be detected in MCF-7 cells after [[ BSC ]] 3g or 3n treatment our results suggest that BSC treated cells die from lethal mitosis.",1814,8
+1815,"Moreover, since reduced levels of p21CIP1 and << Chk2 >> proteins but no change in p53 levels could be detected in MCF-7 cells after [[ BSC ]] 3g or 3n treatment our results suggest that BSC treated cells die from lethal mitosis.",1815,8
+1816,A one-pot domino synthesis and discovery of highly functionalized << dihydrobenzo[b]thiophenes >> as [[ AChE ]] inhibitors.,1816,0
+1817,"These compounds were evaluated for their acetylcholinesterase (AChE) inhibitory activity and << 5-amino-2,7-bis(4-methoxyphenyl)-2,3-dihydrobenzo[b]thiophene-4,6-dicarbonitrile >> was found to be the most potent against [[ AChE ]] with IC50 4.16 μmol/L.",1817,0
+1818,"Furthermore, knockdown of OPN enhanced cell death caused by other drugs, including << paclitaxel >>, doxorubicin, actinomycin-D, and rapamycin, which are also [[ P-gp ]] substrates.",1818,5
+1819,"Furthermore, knockdown of OPN enhanced cell death caused by other drugs, including paclitaxel, << doxorubicin >>, actinomycin-D, and rapamycin, which are also [[ P-gp ]] substrates.",1819,5
+1820,"Furthermore, knockdown of OPN enhanced cell death caused by other drugs, including paclitaxel, doxorubicin, << actinomycin-D >>, and rapamycin, which are also [[ P-gp ]] substrates.",1820,5
+1821,"Furthermore, knockdown of OPN enhanced cell death caused by other drugs, including paclitaxel, doxorubicin, actinomycin-D, and << rapamycin >>, which are also [[ P-gp ]] substrates.",1821,5
+1822,"Compared with normally-fed counterparts, PM-CP rats exhibited higher glutathione S-transferase, aminopeptidase N and cysteine S-conjugate beta-lyase (CCBL) and lower gamma-glutamyltransferase activities, PM-FU rats exhibited decreased dihydropyrimidine dehydrogenase and cytochrome P450 1A1/2 activities and PM-<< MMC >> rats showed higher [[ quinone reductase ]] and depleted xanthine oxidase activities.",1822,9
+1823,"Compared with normally-fed counterparts, PM-CP rats exhibited higher glutathione S-transferase, aminopeptidase N and cysteine S-conjugate beta-lyase (CCBL) and lower gamma-glutamyltransferase activities, PM-FU rats exhibited decreased dihydropyrimidine dehydrogenase and cytochrome P450 1A1/2 activities and PM-<< MMC >> rats showed higher quinone reductase and depleted [[ xanthine oxidase ]] activities.",1823,0
+1824,"Conclusively, protein malnutrition alters CP, FU and << MMC >> metabolism in rat stomach by enhancing [[ CCBL ]] pathway for CP activation, delaying FU elimination and activating two-electron reduction of MMC, potentiating their gastrotoxicity.",1824,5
+1825,"N-acetylcysteine (NAC, 33 mM) and the c-jun N-terminal kinase (<< JNK >>) inhibitor ([[ SP600125 ]], 33 μM) further decreased the viability in the presence of DEP (200 μg/ml) and 3.3% FCS.",1825,0
+1826,"N-acetylcysteine (NAC, 33 mM) and the << c-jun N-terminal kinase >> (JNK) inhibitor ([[ SP600125 ]], 33 μM) further decreased the viability in the presence of DEP (200 μg/ml) and 3.3% FCS.",1826,0
+1827,<< HENA >> activated the [[ BK (cbv1 + β1) channels ]] cloned from rat cerebral artery myocytes with a potency (EC50 = 53 μM) similar to and an efficacy (×2.5 potentiation) significantly greater than that of LCA.,1827,9
+1828,HENA activated the << BK (cbv1 + β1) channels >> cloned from rat cerebral artery myocytes with a potency (EC50 = 53 μM) similar to and an efficacy (×2.5 potentiation) significantly greater than that of [[ LCA ]].,1828,9
+1829,"<< HENA >> failed to activate the channels made of cbv1 + β2, β3, β4, or β1T169A, indicating that this drug selectively targets [[ β1-containing BK channels ]] via the BK β1 steroid-sensing site.",1829,9
+1830,"Assessment of the abuse liability of << ABT-288 >>, a novel [[ histamine H3 receptor ]] antagonist.",1830,1
+1831,"RATIONALE: << Histamine H3 receptor >> antagonists, such as [[ ABT-288 ]], have been shown to possess cognitive-enhancing and wakefulness-promoting effects.",1831,1
+1832,"CONCLUSIONS: The sum of these preclinical data, the first of their kind applied to H3 antagonists, indicates that << ABT-288 >> is unlikely to possess a high potential for abuse in the human population and suggests that [[ H3 ]] antagonists, as a class, are similar in this regard.",1832,1
+1833,Uptake of << estrone-3-sulfate >> (5 nM) by [[ OATP1B1 ]] was reduced by 82%-95%.,1833,5
+1834,"This methodology was subsequently used to assess the relative contribution of << OATP1B1 >> uptake in human hepatocytes for olmesartan (42%-62%), valsartan (28%-81%), rosuvastatin (64%-72%), [[ pitavastatin ]] (84%-98%) and lopinavir (64%-89%).",1834,5
+1835,"This methodology was subsequently used to assess the relative contribution of << OATP1B1 >> uptake in human hepatocytes for olmesartan (42%-62%), valsartan (28%-81%), rosuvastatin (64%-72%), pitavastatin (84%-98%) and [[ lopinavir ]] (64%-89%).",1835,5
+1836,"This methodology was subsequently used to assess the relative contribution of << OATP1B1 >> uptake in human hepatocytes for [[ olmesartan ]] (42%-62%), valsartan (28%-81%), rosuvastatin (64%-72%), pitavastatin (84%-98%) and lopinavir (64%-89%).",1836,5
+1837,"This methodology was subsequently used to assess the relative contribution of << OATP1B1 >> uptake in human hepatocytes for olmesartan (42%-62%), [[ valsartan ]] (28%-81%), rosuvastatin (64%-72%), pitavastatin (84%-98%) and lopinavir (64%-89%).",1837,5
+1838,"This methodology was subsequently used to assess the relative contribution of << OATP1B1 >> uptake in human hepatocytes for olmesartan (42%-62%), valsartan (28%-81%), [[ rosuvastatin ]] (64%-72%), pitavastatin (84%-98%) and lopinavir (64%-89%).",1838,5
+1839,Oral << l-glutamine >> increases active [[ GLP-1 ]] (7-36) amide secretion and improves glycemic control in stretpozotocin-nicotinamide induced diabetic rats.,1839,6
+1840,The objective of the present investigation was to evaluate << l-glutamine >> increases [[ glucagon like peptide-1 ]] (GLP-1) (7-36) amide secretion in streptozotocin-nicotinamide (STZ-NTM) induced diabetic Sprague Dawley rats.,1840,6
+1841,The objective of the present investigation was to evaluate << l-glutamine >> increases glucagon like peptide-1 ([[ GLP-1 ]]) (7-36) amide secretion in streptozotocin-nicotinamide (STZ-NTM) induced diabetic Sprague Dawley rats.,1841,6
+1842,"<< l-glutamine >> decreased plasma glucose, increased plasma and pancreatic [[ insulin ]], increased plasma and colonic active GLP-1 (7-36) amide secretion as well as decreased oxidative stress in streptozotocin-nicotinamide induced diabetic rats.",1842,6
+1843,"<< l-glutamine >> decreased plasma glucose, increased plasma and pancreatic insulin, increased plasma and colonic active [[ GLP-1 ]] (7-36) amide secretion as well as decreased oxidative stress in streptozotocin-nicotinamide induced diabetic rats.",1843,6
+1844,"In the present study, << hinokitiol >> (1 and 2μM) inhibited the [[ collagen ]]-induced aggregation of human platelets, but did not inhibit the activation of platelets by other agonists, including thrombin, arachidonic acid, and ADP.",1844,0
+1845,"<< Hinokitiol >> inhibited the phosphorylation of [[ phospholipase C (PLC)γ2 ]], protein kinase C (PKC), mitogen-activated protein kinases (MAPKs), and Akt in collagen-activated human platelets, and significantly reduced intracellular calcium mobilization and hydroxyl radical (OH) formation.",1845,0
+1846,"<< Hinokitiol >> inhibited the phosphorylation of phospholipase C (PLC)γ2, [[ protein kinase C ]] (PKC), mitogen-activated protein kinases (MAPKs), and Akt in collagen-activated human platelets, and significantly reduced intracellular calcium mobilization and hydroxyl radical (OH) formation.",1846,0
+1847,"<< Hinokitiol >> inhibited the phosphorylation of phospholipase C (PLC)γ2, protein kinase C ([[ PKC ]]), mitogen-activated protein kinases (MAPKs), and Akt in collagen-activated human platelets, and significantly reduced intracellular calcium mobilization and hydroxyl radical (OH) formation.",1847,0
+1848,"<< Hinokitiol >> inhibited the phosphorylation of phospholipase C (PLC)γ2, protein kinase C (PKC), [[ mitogen-activated protein kinases ]] (MAPKs), and Akt in collagen-activated human platelets, and significantly reduced intracellular calcium mobilization and hydroxyl radical (OH) formation.",1848,0
+1849,"<< Hinokitiol >> inhibited the phosphorylation of phospholipase C (PLC)γ2, protein kinase C (PKC), mitogen-activated protein kinases ([[ MAPKs ]]), and Akt in collagen-activated human platelets, and significantly reduced intracellular calcium mobilization and hydroxyl radical (OH) formation.",1849,0
+1850,"<< Hinokitiol >> inhibited the phosphorylation of phospholipase C (PLC)γ2, protein kinase C (PKC), mitogen-activated protein kinases (MAPKs), and [[ Akt ]] in collagen-activated human platelets, and significantly reduced intracellular calcium mobilization and hydroxyl radical (OH) formation.",1850,0
+1851,"<< Hinokitiol >> inhibited the phosphorylation of phospholipase C (PLC)γ2, protein kinase C (PKC), mitogen-activated protein kinases (MAPKs), and Akt in [[ collagen ]]-activated human platelets, and significantly reduced intracellular calcium mobilization and hydroxyl radical (OH) formation.",1851,0
+1852,<< Hinokitiol >> also reduced the [[ PKC ]] activation and platelet aggregation stimulated by PDBu.,1852,0
+1853,"In conclusion, << hinokitiol >> may inhibit platelet activation by inhibiting the [[ PLCγ2 ]]-PKC cascade and hydroxyl radical formation, followed by suppressing the activation of MAPKs and Akt.",1853,0
+1854,"In conclusion, << hinokitiol >> may inhibit platelet activation by inhibiting the PLCγ2-[[ PKC ]] cascade and hydroxyl radical formation, followed by suppressing the activation of MAPKs and Akt.",1854,0
+1855,"In conclusion, << hinokitiol >> may inhibit platelet activation by inhibiting the PLCγ2-PKC cascade and hydroxyl radical formation, followed by suppressing the activation of [[ MAPKs ]] and Akt.",1855,0
+1856,"In conclusion, << hinokitiol >> may inhibit platelet activation by inhibiting the PLCγ2-PKC cascade and hydroxyl radical formation, followed by suppressing the activation of MAPKs and [[ Akt ]].",1856,0
+1857,Novel << 5-(benzyloxy)pyridin-2(1H)-one >> derivatives as potent [[ c-Met ]] inhibitors.,1857,0
+1858,"Design, Synthesis, and Pharmacological Characterization of Novel << Endomorphin-1 >> Analogues as Extremely Potent [[ μ-Opioid ]] Agonists.",1858,2
+1859,"Furthermore, no impact on cytokine release (i.e., on IL-10, IL-6, IL-12/23p40 and TNFα levels) was seen in LPS-stimulated human PBMCs, except with << JWH-210 >> and JWH-122 which caused a decrease of [[ TNFα ]] and IL-12/23p40.",1859,8
+1860,"Furthermore, no impact on cytokine release (i.e., on IL-10, IL-6, IL-12/23p40 and TNFα levels) was seen in LPS-stimulated human PBMCs, except with << JWH-210 >> and JWH-122 which caused a decrease of TNFα and [[ IL-12 ]]/23p40.",1860,8
+1861,"Furthermore, no impact on cytokine release (i.e., on IL-10, IL-6, IL-12/23p40 and TNFα levels) was seen in LPS-stimulated human PBMCs, except with << JWH-210 >> and JWH-122 which caused a decrease of TNFα and IL-12/[[ 23p40 ]].",1861,8
+1862,"Furthermore, no impact on cytokine release (i.e., on IL-10, IL-6, IL-12/23p40 and TNFα levels) was seen in LPS-stimulated human PBMCs, except with JWH-210 and << JWH-122 >> which caused a decrease of [[ TNFα ]] and IL-12/23p40.",1862,8
+1863,"Furthermore, no impact on cytokine release (i.e., on IL-10, IL-6, IL-12/23p40 and TNFα levels) was seen in LPS-stimulated human PBMCs, except with JWH-210 and << JWH-122 >> which caused a decrease of TNFα and [[ IL-12 ]]/23p40.",1863,8
+1864,"Furthermore, no impact on cytokine release (i.e., on IL-10, IL-6, IL-12/23p40 and TNFα levels) was seen in LPS-stimulated human PBMCs, except with JWH-210 and << JWH-122 >> which caused a decrease of TNFα and IL-12/[[ 23p40 ]].",1864,8
+1865,<< AlCl3 >> markedly reduced AA performance and activities of [[ cytochrome c oxidase ]] (COX) and acetylcholinesterase (AChE) in all regions.,1865,0
+1866,<< AlCl3 >> markedly reduced AA performance and activities of cytochrome c oxidase ([[ COX ]]) and acetylcholinesterase (AChE) in all regions.,1866,0
+1867,<< AlCl3 >> markedly reduced AA performance and activities of cytochrome c oxidase (COX) and [[ acetylcholinesterase ]] (AChE) in all regions.,1867,0
+1868,<< AlCl3 >> markedly reduced AA performance and activities of cytochrome c oxidase (COX) and acetylcholinesterase ([[ AChE ]]) in all regions.,1868,0
+1869,"GTLE pretreatment completely reversed the damaging effects of << AlCl3 >> on AA and [[ superoxide dismutase ]] activity, markedly corrected COX and AChE activities, and moderately improved TGC.",1869,0
+1870,"GTLE pretreatment completely reversed the damaging effects of << AlCl3 >> on AA and superoxide dismutase activity, markedly corrected [[ COX ]] and AChE activities, and moderately improved TGC.",1870,0
+1871,"GTLE pretreatment completely reversed the damaging effects of << AlCl3 >> on AA and superoxide dismutase activity, markedly corrected COX and [[ AChE ]] activities, and moderately improved TGC.",1871,0
+1872,Our study demonstrated that << curcumin >> inhibited OVA-induced increases in eosinophil count; interleukin (IL)-17A level were recovered in bronchoalveolar lavage fluid increased [[ IL-10 ]] level in bronchoalveolar lavage fluid.,1872,6
+1873,Our study demonstrated that << curcumin >> inhibited [[ OVA ]]-induced increases in eosinophil count; interleukin (IL)-17A level were recovered in bronchoalveolar lavage fluid increased IL-10 level in bronchoalveolar lavage fluid.,1873,0
+1874,Our study demonstrated that << curcumin >> inhibited OVA-induced increases in eosinophil count; [[ interleukin (IL)-17A ]] level were recovered in bronchoalveolar lavage fluid increased IL-10 level in bronchoalveolar lavage fluid.,1874,0
+1875,Histological studies demonstrated that << curcumin >> substantially inhibited [[ OVA ]]-induced eosinophilia in lung tissue.,1875,0
+1876,The results in vivo show << ovalbumin >>-induced significantly broke Treg/Th17 balance; [[ curcumin ]] treatments markedly attenuated the inflammatory in asthma model by regulating Treg/Th17 balance.,1876,0
+1877,Synthesis of a << DOTA >> (Gd(3+))-conjugate of [[ proton-pump ]] inhibitor pantoprazole for gastric wall imaging studies.,1877,0
+1878,Synthesis of a DOTA (<< Gd(3+) >>)-conjugate of [[ proton-pump ]] inhibitor pantoprazole for gastric wall imaging studies.,1878,0
+1879,Synthesis of a DOTA (Gd(3+))-conjugate of << proton-pump >> inhibitor [[ pantoprazole ]] for gastric wall imaging studies.,1879,0
+1880,"To overcome this limitation, we de novo synthesized a conjugate that covalently combines a << Gd >>-based MRI contrast agent, encaged with a chelating agent (DOTA), with pantoprazole, which is a widely used [[ proton pump ]] inhibitor that binds to proton pumps in the stomach and colon.",1880,0
+1881,"To overcome this limitation, we de novo synthesized a conjugate that covalently combines a Gd-based MRI contrast agent, encaged with a chelating agent (<< DOTA >>), with pantoprazole, which is a widely used [[ proton pump ]] inhibitor that binds to proton pumps in the stomach and colon.",1881,0
+1882,"To overcome this limitation, we de novo synthesized a conjugate that covalently combines a Gd-based MRI contrast agent, encaged with a chelating agent (DOTA), with << pantoprazole >>, which is a widely used [[ proton pump ]] inhibitor that binds to proton pumps in the stomach and colon.",1882,0
+1883,"Second, EPSCs were recorded from rat hippocampal slices before and after their superfusion with the reversible << AChE >> inhibitor [[ donepezil ]] (100nM).",1883,0
+1884,A Nanogram Dose of the << CYP3A >> Probe Substrate [[ Midazolam ]] to Evaluate Drug Interactions.,1884,5
+1885,We then evaluated the interactions with the << CYP3A >> inhibitor [[ ketoconazole ]] (400 mg q.d.) after nanogram and regular doses of midazolam.,1885,0
+1886,<< CYP3A5 >> carrier status had no influence on midazolam oral clearance or its inhibition by [[ ketoconazole ]].,1886,0
+1887,<< CYP3A5 >> carrier status had no influence on [[ midazolam ]] oral clearance or its inhibition by ketoconazole.,1887,5
+1888,Metabolism of << Beclomethasone Dipropionate >> by [[ Cytochrome P450 3A ]] Enzymes.,1888,5
+1889,It is possible that variations in << cytochrome P450 3A >> enzyme-mediated metabolism of [[ BDP ]] may contribute to this phenomenon.,1889,5
+1890,"This hypothesis was explored by evaluating the contributions of CYP3A4, 3A5, 3A7, and << esterase >> enzymes in the metabolism of [[ BDP ]] in vitro and relating metabolism to changes in CYP3A enzyme mRNA expression via the glucocorticoid receptor in lung and liver cells.",1890,5
+1891,<< CYP3A4 >> and CYP3A5 metabolized [[ BDP ]] via hydroxylation ([M4] and [M6]) and dehydrogenation ([M5]) at similar rates; CYP3A7 did not metabolize BDP.,1891,5
+1892,CYP3A4 and << CYP3A5 >> metabolized [[ BDP ]] via hydroxylation ([M4] and [M6]) and dehydrogenation ([M5]) at similar rates; CYP3A7 did not metabolize BDP.,1892,5
+1893,These studies show that << CYP3A4 >> and CYP3A5 metabolize [[ BDP ]] to inactive metabolites and suggest that differences in the expression or function of these enzymes in the lung and/or liver could influence BDP disposition in humans.,1893,5
+1894,These studies show that CYP3A4 and << CYP3A5 >> metabolize [[ BDP ]] to inactive metabolites and suggest that differences in the expression or function of these enzymes in the lung and/or liver could influence BDP disposition in humans.,1894,5
+1895,"In macrophages, levels of << TNF-α >>, IFN-γ, NO, IL-6 and IL-10 were increased by [[ CDM ]] used alone or in combination with HSV-2.",1895,6
+1896,"In macrophages, levels of TNF-α, << IFN-γ >>, NO, IL-6 and IL-10 were increased by [[ CDM ]] used alone or in combination with HSV-2.",1896,6
+1897,"In macrophages, levels of TNF-α, IFN-γ, NO, << IL-6 >> and IL-10 were increased by [[ CDM ]] used alone or in combination with HSV-2.",1897,6
+1898,"In macrophages, levels of TNF-α, IFN-γ, NO, IL-6 and << IL-10 >> were increased by [[ CDM ]] used alone or in combination with HSV-2.",1898,6
+1899,"Besides, << CDM >> not only synergized [[ TNF-α ]] production combined with IFN-γ, but also prolonged its expression in time.",1899,6
+1900,"Besides, << CDM >> not only synergized TNF-α production combined with [[ IFN-γ ]], but also prolonged its expression in time.",1900,6
+1901,"Results indicate that << CDM >> inhibits HSV-2 multiplication in epithelial cells and also increases [[ cytokine ]] production in macrophages, both important actions to the clearance of infecting virus in the mouse vagina.",1901,6
+1902,Intestinal and hepatic first-pass extraction of the << 11β-HSD1 >> inhibitor [[ AMG 221 ]] in rats with chronic vascular catheters.,1902,0
+1903,"A catheterized rat model was used to define the intestinal and hepatic components of oral bioavailability for an << 11β-HSD1 >> inhibitor, [[ AMG 221 ]].",1903,0
+1904,"In DU-PM cells with acquired resistance to << elisidepsin >>, ErbB3 expression was decreased, while [[ Bcl2 ]] was increased.",1904,6
+1905,"In DU-PM cells with acquired resistance to << elisidepsin >>, [[ ErbB3 ]] expression was decreased, while Bcl2 was increased.",1905,8
+1906,"Administration of << bicuculline >>, a [[ GABAA ]] inhibitor, isolated a single response to ω-agatoxin, which was characterized by a reduction in network activity.",1906,0
+1907,"Administration of << bicuculline >>, a GABAA inhibitor, isolated a single response to [[ ω-agatoxin ]], which was characterized by a reduction in network activity.",1907,0
+1908,"<< tert-Butylcarbamate >>-Containing [[ Histone Deacetylase ]] Inhibitors: Apoptosis Induction, Cytodifferentiation, and Antiproliferative Activities in Cancer Cells.",1908,0
+1909,"Herein we report novel pyrrole- and benzene-based hydroxamates (8, 10) and 2'-aminoanilides (9, 11) bearing the << tert-butylcarbamate >> group at the CAP moiety as [[ histone deacetylase ]] (HDAC) inhibitors.",1909,0
+1910,"Herein we report novel pyrrole- and benzene-based hydroxamates (8, 10) and 2'-aminoanilides (9, 11) bearing the << tert-butylcarbamate >> group at the CAP moiety as histone deacetylase ([[ HDAC ]]) inhibitors.",1910,0
+1911,"Herein we report novel << pyrrole >>- and benzene-based hydroxamates (8, 10) and 2'-aminoanilides (9, 11) bearing the tert-butylcarbamate group at the CAP moiety as [[ histone deacetylase ]] (HDAC) inhibitors.",1911,0
+1912,"Herein we report novel << pyrrole >>- and benzene-based hydroxamates (8, 10) and 2'-aminoanilides (9, 11) bearing the tert-butylcarbamate group at the CAP moiety as histone deacetylase ([[ HDAC ]]) inhibitors.",1912,0
+1913,"Herein we report novel pyrrole- and << benzene >>-based hydroxamates (8, 10) and 2'-aminoanilides (9, 11) bearing the tert-butylcarbamate group at the CAP moiety as [[ histone deacetylase ]] (HDAC) inhibitors.",1913,0
+1914,"Herein we report novel pyrrole- and << benzene >>-based hydroxamates (8, 10) and 2'-aminoanilides (9, 11) bearing the tert-butylcarbamate group at the CAP moiety as histone deacetylase ([[ HDAC ]]) inhibitors.",1914,0
+1915,"Herein we report novel pyrrole- and benzene-based << hydroxamates >> (8, 10) and 2'-aminoanilides (9, 11) bearing the tert-butylcarbamate group at the CAP moiety as [[ histone deacetylase ]] (HDAC) inhibitors.",1915,0
+1916,"Herein we report novel pyrrole- and benzene-based << hydroxamates >> (8, 10) and 2'-aminoanilides (9, 11) bearing the tert-butylcarbamate group at the CAP moiety as histone deacetylase ([[ HDAC ]]) inhibitors.",1916,0
+1917,"Herein we report novel pyrrole- and benzene-based hydroxamates (8, 10) and << 2'-aminoanilides >> (9, 11) bearing the tert-butylcarbamate group at the CAP moiety as [[ histone deacetylase ]] (HDAC) inhibitors.",1917,0
+1918,"Herein we report novel pyrrole- and benzene-based hydroxamates (8, 10) and << 2'-aminoanilides >> (9, 11) bearing the tert-butylcarbamate group at the CAP moiety as histone deacetylase ([[ HDAC ]]) inhibitors.",1918,0
+1919,"Compounds 8 b and 10 c selectively inhibited HDAC6 at the nanomolar level, whereas the other << hydroxamates >> effected an increase in [[ acetyl-α-tubulin ]] levels in human acute myeloid leukemia U937 cells.",1919,6
+1920,Discovery of a synthetic << Aminopeptidase N >> inhibitor [[ LB-4b ]] as a potential anticancer agent.,1920,0
+1921,<< LB-4b >> is the first synthetic [[ APN ]] inhibitor to be evaluated for both of its anti-invasion and anti-angiogenesis effects.,1921,0
+1922,"As a potent synthetic << APN >> inhibitor (IC50=850nM, versus [[ bestatin ]] of 8.1μM), LB-4b was determined to have more significant block effects to cancer cell invasion and angiogenesis than bestatin.",1922,0
+1923,"As a potent synthetic << APN >> inhibitor (IC50=850nM, versus bestatin of 8.1μM), [[ LB-4b ]] was determined to have more significant block effects to cancer cell invasion and angiogenesis than bestatin.",1923,0
+1924,"As a potent synthetic << APN >> inhibitor (IC50=850nM, versus bestatin of 8.1μM), LB-4b was determined to have more significant block effects to cancer cell invasion and angiogenesis than [[ bestatin ]].",1924,0
+1925,Both types of granules contain << catechol oxidase >> that catalyzes oxidative cross-linking of [[ L-DOPA ]].,1925,5
+1926,"Under << NaCl >> and sorbitol stresses, [[ catalase ]] (CAT) activity in wnk8 mutant was 1.92- and 3.7-times of that in Col-0, respectively.",1926,9
+1927,"Under << NaCl >> and sorbitol stresses, catalase ([[ CAT ]]) activity in wnk8 mutant was 1.92- and 3.7-times of that in Col-0, respectively.",1927,9
+1928,"Under NaCl and << sorbitol >> stresses, [[ catalase ]] (CAT) activity in wnk8 mutant was 1.92- and 3.7-times of that in Col-0, respectively.",1928,9
+1929,"Under NaCl and << sorbitol >> stresses, catalase ([[ CAT ]]) activity in wnk8 mutant was 1.92- and 3.7-times of that in Col-0, respectively.",1929,9
+1930,Immunofluorescence staining and western blotting demonstrated that << cilostazol >> treatment reduced GFAP and [[ VEGF ]] expression in the retinas of OLETF rats.,1930,8
+1931,Immunofluorescence staining and western blotting demonstrated that << cilostazol >> treatment reduced [[ GFAP ]] and VEGF expression in the retinas of OLETF rats.,1931,8
+1932,"Other dams received 1.8ng/kg/day of a mixture of << aryl hydrocarbon receptor >> (AhR) agonists (non-ortho PCBs, PC-dibenzodioxins and [[ PC-dibenzofurans ]]) without or with 0.5M (0.5MAhR).",1932,2
+1933,"Other dams received 1.8ng/kg/day of a mixture of << aryl hydrocarbon receptor >> (AhR) agonists ([[ non-ortho PCB ]]s, PC-dibenzodioxins and PC-dibenzofurans) without or with 0.5M (0.5MAhR).",1933,2
+1934,"Other dams received 1.8ng/kg/day of a mixture of << aryl hydrocarbon receptor >> (AhR) agonists (non-ortho PCBs, [[ PC-dibenzodioxins ]] and PC-dibenzofurans) without or with 0.5M (0.5MAhR).",1934,2
+1935,"Discovery of a series of novel << 5H-pyrrolo[2,3-b]pyrazine-2-phenyl ethers >>, as potent [[ JAK3 ]] kinase inhibitors.",1935,0
+1936,"Discovery of a series of novel << 5H-pyrrolo[2,3-b]pyrazine-2-phenyl ethers >>, as potent JAK3 [[ kinase ]] inhibitors.",1936,0
+1937,"We report the discovery of a novel series of ATP-competitive << Janus kinase 3 >> (JAK3) inhibitors based on the [[ 5H-pyrrolo[2,3-b]pyrazine ]] scaffold.",1937,0
+1938,"We report the discovery of a novel series of ATP-competitive Janus kinase 3 (<< JAK3 >>) inhibitors based on the [[ 5H-pyrrolo[2,3-b]pyrazine ]] scaffold.",1938,0
+1939,<< Arsenic trioxide >> depletes cancer stem-like cells and inhibits repopulation of neurosphere derived from glioblastoma by downregulation of [[ Notch ]] pathway.,1939,0
+1940,<< ATO >> inhibited the phosphorylation and activation of AKT and STAT3 through [[ Notch ]] signaling blockade.,1940,8
+1941,<< ATO >> inhibited the phosphorylation and activation of AKT and [[ STAT3 ]] through Notch signaling blockade.,1941,0
+1942,<< ATO >> inhibited the phosphorylation and activation of [[ AKT ]] and STAT3 through Notch signaling blockade.,1942,0
+1943,These data show that the << ATO >> is a promising new approach to decrease glioblastoma proliferation and recurrence by downregulation of [[ Notch ]] pathway.,1943,0
+1944,"The high fat diet significantly increased hepatic mRNA expressions of << PPARγ >>, SREBP1C and SCD-1 genes in comparison to the control diet, which was subsequently reversed by supplementation with [[ fisetin ]].",1944,8
+1945,"The high fat diet significantly increased hepatic mRNA expressions of PPARγ, << SREBP1C >> and SCD-1 genes in comparison to the control diet, which was subsequently reversed by supplementation with [[ fisetin ]].",1945,8
+1946,"The high fat diet significantly increased hepatic mRNA expressions of PPARγ, SREBP1C and << SCD-1 >> genes in comparison to the control diet, which was subsequently reversed by supplementation with [[ fisetin ]].",1946,8
+1947,"In addition, << fisetin >> supplementation significantly reduced hepatic mRNA abundance of [[ FAS ]], ATPCL and G6Pase compared to the control group.",1947,8
+1948,"In addition, << fisetin >> supplementation significantly reduced hepatic mRNA abundance of FAS, [[ ATPCL ]] and G6Pase compared to the control group.",1948,8
+1949,"In addition, << fisetin >> supplementation significantly reduced hepatic mRNA abundance of FAS, ATPCL and [[ G6Pase ]] compared to the control group.",1949,8
+1950,"Finally, epididymal mRNA abundance of << GLUT4 >> was significantly increased by [[ fisetin ]] supplementation, compared to levels in the control and HF groups.",1950,6
+1951,Enhancement of << GLUT4 >> expression by [[ fisetin ]] was further confirmed in differentiated 3T3-L1 adipocytes.,1951,6
+1952,Western blot assay demonstrated that << DICO >> decreased Bcl-2 level and induced [[ Bax ]] translocation to cause cytochrome c release.,1952,6
+1953,Western blot assay demonstrated that << DICO >> decreased Bcl-2 level and induced Bax translocation to cause [[ cytochrome c ]] release.,1953,6
+1954,Western blot assay demonstrated that << DICO >> decreased [[ Bcl-2 ]] level and induced Bax translocation to cause cytochrome c release.,1954,8
+1955,<< Quercetin >> and rutin also increased [[ alkaline phosphatase ]] activity by about 150 and 240% and demonstrated mineralization up to 110 and 200% respectively as compared to control (which was considered as 100%).,1955,9
+1956,Quercetin and << rutin >> also increased [[ alkaline phosphatase ]] activity by about 150 and 240% and demonstrated mineralization up to 110 and 200% respectively as compared to control (which was considered as 100%).,1956,9
+1957,"Further, both the << flavonoids >> were also found to increase the expression of some of the prominent markers for differentiation of osteoblast like [[ osteopontin ]], osterix, RunX2, osteoprotegerin and osteocalcin.",1957,6
+1958,"Further, both the << flavonoids >> were also found to increase the expression of some of the prominent markers for differentiation of osteoblast like osteopontin, [[ osterix ]], RunX2, osteoprotegerin and osteocalcin.",1958,6
+1959,"Further, both the << flavonoids >> were also found to increase the expression of some of the prominent markers for differentiation of osteoblast like osteopontin, osterix, [[ RunX2 ]], osteoprotegerin and osteocalcin.",1959,6
+1960,"Further, both the << flavonoids >> were also found to increase the expression of some of the prominent markers for differentiation of osteoblast like osteopontin, osterix, RunX2, [[ osteoprotegerin ]] and osteocalcin.",1960,6
+1961,"Further, both the << flavonoids >> were also found to increase the expression of some of the prominent markers for differentiation of osteoblast like osteopontin, osterix, RunX2, osteoprotegerin and [[ osteocalcin ]].",1961,6
+1962,"<< Cytochrome P450 2E1 >> (CYP 450 2E1), activity was determined as hydroxylation of [[ aniline ]] in liver microsomes.",1962,5
+1963,"Cytochrome P450 2E1 (<< CYP 450 2E1 >>), activity was determined as hydroxylation of [[ aniline ]] in liver microsomes.",1963,5
+1964,"Serum markers of liver damage (<< AST >>, ALT, ALP and Bilirubin) were increased by [[ CCl4 ]] and TAA intoxication (p<0.001), whereas co-treatment with NAC reversed such changes (p<0.001).",1964,6
+1965,"Serum markers of liver damage (AST, << ALT >>, ALP and Bilirubin) were increased by [[ CCl4 ]] and TAA intoxication (p<0.001), whereas co-treatment with NAC reversed such changes (p<0.001).",1965,6
+1966,"Serum markers of liver damage (AST, ALT, << ALP >> and Bilirubin) were increased by [[ CCl4 ]] and TAA intoxication (p<0.001), whereas co-treatment with NAC reversed such changes (p<0.001).",1966,6
+1967,"Serum markers of liver damage (<< AST >>, ALT, ALP and Bilirubin) were increased by CCl4 and [[ TAA ]] intoxication (p<0.001), whereas co-treatment with NAC reversed such changes (p<0.001).",1967,6
+1968,"Serum markers of liver damage (AST, << ALT >>, ALP and Bilirubin) were increased by CCl4 and [[ TAA ]] intoxication (p<0.001), whereas co-treatment with NAC reversed such changes (p<0.001).",1968,6
+1969,"Serum markers of liver damage (AST, ALT, << ALP >> and Bilirubin) were increased by CCl4 and [[ TAA ]] intoxication (p<0.001), whereas co-treatment with NAC reversed such changes (p<0.001).",1969,6
+1970,"Serum markers of liver damage (<< AST >>, ALT, ALP and Bilirubin) were increased by CCl4 and TAA intoxication (p<0.001), whereas co-treatment with [[ NAC ]] reversed such changes (p<0.001).",1970,8
+1971,"Serum markers of liver damage (AST, << ALT >>, ALP and Bilirubin) were increased by CCl4 and TAA intoxication (p<0.001), whereas co-treatment with [[ NAC ]] reversed such changes (p<0.001).",1971,8
+1972,"Serum markers of liver damage (AST, ALT, << ALP >> and Bilirubin) were increased by CCl4 and TAA intoxication (p<0.001), whereas co-treatment with [[ NAC ]] reversed such changes (p<0.001).",1972,8
+1973,"LPO was increased while as GSH, << CAT >> and GPx decreased by the administration of CCl4 and TAA (p<0.001); co-administration of [[ NAC ]] restored these liver markers to normal levels (p<0.001).",1973,6
+1974,"LPO was increased while as GSH, CAT and << GPx >> decreased by the administration of CCl4 and TAA (p<0.001); co-administration of [[ NAC ]] restored these liver markers to normal levels (p<0.001).",1974,6
+1975,"This report concerns the marked up-regulation in differentiated CaCo-2 colonic epithelial cells of two key inflammatory << interleukins >>, IL-6 and IL-8, caused by a mixture of [[ oxysterols ]] representative of a high cholesterol diet.",1975,6
+1976,"This report concerns the marked up-regulation in differentiated CaCo-2 colonic epithelial cells of two key inflammatory interleukins, << IL-6 >> and IL-8, caused by a mixture of [[ oxysterols ]] representative of a high cholesterol diet.",1976,6
+1977,"This report concerns the marked up-regulation in differentiated CaCo-2 colonic epithelial cells of two key inflammatory interleukins, IL-6 and << IL-8 >>, caused by a mixture of [[ oxysterols ]] representative of a high cholesterol diet.",1977,6
+1978,"This report concerns the marked up-regulation in differentiated CaCo-2 colonic epithelial cells of two key inflammatory << interleukins >>, IL-6 and IL-8, caused by a mixture of oxysterols representative of a high [[ cholesterol ]] diet.",1978,6
+1979,"This report concerns the marked up-regulation in differentiated CaCo-2 colonic epithelial cells of two key inflammatory interleukins, << IL-6 >> and IL-8, caused by a mixture of oxysterols representative of a high [[ cholesterol ]] diet.",1979,6
+1980,"This report concerns the marked up-regulation in differentiated CaCo-2 colonic epithelial cells of two key inflammatory interleukins, IL-6 and << IL-8 >>, caused by a mixture of oxysterols representative of a high [[ cholesterol ]] diet.",1980,6
+1981,"<< Oxysterol >>-dependent [[ NOX1 ]] activation, as well as interleukin synthesis, were completely prevented by Cannonau red wine extract that contains an abundant phenolic fraction, in particular phenolic acids and flavonoids.",1981,9
+1982,"<< Oxysterol >>-dependent NOX1 activation, as well as [[ interleukin ]] synthesis, were completely prevented by Cannonau red wine extract that contains an abundant phenolic fraction, in particular phenolic acids and flavonoids.",1982,6
+1983,"Oxysterol-dependent NOX1 activation, as well as << interleukin >> synthesis, were completely prevented by Cannonau red wine extract that contains an abundant phenolic fraction, in particular [[ phenolic acids ]] and flavonoids.",1983,8
+1984,"Oxysterol-dependent NOX1 activation, as well as << interleukin >> synthesis, were completely prevented by Cannonau red wine extract that contains an abundant phenolic fraction, in particular phenolic acids and [[ flavonoids ]].",1984,8
+1985,"Oxysterol-dependent << NOX1 >> activation, as well as interleukin synthesis, were completely prevented by Cannonau red wine extract that contains an abundant phenolic fraction, in particular [[ phenolic acids ]] and flavonoids.",1985,0
+1986,"Oxysterol-dependent << NOX1 >> activation, as well as interleukin synthesis, were completely prevented by Cannonau red wine extract that contains an abundant phenolic fraction, in particular phenolic acids and [[ flavonoids ]].",1986,0
+1987,"Conversely, cell pre-treatment with Vermentino white wine extract with smaller phenolic fraction showed only a partial NOX1 down-regulation and was ineffective in << interleukin >> synthesis induced by dietary [[ oxysterols ]].",1987,6
+1988,"Conversely, cell pre-treatment with Vermentino white wine extract with smaller phenolic fraction showed only a partial << NOX1 >> down-regulation and was ineffective in interleukin synthesis induced by dietary [[ oxysterols ]].",1988,7
+1989,"Besides this direct activity, an excess of phenolic compounds detectable in red wine, may exert an additional indirect action by blocking << oxysterol >>-related [[ NOX1 ]] induction, thus totally preventing the pro-oxidant and pro-inflammatory events triggered by dietary oxysterols.",1989,9
+1990,"Besides this direct activity, an excess of << phenolic >> compounds detectable in red wine, may exert an additional indirect action by blocking oxysterol-related [[ NOX1 ]] induction, thus totally preventing the pro-oxidant and pro-inflammatory events triggered by dietary oxysterols.",1990,0
+1991,<< Arsenic >> inhibits autophagic flux activating the [[ Nrf2 ]]-Keap1 pathway in a p62-dependent manner.,1991,9
+1992,<< Arsenic >> inhibits autophagic flux activating the Nrf2-[[ Keap1 ]] pathway in a p62-dependent manner.,1992,9
+1993,"<< Arsenic >> deregulates the autophagic pathway through blockage of autophagic flux, resulting in accumulation of autophagosomes and sequestration of [[ p62 ]], Keap1, and LC3.",1993,8
+1994,"<< Arsenic >> deregulates the autophagic pathway through blockage of autophagic flux, resulting in accumulation of autophagosomes and sequestration of p62, [[ Keap1 ]], and LC3.",1994,8
+1995,"<< Arsenic >> deregulates the autophagic pathway through blockage of autophagic flux, resulting in accumulation of autophagosomes and sequestration of p62, Keap1, and [[ LC3 ]].",1995,8
+1996,"Thus, << arsenic >> activates [[ Nrf2 ]] through a non-canonical mechanism (p62-dependent), leading to a chronic, sustained activation of Nrf2.",1996,9
+1997,"Thus, << arsenic >> activates Nrf2 through a non-canonical mechanism (p62-dependent), leading to a chronic, sustained activation of [[ Nrf2 ]].",1997,9
+1998,"In contrast, activation of << Nrf2 >> by [[ sulforaphane ]] and tert-butylhydroquinone depend upon Keap1-C151 and not p62 (the canonical mechanism).",1998,9
+1999,"In contrast, activation of << Nrf2 >> by sulforaphane and [[ tert-butylhydroquinone ]] depend upon Keap1-C151 and not p62 (the canonical mechanism).",1999,9
+2000,"Collectively, these findings provide evidence that << arsenic >> causes prolonged activation of [[ Nrf2 ]] through autophagy dysfunction, possibly providing a similar scenario to constitutive activation of Nrf2 found in certain human cancers.",2000,9
+2001,"Collectively, these findings provide evidence that << arsenic >> causes prolonged activation of Nrf2 through autophagy dysfunction, possibly providing a similar scenario to constitutive activation of [[ Nrf2 ]] found in certain human cancers.",2001,9
+2002,"Ovarian AR was not influenced by either treatment, and oviduct << AR >> was reduced after [[ ethanol ]]-melatonin combination.",2002,8
+2003,"Ovarian AR was not influenced by either treatment, and oviduct << AR >> was reduced after ethanol-[[ melatonin ]] combination.",2003,8
+2004,"Oviduct << ER-α >>, ER-β and uterine ER-β were down-regulated by either [[ ethanol ]] or melatonin.",2004,8
+2005,"Oviduct ER-α, << ER-β >> and uterine ER-β were down-regulated by either [[ ethanol ]] or melatonin.",2005,8
+2006,"Oviduct ER-α, ER-β and uterine << ER-β >> were down-regulated by either [[ ethanol ]] or melatonin.",2006,8
+2007,"Oviduct << ER-α >>, ER-β and uterine ER-β were down-regulated by either ethanol or [[ melatonin ]].",2007,8
+2008,"Oviduct ER-α, << ER-β >> and uterine ER-β were down-regulated by either ethanol or [[ melatonin ]].",2008,8
+2009,"Oviduct ER-α, ER-β and uterine << ER-β >> were down-regulated by either ethanol or [[ melatonin ]].",2009,8
+2010,"Conversely, ovarian PRA and PRB were positively regulated by ethanol and ethanol-melatonin combination, whereas << PRA >> was down-regulated in the uterus and oviduct after [[ ethanol ]] consumption.",2010,8
+2011,<< MT1R >> was increased in ovaries and uteri of [[ melatonin ]]-treated rats.,2011,6
+2012,"Intraplantar or intrathecal administered Phα1β reduced both nocifensive behavior and mechanical hypersensitivity induced by capsaicin similarly to that observed with << SB366791 >>, a specific [[ TRPV1 ]] antagonist.",2012,1
+2013,"Recently, the << c-Abl >> kinase inhibitor [[ imatinib mesylate ]] (imatinib) has become the focus of research as a fertoprotective drug against cisplatin.",2013,0
+2014,"Recently, the c-Abl << kinase >> inhibitor [[ imatinib mesylate ]] (imatinib) has become the focus of research as a fertoprotective drug against cisplatin.",2014,0
+2015,"Recently, the << c-Abl >> kinase inhibitor imatinib mesylate ([[ imatinib ]]) has become the focus of research as a fertoprotective drug against cisplatin.",2015,0
+2016,"Recently, the c-Abl << kinase >> inhibitor imatinib mesylate ([[ imatinib ]]) has become the focus of research as a fertoprotective drug against cisplatin.",2016,0
+2017,"We found that, before apoptosis, << cisplatin >> induces [[ c-Abl ]] and TAp73 expression in the oocyte.",2017,6
+2018,"We found that, before apoptosis, << cisplatin >> induces c-Abl and [[ TAp73 ]] expression in the oocyte.",2018,6
+2019,"While imatinib was unable to block << cisplatin >>-induced DNA damage and damage response, such as the upregulation of [[ p53 ]], imatinib inhibited the cisplatin-induced nuclear accumulation of c-Abl/TAp73 and the subsequent downregulation of TAp63 and upregulation of Bax, thereby abrogating oocyte cell death.",2019,6
+2020,"While imatinib was unable to block cisplatin-induced DNA damage and damage response, such as the upregulation of p53, << imatinib >> inhibited the cisplatin-induced nuclear accumulation of c-Abl/TAp73 and the subsequent downregulation of [[ TAp63 ]] and upregulation of Bax, thereby abrogating oocyte cell death.",2020,6
+2021,"While imatinib was unable to block cisplatin-induced DNA damage and damage response, such as the upregulation of p53, imatinib inhibited the << cisplatin >>-induced nuclear accumulation of [[ c-Abl ]]/TAp73 and the subsequent downregulation of TAp63 and upregulation of Bax, thereby abrogating oocyte cell death.",2021,6
+2022,"While imatinib was unable to block cisplatin-induced DNA damage and damage response, such as the upregulation of p53, imatinib inhibited the << cisplatin >>-induced nuclear accumulation of c-Abl/[[ TAp73 ]] and the subsequent downregulation of TAp63 and upregulation of Bax, thereby abrogating oocyte cell death.",2022,6
+2023,"While imatinib was unable to block cisplatin-induced DNA damage and damage response, such as the upregulation of p53, imatinib inhibited the << cisplatin >>-induced nuclear accumulation of c-Abl/TAp73 and the subsequent downregulation of TAp63 and upregulation of [[ Bax ]], thereby abrogating oocyte cell death.",2023,6
+2024,"While imatinib was unable to block cisplatin-induced DNA damage and damage response, such as the upregulation of p53, << imatinib >> inhibited the cisplatin-induced nuclear accumulation of [[ c-Abl ]]/TAp73 and the subsequent downregulation of TAp63 and upregulation of Bax, thereby abrogating oocyte cell death.",2024,8
+2025,"While imatinib was unable to block cisplatin-induced DNA damage and damage response, such as the upregulation of p53, << imatinib >> inhibited the cisplatin-induced nuclear accumulation of c-Abl/[[ TAp73 ]] and the subsequent downregulation of TAp63 and upregulation of Bax, thereby abrogating oocyte cell death.",2025,8
+2026,"While imatinib was unable to block cisplatin-induced DNA damage and damage response, such as the upregulation of p53, << imatinib >> inhibited the cisplatin-induced nuclear accumulation of c-Abl/TAp73 and the subsequent downregulation of TAp63 and upregulation of [[ Bax ]], thereby abrogating oocyte cell death.",2026,8
+2027,"While imatinib was unable to block cisplatin-induced DNA damage and damage response, such as the upregulation of p53, imatinib inhibited the << cisplatin >>-induced nuclear accumulation of c-Abl/TAp73 and the subsequent downregulation of [[ TAp63 ]] and upregulation of Bax, thereby abrogating oocyte cell death.",2027,8
+2028,"Surprisingly, the conditional deletion of Trp63, but not ΔNp63, in oocytes inhibited apoptosis, as well as the accumulation of << c-Abl >> and TAp73 caused by [[ cisplatin ]].",2028,6
+2029,"Surprisingly, the conditional deletion of Trp63, but not ΔNp63, in oocytes inhibited apoptosis, as well as the accumulation of c-Abl and << TAp73 >> caused by [[ cisplatin ]].",2029,6
+2030,"The expression kinetics of TAp63, c-Abl and TAp73 suggest that << cisplatin >> activates [[ TAp63 ]]-dependent expression of c-Abl and TAp73 and, in turn, the activation of TAp73 by c-Abl-induced BAX expression.",2030,9
+2031,"The expression kinetics of TAp63, c-Abl and TAp73 suggest that << cisplatin >> activates TAp63-dependent expression of c-Abl and TAp73 and, in turn, the activation of [[ TAp73 ]] by c-Abl-induced BAX expression.",2031,9
+2032,"The expression kinetics of TAp63, c-Abl and TAp73 suggest that << cisplatin >> activates TAp63-dependent expression of c-Abl and TAp73 and, in turn, the activation of TAp73 by [[ c-Abl ]]-induced BAX expression.",2032,9
+2033,"The expression kinetics of TAp63, c-Abl and TAp73 suggest that << cisplatin >> activates TAp63-dependent expression of [[ c-Abl ]] and TAp73 and, in turn, the activation of TAp73 by c-Abl-induced BAX expression.",2033,6
+2034,"The expression kinetics of TAp63, c-Abl and TAp73 suggest that << cisplatin >> activates TAp63-dependent expression of c-Abl and [[ TAp73 ]] and, in turn, the activation of TAp73 by c-Abl-induced BAX expression.",2034,6
+2035,"The expression kinetics of TAp63, c-Abl and TAp73 suggest that << cisplatin >> activates TAp63-dependent expression of c-Abl and TAp73 and, in turn, the activation of TAp73 by c-Abl-induced [[ BAX ]] expression.",2035,6
+2036,"Our findings indicate that << imatinib >> protects oocytes from cisplatin-induced cell death by inhibiting c-Abl [[ kinase ]], which would otherwise activate TAp73-BAX-mediated apoptosis.",2036,9
+2037,"Our findings indicate that imatinib protects oocytes from << cisplatin >>-induced cell death by inhibiting [[ c-Abl ]] kinase, which would otherwise activate TAp73-BAX-mediated apoptosis.",2037,9
+2038,"Our findings indicate that imatinib protects oocytes from << cisplatin >>-induced cell death by inhibiting c-Abl [[ kinase ]], which would otherwise activate TAp73-BAX-mediated apoptosis.",2038,9
+2039,"Our findings indicate that imatinib protects oocytes from << cisplatin >>-induced cell death by inhibiting c-Abl kinase, which would otherwise activate [[ TAp73 ]]-BAX-mediated apoptosis.",2039,9
+2040,"Our findings indicate that imatinib protects oocytes from << cisplatin >>-induced cell death by inhibiting c-Abl kinase, which would otherwise activate TAp73-[[ BAX ]]-mediated apoptosis.",2040,9
+2041,"Our findings indicate that << imatinib >> protects oocytes from cisplatin-induced cell death by inhibiting [[ c-Abl ]] kinase, which would otherwise activate TAp73-BAX-mediated apoptosis.",2041,0
+2042,"Our findings indicate that << imatinib >> protects oocytes from cisplatin-induced cell death by inhibiting c-Abl kinase, which would otherwise activate [[ TAp73 ]]-BAX-mediated apoptosis.",2042,0
+2043,"Our findings indicate that << imatinib >> protects oocytes from cisplatin-induced cell death by inhibiting c-Abl kinase, which would otherwise activate TAp73-[[ BAX ]]-mediated apoptosis.",2043,0
+2044,"Thus, << imatinib >> and other [[ c-Abl ]] kinase inhibitors provide an intriguing new way to halt cisplatin-induced oocyte death in early follicles and perhaps conserve the endocrine function of the ovary against chemotherapy.Cell Death and Differentiation advance online publication, 19 April 2013; doi:10.1038/cdd.2013.31.",2044,0
+2045,"Thus, << imatinib >> and other c-Abl [[ kinase ]] inhibitors provide an intriguing new way to halt cisplatin-induced oocyte death in early follicles and perhaps conserve the endocrine function of the ovary against chemotherapy.Cell Death and Differentiation advance online publication, 19 April 2013; doi:10.1038/cdd.2013.31.",2045,0
+2046,"Among the possible transporters involved in the uptake of << Cd(2+) >> and Mn(2+), the expression of ZIP8 (Zrt-, Irt-related protein 8), encoded by [[ Slc39a8 ]], showed a marked suppression in both RBL-Cdr and RBL-Mnr cells.",2046,5
+2047,"Among the possible transporters involved in the uptake of << Cd(2+) >> and Mn(2+), the expression of [[ ZIP8 ]] (Zrt-, Irt-related protein 8), encoded by Slc39a8, showed a marked suppression in both RBL-Cdr and RBL-Mnr cells.",2047,5
+2048,"Among the possible transporters involved in the uptake of << Cd(2+) >> and Mn(2+), the expression of ZIP8 ([[ Zrt-, Irt-related protein 8 ]]), encoded by Slc39a8, showed a marked suppression in both RBL-Cdr and RBL-Mnr cells.",2048,5
+2049,"Among the possible transporters involved in the uptake of Cd(2+) and << Mn(2+) >>, the expression of ZIP8 (Zrt-, Irt-related protein 8), encoded by [[ Slc39a8 ]], showed a marked suppression in both RBL-Cdr and RBL-Mnr cells.",2049,5
+2050,"Among the possible transporters involved in the uptake of Cd(2+) and << Mn(2+) >>, the expression of [[ ZIP8 ]] (Zrt-, Irt-related protein 8), encoded by Slc39a8, showed a marked suppression in both RBL-Cdr and RBL-Mnr cells.",2050,5
+2051,"Among the possible transporters involved in the uptake of Cd(2+) and << Mn(2+) >>, the expression of ZIP8 ([[ Zrt-, Irt-related protein 8 ]]), encoded by Slc39a8, showed a marked suppression in both RBL-Cdr and RBL-Mnr cells.",2051,5
+2052,These results suggest that << ZIP8 >> plays a pivotal role in the transport and toxicity of [[ Cd(2+) ]] and Mn(2+) in RBL-2H3 cells.,2052,5
+2053,These results suggest that << ZIP8 >> plays a pivotal role in the transport and toxicity of Cd(2+) and [[ Mn(2+) ]] in RBL-2H3 cells.,2053,5
+2054,"Optimization of a 1,5-dihydrobenzo[b][1,4]diazepine-2,4-dione series of << HIV capsid >> assembly inhibitors 2: Structure-activity relationships (SAR) of the C3-[[ phenyl ]] moiety.",2054,0
+2055,"Optimization of a << 1,5-dihydrobenzo[b][1,4]diazepine-2,4-dione >> series of [[ HIV capsid ]] assembly inhibitors 2: Structure-activity relationships (SAR) of the C3-phenyl moiety.",2055,0
+2056,"Detailed structure-activity relationships of the C3-phenyl moiety that allow for the optimization of antiviral potency of a series of << 1,5-dihydrobenzo[b][1,4]diazepine-2,4-dione >> inhibitors of [[ HIV capsid ]] (CA) assembly are described.",2056,0
+2057,"Detailed structure-activity relationships of the C3-phenyl moiety that allow for the optimization of antiviral potency of a series of << 1,5-dihydrobenzo[b][1,4]diazepine-2,4-dione >> inhibitors of HIV capsid ([[ CA ]]) assembly are described.",2057,0
+2058,<< Arsenic >> upregulates the expression of [[ angiotensin II Type I receptor ]] in mouse aortic endothelial cells.,2058,6
+2059,"Quantitative real-time PCR analysis revealed significant increases in the mRNA levels of 2 << AT1R >> subtypes, AT1AR and AT1BR following [[ sodium arsenite ]] (SA) treatment.",2059,6
+2060,"Quantitative real-time PCR analysis revealed significant increases in the mRNA levels of 2 AT1R subtypes, << AT1AR >> and AT1BR following [[ sodium arsenite ]] (SA) treatment.",2060,6
+2061,"Quantitative real-time PCR analysis revealed significant increases in the mRNA levels of 2 AT1R subtypes, AT1AR and << AT1BR >> following [[ sodium arsenite ]] (SA) treatment.",2061,6
+2062,"Finally, SA-induced << AT1R >> expression was found to be prevented both by NAC and specific JNK inhibitor, [[ SP6001325 ]], strongly indicating that AT1R upregulation is a result of the ROS-mediated activation of the JNK signaling pathway.",2062,8
+2063,"Finally, SA-induced AT1R expression was found to be prevented both by NAC and specific << JNK >> inhibitor, [[ SP6001325 ]], strongly indicating that AT1R upregulation is a result of the ROS-mediated activation of the JNK signaling pathway.",2063,0
+2064,"Taken together, our results indicate that << arsenic >> indeed upregulates the [[ AT1R ]] expression, thus highlighting a role of arsenic-induced aberrant AT1R signaling in the pathogenesis of hypertension.",2064,6
+2065,"Taken together, our results indicate that arsenic indeed upregulates the AT1R expression, thus highlighting a role of << arsenic >>-induced aberrant [[ AT1R ]] signaling in the pathogenesis of hypertension.",2065,6
+2066,"The mRNA levels of << SOD1 >>, CAT, GPx and Txnrd1 were increased significantly (P<0.05) in the combined [[ Na2SeO3 ]]+NaAsO2 treatment group.",2066,6
+2067,"The mRNA levels of SOD1, << CAT >>, GPx and Txnrd1 were increased significantly (P<0.05) in the combined [[ Na2SeO3 ]]+NaAsO2 treatment group.",2067,6
+2068,"The mRNA levels of SOD1, CAT, << GPx >> and Txnrd1 were increased significantly (P<0.05) in the combined [[ Na2SeO3 ]]+NaAsO2 treatment group.",2068,6
+2069,"The mRNA levels of << SOD1 >>, CAT, GPx and Txnrd1 were increased significantly (P<0.05) in the combined Na2SeO3+[[ NaAsO2 ]] treatment group.",2069,8
+2070,"The mRNA levels of SOD1, << CAT >>, GPx and Txnrd1 were increased significantly (P<0.05) in the combined Na2SeO3+[[ NaAsO2 ]] treatment group.",2070,8
+2071,"The mRNA levels of SOD1, CAT, << GPx >> and Txnrd1 were increased significantly (P<0.05) in the combined Na2SeO3+[[ NaAsO2 ]] treatment group.",2071,8
+2072,"The mRNA levels of SOD1, CAT, GPx and << Txnrd1 >> were increased significantly (P<0.05) in the combined Na2SeO3+[[ NaAsO2 ]] treatment group.",2072,8
+2073,"The mRNA levels of SOD1, CAT, GPx and << Txnrd1 >> were increased significantly (P<0.05) in the combined [[ Na2SeO3 ]]+NaAsO2 treatment group.",2073,8
+2074,The expressions of << HSP70 >> and HO-1 were significantly (P<0.05) increased in the [[ NaAsO2 ]] group and reduced in the combined treatment group.,2074,6
+2075,The expressions of HSP70 and << HO-1 >> were significantly (P<0.05) increased in the [[ NaAsO2 ]] group and reduced in the combined treatment group.,2075,6
+2076,"From the 10 isolated compounds, << methyl-3,5-di-O-caffeoylquinate >> showed the most potent inhibition, with IC50 values of 0.30 and 0.67 μM for [[ rAR ]] and rhAR, respectively.",2076,0
+2077,"From the 10 isolated compounds, << methyl-3,5-di-O-caffeoylquinate >> showed the most potent inhibition, with IC50 values of 0.30 and 0.67 μM for rAR and [[ rhAR ]], respectively.",2077,0
+2078,"In the kinetic analyses using Lineweaver-Burk plots of 1/velocity and 1/substrate, << methyl-3,5-di-O-caffeoylquinate >> showed competitive inhibition of [[ rhAR ]].",2078,0
+2079,Recent observations revealed that << human UDP-glucuronosyltransferase (UGT) 2B10 >> catalyzes N-glucuronidation of [[ amine ]]-containing compounds.,2079,5
+2080,"Using recombinant << UGT2B10 >>, we found that it catalyzes the N-glucuronidation of [[ amitriptyline ]], imipramine, ketotifen, pizotifen, olanzapine, diphenhydramine, tamoxifen, ketoconazole and midazolam.",2080,5
+2081,"Using recombinant << UGT2B10 >>, we found that it catalyzes the N-glucuronidation of amitriptyline, [[ imipramine ]], ketotifen, pizotifen, olanzapine, diphenhydramine, tamoxifen, ketoconazole and midazolam.",2081,5
+2082,"Using recombinant << UGT2B10 >>, we found that it catalyzes the N-glucuronidation of amitriptyline, imipramine, [[ ketotifen ]], pizotifen, olanzapine, diphenhydramine, tamoxifen, ketoconazole and midazolam.",2082,5
+2083,"Using recombinant << UGT2B10 >>, we found that it catalyzes the N-glucuronidation of amitriptyline, imipramine, ketotifen, [[ pizotifen ]], olanzapine, diphenhydramine, tamoxifen, ketoconazole and midazolam.",2083,5
+2084,"Using recombinant << UGT2B10 >>, we found that it catalyzes the N-glucuronidation of amitriptyline, imipramine, ketotifen, pizotifen, [[ olanzapine ]], diphenhydramine, tamoxifen, ketoconazole and midazolam.",2084,5
+2085,"Using recombinant << UGT2B10 >>, we found that it catalyzes the N-glucuronidation of amitriptyline, imipramine, ketotifen, pizotifen, olanzapine, [[ diphenhydramine ]], tamoxifen, ketoconazole and midazolam.",2085,5
+2086,"Using recombinant << UGT2B10 >>, we found that it catalyzes the N-glucuronidation of amitriptyline, imipramine, ketotifen, pizotifen, olanzapine, diphenhydramine, [[ tamoxifen ]], ketoconazole and midazolam.",2086,5
+2087,"Using recombinant << UGT2B10 >>, we found that it catalyzes the N-glucuronidation of amitriptyline, imipramine, ketotifen, pizotifen, olanzapine, diphenhydramine, tamoxifen, [[ ketoconazole ]] and midazolam.",2087,5
+2088,"Using recombinant << UGT2B10 >>, we found that it catalyzes the N-glucuronidation of amitriptyline, imipramine, ketotifen, pizotifen, olanzapine, diphenhydramine, tamoxifen, ketoconazole and [[ midazolam ]].",2088,5
+2089,"This group of drugs contains secondary or primary amines, and these results suggest that << UGT2B10 >> preferably conjugates [[ tertiary amines ]].",2089,5
+2090,"Kinetic analyses revealed that the affinity and clearance of << UGT2B10 >> for [[ amitriptyline ]], imipramine, and diphenhydramine are significantly higher than the corresponding values of UGT1A4 and UGT1A3, although the Vmax values of UGT1A4 toward these drugs are considerably higher.",2090,5
+2091,"Kinetic analyses revealed that the affinity and clearance of UGT2B10 for << amitriptyline >>, imipramine, and diphenhydramine are significantly higher than the corresponding values of [[ UGT1A4 ]] and UGT1A3, although the Vmax values of UGT1A4 toward these drugs are considerably higher.",2091,5
+2092,"Kinetic analyses revealed that the affinity and clearance of UGT2B10 for << amitriptyline >>, imipramine, and diphenhydramine are significantly higher than the corresponding values of UGT1A4 and UGT1A3, although the Vmax values of [[ UGT1A4 ]] toward these drugs are considerably higher.",2092,5
+2093,"Kinetic analyses revealed that the affinity and clearance of << UGT2B10 >> for amitriptyline, [[ imipramine ]], and diphenhydramine are significantly higher than the corresponding values of UGT1A4 and UGT1A3, although the Vmax values of UGT1A4 toward these drugs are considerably higher.",2093,5
+2094,"Kinetic analyses revealed that the affinity and clearance of UGT2B10 for amitriptyline, << imipramine >>, and diphenhydramine are significantly higher than the corresponding values of [[ UGT1A4 ]] and UGT1A3, although the Vmax values of UGT1A4 toward these drugs are considerably higher.",2094,5
+2095,"Kinetic analyses revealed that the affinity and clearance of UGT2B10 for amitriptyline, << imipramine >>, and diphenhydramine are significantly higher than the corresponding values of UGT1A4 and [[ UGT1A3 ]], although the Vmax values of UGT1A4 toward these drugs are considerably higher.",2095,5
+2096,"Kinetic analyses revealed that the affinity and clearance of UGT2B10 for amitriptyline, << imipramine >>, and diphenhydramine are significantly higher than the corresponding values of UGT1A4 and UGT1A3, although the Vmax values of [[ UGT1A4 ]] toward these drugs are considerably higher.",2096,5
+2097,"Kinetic analyses revealed that the affinity and clearance of << UGT2B10 >> for amitriptyline, imipramine, and [[ diphenhydramine ]] are significantly higher than the corresponding values of UGT1A4 and UGT1A3, although the Vmax values of UGT1A4 toward these drugs are considerably higher.",2097,5
+2098,"Kinetic analyses revealed that the affinity and clearance of UGT2B10 for amitriptyline, imipramine, and << diphenhydramine >> are significantly higher than the corresponding values of [[ UGT1A4 ]] and UGT1A3, although the Vmax values of UGT1A4 toward these drugs are considerably higher.",2098,5
+2099,"Kinetic analyses revealed that the affinity and clearance of UGT2B10 for amitriptyline, imipramine, and << diphenhydramine >> are significantly higher than the corresponding values of UGT1A4 and [[ UGT1A3 ]], although the Vmax values of UGT1A4 toward these drugs are considerably higher.",2099,5
+2100,"Kinetic analyses revealed that the affinity and clearance of UGT2B10 for amitriptyline, imipramine, and << diphenhydramine >> are significantly higher than the corresponding values of UGT1A4 and UGT1A3, although the Vmax values of [[ UGT1A4 ]] toward these drugs are considerably higher.",2100,5
+2101,"In conclusion, this study expands the understanding of the substrate specificity of << UGT2B10 >>, highlighting its preference for [[ tertiary amines ]] with higher affinities and clearance values than those of UGT1A4 and UGT1A3.",2101,5
+2102,"In conclusion, this study expands the understanding of the substrate specificity of UGT2B10, highlighting its preference for << tertiary amines >> with higher affinities and clearance values than those of [[ UGT1A4 ]] and UGT1A3.",2102,5
+2103,"In conclusion, this study expands the understanding of the substrate specificity of UGT2B10, highlighting its preference for << tertiary amines >> with higher affinities and clearance values than those of UGT1A4 and [[ UGT1A3 ]].",2103,5
+2104,"<< SB225002 >> (SB) is an IL-8 receptor B (IL-8RB) antagonist that has previously been shown to inhibit [[ IL-8 ]]-based cancer cell invasion, and to possess in vivo anti-inflammatory and anti-nociceptive effects.",2104,0
+2105,"<< SB225002 >> (SB) is an [[ IL-8 receptor B ]] (IL-8RB) antagonist that has previously been shown to inhibit IL-8-based cancer cell invasion, and to possess in vivo anti-inflammatory and anti-nociceptive effects.",2105,1
+2106,"<< SB225002 >> (SB) is an IL-8 receptor B ([[ IL-8RB ]]) antagonist that has previously been shown to inhibit IL-8-based cancer cell invasion, and to possess in vivo anti-inflammatory and anti-nociceptive effects.",2106,1
+2107,"Of note, << SB265610 >> which is a close structural analogue of SB225002 with a potent [[ IL-8RB ]] antagonistic activity did not exhibit a similar antimitotic activity.",2107,1
+2108,"Of note, SB265610 which is a close structural analogue of << SB225002 >> with a potent [[ IL-8RB ]] antagonistic activity did not exhibit a similar antimitotic activity.",2108,1
+2109,"In support of this observation, elongation can be reversed by the << tyrosine kinase >> inhibitor [[ SU5402 ]], mRNA for the FGFR antagonist sprouty4, or FGF8 morpholino.",2109,0
+2110,<< Caffeic Acid Phenethyl Ester >> Suppresses Proliferation and Survival of TW2.6 Human Oral Cancer Cells via Inhibition of [[ Akt ]] Signaling.,2110,8
+2111,"Treatment with << CAPE >> decreased protein abundance of Akt, Akt1, Akt2, Akt3, phospho-Akt Ser473, phospho-Akt Thr 308, GSK3β, FOXO1, FOXO3a, phospho-FOXO1 Thr24, phospho-FoxO3a Thr32, NF-κB, phospho-NF-κB Ser536, Rb, phospho-Rb Ser807/811, Skp2, and cyclin D1, but increased cell cycle inhibitor [[ p27Kip ]].",2111,6
+2112,"Treatment with << CAPE >> decreased protein abundance of [[ Akt ]], Akt1, Akt2, Akt3, phospho-Akt Ser473, phospho-Akt Thr 308, GSK3β, FOXO1, FOXO3a, phospho-FOXO1 Thr24, phospho-FoxO3a Thr32, NF-κB, phospho-NF-κB Ser536, Rb, phospho-Rb Ser807/811, Skp2, and cyclin D1, but increased cell cycle inhibitor p27Kip.",2112,8
+2113,"Treatment with << CAPE >> decreased protein abundance of Akt, [[ Akt1 ]], Akt2, Akt3, phospho-Akt Ser473, phospho-Akt Thr 308, GSK3β, FOXO1, FOXO3a, phospho-FOXO1 Thr24, phospho-FoxO3a Thr32, NF-κB, phospho-NF-κB Ser536, Rb, phospho-Rb Ser807/811, Skp2, and cyclin D1, but increased cell cycle inhibitor p27Kip.",2113,8
+2114,"Treatment with << CAPE >> decreased protein abundance of Akt, Akt1, [[ Akt2 ]], Akt3, phospho-Akt Ser473, phospho-Akt Thr 308, GSK3β, FOXO1, FOXO3a, phospho-FOXO1 Thr24, phospho-FoxO3a Thr32, NF-κB, phospho-NF-κB Ser536, Rb, phospho-Rb Ser807/811, Skp2, and cyclin D1, but increased cell cycle inhibitor p27Kip.",2114,8
+2115,"Treatment with << CAPE >> decreased protein abundance of Akt, Akt1, Akt2, [[ Akt3 ]], phospho-Akt Ser473, phospho-Akt Thr 308, GSK3β, FOXO1, FOXO3a, phospho-FOXO1 Thr24, phospho-FoxO3a Thr32, NF-κB, phospho-NF-κB Ser536, Rb, phospho-Rb Ser807/811, Skp2, and cyclin D1, but increased cell cycle inhibitor p27Kip.",2115,8
+2116,"Treatment with << CAPE >> decreased protein abundance of Akt, Akt1, Akt2, Akt3, [[ phospho-Akt ]] Ser473, phospho-Akt Thr 308, GSK3β, FOXO1, FOXO3a, phospho-FOXO1 Thr24, phospho-FoxO3a Thr32, NF-κB, phospho-NF-κB Ser536, Rb, phospho-Rb Ser807/811, Skp2, and cyclin D1, but increased cell cycle inhibitor p27Kip.",2116,8
+2117,"Treatment with << CAPE >> decreased protein abundance of Akt, Akt1, Akt2, Akt3, phospho-Akt Ser473, [[ phospho-Akt ]] Thr 308, GSK3β, FOXO1, FOXO3a, phospho-FOXO1 Thr24, phospho-FoxO3a Thr32, NF-κB, phospho-NF-κB Ser536, Rb, phospho-Rb Ser807/811, Skp2, and cyclin D1, but increased cell cycle inhibitor p27Kip.",2117,8
+2118,"Treatment with << CAPE >> decreased protein abundance of Akt, Akt1, Akt2, Akt3, phospho-Akt Ser473, phospho-Akt Thr 308, [[ GSK3β ]], FOXO1, FOXO3a, phospho-FOXO1 Thr24, phospho-FoxO3a Thr32, NF-κB, phospho-NF-κB Ser536, Rb, phospho-Rb Ser807/811, Skp2, and cyclin D1, but increased cell cycle inhibitor p27Kip.",2118,8
+2119,"Treatment with << CAPE >> decreased protein abundance of Akt, Akt1, Akt2, Akt3, phospho-Akt Ser473, phospho-Akt Thr 308, GSK3β, [[ FOXO1 ]], FOXO3a, phospho-FOXO1 Thr24, phospho-FoxO3a Thr32, NF-κB, phospho-NF-κB Ser536, Rb, phospho-Rb Ser807/811, Skp2, and cyclin D1, but increased cell cycle inhibitor p27Kip.",2119,8
+2120,"Treatment with << CAPE >> decreased protein abundance of Akt, Akt1, Akt2, Akt3, phospho-Akt Ser473, phospho-Akt Thr 308, GSK3β, FOXO1, [[ FOXO3a ]], phospho-FOXO1 Thr24, phospho-FoxO3a Thr32, NF-κB, phospho-NF-κB Ser536, Rb, phospho-Rb Ser807/811, Skp2, and cyclin D1, but increased cell cycle inhibitor p27Kip.",2120,8
+2121,"Treatment with << CAPE >> decreased protein abundance of Akt, Akt1, Akt2, Akt3, phospho-Akt Ser473, phospho-Akt Thr 308, GSK3β, FOXO1, FOXO3a, [[ phospho-FOXO1 ]] Thr24, phospho-FoxO3a Thr32, NF-κB, phospho-NF-κB Ser536, Rb, phospho-Rb Ser807/811, Skp2, and cyclin D1, but increased cell cycle inhibitor p27Kip.",2121,8
+2122,"Treatment with << CAPE >> decreased protein abundance of Akt, Akt1, Akt2, Akt3, phospho-Akt Ser473, phospho-Akt Thr 308, GSK3β, FOXO1, FOXO3a, phospho-FOXO1 Thr24, [[ phospho-FoxO3a ]] Thr32, NF-κB, phospho-NF-κB Ser536, Rb, phospho-Rb Ser807/811, Skp2, and cyclin D1, but increased cell cycle inhibitor p27Kip.",2122,8
+2123,"Treatment with << CAPE >> decreased protein abundance of Akt, Akt1, Akt2, Akt3, phospho-Akt Ser473, phospho-Akt Thr 308, GSK3β, FOXO1, FOXO3a, phospho-FOXO1 Thr24, phospho-FoxO3a Thr32, [[ NF-κB ]], phospho-NF-κB Ser536, Rb, phospho-Rb Ser807/811, Skp2, and cyclin D1, but increased cell cycle inhibitor p27Kip.",2123,8
+2124,"Treatment with << CAPE >> decreased protein abundance of Akt, Akt1, Akt2, Akt3, phospho-Akt Ser473, phospho-Akt Thr 308, GSK3β, FOXO1, FOXO3a, phospho-FOXO1 Thr24, phospho-FoxO3a Thr32, NF-κB, [[ phospho-NF-κB ]] Ser536, Rb, phospho-Rb Ser807/811, Skp2, and cyclin D1, but increased cell cycle inhibitor p27Kip.",2124,8
+2125,"Treatment with << CAPE >> decreased protein abundance of Akt, Akt1, Akt2, Akt3, phospho-Akt Ser473, phospho-Akt Thr 308, GSK3β, FOXO1, FOXO3a, phospho-FOXO1 Thr24, phospho-FoxO3a Thr32, NF-κB, phospho-NF-κB Ser536, [[ Rb ]], phospho-Rb Ser807/811, Skp2, and cyclin D1, but increased cell cycle inhibitor p27Kip.",2125,8
+2126,"Treatment with << CAPE >> decreased protein abundance of Akt, Akt1, Akt2, Akt3, phospho-Akt Ser473, phospho-Akt Thr 308, GSK3β, FOXO1, FOXO3a, phospho-FOXO1 Thr24, phospho-FoxO3a Thr32, NF-κB, phospho-NF-κB Ser536, Rb, [[ phospho-Rb ]] Ser807/811, Skp2, and cyclin D1, but increased cell cycle inhibitor p27Kip.",2126,8
+2127,"Treatment with << CAPE >> decreased protein abundance of Akt, Akt1, Akt2, Akt3, phospho-Akt Ser473, phospho-Akt Thr 308, GSK3β, FOXO1, FOXO3a, phospho-FOXO1 Thr24, phospho-FoxO3a Thr32, NF-κB, phospho-NF-κB Ser536, Rb, phospho-Rb Ser807/811, [[ Skp2 ]], and cyclin D1, but increased cell cycle inhibitor p27Kip.",2127,8
+2128,"Treatment with << CAPE >> decreased protein abundance of Akt, Akt1, Akt2, Akt3, phospho-Akt Ser473, phospho-Akt Thr 308, GSK3β, FOXO1, FOXO3a, phospho-FOXO1 Thr24, phospho-FoxO3a Thr32, NF-κB, phospho-NF-κB Ser536, Rb, phospho-Rb Ser807/811, Skp2, and [[ cyclin D1 ]], but increased cell cycle inhibitor p27Kip.",2128,8
+2129,Here we show that << fisetin >> rapidly increases the levels of both [[ Nrf2 ]] and ATF4 as well as Nrf2- and ATF4-dependent gene transcription via distinct mechanisms.,2129,6
+2130,Here we show that << fisetin >> rapidly increases the levels of both Nrf2 and [[ ATF4 ]] as well as Nrf2- and ATF4-dependent gene transcription via distinct mechanisms.,2130,6
+2131,Here we show that << fisetin >> rapidly increases the levels of both Nrf2 and ATF4 as well as [[ Nrf2 ]]- and ATF4-dependent gene transcription via distinct mechanisms.,2131,6
+2132,Here we show that << fisetin >> rapidly increases the levels of both Nrf2 and ATF4 as well as Nrf2- and [[ ATF4 ]]-dependent gene transcription via distinct mechanisms.,2132,6
+2133,"Although << fisetin >> greatly increases the stability of both [[ Nrf2 ]] and ATF4, only the effect on ATF4 is dependent on protein kinase activity.",2133,6
+2134,"Although << fisetin >> greatly increases the stability of both Nrf2 and [[ ATF4 ]], only the effect on ATF4 is dependent on protein kinase activity.",2134,6
+2135,"<< Cynomolgus FMO1 >>, FMO2, FMO3, and FMO5 metabolized [[ benzydamine ]], and FMO1/FMO3 and FMO3 also metabolized methimazole and trimethylamine, respectively.",2135,5
+2136,"Cynomolgus FMO1, << FMO2 >>, FMO3, and FMO5 metabolized [[ benzydamine ]], and FMO1/FMO3 and FMO3 also metabolized methimazole and trimethylamine, respectively.",2136,5
+2137,"Cynomolgus FMO1, FMO2, << FMO3 >>, and FMO5 metabolized [[ benzydamine ]], and FMO1/FMO3 and FMO3 also metabolized methimazole and trimethylamine, respectively.",2137,5
+2138,"Cynomolgus FMO1, FMO2, FMO3, and << FMO5 >> metabolized [[ benzydamine ]], and FMO1/FMO3 and FMO3 also metabolized methimazole and trimethylamine, respectively.",2138,5
+2139,"Cynomolgus FMO1, FMO2, FMO3, and FMO5 metabolized benzydamine, and << FMO1 >>/FMO3 and FMO3 also metabolized [[ methimazole ]] and trimethylamine, respectively.",2139,5
+2140,"Cynomolgus FMO1, FMO2, FMO3, and FMO5 metabolized benzydamine, and FMO1/<< FMO3 >> and FMO3 also metabolized [[ methimazole ]] and trimethylamine, respectively.",2140,5
+2141,"Cynomolgus FMO1, FMO2, FMO3, and FMO5 metabolized benzydamine, and FMO1/FMO3 and << FMO3 >> also metabolized [[ methimazole ]] and trimethylamine, respectively.",2141,5
+2142,"Cynomolgus FMO1, FMO2, FMO3, and FMO5 metabolized benzydamine, and << FMO1 >>/FMO3 and FMO3 also metabolized methimazole and [[ trimethylamine ]], respectively.",2142,5
+2143,"Cynomolgus FMO1, FMO2, FMO3, and FMO5 metabolized benzydamine, and FMO1/<< FMO3 >> and FMO3 also metabolized methimazole and [[ trimethylamine ]], respectively.",2143,5
+2144,"Cynomolgus FMO1, FMO2, FMO3, and FMO5 metabolized benzydamine, and FMO1/FMO3 and << FMO3 >> also metabolized methimazole and [[ trimethylamine ]], respectively.",2144,5
+2145,"Rates of << benzydamine >> N-oxygenation (catalyzed by [[ FMO3 ]]) varied (approximately 20-fold) among the 28 cynomolgus livers and were significantly correlated with FMO3 protein expression, indicating that the inter-animal variations in benzydamine N-oxygenation might be partly accounted for by the variable FMO3 expression.",2145,5
+2146,"Rates of benzydamine << N >>-oxygenation (catalyzed by [[ FMO3 ]]) varied (approximately 20-fold) among the 28 cynomolgus livers and were significantly correlated with FMO3 protein expression, indicating that the inter-animal variations in benzydamine N-oxygenation might be partly accounted for by the variable FMO3 expression.",2146,5
+2147,"Rates of benzydamine N-oxygenation (catalyzed by FMO3) varied (approximately 20-fold) among the 28 cynomolgus livers and were significantly correlated with FMO3 protein expression, indicating that the inter-animal variations in << benzydamine >> N-oxygenation might be partly accounted for by the variable [[ FMO3 ]] expression.",2147,5
+2148,"Rates of benzydamine N-oxygenation (catalyzed by FMO3) varied (approximately 20-fold) among the 28 cynomolgus livers and were significantly correlated with FMO3 protein expression, indicating that the inter-animal variations in benzydamine << N >>-oxygenation might be partly accounted for by the variable [[ FMO3 ]] expression.",2148,5
+2149,"<< Cynomolgus FMO6 >> metabolized [[ benzydamine ]] only slightly, but minimal expression of FMO6 in all tissue precludes the importance of FMO6 in drug metabolism, unlike cynomolgus FMO1, FMO2, FMO3, and FMO5 which were all functional.",2149,5
+2150,"Cynomolgus FMO6 metabolized << benzydamine >> only slightly, but minimal expression of FMO6 in all tissue precludes the importance of FMO6 in drug metabolism, unlike cynomolgus [[ FMO1 ]], FMO2, FMO3, and FMO5 which were all functional.",2150,5
+2151,"Cynomolgus FMO6 metabolized << benzydamine >> only slightly, but minimal expression of FMO6 in all tissue precludes the importance of FMO6 in drug metabolism, unlike cynomolgus FMO1, [[ FMO2 ]], FMO3, and FMO5 which were all functional.",2151,5
+2152,"Cynomolgus FMO6 metabolized << benzydamine >> only slightly, but minimal expression of FMO6 in all tissue precludes the importance of FMO6 in drug metabolism, unlike cynomolgus FMO1, FMO2, [[ FMO3 ]], and FMO5 which were all functional.",2152,5
+2153,"Cynomolgus FMO6 metabolized << benzydamine >> only slightly, but minimal expression of FMO6 in all tissue precludes the importance of FMO6 in drug metabolism, unlike cynomolgus FMO1, FMO2, FMO3, and [[ FMO5 ]] which were all functional.",2153,5
+2154,Activation of << AMPK >> using [[ AICAR ]] resulted in STIM1 phosphorylation on serine residues and prevented PAR-1-induced Ca2+ entry.,2154,9
+2155,Activation of AMPK using << AICAR >> resulted in [[ STIM1 ]] phosphorylation on serine residues and prevented PAR-1-induced Ca2+ entry.,2155,9
+2156,Activation of AMPK using << AICAR >> resulted in STIM1 phosphorylation on serine residues and prevented [[ PAR-1 ]]-induced Ca2+ entry.,2156,8
+2157,"Further, << AICAR >> pretreatment blocked [[ PAR-1 ]]-induced increase in permeability of mouse-lung microvessels.",2157,0
+2158,"Interestingly, << SB203580 >>, a selective inhibitor of [[ p38 ]] MAPK, blocked STIM1 phosphorylation and led to sustained STIM1-puncta formation and Ca2+ entry.",2158,0
+2159,"Interestingly, << SB203580 >>, a selective inhibitor of p38 [[ MAPK ]], blocked STIM1 phosphorylation and led to sustained STIM1-puncta formation and Ca2+ entry.",2159,0
+2160,"Interestingly, << SB203580 >>, a selective inhibitor of p38 MAPK, blocked [[ STIM1 ]] phosphorylation and led to sustained STIM1-puncta formation and Ca2+ entry.",2160,0
+2161,"Mitochondria in the steroidogenic cells of the adrenal, gonad, placenta and brain contain the << cholesterol >> side-chain cleavage enzyme, [[ P450scc ]], and its two electron-transfer partners, ferredoxin reductase and ferredoxin.",2161,5
+2162,"The precise fashion in which these proteins interact and move << cholesterol >> from the OMM to [[ P450scc ]], and the means by which cholesterol is loaded into the OMM, remain unclear.",2162,5
+2163,<< Matrix Metalloproteinase >> Inhibitors Based on the [[ 3-Mercaptopyrrolidine ]] Core.,2163,0
+2164,"New series of << pyrrolidine mercaptosulfide >>, 2-mercaptocyclopentane arylsulfonamide, and 3-mercapto-4-arylsulfonamido pyrrolidine [[ matrix metalloproteinase ]] inhibitors (MMPIs) were designed, synthesized, and evaluated.",2164,0
+2165,"New series of pyrrolidine mercaptosulfide, << 2-mercaptocyclopentane arylsulfonamide >>, and 3-mercapto-4-arylsulfonamido pyrrolidine [[ matrix metalloproteinase ]] inhibitors (MMPIs) were designed, synthesized, and evaluated.",2165,0
+2166,"New series of pyrrolidine mercaptosulfide, 2-mercaptocyclopentane arylsulfonamide, and << 3-mercapto-4-arylsulfonamido pyrrolidine >> [[ matrix metalloproteinase ]] inhibitors (MMPIs) were designed, synthesized, and evaluated.",2166,0
+2167,"Exhibiting unique properties over other MMPIs (e.g., << hydroxamates >>), these newly reported compounds are capable of modulating activities of several [[ MMPs ]] in the low nanomolar range, including MMP-2 (~2 to 50 nM), MMP-13 (~2 to 50 nM), and MMP-14 (~4 to 60 nM).",2167,0
+2168,"Exhibiting unique properties over other MMPIs (e.g., << hydroxamates >>), these newly reported compounds are capable of modulating activities of several MMPs in the low nanomolar range, including [[ MMP-2 ]] (~2 to 50 nM), MMP-13 (~2 to 50 nM), and MMP-14 (~4 to 60 nM).",2168,0
+2169,"Exhibiting unique properties over other MMPIs (e.g., << hydroxamates >>), these newly reported compounds are capable of modulating activities of several MMPs in the low nanomolar range, including MMP-2 (~2 to 50 nM), [[ MMP-13 ]] (~2 to 50 nM), and MMP-14 (~4 to 60 nM).",2169,0
+2170,"Exhibiting unique properties over other MMPIs (e.g., << hydroxamates >>), these newly reported compounds are capable of modulating activities of several MMPs in the low nanomolar range, including MMP-2 (~2 to 50 nM), MMP-13 (~2 to 50 nM), and [[ MMP-14 ]] (~4 to 60 nM).",2170,0
+2171,"Recent literature shows that Brassica vegetables (Cruciferae) possess therapeutic effects particularly ascribed due to their content in glucosinolates, which upon << myrosinase >> hydrolysis release the corresponding [[ isothiocyanates ]].",2171,4
+2172,"Recent literature shows that Brassica vegetables (Cruciferae) possess therapeutic effects particularly ascribed due to their content in << glucosinolates >>, which upon [[ myrosinase ]] hydrolysis release the corresponding isothiocyanates.",2172,5
+2173,"RESULTS: By Western blot analysis of spinal cord tissues, we have demonstrated that treatment with bioactive << RS -GRA >> significantly decreased nuclear factor (NF)-kB translocation, pro-inflammatory cytokine production such as [[ interleukin-1β ]] (IL-1β), and apoptosis (Bax and caspase 3 expression).",2173,8
+2174,"RESULTS: By Western blot analysis of spinal cord tissues, we have demonstrated that treatment with bioactive << RS -GRA >> significantly decreased nuclear factor (NF)-kB translocation, pro-inflammatory cytokine production such as interleukin-1β ([[ IL-1β ]]), and apoptosis (Bax and caspase 3 expression).",2174,8
+2175,"RESULTS: By Western blot analysis of spinal cord tissues, we have demonstrated that treatment with bioactive << RS -GRA >> significantly decreased nuclear factor (NF)-kB translocation, pro-inflammatory cytokine production such as interleukin-1β (IL-1β), and apoptosis ([[ Bax ]] and caspase 3 expression).",2175,8
+2176,"RESULTS: By Western blot analysis of spinal cord tissues, we have demonstrated that treatment with bioactive << RS -GRA >> significantly decreased nuclear factor (NF)-kB translocation, pro-inflammatory cytokine production such as interleukin-1β (IL-1β), and apoptosis (Bax and [[ caspase 3 ]] expression).",2176,8
+2177,"RESULTS: By Western blot analysis of spinal cord tissues, we have demonstrated that treatment with bioactive << RS -GRA >> significantly decreased [[ nuclear factor (NF)-kB ]] translocation, pro-inflammatory cytokine production such as interleukin-1β (IL-1β), and apoptosis (Bax and caspase 3 expression).",2177,8
+2178,"RESULTS: By Western blot analysis of spinal cord tissues, we have demonstrated that treatment with bioactive << RS -GRA >> significantly decreased nuclear factor (NF)-kB translocation, pro-inflammatory [[ cytokine ]] production such as interleukin-1β (IL-1β), and apoptosis (Bax and caspase 3 expression).",2178,8
+2179,"Herein, we investigated the effect of a natural neuroprotective flavonoid, calycopterin, on << H2O2 >>-induced disruption of [[ phase II detoxifying enzyme ]] system and cAMP response element binding protein (CREB) phosphorylation.",2179,3
+2180,"Herein, we investigated the effect of a natural neuroprotective flavonoid, calycopterin, on << H2O2 >>-induced disruption of phase II detoxifying enzyme system and [[ cAMP response element binding protein ]] (CREB) phosphorylation.",2180,0
+2181,"Herein, we investigated the effect of a natural neuroprotective flavonoid, calycopterin, on << H2O2 >>-induced disruption of phase II detoxifying enzyme system and cAMP response element binding protein ([[ CREB ]]) phosphorylation.",2181,0
+2182,"In H2O2-treated cells, << calycopterin >> also suppressed [[ cytochrome C ]] release to cytosol that is necessary for maintaining mitochondrial homeostasis in survived cells.",2182,8
+2183,"Moreover, << calycopterin >>, in presence of H2O2 inhibited the decrease caused by oxidative stress in stress-sensing transcription factors, [[ CREB ]] and Nrf2, which play an important role in antioxidant capacity of the cell.",2183,6
+2184,"Moreover, << calycopterin >>, in presence of H2O2 inhibited the decrease caused by oxidative stress in stress-sensing transcription factors, CREB and [[ Nrf2 ]], which play an important role in antioxidant capacity of the cell.",2184,6
+2185,There was also an increase in << γ-GCS >> and HO-1 levels in [[ calycopterin ]] pretreated cells.,2185,6
+2186,There was also an increase in γ-GCS and << HO-1 >> levels in [[ calycopterin ]] pretreated cells.,2186,6
+2187,"In the presence of H2O2, << calycopterin >> inhibited decrease in GSH level and [[ SOD ]] activity.",2187,9
+2188,<< Indoxyl 3-sulfate >> stimulates Th17 differentiation enhancing phosphorylation of [[ c-Src ]] and STAT3 to worsen experimental autoimmune encephalomyelitis.,2188,9
+2189,<< Indoxyl 3-sulfate >> stimulates Th17 differentiation enhancing phosphorylation of c-Src and [[ STAT3 ]] to worsen experimental autoimmune encephalomyelitis.,2189,9
+2190,"In the present study, using in vitro Th17 differentiation model, we examined effects of << AhR >> activation by [[ indoxyl 3-sulfate ]] (I3S), a uremic toxin, on Th17 differentiation and investigated underlying mechanisms.",2190,9
+2191,"In the present study, using in vitro Th17 differentiation model, we examined effects of << AhR >> activation by indoxyl 3-sulfate ([[ I3S ]]), a uremic toxin, on Th17 differentiation and investigated underlying mechanisms.",2191,9
+2192,"<< I3S >> increased expression of [[ RORγt ]], the master transcription factor for Th17 differentiation, and stimulated Th17 differentiation, in a comparative manner as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a prototypical AhR ligand.",2192,6
+2193,"Activation of << STAT3 >>, which is phosphorylated by the IL-6 signaling pathways and thus is necessary for Th17 differentiation, was strongly stimulated by I3S and [[ TCDD ]].",2193,9
+2194,"Activation of STAT3, which is phosphorylated by the << IL-6 >> signaling pathways and thus is necessary for Th17 differentiation, was strongly stimulated by I3S and [[ TCDD ]].",2194,9
+2195,"Activation of << STAT3 >>, which is phosphorylated by the IL-6 signaling pathways and thus is necessary for Th17 differentiation, was strongly stimulated by [[ I3S ]] and TCDD.",2195,9
+2196,"Activation of STAT3, which is phosphorylated by the << IL-6 >> signaling pathways and thus is necessary for Th17 differentiation, was strongly stimulated by [[ I3S ]] and TCDD.",2196,9
+2197,"Phosphorylation of << c-Src >>, which was shown to be activated by AhR ligands, was also increased by [[ I3S ]] and TCDD, and blocking of c-Src activity by 4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo[3,4-d]pyrimidine (PP2) inhibited phosphorylation of both c-Src and STAT3, raising a possibility that stimulatory activities of I3S and TCDD on Th17 differentiation could be exerted via increased phosphorylation of c-Src, which in turn stimulates STAT3 activation.",2197,9
+2198,"Phosphorylation of << c-Src >>, which was shown to be activated by AhR ligands, was also increased by I3S and [[ TCDD ]], and blocking of c-Src activity by 4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo[3,4-d]pyrimidine (PP2) inhibited phosphorylation of both c-Src and STAT3, raising a possibility that stimulatory activities of I3S and TCDD on Th17 differentiation could be exerted via increased phosphorylation of c-Src, which in turn stimulates STAT3 activation.",2198,9
+2199,"Phosphorylation of c-Src, which was shown to be activated by AhR ligands, was also increased by I3S and TCDD, and blocking of c-Src activity by 4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo[3,4-d]pyrimidine (PP2) inhibited phosphorylation of both c-Src and STAT3, raising a possibility that stimulatory activities of << I3S >> and TCDD on Th17 differentiation could be exerted via increased phosphorylation of [[ c-Src ]], which in turn stimulates STAT3 activation.",2199,9
+2200,"Phosphorylation of c-Src, which was shown to be activated by AhR ligands, was also increased by I3S and TCDD, and blocking of c-Src activity by 4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo[3,4-d]pyrimidine (PP2) inhibited phosphorylation of both c-Src and STAT3, raising a possibility that stimulatory activities of << I3S >> and TCDD on Th17 differentiation could be exerted via increased phosphorylation of c-Src, which in turn stimulates [[ STAT3 ]] activation.",2200,9
+2201,"Phosphorylation of c-Src, which was shown to be activated by AhR ligands, was also increased by I3S and TCDD, and blocking of c-Src activity by 4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo[3,4-d]pyrimidine (PP2) inhibited phosphorylation of both c-Src and STAT3, raising a possibility that stimulatory activities of I3S and << TCDD >> on Th17 differentiation could be exerted via increased phosphorylation of [[ c-Src ]], which in turn stimulates STAT3 activation.",2201,9
+2202,"Phosphorylation of c-Src, which was shown to be activated by AhR ligands, was also increased by I3S and TCDD, and blocking of c-Src activity by 4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo[3,4-d]pyrimidine (PP2) inhibited phosphorylation of both c-Src and STAT3, raising a possibility that stimulatory activities of I3S and << TCDD >> on Th17 differentiation could be exerted via increased phosphorylation of c-Src, which in turn stimulates [[ STAT3 ]] activation.",2202,9
+2203,"Phosphorylation of c-Src, which was shown to be activated by AhR ligands, was also increased by I3S and TCDD, and blocking of << c-Src >> activity by [[ 4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo[3,4-d]pyrimidine ]] (PP2) inhibited phosphorylation of both c-Src and STAT3, raising a possibility that stimulatory activities of I3S and TCDD on Th17 differentiation could be exerted via increased phosphorylation of c-Src, which in turn stimulates STAT3 activation.",2203,0
+2204,"Phosphorylation of c-Src, which was shown to be activated by AhR ligands, was also increased by I3S and TCDD, and blocking of c-Src activity by << 4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo[3,4-d]pyrimidine >> (PP2) inhibited phosphorylation of both [[ c-Src ]] and STAT3, raising a possibility that stimulatory activities of I3S and TCDD on Th17 differentiation could be exerted via increased phosphorylation of c-Src, which in turn stimulates STAT3 activation.",2204,0
+2205,"Phosphorylation of c-Src, which was shown to be activated by AhR ligands, was also increased by I3S and TCDD, and blocking of c-Src activity by << 4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo[3,4-d]pyrimidine >> (PP2) inhibited phosphorylation of both c-Src and [[ STAT3 ]], raising a possibility that stimulatory activities of I3S and TCDD on Th17 differentiation could be exerted via increased phosphorylation of c-Src, which in turn stimulates STAT3 activation.",2205,0
+2206,"Finally, we found that << I3S >> worsened experimental autoimmune encephalomyelitis (EAE), which is primarily mediated by Th17 cells, enhancing the frequency of [[ IL-17 ]]-producing cells in draining lymph nodes.",2206,6
+2207,<< TCDD >> induces the expression of [[ insulin-like growth factor binding protein 4 ]] in 5L rat hepatoma cells: a cautionary tale of the use of this cell line in studies on dioxin toxicity.,2207,6
+2208,"By ""working upwards"" from mTOR, we observed that << TCDD >> inhibited endogenous and IGF-I-induced [[ AKT ]] and ERK activation by interfering with tyrosine phosphorylation of insulin receptor substrate 1.",2208,8
+2209,"By ""working upwards"" from mTOR, we observed that << TCDD >> inhibited endogenous and IGF-I-induced AKT and [[ ERK ]] activation by interfering with tyrosine phosphorylation of insulin receptor substrate 1.",2209,8
+2210,"By ""working upwards"" from mTOR, we observed that << TCDD >> inhibited endogenous and [[ IGF-I ]]-induced AKT and ERK activation by interfering with tyrosine phosphorylation of insulin receptor substrate 1.",2210,0
+2211,This inhibition was mediated by a << TCDD >>-induced secreted factor which was identified as [[ insulin-like growth factor binding protein 4 ]] (IGFBP-4).,2211,7
+2212,This inhibition was mediated by a << TCDD >>-induced secreted factor which was identified as insulin-like growth factor binding protein 4 ([[ IGFBP-4 ]]).,2212,7
+2213,The induction of IGFBP-4 protein was dependent on a functional aryl hydrocarbon receptor and was preceded by a rapid increase in the level of << IGFBP-4 >> mRNA indicating that IGFBP-4 is a previously unknown transcriptional target of [[ TCDD ]] in 5L cells.,2213,8
+2214,The observations suggest that in 5L cells the Igfbp-4 gene may have got under the control of a promoter containing dioxin responsive element(s) leading to the induction of << IGFBP-4 >> by [[ TCDD ]].,2214,7
+2215,"Although numerous mechanisms of action of << pimozide >> and thioridazine have been identified, both drugs are [[ calmodulin ]] antagonists at drug concentrations that inhibit breast cancer cell growth in vitro.",2215,1
+2216,"Although numerous mechanisms of action of pimozide and << thioridazine >> have been identified, both drugs are [[ calmodulin ]] antagonists at drug concentrations that inhibit breast cancer cell growth in vitro.",2216,1
+2217,Inhibition of MCF-7 cell growth by the selective calmodulin antagonists W-13 and W-12 is consistent with a role for << calmodulin >> antagonism in the broad growth-inhibitory properties of [[ pimozide ]].,2217,0
+2218,Inhibition of MCF-7 cell growth by the selective << calmodulin >> antagonists [[ W-13 ]] and W-12 is consistent with a role for calmodulin antagonism in the broad growth-inhibitory properties of pimozide.,2218,1
+2219,Inhibition of MCF-7 cell growth by the selective << calmodulin >> antagonists W-13 and [[ W-12 ]] is consistent with a role for calmodulin antagonism in the broad growth-inhibitory properties of pimozide.,2219,1
+2220,"Levels of homovanillic acid (HVA), dihydroxyphenylacetic acid (DOPAC) and dihydroxyphenylglycol (DHPG) in plasma and the striatium were measured after inhibition of monoamine oxidase type A (MAO-A) by clorgyline (4 mg/kg i.p.), << MAO-B >> by [[ (-)deprenyl ]] (1 mg/kg i.p.), both MAO-A and MAO-B by nialamide (75 mg/kg i.p.) or peripheral neuronal MAO by debrisoquin (40 mg/kg i.p.).",2220,0
+2221,"Levels of homovanillic acid (HVA), dihydroxyphenylacetic acid (DOPAC) and dihydroxyphenylglycol (DHPG) in plasma and the striatium were measured after inhibition of monoamine oxidase type A (MAO-A) by clorgyline (4 mg/kg i.p.), MAO-B by (-)deprenyl (1 mg/kg i.p.), both << MAO-A >> and MAO-B by [[ nialamide ]] (75 mg/kg i.p.) or peripheral neuronal MAO by debrisoquin (40 mg/kg i.p.).",2221,0
+2222,"Levels of homovanillic acid (HVA), dihydroxyphenylacetic acid (DOPAC) and dihydroxyphenylglycol (DHPG) in plasma and the striatium were measured after inhibition of monoamine oxidase type A (MAO-A) by clorgyline (4 mg/kg i.p.), MAO-B by (-)deprenyl (1 mg/kg i.p.), both MAO-A and << MAO-B >> by [[ nialamide ]] (75 mg/kg i.p.) or peripheral neuronal MAO by debrisoquin (40 mg/kg i.p.).",2222,0
+2223,"Levels of homovanillic acid (HVA), dihydroxyphenylacetic acid (DOPAC) and dihydroxyphenylglycol (DHPG) in plasma and the striatium were measured after inhibition of monoamine oxidase type A (MAO-A) by clorgyline (4 mg/kg i.p.), MAO-B by (-)deprenyl (1 mg/kg i.p.), both MAO-A and MAO-B by nialamide (75 mg/kg i.p.) or peripheral neuronal << MAO >> by [[ debrisoquin ]] (40 mg/kg i.p.).",2223,0
+2224,"Levels of homovanillic acid (HVA), dihydroxyphenylacetic acid (DOPAC) and dihydroxyphenylglycol (DHPG) in plasma and the striatium were measured after inhibition of << monoamine oxidase type A >> (MAO-A) by [[ clorgyline ]] (4 mg/kg i.p.), MAO-B by (-)deprenyl (1 mg/kg i.p.), both MAO-A and MAO-B by nialamide (75 mg/kg i.p.) or peripheral neuronal MAO by debrisoquin (40 mg/kg i.p.).",2224,0
+2225,"Levels of homovanillic acid (HVA), dihydroxyphenylacetic acid (DOPAC) and dihydroxyphenylglycol (DHPG) in plasma and the striatium were measured after inhibition of monoamine oxidase type A (<< MAO-A >>) by [[ clorgyline ]] (4 mg/kg i.p.), MAO-B by (-)deprenyl (1 mg/kg i.p.), both MAO-A and MAO-B by nialamide (75 mg/kg i.p.) or peripheral neuronal MAO by debrisoquin (40 mg/kg i.p.).",2225,0
+2226,The results suggest that most of the << HVA >> in plasma is derived from deamination of DA by [[ MAO-A ]] in peripheral neurons; that DOPAC in plasma is derived from cells outside the central nervous system; that DHPG in plasma is derived virtually exclusively from the metabolism of norepinephrine in sympathetic nerve endings and that residual levels of HVA after treatment with debrisoquin provide an improved but limited indication of central dopaminergic activity.,2226,4
+2227,The results suggest that most of the HVA in plasma is derived from deamination of << DA >> by [[ MAO-A ]] in peripheral neurons; that DOPAC in plasma is derived from cells outside the central nervous system; that DHPG in plasma is derived virtually exclusively from the metabolism of norepinephrine in sympathetic nerve endings and that residual levels of HVA after treatment with debrisoquin provide an improved but limited indication of central dopaminergic activity.,2227,5
+2228,"After << loperamide >> administration ACTH levels fell to a nadir of 135 +/- 76 pg/ml, and then CRH was still able to induce an [[ ACTH ]] increase; the pattern of ACTH response to CRH was slightly delayed.",2228,6
+2229,"After << loperamide >> administration [[ ACTH ]] levels fell to a nadir of 135 +/- 76 pg/ml, and then CRH was still able to induce an ACTH increase; the pattern of ACTH response to CRH was slightly delayed.",2229,8
+2230,"<< Ambenonium >> is known to be an inhibitor of [[ acetylcholinesterase ]], and recent data have shown this drug to antagonize muscarinic receptors as well.",2230,0
+2231,"<< Ambenonium >> is known to be an inhibitor of acetylcholinesterase, and recent data have shown this drug to antagonize [[ muscarinic receptors ]] as well.",2231,1
+2232,"Ambenonium was a less potent antagonist of tissue responses to acetylcholine, and the underestimation in the pKB (as compared to that obtained with bethanechol) could be eliminated by prior treatment of tissues with the << acetylcholinesterase >> inhibitor [[ neostigmine ]].",2232,0
+2233,These data suggested that << ambenonium >> had a dual effect on tissue responses to acetylcholine-producing potentiation by blockade of [[ acetylcholinesterase ]] and concomitant antagonism by blockade of muscarinic receptors.,2233,0
+2234,These data suggested that << ambenonium >> had a dual effect on tissue responses to acetylcholine-producing potentiation by blockade of acetylcholinesterase and concomitant antagonism by blockade of [[ muscarinic receptors ]].,2234,0
+2235,These data suggested that ambenonium had a dual effect on tissue responses to << acetylcholine >>-producing potentiation by blockade of [[ acetylcholinesterase ]] and concomitant antagonism by blockade of muscarinic receptors.,2235,2
+2236,These data suggested that << ambenonium >> had a dual effect on tissue responses to acetylcholine-producing potentiation by blockade of acetylcholinesterase and concomitant antagonism by blockade of [[ muscarinic receptors ]].,2236,1
+2237,"However, << betaxolol >> produces less systemic beta 2- and possibly [[ beta 1-adrenergic receptor ]] blockade than either timolol or levobunolol.",2237,0
+2238,"However, betaxolol produces less systemic beta 2- and possibly << beta 1-adrenergic receptor >> blockade than either [[ timolol ]] or levobunolol.",2238,0
+2239,"However, betaxolol produces less systemic beta 2- and possibly << beta 1-adrenergic receptor >> blockade than either timolol or [[ levobunolol ]].",2239,0
+2240,"<< Tyrosinase >> catalyzes an unusual oxidative decarboxylation of [[ 3,4-dihydroxymandelate ]].",2240,5
+2241,<< Tyrosinase >> usually catalyzes the conversion of [[ monophenols ]] to o-diphenols and oxidation of diphenols to the corresponding quinones.,2241,5
+2242,<< Tyrosinase >> usually catalyzes the conversion of monophenols to o-diphenols and oxidation of [[ diphenols ]] to the corresponding quinones.,2242,5
+2243,"<< Phenol oxidase >> inhibitors such as [[ phenylthiourea ]], potassium cyanide, and sodium azide inhibited the reaction drastically, suggesting the participation of the active site copper of the enzyme in the catalysis.",2243,0
+2244,"<< Phenol oxidase >> inhibitors such as phenylthiourea, [[ potassium cyanide ]], and sodium azide inhibited the reaction drastically, suggesting the participation of the active site copper of the enzyme in the catalysis.",2244,0
+2245,"<< Phenol oxidase >> inhibitors such as phenylthiourea, potassium cyanide, and [[ sodium azide ]] inhibited the reaction drastically, suggesting the participation of the active site copper of the enzyme in the catalysis.",2245,0
+2246,"<< Mimosine >>, a well-known competitive inhibitor of [[ tyrosinase ]], competitively inhibited the new reaction also.",2246,0
+2247,"Present studies demonstrate that << mushroom tyrosinase >> will also catalyze [[ quinone methide ]] production with the same active site copper if a suitable substrate such as 3,4-dihydroxymandelic acid is provided.",2247,4
+2248,"Present studies demonstrate that << mushroom tyrosinase >> will also catalyze quinone methide production with the same active site copper if a suitable substrate such as [[ 3,4-dihydroxymandelic acid ]] is provided.",2248,5
+2249,"The activation of human [Glu1]plasminogen [( Glu1]Pg) by human recombinant (rec) two-chain tissue plasminogen activator (<< t-PA >>) is inhibited by Cl-, at physiological concentrations, and stimulated by [[ epsilon-aminocaproic acid ]] (EACA), as well as fibrin(ogen).",2249,9
+2250,"The activation of << human [Glu1]plasminogen >> [( Glu1]Pg) by human recombinant (rec) two-chain tissue plasminogen activator (t-PA) is inhibited by Cl-, at physiological concentrations, and stimulated by [[ epsilon-aminocaproic acid ]] (EACA), as well as fibrin(ogen).",2250,9
+2251,"The activation of human [Glu1]plasminogen [<< ( Glu1]Pg >>) by human recombinant (rec) two-chain tissue plasminogen activator (t-PA) is inhibited by Cl-, at physiological concentrations, and stimulated by [[ epsilon-aminocaproic acid ]] (EACA), as well as fibrin(ogen).",2251,9
+2252,"The activation of human [Glu1]plasminogen [( Glu1]Pg) by human recombinant (rec) two-chain << tissue plasminogen activator >> (t-PA) is inhibited by Cl-, at physiological concentrations, and stimulated by [[ epsilon-aminocaproic acid ]] (EACA), as well as fibrin(ogen).",2252,9
+2253,"The activation of human [Glu1]plasminogen [( Glu1]Pg) by human recombinant (rec) two-chain tissue plasminogen activator (<< t-PA >>) is inhibited by Cl-, at physiological concentrations, and stimulated by epsilon-aminocaproic acid ([[ EACA ]]), as well as fibrin(ogen).",2253,9
+2254,"The activation of << human [Glu1]plasminogen >> [( Glu1]Pg) by human recombinant (rec) two-chain tissue plasminogen activator (t-PA) is inhibited by Cl-, at physiological concentrations, and stimulated by epsilon-aminocaproic acid ([[ EACA ]]), as well as fibrin(ogen).",2254,9
+2255,"The activation of human [Glu1]plasminogen [<< ( Glu1]Pg >>) by human recombinant (rec) two-chain tissue plasminogen activator (t-PA) is inhibited by Cl-, at physiological concentrations, and stimulated by epsilon-aminocaproic acid ([[ EACA ]]), as well as fibrin(ogen).",2255,9
+2256,"The activation of human [Glu1]plasminogen [( Glu1]Pg) by human recombinant (rec) two-chain << tissue plasminogen activator >> (t-PA) is inhibited by Cl-, at physiological concentrations, and stimulated by epsilon-aminocaproic acid ([[ EACA ]]), as well as fibrin(ogen).",2256,9
+2257,"The activation of human [Glu1]plasminogen [( Glu1]Pg) by human recombinant (rec) two-chain tissue plasminogen activator (<< t-PA >>) is inhibited by [[ Cl- ]], at physiological concentrations, and stimulated by epsilon-aminocaproic acid (EACA), as well as fibrin(ogen).",2257,0
+2258,"The activation of << human [Glu1]plasminogen >> [( Glu1]Pg) by human recombinant (rec) two-chain tissue plasminogen activator (t-PA) is inhibited by [[ Cl- ]], at physiological concentrations, and stimulated by epsilon-aminocaproic acid (EACA), as well as fibrin(ogen).",2258,0
+2259,"The activation of human [Glu1]plasminogen [<< ( Glu1]Pg >>) by human recombinant (rec) two-chain tissue plasminogen activator (t-PA) is inhibited by [[ Cl- ]], at physiological concentrations, and stimulated by epsilon-aminocaproic acid (EACA), as well as fibrin(ogen).",2259,0
+2260,"The activation of human [Glu1]plasminogen [( Glu1]Pg) by human recombinant (rec) two-chain << tissue plasminogen activator >> (t-PA) is inhibited by [[ Cl- ]], at physiological concentrations, and stimulated by epsilon-aminocaproic acid (EACA), as well as fibrin(ogen).",2260,0
+2261,"The presence of << Cl- >> inhibits the stimulation of [[ [Glu1]Pg ]] activation that would normally occur in the presence of fibrinogen, a result of possible importance to the observation that some degree of systemic fibrinogenolysis accompanies therapeutic use of tissue plasminogen activator.",2261,0
+2262,Sodium-dependent << norepinephrine >>-induced currents in [[ norepinephrine-transporter ]]-transfected HEK-293 cells blocked by cocaine and antidepressants.,2262,9
+2263,Sodium-dependent norepinephrine-induced currents in << norepinephrine-transporter >>-transfected HEK-293 cells blocked by [[ cocaine ]] and antidepressants.,2263,0
+2264,"Whole-cell voltage-clamp of << hNET >>-293 cells reveals [[ NE ]]-induced, Na(+)-dependent currents blocked by antidepressants and cocaine that are absent in parental cells.",2264,9
+2265,"Whole-cell voltage-clamp of << hNET >>-293 cells reveals NE-induced, Na(+)-dependent currents blocked by antidepressants and [[ cocaine ]] that are absent in parental cells.",2265,0
+2266,"To explain our observations, we propose that << hNETs >> function as ion-gated ligand channels with an indefinite stoichiometry relating ion flux to [[ NE ]] transport.",2266,5
+2267,BACKGROUND: The active metabolite of the anti-inflammatory drug << nabumetone >> has been characterized as a selective inhibitor of the inducible [[ prostaglandin H synthase ]] (PGHS).,2267,0
+2268,BACKGROUND: The active metabolite of the anti-inflammatory drug << nabumetone >> has been characterized as a selective inhibitor of the inducible prostaglandin H synthase ([[ PGHS ]]).,2268,0
+2269,"Moreover, the production of << TXB2 >> during whole blood clotting was assessed as an index of the [[ cyclooxygenase ]] activity of platelet PGHS-1 ex vivo.",2269,4
+2270,"Moreover, the production of << TXB2 >> during whole blood clotting was assessed as an index of the cyclooxygenase activity of platelet [[ PGHS-1 ]] ex vivo.",2270,4
+2271,"The daily administration of low-dose << aspirin >> (40 mg), a selective inhibitor of platelet [[ PGHS-1 ]], caused a cumulative inhibition of urinary 11-dehydro-TXB2 and whole blood TXB2 production that recovered with a timecourse consistent with platelet turnover.",2271,0
+2272,"The daily administration of low-dose aspirin (40 mg), a selective inhibitor of platelet << PGHS-1 >>, caused a cumulative inhibition of urinary [[ 11-dehydro-TXB2 ]] and whole blood TXB2 production that recovered with a timecourse consistent with platelet turnover.",2272,4
+2273,"The daily administration of low-dose aspirin (40 mg), a selective inhibitor of platelet << PGHS-1 >>, caused a cumulative inhibition of urinary 11-dehydro-TXB2 and whole blood [[ TXB2 ]] production that recovered with a timecourse consistent with platelet turnover.",2273,4
+2274,CONCLUSIONS: << Nabumetone >> does dose-dependently inhibit the [[ cyclooxygenase ]] activity of platelet PGHS-1 of healthy subjects both in vivo and ex vivo.,2274,0
+2275,CONCLUSIONS: << Nabumetone >> does dose-dependently inhibit the cyclooxygenase activity of platelet [[ PGHS-1 ]] of healthy subjects both in vivo and ex vivo.,2275,0
+2276,"Preclinical efficacy of << emedastine >>, a potent, selective [[ histamine H1 ]] antagonist for topical ocular use.",2276,1
+2277,"(2) Exposure histories vary in secondary 11q23 leukemia, as the only << topoisomerase II >> inhibitor was [[ dactinomycin ]] in one case, and, in another case, no topoisomerase II inhibitor was administered.",2277,0
+2278,"<< Indomethacin >>, piroxicam, and sulindac sulfide were found to preferentially inhibit [[ PGHS-1 ]].",2278,0
+2279,"Indomethacin, << piroxicam >>, and sulindac sulfide were found to preferentially inhibit [[ PGHS-1 ]].",2279,0
+2280,"Indomethacin, piroxicam, and << sulindac sulfide >> were found to preferentially inhibit [[ PGHS-1 ]].",2280,0
+2281,"<< 6-Methoxy-2-naphthylacetic acid >>, the active metabolite of Relafen, inhibits murine [[ PGHS-2 ]] preferentially.",2281,0
+2282,"6-Methoxy-2-naphthylacetic acid, the active metabolite of << Relafen >>, inhibits murine [[ PGHS-2 ]] preferentially.",2282,0
+2283,"<< Aspirin >> irreversibly inhibits [[ PGHS-1 ]], preventing this isozyme from forming PGH2 or any other oxygenated product; in contrast, aspirin treatment of PGHS-2 causes this enzyme to form 15-hydroxy-5c,8c,11c,13t-eicosatetraenoic acid (15-HETE) instead of PGH2.",2283,0
+2284,"Aspirin irreversibly inhibits PGHS-1, preventing this isozyme from forming PGH2 or any other oxygenated product; in contrast, aspirin treatment of << PGHS-2 >> causes this enzyme to form 15-hydroxy-5c,8c,11c,13t-eicosatetraenoic acid ([[ 15-HETE ]]) instead of PGH2.",2284,4
+2285,"Aspirin irreversibly inhibits PGHS-1, preventing this isozyme from forming PGH2 or any other oxygenated product; in contrast, aspirin treatment of << PGHS-2 >> causes this enzyme to form [[ 15-hydroxy-5c,8c,11c,13t-eicosatetraenoic acid ]] (15-HETE) instead of PGH2.",2285,4
+2286,"Anorexia induced by (+)-amphetamine, phentermine, diethylpropion and phenylpropanolamine seems to be the result of their ability to increase the release of noradrenaline and/or dopamine from nerve terminals and inhibit their reuptake or, in the case of << phenylpropanolamine >>, to stimulate directly [[ alpha 1-adrenoceptors ]].",2286,9
+2287,"Under these conditions, blockade of << monoamine oxidase >> with [[ pargyline ]] (100 microM for 15 min) caused a leftward displacement of concentration-effect curves for both 5-methoxytryptamine (5-MeO-T) and tryptamine.",2287,0
+2288,"In addition several ligands known to act as agonists at either << 5-HT2A >> or 5-HT2C receptors including 1-m-chlorophenylpiperazine (m-CPP), [[ Ru 24969 ]], MK 212 and SCH 23390 were also agonists in rat fundus whilst sumatriptan, renzapride and 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) were very weak or inactive.",2288,2
+2289,"In addition several ligands known to act as agonists at either 5-HT2A or << 5-HT2C >> receptors including 1-m-chlorophenylpiperazine (m-CPP), [[ Ru 24969 ]], MK 212 and SCH 23390 were also agonists in rat fundus whilst sumatriptan, renzapride and 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) were very weak or inactive.",2289,2
+2290,"In addition several ligands known to act as agonists at either << 5-HT2A >> or 5-HT2C receptors including 1-m-chlorophenylpiperazine (m-CPP), Ru 24969, [[ MK 212 ]] and SCH 23390 were also agonists in rat fundus whilst sumatriptan, renzapride and 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) were very weak or inactive.",2290,2
+2291,"In addition several ligands known to act as agonists at either 5-HT2A or << 5-HT2C >> receptors including 1-m-chlorophenylpiperazine (m-CPP), Ru 24969, [[ MK 212 ]] and SCH 23390 were also agonists in rat fundus whilst sumatriptan, renzapride and 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) were very weak or inactive.",2291,2
+2292,"In addition several ligands known to act as agonists at either << 5-HT2A >> or 5-HT2C receptors including 1-m-chlorophenylpiperazine (m-CPP), Ru 24969, MK 212 and [[ SCH 23390 ]] were also agonists in rat fundus whilst sumatriptan, renzapride and 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) were very weak or inactive.",2292,2
+2293,"In addition several ligands known to act as agonists at either 5-HT2A or << 5-HT2C >> receptors including 1-m-chlorophenylpiperazine (m-CPP), Ru 24969, MK 212 and [[ SCH 23390 ]] were also agonists in rat fundus whilst sumatriptan, renzapride and 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) were very weak or inactive.",2293,2
+2294,"In addition several ligands known to act as agonists at either << 5-HT2A >> or 5-HT2C receptors including [[ 1-m-chlorophenylpiperazine ]] (m-CPP), Ru 24969, MK 212 and SCH 23390 were also agonists in rat fundus whilst sumatriptan, renzapride and 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) were very weak or inactive.",2294,2
+2295,"In addition several ligands known to act as agonists at either 5-HT2A or << 5-HT2C >> receptors including [[ 1-m-chlorophenylpiperazine ]] (m-CPP), Ru 24969, MK 212 and SCH 23390 were also agonists in rat fundus whilst sumatriptan, renzapride and 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) were very weak or inactive.",2295,2
+2296,"In addition several ligands known to act as agonists at either << 5-HT2A >> or 5-HT2C receptors including 1-m-chlorophenylpiperazine ([[ m-CPP ]]), Ru 24969, MK 212 and SCH 23390 were also agonists in rat fundus whilst sumatriptan, renzapride and 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) were very weak or inactive.",2296,2
+2297,"In addition several ligands known to act as agonists at either 5-HT2A or << 5-HT2C >> receptors including 1-m-chlorophenylpiperazine ([[ m-CPP ]]), Ru 24969, MK 212 and SCH 23390 were also agonists in rat fundus whilst sumatriptan, renzapride and 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) were very weak or inactive.",2297,2
+2298,Phorbol esters and << norepinephrine >> destabilize [[ alpha 1B-adrenergic receptor ]] mRNA in vascular smooth muscle cells.,2298,8
+2299,The mechanism by which << norepinephrine >> (NE) down-regulates [[ alpha 1B-adrenergic receptor ]] (alpha-AR) mRNA was studied in rabbit aortic smooth muscle cells.,2299,8
+2300,The mechanism by which << norepinephrine >> (NE) down-regulates alpha 1B-adrenergic receptor ([[ alpha-AR ]]) mRNA was studied in rabbit aortic smooth muscle cells.,2300,8
+2301,The mechanism by which norepinephrine (<< NE >>) down-regulates [[ alpha 1B-adrenergic receptor ]] (alpha-AR) mRNA was studied in rabbit aortic smooth muscle cells.,2301,8
+2302,The mechanism by which norepinephrine (<< NE >>) down-regulates alpha 1B-adrenergic receptor ([[ alpha-AR ]]) mRNA was studied in rabbit aortic smooth muscle cells.,2302,8
+2303,"<< NE >>, phorbol esters, and bradykinin each decreased [[ alpha-AR ]] mRNA levels by 70-80%.",2303,8
+2304,"NE, << phorbol esters >>, and bradykinin each decreased [[ alpha-AR ]] mRNA levels by 70-80%.",2304,8
+2305,The << protein kinase C >> inhibitor [[ (+)-1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride ]] (H-7) abolished the effects of phorbol esters and NE and decreased basal mRNA levels by 52 +/- 3%.,2305,0
+2306,The << protein kinase C >> inhibitor (+)-1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride ([[ H-7 ]]) abolished the effects of phorbol esters and NE and decreased basal mRNA levels by 52 +/- 3%.,2306,0
+2307,Neither ryanodine nor << EGTA >> inhibited down-regulation of [[ alpha-AR ]] mRNA by NE.,2307,6
+2308,Neither << ryanodine >> nor EGTA inhibited down-regulation of [[ alpha-AR ]] mRNA by NE.,2308,6
+2309,Neither ryanodine nor EGTA inhibited down-regulation of << alpha-AR >> mRNA by [[ NE ]].,2309,8
+2310,<< Actinomycin D >> caused [[ alpha-AR ]] mRNA level to decrease with a half-life of 3.2 +/- 0.4 h and blocked the effect of H-7 to decrease basal alpha-AR mRNA level.,2310,8
+2311,<< Actinomycin D >> caused alpha-AR mRNA level to decrease with a half-life of 3.2 +/- 0.4 h and blocked the effect of H-7 to decrease basal [[ alpha-AR ]] mRNA level.,2311,8
+2312,Both << NE >> and phorbol esters increased the rate of [[ alpha-AR ]] mRNA degradation.,2312,8
+2313,Both NE and << phorbol esters >> increased the rate of [[ alpha-AR ]] mRNA degradation.,2313,8
+2314,"In << NE >>-desensitized cells, phorbol esters and bradykinin each caused the expected down-regulation of [[ alpha-AR ]] mRNA.",2314,8
+2315,"In NE-desensitized cells, << phorbol esters >> and bradykinin each caused the expected down-regulation of [[ alpha-AR ]] mRNA.",2315,8
+2316,The << protein phosphatase >> inhibitor [[ okadaic acid ]] prolonged the normally transient effect of NE for at least 24 h.,2316,0
+2317,The specific binding is displaced by the selective << 5-HT1D >> agonist [[ sumatriptan ]] but not by the mixed 5-HT1A/1D agonist 5-carboxyamidotryptamine.,2317,2
+2318,HeLa cells transfected with the MR77 gene exhibited inhibition of << adenylate cyclase >> in response to [[ serotonin ]].,2318,0
+2319,"The antiarrhythmic effects of exogenous adenosine and Valsalva on this form of VT may be due to receptor-mediated inhibition of adenylate cyclase or to noncardiac receptor-mediated effects, i.e., exogenous << adenosine >> may modulate VT through alterations in autonomic tone by activation of arterial [[ chemoreceptors ]], and Valsalva has been shown to decrease venous return, resulting in a reduction in cardiac dimensions and myocardial stretch.",2319,9
+2320,"VT recurred with the addition of << aminophylline >>, a competitive [[ adenosine A1-receptor ]] antagonist.",2320,1
+2321,"Edrophonium (10 mg i.v.), a cholinesterase inhibitor that potentiates the effects of acetylcholine at the << muscarinic cholinergic receptor >>, terminated VT in four of four patients, an effect that was reversed by [[ atropine ]].",2321,3
+2322,"<< Edrophonium >> (10 mg i.v.), a [[ cholinesterase ]] inhibitor that potentiates the effects of acetylcholine at the muscarinic cholinergic receptor, terminated VT in four of four patients, an effect that was reversed by atropine.",2322,0
+2323,<< Amantadine >> induces [[ c-fos ]] in rat striatum: reversal with dopamine D1 and NMDA receptor antagonists.,2323,6
+2324,"<< Amantadine >> (1-aminoadamantane) induced [[ Fos ]] expression in the central, dorsal-medial and ventral-medial part of the striatum.",2324,6
+2325,"Amantadine (<< 1-aminoadamantane >>) induced [[ Fos ]] expression in the central, dorsal-medial and ventral-medial part of the striatum.",2325,6
+2326,The distribution pattern of << Fos >> induced by [[ amantadine ]] was more similar to those seen with dopaminomimetics than with N-methyl-D-aspartate (NMDA) receptor antagonists.,2326,6
+2327,"Pretreatment with the dopamine D1 receptor antagonist, SCH23390, and the NMDA receptor antagonist, MK-801, blocked << amantadine >> induction of [[ Fos ]] in the striatum.",2327,6
+2328,"Pretreatment with the dopamine D1 receptor antagonist, << SCH23390 >>, and the NMDA receptor antagonist, MK-801, blocked amantadine induction of [[ Fos ]] in the striatum.",2328,8
+2329,"Pretreatment with the dopamine D1 receptor antagonist, SCH23390, and the NMDA receptor antagonist, << MK-801 >>, blocked amantadine induction of [[ Fos ]] in the striatum.",2329,8
+2330,"Pretreatment with the << dopamine D1 receptor >> antagonist, [[ SCH23390 ]], and the NMDA receptor antagonist, MK-801, blocked amantadine induction of Fos in the striatum.",2330,1
+2331,"Pretreatment with the dopamine D1 receptor antagonist, SCH23390, and the << NMDA receptor >> antagonist, [[ MK-801 ]], blocked amantadine induction of Fos in the striatum.",2331,1
+2332,"However, << amantadine >> induction of [[ Fos ]] in the striatum was unaffected by the dopamine D2 receptor antagonist, sulpiride.",2332,6
+2333,"However, amantadine induction of Fos in the striatum was unaffected by the << dopamine D2 receptor >> antagonist, [[ sulpiride ]].",2333,1
+2334,These results suggest that << amantadine >> induction of [[ Fos ]] in the rat striatum is related to dopamine D1 and NMDA receptors.,2334,6
+2335,"After CFVs were observed for 30 min, the animals were randomly divided in four groups: 5 animals received via a small catheter (26G) placed proximally to the stenosis, an intra-arterial infusion of human recombinant FVIIai (0.1 mg/kg/min for 10 min); 9 animals received AP-1, a monoclonal antibody against rabbit TF (0.1 mg/kg i.v. bolus); 7 animals received ridogrel, a dual thromboxane A2 synthetase inhibitor and thromboxane A2 receptor antagonist (10 mg/kg i.v. bolus); finally, 8 rabbits received << aurintrycarboxilic acid >> (ATA), an inhibitor of platelet [[ glycoprotein Ib ]]/von Willebrand factor interaction (10 mg/kg i.v. bolus).",2335,0
+2336,"After CFVs were observed for 30 min, the animals were randomly divided in four groups: 5 animals received via a small catheter (26G) placed proximally to the stenosis, an intra-arterial infusion of human recombinant FVIIai (0.1 mg/kg/min for 10 min); 9 animals received AP-1, a monoclonal antibody against rabbit TF (0.1 mg/kg i.v. bolus); 7 animals received ridogrel, a dual thromboxane A2 synthetase inhibitor and thromboxane A2 receptor antagonist (10 mg/kg i.v. bolus); finally, 8 rabbits received << aurintrycarboxilic acid >> (ATA), an inhibitor of platelet glycoprotein Ib/[[ von Willebrand factor ]] interaction (10 mg/kg i.v. bolus).",2336,0
+2337,"After CFVs were observed for 30 min, the animals were randomly divided in four groups: 5 animals received via a small catheter (26G) placed proximally to the stenosis, an intra-arterial infusion of human recombinant FVIIai (0.1 mg/kg/min for 10 min); 9 animals received AP-1, a monoclonal antibody against rabbit TF (0.1 mg/kg i.v. bolus); 7 animals received ridogrel, a dual thromboxane A2 synthetase inhibitor and thromboxane A2 receptor antagonist (10 mg/kg i.v. bolus); finally, 8 rabbits received aurintrycarboxilic acid (<< ATA >>), an inhibitor of platelet [[ glycoprotein Ib ]]/von Willebrand factor interaction (10 mg/kg i.v. bolus).",2337,0
+2338,"After CFVs were observed for 30 min, the animals were randomly divided in four groups: 5 animals received via a small catheter (26G) placed proximally to the stenosis, an intra-arterial infusion of human recombinant FVIIai (0.1 mg/kg/min for 10 min); 9 animals received AP-1, a monoclonal antibody against rabbit TF (0.1 mg/kg i.v. bolus); 7 animals received ridogrel, a dual thromboxane A2 synthetase inhibitor and thromboxane A2 receptor antagonist (10 mg/kg i.v. bolus); finally, 8 rabbits received aurintrycarboxilic acid (<< ATA >>), an inhibitor of platelet glycoprotein Ib/[[ von Willebrand factor ]] interaction (10 mg/kg i.v. bolus).",2338,0
+2339,"These events are stimulated by NE and by guanethidine, an << hNET >> substrate, and they are blocked by [[ cocaine ]] and the antidepressant desipramine.",2339,0
+2340,"These events are stimulated by NE and by guanethidine, an << hNET >> substrate, and they are blocked by cocaine and the antidepressant [[ desipramine ]].",2340,0
+2341,"These events are stimulated by << NE >> and by guanethidine, an [[ hNET ]] substrate, and they are blocked by cocaine and the antidepressant desipramine.",2341,5
+2342,"These events are stimulated by NE and by << guanethidine >>, an [[ hNET ]] substrate, and they are blocked by cocaine and the antidepressant desipramine.",2342,5
+2343,Voltage-clamp data combined with << NE >> uptake data from these same cells indicate that [[ hNETs ]] have two functional modes of conduction: a classical transporter mode (T-mode) and a novel channel mode (C-mode).,2343,5
+2344,"In extending these initial findings, we have shown that cardiac fibrosis (i) is not reversed by correction of mineralocorticoid-induced hypokalemia; (ii) appears not to involve the plasma or tissue renin-angiotensin systems, as fibrosis is largely unaffected by concurrent administration of Losartan or Perindopril; (iii) is independent of cardiac hypertrophy, in that it is equally seen in right and left ventricles, and in rats rendered hypertensive without cardiac hypertrophy by the administration of 9 alpha-fluorocortisol; (iv) is independent of elevated blood pressure, in that it is found in normotensive animals infused peripherally with aldosterone and intracerebroventricularly with the << mineralocorticoid receptor >> (MR) antagonist [[ RU28318 ]]; (v) is via classical MR, in that it is blocked by concurrent administration of the MR antagonist potassium canrenoate; and (vi) may or may not be a direct cardiac effect, inasmuch as data for in vivo effects on collagen formation by cardiac fibroblasts are conflicting.",2344,1
+2345,"In extending these initial findings, we have shown that cardiac fibrosis (i) is not reversed by correction of mineralocorticoid-induced hypokalemia; (ii) appears not to involve the plasma or tissue renin-angiotensin systems, as fibrosis is largely unaffected by concurrent administration of Losartan or Perindopril; (iii) is independent of cardiac hypertrophy, in that it is equally seen in right and left ventricles, and in rats rendered hypertensive without cardiac hypertrophy by the administration of 9 alpha-fluorocortisol; (iv) is independent of elevated blood pressure, in that it is found in normotensive animals infused peripherally with aldosterone and intracerebroventricularly with the mineralocorticoid receptor (<< MR >>) antagonist [[ RU28318 ]]; (v) is via classical MR, in that it is blocked by concurrent administration of the MR antagonist potassium canrenoate; and (vi) may or may not be a direct cardiac effect, inasmuch as data for in vivo effects on collagen formation by cardiac fibroblasts are conflicting.",2345,1
+2346,"In extending these initial findings, we have shown that cardiac fibrosis (i) is not reversed by correction of mineralocorticoid-induced hypokalemia; (ii) appears not to involve the plasma or tissue renin-angiotensin systems, as fibrosis is largely unaffected by concurrent administration of Losartan or Perindopril; (iii) is independent of cardiac hypertrophy, in that it is equally seen in right and left ventricles, and in rats rendered hypertensive without cardiac hypertrophy by the administration of 9 alpha-fluorocortisol; (iv) is independent of elevated blood pressure, in that it is found in normotensive animals infused peripherally with aldosterone and intracerebroventricularly with the mineralocorticoid receptor (MR) antagonist RU28318; (v) is via classical << MR >>, in that it is blocked by concurrent administration of the MR antagonist [[ potassium canrenoate ]]; and (vi) may or may not be a direct cardiac effect, inasmuch as data for in vivo effects on collagen formation by cardiac fibroblasts are conflicting.",2346,1
+2347,"In extending these initial findings, we have shown that cardiac fibrosis (i) is not reversed by correction of mineralocorticoid-induced hypokalemia; (ii) appears not to involve the plasma or tissue renin-angiotensin systems, as fibrosis is largely unaffected by concurrent administration of Losartan or Perindopril; (iii) is independent of cardiac hypertrophy, in that it is equally seen in right and left ventricles, and in rats rendered hypertensive without cardiac hypertrophy by the administration of 9 alpha-fluorocortisol; (iv) is independent of elevated blood pressure, in that it is found in normotensive animals infused peripherally with aldosterone and intracerebroventricularly with the mineralocorticoid receptor (MR) antagonist RU28318; (v) is via classical MR, in that it is blocked by concurrent administration of the << MR >> antagonist [[ potassium canrenoate ]]; and (vi) may or may not be a direct cardiac effect, inasmuch as data for in vivo effects on collagen formation by cardiac fibroblasts are conflicting.",2347,1
+2348,<< Amezinium >> and debrisoquine are substrates of uptake1 and potent inhibitors of [[ monoamine oxidase ]] in perfused lungs of rats.,2348,0
+2349,Amezinium and << debrisoquine >> are substrates of uptake1 and potent inhibitors of [[ monoamine oxidase ]] in perfused lungs of rats.,2349,0
+2350,<< Amezinium >> and debrisoquine are substrates of [[ uptake1 ]] and potent inhibitors of monoamine oxidase in perfused lungs of rats.,2350,5
+2351,Amezinium and << debrisoquine >> are substrates of [[ uptake1 ]] and potent inhibitors of monoamine oxidase in perfused lungs of rats.,2351,5
+2352,"Previous studies have resulted in the classification of << amezinium >> as a selective inhibitor of neuronal [[ monoamine oxidase ]] (MAO), because it is a much more potent MAO inhibitor in intact tissues, in which it is accumulated in noradrenergic neurones by uptake1, than in tissue homogenates.",2352,0
+2353,"Previous studies have resulted in the classification of << amezinium >> as a selective inhibitor of neuronal monoamine oxidase ([[ MAO ]]), because it is a much more potent MAO inhibitor in intact tissues, in which it is accumulated in noradrenergic neurones by uptake1, than in tissue homogenates.",2353,0
+2354,"Previous studies have resulted in the classification of << amezinium >> as a selective inhibitor of neuronal monoamine oxidase (MAO), because it is a much more potent [[ MAO ]] inhibitor in intact tissues, in which it is accumulated in noradrenergic neurones by uptake1, than in tissue homogenates.",2354,0
+2355,"In addition, another drug that is both a substrate of uptake1 and a << MAO >> inhibitor, [[ debrisoquine ]], was investigated in the study.",2355,0
+2356,"In addition, another drug that is both a substrate of << uptake1 >> and a MAO inhibitor, [[ debrisoquine ]], was investigated in the study.",2356,5
+2357,"When MAO-B was also inhibited, 10 nmol/l << amezinium >> caused 84% inhibition of the deamination of noradrenaline by [[ MAO-A ]] in the lungs.",2357,0
+2358,"The results when considered with previous reports in the literature show that << amezinium >> is about 1000 times more potent and debrisoquine is about 20 times more potent for [[ MAO ]] inhibition in rat lungs than in tissue homogenates, and the reason for their high potencies in the intact lungs is transport and accumulation of the drugs in the pulmonary endothelial cells by uptake1.",2358,0
+2359,"The results when considered with previous reports in the literature show that amezinium is about 1000 times more potent and << debrisoquine >> is about 20 times more potent for [[ MAO ]] inhibition in rat lungs than in tissue homogenates, and the reason for their high potencies in the intact lungs is transport and accumulation of the drugs in the pulmonary endothelial cells by uptake1.",2359,0
+2360,"The results when considered with previous reports in the literature show that << amezinium >> is about 1000 times more potent and debrisoquine is about 20 times more potent for MAO inhibition in rat lungs than in tissue homogenates, and the reason for their high potencies in the intact lungs is transport and accumulation of the drugs in the pulmonary endothelial cells by [[ uptake1 ]].",2360,5
+2361,"The results when considered with previous reports in the literature show that amezinium is about 1000 times more potent and << debrisoquine >> is about 20 times more potent for MAO inhibition in rat lungs than in tissue homogenates, and the reason for their high potencies in the intact lungs is transport and accumulation of the drugs in the pulmonary endothelial cells by [[ uptake1 ]].",2361,5
+2362,"<< Amezinium >> is much less potent as a [[ MAO ]] inhibitor in cells with the uptake2 transporter, such as the myocardial cells of the heart.",2362,0
+2363,"<< Amezinium >> is much less potent as a MAO inhibitor in cells with the [[ uptake2 transporter ]], such as the myocardial cells of the heart.",2363,5
+2364,The results also confirmed previous reports that << amezinium >> is highly selective for [[ MAO-A ]].,2364,0
+2365,"We have investigated the effects of << CP-99,994 >> [(+)-(2s,3s)-3-(2-methoxybenzylamino)-2-phenylpiperidine], a [[ tachykinin NK1 receptor ]] antagonist, HOE 140 (D-Arg[Hyp3,Thi5,D-Tic7,Oic8]bradykinin), a bradykinin B2 receptor antagonist, and ketotifen (4-(1-methyl-4-piperidylidene)4 H-benzo[4,5]cycloheptal[1,2-b]thiophen-10(9H)-one hydrogen fumarate), a histamine H1 receptor antagonist with mast cell-stabilizing properties, on microvascular leakage induced by gaseous formaldehyde.",2365,1
+2366,"We have investigated the effects of CP-99,994 << [(+)-(2s,3s)-3-(2-methoxybenzylamino)-2-phenylpiperidine] >>, a [[ tachykinin NK1 receptor ]] antagonist, HOE 140 (D-Arg[Hyp3,Thi5,D-Tic7,Oic8]bradykinin), a bradykinin B2 receptor antagonist, and ketotifen (4-(1-methyl-4-piperidylidene)4 H-benzo[4,5]cycloheptal[1,2-b]thiophen-10(9H)-one hydrogen fumarate), a histamine H1 receptor antagonist with mast cell-stabilizing properties, on microvascular leakage induced by gaseous formaldehyde.",2366,1
+2367,"We have investigated the effects of CP-99,994 [(+)-(2s,3s)-3-(2-methoxybenzylamino)-2-phenylpiperidine], a tachykinin NK1 receptor antagonist, << HOE 140 >> (D-Arg[Hyp3,Thi5,D-Tic7,Oic8]bradykinin), a [[ bradykinin B2 receptor ]] antagonist, and ketotifen (4-(1-methyl-4-piperidylidene)4 H-benzo[4,5]cycloheptal[1,2-b]thiophen-10(9H)-one hydrogen fumarate), a histamine H1 receptor antagonist with mast cell-stabilizing properties, on microvascular leakage induced by gaseous formaldehyde.",2367,1
+2368,"We have investigated the effects of CP-99,994 [(+)-(2s,3s)-3-(2-methoxybenzylamino)-2-phenylpiperidine], a tachykinin NK1 receptor antagonist, HOE 140 << (D-Arg[Hyp3,Thi5,D-Tic7,Oic8]bradykinin) >>, a [[ bradykinin B2 receptor ]] antagonist, and ketotifen (4-(1-methyl-4-piperidylidene)4 H-benzo[4,5]cycloheptal[1,2-b]thiophen-10(9H)-one hydrogen fumarate), a histamine H1 receptor antagonist with mast cell-stabilizing properties, on microvascular leakage induced by gaseous formaldehyde.",2368,1
+2369,"We have investigated the effects of CP-99,994 [(+)-(2s,3s)-3-(2-methoxybenzylamino)-2-phenylpiperidine], a tachykinin NK1 receptor antagonist, HOE 140 (D-Arg[Hyp3,Thi5,D-Tic7,Oic8]bradykinin), a bradykinin B2 receptor antagonist, and << ketotifen >> (4-(1-methyl-4-piperidylidene)4 H-benzo[4,5]cycloheptal[1,2-b]thiophen-10(9H)-one hydrogen fumarate), a [[ histamine H1 receptor ]] antagonist with mast cell-stabilizing properties, on microvascular leakage induced by gaseous formaldehyde.",2369,1
+2370,"We have investigated the effects of CP-99,994 [(+)-(2s,3s)-3-(2-methoxybenzylamino)-2-phenylpiperidine], a tachykinin NK1 receptor antagonist, HOE 140 (D-Arg[Hyp3,Thi5,D-Tic7,Oic8]bradykinin), a bradykinin B2 receptor antagonist, and ketotifen << (4-(1-methyl-4-piperidylidene)4 H-benzo[4,5]cycloheptal[1,2-b]thiophen-10(9H)-one hydrogen fumarate) >>, a [[ histamine H1 receptor ]] antagonist with mast cell-stabilizing properties, on microvascular leakage induced by gaseous formaldehyde.",2370,1
+2371,Molecular determinants of << dofetilide >> block of [[ HERG ]] K+ channels.,2371,0
+2372,Molecular determinants of << dofetilide >> block of HERG [[ K+ channels ]].,2372,0
+2373,"<< HERG >>/IKr channels are a prime target for the pharmacological management of arrhythmias and are selectively blocked by class III antiarrhythmic methanesulfonanilide drugs, such as dofetilide, [[ E4031 ]], and MK-499, at submicromolar concentrations.",2373,0
+2374,"HERG/<< IKr >> channels are a prime target for the pharmacological management of arrhythmias and are selectively blocked by class III antiarrhythmic methanesulfonanilide drugs, such as dofetilide, [[ E4031 ]], and MK-499, at submicromolar concentrations.",2374,0
+2375,"<< HERG >>/IKr channels are a prime target for the pharmacological management of arrhythmias and are selectively blocked by class III antiarrhythmic methanesulfonanilide drugs, such as dofetilide, E4031, and [[ MK-499 ]], at submicromolar concentrations.",2375,0
+2376,"HERG/<< IKr >> channels are a prime target for the pharmacological management of arrhythmias and are selectively blocked by class III antiarrhythmic methanesulfonanilide drugs, such as dofetilide, E4031, and [[ MK-499 ]], at submicromolar concentrations.",2376,0
+2377,"<< HERG >>/IKr channels are a prime target for the pharmacological management of arrhythmias and are selectively blocked by class III antiarrhythmic [[ methanesulfonanilide ]] drugs, such as dofetilide, E4031, and MK-499, at submicromolar concentrations.",2377,0
+2378,"HERG/<< IKr >> channels are a prime target for the pharmacological management of arrhythmias and are selectively blocked by class III antiarrhythmic [[ methanesulfonanilide ]] drugs, such as dofetilide, E4031, and MK-499, at submicromolar concentrations.",2378,0
+2379,"<< HERG >>/IKr channels are a prime target for the pharmacological management of arrhythmias and are selectively blocked by class III antiarrhythmic methanesulfonanilide drugs, such as [[ dofetilide ]], E4031, and MK-499, at submicromolar concentrations.",2379,0
+2380,"HERG/<< IKr >> channels are a prime target for the pharmacological management of arrhythmias and are selectively blocked by class III antiarrhythmic methanesulfonanilide drugs, such as [[ dofetilide ]], E4031, and MK-499, at submicromolar concentrations.",2380,0
+2381,Treatment using a combination of testosterone and the << aromatase >> inhibitor [[ testolactone ]] may have significantly better effects on sexual function and also seizure frequency than testosterone alone.,2381,0
+2382,"A case of therapy-related acute myeloblastic leukemia with t(16;21)(q24;q22) after chemotherapy with << DNA-topoisomerase II >> inhibitors, [[ etoposide ]] and mitoxantrone, and the alkylating agent, cyclophosphamide.",2382,0
+2383,"A case of therapy-related acute myeloblastic leukemia with t(16;21)(q24;q22) after chemotherapy with << DNA-topoisomerase II >> inhibitors, etoposide and [[ mitoxantrone ]], and the alkylating agent, cyclophosphamide.",2383,0
+2384,"A 59-year-old female suffering from malignant lymphoma developed therapy-related acute myeloblastic leukemia (t-AML) after chemotherapy consisting of treatment with << DNA-topoisomerase II >> inhibitors, [[ etoposide ]] and mitoxantrone, and an alkylating agent, cyclophosphamide.",2384,0
+2385,"A 59-year-old female suffering from malignant lymphoma developed therapy-related acute myeloblastic leukemia (t-AML) after chemotherapy consisting of treatment with << DNA-topoisomerase II >> inhibitors, etoposide and [[ mitoxantrone ]], and an alkylating agent, cyclophosphamide.",2385,0
+2386,"<< Selegiline >> (deprenyl), a selective, irreversible inhibitor of [[ monoamine oxidase type B ]] (MAO-B) is widely used in the treatment of Parkinson's disease.",2386,0
+2387,"<< Selegiline >> (deprenyl), a selective, irreversible inhibitor of monoamine oxidase type B ([[ MAO-B ]]) is widely used in the treatment of Parkinson's disease.",2387,0
+2388,"Selegiline (<< deprenyl >>), a selective, irreversible inhibitor of [[ monoamine oxidase type B ]] (MAO-B) is widely used in the treatment of Parkinson's disease.",2388,0
+2389,"Selegiline (<< deprenyl >>), a selective, irreversible inhibitor of monoamine oxidase type B ([[ MAO-B ]]) is widely used in the treatment of Parkinson's disease.",2389,0
+2390,"Unlike the nonselective << MAO >> inhibitors, [[ selegiline ]] does not significantly potentiate tyramine-induced hypertension (the 'cheese effect') at the dosages (5 to 10 mg daily) used for the treatment of Parkinson's disease.",2390,0
+2391,"A low tyramine diet is recommended if << selegiline >> is used together with nonselective [[ MAO ]] inhibitors or the selective, reversible MAO-A inhibitor, moclobemide.",2391,0
+2392,"A low tyramine diet is recommended if selegiline is used together with nonselective MAO inhibitors or the selective, reversible << MAO-A >> inhibitor, [[ moclobemide ]].",2392,0
+2393,<< Ibuprofen >> inhibits [[ cystic fibrosis transmembrane conductance regulator ]]-mediated Cl- secretion.,2393,0
+2394,<< Ibuprofen >> (300 microM) reduced [[ CFTR ]] Cl- current by 60+/-16% and this was explained by a short-lived block (approximately 1.2 ms) which causes an apparent reduction in single channel amplitude from 1.07+/-0.04 pA to 0.59+/-0.04 pA (n = 3).,2394,0
+2395,"Similarly, << salicylic acid >> (3 mM) reduced [[ CFTR ]] Cl- current by 50+/-8% with an apparent reduction in single channel amplitude from 1.08+/-0.03 pA to 0.48+/-0.06 pA (n = 4).",2395,0
+2396,"Based on these results, we conclude that the NSAIDs << ibuprofen >> and salicylic acid inhibit cAMP-mediated Cl- secretion in human colonic and airway epithelia via a direct inhibition of [[ CFTR ]] Cl- channels as well as basolateral membrane K+ channels.",2396,0
+2397,"Based on these results, we conclude that the NSAIDs << ibuprofen >> and salicylic acid inhibit cAMP-mediated Cl- secretion in human colonic and airway epithelia via a direct inhibition of CFTR [[ Cl- channels ]] as well as basolateral membrane K+ channels.",2397,0
+2398,"Based on these results, we conclude that the NSAIDs << ibuprofen >> and salicylic acid inhibit cAMP-mediated Cl- secretion in human colonic and airway epithelia via a direct inhibition of CFTR Cl- channels as well as basolateral membrane [[ K+ channels ]].",2398,0
+2399,"Based on these results, we conclude that the NSAIDs ibuprofen and << salicylic acid >> inhibit cAMP-mediated Cl- secretion in human colonic and airway epithelia via a direct inhibition of [[ CFTR ]] Cl- channels as well as basolateral membrane K+ channels.",2399,0
+2400,"Based on these results, we conclude that the NSAIDs ibuprofen and << salicylic acid >> inhibit cAMP-mediated Cl- secretion in human colonic and airway epithelia via a direct inhibition of CFTR [[ Cl- channels ]] as well as basolateral membrane K+ channels.",2400,0
+2401,"Based on these results, we conclude that the NSAIDs ibuprofen and << salicylic acid >> inhibit cAMP-mediated Cl- secretion in human colonic and airway epithelia via a direct inhibition of CFTR Cl- channels as well as basolateral membrane [[ K+ channels ]].",2401,0
+2402,"Additional neuroendocrine experiments in a parallel group of rats revealed a dose-related increase in << plasma prolactin >> and ACTH levels after i.v. [[ mCPP ]], pointing to a general state of arousal in these mCPP-treated animals.",2402,6
+2403,"Additional neuroendocrine experiments in a parallel group of rats revealed a dose-related increase in plasma prolactin and << ACTH >> levels after i.v. [[ mCPP ]], pointing to a general state of arousal in these mCPP-treated animals.",2403,6
+2404,"These data indicate that mixed 5-HT1/5-HT2 receptor antagonists such as pizotifen and methysergide, and mixed 5-HT and catecholamine antagonists such as mianserin and mirtazapine are more potent antagonists of mCPP-induced behavioural inhibition in rats than the more selective << 5-HT2A >>/5-HT2C antagonist [[ ritanserin ]].",2404,1
+2405,"These data indicate that mixed 5-HT1/5-HT2 receptor antagonists such as pizotifen and methysergide, and mixed 5-HT and catecholamine antagonists such as mianserin and mirtazapine are more potent antagonists of mCPP-induced behavioural inhibition in rats than the more selective 5-HT2A/<< 5-HT2C >> antagonist [[ ritanserin ]].",2405,1
+2406,"These data indicate that mixed << 5-HT1 >>/5-HT2 receptor antagonists such as [[ pizotifen ]] and methysergide, and mixed 5-HT and catecholamine antagonists such as mianserin and mirtazapine are more potent antagonists of mCPP-induced behavioural inhibition in rats than the more selective 5-HT2A/5-HT2C antagonist ritanserin.",2406,1
+2407,"These data indicate that mixed 5-HT1/<< 5-HT2 >> receptor antagonists such as [[ pizotifen ]] and methysergide, and mixed 5-HT and catecholamine antagonists such as mianserin and mirtazapine are more potent antagonists of mCPP-induced behavioural inhibition in rats than the more selective 5-HT2A/5-HT2C antagonist ritanserin.",2407,1
+2408,"These data indicate that mixed << 5-HT1 >>/5-HT2 receptor antagonists such as pizotifen and [[ methysergide ]], and mixed 5-HT and catecholamine antagonists such as mianserin and mirtazapine are more potent antagonists of mCPP-induced behavioural inhibition in rats than the more selective 5-HT2A/5-HT2C antagonist ritanserin.",2408,1
+2409,"These data indicate that mixed 5-HT1/<< 5-HT2 >> receptor antagonists such as pizotifen and [[ methysergide ]], and mixed 5-HT and catecholamine antagonists such as mianserin and mirtazapine are more potent antagonists of mCPP-induced behavioural inhibition in rats than the more selective 5-HT2A/5-HT2C antagonist ritanserin.",2409,1
+2410,"The cardiovascular effects of three different << acetylcholinesterase >> inhibitors: [[ physostigmine ]], tacrine and rivastigmine injected by intravenous (i.v.) route were compared in freely moving Wistar rats.",2410,0
+2411,"The cardiovascular effects of three different << acetylcholinesterase >> inhibitors: physostigmine, [[ tacrine ]] and rivastigmine injected by intravenous (i.v.) route were compared in freely moving Wistar rats.",2411,0
+2412,"The cardiovascular effects of three different << acetylcholinesterase >> inhibitors: physostigmine, tacrine and [[ rivastigmine ]] injected by intravenous (i.v.) route were compared in freely moving Wistar rats.",2412,0
+2413,<< Tacrine >> was chosen as a model to study the mechanisms underlying the cardiovascular effects of i.v. [[ cholinesterase ]] inhibitors.,2413,0
+2414,"The << alpha1-adrenoceptor >> antagonist [[ prazosin ]] or the vasopressin V1 receptor antagonist, [beta-mercapto-beta,beta-cyclopenta-methylenepropionyl1, O-Me-Tyr2, Arg8] vasopressin partially but significantly reduced tacrine pressor effect and mostly abolished it when administered concomitantly.",2414,1
+2415,"The alpha1-adrenoceptor antagonist prazosin or the << vasopressin V1 receptor >> antagonist, [[ [beta-mercapto-beta,beta-cyclopenta-methylenepropionyl1, O-Me-Tyr2, Arg8] vasopressin ]] partially but significantly reduced tacrine pressor effect and mostly abolished it when administered concomitantly.",2415,1
+2416,"The tacrine pressor response was inhibited in a dose-dependent manner by the i.c.v. administration of the non-selective << muscarinic receptor >> antagonist [[ atropine ]] (ID50 = 1.45 microg), the muscarinic M1 receptor antagonist pirenzepine (ID50 = 4.33 microg), the muscarinic M2 receptor antagonist methoctramine (ID50 = 1.39 microg) and the muscarinic M3 receptor antagonist para-fluoro-hexahydro-sila-difenidol (ID50 = 31.19 microg).",2416,1
+2417,"The tacrine pressor response was inhibited in a dose-dependent manner by the i.c.v. administration of the non-selective muscarinic receptor antagonist atropine (ID50 = 1.45 microg), the << muscarinic M1 receptor >> antagonist [[ pirenzepine ]] (ID50 = 4.33 microg), the muscarinic M2 receptor antagonist methoctramine (ID50 = 1.39 microg) and the muscarinic M3 receptor antagonist para-fluoro-hexahydro-sila-difenidol (ID50 = 31.19 microg).",2417,1
+2418,"The tacrine pressor response was inhibited in a dose-dependent manner by the i.c.v. administration of the non-selective muscarinic receptor antagonist atropine (ID50 = 1.45 microg), the muscarinic M1 receptor antagonist pirenzepine (ID50 = 4.33 microg), the << muscarinic M2 receptor >> antagonist [[ methoctramine ]] (ID50 = 1.39 microg) and the muscarinic M3 receptor antagonist para-fluoro-hexahydro-sila-difenidol (ID50 = 31.19 microg).",2418,1
+2419,"The tacrine pressor response was inhibited in a dose-dependent manner by the i.c.v. administration of the non-selective muscarinic receptor antagonist atropine (ID50 = 1.45 microg), the muscarinic M1 receptor antagonist pirenzepine (ID50 = 4.33 microg), the muscarinic M2 receptor antagonist methoctramine (ID50 = 1.39 microg) and the << muscarinic M3 receptor >> antagonist [[ para-fluoro-hexahydro-sila-difenidol ]] (ID50 = 31.19 microg).",2419,1
+2420,"State-dependent << cocaine >> block of [[ sodium channel ]] isoforms, chimeras, and channels coexpressed with the beta1 subunit.",2420,0
+2421,<< Cocaine >> block of [[ human cardiac (hH1) ]] and rat skeletal (mu1) muscle sodium channels was examined under whole-cell voltage clamp in transiently transfected HEK293t cells.,2421,0
+2422,<< Cocaine >> block of human cardiac (hH1) and [[ rat skeletal (mu1) muscle sodium channels ]] was examined under whole-cell voltage clamp in transiently transfected HEK293t cells.,2422,0
+2423,"<< Cocaine >> block of [[ hH1 channels ]] was greater than block of mu1 channels at voltages between -120 mV and -90 mV, suggesting that greater steady-state inactivation of hH1 channels in this voltage range makes them more susceptible to cocaine block.",2423,0
+2424,"<< Cocaine >> block of hH1 channels was greater than block of [[ mu1 channels ]] at voltages between -120 mV and -90 mV, suggesting that greater steady-state inactivation of hH1 channels in this voltage range makes them more susceptible to cocaine block.",2424,0
+2425,"<< Cocaine >> block of hH1 channels was greater than block of mu1 channels at voltages between -120 mV and -90 mV, suggesting that greater steady-state inactivation of [[ hH1 channels ]] in this voltage range makes them more susceptible to cocaine block.",2425,0
+2426,"Cocaine block of hH1 channels was greater than block of mu1 channels at voltages between -120 mV and -90 mV, suggesting that greater steady-state inactivation of << hH1 channels >> in this voltage range makes them more susceptible to [[ cocaine ]] block.",2426,0