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.


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.


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 ]].


Reversal of inhibition by << D2 >> agonist quinpirole was produced by serotonin (50 µM) and by [[ neurotensin ]] (5-10 nM).


Reversal of inhibition by << D2 >> agonist quinpirole was produced by [[ serotonin ]] (50 µM) and by neurotensin (5-10 nM).


Reversal of inhibition by << D2 >> agonist [[ quinpirole ]] was produced by serotonin (50 µM) and by neurotensin (5-10 nM).


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).


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 ]]).


<< RSV >> targets and activates the [[ NAD(+)-dependent protein deacetylase SIRT1 ]]; in turn, SIRT1 induces an intracellular antioxidative mechanism by inducing mitochondrial superoxide dismutase (SOD2).


<< RSV >> targets and activates the NAD(+)-dependent protein deacetylase SIRT1; in turn, [[ SIRT1 ]] induces an intracellular antioxidative mechanism by inducing mitochondrial superoxide dismutase (SOD2).


<< RSV >> targets and activates the NAD(+)-dependent protein deacetylase SIRT1; in turn, SIRT1 induces an intracellular antioxidative mechanism by inducing [[ mitochondrial superoxide dismutase ]] (SOD2).


<< RSV >> targets and activates the NAD(+)-dependent protein deacetylase SIRT1; in turn, SIRT1 induces an intracellular antioxidative mechanism by inducing mitochondrial superoxide dismutase ([[ SOD2 ]]).


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.


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.


Hydrophobic amino acids in the hinge region of the 5A apolipoprotein mimetic peptide are essential for promoting << cholesterol >> efflux by the [[ ABCA1 ]] transporter.


The bihelical << apolipoprotein mimetic peptide 5A >> effluxes [[ cholesterol ]] from cells and reduces inflammation and atherosclerosis in animal models.


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


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 ]].


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.


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.


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.


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.


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 ]].


<< L-BMAA >> induced ER stress and enhanced [[ caspase 12 ]] cleavage in human neuroblastoma SH-SY5Y cells at low nonexcitotoxic concentrations.


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.


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.


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.


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.


<< Ribavirin >>-induced intracellular GTP depletion activates transcription elongation in [[ coagulation factor VII ]] gene expression.


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.


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.


In the present study, we investigated the molecular mechanism of << ribavirin >>-induced up-regulation of [[ F7 ]] expression in HepG2 (human hepatoma cell line).


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.


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.


<< Ribavirin >> unregulated [[ ELL ]] (eleven-nineteen lysine-rich leukaemia) 3 mRNA expression before F7 up-regulation.


<< Ribavirin >> unregulated ELL ([[ eleven-nineteen lysine-rich leukaemia) 3 ]] mRNA expression before F7 up-regulation.


<< Ribavirin >> unregulated ELL (eleven-nineteen lysine-rich leukaemia) 3 mRNA expression before [[ F7 ]] up-regulation.


We observed that << ribavirin >> enhanced [[ ELL3 ]] recruitment to F7, whereas knockdown of ELL3 diminished ribavirin-induced FVII mRNA up-regulation.


We observed that << ribavirin >> enhanced ELL3 recruitment to [[ F7 ]], whereas knockdown of ELL3 diminished ribavirin-induced FVII mRNA up-regulation.


We observed that ribavirin enhanced ELL3 recruitment to F7, whereas knockdown of ELL3 diminished << ribavirin >>-induced [[ FVII ]] mRNA up-regulation.


<< Ribavirin >> also enhanced recruitment of [[ CDK9 ]] (cyclin-dependent kinase 9) and AFF4 to F7.


<< Ribavirin >> also enhanced recruitment of CDK9 ([[ cyclin-dependent kinase 9 ]]) and AFF4 to F7.


<< Ribavirin >> also enhanced recruitment of CDK9 (cyclin-dependent kinase 9) and [[ AFF4 ]] to F7.


<< Ribavirin >> also enhanced recruitment of CDK9 (cyclin-dependent kinase 9) and AFF4 to [[ F7 ]].


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


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 ]].


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 ]].


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 ]].


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.


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.


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 ]].


<< Fingolimod >> (FTY720), a novel drug approved for the treatment of relapsing-remitting multiple sclerosis, activates different [[ sphingosine-1-phosphate receptor ]] (S1PR) subtypes.


<< Fingolimod >> (FTY720), a novel drug approved for the treatment of relapsing-remitting multiple sclerosis, activates different sphingosine-1-phosphate receptor ([[ S1PR ]]) subtypes.


Fingolimod (<< FTY720 >>), a novel drug approved for the treatment of relapsing-remitting multiple sclerosis, activates different [[ sphingosine-1-phosphate receptor ]] (S1PR) subtypes.


Fingolimod (<< FTY720 >>), a novel drug approved for the treatment of relapsing-remitting multiple sclerosis, activates different sphingosine-1-phosphate receptor ([[ S1PR ]]) subtypes.


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.


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.


Pharmacokinetics and metabolism of << [(14)C]anagliptin >>, a novel [[ dipeptidyl peptidase-4 ]] inhibitor, in humans.


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.


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.


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.


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.


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.


Antiretroviral << protease >> inhibitors [[ lopinavir ]] (LPV) and ritonavir (RTV) are reported BSEP inhibitors.


Antiretroviral protease inhibitors << lopinavir >> (LPV) and ritonavir (RTV) are reported [[ BSEP ]] inhibitors.


Antiretroviral << protease >> inhibitors lopinavir ([[ LPV ]]) and ritonavir (RTV) are reported BSEP inhibitors.


Antiretroviral protease inhibitors lopinavir (<< LPV >>) and ritonavir (RTV) are reported [[ BSEP ]] inhibitors.


Antiretroviral << protease >> inhibitors lopinavir (LPV) and [[ ritonavir ]] (RTV) are reported BSEP inhibitors.


Antiretroviral protease inhibitors lopinavir (LPV) and << ritonavir >> (RTV) are reported [[ BSEP ]] inhibitors.


Antiretroviral << protease >> inhibitors lopinavir (LPV) and ritonavir ([[ RTV ]]) are reported BSEP inhibitors.


Antiretroviral protease inhibitors lopinavir (LPV) and ritonavir (<< RTV >>) are reported [[ BSEP ]] inhibitors.


<< GHRP-6 >> is a [[ growth hormone ]] secretagogue that also enhances tissue viability in different organs.


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).


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).


<< Ibandronate >> increases the expression of the pro-apoptotic gene [[ FAS ]] by epigenetic mechanisms in tumor cells.


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.


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 ]].


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.


The AhR target gene << CYP1A1 >> mRNA expression was induced by [[ TCDD ]], but was not affected by the AR CAG length.


TCDD had no effect on AR activity in PC-3 cells, whereas the shortest << AR >> variant was induced by [[ TCDD ]] in PNT1A cells.


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 ]].


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).


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).


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).


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).


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 ]]).


Contributions of << rat Ctr1 >> to the uptake and toxicity of [[ copper ]] and platinum anticancer drugs in dorsal root ganglion neurons.


Contributions of << rat Ctr1 >> to the uptake and toxicity of copper and [[ platinum ]] anticancer drugs in dorsal root ganglion neurons.


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


In conclusion, << rCtr1 >> can transport copper and [[ platinum ]] drugs, and sensitizes cells to their cytotoxicities.


In conclusion, << rCtr1 >> can transport [[ copper ]] and platinum drugs, and sensitizes cells to their cytotoxicities.


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.


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 ]].


Examination of phosphorylation in << retinoblastoma (Rb) protein >>, we found an inhibitory effect by [[ glucosamine ]] at 20 and 50 mM.


<< 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.


<< 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.


<< 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.


In addition, << glucosamine >> attenuated p21 protein stability via the proteasomal proteolytic pathway, as well as inducing [[ p21 ]] nuclear accumulation.


In addition, << glucosamine >> attenuated [[ p21 ]] protein stability via the proteasomal proteolytic pathway, as well as inducing p21 nuclear accumulation.


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.


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.


Characterization of substituted << phenylpropylamides >> as highly selective agonists at the [[ melatonin MT2 receptor ]].


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.


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.


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.


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.


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.


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.


<< CYP3A5 >>, which is particularly relevant to GC metabolism in the lungs, was also shown to efficiently metabolize [[ triamcinolone acetonide ]], budesonide, and fluticasone propionate.


<< CYP3A5 >>, which is particularly relevant to GC metabolism in the lungs, was also shown to efficiently metabolize triamcinolone acetonide, [[ budesonide ]], and fluticasone propionate.


<< CYP3A5 >>, which is particularly relevant to GC metabolism in the lungs, was also shown to efficiently metabolize triamcinolone acetonide, budesonide, and [[ fluticasone propionate ]].


In contrast, << flunisolide >> was only metabolized via [[ CYP3A4 ]], with no significant turnover by CYP3A5 or CYP3A7.


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.


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.


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.


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.


Moreover, activation of the << ERK >> and CREB signaling pathway in the hippocampus might be involved in [[ METH ]]-induced spatial memory changes.


Moreover, activation of the ERK and << CREB >> signaling pathway in the hippocampus might be involved in [[ METH ]]-induced spatial memory changes.


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 ]].


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 ]].


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 ]].


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.


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.


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).


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 ]]).


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 ]].


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.


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.


The treatment also prevented the high << cholesterol >> diet-induced increase in serum [[ creatine kinase ]], total and isoforms, markers of neurological, cardiac and muscular damage.


GIP potentiates << glucose >>-stimulated [[ insulin ]] secretion and induces energy accumulation into adipose tissue, resulting in obesity.


Diet, physical exercise and << Orlistat >> administration increase serum [[ Anti-Müllerian Hormone ]] (AMH) levels in women with polycystic ovary syndrome (PCOS).


Diet, physical exercise and << Orlistat >> administration increase serum Anti-Müllerian Hormone ([[ AMH ]]) levels in women with polycystic ovary syndrome (PCOS).


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.


Moreover, << 1,25(OH)(2)D(3) >> decreased expression of [[ Oat1 ]] and Oat3 in rat kidney.


Moreover, << 1,25(OH)(2)D(3) >> decreased expression of Oat1 and [[ Oat3 ]] in rat kidney.


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.


<< 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.


<< 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.


<< ISO >> significantly inhibited the levels of ERK1/2 kinase and increased the expression of [[ JNK ]] and p38 kinases.


<< ISO >> significantly inhibited the levels of ERK1/2 kinase and increased the expression of JNK and [[ p38 ]] kinases.


<< ISO >> significantly inhibited the levels of ERK1/2 kinase and increased the expression of JNK and p38 [[ kinases ]].


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.


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.


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.


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.


While SP600125 (a << JNK >> inhibitor) and SB203580 (a p38 inhibitor) markedly prevented the expression of these proteins induced by [[ ISO ]].


While SP600125 (a JNK inhibitor) and SB203580 (a << p38 >> inhibitor) markedly prevented the expression of these proteins induced by [[ ISO ]].


While << SP600125 >> (a [[ JNK ]] inhibitor) and SB203580 (a p38 inhibitor) markedly prevented the expression of these proteins induced by ISO.


While SP600125 (a JNK inhibitor) and << SB203580 >> (a [[ p38 ]] inhibitor) markedly prevented the expression of these proteins induced by ISO.


<< NAC >> also suppressed the p-[[ JNK ]] and p-p38, but failed to reverse the effects of ISO.


<< NAC >> also suppressed the p-JNK and [[ p-p38 ]], but failed to reverse the effects of ISO.


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


Optimization of << 5-hydroxytryptamines >> as dual function inhibitors targeting [[ phospholipase A2 ]] and leukotriene A4 hydrolase.


Optimization of << 5-hydroxytryptamines >> as dual function inhibitors targeting phospholipase A2 and [[ leukotriene A4 hydrolase ]].


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.


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.


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.


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.


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.


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.


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.


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.


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.


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 ]].


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.


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 ]].


<< 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.


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.


Dietary << carbohydrates >> increase [[ SCD-1 ]] gene expression in liver by sterol response element binding protein (SREBP)-1c-dependent and SREBP-1c -independent pathways.


Previous report demonstrated that << thyroid hormone >> (TH) negatively regulates [[ mouse SCD-1 gene promoter ]] before SREBP-1c was revealed.


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.


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.


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.


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.


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.


Finally, chronic administration of << metformin >> in diabetic mice restored cardiac autophagy by activating [[ JNK1 ]]-Bcl-2 pathways and dissociating Beclin1 and Bcl-2.


Finally, chronic administration of << metformin >> in diabetic mice restored cardiac autophagy by activating JNK1-[[ Bcl-2 ]] pathways and dissociating Beclin1 and Bcl-2.


<< 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.


<< 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.


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.


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.


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.


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.


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).


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).


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).


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).


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


<< Orlistat >> has been the most used anti-obesity drug and the mechanism of its action is to reduce lipid absorption by inhibiting gastrointestinal [[ lipases ]].


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.


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.


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.


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.


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.


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 ]].


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 ]].


Inhibition of this << carboxylesterase >> probably presents a major source for altered therapeutic activity of these medicines if co-administered with [[ orlistat ]].


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.


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.


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.


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.


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.


<< 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.


<< 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.


<< 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.


<< 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.


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 ]].


<< PKAA >>/anti-TNF-α siRNA nanocomplexes significantly reduced the [[ ALT ]] (alanine transaminase) and the hepatic cellular damages in APAP-intoxicated mice.


<< PKAA >>/anti-TNF-α siRNA nanocomplexes significantly reduced the ALT ([[ alanine transaminase ]]) and the hepatic cellular damages in APAP-intoxicated mice.


Wogonin inhibits << H2O2 >>-induced vascular permeability through suppressing the phosphorylation of [[ caveolin-1 ]].


<< Wogonin >> inhibits H2O2-induced vascular permeability through suppressing the phosphorylation of [[ caveolin-1 ]].


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.


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.


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.


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.


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.


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.


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.


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 ]].


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.


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.


Moreover, wogonin repressed << anisomycin >>-induced phosphorylation of [[ p38 ]], cav-1 and vascular permeability.


Moreover, wogonin repressed << anisomycin >>-induced phosphorylation of p38, [[ cav-1 ]] and vascular permeability.


Moreover, << wogonin >> repressed anisomycin-induced phosphorylation of [[ p38 ]], cav-1 and vascular permeability.


Moreover, << wogonin >> repressed anisomycin-induced phosphorylation of p38, [[ cav-1 ]] and vascular permeability.


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.


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.


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.


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 ]].


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 ]].


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 ]].


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 ]].


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 ]].


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 ]].


We used << nutlin-3 >>, a well-known disruptor of [[ p53 ]]-Mdm2 interaction, to validate the specificity of the assay.


We used << nutlin-3 >>, a well-known disruptor of p53-[[ Mdm2 ]] interaction, to validate the specificity of the assay.


The reduction of BiFC signal mediated by << nutlin-3 >> was correlated with an increase in [[ Puma ]] transactivation, PARP cleavage, and cell death.


The reduction of BiFC signal mediated by << nutlin-3 >> was correlated with an increase in Puma transactivation, [[ PARP ]] cleavage, and cell death.


<< 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.


<< 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.


<< 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.


<< 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.


<< 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.


<< 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.


<< 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.


<< 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.


<< 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.


This was confirmed on adding << LY294002 >> the [[ PI3K ]] inhibitor which abolished the protection.


<< 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.


<< 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.


<< 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.


<< 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.


Increased urinary excretion of << albumin >>, hemopexin, transferrin and VDBP correlates with chronic sensitization to [[ gentamicin ]] nephrotoxicity in rats.


Increased urinary excretion of albumin, << hemopexin >>, transferrin and VDBP correlates with chronic sensitization to [[ gentamicin ]] nephrotoxicity in rats.


Increased urinary excretion of albumin, hemopexin, << transferrin >> and VDBP correlates with chronic sensitization to [[ gentamicin ]] nephrotoxicity in rats.


Increased urinary excretion of albumin, hemopexin, transferrin and << VDBP >> correlates with chronic sensitization to [[ gentamicin ]] nephrotoxicity in rats.


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.


<< 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)).


<< 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)).


<< 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)).


<< 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)).


Additionally, << DPEP >> suppressed the production of inflammatory [[ cytokines ]], including tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6.


Additionally, << DPEP >> suppressed the production of inflammatory cytokines, including [[ tumor necrosis factor-α ]] (TNF-α), interleukin (IL)-1β, and IL-6.


Additionally, << DPEP >> suppressed the production of inflammatory cytokines, including tumor necrosis factor-α ([[ TNF-α ]]), interleukin (IL)-1β, and IL-6.


Additionally, << DPEP >> suppressed the production of inflammatory cytokines, including tumor necrosis factor-α (TNF-α), [[ interleukin (IL)-1β ]], and IL-6.


Additionally, << DPEP >> suppressed the production of inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and [[ IL-6 ]].


<< DPEP >> inhibited LPS-induced phosphorylation of [[ ERK ]], JNK, and p38.


<< DPEP >> inhibited LPS-induced phosphorylation of ERK, [[ JNK ]], and p38.


<< DPEP >> inhibited LPS-induced phosphorylation of ERK, JNK, and [[ p38 ]].


Furthermore, << DPEP >> inhibited the LPS-induced phosphorylation of inhibitor κB (IκB)-α and NF-κB [[ p50 ]].


Furthermore, << DPEP >> inhibited the LPS-induced phosphorylation of [[ inhibitor κB (IκB)-α ]] and NF-κB p50.


Furthermore, << DPEP >> inhibited the LPS-induced phosphorylation of inhibitor κB (IκB)-α and [[ NF-κB ]] p50.


Taken together, the results of this study demonstrate that << DPEP >> inhibits LPS-stimulated inflammation by blocking the [[ NF-κB ]] and MAPK pathways in macrophages.


Taken together, the results of this study demonstrate that << DPEP >> inhibits LPS-stimulated inflammation by blocking the NF-κB and [[ MAPK ]] pathways in macrophages.


This leads to decreased expression of << glutamate aspartate transporter >>, which in turn reduces [[ glutamate ]] transport.


<< Tetrahydropyrroloquinolinone >> type dual inhibitors of [[ aromatase ]]/aldosterone synthase as a novel strategy for breast cancer patients with elevated cardiovascular risks.


<< Tetrahydropyrroloquinolinone >> type dual inhibitors of aromatase/[[ aldosterone synthase ]] as a novel strategy for breast cancer patients with elevated cardiovascular risks.


Furthermore, << MDZ >> caused mechanism-based inactivation of [[ cytochrome P450 3A ]]-dependent TRZ 1'-hydroxylation in mouse, rat and human intestinal microsomes with similar potencies.


Furthermore, MDZ caused mechanism-based inactivation of << cytochrome P450 3A >>-dependent [[ TRZ ]] 1'-hydroxylation in mouse, rat and human intestinal microsomes with similar potencies.


<< Tamoxifen >> represses miR-200 microRNAs and promotes epithelial-to-mesenchymal transition by up-regulating [[ c-Myc ]] in endometrial carcinoma cell lines.


<< Tamoxifen >> represses [[ miR-200 ]] microRNAs and promotes epithelial-to-mesenchymal transition by up-regulating c-Myc in endometrial carcinoma cell lines.


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


Synthesis and dual biological effects of << hydroxycinnamoyl phenylalanyl >>/prolyl hydroxamic acid derivatives as [[ tyrosinase ]] inhibitor and antioxidant.


Synthesis and dual biological effects of hydroxycinnamoyl phenylalanyl/<< prolyl hydroxamic acid >> derivatives as [[ tyrosinase ]] inhibitor and antioxidant.


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.


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.


In addition, derivatives of << caffeic acid >> and sinapic acid efficiently inhibited [[ tyrosinase ]] activity and reduced melanin content in melanocytes Mel-Ab cell.


In addition, derivatives of caffeic acid and << sinapic acid >> efficiently inhibited [[ tyrosinase ]] activity and reduced melanin content in melanocytes Mel-Ab cell.


<< 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.


<< 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.


<< Pb >> and BaP treatments significantly increased active [[ caspase-3 ]] levels in a time-dependent manner.


Pb and << BaP >> treatments significantly increased active [[ caspase-3 ]] levels in a time-dependent manner.


<< 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.


<< 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.


<< TAA >> also increased the numbers of ED2(+), [[ cyclooxygenase-2 ]](+), and heme oxygenase-1(+) liver cells, as well as the number of CD3(+) lymphocytes.


<< TAA >> also increased the numbers of ED2(+), cyclooxygenase-2(+), and [[ heme oxygenase-1 ]](+) liver cells, as well as the number of CD3(+) lymphocytes.


<< TAA >> also increased the numbers of ED2(+), cyclooxygenase-2(+), and heme oxygenase-1(+) liver cells, as well as the number of [[ CD3 ]](+) lymphocytes.


<< ICA-105574 >> interacts with a common binding site to elicit opposite effects on inactivation gating of [[ EAG ]] and ERG potassium channels.


<< ICA-105574 >> interacts with a common binding site to elicit opposite effects on inactivation gating of EAG and [[ ERG ]] potassium channels.


<< ICA-105574 >> interacts with a common binding site to elicit opposite effects on inactivation gating of EAG and ERG [[ potassium channels ]].


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.


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.


<< ICA >> is a mixed agonist of mutant [[ EAG ]] and EAG/ERG chimera channels that inactivate by a combination of slow and fast mechanisms.


<< ICA >> is a mixed agonist of mutant EAG and [[ EAG ]]/ERG chimera channels that inactivate by a combination of slow and fast mechanisms.


<< ICA >> is a mixed agonist of mutant EAG and EAG/[[ ERG ]] chimera channels that inactivate by a combination of slow and fast mechanisms.


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 ]].


However the << α7 receptor >> antagonist [[ methyllycaconitine ]] was unable to reverse these anxiety-like effects seen with PNU-282987.


<< Carnitine palmitoyltransferase 2 >> and carnitine/acylcarnitine translocase are involved in the mitochondrial synthesis and export of [[ acylcarnitines ]].


Carnitine palmitoyltransferase 2 and << carnitine/acylcarnitine translocase >> are involved in the mitochondrial synthesis and export of [[ acylcarnitines ]].


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.


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.


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.


PURPOSE: To characterise further the previously observed cytochrome P450 3A4 (CYP3A4) interaction of the dual << orexin receptor >> antagonist [[ almorexant ]].


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.


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.


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.


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.


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.


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.


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.


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.


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.


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.


<< Methadone >> N-demethylation in vitro is catalyzed by hepatic cytochrome P4502B6 (CYP2B6) and CYP3A4, but clinical disposition is often attributed to [[ CYP3A4 ]].


<< Methadone >> N-demethylation in vitro is catalyzed by hepatic [[ cytochrome P4502B6 ]] (CYP2B6) and CYP3A4, but clinical disposition is often attributed to CYP3A4.


<< Methadone >> N-demethylation in vitro is catalyzed by hepatic cytochrome P4502B6 ([[ CYP2B6 ]]) and CYP3A4, but clinical disposition is often attributed to CYP3A4.


<< Methadone >> N-demethylation in vitro is catalyzed by hepatic cytochrome P4502B6 (CYP2B6) and [[ CYP3A4 ]], but clinical disposition is often attributed to CYP3A4.


Methadone << N >>-demethylation in vitro is catalyzed by hepatic cytochrome P4502B6 (CYP2B6) and CYP3A4, but clinical disposition is often attributed to [[ CYP3A4 ]].


Methadone << N >>-demethylation in vitro is catalyzed by hepatic [[ cytochrome P4502B6 ]] (CYP2B6) and CYP3A4, but clinical disposition is often attributed to CYP3A4.


Methadone << N >>-demethylation in vitro is catalyzed by hepatic cytochrome P4502B6 ([[ CYP2B6 ]]) and CYP3A4, but clinical disposition is often attributed to CYP3A4.


Methadone << N >>-demethylation in vitro is catalyzed by hepatic cytochrome P4502B6 (CYP2B6) and [[ CYP3A4 ]], but clinical disposition is often attributed to CYP3A4.


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.


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.


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.


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.


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.


CYP2B6 inhibition reduces methadone N-demethylation and clearance, and alters methadone concentrations, demonstrating an important role for << CYP2B6 >> in clinical [[ methadone ]] disposition.


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.


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.


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.


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.


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.


Moreover, the D2R inhibitor << raclopride >> blocked the increase of both [[ GDNF ]] and Zif268 expression following potassium-evoked dopamine release in SH-SY5Y cells.


Moreover, the D2R inhibitor << raclopride >> blocked the increase of both GDNF and [[ Zif268 ]] expression following potassium-evoked dopamine release in SH-SY5Y cells.


Moreover, the << D2R >> inhibitor [[ raclopride ]] blocked the increase of both GDNF and Zif268 expression following potassium-evoked dopamine release in SH-SY5Y cells.


Synthesis and biological evaluation of << 1,3,4-thiadiazole >> analogues as novel [[ AChE ]] and BuChE inhibitors.


Synthesis and biological evaluation of << 1,3,4-thiadiazole >> analogues as novel AChE and [[ BuChE ]] inhibitors.


In this paper a series of new << 1,3,4-thiadiazole >> derivatives has been designed, synthesized and evaluated as the [[ acetyl- and butyrylcholinesterase ]] inhibitors.


<< LY294002 >>, a specific PI3K/AKT inhibitor, selectively activated the [[ p38 ]] MAPK kinase pathway and enhanced c-Jun phosphorylation, but did not activate JNK.


<< LY294002 >>, a specific PI3K/AKT inhibitor, selectively activated the p38 [[ MAPK ]] kinase pathway and enhanced c-Jun phosphorylation, but did not activate JNK.


<< LY294002 >>, a specific PI3K/AKT inhibitor, selectively activated the p38 MAPK [[ kinase ]] pathway and enhanced c-Jun phosphorylation, but did not activate JNK.


<< LY294002 >>, a specific PI3K/AKT inhibitor, selectively activated the p38 MAPK kinase pathway and enhanced [[ c-Jun ]] phosphorylation, but did not activate JNK.


<< LY294002 >>, a specific [[ PI3K ]]/AKT inhibitor, selectively activated the p38 MAPK kinase pathway and enhanced c-Jun phosphorylation, but did not activate JNK.


<< LY294002 >>, a specific PI3K/[[ AKT ]] inhibitor, selectively activated the p38 MAPK kinase pathway and enhanced c-Jun phosphorylation, but did not activate JNK.


The pharmacological inhibitors << SB203580 >> ([[ p38 ]] inhibitor) and SP600125 (a JNK inhibitor) protected primary cultures of rat CGCs from LY294002-induced apoptosis.


The pharmacological inhibitors SB203580 (p38 inhibitor) and << SP600125 >> (a [[ JNK ]] inhibitor) protected primary cultures of rat CGCs from LY294002-induced apoptosis.


Today, we used << cobalt chloride >>, a hypoxia mimetic that inhibits proteasomal [[ HIF-1 ]] degradation and generates reactive oxygen species (ROS).


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.


Cellular responses to DNA damage induced by << etoposide >> or doxorubicin include down-regulation of endogenous supervillin coincident with increases in [[ p53 ]].


Cellular responses to DNA damage induced by etoposide or << doxorubicin >> include down-regulation of endogenous supervillin coincident with increases in [[ p53 ]].


Cellular responses to DNA damage induced by << etoposide >> or doxorubicin include down-regulation of endogenous [[ supervillin ]] coincident with increases in p53.


Cellular responses to DNA damage induced by etoposide or << doxorubicin >> include down-regulation of endogenous [[ supervillin ]] coincident with increases in p53.


Novel << acylethanolamide >> derivatives that modulate body weight through enhancement of hypothalamic pro-opiomelanocortin ([[ POMC ]]) and/or decreased neuropeptide Y (NPY).


Novel << acylethanolamide >> derivatives that modulate body weight through enhancement of hypothalamic [[ pro-opiomelanocortin ]] (POMC) and/or decreased neuropeptide Y (NPY).


Novel << acylethanolamide >> derivatives that modulate body weight through enhancement of hypothalamic pro-opiomelanocortin (POMC) and/or decreased [[ neuropeptide Y ]] (NPY).


Novel << acylethanolamide >> derivatives that modulate body weight through enhancement of hypothalamic pro-opiomelanocortin (POMC) and/or decreased neuropeptide Y ([[ NPY ]]).


<< 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.


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.


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.


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.


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.


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.


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.


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.


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 ]].


<< 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.


<< 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.


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.


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.


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.


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.


Treatment of these cells with << Paeoniflorin >> significantly induced [[ HO-1 ]] expression.


The << Paeoniflorin >>-induced [[ HO-1 ]] expression was abrogated by Nrf2 siRNA.


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.


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.


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.


Our findings confirmed that << Paeoniflorin >> protected EA.hy926 cells against radiation-induced injury through the [[ Nrf2 ]]/HO-1 pathway.


Our findings confirmed that << Paeoniflorin >> protected EA.hy926 cells against radiation-induced injury through the Nrf2/[[ HO-1 ]] pathway.


<< 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.


<< 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.


<< Rolapitant >> and netupitant are other [[ NK1 receptor ]] antagonists that are currently in phase III clinical trials.


Rolapitant and << netupitant >> are other [[ NK1 receptor ]] antagonists that are currently in phase III clinical trials.


Moderate inhibitory effect of << LDL >>-C oxidation by [[ phytosteryl phenolates ]] was observed.


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.


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.