SC-51089 (10(-5) M), a selective EP1-receptor antagonist, showed no effect on the PGE1- or PGE2-induced inhibition of the HVA ICa, thereby indicating that << PGE1 >>- and PGE2-induced inhibition of the [[ HVA Ca2+ channels ]] is possibly mediated by the EP3 receptor.


SC-51089 (10(-5) M), a selective EP1-receptor antagonist, showed no effect on the PGE1- or PGE2-induced inhibition of the HVA ICa, thereby indicating that PGE1- and << PGE2 >>-induced inhibition of the [[ HVA Ca2+ channels ]] is possibly mediated by the EP3 receptor.


<< SC-51089 >> (10(-5) M), a selective [[ EP1-receptor ]] antagonist, showed no effect on the PGE1- or PGE2-induced inhibition of the HVA ICa, thereby indicating that PGE1- and PGE2-induced inhibition of the HVA Ca2+ channels is possibly mediated by the EP3 receptor.


The inhibitory effect of PGE1 or sulprostone was prevented by pretreatment with pertussis toxin [islet activating protein (IAP)] or phorbol-12-myristate-13-acetate (PMA), and the << protein kinase C >> (PKC) inhibitor [[ chelerythrine ]] blocked the action of PMA.


The inhibitory effect of PGE1 or sulprostone was prevented by pretreatment with pertussis toxin [islet activating protein (IAP)] or phorbol-12-myristate-13-acetate (PMA), and the protein kinase C (<< PKC >>) inhibitor [[ chelerythrine ]] blocked the action of PMA.


It was concluded that << PGE1 >> selectively reduces both N- and R-type Ca2+ currents by activating a [[ G-protein ]] probably through the EP3 receptor in paratracheal ganglion cells.


Inhibition of << MCP-1 >> and MIP-2 transcription and translation by [[ mimosine ]] in muscle tissue infected with the parasite Trichinella spiralis.


Inhibition of MCP-1 and << MIP-2 >> transcription and translation by [[ mimosine ]] in muscle tissue infected with the parasite Trichinella spiralis.


In addition, we found that << MCP-1 >> transcription and translation was completely inhibited by [[ mimosine ]], while MIP-2 transcription and translation was partially inhibited at 30 and 40 days; yet it was totally inhibited after 10 and 20 days in encysted diaphragm tissue infected by T. spiralis.


In addition, we found that MCP-1 transcription and translation was completely inhibited by << mimosine >>, while [[ MIP-2 ]] transcription and translation was partially inhibited at 30 and 40 days; yet it was totally inhibited after 10 and 20 days in encysted diaphragm tissue infected by T. spiralis.


This is described in a case study of the expedited review and approval of << peramivir >>, a novel [[ neuraminidase ]] inhibitor, in Japan in the context of the emergence of new strain of influenza in 2009.


The influence of sex, ethnicity, and << CYP2B6 >> genotype on [[ bupropion ]] metabolism as an index of hepatic CYP2B6 activity in humans.


To identify important covariates associated with interindividual variation in CYP2B6 activity in vivo, we evaluated these effects in healthy volunteers using << bupropion >> (Wellbutrin SR GlaxoSmithKline, Research Triangle Park, NC) as a [[ CYP2B6 ]] probe substrate.


To identify important covariates associated with interindividual variation in CYP2B6 activity in vivo, we evaluated these effects in healthy volunteers using bupropion (<< Wellbutrin SR >> GlaxoSmithKline, Research Triangle Park, NC) as a [[ CYP2B6 ]] probe substrate.


These results suggest that << CYP2B6 >> genotype is the most important patient variable for predicting the level of CYP2B6 activity in women, when measured by the metabolism of [[ bupropion ]].


These results suggest that CYP2B6 genotype is the most important patient variable for predicting the level of << CYP2B6 >> activity in women, when measured by the metabolism of [[ bupropion ]].


The << bupropion >> metabolic ratio appears to detect known differences in [[ CYP2B6 ]] activity associated with genetic polymorphism, across different ethnic groups.


The identification of the << succinate receptor >> SUCNR1 in platelets is of particular interest, because physiologically relevant concentrations of [[ succinate ]] were shown to potentiate the effect of low doses of a variety of platelet agonists.


The identification of the succinate receptor << SUCNR1 >> in platelets is of particular interest, because physiologically relevant concentrations of [[ succinate ]] were shown to potentiate the effect of low doses of a variety of platelet agonists.


<< β-ionone >> was also shown to induce the expression of cleaved-[[ caspase-3 ]] and inhibit bcl-2 expression in SGC-7901 cells in a dose-dependent manner.


<< β-ionone >> was also shown to induce the expression of cleaved-caspase-3 and inhibit [[ bcl-2 ]] expression in SGC-7901 cells in a dose-dependent manner.


The significantly decreased levels of << p-PI3K >> and p-AKT expression were observed in SGC-7901 cells after [[ β-ionone ]] treatments in a time- and dose-dependent manner (P < 0.01).


The significantly decreased levels of p-PI3K and << p-AKT >> expression were observed in SGC-7901 cells after [[ β-ionone ]] treatments in a time- and dose-dependent manner (P < 0.01).


However, AII receptor blockers differ from ACE inhibitors with respect to side effects, and induce less cough, a side effect which may be related to bradykinin or other mediators such as substance P. Within the class of << AII >> blockers, [[ eprosartan ]] differs from other currently available agents in terms of chemical structure, as it is a non-biphenyl, non-tetrazole, non-peptide antagonist with a dual pharmacological mode of action.


In clinical trials, eprosartan has been demonstrated to be at least as effective in reducing blood pressure as the << ACE >> inhibitor [[ enalapril ]], and has significantly lower side effects.


Reductive detoxification of << arylhydroxylamine >> carcinogens by human NADH cytochrome b5 reductase and [[ cytochrome b5 ]].


Reductive detoxification of << arylhydroxylamine >> carcinogens by [[ human NADH cytochrome b5 reductase ]] and cytochrome b5.


On the basis of our findings with structurally similar arylhydroxylamine metabolites of therapeutic drugs, we hypothesized that the reductive detoxification of << arylhydroxylamine >> carcinogens was catalyzed by [[ NADH cytochrome b5 reductase ]] (b5R) and cytochrome b5 (cyt b5).


On the basis of our findings with structurally similar arylhydroxylamine metabolites of therapeutic drugs, we hypothesized that the reductive detoxification of << arylhydroxylamine >> carcinogens was catalyzed by NADH cytochrome b5 reductase ([[ b5R ]]) and cytochrome b5 (cyt b5).


On the basis of our findings with structurally similar arylhydroxylamine metabolites of therapeutic drugs, we hypothesized that the reductive detoxification of << arylhydroxylamine >> carcinogens was catalyzed by NADH cytochrome b5 reductase (b5R) and [[ cytochrome b5 ]] (cyt b5).


On the basis of our findings with structurally similar arylhydroxylamine metabolites of therapeutic drugs, we hypothesized that the reductive detoxification of << arylhydroxylamine >> carcinogens was catalyzed by NADH cytochrome b5 reductase (b5R) and cytochrome b5 ([[ cyt b5 ]]).


We found that reduction of the carcinogenic << hydroxylamines >> of the aromatic amine 4-aminobiphenyl (4-ABP; found in cigarette smoke) and the heterocyclic amine 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine (PhIP; found in grilled meats) was indeed catalyzed by a purified system containing only [[ human b5R ]] and cyt b5.


We found that reduction of the carcinogenic << hydroxylamines >> of the aromatic amine 4-aminobiphenyl (4-ABP; found in cigarette smoke) and the heterocyclic amine 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine (PhIP; found in grilled meats) was indeed catalyzed by a purified system containing only human b5R and [[ cyt b5 ]].


We found that reduction of the carcinogenic hydroxylamines of the << aromatic amine >> 4-aminobiphenyl (4-ABP; found in cigarette smoke) and the heterocyclic amine 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine (PhIP; found in grilled meats) was indeed catalyzed by a purified system containing only [[ human b5R ]] and cyt b5.


We found that reduction of the carcinogenic hydroxylamines of the << aromatic amine >> 4-aminobiphenyl (4-ABP; found in cigarette smoke) and the heterocyclic amine 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine (PhIP; found in grilled meats) was indeed catalyzed by a purified system containing only human b5R and [[ cyt b5 ]].


We found that reduction of the carcinogenic hydroxylamines of the aromatic amine << 4-aminobiphenyl >> (4-ABP; found in cigarette smoke) and the heterocyclic amine 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine (PhIP; found in grilled meats) was indeed catalyzed by a purified system containing only [[ human b5R ]] and cyt b5.


We found that reduction of the carcinogenic hydroxylamines of the aromatic amine << 4-aminobiphenyl >> (4-ABP; found in cigarette smoke) and the heterocyclic amine 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine (PhIP; found in grilled meats) was indeed catalyzed by a purified system containing only human b5R and [[ cyt b5 ]].


We found that reduction of the carcinogenic hydroxylamines of the aromatic amine 4-aminobiphenyl (<< 4-ABP >>; found in cigarette smoke) and the heterocyclic amine 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine (PhIP; found in grilled meats) was indeed catalyzed by a purified system containing only [[ human b5R ]] and cyt b5.


We found that reduction of the carcinogenic hydroxylamines of the aromatic amine 4-aminobiphenyl (<< 4-ABP >>; found in cigarette smoke) and the heterocyclic amine 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine (PhIP; found in grilled meats) was indeed catalyzed by a purified system containing only human b5R and [[ cyt b5 ]].


We found that reduction of the carcinogenic hydroxylamines of the aromatic amine 4-aminobiphenyl (4-ABP; found in cigarette smoke) and the << heterocyclic amine >> 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine (PhIP; found in grilled meats) was indeed catalyzed by a purified system containing only [[ human b5R ]] and cyt b5.


We found that reduction of the carcinogenic hydroxylamines of the aromatic amine 4-aminobiphenyl (4-ABP; found in cigarette smoke) and the << heterocyclic amine >> 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine (PhIP; found in grilled meats) was indeed catalyzed by a purified system containing only human b5R and [[ cyt b5 ]].


We found that reduction of the carcinogenic hydroxylamines of the aromatic amine 4-aminobiphenyl (4-ABP; found in cigarette smoke) and the heterocyclic amine << 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine >> (PhIP; found in grilled meats) was indeed catalyzed by a purified system containing only [[ human b5R ]] and cyt b5.


We found that reduction of the carcinogenic hydroxylamines of the aromatic amine 4-aminobiphenyl (4-ABP; found in cigarette smoke) and the heterocyclic amine << 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine >> (PhIP; found in grilled meats) was indeed catalyzed by a purified system containing only human b5R and [[ cyt b5 ]].


We found that reduction of the carcinogenic hydroxylamines of the aromatic amine 4-aminobiphenyl (4-ABP; found in cigarette smoke) and the heterocyclic amine 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine (<< PhIP >>; found in grilled meats) was indeed catalyzed by a purified system containing only [[ human b5R ]] and cyt b5.


We found that reduction of the carcinogenic hydroxylamines of the aromatic amine 4-aminobiphenyl (4-ABP; found in cigarette smoke) and the heterocyclic amine 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine (<< PhIP >>; found in grilled meats) was indeed catalyzed by a purified system containing only human b5R and [[ cyt b5 ]].


Polyclonal antisera to either << b5R >> or cyt b5 significantly inhibited [[ N-hydroxy-4-aminobiphenyl ]] (NHOH-4-ABP) reduction by 95 and 89%, respectively, and immunoreactive cyt b5 protein content in individual HLM was significantly correlated with individual reduction of both NHOH-4-ABP and N-hydroxy-PhIP (NHOH-PhIP).


Polyclonal antisera to either b5R or << cyt b5 >> significantly inhibited [[ N-hydroxy-4-aminobiphenyl ]] (NHOH-4-ABP) reduction by 95 and 89%, respectively, and immunoreactive cyt b5 protein content in individual HLM was significantly correlated with individual reduction of both NHOH-4-ABP and N-hydroxy-PhIP (NHOH-PhIP).


Polyclonal antisera to either << b5R >> or cyt b5 significantly inhibited N-hydroxy-4-aminobiphenyl ([[ NHOH-4-ABP ]]) reduction by 95 and 89%, respectively, and immunoreactive cyt b5 protein content in individual HLM was significantly correlated with individual reduction of both NHOH-4-ABP and N-hydroxy-PhIP (NHOH-PhIP).


Polyclonal antisera to either b5R or << cyt b5 >> significantly inhibited N-hydroxy-4-aminobiphenyl ([[ NHOH-4-ABP ]]) reduction by 95 and 89%, respectively, and immunoreactive cyt b5 protein content in individual HLM was significantly correlated with individual reduction of both NHOH-4-ABP and N-hydroxy-PhIP (NHOH-PhIP).


Clinical effects of << pranlukast >>, an oral [[ leukotriene receptor ]] antagonist, in mild-to-moderate asthma: a 4 week randomized multicentre controlled trial.


<< Pranlukast >> is a new, orally active, selective inhibitor of [[ CysLt1 ]] leukotriene receptor.


<< Pranlukast >> is a new, orally active, selective inhibitor of CysLt1 [[ leukotriene receptor ]].


We used mutagenesis of these residues, combined with an investigation of << hERG >> block by close analogs of [[ clofilium ]] and ibutilide, to assess how specific alterations in drug structure affected potency and binding interactions.


We used mutagenesis of these residues, combined with an investigation of << hERG >> block by close analogs of clofilium and [[ ibutilide ]], to assess how specific alterations in drug structure affected potency and binding interactions.


<< Parathion >> is a [[ cholinesterase ]] inhibitor that induces the hydrolysis of body choline esters, including acetylcholine at cholinergic synapses.


There was also an increase in << c-kit >>, Trio, Rho-A, Rac-3, EGFR, Notch-4, Dvl-2, Ezrin, beta catenin and mutant p53 protein expression in the [[ parathion ]]-treated cells.


There was also an increase in c-kit, << Trio >>, Rho-A, Rac-3, EGFR, Notch-4, Dvl-2, Ezrin, beta catenin and mutant p53 protein expression in the [[ parathion ]]-treated cells.


There was also an increase in c-kit, Trio, << Rho-A >>, Rac-3, EGFR, Notch-4, Dvl-2, Ezrin, beta catenin and mutant p53 protein expression in the [[ parathion ]]-treated cells.


There was also an increase in c-kit, Trio, Rho-A, << Rac-3 >>, EGFR, Notch-4, Dvl-2, Ezrin, beta catenin and mutant p53 protein expression in the [[ parathion ]]-treated cells.


There was also an increase in c-kit, Trio, Rho-A, Rac-3, EGFR, << Notch-4 >>, Dvl-2, Ezrin, beta catenin and mutant p53 protein expression in the [[ parathion ]]-treated cells.


There was also an increase in c-kit, Trio, Rho-A, Rac-3, EGFR, Notch-4, << Dvl-2 >>, Ezrin, beta catenin and mutant p53 protein expression in the [[ parathion ]]-treated cells.


There was also an increase in c-kit, Trio, Rho-A, Rac-3, EGFR, Notch-4, Dvl-2, << Ezrin >>, beta catenin and mutant p53 protein expression in the [[ parathion ]]-treated cells.


There was also an increase in c-kit, Trio, Rho-A, Rac-3, EGFR, Notch-4, Dvl-2, Ezrin, << beta catenin >> and mutant p53 protein expression in the [[ parathion ]]-treated cells.


There was also an increase in c-kit, Trio, Rho-A, Rac-3, EGFR, Notch-4, Dvl-2, Ezrin, beta catenin and mutant << p53 >> protein expression in the [[ parathion ]]-treated cells.


<< N-Acetylglucosamine-1-phosphodiester alpha-N-Acetylglucosaminidase >> (EC 3.1.4.45; phosphodiester alpha-GlcNAcase) catalyzes the second step in the synthesis of the [[ mannose 6-phosphate ]] determinant required for efficient intracellular targeting of newly synthesized lysosomal hydrolases to the lysosome.


N-Acetylglucosamine-1-phosphodiester alpha-N-Acetylglucosaminidase (<< EC 3.1.4.45 >>; phosphodiester alpha-GlcNAcase) catalyzes the second step in the synthesis of the [[ mannose 6-phosphate ]] determinant required for efficient intracellular targeting of newly synthesized lysosomal hydrolases to the lysosome.


N-Acetylglucosamine-1-phosphodiester alpha-N-Acetylglucosaminidase (EC 3.1.4.45; << phosphodiester alpha-GlcNAcase >>) catalyzes the second step in the synthesis of the [[ mannose 6-phosphate ]] determinant required for efficient intracellular targeting of newly synthesized lysosomal hydrolases to the lysosome.


The purified << phosphodiester alpha-GlcNAcase >> has a specific activity of 498 micromol of [[ [3H]GlcNAc-alpha-phosphomannose-alpha-methyl ]] cleaved per h per mg of protein using 0.5 mM [3H]GlcNAc-alpha-phosphomannose-alpha-methyl as substrate.


The purified << phosphodiester alpha-GlcNAcase >> has a specific activity of 498 micromol of [3H]GlcNAc-alpha-phosphomannose-alpha-methyl cleaved per h per mg of protein using 0.5 mM [[ [3H]GlcNAc-alpha-phosphomannose-alpha-methyl ]] as substrate.


In the in vitro assay, << kinsenoside >> (20 and 50μg/mL) markedly inhibited changes in various biochemical substances (nitric oxide (NO), [[ lactic dehydrogenase ]] (LDH), superoxide dismutase (SOD), and catalase (CAT)) in human umbilical vein endothelial cells (HUVECs) damaged by high glucose (35mM) and restored vascular endothelial structure by balancing the matrix metalloproteinases-the tissue inhibitors of matrix metalloproteinases (MMP-TIMP) system.


In the in vitro assay, << kinsenoside >> (20 and 50μg/mL) markedly inhibited changes in various biochemical substances (nitric oxide (NO), lactic dehydrogenase ([[ LDH ]]), superoxide dismutase (SOD), and catalase (CAT)) in human umbilical vein endothelial cells (HUVECs) damaged by high glucose (35mM) and restored vascular endothelial structure by balancing the matrix metalloproteinases-the tissue inhibitors of matrix metalloproteinases (MMP-TIMP) system.


In the in vitro assay, << kinsenoside >> (20 and 50μg/mL) markedly inhibited changes in various biochemical substances (nitric oxide (NO), lactic dehydrogenase (LDH), [[ superoxide dismutase ]] (SOD), and catalase (CAT)) in human umbilical vein endothelial cells (HUVECs) damaged by high glucose (35mM) and restored vascular endothelial structure by balancing the matrix metalloproteinases-the tissue inhibitors of matrix metalloproteinases (MMP-TIMP) system.


In the in vitro assay, << kinsenoside >> (20 and 50μg/mL) markedly inhibited changes in various biochemical substances (nitric oxide (NO), lactic dehydrogenase (LDH), superoxide dismutase ([[ SOD ]]), and catalase (CAT)) in human umbilical vein endothelial cells (HUVECs) damaged by high glucose (35mM) and restored vascular endothelial structure by balancing the matrix metalloproteinases-the tissue inhibitors of matrix metalloproteinases (MMP-TIMP) system.


In the in vitro assay, << kinsenoside >> (20 and 50μg/mL) markedly inhibited changes in various biochemical substances (nitric oxide (NO), lactic dehydrogenase (LDH), superoxide dismutase (SOD), and [[ catalase ]] (CAT)) in human umbilical vein endothelial cells (HUVECs) damaged by high glucose (35mM) and restored vascular endothelial structure by balancing the matrix metalloproteinases-the tissue inhibitors of matrix metalloproteinases (MMP-TIMP) system.


In the in vitro assay, << kinsenoside >> (20 and 50μg/mL) markedly inhibited changes in various biochemical substances (nitric oxide (NO), lactic dehydrogenase (LDH), superoxide dismutase (SOD), and catalase ([[ CAT ]])) in human umbilical vein endothelial cells (HUVECs) damaged by high glucose (35mM) and restored vascular endothelial structure by balancing the matrix metalloproteinases-the tissue inhibitors of matrix metalloproteinases (MMP-TIMP) system.


The vascular protective effects of << kinsenoside >> were speculated to be attributed to oxidative stress inhibition and the reduction of [[ nuclear factor kappa B ]] (NF-κB) mRNA expression levels in high glucose conditions.


The vascular protective effects of << kinsenoside >> were speculated to be attributed to oxidative stress inhibition and the reduction of nuclear factor kappa B ([[ NF-κB ]]) mRNA expression levels in high glucose conditions.


<< Tolbutamide >> and gliclazide block the K(ATP) channel K(ir)6.2/Sur1, causing membrane depolarization and stimulating [[ insulin ]] secretion in pancreatic beta cells.


<< Tolbutamide >> and gliclazide block the [[ K(ATP) channel ]] K(ir)6.2/Sur1, causing membrane depolarization and stimulating insulin secretion in pancreatic beta cells.


<< Tolbutamide >> and gliclazide block the K(ATP) channel [[ K(ir)6.2 ]]/Sur1, causing membrane depolarization and stimulating insulin secretion in pancreatic beta cells.


<< Tolbutamide >> and gliclazide block the K(ATP) channel K(ir)6.2/[[ Sur1 ]], causing membrane depolarization and stimulating insulin secretion in pancreatic beta cells.


<< Insulin >> secretion stimulated by both 200 μM [[ tolbutamide ]] and 20 μM gliclazide, concentrations that had equivalent effects on membrane potential, was inhibited by thapsigargin (1 μM) or the L-type Ca(2+) channel blocker nicardipine (2 μM) and was potentiated by 8-pCPT-2'-O-Me-cAMP-AM at concentrations ≥2 μM in INS-1 cells.


<< Insulin >> secretion stimulated by both 200 μM tolbutamide and 20 μM [[ gliclazide ]], concentrations that had equivalent effects on membrane potential, was inhibited by thapsigargin (1 μM) or the L-type Ca(2+) channel blocker nicardipine (2 μM) and was potentiated by 8-pCPT-2'-O-Me-cAMP-AM at concentrations ≥2 μM in INS-1 cells.


<< Insulin >> secretion stimulated by both 200 μM tolbutamide and 20 μM gliclazide, concentrations that had equivalent effects on membrane potential, was inhibited by thapsigargin (1 μM) or the L-type Ca(2+) channel blocker nicardipine (2 μM) and was potentiated by [[ 8-pCPT-2'-O-Me-cAMP-AM ]] at concentrations ≥2 μM in INS-1 cells.


<< Insulin >> secretion stimulated by both 200 μM tolbutamide and 20 μM gliclazide, concentrations that had equivalent effects on membrane potential, was inhibited by [[ thapsigargin ]] (1 μM) or the L-type Ca(2+) channel blocker nicardipine (2 μM) and was potentiated by 8-pCPT-2'-O-Me-cAMP-AM at concentrations ≥2 μM in INS-1 cells.


<< Insulin >> secretion stimulated by both 200 μM tolbutamide and 20 μM gliclazide, concentrations that had equivalent effects on membrane potential, was inhibited by thapsigargin (1 μM) or the L-type Ca(2+) channel blocker [[ nicardipine ]] (2 μM) and was potentiated by 8-pCPT-2'-O-Me-cAMP-AM at concentrations ≥2 μM in INS-1 cells.


Insulin secretion stimulated by both 200 μM tolbutamide and 20 μM gliclazide, concentrations that had equivalent effects on membrane potential, was inhibited by thapsigargin (1 μM) or the << L-type Ca(2+) channel >> blocker [[ nicardipine ]] (2 μM) and was potentiated by 8-pCPT-2'-O-Me-cAMP-AM at concentrations ≥2 μM in INS-1 cells.


Both << tolbutamide >> and gliclazide stimulated [[ phospholipase C ]] activity; however, only gliclazide did so independently of its activity at K(ATP) channels, and this activity was partially inhibited by pertussis toxin.


Both tolbutamide and << gliclazide >> stimulated [[ phospholipase C ]] activity; however, only gliclazide did so independently of its activity at K(ATP) channels, and this activity was partially inhibited by pertussis toxin.


Both tolbutamide and gliclazide stimulated phospholipase C activity; however, only << gliclazide >> did so independently of its activity at [[ K(ATP) channels ]], and this activity was partially inhibited by pertussis toxin.


8-pCPT-2'-O-Me-cAMP-AM potentiation of << insulin >> secretion stimulated by tolbutamide was markedly inhibited by 2-APB (25 μM) and enhanced by the PKC inhibitor [[ bisindolylmaleimide I ]] (1 μM).


<< 8-pCPT-2'-O-Me-cAMP-AM >> potentiation of [[ insulin ]] secretion stimulated by tolbutamide was markedly inhibited by 2-APB (25 μM) and enhanced by the PKC inhibitor bisindolylmaleimide I (1 μM).


8-pCPT-2'-O-Me-cAMP-AM potentiation of << insulin >> secretion stimulated by [[ tolbutamide ]] was markedly inhibited by 2-APB (25 μM) and enhanced by the PKC inhibitor bisindolylmaleimide I (1 μM).


8-pCPT-2'-O-Me-cAMP-AM potentiation of << insulin >> secretion stimulated by tolbutamide was markedly inhibited by [[ 2-APB ]] (25 μM) and enhanced by the PKC inhibitor bisindolylmaleimide I (1 μM).


8-pCPT-2'-O-Me-cAMP-AM potentiation of insulin secretion stimulated by tolbutamide was markedly inhibited by 2-APB (25 μM) and enhanced by the << PKC >> inhibitor [[ bisindolylmaleimide I ]] (1 μM).


Our data demonstrate that the actions of both tolbutamide and gliclazide are strongly potentiated by 8-pCPT-2'-O-Me-cAMP-AM, that << gliclazide >> can stimulate [[ phospholipase C ]] activity via a partially pertussis toxin-sensitive mechanism, and that 8-pCPT-2'-O-Me-cAMP-AM potentiation of tolbutamide action may involve activation of a 2-APB-sensitive Ca(2+) influx.


Phosphorylation of << AMPK >> at Thr172 increased by 1.4-fold within 5 min, and remained elevated throughout a 30-min time course, in response to [[ 2-deoxyglucose ]].


Phosphorylation of ER-stress marker << eIF2α >> was also increased but only at 30 min of [[ 2-deoxyglucose ]] exposure.


<< 2-Deoxyglucose >> increased phosphorylation of tuberous sclerosis complex 2 (TSC2) on AMPK consensus sites but did not change the amount of TSC1 bound to [[ TSC2 ]].


<< 2-Deoxyglucose >> increased phosphorylation of [[ tuberous sclerosis complex 2 ]] (TSC2) on AMPK consensus sites but did not change the amount of TSC1 bound to TSC2.


<< 2-Deoxyglucose >> increased phosphorylation of tuberous sclerosis complex 2 ([[ TSC2 ]]) on AMPK consensus sites but did not change the amount of TSC1 bound to TSC2.


<< 2-Deoxyglucose >> increased phosphorylation of tuberous sclerosis complex 2 (TSC2) on [[ AMPK ]] consensus sites but did not change the amount of TSC1 bound to TSC2.


<< Conivaptan >>: a dual [[ vasopressin receptor v1a/v2 ]] antagonist [corrected].


<< Conivaptan >> is a nonpeptide dual [[ V1a/V2 AVP receptor ]] antagonist.


<< H1-receptor >> antagonists have been utilized, following their initial chemical synthesis in 1933, both in the treatment of conditions in which histamine is considered to be of pathogenic importance and conversely to help elucidate the role of [[ histamine ]] in disease, through an evaluation of their influence on disease expression.


<< H1-receptor >> antagonists have been utilized, following their initial chemical synthesis in 1933, both in the treatment of conditions in which [[ histamine ]] is considered to be of pathogenic importance and conversely to help elucidate the role of histamine in disease, through an evaluation of their influence on disease expression.


While there is considerable indirect evidence to implicate << histamine >> in the pathogenesis of asthma, a critical evaluation of [[ H1-receptor ]] antagonism in this condition has, until recently, proved difficult, as many of the early H1-receptor antagonists possessed additional actions, such as anti-cholinergic, local anaesthetic, alpha-adrenoceptor antagonistic and anti-serotonin activity.


While there is considerable indirect evidence to implicate << histamine >> in the pathogenesis of asthma, a critical evaluation of H1-receptor antagonism in this condition has, until recently, proved difficult, as many of the early [[ H1-receptor ]] antagonists possessed additional actions, such as anti-cholinergic, local anaesthetic, alpha-adrenoceptor antagonistic and anti-serotonin activity.


The recent development of << H1-receptor >> antagonists devoid of clinical sedative effects has enabled the administration of doses of H1-antihistamines which achieve a greater degree of H1-receptor blockade within the airways, thus permitting a better appraisal of the role of [[ histamine ]] in this condition.


The recent development of H1-receptor antagonists devoid of clinical sedative effects has enabled the administration of doses of H1-antihistamines which achieve a greater degree of << H1-receptor >> blockade within the airways, thus permitting a better appraisal of the role of [[ histamine ]] in this condition.


<< Cholesterol esterase >> (CE) induced surface erosion of poly(ethylene carbonate) ([[ PEC ]]) and drug release from PEC under mild physiological environment was investigated.


Cholesterol esterase (<< CE >>) induced surface erosion of poly(ethylene carbonate) ([[ PEC ]]) and drug release from PEC under mild physiological environment was investigated.


<< Cholesterol esterase >> (CE) induced surface erosion of [[ poly(ethylene carbonate) ]] (PEC) and drug release from PEC under mild physiological environment was investigated.


Cholesterol esterase (<< CE >>) induced surface erosion of [[ poly(ethylene carbonate) ]] (PEC) and drug release from PEC under mild physiological environment was investigated.


Intravenous << arginine >> significantly increased the acute [[ glucagon ]] response (129 +/- 12 vs 36 +/- 6 ng/l in controls; p < 0.01), notably without affecting plasma glucose.


Isolated islets displayed improved << glucose >>-stimulated [[ insulin ]] secretion after GRA treatment (0.061 +/- 0.007 vs 0.030 +/- 0.004 pmol islet(-1) h(-1) at 16.7 mmol/l glucose; p < 0.001), without affecting islet glucose oxidation.


<< PIP5K1B >> encodes phosphatidylinositol 4-phosphate 5-kinase β type I (pip5k1β), an enzyme functionally linked to actin cytoskeleton dynamics that phosphorylates phosphatidylinositol 4-phosphate [PI(4)P] to generate [[ phosphatidylinositol-4,5-bisphosphate ]] [PI(4,5)P2].


PIP5K1B encodes << phosphatidylinositol 4-phosphate 5-kinase β type I >> (pip5k1β), an enzyme functionally linked to actin cytoskeleton dynamics that phosphorylates phosphatidylinositol 4-phosphate [PI(4)P] to generate [[ phosphatidylinositol-4,5-bisphosphate ]] [PI(4,5)P2].


PIP5K1B encodes phosphatidylinositol 4-phosphate 5-kinase β type I (<< pip5k1β >>), an enzyme functionally linked to actin cytoskeleton dynamics that phosphorylates phosphatidylinositol 4-phosphate [PI(4)P] to generate [[ phosphatidylinositol-4,5-bisphosphate ]] [PI(4,5)P2].


<< PIP5K1B >> encodes phosphatidylinositol 4-phosphate 5-kinase β type I (pip5k1β), an enzyme functionally linked to actin cytoskeleton dynamics that phosphorylates phosphatidylinositol 4-phosphate [PI(4)P] to generate phosphatidylinositol-4,5-bisphosphate [[[ PI(4,5)P2 ]]].


PIP5K1B encodes << phosphatidylinositol 4-phosphate 5-kinase β type I >> (pip5k1β), an enzyme functionally linked to actin cytoskeleton dynamics that phosphorylates phosphatidylinositol 4-phosphate [PI(4)P] to generate phosphatidylinositol-4,5-bisphosphate [[[ PI(4,5)P2 ]]].


PIP5K1B encodes phosphatidylinositol 4-phosphate 5-kinase β type I (<< pip5k1β >>), an enzyme functionally linked to actin cytoskeleton dynamics that phosphorylates phosphatidylinositol 4-phosphate [PI(4)P] to generate phosphatidylinositol-4,5-bisphosphate [[[ PI(4,5)P2 ]]].


<< PIP5K1B >> encodes phosphatidylinositol 4-phosphate 5-kinase β type I (pip5k1β), an enzyme functionally linked to actin cytoskeleton dynamics that phosphorylates [[ phosphatidylinositol 4-phosphate ]] [PI(4)P] to generate phosphatidylinositol-4,5-bisphosphate [PI(4,5)P2].


PIP5K1B encodes << phosphatidylinositol 4-phosphate 5-kinase β type I >> (pip5k1β), an enzyme functionally linked to actin cytoskeleton dynamics that phosphorylates [[ phosphatidylinositol 4-phosphate ]] [PI(4)P] to generate phosphatidylinositol-4,5-bisphosphate [PI(4,5)P2].


PIP5K1B encodes phosphatidylinositol 4-phosphate 5-kinase β type I (<< pip5k1β >>), an enzyme functionally linked to actin cytoskeleton dynamics that phosphorylates [[ phosphatidylinositol 4-phosphate ]] [PI(4)P] to generate phosphatidylinositol-4,5-bisphosphate [PI(4,5)P2].


<< PIP5K1B >> encodes phosphatidylinositol 4-phosphate 5-kinase β type I (pip5k1β), an enzyme functionally linked to actin cytoskeleton dynamics that phosphorylates phosphatidylinositol 4-phosphate [[[ PI(4)P ]]] to generate phosphatidylinositol-4,5-bisphosphate [PI(4,5)P2].


PIP5K1B encodes << phosphatidylinositol 4-phosphate 5-kinase β type I >> (pip5k1β), an enzyme functionally linked to actin cytoskeleton dynamics that phosphorylates phosphatidylinositol 4-phosphate [[[ PI(4)P ]]] to generate phosphatidylinositol-4,5-bisphosphate [PI(4,5)P2].


PIP5K1B encodes phosphatidylinositol 4-phosphate 5-kinase β type I (<< pip5k1β >>), an enzyme functionally linked to actin cytoskeleton dynamics that phosphorylates phosphatidylinositol 4-phosphate [[[ PI(4)P ]]] to generate phosphatidylinositol-4,5-bisphosphate [PI(4,5)P2].


Accordingly, loss of << pip5k1β >> function in FRDA cells was accompanied by decreased [[ PI(4,5)P2 ]] levels and was shown instrumental for destabilization of the actin network and delayed cell spreading.


The expression of << regucalcin >> is stimulated through the action of insulin in liver cells in vitro and in vivo and it is decreased in the liver of rats with type I diabetes induced by [[ streptozotocin ]] administration in vivo.


<< AMPK >> activators [[ metformin ]] and AICAR partly prevented the cell cycle block, oxidative stress and apoptosis induced by compound C.


<< AMPK >> activators metformin and [[ AICAR ]] partly prevented the cell cycle block, oxidative stress and apoptosis induced by compound C.


<< Indomethacin >> treatment led to an increase in lipid peroxidation, [[ glutathione peroxidase ]] and glucose-6-phosphate dehydrogenase activities and to a decrease in catalase activity and glutathione levels in gastric mucosa.


<< Indomethacin >> treatment led to an increase in lipid peroxidation, glutathione peroxidase and [[ glucose-6-phosphate dehydrogenase ]] activities and to a decrease in catalase activity and glutathione levels in gastric mucosa.


<< Indomethacin >> treatment led to an increase in lipid peroxidation, glutathione peroxidase and glucose-6-phosphate dehydrogenase activities and to a decrease in [[ catalase ]] activity and glutathione levels in gastric mucosa.


Reversible inhibition of << human carboxylesterases >> by [[ acyl glucuronides ]].


<< Carboxylesterases >> hydrolyze esters, amides, and thioesters to produce carboxylic acids and resulting [[ alcohols ]], amines, and thiols, respectively.


<< Carboxylesterases >> hydrolyze esters, amides, and thioesters to produce [[ carboxylic acids ]] and resulting alcohols, amines, and thiols, respectively.


<< Carboxylesterases >> hydrolyze esters, amides, and thioesters to produce carboxylic acids and resulting alcohols, [[ amines ]], and thiols, respectively.


<< Carboxylesterases >> hydrolyze esters, amides, and thioesters to produce carboxylic acids and resulting alcohols, amines, and [[ thiols ]], respectively.


<< Carboxylesterases >> hydrolyze [[ esters ]], amides, and thioesters to produce carboxylic acids and resulting alcohols, amines, and thiols, respectively.


<< Carboxylesterases >> hydrolyze esters, [[ amides ]], and thioesters to produce carboxylic acids and resulting alcohols, amines, and thiols, respectively.


<< Carboxylesterases >> hydrolyze esters, amides, and [[ thioesters ]] to produce carboxylic acids and resulting alcohols, amines, and thiols, respectively.


<< Uridine 5'-diphosphate- glucuronosyltransferases >> are colocalized with carboxylesterases and have the potential to further metabolize carboxylic acids to [[ acyl glucuronides ]], but it is currently unknown if acyl glucuronides, being esters, also interact with carboxylesterases.


Uridine 5'-diphosphate- glucuronosyltransferases are colocalized with << carboxylesterases >> and have the potential to further metabolize carboxylic acids to [[ acyl glucuronides ]], but it is currently unknown if acyl glucuronides, being esters, also interact with carboxylesterases.


<< Uridine 5'-diphosphate- glucuronosyltransferases >> are colocalized with carboxylesterases and have the potential to further metabolize carboxylic acids to acyl glucuronides, but it is currently unknown if [[ acyl glucuronides ]], being esters, also interact with carboxylesterases.


<< Uridine 5'-diphosphate- glucuronosyltransferases >> are colocalized with carboxylesterases and have the potential to further metabolize [[ carboxylic acids ]] to acyl glucuronides, but it is currently unknown if acyl glucuronides, being esters, also interact with carboxylesterases.


Uridine 5'-diphosphate- glucuronosyltransferases are colocalized with << carboxylesterases >> and have the potential to further metabolize [[ carboxylic acids ]] to acyl glucuronides, but it is currently unknown if acyl glucuronides, being esters, also interact with carboxylesterases.


Objective: This study explores the ability of << acyl glucuronides >> to act as substrates or inhibitors of [[ human carboxylesterases 1 ]] (hCES1) and 2 (hCES2).


Objective: This study explores the ability of << acyl glucuronides >> to act as substrates or inhibitors of human carboxylesterases 1 ([[ hCES1 ]]) and 2 (hCES2).


Objective: This study explores the ability of << acyl glucuronides >> to act as substrates or inhibitors of human carboxylesterases 1 (hCES1) and 2 ([[ hCES2 ]]).


Methods: The stability of six << acyl glucuronides >> in the presence of [[ hCES1 ]], hCES2, and buffer alone (100 mM potassium phosphate, pH 7.4, 37°C) were investigated.


Methods: The stability of six << acyl glucuronides >> in the presence of hCES1, [[ hCES2 ]], and buffer alone (100 mM potassium phosphate, pH 7.4, 37°C) were investigated.


Diclofenac-β-d-glucuronide, << clopidogrel-β-d-glucuronide >>, ibuprofen-β-d-glucuronide, (R)-naproxen-β-d-glucuronide, and (S)-naproxen-β-d-glucuronide selectively inhibited [[ hCES1 ]], with Ki values of 4.32 ± 0.47, 24.8 ± 4.2, 355 ± 38, 468 ± 21, 707 ± 64 µM, respectively, but did not significantly inhibit hCES2.


Diclofenac-β-d-glucuronide, clopidogrel-β-d-glucuronide, << ibuprofen-β-d-glucuronide >>, (R)-naproxen-β-d-glucuronide, and (S)-naproxen-β-d-glucuronide selectively inhibited [[ hCES1 ]], with Ki values of 4.32 ± 0.47, 24.8 ± 4.2, 355 ± 38, 468 ± 21, 707 ± 64 µM, respectively, but did not significantly inhibit hCES2.


Diclofenac-β-d-glucuronide, clopidogrel-β-d-glucuronide, ibuprofen-β-d-glucuronide, << (R)-naproxen-β-d-glucuronide >>, and (S)-naproxen-β-d-glucuronide selectively inhibited [[ hCES1 ]], with Ki values of 4.32 ± 0.47, 24.8 ± 4.2, 355 ± 38, 468 ± 21, 707 ± 64 µM, respectively, but did not significantly inhibit hCES2.


Diclofenac-β-d-glucuronide, clopidogrel-β-d-glucuronide, ibuprofen-β-d-glucuronide, (R)-naproxen-β-d-glucuronide, and << (S)-naproxen-β-d-glucuronide >> selectively inhibited [[ hCES1 ]], with Ki values of 4.32 ± 0.47, 24.8 ± 4.2, 355 ± 38, 468 ± 21, 707 ± 64 µM, respectively, but did not significantly inhibit hCES2.


<< Diclofenac-β-d-glucuronide >>, clopidogrel-β-d-glucuronide, ibuprofen-β-d-glucuronide, (R)-naproxen-β-d-glucuronide, and (S)-naproxen-β-d-glucuronide selectively inhibited [[ hCES1 ]], with Ki values of 4.32 ± 0.47, 24.8 ± 4.2, 355 ± 38, 468 ± 21, 707 ± 64 µM, respectively, but did not significantly inhibit hCES2.


Conclusion: Drug-drug interaction studies may be warranted for drugs that metabolize to << acyl glucuronides >> due to the potential inhibition of [[ hCESs ]].


Furthermore, << DOX >>-treated WT and p65(-/-) MEFs differed in their expression of various apoptosis-associated molecules, when the former demonstrated a decrease in the percentage of [[ p65 ]]-positive and a more prominent decrease in the percentage of p53-positive cells, while a decreased percentage of IκBα-positive and a more prominent decrease in the percentage of bcl-2-positive cells was detected among the latter.


RESULTS: << DZN >> induced histophatological damages and elevated the level of cardiac marker [[ CK-MB ]].


Crocin (25 and 50mg/kg) or vitamin E improved histopathological damages, decreased MDA and CK-MB, increased GSH content and attenuated the increase of Bax/Bcl2 ratio, activation of << caspase 3 >> and release of cytochrome c to the cytosol induced by [[ DZN ]].


<< Crocin >> (25 and 50mg/kg) or vitamin E improved histopathological damages, decreased MDA and CK-MB, increased GSH content and attenuated the increase of Bax/Bcl2 ratio, activation of [[ caspase 3 ]] and release of cytochrome c to the cytosol induced by DZN.


Crocin (25 and 50mg/kg) or << vitamin E >> improved histopathological damages, decreased MDA and CK-MB, increased GSH content and attenuated the increase of Bax/Bcl2 ratio, activation of [[ caspase 3 ]] and release of cytochrome c to the cytosol induced by DZN.


Crocin (25 and 50mg/kg) or vitamin E improved histopathological damages, decreased MDA and CK-MB, increased GSH content and attenuated the increase of Bax/Bcl2 ratio, activation of caspase 3 and release of << cytochrome c >> to the cytosol induced by [[ DZN ]].


Crocin (25 and 50mg/kg) or vitamin E improved histopathological damages, decreased MDA and CK-MB, increased GSH content and attenuated the increase of << Bax >>/Bcl2 ratio, activation of caspase 3 and release of cytochrome c to the cytosol induced by [[ DZN ]].


<< Crocin >> (25 and 50mg/kg) or vitamin E improved histopathological damages, decreased MDA and CK-MB, increased GSH content and attenuated the increase of Bax/Bcl2 ratio, activation of caspase 3 and release of [[ cytochrome c ]] to the cytosol induced by DZN.


Crocin (25 and 50mg/kg) or vitamin E improved histopathological damages, decreased MDA and CK-MB, increased GSH content and attenuated the increase of Bax/<< Bcl2 >> ratio, activation of caspase 3 and release of cytochrome c to the cytosol induced by [[ DZN ]].


<< Crocin >> (25 and 50mg/kg) or vitamin E improved histopathological damages, decreased MDA and [[ CK-MB ]], increased GSH content and attenuated the increase of Bax/Bcl2 ratio, activation of caspase 3 and release of cytochrome c to the cytosol induced by DZN.


<< Crocin >> (25 and 50mg/kg) or vitamin E improved histopathological damages, decreased MDA and CK-MB, increased GSH content and attenuated the increase of [[ Bax ]]/Bcl2 ratio, activation of caspase 3 and release of cytochrome c to the cytosol induced by DZN.


<< Crocin >> (25 and 50mg/kg) or vitamin E improved histopathological damages, decreased MDA and CK-MB, increased GSH content and attenuated the increase of Bax/[[ Bcl2 ]] ratio, activation of caspase 3 and release of cytochrome c to the cytosol induced by DZN.


Crocin (25 and 50mg/kg) or << vitamin E >> improved histopathological damages, decreased MDA and [[ CK-MB ]], increased GSH content and attenuated the increase of Bax/Bcl2 ratio, activation of caspase 3 and release of cytochrome c to the cytosol induced by DZN.


Crocin (25 and 50mg/kg) or << vitamin E >> improved histopathological damages, decreased MDA and CK-MB, increased GSH content and attenuated the increase of [[ Bax ]]/Bcl2 ratio, activation of caspase 3 and release of cytochrome c to the cytosol induced by DZN.


Crocin (25 and 50mg/kg) or << vitamin E >> improved histopathological damages, decreased MDA and CK-MB, increased GSH content and attenuated the increase of Bax/[[ Bcl2 ]] ratio, activation of caspase 3 and release of cytochrome c to the cytosol induced by DZN.


Effect of << fenoterol >>-induced constitutive [[ beta(2)-adrenoceptor ]] activity on contractile receptor function in airway smooth muscle.


In the present study, we investigated the effect of << fenoterol >>-induced constitutive [[ beta(2)-adrenoceptor ]] activity on muscarinic receptor agonist- and histamine-induced bovine tracheal smooth muscle contractions.


After extensive washout (3 h, 37 degrees C), isometric contractions were measured to the full muscarinic receptor agonist methacholine, the partial << muscarinic receptor >> agonist [[ 4-(m-chlorophenyl-carbamoyloxy)-2-butynyltrimethylammonium ]] (McN-A-343) and histamine.


After extensive washout (3 h, 37 degrees C), isometric contractions were measured to the full muscarinic receptor agonist methacholine, the partial << muscarinic receptor >> agonist 4-(m-chlorophenyl-carbamoyloxy)-2-butynyltrimethylammonium (McN-A-343) and [[ histamine ]].


After extensive washout (3 h, 37 degrees C), isometric contractions were measured to the full << muscarinic receptor >> agonist [[ methacholine ]], the partial muscarinic receptor agonist 4-(m-chlorophenyl-carbamoyloxy)-2-butynyltrimethylammonium (McN-A-343) and histamine.


In conclusion, << fenoterol >>-induced constitutive [[ beta(2)-adrenoceptor ]] activity reduces muscarinic receptor agonist- and histamine-induced contractions of bovine tracheal smooth muscle, which can be reversed by the inverse agonist timolol.


In conclusion, fenoterol-induced constitutive << beta(2)-adrenoceptor >> activity reduces muscarinic receptor agonist- and histamine-induced contractions of bovine tracheal smooth muscle, which can be reversed by the inverse agonist [[ timolol ]].


<< Beta-glucogallin >> reduces the expression of lipopolysaccharide-induced inflammatory markers by inhibition of [[ aldose reductase ]] in murine macrophages and ocular tissues.


<< Aldose reductase >> (AR) catalyzes the reduction of toxic lipid aldehydes to their [[ alcohol ]] products and mediates inflammatory signals triggered by lipopolysaccharide (LPS).


Aldose reductase (<< AR >>) catalyzes the reduction of toxic lipid aldehydes to their [[ alcohol ]] products and mediates inflammatory signals triggered by lipopolysaccharide (LPS).


<< Aldose reductase >> (AR) catalyzes the reduction of toxic lipid [[ aldehydes ]] to their alcohol products and mediates inflammatory signals triggered by lipopolysaccharide (LPS).


Aldose reductase (<< AR >>) catalyzes the reduction of toxic lipid [[ aldehydes ]] to their alcohol products and mediates inflammatory signals triggered by lipopolysaccharide (LPS).


<< Beta-glucogallin >> (BGG), a recently described [[ AR ]] inhibitor, was purified from extracts of the Indian gooseberry (Emblica officinalis).


Beta-glucogallin (<< BGG >>), a recently described [[ AR ]] inhibitor, was purified from extracts of the Indian gooseberry (Emblica officinalis).


In this study, we found that << BGG >> showed low cytotoxicity in Raw264.7 murine macrophages and effectively inhibited [[ AR ]] activity as measured by a decrease in sorbitol accumulation.


In addition, << BGG >>-mediated inhibition of AR prevented LPS-induced activation of [[ JNK ]] and p38 and lowered ROS levels, which could inhibit LPS-induced apoptosis.


In addition, << BGG >>-mediated inhibition of AR prevented LPS-induced activation of JNK and [[ p38 ]] and lowered ROS levels, which could inhibit LPS-induced apoptosis.


In addition, << BGG >>-mediated inhibition of [[ AR ]] prevented LPS-induced activation of JNK and p38 and lowered ROS levels, which could inhibit LPS-induced apoptosis.


Exogenous << C2-ceramide >> activates [[ c-fos serum response element ]] via Rac-dependent signalling pathway.


Treatment of Rat-2 fibroblast cells with << C2-ceramide >> caused the stimulation of [[ c-fos SRE ]]-dependent reporter gene activity in a dose- and time-dependent manner by transient transfection analysis.


Next, we examined the role of Rho family GTPases in the << ceramide >>-induced signalling to [[ SRE ]] activation.


By reporter gene analysis following transient transfections with various plasmids expressing a dominant negative mutant form of Cdc42, Rac1 or RhoA, << C2-ceramide >>-induced [[ SRE ]] activation was shown to be selectively repressed by pEXV-RacN17 encoding a dominant negative mutant of Rac1, suggesting that Rac activity is essential for the signalling cascade of ceramide to the nucleus.


In a further study to analyse the downstream mediator of Rac in the ceramide-signalling pathway, we observed that either pretreatment with mepacrine, a potent and specific inhibitor of phospholipase A2, or co-transfection with antisense cytosolic phospholipase A2 (cPLA2) oligonucleotide repressed the << C2-ceramide >>-induced [[ SRE ]] activation selectively, implying a critical role of cPLA2 in C2-ceramide-induced signalling to nucleus.


Consistent with these results, the translocation of cPLA2 protein as well as the release of << arachidonic acid >>, a principal product of [[ phospholipase A2 ]], was rapidly induced by the addition of C2-ceramide in a Rac-dependent manner.


Together, our findings suggest the critical role of 'Rac and subsequent activation of << phospholipase A2 >>' in [[ ceramide ]]-signalling to nucleus.


Effect of << ramelteon >> (TAK-375), a selective [[ MT1/MT2 receptor ]] agonist, on motor performance in mice.


Effect of ramelteon (<< TAK-375 >>), a selective [[ MT1/MT2 receptor ]] agonist, on motor performance in mice.


Effect of (S)-N-[2-(1,6,7,8-tetrahydro-2H-indeno-[5,4-b]furan-8-yl)ethyl]propionamide (<< ramelteon >>, TAK-375), a selective [[ MT1/MT2 receptor ]] agonist, on motor coordination was studied using rota-rod performance in mice.


Effect of (S)-N-[2-(1,6,7,8-tetrahydro-2H-indeno-[5,4-b]furan-8-yl)ethyl]propionamide (ramelteon, << TAK-375 >>), a selective [[ MT1/MT2 receptor ]] agonist, on motor coordination was studied using rota-rod performance in mice.


Effect of << (S)-N-[2-(1,6,7,8-tetrahydro-2H-indeno-[5,4-b]furan-8-yl)ethyl]propionamide >> (ramelteon, TAK-375), a selective [[ MT1/MT2 receptor ]] agonist, on motor coordination was studied using rota-rod performance in mice.


Synthesis and cancer stem cell-based activity of substituted << 5-morpholino-7H-thieno[3,2-b]pyran-7-ones >> designed as next generation [[ PI3K ]] inhibitors.


Our previous work, built on the early pioneering multikinase inhibitor << LY294002 >>, resulted in the only [[ PI3K ]] vascular-targeted PI3K inhibitor prodrug, SF1126, which has now completed Phase I clinical trials.


Our previous work, built on the early pioneering multikinase inhibitor << LY294002 >>, resulted in the only PI3K vascular-targeted [[ PI3K ]] inhibitor prodrug, SF1126, which has now completed Phase I clinical trials.


Our previous work, built on the early pioneering multikinase inhibitor LY294002, resulted in the only << PI3K >> vascular-targeted PI3K inhibitor prodrug, [[ SF1126 ]], which has now completed Phase I clinical trials.


Our previous work, built on the early pioneering multikinase inhibitor LY294002, resulted in the only PI3K vascular-targeted << PI3K >> inhibitor prodrug, [[ SF1126 ]], which has now completed Phase I clinical trials.


This work resulted in the discovery of the << 5-morpholino-7H-thieno[3,2-b]pyran-7-one >> system as the foundation of a new compound class of potential [[ PI3K ]] inhibitors having improved potency toward PI3K.


This work resulted in the discovery of the << 5-morpholino-7H-thieno[3,2-b]pyran-7-one >> system as the foundation of a new compound class of potential PI3K inhibitors having improved potency toward [[ PI3K ]].


<< CP-690550 >>, a [[ JAK3 ]] inhibitor is currently in phase II clinical trials.FK778, is a synthetic malononitrilamide that targets the critical enzyme of the de novo pyrimidine synthesis, dihydroorotic acid dehydrogenase, and receptor-associated tyrosine kinases has completed phase II trials.


Firstly, the V(max) of << GAD >> was increased when ApoCaM was present whereas the affinity for the substrate, [[ glutamate ]], was not affected.


Hydrogen sulphide (<< H(2)S >>) is synthesized from L-cysteine via the action of cystathionine-gamma-lyase ([[ CSE ]]) and cystathionine-beta-synthase (CBS).


Hydrogen sulphide (<< H(2)S >>) is synthesized from L-cysteine via the action of cystathionine-gamma-lyase (CSE) and [[ cystathionine-beta-synthase ]] (CBS).


Hydrogen sulphide (<< H(2)S >>) is synthesized from L-cysteine via the action of cystathionine-gamma-lyase (CSE) and cystathionine-beta-synthase ([[ CBS ]]).


Hydrogen sulphide (<< H(2)S >>) is synthesized from L-cysteine via the action of [[ cystathionine-gamma-lyase ]] (CSE) and cystathionine-beta-synthase (CBS).


<< Hydrogen sulphide >> (H(2)S) is synthesized from L-cysteine via the action of cystathionine-gamma-lyase ([[ CSE ]]) and cystathionine-beta-synthase (CBS).


<< Hydrogen sulphide >> (H(2)S) is synthesized from L-cysteine via the action of cystathionine-gamma-lyase (CSE) and [[ cystathionine-beta-synthase ]] (CBS).


<< Hydrogen sulphide >> (H(2)S) is synthesized from L-cysteine via the action of cystathionine-gamma-lyase (CSE) and cystathionine-beta-synthase ([[ CBS ]]).


<< Hydrogen sulphide >> (H(2)S) is synthesized from L-cysteine via the action of [[ cystathionine-gamma-lyase ]] (CSE) and cystathionine-beta-synthase (CBS).


Hydrogen sulphide (H(2)S) is synthesized from << L-cysteine >> via the action of cystathionine-gamma-lyase ([[ CSE ]]) and cystathionine-beta-synthase (CBS).


Hydrogen sulphide (H(2)S) is synthesized from << L-cysteine >> via the action of cystathionine-gamma-lyase (CSE) and [[ cystathionine-beta-synthase ]] (CBS).


Hydrogen sulphide (H(2)S) is synthesized from << L-cysteine >> via the action of cystathionine-gamma-lyase (CSE) and cystathionine-beta-synthase ([[ CBS ]]).


Hydrogen sulphide (H(2)S) is synthesized from << L-cysteine >> via the action of [[ cystathionine-gamma-lyase ]] (CSE) and cystathionine-beta-synthase (CBS).


In this study, we investigated the presence of H(2)S and the expression of << H(2)S >> synthesizing enzymes, [[ CSE ]] and CBS, in isolated mouse pancreatic acini.


In this study, we investigated the presence of H(2)S and the expression of << H(2)S >> synthesizing enzymes, CSE and [[ CBS ]], in isolated mouse pancreatic acini.


<< Caerulein >> increased the levels of H(2)S and [[ CSE ]] mRNA expression while CBS mRNA expression was decreased.


<< Caerulein >> increased the levels of H(2)S and CSE mRNA expression while [[ CBS ]] mRNA expression was decreased.


In addition, cells pre-treated with << DL-propargylglycine >> (PAG, 3 mM), a [[ CSE ]] inhibitor, reduced the formation of H(2)S in caerulein treated cells, suggesting that CSE may be the main enzyme involved in H(2)S formation in mouse acinar cells.


In addition, cells pre-treated with DL-propargylglycine (<< PAG >>, 3 mM), a [[ CSE ]] inhibitor, reduced the formation of H(2)S in caerulein treated cells, suggesting that CSE may be the main enzyme involved in H(2)S formation in mouse acinar cells.


In addition, cells pre-treated with DL-propargylglycine (PAG, 3 mM), a CSE inhibitor, reduced the formation of H(2)S in caerulein treated cells, suggesting that << CSE >> may be the main enzyme involved in [[ H(2)S ]] formation in mouse acinar cells.


Furthermore, << substance P >> (SP) concentration in the acini and expression of SP gene (preprotachykinin-A, PPT-A) and neurokinin-1 receptor (NK-1R), the primary receptor for SP, are increased in secretagogue [[ caerulein ]]-treated acinar cells.


Furthermore, substance P (<< SP >>) concentration in the acini and expression of SP gene (preprotachykinin-A, PPT-A) and neurokinin-1 receptor (NK-1R), the primary receptor for SP, are increased in secretagogue [[ caerulein ]]-treated acinar cells.


Furthermore, substance P (SP) concentration in the acini and expression of << SP >> gene (preprotachykinin-A, PPT-A) and neurokinin-1 receptor (NK-1R), the primary receptor for SP, are increased in secretagogue [[ caerulein ]]-treated acinar cells.


Furthermore, substance P (SP) concentration in the acini and expression of SP gene (<< preprotachykinin-A >>, PPT-A) and neurokinin-1 receptor (NK-1R), the primary receptor for SP, are increased in secretagogue [[ caerulein ]]-treated acinar cells.


Furthermore, substance P (SP) concentration in the acini and expression of SP gene (preprotachykinin-A, << PPT-A >>) and neurokinin-1 receptor (NK-1R), the primary receptor for SP, are increased in secretagogue [[ caerulein ]]-treated acinar cells.


Furthermore, substance P (SP) concentration in the acini and expression of SP gene (preprotachykinin-A, PPT-A) and << neurokinin-1 receptor >> (NK-1R), the primary receptor for SP, are increased in secretagogue [[ caerulein ]]-treated acinar cells.


Furthermore, substance P (SP) concentration in the acini and expression of SP gene (preprotachykinin-A, PPT-A) and neurokinin-1 receptor (<< NK-1R >>), the primary receptor for SP, are increased in secretagogue [[ caerulein ]]-treated acinar cells.


Inhibition of endogenous production of << H(2)S >> by PAG significantly suppressed [[ SP ]] concentration, PPT-A expression and NK1-R expression in the acini.


Inhibition of endogenous production of << H(2)S >> by PAG significantly suppressed SP concentration, [[ PPT-A ]] expression and NK1-R expression in the acini.


Inhibition of endogenous production of << H(2)S >> by PAG significantly suppressed SP concentration, PPT-A expression and [[ NK1-R ]] expression in the acini.


To determine whether H(2)S itself provoked inflammation in acinar cells, the cells were treated with H(2)S donor drug, << sodium hydrosulphide >> (NaHS), (10, 50 and 100 muM), that resulted in a significant increase in [[ SP ]] concentration and expression of PPT-A and NK1-R in acinar cells.


To determine whether H(2)S itself provoked inflammation in acinar cells, the cells were treated with H(2)S donor drug, << sodium hydrosulphide >> (NaHS), (10, 50 and 100 muM), that resulted in a significant increase in SP concentration and expression of [[ PPT-A ]] and NK1-R in acinar cells.


To determine whether H(2)S itself provoked inflammation in acinar cells, the cells were treated with H(2)S donor drug, << sodium hydrosulphide >> (NaHS), (10, 50 and 100 muM), that resulted in a significant increase in SP concentration and expression of PPT-A and [[ NK1-R ]] in acinar cells.


To determine whether H(2)S itself provoked inflammation in acinar cells, the cells were treated with H(2)S donor drug, sodium hydrosulphide (<< NaHS >>), (10, 50 and 100 muM), that resulted in a significant increase in [[ SP ]] concentration and expression of PPT-A and NK1-R in acinar cells.


To determine whether H(2)S itself provoked inflammation in acinar cells, the cells were treated with H(2)S donor drug, sodium hydrosulphide (<< NaHS >>), (10, 50 and 100 muM), that resulted in a significant increase in SP concentration and expression of [[ PPT-A ]] and NK1-R in acinar cells.


To determine whether H(2)S itself provoked inflammation in acinar cells, the cells were treated with H(2)S donor drug, sodium hydrosulphide (<< NaHS >>), (10, 50 and 100 muM), that resulted in a significant increase in SP concentration and expression of PPT-A and [[ NK1-R ]] in acinar cells.


These results suggest that the pro-inflammatory effect of << H(2)S >> may be mediated by [[ SP ]]-NK-1R related pathway in mouse pancreatic acinar cells.


These results suggest that the pro-inflammatory effect of << H(2)S >> may be mediated by SP-[[ NK-1R ]] related pathway in mouse pancreatic acinar cells.


The results showed that administration of << AlCl3 >> resulted in a significant elevation in the levels of AchE activity, [[ CRP ]], NF-κB, and MCP-1 accompanied with a significant depletion in the Ach level.


The results showed that administration of << AlCl3 >> resulted in a significant elevation in the levels of AchE activity, CRP, [[ NF-κB ]], and MCP-1 accompanied with a significant depletion in the Ach level.


The results showed that administration of << AlCl3 >> resulted in a significant elevation in the levels of AchE activity, CRP, NF-κB, and [[ MCP-1 ]] accompanied with a significant depletion in the Ach level.


The results showed that administration of << AlCl3 >> resulted in a significant elevation in the levels of [[ AchE ]] activity, CRP, NF-κB, and MCP-1 accompanied with a significant depletion in the Ach level.


6-DHSG was metabolised by GSH to form a GSH conjugate (<< GS-6-DHSG >>) in RAW 264.7 cells, via a potential mechanism involving the catalytic activity of [[ glutathione-S-transferase ]] (GST).


6-DHSG was metabolised by GSH to form a GSH conjugate (<< GS-6-DHSG >>) in RAW 264.7 cells, via a potential mechanism involving the catalytic activity of glutathione-S-transferase ([[ GST ]]).


<< 6-DHSG >> was metabolised by GSH to form a GSH conjugate (GS-6-DHSG) in RAW 264.7 cells, via a potential mechanism involving the catalytic activity of [[ glutathione-S-transferase ]] (GST).


<< 6-DHSG >> was metabolised by GSH to form a GSH conjugate (GS-6-DHSG) in RAW 264.7 cells, via a potential mechanism involving the catalytic activity of glutathione-S-transferase ([[ GST ]]).


The concentration response to << levcromakalim >> (LEVC), a [[ K(ATP) channel ]] opener, was significantly shifted to the left in the inflamed smooth-muscle cells.


The concentration response to levcromakalim (<< LEVC >>), a [[ K(ATP) channel ]] opener, was significantly shifted to the left in the inflamed smooth-muscle cells.


Sulfhydration of << sulfonylurea receptor 2B >> (SUR2B) was induced by [[ NaHS ]] and colonic inflammation.


Sulfhydration of sulfonylurea receptor 2B (<< SUR2B >>) was induced by [[ NaHS ]] and colonic inflammation.


Pharmacological treatment has been studied and it could be demonstrated, that some mutant currents may be insufficiently suppressed by drugs targeted to block the specific current such as, e.g., << sotalol >> or ibutilide in patients with a mutation in the [[ IKr ]]-coding gene KCNH2 (HERG).


Pharmacological treatment has been studied and it could be demonstrated, that some mutant currents may be insufficiently suppressed by drugs targeted to block the specific current such as, e.g., << sotalol >> or ibutilide in patients with a mutation in the IKr-coding gene [[ KCNH2 ]] (HERG).


Pharmacological treatment has been studied and it could be demonstrated, that some mutant currents may be insufficiently suppressed by drugs targeted to block the specific current such as, e.g., << sotalol >> or ibutilide in patients with a mutation in the IKr-coding gene KCNH2 ([[ HERG ]]).


Pharmacological treatment has been studied and it could be demonstrated, that some mutant currents may be insufficiently suppressed by drugs targeted to block the specific current such as, e.g., sotalol or << ibutilide >> in patients with a mutation in the [[ IKr ]]-coding gene KCNH2 (HERG).


Pharmacological treatment has been studied and it could be demonstrated, that some mutant currents may be insufficiently suppressed by drugs targeted to block the specific current such as, e.g., sotalol or << ibutilide >> in patients with a mutation in the IKr-coding gene [[ KCNH2 ]] (HERG).


Pharmacological treatment has been studied and it could be demonstrated, that some mutant currents may be insufficiently suppressed by drugs targeted to block the specific current such as, e.g., sotalol or << ibutilide >> in patients with a mutation in the IKr-coding gene KCNH2 ([[ HERG ]]).


Although inhibition of << LH >> release can be achieved by [[ estrogen ]] and progestins, an optimal inhibitory effect on the prostate is obtained by the combined administration of the antiandrogen with an LHRH agonist that causes a specific blockage of testicular androgen biosynthesis as well as an inhibition of the LH responsiveness to LHRH.


Although inhibition of << LH >> release can be achieved by estrogen and [[ progestins ]], an optimal inhibitory effect on the prostate is obtained by the combined administration of the antiandrogen with an LHRH agonist that causes a specific blockage of testicular androgen biosynthesis as well as an inhibition of the LH responsiveness to LHRH.


Mechanisms of << cefadroxil >> uptake in the choroid plexus: studies in wild-type and [[ PEPT2 ]] knockout mice.


The choroid plexus uptake of << [(3)H]cefadroxil >> was studied in [[ peptide transporter 2 ]] (PEPT2) wild-type and null mice as a function of temperature, transport inhibitors, pH, and saturability.


The choroid plexus uptake of << [(3)H]cefadroxil >> was studied in peptide transporter 2 ([[ PEPT2 ]]) wild-type and null mice as a function of temperature, transport inhibitors, pH, and saturability.


At normal pH (7.4) and temperature (37 degrees C), the uptake of 1 microM << cefadroxil >> was reduced by 83% in [[ PEPT2 ]](-/-) mice as compared with PEPT2(+/+) mice (p < 0.001).


At normal pH (7.4) and temperature (37 degrees C), the uptake of 1 microM << cefadroxil >> was reduced by 83% in PEPT2(-/-) mice as compared with [[ PEPT2 ]](+/+) mice (p < 0.001).


Glycylsarcosine coadministration could inhibit the uptake of << cefadroxil >> in [[ PEPT2 ]](+/+) mice (p < 0.01) but not PEPT2(-/-) mice.


Glycylsarcosine coadministration could inhibit the uptake of << cefadroxil >> in PEPT2(+/+) mice (p < 0.01) but not [[ PEPT2 ]](-/-) mice.


Although a proton-stimulated uptake of << cefadroxil >> was demonstrated in [[ PEPT2 ]](+/+) mice (pH 6.5 versus pH 7.4; p < 0.01), no pH dependence was observed in PEPT2(-/-) mice.


Although a proton-stimulated uptake of << cefadroxil >> was demonstrated in PEPT2(+/+) mice (pH 6.5 versus pH 7.4; p < 0.01), no pH dependence was observed in [[ PEPT2 ]](-/-) mice.


These findings demonstrate that << PEPT2 >> is the primary transporter responsible for [[ cefadroxil ]] uptake in the choroid plexus.


The effects of the << adenosine A3 receptor >> agonist [[ IB-MECA ]] on sodium taurocholate-induced experimental acute pancreatitis.


The experiments were performed on 80 male Wistar rats, 58 of which survived, subdivided into 3 groups: C-control rats, I-EAP group, and II-EAP group treated with the << adenosine A3 receptor >> agonist [[ IB-MECA ]] (1-deoxy-1-6[[(3-iodophenyl) methyl]amino]-9H-purin-9-yl)-N-methyl-B-D-ribofuronamide at a dose of 0.75 mg/kg b.w.


The experiments were performed on 80 male Wistar rats, 58 of which survived, subdivided into 3 groups: C-control rats, I-EAP group, and II-EAP group treated with the << adenosine A3 receptor >> agonist IB-MECA [[ (1-deoxy-1-6[[(3-iodophenyl) methyl]amino]-9H-purin-9-yl)-N-methyl-B-D-ribofuronamide ]] at a dose of 0.75 mg/kg b.w.


In the << IB-MECA >> group, [[ α-amylase ]] activity was decreased with statistically high significance compared to group I.


The use of << A3 receptor >> agonist [[ IB-MECA ]] attenuates EAP.


<< Pyrrolopyrazines >> as Selective [[ Spleen Tyrosine Kinase ]] Inhibitors.


We describe the discovery of several << pyrrolopyrazines >> as potent and selective [[ Syk ]] inhibitors and the efforts that eventually led to the desired improvements in physicochemical properties and human whole blood potencies.


<< Ozone >> plus PM(2.5) exposure, however, induced [[ CRP ]], IL-6, CK, LDH and MDA increase, SOD and HRV decrease significantly in a dose-response way.


<< Ozone >> plus PM(2.5) exposure, however, induced CRP, [[ IL-6 ]], CK, LDH and MDA increase, SOD and HRV decrease significantly in a dose-response way.


<< Ozone >> plus PM(2.5) exposure, however, induced CRP, IL-6, [[ CK ]], LDH and MDA increase, SOD and HRV decrease significantly in a dose-response way.


<< Ozone >> plus PM(2.5) exposure, however, induced CRP, IL-6, CK, [[ LDH ]] and MDA increase, SOD and HRV decrease significantly in a dose-response way.


<< Ozone >> plus PM(2.5) exposure, however, induced CRP, IL-6, CK, LDH and MDA increase, [[ SOD ]] and HRV decrease significantly in a dose-response way.


<< Flavopiridol >>, a [[ cyclin-dependent kinase ]] inhibitor, arrests cell division and causes apoptosis in non-small lung cancer cells [283660].


In ex vivo experiments with tumor cells from refractory chronic lymphoblastic leukemia, dose-dependent << CDK2 >> inhibition associated with apoptotic changes was seen at concentrations greater than 100 nM of [[ flavopiridol ]].


<< Flavopiridol >> inhibits [[ CDK ]] with an IC50 value of 0.4 mM [285707].


<< Carbonic anhydrase >> inhibitors: [[ aromatic and heterocyclic sulfonamides ]] incorporating adamantyl moieties with strong anticonvulsant activity.


<< Carbonic anhydrase >> inhibitors: aromatic and heterocyclic sulfonamides incorporating [[ adamantyl ]] moieties with strong anticonvulsant activity.


Some of these derivatives showed good inhibitory potency against two << human CA >> isozymes involved in important physiological processes, CA I, and CA II, of the same order of magnitude as the clinically used drugs acetazolamide and [[ methazolamide ]].


Some of these derivatives showed good inhibitory potency against two human CA isozymes involved in important physiological processes, << CA I >>, and CA II, of the same order of magnitude as the clinically used drugs acetazolamide and [[ methazolamide ]].


Some of these derivatives showed good inhibitory potency against two human CA isozymes involved in important physiological processes, CA I, and << CA II >>, of the same order of magnitude as the clinically used drugs acetazolamide and [[ methazolamide ]].


Some of these derivatives showed good inhibitory potency against two << human CA >> isozymes involved in important physiological processes, CA I, and CA II, of the same order of magnitude as the clinically used drugs [[ acetazolamide ]] and methazolamide.


Some of these derivatives showed good inhibitory potency against two human CA isozymes involved in important physiological processes, << CA I >>, and CA II, of the same order of magnitude as the clinically used drugs [[ acetazolamide ]] and methazolamide.


Some of these derivatives showed good inhibitory potency against two human CA isozymes involved in important physiological processes, CA I, and << CA II >>, of the same order of magnitude as the clinically used drugs [[ acetazolamide ]] and methazolamide.


BACKGROUND AND AIMS: << Glutamic acid decarboxylase >> (GAD, EC 4.1.1.15) catalyses the conversion of glutamate to [[ gamma-aminobutyric acid ]] (GABA).


BACKGROUND AND AIMS: Glutamic acid decarboxylase (<< GAD >>, EC 4.1.1.15) catalyses the conversion of glutamate to [[ gamma-aminobutyric acid ]] (GABA).


BACKGROUND AND AIMS: Glutamic acid decarboxylase (GAD, << EC 4.1.1.15 >>) catalyses the conversion of glutamate to [[ gamma-aminobutyric acid ]] (GABA).


BACKGROUND AND AIMS: << Glutamic acid decarboxylase >> (GAD, EC 4.1.1.15) catalyses the conversion of glutamate to gamma-aminobutyric acid ([[ GABA ]]).


BACKGROUND AND AIMS: Glutamic acid decarboxylase (<< GAD >>, EC 4.1.1.15) catalyses the conversion of glutamate to gamma-aminobutyric acid ([[ GABA ]]).


BACKGROUND AND AIMS: Glutamic acid decarboxylase (GAD, << EC 4.1.1.15 >>) catalyses the conversion of glutamate to gamma-aminobutyric acid ([[ GABA ]]).


BACKGROUND AND AIMS: << Glutamic acid decarboxylase >> (GAD, EC 4.1.1.15) catalyses the conversion of [[ glutamate ]] to gamma-aminobutyric acid (GABA).


BACKGROUND AND AIMS: Glutamic acid decarboxylase (<< GAD >>, EC 4.1.1.15) catalyses the conversion of [[ glutamate ]] to gamma-aminobutyric acid (GABA).


BACKGROUND AND AIMS: Glutamic acid decarboxylase (GAD, << EC 4.1.1.15 >>) catalyses the conversion of [[ glutamate ]] to gamma-aminobutyric acid (GABA).


FCEO significantly inhibited << nitric oxide >> (NO) and prostaglandin E2 (PGE2) by suppressing the protein expression of [[ inducible nitric oxide synthase ]] (iNOS) and cyclooxygenase (COX)-2, respectively.


FCEO significantly inhibited << nitric oxide >> (NO) and prostaglandin E2 (PGE2) by suppressing the protein expression of inducible nitric oxide synthase ([[ iNOS ]]) and cyclooxygenase (COX)-2, respectively.


FCEO significantly inhibited nitric oxide (<< NO >>) and prostaglandin E2 (PGE2) by suppressing the protein expression of [[ inducible nitric oxide synthase ]] (iNOS) and cyclooxygenase (COX)-2, respectively.


FCEO significantly inhibited nitric oxide (<< NO >>) and prostaglandin E2 (PGE2) by suppressing the protein expression of inducible nitric oxide synthase ([[ iNOS ]]) and cyclooxygenase (COX)-2, respectively.


FCEO significantly inhibited nitric oxide (NO) and << prostaglandin E2 >> (PGE2) by suppressing the protein expression of inducible nitric oxide synthase (iNOS) and [[ cyclooxygenase (COX)-2 ]], respectively.


FCEO significantly inhibited nitric oxide (NO) and prostaglandin E2 (<< PGE2 >>) by suppressing the protein expression of inducible nitric oxide synthase (iNOS) and [[ cyclooxygenase (COX)-2 ]], respectively.


<< Amrinone >> and milrinone, selective PDE3 inhibitors, suppressed [[ TNF ]] secretion to a lesser extent.


Amrinone and << milrinone >>, selective PDE3 inhibitors, suppressed [[ TNF ]] secretion to a lesser extent.


<< Amrinone >> and milrinone, selective [[ PDE3 ]] inhibitors, suppressed TNF secretion to a lesser extent.


Amrinone and << milrinone >>, selective [[ PDE3 ]] inhibitors, suppressed TNF secretion to a lesser extent.


The effects of << theophylline >> (unspecific [[ PDE ]] inhibitor), vinpocetine (PDE1 inhibitor), EHNA (PDE2 inhibitor) and the PDE5 inhibitors zaprinast and E 4021 were weak.


The effects of theophylline (unspecific PDE inhibitor), << vinpocetine >> ([[ PDE1 ]] inhibitor), EHNA (PDE2 inhibitor) and the PDE5 inhibitors zaprinast and E 4021 were weak.


The effects of theophylline (unspecific PDE inhibitor), vinpocetine (PDE1 inhibitor), EHNA (PDE2 inhibitor) and the << PDE5 >> inhibitors [[ zaprinast ]] and E 4021 were weak.


The effects of theophylline (unspecific PDE inhibitor), vinpocetine (PDE1 inhibitor), EHNA (PDE2 inhibitor) and the << PDE5 >> inhibitors zaprinast and [[ E 4021 ]] were weak.


In human blood, the tested glucocorticoids << beclomethasone >>, dexamethasone and fluticasone inhibited the LPS induced [[ TNF ]] release potently in a concentration dependent manner, whereas in dispersed human nasal polyp cells, the effect of the glucocorticoids on allergically induced TNF release, with the exception of dexamethasone, was much less pronounced.


In human blood, the tested glucocorticoids beclomethasone, << dexamethasone >> and fluticasone inhibited the LPS induced [[ TNF ]] release potently in a concentration dependent manner, whereas in dispersed human nasal polyp cells, the effect of the glucocorticoids on allergically induced TNF release, with the exception of dexamethasone, was much less pronounced.


In human blood, the tested glucocorticoids beclomethasone, dexamethasone and << fluticasone >> inhibited the LPS induced [[ TNF ]] release potently in a concentration dependent manner, whereas in dispersed human nasal polyp cells, the effect of the glucocorticoids on allergically induced TNF release, with the exception of dexamethasone, was much less pronounced.


In human blood, the tested glucocorticoids << beclomethasone >>, dexamethasone and fluticasone inhibited the LPS induced TNF release potently in a concentration dependent manner, whereas in dispersed human nasal polyp cells, the effect of the glucocorticoids on allergically induced [[ TNF ]] release, with the exception of dexamethasone, was much less pronounced.


In human blood, the tested glucocorticoids beclomethasone, << dexamethasone >> and fluticasone inhibited the LPS induced TNF release potently in a concentration dependent manner, whereas in dispersed human nasal polyp cells, the effect of the glucocorticoids on allergically induced [[ TNF ]] release, with the exception of dexamethasone, was much less pronounced.


In human blood, the tested glucocorticoids beclomethasone, dexamethasone and << fluticasone >> inhibited the LPS induced TNF release potently in a concentration dependent manner, whereas in dispersed human nasal polyp cells, the effect of the glucocorticoids on allergically induced [[ TNF ]] release, with the exception of dexamethasone, was much less pronounced.


The selective PDE 4 inhibitors, and to a certain extent the PDE3 inhibitors amrinone and << milrinone >>, reduced the [[ GM-CSF ]] release in a concentration dependent manner.


The selective PDE 4 inhibitors, and to a certain extent the PDE3 inhibitors << amrinone >> and milrinone, reduced the [[ GM-CSF ]] release in a concentration dependent manner.


The selective << PDE 4 >> inhibitors, and to a certain extent the PDE3 inhibitors amrinone and [[ milrinone ]], reduced the GM-CSF release in a concentration dependent manner.


The selective PDE 4 inhibitors, and to a certain extent the << PDE3 >> inhibitors amrinone and [[ milrinone ]], reduced the GM-CSF release in a concentration dependent manner.


The selective << PDE 4 >> inhibitors, and to a certain extent the PDE3 inhibitors [[ amrinone ]] and milrinone, reduced the GM-CSF release in a concentration dependent manner.


The selective PDE 4 inhibitors, and to a certain extent the << PDE3 >> inhibitors [[ amrinone ]] and milrinone, reduced the GM-CSF release in a concentration dependent manner.


Activating << glucocorticoid receptor >>-ERK signaling pathway contributes to [[ ginsenoside Rg1 ]] protection against β-amyloid peptide-induced human endothelial cells apoptosis.


Activating glucocorticoid receptor-<< ERK >> signaling pathway contributes to [[ ginsenoside Rg1 ]] protection against β-amyloid peptide-induced human endothelial cells apoptosis.


Activating glucocorticoid receptor-ERK signaling pathway contributes to << ginsenoside Rg1 >> protection against [[ β-amyloid peptide ]]-induced human endothelial cells apoptosis.


<< Rg1 >> attenuated the Aβ25-35-associated mitochondrial apoptotic events, accompanied by inhibiting [[ HIF-1α ]] expression followed by intracellular reactive nitrogen species generation, and protein nitrotyrosination.


<< Rg1 >> attenuated the [[ Aβ25-35 ]]-associated mitochondrial apoptotic events, accompanied by inhibiting HIF-1α expression followed by intracellular reactive nitrogen species generation, and protein nitrotyrosination.


These protective effects were abolished by glucocorticoid receptor (GR) antagonist RU486 or << p-ERK >> inhibitor [[ U0126 ]] rather than estrogen receptor α antagonist ICI 82,780.


These protective effects were abolished by glucocorticoid receptor (GR) antagonist RU486 or p-ERK inhibitor U0126 rather than << estrogen receptor α >> antagonist [[ ICI 82,780 ]].


These protective effects were abolished by << glucocorticoid receptor >> (GR) antagonist [[ RU486 ]] or p-ERK inhibitor U0126 rather than estrogen receptor α antagonist ICI 82,780.


These protective effects were abolished by glucocorticoid receptor (<< GR >>) antagonist [[ RU486 ]] or p-ERK inhibitor U0126 rather than estrogen receptor α antagonist ICI 82,780.


Taken together, our results suggested that << Rg1 >> protected against Aβ25-35-induced apoptosis at least in part by two complementary GR-dependent [[ ERK ]] phosphorylation pathways: (1) down-regulating HIF-1α initiated protein nitrotyrosination, and (2) inhibiting mitochondrial apoptotic cascades.


Taken together, our results suggested that << Rg1 >> protected against Aβ25-35-induced apoptosis at least in part by two complementary GR-dependent ERK phosphorylation pathways: (1) down-regulating [[ HIF-1α ]] initiated protein nitrotyrosination, and (2) inhibiting mitochondrial apoptotic cascades.


Taken together, our results suggested that << Rg1 >> protected against [[ Aβ25-35 ]]-induced apoptosis at least in part by two complementary GR-dependent ERK phosphorylation pathways: (1) down-regulating HIF-1α initiated protein nitrotyrosination, and (2) inhibiting mitochondrial apoptotic cascades.


These data provided a novel insight to the mechanisms of << Rg1 >>protective effects on [[ Aβ25-35 ]]-induced endothelial cells apoptosis, suggesting that GR-ERK signaling pathway might play an important role in it.


Effectiveness of << endopeptidase >> inhibition ([[ candoxatril ]]) in congestive heart failure.


<< Candoxatril >> is a novel, orally active inhibitor of [[ neutral endopeptidase ]] EC 3.4.24.11, the enzyme that degrades atrial natriuretic peptide (ANP).


<< Candoxatril >> is a novel, orally active inhibitor of neutral endopeptidase [[ EC 3.4.24.11 ]], the enzyme that degrades atrial natriuretic peptide (ANP).


On study day 1, << candoxatril >> acutely increased plasma [[ ANP ]] levels, suppressed aldosterone and decreased right atrial and pulmonary capillary wedge pressures.


On study day 10, the acute effects of << candoxatril >> were similar to those on day 1 (i.e., [[ ANP ]] was further increased, aldosterone was suppressed, and right and left ventricular filling pressures were decreased).


<< Type 2 11β-hydroxysteroid dehydrogenase >> encoded by the HSD11B2 gene converts [[ cortisol ]] to inactive cortisone, and alteration in this enzymatic activity might affect glucose homeostasis by affecting circulating levels or tissue availability of glucocorticoids.


Type 2 11β-hydroxysteroid dehydrogenase encoded by the << HSD11B2 >> gene converts [[ cortisol ]] to inactive cortisone, and alteration in this enzymatic activity might affect glucose homeostasis by affecting circulating levels or tissue availability of glucocorticoids.


<< Type 2 11β-hydroxysteroid dehydrogenase >> encoded by the HSD11B2 gene converts cortisol to inactive [[ cortisone ]], and alteration in this enzymatic activity might affect glucose homeostasis by affecting circulating levels or tissue availability of glucocorticoids.


Type 2 11β-hydroxysteroid dehydrogenase encoded by the << HSD11B2 >> gene converts cortisol to inactive [[ cortisone ]], and alteration in this enzymatic activity might affect glucose homeostasis by affecting circulating levels or tissue availability of glucocorticoids.


The << alpha(1)-adrenoceptor >> antagonist, [[ tamsulosin ]], is selective for alpha(1A)- and alpha(1D)- over alpha(1B)-adrenoceptors.


The alpha(1)-adrenoceptor antagonist, << tamsulosin >>, is selective for [[ alpha(1A)- and alpha(1D)- over alpha(1B)-adrenoceptors ]].


The obtained results showed that << pioglitazone >> improved the renal function, structural changes, renal malondialdehyde (MDA), [[ tumor necrosis factor alpha ]] (TNF-α), nuclear factor kappa B (NF-κB) genes expression in cisplatin injected rats.


The obtained results showed that << pioglitazone >> improved the renal function, structural changes, renal malondialdehyde (MDA), tumor necrosis factor alpha ([[ TNF-α ]]), nuclear factor kappa B (NF-κB) genes expression in cisplatin injected rats.


The obtained results showed that << pioglitazone >> improved the renal function, structural changes, renal malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), [[ nuclear factor kappa B ]] (NF-κB) genes expression in cisplatin injected rats.


The obtained results showed that << pioglitazone >> improved the renal function, structural changes, renal malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), nuclear factor kappa B ([[ NF-κB ]]) genes expression in cisplatin injected rats.


The obtained results showed that pioglitazone improved the renal function, structural changes, renal malondialdehyde (MDA), << tumor necrosis factor alpha >> (TNF-α), nuclear factor kappa B (NF-κB) genes expression in [[ cisplatin ]] injected rats.


The obtained results showed that pioglitazone improved the renal function, structural changes, renal malondialdehyde (MDA), tumor necrosis factor alpha (<< TNF-α >>), nuclear factor kappa B (NF-κB) genes expression in [[ cisplatin ]] injected rats.


The obtained results showed that pioglitazone improved the renal function, structural changes, renal malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), << nuclear factor kappa B >> (NF-κB) genes expression in [[ cisplatin ]] injected rats.


The obtained results showed that pioglitazone improved the renal function, structural changes, renal malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), nuclear factor kappa B (<< NF-κB >>) genes expression in [[ cisplatin ]] injected rats.


<< Sulindac >> metabolites simultaneously (a) increase cellular cyclic GMP and subsequently activate [[ cyclic GMP-dependent protein kinase ]] (PKG); (b) activate c-jun NH2-terminal kinase (JNK); (c) inhibit extracellular signal-regulated kinase 1/2 (ERK1/2); and (d) decrease beta-catenin protein expression at times and doses consistent with apoptosis.


<< Sulindac >> metabolites simultaneously (a) increase cellular cyclic GMP and subsequently activate cyclic GMP-dependent protein kinase ([[ PKG ]]); (b) activate c-jun NH2-terminal kinase (JNK); (c) inhibit extracellular signal-regulated kinase 1/2 (ERK1/2); and (d) decrease beta-catenin protein expression at times and doses consistent with apoptosis.


<< Sulindac >> metabolites simultaneously (a) increase cellular cyclic GMP and subsequently activate cyclic GMP-dependent protein kinase (PKG); (b) activate c-jun NH2-terminal kinase (JNK); (c) inhibit extracellular signal-regulated kinase 1/2 (ERK1/2); and (d) decrease [[ beta-catenin ]] protein expression at times and doses consistent with apoptosis.


<< Sulindac >> metabolites simultaneously (a) increase cellular cyclic GMP and subsequently activate cyclic GMP-dependent protein kinase (PKG); (b) activate [[ c-jun NH2-terminal kinase ]] (JNK); (c) inhibit extracellular signal-regulated kinase 1/2 (ERK1/2); and (d) decrease beta-catenin protein expression at times and doses consistent with apoptosis.


<< Sulindac >> metabolites simultaneously (a) increase cellular cyclic GMP and subsequently activate cyclic GMP-dependent protein kinase (PKG); (b) activate c-jun NH2-terminal kinase ([[ JNK ]]); (c) inhibit extracellular signal-regulated kinase 1/2 (ERK1/2); and (d) decrease beta-catenin protein expression at times and doses consistent with apoptosis.


Cotreatment with << U0126 >> and YC-1 synergistically increases apoptosis in colorectal cancer cells and recapitulates the effects of sulindac treatment on ERK1/2, [[ JNK ]], and beta-catenin.


Cotreatment with U0126 and << YC-1 >> synergistically increases apoptosis in colorectal cancer cells and recapitulates the effects of sulindac treatment on ERK1/2, [[ JNK ]], and beta-catenin.


Cotreatment with U0126 and YC-1 synergistically increases apoptosis in colorectal cancer cells and recapitulates the effects of << sulindac >> treatment on ERK1/2, [[ JNK ]], and beta-catenin.


Cotreatment with << U0126 >> and YC-1 synergistically increases apoptosis in colorectal cancer cells and recapitulates the effects of sulindac treatment on ERK1/2, JNK, and [[ beta-catenin ]].


Cotreatment with U0126 and << YC-1 >> synergistically increases apoptosis in colorectal cancer cells and recapitulates the effects of sulindac treatment on ERK1/2, JNK, and [[ beta-catenin ]].


Cotreatment with U0126 and YC-1 synergistically increases apoptosis in colorectal cancer cells and recapitulates the effects of << sulindac >> treatment on ERK1/2, JNK, and [[ beta-catenin ]].


Synthesis and antagonistic activity at << muscarinic receptor >> subtypes of some 2-carbonyl derivatives of [[ diphenidol ]].


Synthesis and antagonistic activity at << muscarinic receptor >> subtypes of some [[ 2-carbonyl ]] derivatives of diphenidol.


A series of 2-carbonyl analogues of the muscarinic antagonist << diphenidol >> bearing 1-substituents of different lipophilic, electronic, and steric properties was synthesized and their affinity for the [[ M2 and M3 muscarinic receptor ]] subtypes was evaluated by functional tests.


This work showed that appropriate structural modification of << diphenidol >> can lead to [[ M2 ]]-selective muscarinic antagonists of possible interest in the field of Alzheimer's disease.


Activation of an apoptotic signal transduction pathway involved in the upregulation of << calpain >> and apoptosis-inducing factor in [[ aldosterone ]]-induced primary cultured cardiomyocytes.


Activation of an apoptotic signal transduction pathway involved in the upregulation of calpain and << apoptosis-inducing factor >> in [[ aldosterone ]]-induced primary cultured cardiomyocytes.


In this study, aldosterone (<< ALD >>)-induced apoptosis of cardiomyocyte was evaluated based on the previous studies, and the roles of [[ calpain ]] signaling were clarified.


In this study, << aldosterone >> (ALD)-induced apoptosis of cardiomyocyte was evaluated based on the previous studies, and the roles of [[ calpain ]] signaling were clarified.


<< ALD >> increased calpain expression and [[ caspase-3 ]] activity and promoted Bid cleavage.


<< ALD >> increased [[ calpain ]] expression and caspase-3 activity and promoted Bid cleavage.


The upregulation of calpain, tBid and << caspase-3 >> activity were further inhibited by treatment with EGTA in the presence of [[ ALD ]].


The upregulation of << calpain >>, tBid and caspase-3 activity were further inhibited by treatment with EGTA in the presence of [[ ALD ]].


The upregulation of calpain, << tBid >> and caspase-3 activity were further inhibited by treatment with EGTA in the presence of [[ ALD ]].


The upregulation of << calpain >>, tBid and caspase-3 activity were further inhibited by treatment with [[ EGTA ]] in the presence of ALD.


The upregulation of calpain, << tBid >> and caspase-3 activity were further inhibited by treatment with [[ EGTA ]] in the presence of ALD.


The upregulation of calpain, tBid and << caspase-3 >> activity were further inhibited by treatment with [[ EGTA ]] in the presence of ALD.


Additionally, << AIF >> levels in the cytosol decreased due to [[ EGTA ]] but not due to calpeptin.


Furthermore, treatment with spironoclactone not only attenuated the pro-apoptotic effect of ALD but reversed the << ALD >>-induced increase of [[ calpain ]] and AIF levels.


Furthermore, treatment with spironoclactone not only attenuated the pro-apoptotic effect of ALD but reversed the << ALD >>-induced increase of calpain and [[ AIF ]] levels.


Furthermore, treatment with << spironoclactone >> not only attenuated the pro-apoptotic effect of ALD but reversed the ALD-induced increase of [[ calpain ]] and AIF levels.


Furthermore, treatment with << spironoclactone >> not only attenuated the pro-apoptotic effect of ALD but reversed the ALD-induced increase of calpain and [[ AIF ]] levels.


<< Loperamide >> is a peripheral opiate agonist able to inhibit [[ ACTH ]] secretion.


In all patients << loperamide >> induced a significant fall in plasma [[ ACTH ]] levels.


CRH caused a rise in plasma ACTH after both loperamide (from 30 +/- 16.6 to a peak of 108 +/- 31 pmol/l) and placebo (from 98.5 +/- 47 to 211 +/- 61.7 pmol/l): the interaction between treatments and time was significant, and the first phase of << CRH >>-induced ACTH secretion was significantly lower after [[ loperamide ]].


CRH caused a rise in plasma ACTH after both loperamide (from 30 +/- 16.6 to a peak of 108 +/- 31 pmol/l) and placebo (from 98.5 +/- 47 to 211 +/- 61.7 pmol/l): the interaction between treatments and time was significant, and the first phase of CRH-induced << ACTH >> secretion was significantly lower after [[ loperamide ]].


<< CCl(4) >> intoxication caused hepatic necrosis and increased serum [[ ALT ]] activity.


<< CCl(4) >> administration triggered inflammatory response in mice livers by activating [[ nuclear factor-kappaB ]] (NF-κB), which coincided with the induction of tumor necrosis factor-alpha (TNF-α) and cyclooxygenase-2 (COX-2).


<< CCl(4) >> administration triggered inflammatory response in mice livers by activating nuclear factor-kappaB ([[ NF-κB ]]), which coincided with the induction of tumor necrosis factor-alpha (TNF-α) and cyclooxygenase-2 (COX-2).


<< CCl(4) >> administration triggered inflammatory response in mice livers by activating nuclear factor-kappaB (NF-κB), which coincided with the induction of [[ tumor necrosis factor-alpha ]] (TNF-α) and cyclooxygenase-2 (COX-2).


<< CCl(4) >> administration triggered inflammatory response in mice livers by activating nuclear factor-kappaB (NF-κB), which coincided with the induction of tumor necrosis factor-alpha ([[ TNF-α ]]) and cyclooxygenase-2 (COX-2).


<< CCl(4) >> administration triggered inflammatory response in mice livers by activating nuclear factor-kappaB (NF-κB), which coincided with the induction of tumor necrosis factor-alpha (TNF-α) and [[ cyclooxygenase-2 ]] (COX-2).


<< CCl(4) >> administration triggered inflammatory response in mice livers by activating nuclear factor-kappaB (NF-κB), which coincided with the induction of tumor necrosis factor-alpha (TNF-α) and cyclooxygenase-2 ([[ COX-2 ]]).


Furthermore, RA significantly inhibited the << CCl(4) >>-induced apoptosis, which was evident from decreased cleavage of [[ caspase-3 ]].


Pre-clinical pharmacology of << zolmitriptan >> (Zomig; formerly 311C90), a centrally and peripherally acting [[ 5HT1B/1D ]] agonist for migraine.


Pre-clinical pharmacology of zolmitriptan (<< Zomig >>; formerly 311C90), a centrally and peripherally acting [[ 5HT1B/1D ]] agonist for migraine.


Pre-clinical pharmacology of zolmitriptan (Zomig; formerly << 311C90 >>), a centrally and peripherally acting [[ 5HT1B/1D ]] agonist for migraine.


Zolmitriptan (Zomig; formerly << 311C90 >>) is a novel [[ 5-hydroxytryptamine (5HT)1B/1D ]] receptor agonist with proven efficacy in the acute treatment of migraine with or without preceding aura.


<< Zolmitriptan >> (Zomig; formerly 311C90) is a novel [[ 5-hydroxytryptamine (5HT)1B/1D ]] receptor agonist with proven efficacy in the acute treatment of migraine with or without preceding aura.


Zolmitriptan (<< Zomig >>; formerly 311C90) is a novel [[ 5-hydroxytryptamine (5HT)1B/1D ]] receptor agonist with proven efficacy in the acute treatment of migraine with or without preceding aura.


These actions are consistent with a pre-junctional inhibition of neuropeptide release from perivascular afferents of the trigeminal nerve, as confirmed by independent studies showing that << zolmitriptan >> blocks elevations of [[ calcitonin-gene-related peptide ]] in jugular venous blood during electrical stimulation of the trigeminal ganglion.


It has been reported that oligomeric << procyanidins >> of lotus seedpod (LSOPC) is effective in the alleviation of Alzheimer's disease and diabetes through its antioxidant and [[ insulin ]]-potentiating activities.


They all expressed ASS, but not ornithine transcarbamylase (OTC), the enzyme that converts ornithine, the product of degradation of arginine with << rhArg >>, to [[ citrulline ]], which is converted back to arginine via ASS.


They all expressed ASS, but not << ornithine transcarbamylase >> (OTC), the enzyme that converts [[ ornithine ]], the product of degradation of arginine with rhArg, to citrulline, which is converted back to arginine via ASS.


They all expressed ASS, but not ornithine transcarbamylase (<< OTC >>), the enzyme that converts [[ ornithine ]], the product of degradation of arginine with rhArg, to citrulline, which is converted back to arginine via ASS.


They all expressed ASS, but not ornithine transcarbamylase (OTC), the enzyme that converts ornithine, the product of degradation of << arginine >> with [[ rhArg ]], to citrulline, which is converted back to arginine via ASS.


They all expressed ASS, but not ornithine transcarbamylase (OTC), the enzyme that converts ornithine, the product of degradation of arginine with rhArg, to citrulline, which is converted back to << arginine >> via [[ ASS ]].


This surprising correlation between the lack of OTC expression and sensitivity of ASS-positive HCC cells shows that OTC-deficient HCCs are sensitive to << rhArg >>-mediated [[ arginine ]] depletion.


Therefore, pretreatment tumor gene expression profiling of ASS and OTC could aid in predicting tumor response to << arginine >> depletion with [[ arginine-depleting enzymes ]].


To establish the relative importance of these subtypes, we compared the effects of sumatriptan with those of a selective << 5-HT1F >> receptor agonist ([[ LY 344864 ]]) on c-fos protein expression in the trigeminal nucleus caudalis.


<< c-fos >> expression was induced in urethane-anaesthetized rats by intracisternal [[ capsaicin ]] administration.


Sumatriptan and LY 344864 decreased the number of << capsaicin >>-induced [[ c-fos ]]-like immunoreactive cells within trigeminal nucleus caudalis (ID50 = 0.04 and 0.6 mg kg(-1)).


<< Sumatriptan >> and LY 344864 decreased the number of capsaicin-induced [[ c-fos ]]-like immunoreactive cells within trigeminal nucleus caudalis (ID50 = 0.04 and 0.6 mg kg(-1)).


Sumatriptan and << LY 344864 >> decreased the number of capsaicin-induced [[ c-fos ]]-like immunoreactive cells within trigeminal nucleus caudalis (ID50 = 0.04 and 0.6 mg kg(-1)).


The effect of sumatriptan, but not of LY 344864, was prevented by pretreatment with the antagonist << SDZ 21-009 >>, which displays high affinity for [[ rat 5-HT1B ]] receptors.


The involvement of << EP1 >> and EP2 receptors is indicated by studies with the EP1 selective agonist [[ 17-phenyl trinor PGE2 ]], and the EP2 selective agonist butaprost (which stimulate), as well as by studies with the antagonists SC-51089 (EP1 specific) and AH 6809 (EP1 and EP2 specific).


The involvement of EP1 and EP2 receptors is indicated by studies with the << EP1 >> selective agonist [[ 17-phenyl trinor PGE2 ]], and the EP2 selective agonist butaprost (which stimulate), as well as by studies with the antagonists SC-51089 (EP1 specific) and AH 6809 (EP1 and EP2 specific).


The involvement of EP1 and << EP2 receptors >> is indicated by studies with the EP1 selective agonist 17-phenyl trinor PGE2, and the EP2 selective agonist [[ butaprost ]] (which stimulate), as well as by studies with the antagonists SC-51089 (EP1 specific) and AH 6809 (EP1 and EP2 specific).


The involvement of EP1 and EP2 receptors is indicated by studies with the EP1 selective agonist 17-phenyl trinor PGE2, and the << EP2 >> selective agonist [[ butaprost ]] (which stimulate), as well as by studies with the antagonists SC-51089 (EP1 specific) and AH 6809 (EP1 and EP2 specific).


The involvement of << EP1 >> and EP2 receptors is indicated by studies with the EP1 selective agonist 17-phenyl trinor PGE2, and the EP2 selective agonist butaprost (which stimulate), as well as by studies with the antagonists [[ SC-51089 ]] (EP1 specific) and AH 6809 (EP1 and EP2 specific).


The involvement of EP1 and EP2 receptors is indicated by studies with the << EP1 >> selective agonist 17-phenyl trinor PGE2, and the EP2 selective agonist butaprost (which stimulate), as well as by studies with the antagonists [[ SC-51089 ]] (EP1 specific) and AH 6809 (EP1 and EP2 specific).


The involvement of EP1 and EP2 receptors is indicated by studies with the EP1 selective agonist 17-phenyl trinor PGE2, and the EP2 selective agonist butaprost (which stimulate), as well as by studies with the antagonists << SC-51089 >> (EP1 specific) and AH 6809 ([[ EP1 ]] and EP2 specific).


The involvement of << EP1 >> and EP2 receptors is indicated by studies with the EP1 selective agonist 17-phenyl trinor PGE2, and the EP2 selective agonist butaprost (which stimulate), as well as by studies with the antagonists SC-51089 (EP1 specific) and [[ AH 6809 ]] (EP1 and EP2 specific).


The involvement of EP1 and << EP2 receptors >> is indicated by studies with the EP1 selective agonist 17-phenyl trinor PGE2, and the EP2 selective agonist butaprost (which stimulate), as well as by studies with the antagonists SC-51089 (EP1 specific) and [[ AH 6809 ]] (EP1 and EP2 specific).


The involvement of EP1 and EP2 receptors is indicated by studies with the << EP1 >> selective agonist 17-phenyl trinor PGE2, and the EP2 selective agonist butaprost (which stimulate), as well as by studies with the antagonists SC-51089 (EP1 specific) and [[ AH 6809 ]] (EP1 and EP2 specific).