These findings suggest that << S1P >> activates the [[ PI3K ]]/Akt signaling pathway leading to the promotion of nuclear translocation of β-catenin in osteoblast-like cells, resulting in the upregulation of osteoptotegerin and osteoblast differentiation markers including alkaline phosphatase, probably relating to the inhibition of osteoclast formation and the mineralization, respectively.


These findings suggest that << S1P >> activates the PI3K/[[ Akt ]] signaling pathway leading to the promotion of nuclear translocation of β-catenin in osteoblast-like cells, resulting in the upregulation of osteoptotegerin and osteoblast differentiation markers including alkaline phosphatase, probably relating to the inhibition of osteoclast formation and the mineralization, respectively.


These findings suggest that << S1P >> activates the PI3K/Akt signaling pathway leading to the promotion of nuclear translocation of [[ β-catenin ]] in osteoblast-like cells, resulting in the upregulation of osteoptotegerin and osteoblast differentiation markers including alkaline phosphatase, probably relating to the inhibition of osteoclast formation and the mineralization, respectively.


These findings suggest that << S1P >> activates the PI3K/Akt signaling pathway leading to the promotion of nuclear translocation of β-catenin in osteoblast-like cells, resulting in the upregulation of [[ osteoptotegerin ]] and osteoblast differentiation markers including alkaline phosphatase, probably relating to the inhibition of osteoclast formation and the mineralization, respectively.


These findings suggest that << S1P >> activates the PI3K/Akt signaling pathway leading to the promotion of nuclear translocation of β-catenin in osteoblast-like cells, resulting in the upregulation of osteoptotegerin and osteoblast differentiation markers including [[ alkaline phosphatase ]], probably relating to the inhibition of osteoclast formation and the mineralization, respectively.


<< Plerixafor >>, a [[ CXCR4 ]] antagonist for the mobilization of hematopoietic stem cells.


<< Plerixafor >> (AMD3100, Genzyme Corporation) is a bicyclam molecule that antagonizes the binding of the chemokine [[ stromal cell-derived factor-1 ]] (SDF-1) to its cognate receptor CXCR4.


<< Plerixafor >> (AMD3100, Genzyme Corporation) is a bicyclam molecule that antagonizes the binding of the chemokine stromal cell-derived factor-1 ([[ SDF-1 ]]) to its cognate receptor CXCR4.


<< Plerixafor >> (AMD3100, Genzyme Corporation) is a bicyclam molecule that antagonizes the binding of the chemokine stromal cell-derived factor-1 (SDF-1) to its cognate receptor [[ CXCR4 ]].


<< Plerixafor >> (AMD3100, Genzyme Corporation) is a bicyclam molecule that antagonizes the binding of the [[ chemokine ]] stromal cell-derived factor-1 (SDF-1) to its cognate receptor CXCR4.


Plerixafor (<< AMD3100 >>, Genzyme Corporation) is a bicyclam molecule that antagonizes the binding of the chemokine [[ stromal cell-derived factor-1 ]] (SDF-1) to its cognate receptor CXCR4.


Plerixafor (<< AMD3100 >>, Genzyme Corporation) is a bicyclam molecule that antagonizes the binding of the chemokine stromal cell-derived factor-1 ([[ SDF-1 ]]) to its cognate receptor CXCR4.


Plerixafor (<< AMD3100 >>, Genzyme Corporation) is a bicyclam molecule that antagonizes the binding of the chemokine stromal cell-derived factor-1 (SDF-1) to its cognate receptor [[ CXCR4 ]].


Plerixafor (<< AMD3100 >>, Genzyme Corporation) is a bicyclam molecule that antagonizes the binding of the [[ chemokine ]] stromal cell-derived factor-1 (SDF-1) to its cognate receptor CXCR4.


Plerixafor (AMD3100, Genzyme Corporation) is a << bicyclam >> molecule that antagonizes the binding of the chemokine [[ stromal cell-derived factor-1 ]] (SDF-1) to its cognate receptor CXCR4.


Plerixafor (AMD3100, Genzyme Corporation) is a << bicyclam >> molecule that antagonizes the binding of the chemokine stromal cell-derived factor-1 ([[ SDF-1 ]]) to its cognate receptor CXCR4.


Plerixafor (AMD3100, Genzyme Corporation) is a << bicyclam >> molecule that antagonizes the binding of the chemokine stromal cell-derived factor-1 (SDF-1) to its cognate receptor [[ CXCR4 ]].


Plerixafor (AMD3100, Genzyme Corporation) is a << bicyclam >> molecule that antagonizes the binding of the [[ chemokine ]] stromal cell-derived factor-1 (SDF-1) to its cognate receptor CXCR4.


This stimulation was attenuated by the << Pak >> inhibitor [[ 2,2'-dihydroxy-1,1'-dinaphthyldisulfide ]] (IPA3) or dominant-negative Pak1.


This stimulation was attenuated by the << Pak >> inhibitor 2,2'-dihydroxy-1,1'-dinaphthyldisulfide ([[ IPA3 ]]) or dominant-negative Pak1.


Chronic insulin (24 h) activates NHE3 through the classic << phosphatidylinositol 3-kinase >>-serum- and glucocorticoid-dependent kinase 1 (PI3K-SGK1) pathway as insulin stimulates SGK1 phosphorylation and the insulin effect can be blocked by the PI3K inhibitor [[ wortmannin ]] or a dominant-negative SGK1.


Chronic insulin (24 h) activates NHE3 through the classic phosphatidylinositol 3-kinase-serum- and glucocorticoid-dependent kinase 1 (<< PI3K >>-SGK1) pathway as insulin stimulates SGK1 phosphorylation and the insulin effect can be blocked by the PI3K inhibitor [[ wortmannin ]] or a dominant-negative SGK1.


Chronic insulin (24 h) activates NHE3 through the classic phosphatidylinositol 3-kinase-serum- and glucocorticoid-dependent kinase 1 (PI3K-SGK1) pathway as insulin stimulates SGK1 phosphorylation and the insulin effect can be blocked by the << PI3K >> inhibitor [[ wortmannin ]] or a dominant-negative SGK1.


Results showed that neonatal << quinpirole >> treatment induced [[ D2 ]] priming that was eliminated by olanzapine treatment.


Results showed that neonatal quinpirole treatment induced << D2 >> priming that was eliminated by [[ olanzapine ]] treatment.


Brain tissue analyses revealed that neonatal quinpirole treatment produced a significant decrease in hippocampal << NGF >>, BDNF and ChAT that was eliminated by [[ olanzapine ]] treatment.


Brain tissue analyses revealed that neonatal quinpirole treatment produced a significant decrease in hippocampal NGF, << BDNF >> and ChAT that was eliminated by [[ olanzapine ]] treatment.


Brain tissue analyses revealed that neonatal quinpirole treatment produced a significant decrease in hippocampal NGF, BDNF and << ChAT >> that was eliminated by [[ olanzapine ]] treatment.


Brain tissue analyses revealed that neonatal << quinpirole >> treatment produced a significant decrease in hippocampal [[ NGF ]], BDNF and ChAT that was eliminated by olanzapine treatment.


Brain tissue analyses revealed that neonatal << quinpirole >> treatment produced a significant decrease in hippocampal NGF, [[ BDNF ]] and ChAT that was eliminated by olanzapine treatment.


Brain tissue analyses revealed that neonatal << quinpirole >> treatment produced a significant decrease in hippocampal NGF, BDNF and [[ ChAT ]] that was eliminated by olanzapine treatment.


Neonatal << quinpirole >> treatment produced a significant decrease in [[ BDNF ]] and ChAT in the frontal cortex that was unaffected by olanzapine treatment.


Neonatal << quinpirole >> treatment produced a significant decrease in BDNF and [[ ChAT ]] in the frontal cortex that was unaffected by olanzapine treatment.


These results show that << olanzapine >> eliminates [[ D2 receptor ]] priming and cognitive impairment and also alleviates decreases in neurotrophins and acetylcholinergic markers produced by D2 priming in the hippocampus.


Suppression of << Src >>/ERK and GSK-3/β-catenin signaling by [[ pinosylvin ]] inhibits the growth of human colorectal cancer cells.


Suppression of Src/<< ERK >> and GSK-3/β-catenin signaling by [[ pinosylvin ]] inhibits the growth of human colorectal cancer cells.


Suppression of Src/ERK and << GSK-3 >>/β-catenin signaling by [[ pinosylvin ]] inhibits the growth of human colorectal cancer cells.


Suppression of Src/ERK and GSK-3/<< β-catenin >> signaling by [[ pinosylvin ]] inhibits the growth of human colorectal cancer cells.


<< Pinosylvin >> inhibited the proliferation of HCT 116 cells by arresting transition of cell cycle from G1 to S phase along with the downregulation of cyclin D1, cyclin E, cyclin A, cyclin dependent kinase 2 (CDK2), CDK4, c-Myc, and retinoblastoma protein (pRb), and the upregulation of [[ p21 ]](WAF1/CIP1) and p53.


<< Pinosylvin >> inhibited the proliferation of HCT 116 cells by arresting transition of cell cycle from G1 to S phase along with the downregulation of cyclin D1, cyclin E, cyclin A, cyclin dependent kinase 2 (CDK2), CDK4, c-Myc, and retinoblastoma protein (pRb), and the upregulation of p21([[ WAF1 ]]/CIP1) and p53.


<< Pinosylvin >> inhibited the proliferation of HCT 116 cells by arresting transition of cell cycle from G1 to S phase along with the downregulation of cyclin D1, cyclin E, cyclin A, cyclin dependent kinase 2 (CDK2), CDK4, c-Myc, and retinoblastoma protein (pRb), and the upregulation of p21(WAF1/[[ CIP1 ]]) and p53.


<< Pinosylvin >> inhibited the proliferation of HCT 116 cells by arresting transition of cell cycle from G1 to S phase along with the downregulation of cyclin D1, cyclin E, cyclin A, cyclin dependent kinase 2 (CDK2), CDK4, c-Myc, and retinoblastoma protein (pRb), and the upregulation of p21(WAF1/CIP1) and [[ p53 ]].


<< Pinosylvin >> inhibited the proliferation of HCT 116 cells by arresting transition of cell cycle from G1 to S phase along with the downregulation of [[ cyclin D1 ]], cyclin E, cyclin A, cyclin dependent kinase 2 (CDK2), CDK4, c-Myc, and retinoblastoma protein (pRb), and the upregulation of p21(WAF1/CIP1) and p53.


<< Pinosylvin >> inhibited the proliferation of HCT 116 cells by arresting transition of cell cycle from G1 to S phase along with the downregulation of cyclin D1, [[ cyclin E ]], cyclin A, cyclin dependent kinase 2 (CDK2), CDK4, c-Myc, and retinoblastoma protein (pRb), and the upregulation of p21(WAF1/CIP1) and p53.


<< Pinosylvin >> inhibited the proliferation of HCT 116 cells by arresting transition of cell cycle from G1 to S phase along with the downregulation of cyclin D1, cyclin E, [[ cyclin A ]], cyclin dependent kinase 2 (CDK2), CDK4, c-Myc, and retinoblastoma protein (pRb), and the upregulation of p21(WAF1/CIP1) and p53.


<< Pinosylvin >> inhibited the proliferation of HCT 116 cells by arresting transition of cell cycle from G1 to S phase along with the downregulation of cyclin D1, cyclin E, cyclin A, [[ cyclin dependent kinase 2 ]] (CDK2), CDK4, c-Myc, and retinoblastoma protein (pRb), and the upregulation of p21(WAF1/CIP1) and p53.


<< Pinosylvin >> inhibited the proliferation of HCT 116 cells by arresting transition of cell cycle from G1 to S phase along with the downregulation of cyclin D1, cyclin E, cyclin A, cyclin dependent kinase 2 ([[ CDK2 ]]), CDK4, c-Myc, and retinoblastoma protein (pRb), and the upregulation of p21(WAF1/CIP1) and p53.


<< Pinosylvin >> inhibited the proliferation of HCT 116 cells by arresting transition of cell cycle from G1 to S phase along with the downregulation of cyclin D1, cyclin E, cyclin A, cyclin dependent kinase 2 (CDK2), [[ CDK4 ]], c-Myc, and retinoblastoma protein (pRb), and the upregulation of p21(WAF1/CIP1) and p53.


<< Pinosylvin >> inhibited the proliferation of HCT 116 cells by arresting transition of cell cycle from G1 to S phase along with the downregulation of cyclin D1, cyclin E, cyclin A, cyclin dependent kinase 2 (CDK2), CDK4, [[ c-Myc ]], and retinoblastoma protein (pRb), and the upregulation of p21(WAF1/CIP1) and p53.


<< Pinosylvin >> inhibited the proliferation of HCT 116 cells by arresting transition of cell cycle from G1 to S phase along with the downregulation of cyclin D1, cyclin E, cyclin A, cyclin dependent kinase 2 (CDK2), CDK4, c-Myc, and [[ retinoblastoma protein ]] (pRb), and the upregulation of p21(WAF1/CIP1) and p53.


<< Pinosylvin >> inhibited the proliferation of HCT 116 cells by arresting transition of cell cycle from G1 to S phase along with the downregulation of cyclin D1, cyclin E, cyclin A, cyclin dependent kinase 2 (CDK2), CDK4, c-Myc, and retinoblastoma protein ([[ pRb ]]), and the upregulation of p21(WAF1/CIP1) and p53.


<< Pinosylvin >> was also found to attenuate the activation of proteins involved in f[[ ocal adhesion kinase ]] (FAK)/c-Src/extracellular signal-regulated kinase (ERK) signaling, and phosphoinositide 3-kinase (PI3K)/Akt/ glycogen synthase kinase 3β (GSK-3β) signaling pathway.


<< Pinosylvin >> was also found to attenuate the activation of proteins involved in focal adhesion kinase ([[ FAK ]])/c-Src/extracellular signal-regulated kinase (ERK) signaling, and phosphoinositide 3-kinase (PI3K)/Akt/ glycogen synthase kinase 3β (GSK-3β) signaling pathway.


<< Pinosylvin >> was also found to attenuate the activation of proteins involved in focal adhesion kinase (FAK)/[[ c-Src ]]/extracellular signal-regulated kinase (ERK) signaling, and phosphoinositide 3-kinase (PI3K)/Akt/ glycogen synthase kinase 3β (GSK-3β) signaling pathway.


<< Pinosylvin >> was also found to attenuate the activation of proteins involved in focal adhesion kinase (FAK)/c-Src/[[ extracellular signal-regulated kinase ]] (ERK) signaling, and phosphoinositide 3-kinase (PI3K)/Akt/ glycogen synthase kinase 3β (GSK-3β) signaling pathway.


<< Pinosylvin >> was also found to attenuate the activation of proteins involved in focal adhesion kinase (FAK)/c-Src/extracellular signal-regulated kinase ([[ ERK ]]) signaling, and phosphoinositide 3-kinase (PI3K)/Akt/ glycogen synthase kinase 3β (GSK-3β) signaling pathway.


<< Pinosylvin >> was also found to attenuate the activation of proteins involved in focal adhesion kinase (FAK)/c-Src/extracellular signal-regulated kinase (ERK) signaling, and [[ phosphoinositide 3-kinase ]] (PI3K)/Akt/ glycogen synthase kinase 3β (GSK-3β) signaling pathway.


<< Pinosylvin >> was also found to attenuate the activation of proteins involved in focal adhesion kinase (FAK)/c-Src/extracellular signal-regulated kinase (ERK) signaling, and phosphoinositide 3-kinase ([[ PI3K ]])/Akt/ glycogen synthase kinase 3β (GSK-3β) signaling pathway.


<< Pinosylvin >> was also found to attenuate the activation of proteins involved in focal adhesion kinase (FAK)/c-Src/extracellular signal-regulated kinase (ERK) signaling, and phosphoinositide 3-kinase (PI3K)/[[ Akt ]]/ glycogen synthase kinase 3β (GSK-3β) signaling pathway.


<< Pinosylvin >> was also found to attenuate the activation of proteins involved in focal adhesion kinase (FAK)/c-Src/extracellular signal-regulated kinase (ERK) signaling, and phosphoinositide 3-kinase (PI3K)/Akt/ [[ glycogen synthase kinase 3β ]] (GSK-3β) signaling pathway.


<< Pinosylvin >> was also found to attenuate the activation of proteins involved in focal adhesion kinase (FAK)/c-Src/extracellular signal-regulated kinase (ERK) signaling, and phosphoinositide 3-kinase (PI3K)/Akt/ glycogen synthase kinase 3β ([[ GSK-3β ]]) signaling pathway.


Subsequently, << pinosylvin >> suppressed the nuclear translocation of [[ β-catenin ]], one of downstream molecules of PI3K/Akt/GSK-3β signaling, and these events led to the sequential downregulation of β-catenin-mediated transcription of target genes including BMP4, ID2, survivin, cyclin D1, MMP7, and c-Myc.


Subsequently, << pinosylvin >> suppressed the nuclear translocation of β-catenin, one of downstream molecules of [[ PI3K ]]/Akt/GSK-3β signaling, and these events led to the sequential downregulation of β-catenin-mediated transcription of target genes including BMP4, ID2, survivin, cyclin D1, MMP7, and c-Myc.


Subsequently, << pinosylvin >> suppressed the nuclear translocation of β-catenin, one of downstream molecules of PI3K/[[ Akt ]]/GSK-3β signaling, and these events led to the sequential downregulation of β-catenin-mediated transcription of target genes including BMP4, ID2, survivin, cyclin D1, MMP7, and c-Myc.


Subsequently, << pinosylvin >> suppressed the nuclear translocation of β-catenin, one of downstream molecules of PI3K/Akt/[[ GSK-3β ]] signaling, and these events led to the sequential downregulation of β-catenin-mediated transcription of target genes including BMP4, ID2, survivin, cyclin D1, MMP7, and c-Myc.


Subsequently, << pinosylvin >> suppressed the nuclear translocation of β-catenin, one of downstream molecules of PI3K/Akt/GSK-3β signaling, and these events led to the sequential downregulation of [[ β-catenin ]]-mediated transcription of target genes including BMP4, ID2, survivin, cyclin D1, MMP7, and c-Myc.


Subsequently, << pinosylvin >> suppressed the nuclear translocation of β-catenin, one of downstream molecules of PI3K/Akt/GSK-3β signaling, and these events led to the sequential downregulation of β-catenin-mediated transcription of target genes including [[ BMP4 ]], ID2, survivin, cyclin D1, MMP7, and c-Myc.


Subsequently, << pinosylvin >> suppressed the nuclear translocation of β-catenin, one of downstream molecules of PI3K/Akt/GSK-3β signaling, and these events led to the sequential downregulation of β-catenin-mediated transcription of target genes including BMP4, [[ ID2 ]], survivin, cyclin D1, MMP7, and c-Myc.


Subsequently, << pinosylvin >> suppressed the nuclear translocation of β-catenin, one of downstream molecules of PI3K/Akt/GSK-3β signaling, and these events led to the sequential downregulation of β-catenin-mediated transcription of target genes including BMP4, ID2, [[ survivin ]], cyclin D1, MMP7, and c-Myc.


Subsequently, << pinosylvin >> suppressed the nuclear translocation of β-catenin, one of downstream molecules of PI3K/Akt/GSK-3β signaling, and these events led to the sequential downregulation of β-catenin-mediated transcription of target genes including BMP4, ID2, survivin, [[ cyclin D1 ]], MMP7, and c-Myc.


Subsequently, << pinosylvin >> suppressed the nuclear translocation of β-catenin, one of downstream molecules of PI3K/Akt/GSK-3β signaling, and these events led to the sequential downregulation of β-catenin-mediated transcription of target genes including BMP4, ID2, survivin, cyclin D1, [[ MMP7 ]], and c-Myc.


Subsequently, << pinosylvin >> suppressed the nuclear translocation of β-catenin, one of downstream molecules of PI3K/Akt/GSK-3β signaling, and these events led to the sequential downregulation of β-catenin-mediated transcription of target genes including BMP4, ID2, survivin, cyclin D1, MMP7, and [[ c-Myc ]].


Overall, higher alcohol production was reduced by << ammonium >> supplementation, and this can be correlated with a general downregulation of genes encoding [[ decarboxylases ]] and dehydrogenases of the Ehrlich pathway.


Overall, higher alcohol production was reduced by << ammonium >> supplementation, and this can be correlated with a general downregulation of genes encoding decarboxylases and [[ dehydrogenases ]] of the Ehrlich pathway.


Novel analgesic/anti-inflammatory agents: 1,5-diarylpyrrole nitrooxyalkyl ethers and related compounds as << cyclooxygenase-2 >> inhibiting [[ nitric oxide ]] donors.


Novel analgesic/anti-inflammatory agents: << 1,5-diarylpyrrole nitrooxyalkyl ethers >> and related compounds as [[ cyclooxygenase-2 ]] inhibiting nitric oxide donors.


New classes of << pyrrole >>-derived nitrooxyalkyl inverse esters, carbonates, and ethers (7-10) as [[ COX-2 ]] selective inhibitors and NO donors were synthesized and are herein reported.


New classes of pyrrole-derived << nitrooxyalkyl >> inverse esters, carbonates, and ethers (7-10) as [[ COX-2 ]] selective inhibitors and NO donors were synthesized and are herein reported.


New classes of pyrrole-derived nitrooxyalkyl inverse << esters >>, carbonates, and ethers (7-10) as [[ COX-2 ]] selective inhibitors and NO donors were synthesized and are herein reported.


New classes of pyrrole-derived nitrooxyalkyl inverse esters, << carbonates >>, and ethers (7-10) as [[ COX-2 ]] selective inhibitors and NO donors were synthesized and are herein reported.


New classes of pyrrole-derived nitrooxyalkyl inverse esters, carbonates, and << ethers >> (7-10) as [[ COX-2 ]] selective inhibitors and NO donors were synthesized and are herein reported.


<< Nitrooxy >> derivatives showed NO-dependent vasorelaxing properties, while most of the compounds proved to be very potent and selective [[ COX-2 ]] inhibitors in in vitro experimental models.


The clinical profile of the << angiotensin II receptor >> blocker [[ eprosartan ]].


In clinical trials << eprosartan >> has proven to be at least as effective as the [[ ACE ]] inhibitor enalapril in reducing BP, but with a significantly lower incidence of side effects.


A significant decrease of << aspartate aminotransferase >>, alanine aminotransferase, lactate dehydrogenase (LDH) activities and glutathione (GSH) levels and an increase of malondialdehyde (MDA) quantity was observed after [[ CCl4 ]] and PC administration alone.


A significant decrease of aspartate aminotransferase, << alanine aminotransferase >>, lactate dehydrogenase (LDH) activities and glutathione (GSH) levels and an increase of malondialdehyde (MDA) quantity was observed after [[ CCl4 ]] and PC administration alone.


A significant decrease of aspartate aminotransferase, alanine aminotransferase, << lactate dehydrogenase >> (LDH) activities and glutathione (GSH) levels and an increase of malondialdehyde (MDA) quantity was observed after [[ CCl4 ]] and PC administration alone.


A significant decrease of aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase (<< LDH >>) activities and glutathione (GSH) levels and an increase of malondialdehyde (MDA) quantity was observed after [[ CCl4 ]] and PC administration alone.


In the CCl4 hepatotoxicity model, pre-treatment with PSM or << silymarin >> resulted in significantly increased activities of [[ ethylmorphine-N-demethylase ]] and aniline 4-hydroxylase activity and cytochrome P450, compared to the CCl4 only group.


In the CCl4 hepatotoxicity model, pre-treatment with PSM or << silymarin >> resulted in significantly increased activities of ethylmorphine-N-demethylase and [[ aniline 4-hydroxylase ]] activity and cytochrome P450, compared to the CCl4 only group.


In the CCl4 hepatotoxicity model, pre-treatment with PSM or << silymarin >> resulted in significantly increased activities of ethylmorphine-N-demethylase and aniline 4-hydroxylase activity and [[ cytochrome P450 ]], compared to the CCl4 only group.


In the CCl4 hepatotoxicity model, pre-treatment with PSM or silymarin resulted in significantly increased activities of << ethylmorphine-N-demethylase >> and aniline 4-hydroxylase activity and cytochrome P450, compared to the [[ CCl4 ]] only group.


In the CCl4 hepatotoxicity model, pre-treatment with PSM or silymarin resulted in significantly increased activities of ethylmorphine-N-demethylase and << aniline 4-hydroxylase >> activity and cytochrome P450, compared to the [[ CCl4 ]] only group.


In the CCl4 hepatotoxicity model, pre-treatment with PSM or silymarin resulted in significantly increased activities of ethylmorphine-N-demethylase and aniline 4-hydroxylase activity and << cytochrome P450 >>, compared to the [[ CCl4 ]] only group.


In vitro inhibition of << diacylglycerol acyltransferase >> by [[ prenylflavonoids ]] from Sophora flavescens.


Four prenylflavonoids, kurarinone ( 1), a chalcone of 1, << kuraridin >> ( 2), kurarinol ( 3), kushenol H ( 4) and kushenol K ( 5) isolated from the roots of Sophora flavescens were investigated for their inhibitory effects on [[ diacylglycerol acyltransferase ]] (DGAT).


Four prenylflavonoids, kurarinone ( 1), a chalcone of 1, << kuraridin >> ( 2), kurarinol ( 3), kushenol H ( 4) and kushenol K ( 5) isolated from the roots of Sophora flavescens were investigated for their inhibitory effects on diacylglycerol acyltransferase ([[ DGAT ]]).


Four prenylflavonoids, kurarinone ( 1), a chalcone of 1, kuraridin ( 2), << kurarinol >> ( 3), kushenol H ( 4) and kushenol K ( 5) isolated from the roots of Sophora flavescens were investigated for their inhibitory effects on [[ diacylglycerol acyltransferase ]] (DGAT).


Four prenylflavonoids, kurarinone ( 1), a chalcone of 1, kuraridin ( 2), << kurarinol >> ( 3), kushenol H ( 4) and kushenol K ( 5) isolated from the roots of Sophora flavescens were investigated for their inhibitory effects on diacylglycerol acyltransferase ([[ DGAT ]]).


Four prenylflavonoids, kurarinone ( 1), a chalcone of 1, kuraridin ( 2), kurarinol ( 3), << kushenol H >> ( 4) and kushenol K ( 5) isolated from the roots of Sophora flavescens were investigated for their inhibitory effects on [[ diacylglycerol acyltransferase ]] (DGAT).


Four prenylflavonoids, kurarinone ( 1), a chalcone of 1, kuraridin ( 2), kurarinol ( 3), << kushenol H >> ( 4) and kushenol K ( 5) isolated from the roots of Sophora flavescens were investigated for their inhibitory effects on diacylglycerol acyltransferase ([[ DGAT ]]).


Four prenylflavonoids, kurarinone ( 1), a chalcone of 1, kuraridin ( 2), kurarinol ( 3), kushenol H ( 4) and << kushenol K >> ( 5) isolated from the roots of Sophora flavescens were investigated for their inhibitory effects on [[ diacylglycerol acyltransferase ]] (DGAT).


Four prenylflavonoids, kurarinone ( 1), a chalcone of 1, kuraridin ( 2), kurarinol ( 3), kushenol H ( 4) and << kushenol K >> ( 5) isolated from the roots of Sophora flavescens were investigated for their inhibitory effects on diacylglycerol acyltransferase ([[ DGAT ]]).


Four prenylflavonoids, << kurarinone >> ( 1), a chalcone of 1, kuraridin ( 2), kurarinol ( 3), kushenol H ( 4) and kushenol K ( 5) isolated from the roots of Sophora flavescens were investigated for their inhibitory effects on [[ diacylglycerol acyltransferase ]] (DGAT).


Four prenylflavonoids, << kurarinone >> ( 1), a chalcone of 1, kuraridin ( 2), kurarinol ( 3), kushenol H ( 4) and kushenol K ( 5) isolated from the roots of Sophora flavescens were investigated for their inhibitory effects on diacylglycerol acyltransferase ([[ DGAT ]]).


Four prenylflavonoids, kurarinone ( 1), a << chalcone >> of 1, kuraridin ( 2), kurarinol ( 3), kushenol H ( 4) and kushenol K ( 5) isolated from the roots of Sophora flavescens were investigated for their inhibitory effects on [[ diacylglycerol acyltransferase ]] (DGAT).


Four prenylflavonoids, kurarinone ( 1), a << chalcone >> of 1, kuraridin ( 2), kurarinol ( 3), kushenol H ( 4) and kushenol K ( 5) isolated from the roots of Sophora flavescens were investigated for their inhibitory effects on diacylglycerol acyltransferase ([[ DGAT ]]).


Four << prenylflavonoids >>, kurarinone ( 1), a chalcone of 1, kuraridin ( 2), kurarinol ( 3), kushenol H ( 4) and kushenol K ( 5) isolated from the roots of Sophora flavescens were investigated for their inhibitory effects on [[ diacylglycerol acyltransferase ]] (DGAT).


Four << prenylflavonoids >>, kurarinone ( 1), a chalcone of 1, kuraridin ( 2), kurarinol ( 3), kushenol H ( 4) and kushenol K ( 5) isolated from the roots of Sophora flavescens were investigated for their inhibitory effects on diacylglycerol acyltransferase ([[ DGAT ]]).


The << flavonoids >> inhibited [[ DGAT ]] activity in a dose-dependent manner with IC50 values of 10.9 microM ( 1), 9.8 microM ( 2), 8.6 microM ( 3), 142.0 microM ( 4) and 250 microM ( 5).


These data suggest that the << lavandulyl >> side chain and the position of the hydroxy group are important for high [[ DGAT ]] inhibitory activity.


These data suggest that the lavandulyl side chain and the position of the << hydroxy >> group are important for high [[ DGAT ]] inhibitory activity.


Dexamethasone (DXM) decreased the expression of CXCL-8, VEGF, and iNOS induced by reIL-4, while << 1400W dihydrochloride >> (1400W), a selective inhibitor of iNOS, decreased the expression of [[ E-selectin ]], VEGF, and iNOS.


Dexamethasone (DXM) decreased the expression of CXCL-8, VEGF, and iNOS induced by reIL-4, while << 1400W dihydrochloride >> (1400W), a selective inhibitor of iNOS, decreased the expression of E-selectin, [[ VEGF ]], and iNOS.


Dexamethasone (DXM) decreased the expression of CXCL-8, VEGF, and iNOS induced by reIL-4, while << 1400W dihydrochloride >> (1400W), a selective inhibitor of iNOS, decreased the expression of E-selectin, VEGF, and [[ iNOS ]].


Dexamethasone (DXM) decreased the expression of CXCL-8, VEGF, and iNOS induced by reIL-4, while 1400W dihydrochloride (<< 1400W >>), a selective inhibitor of iNOS, decreased the expression of [[ E-selectin ]], VEGF, and iNOS.


Dexamethasone (DXM) decreased the expression of CXCL-8, VEGF, and iNOS induced by reIL-4, while 1400W dihydrochloride (<< 1400W >>), a selective inhibitor of iNOS, decreased the expression of E-selectin, [[ VEGF ]], and iNOS.


Dexamethasone (DXM) decreased the expression of CXCL-8, VEGF, and iNOS induced by reIL-4, while 1400W dihydrochloride (<< 1400W >>), a selective inhibitor of iNOS, decreased the expression of E-selectin, VEGF, and [[ iNOS ]].


<< Dexamethasone >> (DXM) decreased the expression of [[ CXCL-8 ]], VEGF, and iNOS induced by reIL-4, while 1400W dihydrochloride (1400W), a selective inhibitor of iNOS, decreased the expression of E-selectin, VEGF, and iNOS.


<< Dexamethasone >> (DXM) decreased the expression of CXCL-8, [[ VEGF ]], and iNOS induced by reIL-4, while 1400W dihydrochloride (1400W), a selective inhibitor of iNOS, decreased the expression of E-selectin, VEGF, and iNOS.


<< Dexamethasone >> (DXM) decreased the expression of CXCL-8, VEGF, and [[ iNOS ]] induced by reIL-4, while 1400W dihydrochloride (1400W), a selective inhibitor of iNOS, decreased the expression of E-selectin, VEGF, and iNOS.


Dexamethasone (<< DXM >>) decreased the expression of [[ CXCL-8 ]], VEGF, and iNOS induced by reIL-4, while 1400W dihydrochloride (1400W), a selective inhibitor of iNOS, decreased the expression of E-selectin, VEGF, and iNOS.


Dexamethasone (<< DXM >>) decreased the expression of CXCL-8, [[ VEGF ]], and iNOS induced by reIL-4, while 1400W dihydrochloride (1400W), a selective inhibitor of iNOS, decreased the expression of E-selectin, VEGF, and iNOS.


Dexamethasone (<< DXM >>) decreased the expression of CXCL-8, VEGF, and [[ iNOS ]] induced by reIL-4, while 1400W dihydrochloride (1400W), a selective inhibitor of iNOS, decreased the expression of E-selectin, VEGF, and iNOS.


Dexamethasone (DXM) decreased the expression of CXCL-8, VEGF, and iNOS induced by reIL-4, while << 1400W dihydrochloride >> (1400W), a selective inhibitor of [[ iNOS ]], decreased the expression of E-selectin, VEGF, and iNOS.


Dexamethasone (DXM) decreased the expression of CXCL-8, VEGF, and iNOS induced by reIL-4, while 1400W dihydrochloride (<< 1400W >>), a selective inhibitor of [[ iNOS ]], decreased the expression of E-selectin, VEGF, and iNOS.


<< DXM >> and 1400W attenuated the mRNA expression of [[ E-selectin ]] and iNOS induced by the costimulation of reIL-4, reTNF-alpha, and LPS.


<< DXM >> and 1400W attenuated the mRNA expression of E-selectin and [[ iNOS ]] induced by the costimulation of reIL-4, reTNF-alpha, and LPS.


DXM and << 1400W >> attenuated the mRNA expression of [[ E-selectin ]] and iNOS induced by the costimulation of reIL-4, reTNF-alpha, and LPS.


DXM and << 1400W >> attenuated the mRNA expression of E-selectin and [[ iNOS ]] induced by the costimulation of reIL-4, reTNF-alpha, and LPS.


The beneficial role of << 17beta-estradiol >> on blood pressure, cardiac hypertrophy, vascular [[ osteopontin ]] expression, perivascular fibrosis, and impaired NO-dependent relaxation of isolated aortic rings was completely abrogated by coadministration of medroxyprogesterone acetate.


The beneficial role of 17beta-estradiol on blood pressure, cardiac hypertrophy, vascular << osteopontin >> expression, perivascular fibrosis, and impaired NO-dependent relaxation of isolated aortic rings was completely abrogated by coadministration of [[ medroxyprogesterone acetate ]].


At a low pH (pH 7.4), but not pH 7.9, << ifenprodil >> reduces the mean open time of [[ GluN1 ]]/GluN2B receptors, which may be responsible for its usefulness as a context-dependent inhibitor in conditions like ischemia and stroke, when the pH of the extracellular milieu becomes acidic.


At a low pH (pH 7.4), but not pH 7.9, << ifenprodil >> reduces the mean open time of GluN1/[[ GluN2B ]] receptors, which may be responsible for its usefulness as a context-dependent inhibitor in conditions like ischemia and stroke, when the pH of the extracellular milieu becomes acidic.


Pharmacological doses of the << mTOR >> inhibitor [[ rapamycin ]] reduce albuminura in diabetes.


High << glucose >> (HG) induces apoptosis of podocytes, inhibits AMPK activation, inactivates tuberin and activates [[ mTOR ]].


High << glucose >> (HG) induces apoptosis of podocytes, inhibits AMPK activation, inactivates [[ tuberin ]] and activates mTOR.


High << glucose >> (HG) induces apoptosis of podocytes, inhibits [[ AMPK ]] activation, inactivates tuberin and activates mTOR.


Inhibition of mTOR by low dose << rapamycin >> decreases HG-induced [[ Nox4 ]] and Nox1, NADPH oxidase activity and podocyte apoptosis.


Inhibition of mTOR by low dose << rapamycin >> decreases HG-induced Nox4 and [[ Nox1 ]], NADPH oxidase activity and podocyte apoptosis.


Inhibition of << mTOR >> by low dose [[ rapamycin ]] decreases HG-induced Nox4 and Nox1, NADPH oxidase activity and podocyte apoptosis.


Inhibition of mTOR by low dose << rapamycin >> decreases HG-induced Nox4 and Nox1, [[ NADPH oxidase ]] activity and podocyte apoptosis.


Inhibition of << mTOR >> by small dose of [[ rapamycin ]] reduces podocyte apoptosis, attenuates glomerular injury and albuminuria.


Systemic administration of << beta2-adrenoceptor >> agonists, [[ formoterol ]] and salmeterol, elicit skeletal muscle hypertrophy in rats at micromolar doses.


Systemic administration of << beta2-adrenoceptor >> agonists, formoterol and [[ salmeterol ]], elicit skeletal muscle hypertrophy in rats at micromolar doses.


Two beta(2)-agonists, << formoterol >> and salmeterol, are approved for treating asthma and have an extended duration of action and increased safety, associated with greater [[ beta(2)-adrenoceptor ]] selectivity.


Two beta(2)-agonists, formoterol and << salmeterol >>, are approved for treating asthma and have an extended duration of action and increased safety, associated with greater [[ beta(2)-adrenoceptor ]] selectivity.


A dose of 25 microg kg(-1) day(-1) of << formoterol >> elicited greater EDL and soleus hypertrophy than salmeterol, but resulted in similar [[ beta-adrenoceptor ]] downregulation.


A dose of 25 microg kg(-1) day(-1) of formoterol elicited greater EDL and soleus hypertrophy than << salmeterol >>, but resulted in similar [[ beta-adrenoceptor ]] downregulation.


Clinical utility of << acarbose >>, an [[ alpha-glucosidase ]] inhibitor in cardiometabolic disorders.


<< Acarbose >>, an [[ alpha-glucosidase ]] inhibitor, delays the absorption of carbohydrate from the small intestine, thereby reducing postprandial hyperglycemia.


The values of mean corpuscular hemoglobin concentration and mean corpuscular << hemoglobin >> increased in the [[ STX ]] group.


The values of mean corpuscular << hemoglobin >> concentration and mean corpuscular hemoglobin increased in the [[ STX ]] group.


First, we showed that intracerebroventricular administration of << glucose >> in rats increases [[ DBI ]] expression in hypothalamic glial-like tanycytes.


On phosphorylation of << Ser40 >> by [[ protein kinase A ]], the affinity for H4biopterin increased ([S]0.5 = 11 +/- 2 microM) and the negative cooperativity was amplified (h = 0.27 +/- 0.03).


Disposition of a specific << cyclooxygenase-2 >> inhibitor, [[ valdecoxib ]], in human.


<< Valdecoxib >> is a potent and specific inhibitor of [[ cyclooxygenase-2 ]], which is used for the treatment of rheumatoid arthritis, osteoarthritis, and the dysmenorrhea pain.


In mechanistic studies, << Silibinin >> decreased the protein level of [[ p34cdc2 ]], which might be the possible molecular mechanism of Silibinin efficacy on the growth inhibition in SGC-7901 cells.


In addition, << Silibinin >> caused an increase in [[ p53 ]] and p21 protein level as well as mRNA levels.


In addition, << Silibinin >> caused an increase in p53 and [[ p21 ]] protein level as well as mRNA levels.


4-Hydroxynonenal (<< 4-HNE >>) is a mutagenic alpha,beta-unsaturated aldehyde produced during oxidative injury that is conjugated by several [[ glutathione S-transferase ]] (GST) isoforms.


4-Hydroxynonenal (<< 4-HNE >>) is a mutagenic alpha,beta-unsaturated aldehyde produced during oxidative injury that is conjugated by several glutathione S-transferase ([[ GST ]]) isoforms.


<< 4-Hydroxynonenal >> (4-HNE) is a mutagenic alpha,beta-unsaturated aldehyde produced during oxidative injury that is conjugated by several [[ glutathione S-transferase ]] (GST) isoforms.


<< 4-Hydroxynonenal >> (4-HNE) is a mutagenic alpha,beta-unsaturated aldehyde produced during oxidative injury that is conjugated by several glutathione S-transferase ([[ GST ]]) isoforms.


4-Hydroxynonenal (4-HNE) is a mutagenic << alpha,beta-unsaturated aldehyde >> produced during oxidative injury that is conjugated by several [[ glutathione S-transferase ]] (GST) isoforms.


4-Hydroxynonenal (4-HNE) is a mutagenic << alpha,beta-unsaturated aldehyde >> produced during oxidative injury that is conjugated by several glutathione S-transferase ([[ GST ]]) isoforms.


The alpha class << human GSTA4-4 >> enzyme (hGSTA4-4) has a particularly high catalytic efficiency toward [[ 4-HNE ]] conjugation.


The alpha class human GSTA4-4 enzyme (<< hGSTA4-4 >>) has a particularly high catalytic efficiency toward [[ 4-HNE ]] conjugation.


HepG2 cells transfected with an hGSTA4 vector construct exhibited high steady-state hGSTA4 mRNA, high << GST-4 >>[[ 4-HNE ]] catalytic activities, but lower basal glutathione (GSH) concentrations relative to insert-free vector (control) cells.


Specifically, << hGSTA4 >> cells had significantly higher GSH concentrations when exposed to 5-15 microM [[ 4-HNE ]], but not at 20 microM 4-HNE, suggesting extensive GSH utilization at high concentrations of 4-HNE.


Specifically, << hGSTA4 >> cells had significantly higher GSH concentrations when exposed to 5-15 microM 4-HNE, but not at 20 microM [[ 4-HNE ]], suggesting extensive GSH utilization at high concentrations of 4-HNE.


In summary, our data indicates that over-expression of hGSTA4 at levels conferring high << GST >>-[[ 4-HNE ]] conjugating activity confers a partial growth advantage to HepG2 cells and protects against 4-HNE oxidative injury.


However, the loss of proliferative capacity of << hGSTA4 >> cells challenged with levels of [[ 4-HNE ]] associated with severe oxidative stress indicates a role of other aldehyde metabolizing enzymes, and/or GSH-electrophile transporter proteins, in providing full cellular protection against 4-HNE toxicity.


OBJECTIVE: Preclinical evaluation of << DRF 2655 >>, a peroxisome proliferator-activated receptor alpha (PPARalpha) and [[ PPARgamma ]] agonist, as a body-weight lowering, hypolipidemic and euglycemic agent.


OBJECTIVE: Preclinical evaluation of << DRF 2655 >>, a [[ peroxisome proliferator-activated receptor alpha ]] (PPARalpha) and PPARgamma agonist, as a body-weight lowering, hypolipidemic and euglycemic agent.


OBJECTIVE: Preclinical evaluation of << DRF 2655 >>, a peroxisome proliferator-activated receptor alpha ([[ PPARalpha ]]) and PPARgamma agonist, as a body-weight lowering, hypolipidemic and euglycemic agent.


RESULTS: << DRF 2655 >> showed concentration-dependent transactivation of [[ PPARalpha ]] and PPARgamma.


RESULTS: << DRF 2655 >> showed concentration-dependent transactivation of PPARalpha and [[ PPARgamma ]].


db/db mice treated with << DRF 2655 >> showed 5- and 3.6-fold inhibition in phosphoenolpyruvate carboxykinase and glucose 6-phosphatase activity and 651% and 77% increases in the beta-oxidation enzymes [[ carnitine palmitoyltransferase ]] and carnitine acetyltransferase, respectively.


db/db mice treated with << DRF 2655 >> showed 5- and 3.6-fold inhibition in phosphoenolpyruvate carboxykinase and glucose 6-phosphatase activity and 651% and 77% increases in the beta-oxidation enzymes carnitine palmitoyltransferase and [[ carnitine acetyltransferase ]], respectively.


db/db mice treated with << DRF 2655 >> showed 5- and 3.6-fold inhibition in [[ phosphoenolpyruvate carboxykinase ]] and glucose 6-phosphatase activity and 651% and 77% increases in the beta-oxidation enzymes carnitine palmitoyltransferase and carnitine acetyltransferase, respectively.


db/db mice treated with << DRF 2655 >> showed 5- and 3.6-fold inhibition in phosphoenolpyruvate carboxykinase and [[ glucose 6-phosphatase ]] activity and 651% and 77% increases in the beta-oxidation enzymes carnitine palmitoyltransferase and carnitine acetyltransferase, respectively.


The enzyme << cyclo-oxygenase >> catalyses the oxygenation of arachidonic acid, leading to the formation of [[ prostaglandins ]].


The enzyme << cyclo-oxygenase >> catalyses the oxygenation of [[ arachidonic acid ]], leading to the formation of prostaglandins.


<< hCOX-1 >> had a specific activity of 18.8 mumol of O2/mg with a Km of 13.8 microM for [[ arachidonate ]] and Vmax. of 1500 nmol of O2/nmol of enzyme, whereas hCOX-2 had a specific activity of 12.2 mumol of O2/mg with a Km of 8.7 microM for arachidonate and a Vmax. of 1090 nmol of O2/nmol of enzyme.


hCOX-1 had a specific activity of 18.8 mumol of O2/mg with a Km of 13.8 microM for arachidonate and Vmax. of 1500 nmol of O2/nmol of enzyme, whereas << hCOX-2 >> had a specific activity of 12.2 mumol of O2/mg with a Km of 8.7 microM for [[ arachidonate ]] and a Vmax. of 1090 nmol of O2/nmol of enzyme.


<< Indomethacin >> inhibited both [[ hCOX-1 ]] and hCOX-2, whereas NS-398 and Dup-697 selectively inhibited hCOX-2.


<< Indomethacin >> inhibited both hCOX-1 and [[ hCOX-2 ]], whereas NS-398 and Dup-697 selectively inhibited hCOX-2.


Indomethacin inhibited both hCOX-1 and hCOX-2, whereas << NS-398 >> and Dup-697 selectively inhibited [[ hCOX-2 ]].


Indomethacin inhibited both hCOX-1 and hCOX-2, whereas NS-398 and << Dup-697 >> selectively inhibited [[ hCOX-2 ]].


Both << NS-398 >> and Dup-697 exhibited time-dependent inactivation of [[ hCOX-2 ]], as did indomethacin on both enzymes.


Both NS-398 and << Dup-697 >> exhibited time-dependent inactivation of [[ hCOX-2 ]], as did indomethacin on both enzymes.


Both NS-398 and Dup-697 exhibited time-dependent inactivation of << hCOX-2 >>, as did [[ indomethacin ]] on both enzymes.


The competitive inhibitor of << hCOX-1 >>, [[ mefenamic acid ]], also displayed competitive inhibition of hCOX-2.


The competitive inhibitor of hCOX-1, << mefenamic acid >>, also displayed competitive inhibition of [[ hCOX-2 ]].


<< Doxycycline >> was shown to decrease cerebral [[ MMP-9 ]] activities and angiogenesis induced by vascular endothelial growth factor (VEGF).


<< Doxycycline >> was shown to decrease cerebral MMP-9 activities and angiogenesis induced by [[ vascular endothelial growth factor ]] (VEGF).


<< Doxycycline >> was shown to decrease cerebral MMP-9 activities and angiogenesis induced by vascular endothelial growth factor ([[ VEGF ]]).


Our results have shown that << MMP-9 >> messenger ribonucleic acid (mRNA) expression was inhibited by [[ doxycycline ]] starting at 10 mg/kg/day (P<0.02).


<< Minocycline >> showed more potent inhibition on [[ MMP-9 ]] mRNA expression, starting at 1 (P<0.005) and further at more than 30 (P<0.001) mg/kg/day.


At the enzymatic activity level, << doxycycline >> started to suppress [[ MMP-9 ]] activity at 5 mg/kg/day (P<0.001), while minocycline had an effect at a lower dose, 1 mg/kg/day (P<0.02).


We also assessed the potential relevant signaling pathway in vitro to elucidate the mechanisms underlying the << MMP-9 >> inhibition by [[ tetracyclines ]].


In vitro, << minocycline >>, but not doxycycline, inhibits [[ MMP-9 ]], at least in part, via the extracellular signaling-related kinase 1/2 (ERK1/2)-mediated pathway.


In vitro, minocycline, but not << doxycycline >>, inhibits [[ MMP-9 ]], at least in part, via the extracellular signaling-related kinase 1/2 (ERK1/2)-mediated pathway.


This study provided the evidence that the << tetracyclines >> inhibit stimulated cerebral [[ MMP-9 ]] at multiple levels and are effective at very low doses, offering great potential for therapeutic use.


One major route involves the tetrahydrofolate (THF)-dependent activities of the << glycine decarboxylase complex >> (GDC, EC 2.1.1.10) and serine hydroxymethyltransferase (SHMT, EC 2.1.2.1) with [[ glycine ]] (Gly) as one-carbon (1-C) source.


One major route involves the tetrahydrofolate (THF)-dependent activities of the glycine decarboxylase complex (<< GDC >>, EC 2.1.1.10) and serine hydroxymethyltransferase (SHMT, EC 2.1.2.1) with [[ glycine ]] (Gly) as one-carbon (1-C) source.


One major route involves the tetrahydrofolate (THF)-dependent activities of the glycine decarboxylase complex (GDC, << EC 2.1.1.10 >>) and serine hydroxymethyltransferase (SHMT, EC 2.1.2.1) with [[ glycine ]] (Gly) as one-carbon (1-C) source.


One major route involves the tetrahydrofolate (THF)-dependent activities of the glycine decarboxylase complex (GDC, EC 2.1.1.10) and << serine hydroxymethyltransferase >> (SHMT, EC 2.1.2.1) with [[ glycine ]] (Gly) as one-carbon (1-C) source.


One major route involves the tetrahydrofolate (THF)-dependent activities of the glycine decarboxylase complex (GDC, EC 2.1.1.10) and serine hydroxymethyltransferase (<< SHMT >>, EC 2.1.2.1) with [[ glycine ]] (Gly) as one-carbon (1-C) source.


One major route involves the tetrahydrofolate (THF)-dependent activities of the glycine decarboxylase complex (GDC, EC 2.1.1.10) and serine hydroxymethyltransferase (SHMT, << EC 2.1.2.1 >>) with [[ glycine ]] (Gly) as one-carbon (1-C) source.


One major route involves the tetrahydrofolate (THF)-dependent activities of the << glycine decarboxylase complex >> (GDC, EC 2.1.1.10) and serine hydroxymethyltransferase (SHMT, EC 2.1.2.1) with glycine ([[ Gly ]]) as one-carbon (1-C) source.


One major route involves the tetrahydrofolate (THF)-dependent activities of the glycine decarboxylase complex (<< GDC >>, EC 2.1.1.10) and serine hydroxymethyltransferase (SHMT, EC 2.1.2.1) with glycine ([[ Gly ]]) as one-carbon (1-C) source.


One major route involves the tetrahydrofolate (THF)-dependent activities of the glycine decarboxylase complex (GDC, << EC 2.1.1.10 >>) and serine hydroxymethyltransferase (SHMT, EC 2.1.2.1) with glycine ([[ Gly ]]) as one-carbon (1-C) source.


One major route involves the tetrahydrofolate (THF)-dependent activities of the glycine decarboxylase complex (GDC, EC 2.1.1.10) and << serine hydroxymethyltransferase >> (SHMT, EC 2.1.2.1) with glycine ([[ Gly ]]) as one-carbon (1-C) source.


One major route involves the tetrahydrofolate (THF)-dependent activities of the glycine decarboxylase complex (GDC, EC 2.1.1.10) and serine hydroxymethyltransferase (<< SHMT >>, EC 2.1.2.1) with glycine ([[ Gly ]]) as one-carbon (1-C) source.


One major route involves the tetrahydrofolate (THF)-dependent activities of the glycine decarboxylase complex (GDC, EC 2.1.1.10) and serine hydroxymethyltransferase (SHMT, << EC 2.1.2.1 >>) with glycine ([[ Gly ]]) as one-carbon (1-C) source.


An alternative THF-dependent pathway involves the << C1-THF synthase >>/SHMT activities with [[ formate ]] as 1-C source.


An alternative THF-dependent pathway involves the C1-THF synthase/<< SHMT >> activities with [[ formate ]] as 1-C source.


Firstly, transgenic plants overexpressing << formate dehydrogenase >> (FDH, EC 1.2.1.2) were used to continue our previous studies on the function of FDH in [[ formate ]] metabolism.


Firstly, transgenic plants overexpressing formate dehydrogenase (<< FDH >>, EC 1.2.1.2) were used to continue our previous studies on the function of FDH in [[ formate ]] metabolism.


Firstly, transgenic plants overexpressing formate dehydrogenase (FDH, << EC 1.2.1.2 >>) were used to continue our previous studies on the function of FDH in [[ formate ]] metabolism.


Firstly, transgenic plants overexpressing formate dehydrogenase (FDH, EC 1.2.1.2) were used to continue our previous studies on the function of << FDH >> in [[ formate ]] metabolism.


We concluded that FDH has no direct role in the regulation of the above two pathways of Ser synthesis; the breakdown of formate to << CO(2) >> by the [[ FDH ]] reaction is the primary and preferred fate of the organic acid in Arabidopsis.


We concluded that FDH has no direct role in the regulation of the above two pathways of Ser synthesis; the breakdown of << formate >> to CO(2) by the [[ FDH ]] reaction is the primary and preferred fate of the organic acid in Arabidopsis.


The ratio between the GDC/<< SHMT >> and C1-THF synthase/SHMT pathways of [[ Ser ]] synthesis from [alpha-(13)C]Gly and [(13)C]formate, respectively, in Arabidopsis shoots was 21 : 1; in roots, 9 : 1.


The ratio between the GDC/SHMT and C1-THF synthase/<< SHMT >> pathways of [[ Ser ]] synthesis from [alpha-(13)C]Gly and [(13)C]formate, respectively, in Arabidopsis shoots was 21 : 1; in roots, 9 : 1.


The ratio between the << GDC >>/SHMT and C1-THF synthase/SHMT pathways of Ser synthesis from [[ [alpha-(13)C]Gly ]] and [(13)C]formate, respectively, in Arabidopsis shoots was 21 : 1; in roots, 9 : 1.


The ratio between the GDC/SHMT and << C1-THF synthase >>/SHMT pathways of Ser synthesis from [alpha-(13)C]Gly and [[ [(13)C]formate ]], respectively, in Arabidopsis shoots was 21 : 1; in roots, 9 : 1.


On the other hand, the accumulation of << Ser >> through the C1-THF synthase/[[ SHMT ]] pathway in glyD plants was 2.5-fold greater than that in WT plants.


BACKGROUND: << Rivastigmine >> is a carbamate drug designed to inhibit both [[ acetylcholinesterase ]] and butyrylcholinesterase by reversibly covalently bonding to these enzymes.


BACKGROUND: << Rivastigmine >> is a carbamate drug designed to inhibit both acetylcholinesterase and [[ butyrylcholinesterase ]] by reversibly covalently bonding to these enzymes.


BACKGROUND: Rivastigmine is a << carbamate >> drug designed to inhibit both [[ acetylcholinesterase ]] and butyrylcholinesterase by reversibly covalently bonding to these enzymes.


BACKGROUND: Rivastigmine is a << carbamate >> drug designed to inhibit both acetylcholinesterase and [[ butyrylcholinesterase ]] by reversibly covalently bonding to these enzymes.


<< Topotecan >> is a [[ topoisomerase I ]] inhibitor which is currently evaluated as an adjuvant agent for malignant glioma.


High << p53 >> protein levels, but not genetic or functional p53 status, were associated with increased [[ topotecan ]]-induced DNA/topoisomerase I complex formation.


<< Amiloride >> is a specific inhibitor of [[ uPA ]] but does not inhibit tPA.


The inhibitory effect of endothelin-1 on the contraction induced by 5-HT is abolished by deendothelialization, by the << endothelin ET(B) receptor >> antagonist [[ RES 701-1 ]], by indomethacin, or by glibenclamide.


The potentiation of the contractile effect induced by 5-HT is only somewhat modified by deendothelialization, but abolished by the << thromboxane A2 receptor >> antagonists [[ GR32191 ]] and ridogrel.


The potentiation of the contractile effect induced by 5-HT is only somewhat modified by deendothelialization, but abolished by the << thromboxane A2 receptor >> antagonists GR32191 and [[ ridogrel ]].


A novel class of << quinoxalines >> has been discovered as antagonists of the [[ IgG ]]:FcRn protein-protein interaction through optimization of a hit derived from a virtual ligand-based screen.


A novel class of << quinoxalines >> has been discovered as antagonists of the IgG:[[ FcRn ]] protein-protein interaction through optimization of a hit derived from a virtual ligand-based screen.


<< Agmatine >>, locally synthesized, is an endogenous agonist at [[ imidazoline receptors ]], a noncatecholamine ligand at alpha 2-adrenergic receptors and may act as a neurotransmitter.


(S)-3-(Aminomethyl)-7-(3-hydroxypropoxy)-1-hydroxy-1,3-dihydro-2,1-benzoxaborole (<< GSK2251052 >>) is a novel boron-containing antibiotic that inhibits [[ bacterial leucyl tRNA synthetase ]], and that has been in development for the treatment of serious Gram-negative infections.


<< (S)-3-(Aminomethyl)-7-(3-hydroxypropoxy)-1-hydroxy-1,3-dihydro-2,1-benzoxaborole >> (GSK2251052) is a novel boron-containing antibiotic that inhibits [[ bacterial leucyl tRNA synthetase ]], and that has been in development for the treatment of serious Gram-negative infections.


A combination of in vitro metabolism experiments and a pharmacokinetic study in monkeys with the inhibitor << 4-methylpyrazole >> provided strong evidence that [[ alcohol dehydrogenase ]], potentially in association with aldehyde dehydrogenase, is the primary enzyme involved in the formation of the M3 metabolite.


In functional transport assays, we found that one of the identified molecules, ATM7, increased the reuptake of << serotonin >>, possibly by facilitating the interaction of serotonin with transport-ready conformations of [[ SERT ]] when concentrations of serotonin were low and rate limiting.


In functional transport assays, we found that one of the identified molecules, ATM7, increased the reuptake of serotonin, possibly by facilitating the interaction of << serotonin >> with transport-ready conformations of [[ SERT ]] when concentrations of serotonin were low and rate limiting.


In functional transport assays, we found that one of the identified molecules, ATM7, increased the reuptake of serotonin, possibly by facilitating the interaction of serotonin with transport-ready conformations of << SERT >> when concentrations of [[ serotonin ]] were low and rate limiting.


They display sensitivity to << TK >> inhibitors, including [[ gefitinib ]] and erlotinib.


They display sensitivity to << TK >> inhibitors, including gefitinib and [[ erlotinib ]].


Among the [Fe-S] cluster biosynthetic proteins are included a pyridoxal phosphate-dependent enzyme (<< NifS >>) that is involved in the activation of sulphur from [[ l-cysteine ]], and a molecular scaffold protein (NifU) upon which [Fe-S] cluster precursors are formed.


In addition, the number and area of << glutathione S-transferase placental form >> (GST-P) positive foci and proliferating cell nuclear antigen (PCNA) positive cell ratios in the hepatocytes were significantly increased in the male and female rats that were administered 100mg/kg [[ MEG ]] compared with the control animals.


In addition, the number and area of glutathione S-transferase placental form (<< GST-P >>) positive foci and proliferating cell nuclear antigen (PCNA) positive cell ratios in the hepatocytes were significantly increased in the male and female rats that were administered 100mg/kg [[ MEG ]] compared with the control animals.


In addition, the number and area of glutathione S-transferase placental form (GST-P) positive foci and << proliferating cell nuclear antigen >> (PCNA) positive cell ratios in the hepatocytes were significantly increased in the male and female rats that were administered 100mg/kg [[ MEG ]] compared with the control animals.


In addition, the number and area of glutathione S-transferase placental form (GST-P) positive foci and proliferating cell nuclear antigen (<< PCNA >>) positive cell ratios in the hepatocytes were significantly increased in the male and female rats that were administered 100mg/kg [[ MEG ]] compared with the control animals.


Consumption of << alcohol >> for 8weeks induced severe liver damage with increases in prognostic indicators such as [[ aspartate transaminase ]], alanine transaminase in serum whereas co-administration of CNF suppressed their increases.


Consumption of << alcohol >> for 8weeks induced severe liver damage with increases in prognostic indicators such as aspartate transaminase, [[ alanine transaminase ]] in serum whereas co-administration of CNF suppressed their increases.


Chronic consumption of << alcohol >> also stimulated abrupt increases in pro-inflammatory cytokines such as [[ nuclear factor (NF)-κB ]], tumor necrosis factor (TNF)-α and interleukin (IL)-1β in liver otherwise co-administration of CNF effectively suppressed production of these cytokines dose-dependently.


Chronic consumption of << alcohol >> also stimulated abrupt increases in pro-inflammatory cytokines such as nuclear factor (NF)-κB, [[ tumor necrosis factor (TNF)-α ]] and interleukin (IL)-1β in liver otherwise co-administration of CNF effectively suppressed production of these cytokines dose-dependently.


Chronic consumption of << alcohol >> also stimulated abrupt increases in pro-inflammatory cytokines such as nuclear factor (NF)-κB, tumor necrosis factor (TNF)-α and [[ interleukin (IL)-1β ]] in liver otherwise co-administration of CNF effectively suppressed production of these cytokines dose-dependently.


Dietary << EPA >>/DHA treatment restored endogenous biosynthesis of n-3 derived lipid mediators in obesity while attenuating adipose tissue inflammation and improving [[ insulin ]] sensitivity.


Dietary EPA/<< DHA >> treatment restored endogenous biosynthesis of n-3 derived lipid mediators in obesity while attenuating adipose tissue inflammation and improving [[ insulin ]] sensitivity.


Notably, << 17-HDHA >> treatment reduced adipose tissue expression of inflammatory cytokines, increased [[ adiponectin ]] expression and improved glucose tolerance parallel to insulin sensitivity in obese mice.


Notably, << 17-HDHA >> treatment reduced adipose tissue expression of inflammatory cytokines, increased adiponectin expression and improved glucose tolerance parallel to [[ insulin ]] sensitivity in obese mice.


Notably, << 17-HDHA >> treatment reduced adipose tissue expression of inflammatory [[ cytokines ]], increased adiponectin expression and improved glucose tolerance parallel to insulin sensitivity in obese mice.


Furthermore, we validated the inhibition of << GSK-3β >>/NF-κB signaling following [[ cinobufagin ]] treatment.


Furthermore, we validated the inhibition of GSK-3β/<< NF-κB >> signaling following [[ cinobufagin ]] treatment.


Western blots showed a decrease in nuclear p65 protein expression after exposure to different concentrations of << cinobufagin >>, while the phosphorylation of [[ GSK-3β ]] was simultaneously increased.


Western blots showed a decrease in nuclear << p65 >> protein expression after exposure to different concentrations of [[ cinobufagin ]], while the phosphorylation of GSK-3β was simultaneously increased.


Transduction with constitutively active forms of GSK-3β could protect against the downregulation of p65 and upregulation of cleaved-<< PARP >> that are induced by [[ cinobufagin ]] treatment.


Transduction with constitutively active forms of GSK-3β could protect against the downregulation of << p65 >> and upregulation of cleaved-PARP that are induced by [[ cinobufagin ]] treatment.


However, combined treatment with << cinobufagin >> and SB216367 resulted in a significant reduction in p65 and an increase in cleaved-[[ PARP ]] in U2OS cells.


However, combined treatment with cinobufagin and << SB216367 >> resulted in a significant reduction in p65 and an increase in cleaved-[[ PARP ]] in U2OS cells.


However, combined treatment with << cinobufagin >> and SB216367 resulted in a significant reduction in [[ p65 ]] and an increase in cleaved-PARP in U2OS cells.


However, combined treatment with cinobufagin and << SB216367 >> resulted in a significant reduction in [[ p65 ]] and an increase in cleaved-PARP in U2OS cells.


<< [6]-gingerol >>: a novel [[ AT₁ ]] antagonist for the treatment of cardiovascular disease.


<< [6]-Gingerol >> derived from Zingiber officinale Roscoe (ginger) was identified as a novel [[ angiotensin II type 1 receptor ]] antagonist, with an IC50 value of 8.173 µM.


The major ingredient of ginger, << [6]-gingerol >>, could inhibit [[ angiotensin II type 1 receptor ]] activation, which partially clarified the mechanism of ginger regulating blood pressure and strengthening heart in the cardiovascular system.


In patients who do not reach the LDL-C target, combination therapy with additional << LDL >>-C lowering drugs (e.g. [[ ezetimibe ]], bile acid sequestrants or fibrates) should be considered.


In patients who do not reach the LDL-C target, combination therapy with additional << LDL >>-C lowering drugs (e.g. ezetimibe, [[ bile acid ]] sequestrants or fibrates) should be considered.


In patients who do not reach the LDL-C target, combination therapy with additional << LDL >>-C lowering drugs (e.g. ezetimibe, bile acid sequestrants or [[ fibrates ]]) should be considered.


N(5)-Substituted H(4)biopterin derivatives were not oxidized to products serving as substrates for dihydropteridine reductase and,depending on the substituent, were competitive inhibitors of phenylalanine hydroxylase: << N(5)-methyl >>- and N(5)-hydroxymethyl H(4)biopterin inhibited [[ phenylalanine hydroxylase ]], whereas N(5)-formyl- and N(5)-acetyl H(4)biopterin had no effect.


N(5)-Substituted H(4)biopterin derivatives were not oxidized to products serving as substrates for dihydropteridine reductase and,depending on the substituent, were competitive inhibitors of phenylalanine hydroxylase: N(5)-methyl- and << N(5)-hydroxymethyl H(4)biopterin >> inhibited [[ phenylalanine hydroxylase ]], whereas N(5)-formyl- and N(5)-acetyl H(4)biopterin had no effect.


<< N(5)-Substituted H(4)biopterin >> derivatives were not oxidized to products serving as substrates for [[ dihydropteridine reductase ]] and,depending on the substituent, were competitive inhibitors of phenylalanine hydroxylase: N(5)-methyl- and N(5)-hydroxymethyl H(4)biopterin inhibited phenylalanine hydroxylase, whereas N(5)-formyl- and N(5)-acetyl H(4)biopterin had no effect.


Our data demonstrate differences in the mechanism of stimulation of << phenylalanine hydroxylase >> and nitric oxide synthase by [[ H(4)biopterin ]].


Transfection of the brain cDNA into COS-1 cells resulted in transporter activity that was blocked by the << VMAT >> inhibitor [[ reserpine ]] and a proton ionophore, but not by tetrabenazine, which has a high affinity for VMAT-2.


<< Mitochondrial arginase II >> modulates [[ nitric-oxide ]] synthesis through nonfreely exchangeable L-arginine pools in human endothelial cells.


<< Mitochondrial arginase II >> modulates nitric-oxide synthesis through nonfreely exchangeable [[ L-arginine ]] pools in human endothelial cells.


Reduced synthesis of << nitric oxide >> (NO) contributes to the endothelial dysfunction and may be related to limited availability of L-arginine, the common substrate of [[ constitutive nitric-oxide synthase ]] (NOS) and cytosolic arginase I and mitochondrial arginase II.


Reduced synthesis of << nitric oxide >> (NO) contributes to the endothelial dysfunction and may be related to limited availability of L-arginine, the common substrate of constitutive nitric-oxide synthase ([[ NOS ]]) and cytosolic arginase I and mitochondrial arginase II.


Reduced synthesis of << nitric oxide >> (NO) contributes to the endothelial dysfunction and may be related to limited availability of L-arginine, the common substrate of constitutive nitric-oxide synthase (NOS) and cytosolic [[ arginase I ]] and mitochondrial arginase II.


Reduced synthesis of << nitric oxide >> (NO) contributes to the endothelial dysfunction and may be related to limited availability of L-arginine, the common substrate of constitutive nitric-oxide synthase (NOS) and cytosolic arginase I and [[ mitochondrial arginase II ]].


Reduced synthesis of nitric oxide (<< NO >>) contributes to the endothelial dysfunction and may be related to limited availability of L-arginine, the common substrate of [[ constitutive nitric-oxide synthase ]] (NOS) and cytosolic arginase I and mitochondrial arginase II.


Reduced synthesis of nitric oxide (<< NO >>) contributes to the endothelial dysfunction and may be related to limited availability of L-arginine, the common substrate of constitutive nitric-oxide synthase ([[ NOS ]]) and cytosolic arginase I and mitochondrial arginase II.


Reduced synthesis of nitric oxide (<< NO >>) contributes to the endothelial dysfunction and may be related to limited availability of L-arginine, the common substrate of constitutive nitric-oxide synthase (NOS) and cytosolic [[ arginase I ]] and mitochondrial arginase II.


Reduced synthesis of nitric oxide (<< NO >>) contributes to the endothelial dysfunction and may be related to limited availability of L-arginine, the common substrate of constitutive nitric-oxide synthase (NOS) and cytosolic arginase I and [[ mitochondrial arginase II ]].


Reduced synthesis of nitric oxide (NO) contributes to the endothelial dysfunction and may be related to limited availability of << L-arginine >>, the common substrate of [[ constitutive nitric-oxide synthase ]] (NOS) and cytosolic arginase I and mitochondrial arginase II.


Reduced synthesis of nitric oxide (NO) contributes to the endothelial dysfunction and may be related to limited availability of << L-arginine >>, the common substrate of constitutive nitric-oxide synthase ([[ NOS ]]) and cytosolic arginase I and mitochondrial arginase II.


Reduced synthesis of nitric oxide (NO) contributes to the endothelial dysfunction and may be related to limited availability of << L-arginine >>, the common substrate of constitutive nitric-oxide synthase (NOS) and cytosolic [[ arginase I ]] and mitochondrial arginase II.


Reduced synthesis of nitric oxide (NO) contributes to the endothelial dysfunction and may be related to limited availability of << L-arginine >>, the common substrate of constitutive nitric-oxide synthase (NOS) and cytosolic arginase I and [[ mitochondrial arginase II ]].


To determine whether arginases modulate the endothelial NO synthesis, we investigated the effects of the competitive << arginase >> inhibitor [[ N(omega)-hydroxy-nor-L-arginine ]] (Nor-NOHA) on the activity of NOS, arginases, and L-arginine transporter and on NO release at surface of human umbilical vein endothelial cells (HUVECs).


To determine whether arginases modulate the endothelial NO synthesis, we investigated the effects of the competitive << arginase >> inhibitor N(omega)-hydroxy-nor-L-arginine ([[ Nor-NOHA ]]) on the activity of NOS, arginases, and L-arginine transporter and on NO release at surface of human umbilical vein endothelial cells (HUVECs).


To determine whether << arginases >> modulate the endothelial [[ NO ]] synthesis, we investigated the effects of the competitive arginase inhibitor N(omega)-hydroxy-nor-L-arginine (Nor-NOHA) on the activity of NOS, arginases, and L-arginine transporter and on NO release at surface of human umbilical vein endothelial cells (HUVECs).


In unstimulated cells, << Nor-NOHA >> dose-dependently reduced the [[ arginase ]] activity with maximal inhibition at 20 microM.


When HUVECs were stimulated by thrombin without extracellular L-arginine, << Nor-NOHA >> dose-dependently increased the [[ NOS ]] activity and the NO release with maximal effects at 20 microM.


Extracellular << L-arginine >> also dose-dependently increased NO release and [[ arginase ]] activity.


However, despite activation of L-arginine uptake, the inhibition of << arginase >> activity by [[ Nor-NOHA ]] was still significant.


These data suggest that endothelial << NO >> synthesis depends on the activity of [[ arginase II ]] in mitochondria and l-arginine carriers in cell membrane.


However, pretreatment with agents that block late I(Na), like lidocaine, mexiletine, and << RSD1235 >>, a novel mixed [[ ion channel ]] blocker for the rapid pharmacologic conversion of atrial fibrillation, significantly attenuates the prolonging effects of Class III agents or those induced by ATX-II, a specific toxin that delays Na channel inactivation and amplifies late I(Na) greatly, mimicking LQT3.


The << Na channel >> block caused by [[ lidocaine ]] and RSD1235 can be through the open or inactivated states of the channel, but both equivalently inhibit a late component of Na current (I(Na)), recorded at 22 degrees C using whole-cell patch clamp of Nav 1.5 expressed in HEK cells.


The << Na channel >> block caused by lidocaine and [[ RSD1235 ]] can be through the open or inactivated states of the channel, but both equivalently inhibit a late component of Na current (I(Na)), recorded at 22 degrees C using whole-cell patch clamp of Nav 1.5 expressed in HEK cells.


Depletion of putrescine, spermidine, and spermine by << DL-alpha-difluoromethylornithine >> (DFMO), a specific inhibitor of [[ ornithine decarboxylase ]] (ODC) that is the first rate-limiting enzyme for polyamine biosynthesis, decreased the apoptotic index.


Depletion of putrescine, spermidine, and spermine by << DL-alpha-difluoromethylornithine >> (DFMO), a specific inhibitor of ornithine decarboxylase ([[ ODC ]]) that is the first rate-limiting enzyme for polyamine biosynthesis, decreased the apoptotic index.


Depletion of putrescine, spermidine, and spermine by DL-alpha-difluoromethylornithine (<< DFMO >>), a specific inhibitor of [[ ornithine decarboxylase ]] (ODC) that is the first rate-limiting enzyme for polyamine biosynthesis, decreased the apoptotic index.


Depletion of putrescine, spermidine, and spermine by DL-alpha-difluoromethylornithine (<< DFMO >>), a specific inhibitor of ornithine decarboxylase ([[ ODC ]]) that is the first rate-limiting enzyme for polyamine biosynthesis, decreased the apoptotic index.


Depletion of << putrescine >>, spermidine, and spermine by DL-alpha-difluoromethylornithine (DFMO), a specific inhibitor of [[ ornithine decarboxylase ]] (ODC) that is the first rate-limiting enzyme for polyamine biosynthesis, decreased the apoptotic index.


Depletion of << putrescine >>, spermidine, and spermine by DL-alpha-difluoromethylornithine (DFMO), a specific inhibitor of ornithine decarboxylase ([[ ODC ]]) that is the first rate-limiting enzyme for polyamine biosynthesis, decreased the apoptotic index.


Depletion of putrescine, << spermidine >>, and spermine by DL-alpha-difluoromethylornithine (DFMO), a specific inhibitor of [[ ornithine decarboxylase ]] (ODC) that is the first rate-limiting enzyme for polyamine biosynthesis, decreased the apoptotic index.


Depletion of putrescine, << spermidine >>, and spermine by DL-alpha-difluoromethylornithine (DFMO), a specific inhibitor of ornithine decarboxylase ([[ ODC ]]) that is the first rate-limiting enzyme for polyamine biosynthesis, decreased the apoptotic index.


Depletion of putrescine, spermidine, and << spermine >> by DL-alpha-difluoromethylornithine (DFMO), a specific inhibitor of [[ ornithine decarboxylase ]] (ODC) that is the first rate-limiting enzyme for polyamine biosynthesis, decreased the apoptotic index.


Depletion of putrescine, spermidine, and << spermine >> by DL-alpha-difluoromethylornithine (DFMO), a specific inhibitor of ornithine decarboxylase ([[ ODC ]]) that is the first rate-limiting enzyme for polyamine biosynthesis, decreased the apoptotic index.


Addition of << putrescine >> restored the induction of apoptosis as indicated by an increase in the number of detached cells and [[ caspase 3 ]] activity.


Inhibition of << S-adenosylmethionine decarboxylase >> by a specific inhibitor [[[ diethylglyoxal bis-(guanylhydrazone) ]]; DEGBG] led to depletion of spermidine and spermine with a significant accumulation of putrescine and induction of ODC.


Inhibition of << S-adenosylmethionine decarboxylase >> by a specific inhibitor [diethylglyoxal bis-(guanylhydrazone); [[ DEGBG ]]] led to depletion of spermidine and spermine with a significant accumulation of putrescine and induction of ODC.


Inhibition of << S-adenosylmethionine decarboxylase >> by a specific inhibitor [diethylglyoxal bis-(guanylhydrazone); DEGBG] led to depletion of [[ spermidine ]] and spermine with a significant accumulation of putrescine and induction of ODC.


Inhibition of << S-adenosylmethionine decarboxylase >> by a specific inhibitor [diethylglyoxal bis-(guanylhydrazone); DEGBG] led to depletion of spermidine and [[ spermine ]] with a significant accumulation of putrescine and induction of ODC.


The above results indicate that polyamine depletion delays the onset of apoptosis in IEC-6 cells and confers protection against DNA damaging agents, suggesting that << polyamines >> might be involved in the [[ caspase ]] activating signal cascade.


On the other hand, in patients with a mean serum << carvedilol >> level (Cmin) of less than 2.5 nmol/l up to 2 weeks after the start ofcarvedilol therapy, the degree of reduction in the [[ BNP ]] value after the 3rd month was significantly larger, relative to the patient group with Cmin over 2.5 nmol/l.


On the other hand, in patients with a mean serum carvedilol level (Cmin) of less than 2.5 nmol/l up to 2 weeks after the start of<< carvedilol >> therapy, the degree of reduction in the [[ BNP ]] value after the 3rd month was significantly larger, relative to the patient group with Cmin over 2.5 nmol/l.


Two mechanisms of action have been identified for << A77 1726 >>: inhibition of [[ dihydroorotate dehydrogenase ]] (DHODH) and inhibition of tyrosine kinases.


Two mechanisms of action have been identified for << A77 1726 >>: inhibition of dihydroorotate dehydrogenase ([[ DHODH ]]) and inhibition of tyrosine kinases.


Two mechanisms of action have been identified for << A77 1726 >>: inhibition of dihydroorotate dehydrogenase (DHODH) and inhibition of [[ tyrosine kinases ]].


<< DHODH >> inhibition occurs at lower concentrations of [[ A77 1726 ]] than that of tyrosine kinases and is currently considered the major mode of action.


DHODH inhibition occurs at lower concentrations of << A77 1726 >> than that of [[ tyrosine kinases ]] and is currently considered the major mode of action.


<< L-proline >> accumulation and freeze tolerance of Saccharomyces cerevisiae are caused by a mutation in the PRO1 gene encoding [[ gamma-glutamyl kinase ]].


Interestingly, the allele of PRO1 was shown to enhance the activities of << gamma-glutamyl kinase >> and gamma-glutamyl phosphate reductase, both of which catalyze the first two steps of [[ L-proline ]] synthesis from L-glutamate and which together may form a complex in vivo.


Interestingly, the allele of PRO1 was shown to enhance the activities of gamma-glutamyl kinase and << gamma-glutamyl phosphate reductase >>, both of which catalyze the first two steps of [[ L-proline ]] synthesis from L-glutamate and which together may form a complex in vivo.


Interestingly, the allele of PRO1 was shown to enhance the activities of << gamma-glutamyl kinase >> and gamma-glutamyl phosphate reductase, both of which catalyze the first two steps of L-proline synthesis from [[ L-glutamate ]] and which together may form a complex in vivo.


Interestingly, the allele of PRO1 was shown to enhance the activities of gamma-glutamyl kinase and << gamma-glutamyl phosphate reductase >>, both of which catalyze the first two steps of L-proline synthesis from [[ L-glutamate ]] and which together may form a complex in vivo.


When cultured in liquid minimal medium, yeast cells expressing the mutated << gamma-glutamyl kinase >> were found to accumulate intracellular [[ L-proline ]] and showed a prominent increase in cell viability after freezing at -20 degrees C compared to the viability of cells harboring the wild-type PRO1 gene.


These results suggest that the altered << gamma-glutamyl kinase >> results in stabilization of the complex or has an indirect effect on gamma-glutamyl phosphate reductase activity, which leads to an increase in [[ L-proline ]] production in Saccharomyces cerevisiae.


These results suggest that the altered gamma-glutamyl kinase results in stabilization of the complex or has an indirect effect on << gamma-glutamyl phosphate reductase >> activity, which leads to an increase in [[ L-proline ]] production in Saccharomyces cerevisiae.


Structural optimization of << 2,5-thiophene amides >> as highly potent and selective [[ 17β-hydroxysteroid dehydrogenase type 2 ]] inhibitors for the treatment of osteoporosis.


We report here the optimization of << human 17β-HSD2 >> inhibitors in the [[ 2,5-thiophene amide ]] class by varying the size of the linker (n equals 0 and 2) between the amide moiety and the phenyl group.


While none of the phenethylamides (n = 2) were active, most of the << anilides >> (n = 0) turned out to moderately or strongly inhibit [[ 17β-HSD2 ]].


Multiple exposure to << theophylline >>, a phosphodiesterase ([[ PDE ]]) inhibitor, induces acinar hypertrophy in the salivary gland.


Multiple exposure to << theophylline >>, a [[ phosphodiesterase ]] (PDE) inhibitor, induces acinar hypertrophy in the salivary gland.


<< Theophylline >> exposure resulted in a sustained increase in mRNA expression for [[ CysS ]] and PDE3A, but PDE4D gene expression was unchanged.


<< Theophylline >> exposure resulted in a sustained increase in mRNA expression for CysS and [[ PDE3A ]], but PDE4D gene expression was unchanged.


Terbutaline (Bricanyl) and its prodrug << Bambuterol >> (Bambec) are highly potent [[ beta(2)-adrenoceptor ]] agonists often used in asthma patients.


Terbutaline (Bricanyl) and its prodrug Bambuterol (<< Bambec >>) are highly potent [[ beta(2)-adrenoceptor ]] agonists often used in asthma patients.


<< Terbutaline >> (Bricanyl) and its prodrug Bambuterol (Bambec) are highly potent [[ beta(2)-adrenoceptor ]] agonists often used in asthma patients.


Terbutaline (<< Bricanyl >>) and its prodrug Bambuterol (Bambec) are highly potent [[ beta(2)-adrenoceptor ]] agonists often used in asthma patients.


<< (+/-)-tamsulosin >>, an [[ alpha 1A-adrenoceptor ]] antagonist, inhibits the positive inotropic effect but not the accumulation of inositol phosphates in rabbit heart.


The influence of << (+/-)-tamsulosin >>, a selective [[ alpha 1A-adrenoceptor ]] antagonist, on the positive inotropic effect and the accumulation of inositol phosphates that are induced via alpha 1-adrenoceptors was studied in comparison with that of another alpha 1A-adrenoceptor ligand oxymetazoline in the rabbit ventricular myocardium.


<< Phenylephrine >> elicited a concentration-dependent positive inotropic effect via [[ alpha 1-adrenoceptors ]] in the presence of either (+/-)-bupranolol or S(-)-timolol.


(+/-)-Tamsulosin effectively antagonized the positive inotropic effect of phenylephrine even after inactivation of << alpha 1B-adrenoceptors >> by treatment with [[ chlorethylclonidine ]], which is an indication that the (+/-)-tamsulosin-sensitive subtype belongs to a class resistant to chlorethylclonidine.


(+/-)-Tamsulosin effectively antagonized the positive inotropic effect of << phenylephrine >> even after inactivation of [[ alpha 1B-adrenoceptors ]] by treatment with chlorethylclonidine, which is an indication that the (+/-)-tamsulosin-sensitive subtype belongs to a class resistant to chlorethylclonidine.


<< (+/-)-Tamsulosin >> effectively antagonized the positive inotropic effect of phenylephrine even after inactivation of [[ alpha 1B-adrenoceptors ]] by treatment with chlorethylclonidine, which is an indication that the (+/-)-tamsulosin-sensitive subtype belongs to a class resistant to chlorethylclonidine.


<< (+/-)-Tamsulosin >>, over the range of concentrations at which it antagonized the positive inotropic effect mediated by [[ alpha 1-adrenoceptors ]], did not affect the accumulation of [3H]inositol phosphates that was induced by 10 microM phenylephrine.


These results indicate that the positive inotropic effect, mediated via (+/-)-tamsulosin- and << oxymetazoline >>-sensitive subtype of [[ alpha 1-adrenoceptors ]], is exerted by a subcellular mechanism that is independent of the accumulation of inositol phosphates.


These results indicate that the positive inotropic effect, mediated via << (+/-)-tamsulosin >>- and oxymetazoline-sensitive subtype of [[ alpha 1-adrenoceptors ]], is exerted by a subcellular mechanism that is independent of the accumulation of inositol phosphates.


<< Pterostilbene >> exerts antitumor activity against human osteosarcoma cells by inhibiting the [[ JAK2 ]]/STAT3 signaling pathway.


<< Pterostilbene >> exerts antitumor activity against human osteosarcoma cells by inhibiting the JAK2/[[ STAT3 ]] signaling pathway.


Furthermore, << PTE >> treatment directly inhibited the phosphorylation of JAK2 at Tyr 1007 and the downstream activation of [[ STAT3 ]].


Furthermore, << PTE >> treatment directly inhibited the phosphorylation of [[ JAK2 ]] at Tyr 1007 and the downstream activation of STAT3.


<< PTE >> also down-regulated the expression of STAT3 target genes, including the anti-apoptotic proteins Bcl-xL and Mcl-1, leading to the up-regulation of mitochondrial apoptosis pathway-related proteins ([[ Bax ]], Bak, cytosolic Cytochrome c, and cleaved Caspase3) and cyclin-dependent kinase inhibitors such as p21 and p27.


<< PTE >> also down-regulated the expression of STAT3 target genes, including the anti-apoptotic proteins Bcl-xL and Mcl-1, leading to the up-regulation of mitochondrial apoptosis pathway-related proteins (Bax, [[ Bak ]], cytosolic Cytochrome c, and cleaved Caspase3) and cyclin-dependent kinase inhibitors such as p21 and p27.


<< PTE >> also down-regulated the expression of STAT3 target genes, including the anti-apoptotic proteins Bcl-xL and Mcl-1, leading to the up-regulation of mitochondrial apoptosis pathway-related proteins (Bax, Bak, cytosolic [[ Cytochrome c ]], and cleaved Caspase3) and cyclin-dependent kinase inhibitors such as p21 and p27.


<< PTE >> also down-regulated the expression of STAT3 target genes, including the anti-apoptotic proteins Bcl-xL and Mcl-1, leading to the up-regulation of mitochondrial apoptosis pathway-related proteins (Bax, Bak, cytosolic Cytochrome c, and cleaved [[ Caspase3 ]]) and cyclin-dependent kinase inhibitors such as p21 and p27.


<< PTE >> also down-regulated the expression of STAT3 target genes, including the anti-apoptotic proteins Bcl-xL and Mcl-1, leading to the up-regulation of mitochondrial apoptosis pathway-related proteins (Bax, Bak, cytosolic Cytochrome c, and cleaved Caspase3) and cyclin-dependent kinase inhibitors such as [[ p21 ]] and p27.


<< PTE >> also down-regulated the expression of STAT3 target genes, including the anti-apoptotic proteins Bcl-xL and Mcl-1, leading to the up-regulation of mitochondrial apoptosis pathway-related proteins (Bax, Bak, cytosolic Cytochrome c, and cleaved Caspase3) and cyclin-dependent kinase inhibitors such as p21 and [[ p27 ]].


<< PTE >> also down-regulated the expression of [[ STAT3 ]] target genes, including the anti-apoptotic proteins Bcl-xL and Mcl-1, leading to the up-regulation of mitochondrial apoptosis pathway-related proteins (Bax, Bak, cytosolic Cytochrome c, and cleaved Caspase3) and cyclin-dependent kinase inhibitors such as p21 and p27.


<< PTE >> also down-regulated the expression of STAT3 target genes, including the anti-apoptotic proteins [[ Bcl-xL ]] and Mcl-1, leading to the up-regulation of mitochondrial apoptosis pathway-related proteins (Bax, Bak, cytosolic Cytochrome c, and cleaved Caspase3) and cyclin-dependent kinase inhibitors such as p21 and p27.


<< PTE >> also down-regulated the expression of STAT3 target genes, including the anti-apoptotic proteins Bcl-xL and [[ Mcl-1 ]], leading to the up-regulation of mitochondrial apoptosis pathway-related proteins (Bax, Bak, cytosolic Cytochrome c, and cleaved Caspase3) and cyclin-dependent kinase inhibitors such as p21 and p27.


PTE, used in combination with a known << JAK2 >>/STAT3 inhibitor, [[ AG490 ]], further decreased the viability of osteosarcoma cells.


PTE, used in combination with a known JAK2/<< STAT3 >> inhibitor, [[ AG490 ]], further decreased the viability of osteosarcoma cells.


Taken together, << PTE >> is a potent inhibitor of osteosarcoma cell growth that targets the [[ JAK2 ]]/STAT3 signaling pathway.


Taken together, << PTE >> is a potent inhibitor of osteosarcoma cell growth that targets the JAK2/[[ STAT3 ]] signaling pathway.


These data suggest that inhibition of << JAK2 >>/STAT3 signaling is a novel mechanism of action for [[ PTE ]] during therapeutic intervention in osteosarcoma cancers.


These data suggest that inhibition of JAK2/<< STAT3 >> signaling is a novel mechanism of action for [[ PTE ]] during therapeutic intervention in osteosarcoma cancers.


Furthermore, << sinapic acid >> reduced hepatic hydroxyproline content, which correlated with a reduction in the expression of [[ type I collagen ]] mRNA and histological analysis of collagen in liver tissue.


Additionally, the expression of hepatic fibrosis-related factors such as << α-smooth muscle actin >> and transforming growth factor-β1 (TGF-β1), were reduced in rats treated with [[ sinapic acid ]].


Additionally, the expression of hepatic fibrosis-related factors such as α-smooth muscle actin and << transforming growth factor-β1 >> (TGF-β1), were reduced in rats treated with [[ sinapic acid ]].


Additionally, the expression of hepatic fibrosis-related factors such as α-smooth muscle actin and transforming growth factor-β1 (<< TGF-β1 >>), were reduced in rats treated with [[ sinapic acid ]].


In conclusion, we find that << sinapic acid >> exhibits hepatoprotective and antifibrotic effects against DMN-induced liver injury, most likely due to its antioxidant activities of scavenging radicals, its capacity to suppress [[ TGF-β1 ]] and its ability to attenuate activation of hepatic stellate cells.


<< Thalidomide >> inhibits growth of tumors through [[ COX-2 ]] degradation independent of antiangiogenesis.


<< Thalidomide >> reduced COX-2 expression accompanied by a decrease of bcl-2 protein, TNFalpha, VEGF, GSH and an increased [[ cytochrome c ]], but had no effect on that of COX-1, in MCF-7 and HL-60.


<< Thalidomide >> reduced [[ COX-2 ]] expression accompanied by a decrease of bcl-2 protein, TNFalpha, VEGF, GSH and an increased cytochrome c, but had no effect on that of COX-1, in MCF-7 and HL-60.


<< Thalidomide >> reduced COX-2 expression accompanied by a decrease of [[ bcl-2 ]] protein, TNFalpha, VEGF, GSH and an increased cytochrome c, but had no effect on that of COX-1, in MCF-7 and HL-60.


<< Thalidomide >> reduced COX-2 expression accompanied by a decrease of bcl-2 protein, [[ TNFalpha ]], VEGF, GSH and an increased cytochrome c, but had no effect on that of COX-1, in MCF-7 and HL-60.


<< Thalidomide >> reduced COX-2 expression accompanied by a decrease of bcl-2 protein, TNFalpha, [[ VEGF ]], GSH and an increased cytochrome c, but had no effect on that of COX-1, in MCF-7 and HL-60.


These results demonstrated that << thalidomide >> might inhibit growth of tumors through [[ COX-2 ]] degradation independent of antiangiogenesis.


Results: The administration of << prallethrin >> 1.6% w/w created significant increased changes in the levels of total WBC, lymphocytes, RBC, [[ hemoglobin ]], packed cell volume, platelets, mean corpuscular volume, and mean corpuscular hemoglobin in rats after 24, 48, and 72 h of continuous inhalation; however, there was a significant reduction in neutrophils at transient reduction in the monocytes after 24 and 48 h to return to normal after 72 h.


Results: The administration of << prallethrin >> 1.6% w/w created significant increased changes in the levels of total WBC, lymphocytes, RBC, hemoglobin, packed cell volume, platelets, mean corpuscular volume, and mean corpuscular [[ hemoglobin ]] in rats after 24, 48, and 72 h of continuous inhalation; however, there was a significant reduction in neutrophils at transient reduction in the monocytes after 24 and 48 h to return to normal after 72 h.


Gene expression profiling (GEP) of GIST-S, GIST-R cells and two << IM >> resistant GIST patients demonstrated that [[ KIT ]] is downregulated implying a major role in IM resistance.


Gene expression profiling (GEP) of GIST-S, GIST-R cells and two IM resistant GIST patients demonstrated that << KIT >> is downregulated implying a major role in [[ IM ]] resistance.


Molecular modeling of the kinase domain of mutant c-Kit (V654A) and AXL showed no binding to IM but efficient binding to << MP470 >>, a novel [[ c-Kit ]]/AXL kinase inhibitor.


Molecular modeling of the kinase domain of mutant c-Kit (V654A) and AXL showed no binding to IM but efficient binding to << MP470 >>, a novel c-Kit/[[ AXL ]] kinase inhibitor.


Molecular modeling of the kinase domain of mutant c-Kit (V654A) and AXL showed no binding to IM but efficient binding to << MP470 >>, a novel c-Kit/AXL [[ kinase ]] inhibitor.


INTRODUCTION: In this study, we examined the effects of the << alpha-glucosidase >> inhibitors acarbose and [[ voglibose ]] on postprandial plasma glucose and serum triglyceride levels in patients with type 2 diabetes mellitus.


INTRODUCTION: In this study, we examined the effects of the << alpha-glucosidase >> inhibitors [[ acarbose ]] and voglibose on postprandial plasma glucose and serum triglyceride levels in patients with type 2 diabetes mellitus.


INTRODUCTION: In this study, we examined the effects of the << alpha-glucosidase >> inhibitors acarbose and voglibose on postprandial plasma [[ glucose ]] and serum triglyceride levels in patients with type 2 diabetes mellitus.


Blockade of << JAK >> and ERK pathways with [[ AG490 ]] and U0126, respectively, abrogated the myocardial infarct size reduction by NDP-α-MSH.


Blockade of JAK and << ERK >> pathways with AG490 and [[ U0126 ]], respectively, abrogated the myocardial infarct size reduction by NDP-α-MSH.


The << COX >> pathway generates inflammatory [[ prostaglandins ]], while the 5-LOX pathway generates inflammatory leukotrienes.


The COX pathway generates inflammatory prostaglandins, while the << 5-LOX >> pathway generates inflammatory [[ leukotrienes ]].


They included the COX-1 inhibitor indomethacin; the COX-2 inhibitor NS-398; the mixed COX-1/COX-2 inhibitor ibuprofen; the nitric oxide (NO) derivatives of indomethacin, ibuprofen and flurbiprofen; the << 5-LOX >> inhibitor [[ REV 5901 ]]; and the 5-LOX activating protein (FLAP) inhibitor MK-886.


They included the COX-1 inhibitor indomethacin; the COX-2 inhibitor NS-398; the mixed COX-1/COX-2 inhibitor ibuprofen; the nitric oxide (NO) derivatives of indomethacin, ibuprofen and flurbiprofen; the 5-LOX inhibitor REV 5901; and the << 5-LOX activating protein >> (FLAP) inhibitor [[ MK-886 ]].


They included the COX-1 inhibitor indomethacin; the COX-2 inhibitor NS-398; the mixed COX-1/COX-2 inhibitor ibuprofen; the nitric oxide (NO) derivatives of indomethacin, ibuprofen and flurbiprofen; the 5-LOX inhibitor REV 5901; and the 5-LOX activating protein (<< FLAP >>) inhibitor [[ MK-886 ]].


They included the COX-1 inhibitor indomethacin; the << COX-2 >> inhibitor [[ NS-398 ]]; the mixed COX-1/COX-2 inhibitor ibuprofen; the nitric oxide (NO) derivatives of indomethacin, ibuprofen and flurbiprofen; the 5-LOX inhibitor REV 5901; and the 5-LOX activating protein (FLAP) inhibitor MK-886.


They included the COX-1 inhibitor indomethacin; the COX-2 inhibitor NS-398; the mixed << COX-1 >>/COX-2 inhibitor [[ ibuprofen ]]; the nitric oxide (NO) derivatives of indomethacin, ibuprofen and flurbiprofen; the 5-LOX inhibitor REV 5901; and the 5-LOX activating protein (FLAP) inhibitor MK-886.


They included the COX-1 inhibitor indomethacin; the COX-2 inhibitor NS-398; the mixed COX-1/<< COX-2 >> inhibitor [[ ibuprofen ]]; the nitric oxide (NO) derivatives of indomethacin, ibuprofen and flurbiprofen; the 5-LOX inhibitor REV 5901; and the 5-LOX activating protein (FLAP) inhibitor MK-886.


Additionally, << MPTP >> significantly down-regulated Bcl-2 expression in the mitochondria of dopaminergic cells in the SN, followed by an increase in [[ Bax ]] expression, cytochrome C translocation to the cytosol, andcleaved-caspase-3 expression, whereas these were inhibited by CRE or EB treatment.


Additionally, << MPTP >> significantly down-regulated Bcl-2 expression in the mitochondria of dopaminergic cells in the SN, followed by an increase in Bax expression, cytochrome C translocation to the cytosol, andcleaved-[[ caspase-3 ]] expression, whereas these were inhibited by CRE or EB treatment.


Additionally, << MPTP >> significantly down-regulated [[ Bcl-2 ]] expression in the mitochondria of dopaminergic cells in the SN, followed by an increase in Bax expression, cytochrome C translocation to the cytosol, andcleaved-caspase-3 expression, whereas these were inhibited by CRE or EB treatment.


Add-on therapy with the << DPP-4 >> inhibitor [[ sitagliptin ]] improves glycemic control in insulin-treated Japanese patients with type 2 diabetes mellitus.


The << hemoglobin A1c >> (HbA1c) of all patients improved significantly from 8.1±1.2% to 7.6±1.1% after 12 weeks of add-on therapy with [[ sitagliptin ]] (p<0.01), and the insulin dosage was reduced from 27.3±15.8 U/day to 24.5±16.5 U/day (p<0.001).


The hemoglobin A1c (<< HbA1c >>) of all patients improved significantly from 8.1±1.2% to 7.6±1.1% after 12 weeks of add-on therapy with [[ sitagliptin ]] (p<0.01), and the insulin dosage was reduced from 27.3±15.8 U/day to 24.5±16.5 U/day (p<0.001).


In the present study, we have evaluated possible participation of << monocarboxylate transporters >> (MCTs) responsible for the bidirectional membrane transport of [[ pyruvate ]] in the cytoprotective property in osteoblasts.


In the present study, we have evaluated possible participation of monocarboxylate transporters (<< MCTs >>) responsible for the bidirectional membrane transport of [[ pyruvate ]] in the cytoprotective property in osteoblasts.


<< Mammalian ALDH1B1 >>, another mitochondrial enzyme sharing 72% identity with ALDH2, is also capable of metabolizing [[ acetaldehyde ]] but has a tissue distribution and pattern of activity distinct from that of ALDH2.


Mammalian ALDH1B1, another mitochondrial enzyme sharing 72% identity with << ALDH2 >>, is also capable of metabolizing [[ acetaldehyde ]] but has a tissue distribution and pattern of activity distinct from that of ALDH2.


<< Aspirin >> (ASA) and other non-steroidal anti-inflammatory drugs, which are [[ cyclooxygenase ]] (COX) inhibitors, precipitate asthmatic attacks in ASA-intolerant patients, while sodium salicylate, hardly active on COX by itself, is well tolerated by these patients.


<< Aspirin >> (ASA) and other non-steroidal anti-inflammatory drugs, which are cyclooxygenase ([[ COX ]]) inhibitors, precipitate asthmatic attacks in ASA-intolerant patients, while sodium salicylate, hardly active on COX by itself, is well tolerated by these patients.


Aspirin (<< ASA >>) and other non-steroidal anti-inflammatory drugs, which are [[ cyclooxygenase ]] (COX) inhibitors, precipitate asthmatic attacks in ASA-intolerant patients, while sodium salicylate, hardly active on COX by itself, is well tolerated by these patients.


Aspirin (<< ASA >>) and other non-steroidal anti-inflammatory drugs, which are cyclooxygenase ([[ COX ]]) inhibitors, precipitate asthmatic attacks in ASA-intolerant patients, while sodium salicylate, hardly active on COX by itself, is well tolerated by these patients.


However, salicylate moiety appears to interfere with << aspirin >> inhibitory action on platelets and vascular [[ COX ]].


Although the precise mechanism of the protective action of trilisate is unknown, our data support the possibility of interaction between << salicylate >> and ASA on [[ cyclo-oxygenase ]] locus in the respiratory tract in ASA-intolerant patients.


Although the precise mechanism of the protective action of trilisate is unknown, our data support the possibility of interaction between salicylate and << ASA >> on [[ cyclo-oxygenase ]] locus in the respiratory tract in ASA-intolerant patients.


<< Minocycline >> inhibits [[ cytochrome c ]] release and delays progression of amyotrophic lateral sclerosis in mice.


We find that << minocycline >> inhibits mitochondrial permeability-transition-mediated [[ cytochrome c ]] release.


<< Minocycline >>-mediated inhibition of [[ cytochrome c ]] release is demonstrated in vivo, in cells, and in isolated mitochondria.


Here we studied the effects of the recently developed << monoacylglycerol lipase >> inhibitor [[ JZL184 ]] on basal and stress-induced corticosterone levels in male CD1 mice, and found that this compound dramatically increased basal levels without affecting stress responses.


Considerable attention has focused on the antitumor effect of << histone deacetylase >> inhibitor ([[ Trichostatin A ]], TSA) as well as the coding gene expression-induced apoptosis of cancer cells.


Considerable attention has focused on the antitumor effect of << histone deacetylase >> inhibitor (Trichostatin A, [[ TSA ]]) as well as the coding gene expression-induced apoptosis of cancer cells.


Among these differentially expressed lncRNAs, the greatest change was noted for << uc002mbe.2 >>, which had more than 300 folds induction upon [[ TSA ]] treatment.


<< TSA >> selectively induced [[ uc002mbe.2 ]] in four studied HCC cell lines.


The << TSA >>-induced [[ uc002mbe.2 ]] expression was positively correlated with the apoptotic effect of TSA in HCC cells.


<< Orlistat >>, a new [[ lipase ]] inhibitor for the management of obesity.


<< Orlistat >> treatment also results in modest improvements in total cholesterol, [[ low-density lipoprotein ]], blood pressure, and fasting glucose and insulin concentrations.


<< Orlistat >> treatment also results in modest improvements in total cholesterol, low-density lipoprotein, blood pressure, and fasting glucose and [[ insulin ]] concentrations.


Evidence has accumulated in the last few years that the expression of the << microsomal/peroxidase antigen >> (M/TPO-Ag) in thyroid cells is induced by TSH, through pathways which involve intracellular [[ cAMP ]] accumulation and protein synthesis.


Evidence has accumulated in the last few years that the expression of the microsomal/peroxidase antigen (<< M/TPO-Ag >>) in thyroid cells is induced by TSH, through pathways which involve intracellular [[ cAMP ]] accumulation and protein synthesis.


TSH and << cAMP >> also increase the levels of the specific mRNA for [[ TPO ]] in thyroid cells from different species.


A novel << benzo[d]imidazole >> derivate prevents the development of dextran sulfate sodium-induced murine experimental colitis via inhibition of [[ NLRP3 ]] inflammasome.


In addition, the disease activity index, histopathologic scores and << myeloperoxidase >> activity were also significantly reduced by [[ Fc11a-2 ]] treatment.


Moreover, protein and mRNA levels of DSS-induced proinflammatory << cytokines >> in colon, including TNF-α, IL-1β, IL-18, IL-17A and IFN-γ, were markedly suppressed by [[ Fc11a-2 ]].


Moreover, protein and mRNA levels of DSS-induced proinflammatory cytokines in colon, including << TNF-α >>, IL-1β, IL-18, IL-17A and IFN-γ, were markedly suppressed by [[ Fc11a-2 ]].


Moreover, protein and mRNA levels of DSS-induced proinflammatory cytokines in colon, including TNF-α, << IL-1β >>, IL-18, IL-17A and IFN-γ, were markedly suppressed by [[ Fc11a-2 ]].