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3,700 | 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. | 3,700 | 9 |
3,701 | 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. | 3,701 | 9 |
3,702 | 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. | 3,702 | 6 |
3,703 | 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. | 3,703 | 6 |
3,704 | 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. | 3,704 | 6 |
3,705 | << Plerixafor >>, a [[ CXCR4 ]] antagonist for the mobilization of hematopoietic stem cells. | 3,705 | 1 |
3,706 | << 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. | 3,706 | 0 |
3,707 | << 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. | 3,707 | 0 |
3,708 | << 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 ]]. | 3,708 | 0 |
3,709 | << 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. | 3,709 | 0 |
3,710 | 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. | 3,710 | 0 |
3,711 | 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. | 3,711 | 0 |
3,712 | 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 ]]. | 3,712 | 0 |
3,713 | 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. | 3,713 | 0 |
3,714 | 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. | 3,714 | 0 |
3,715 | 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. | 3,715 | 0 |
3,716 | 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 ]]. | 3,716 | 0 |
3,717 | 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. | 3,717 | 0 |
3,718 | This stimulation was attenuated by the << Pak >> inhibitor [[ 2,2'-dihydroxy-1,1'-dinaphthyldisulfide ]] (IPA3) or dominant-negative Pak1. | 3,718 | 0 |
3,719 | This stimulation was attenuated by the << Pak >> inhibitor 2,2'-dihydroxy-1,1'-dinaphthyldisulfide ([[ IPA3 ]]) or dominant-negative Pak1. | 3,719 | 0 |
3,720 | 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. | 3,720 | 0 |
3,721 | 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. | 3,721 | 0 |
3,722 | 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. | 3,722 | 0 |
3,723 | Results showed that neonatal << quinpirole >> treatment induced [[ D2 ]] priming that was eliminated by olanzapine treatment. | 3,723 | 6 |
3,724 | Results showed that neonatal quinpirole treatment induced << D2 >> priming that was eliminated by [[ olanzapine ]] treatment. | 3,724 | 8 |
3,725 | Brain tissue analyses revealed that neonatal quinpirole treatment produced a significant decrease in hippocampal << NGF >>, BDNF and ChAT that was eliminated by [[ olanzapine ]] treatment. | 3,725 | 6 |
3,726 | Brain tissue analyses revealed that neonatal quinpirole treatment produced a significant decrease in hippocampal NGF, << BDNF >> and ChAT that was eliminated by [[ olanzapine ]] treatment. | 3,726 | 6 |
3,727 | Brain tissue analyses revealed that neonatal quinpirole treatment produced a significant decrease in hippocampal NGF, BDNF and << ChAT >> that was eliminated by [[ olanzapine ]] treatment. | 3,727 | 6 |
3,728 | Brain tissue analyses revealed that neonatal << quinpirole >> treatment produced a significant decrease in hippocampal [[ NGF ]], BDNF and ChAT that was eliminated by olanzapine treatment. | 3,728 | 8 |
3,729 | Brain tissue analyses revealed that neonatal << quinpirole >> treatment produced a significant decrease in hippocampal NGF, [[ BDNF ]] and ChAT that was eliminated by olanzapine treatment. | 3,729 | 8 |
3,730 | Brain tissue analyses revealed that neonatal << quinpirole >> treatment produced a significant decrease in hippocampal NGF, BDNF and [[ ChAT ]] that was eliminated by olanzapine treatment. | 3,730 | 8 |
3,731 | Neonatal << quinpirole >> treatment produced a significant decrease in [[ BDNF ]] and ChAT in the frontal cortex that was unaffected by olanzapine treatment. | 3,731 | 8 |
3,732 | Neonatal << quinpirole >> treatment produced a significant decrease in BDNF and [[ ChAT ]] in the frontal cortex that was unaffected by olanzapine treatment. | 3,732 | 8 |
3,733 | 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. | 3,733 | 8 |
3,734 | Suppression of << Src >>/ERK and GSK-3/β-catenin signaling by [[ pinosylvin ]] inhibits the growth of human colorectal cancer cells. | 3,734 | 3 |
3,735 | Suppression of Src/<< ERK >> and GSK-3/β-catenin signaling by [[ pinosylvin ]] inhibits the growth of human colorectal cancer cells. | 3,735 | 3 |
3,736 | Suppression of Src/ERK and << GSK-3 >>/β-catenin signaling by [[ pinosylvin ]] inhibits the growth of human colorectal cancer cells. | 3,736 | 3 |
3,737 | Suppression of Src/ERK and GSK-3/<< β-catenin >> signaling by [[ pinosylvin ]] inhibits the growth of human colorectal cancer cells. | 3,737 | 3 |
3,738 | << 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. | 3,738 | 7 |
3,739 | << 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. | 3,739 | 7 |
3,740 | << 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. | 3,740 | 7 |
3,741 | << 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 ]]. | 3,741 | 7 |
3,742 | << 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. | 3,742 | 3 |
3,743 | << 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. | 3,743 | 3 |
3,744 | << 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. | 3,744 | 3 |
3,745 | << 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. | 3,745 | 3 |
3,746 | << 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. | 3,746 | 3 |
3,747 | << 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. | 3,747 | 3 |
3,748 | << 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. | 3,748 | 3 |
3,749 | << 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. | 3,749 | 3 |
3,750 | << 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. | 3,750 | 3 |
3,751 | << 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. | 3,751 | 8 |
3,752 | << 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. | 3,752 | 8 |
3,753 | << 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. | 3,753 | 8 |
3,754 | << 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. | 3,754 | 8 |
3,755 | << 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. | 3,755 | 8 |
3,756 | << 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. | 3,756 | 8 |
3,757 | << 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. | 3,757 | 8 |
3,758 | << 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. | 3,758 | 8 |
3,759 | << 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. | 3,759 | 8 |
3,760 | << 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. | 3,760 | 8 |
3,761 | 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. | 3,761 | 8 |
3,762 | 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. | 3,762 | 8 |
3,763 | 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. | 3,763 | 8 |
3,764 | 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. | 3,764 | 8 |
3,765 | 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. | 3,765 | 8 |
3,766 | 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. | 3,766 | 8 |
3,767 | 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. | 3,767 | 8 |
3,768 | 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. | 3,768 | 8 |
3,769 | 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. | 3,769 | 8 |
3,770 | 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. | 3,770 | 8 |
3,771 | 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 ]]. | 3,771 | 8 |
3,772 | 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. | 3,772 | 8 |
3,773 | 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. | 3,773 | 8 |
3,774 | Novel analgesic/anti-inflammatory agents: 1,5-diarylpyrrole nitrooxyalkyl ethers and related compounds as << cyclooxygenase-2 >> inhibiting [[ nitric oxide ]] donors. | 3,774 | 0 |
3,775 | Novel analgesic/anti-inflammatory agents: << 1,5-diarylpyrrole nitrooxyalkyl ethers >> and related compounds as [[ cyclooxygenase-2 ]] inhibiting nitric oxide donors. | 3,775 | 0 |
3,776 | 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. | 3,776 | 0 |
3,777 | 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. | 3,777 | 0 |
3,778 | 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. | 3,778 | 0 |
3,779 | 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. | 3,779 | 0 |
3,780 | 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. | 3,780 | 0 |
3,781 | << 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. | 3,781 | 0 |
3,782 | The clinical profile of the << angiotensin II receptor >> blocker [[ eprosartan ]]. | 3,782 | 0 |
3,783 | 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. | 3,783 | 0 |
3,784 | 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. | 3,784 | 0 |
3,785 | 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. | 3,785 | 0 |
3,786 | 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. | 3,786 | 0 |
3,787 | 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. | 3,787 | 0 |
3,788 | 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. | 3,788 | 9 |
3,789 | 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. | 3,789 | 9 |
3,790 | 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. | 3,790 | 9 |
3,791 | 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. | 3,791 | 9 |
3,792 | 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. | 3,792 | 9 |
3,793 | 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. | 3,793 | 9 |
3,794 | In vitro inhibition of << diacylglycerol acyltransferase >> by [[ prenylflavonoids ]] from Sophora flavescens. | 3,794 | 0 |
3,795 | 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). | 3,795 | 0 |
3,796 | 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 ]]). | 3,796 | 0 |
3,797 | 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). | 3,797 | 0 |
3,798 | 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 ]]). | 3,798 | 0 |
3,799 | 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). | 3,799 | 0 |