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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 ]].

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 ]].

Furthermore, a decreased CD11c(+) macrophage infiltration in colons and inactivation of << caspase-1 >> in peritoneal macrophages were detected in [[ Fc11a ]]-2-treated mice.

The mechanism of action of << Fc11a-2 >> was related to the inhibition of the cleavage of [[ pro-caspase-1 ]], pro-IL-1β and pro-IL-18 which in turn suppressed the activation of NLRP3 inflammasome.

The mechanism of action of << Fc11a-2 >> was related to the inhibition of the cleavage of pro-caspase-1, [[ pro-IL-1β ]] and pro-IL-18 which in turn suppressed the activation of NLRP3 inflammasome.

The mechanism of action of << Fc11a-2 >> was related to the inhibition of the cleavage of pro-caspase-1, pro-IL-1β and [[ pro-IL-18 ]] which in turn suppressed the activation of NLRP3 inflammasome.

The mechanism of action of << Fc11a-2 >> was related to the inhibition of the cleavage of pro-caspase-1, pro-IL-1β and pro-IL-18 which in turn suppressed the activation of [[ NLRP3 ]] inflammasome.

Taken together, our results demonstrate the ability of << Fc11a-2 >> to inhibit [[ NLRP3 ]] inflammasome activation and its potential use in the treatment of inflammatory bowel diseases.

At PND35, the medial prefrontal cortex (mPFC) of rats given << MPH >> showed 55% greater immunoreactivity (-ir) for the catecholamine marker [[ tyrosine hydroxylase ]] (TH), 60% more Nissl-stained cells, and 40% less norepinephrine transporter (NET)-ir density.

At PND35, the medial prefrontal cortex (mPFC) of rats given << MPH >> showed 55% greater immunoreactivity (-ir) for the catecholamine marker tyrosine hydroxylase ([[ TH ]]), 60% more Nissl-stained cells, and 40% less norepinephrine transporter (NET)-ir density.

At PND35, the medial prefrontal cortex (mPFC) of rats given << MPH >> showed 55% greater immunoreactivity (-ir) for the catecholamine marker tyrosine hydroxylase (TH), 60% more Nissl-stained cells, and 40% less [[ norepinephrine transporter ]] (NET)-ir density.

At PND35, the medial prefrontal cortex (mPFC) of rats given << MPH >> showed 55% greater immunoreactivity (-ir) for the catecholamine marker tyrosine hydroxylase (TH), 60% more Nissl-stained cells, and 40% less norepinephrine transporter ([[ NET ]])-ir density.

In hippocampal dentate gyrus, << MPH >>-receiving rats showed a 51% decrease in NET-ir density and a 61% expanded distribution of the new-cell marker PSA-NCAM (polysialylated form of [[ neural cell adhesion molecule ]]).

In hippocampal dentate gyrus, << MPH >>-receiving rats showed a 51% decrease in NET-ir density and a 61% expanded distribution of the new-cell marker PSA-[[ NCAM ]] (polysialylated form of neural cell adhesion molecule).

In hippocampal dentate gyrus, << MPH >>-receiving rats showed a 51% decrease in [[ NET ]]-ir density and a 61% expanded distribution of the new-cell marker PSA-NCAM (polysialylated form of neural cell adhesion molecule).

In medial striatum, TH-ir decreased by 21%, and in hypothalamus << neuropeptide Y >>-ir increased by 10% in [[ MPH ]]-exposed rats.

In medial striatum, << TH >>-ir decreased by 21%, and in hypothalamus neuropeptide Y-ir increased by 10% in [[ MPH ]]-exposed rats.