METHODS: The effect of leukotriene D(4) and the << leukotriene receptor >> antagonist, [[ pranlukast hydrate ]] (ONO-1078) on the regulation of MUC2/5AC gene expression and mucin secretion were observed in human airway NCI-H292 epithelial cells.


METHODS: The effect of leukotriene D(4) and the << leukotriene receptor >> antagonist, pranlukast hydrate ([[ ONO-1078 ]]) on the regulation of MUC2/5AC gene expression and mucin secretion were observed in human airway NCI-H292 epithelial cells.


RESULTS: << Leukotriene D(4) >> upregulated [[ MUC2/5AC ]] gene expression and mucin secretion in a dose dependent pattern.


RESULTS: << Leukotriene D(4) >> upregulated MUC2/5AC gene expression and [[ mucin ]] secretion in a dose dependent pattern.


Pranlukast hydrate (ONO-1078, 100 microM) downregulated the << leukotriene D(4) >>-induced [[ MUC2/5AC ]] gene expression and mucin secretion.


Pranlukast hydrate (ONO-1078, 100 microM) downregulated the << leukotriene D(4) >>-induced MUC2/5AC gene expression and [[ mucin ]] secretion.


<< Pranlukast hydrate >> (ONO-1078, 100 microM) downregulated the leukotriene D(4)-induced [[ MUC2/5AC ]] gene expression and mucin secretion.


<< Pranlukast hydrate >> (ONO-1078, 100 microM) downregulated the leukotriene D(4)-induced MUC2/5AC gene expression and [[ mucin ]] secretion.


Pranlukast hydrate (<< ONO-1078 >>, 100 microM) downregulated the leukotriene D(4)-induced [[ MUC2/5AC ]] gene expression and mucin secretion.


Pranlukast hydrate (<< ONO-1078 >>, 100 microM) downregulated the leukotriene D(4)-induced MUC2/5AC gene expression and [[ mucin ]] secretion.


We studied in a clinical trial whether isolated isoflavone treatment in postmenopausal women could affect reverse cholesterol transport as evaluated by << adenosine triphosphate-binding cassette A1 >>- (ABCA1), dependent [[ cholesterol ]] efflux from macrophages.


We studied in a clinical trial whether isolated isoflavone treatment in postmenopausal women could affect reverse cholesterol transport as evaluated by adenosine triphosphate-binding cassette A1- (<< ABCA1 >>), dependent [[ cholesterol ]] efflux from macrophages.


[H]-Cholesterol-labeled J774 macrophage cells, with and without ABCA1 up-regulation, were incubated with the samples, and << ABCA1 >>-dependent [[ cholesterol ]] efflux and serum lipid and lipoprotein levels were assessed.


Thus, isoflavone supplementation did not affect << ABCA1 >>-dependent [[ cholesterol ]] efflux to serum.


However, as a novel finding, << isoflavone >> treatment increased a subclass of [[ high-density lipoprotein ]], the pre-beta high-density lipoprotein levels by 18% without affecting any other serum lipid concentrations.


However, as a novel finding, << isoflavone >> treatment increased a subclass of high-density lipoprotein, the [[ pre-beta high-density lipoprotein ]] levels by 18% without affecting any other serum lipid concentrations.


<< ABCA1 >>-facilitated [[ cholesterol ]] efflux and lipid parameters did not differ between equol-producing and non-equol-producing women.


CONCLUSION: In postmenopausal women, isolated << isoflavone >> treatment does not affect ABCA1-dependent cholesterol efflux potential from macrophages but increases circulating [[ pre-beta high-density lipoprotein ]] level, which could provide beneficial vascular effects.


CONCLUSION: In postmenopausal women, isolated isoflavone treatment does not affect << ABCA1 >>-dependent [[ cholesterol ]] efflux potential from macrophages but increases circulating pre-beta high-density lipoprotein level, which could provide beneficial vascular effects.


The ability of << sorafenib >> to inhibit oncogenic [[ PDGFRbeta ]] and FLT3 mutants and overcome resistance to other small molecule inhibitors.


The ability of << sorafenib >> to inhibit oncogenic PDGFRbeta and [[ FLT3 ]] mutants and overcome resistance to other small molecule inhibitors.


<< Sorafenib >> (BAY43-9006, Nexavar) is a small molecule [[ B-RAF ]] inhibitor that is used for the treatment of renal cell carcinoma, and has been shown to have activity against receptor tyrosine kinases from the platelet-derived growth factor receptor (PDGFR) and vascular endothelial growth factor receptor (VEGFR) families.


Sorafenib (<< BAY43-9006 >>, Nexavar) is a small molecule [[ B-RAF ]] inhibitor that is used for the treatment of renal cell carcinoma, and has been shown to have activity against receptor tyrosine kinases from the platelet-derived growth factor receptor (PDGFR) and vascular endothelial growth factor receptor (VEGFR) families.


Sorafenib (BAY43-9006, << Nexavar >>) is a small molecule [[ B-RAF ]] inhibitor that is used for the treatment of renal cell carcinoma, and has been shown to have activity against receptor tyrosine kinases from the platelet-derived growth factor receptor (PDGFR) and vascular endothelial growth factor receptor (VEGFR) families.


We investigated the efficacy of << sorafenib >> at inhibiting mutants of the [[ receptor tyrosine kinases ]] PDGFRbeta, KIT, and FLT3, which are implicated in the pathogenesis of myeloid malignancies.


We investigated the efficacy of << sorafenib >> at inhibiting mutants of the receptor tyrosine kinases [[ PDGFRbeta ]], KIT, and FLT3, which are implicated in the pathogenesis of myeloid malignancies.


We investigated the efficacy of << sorafenib >> at inhibiting mutants of the receptor tyrosine kinases PDGFRbeta, [[ KIT ]], and FLT3, which are implicated in the pathogenesis of myeloid malignancies.


We investigated the efficacy of << sorafenib >> at inhibiting mutants of the receptor tyrosine kinases PDGFRbeta, KIT, and [[ FLT3 ]], which are implicated in the pathogenesis of myeloid malignancies.


RESULTS: We show that << sorafenib >> is a potent inhibitor of [[ ETV6 ]]-PDGFRbeta and FLT3 mutants, including some of the mutants that confer resistance to PKC412 and other FLT3 inhibitors.


RESULTS: We show that << sorafenib >> is a potent inhibitor of ETV6-[[ PDGFRbeta ]] and FLT3 mutants, including some of the mutants that confer resistance to PKC412 and other FLT3 inhibitors.


RESULTS: We show that << sorafenib >> is a potent inhibitor of ETV6-PDGFRbeta and [[ FLT3 ]] mutants, including some of the mutants that confer resistance to PKC412 and other FLT3 inhibitors.


RESULTS: We show that << sorafenib >> is a potent inhibitor of ETV6-PDGFRbeta and FLT3 mutants, including some of the mutants that confer resistance to PKC412 and other [[ FLT3 ]] inhibitors.


<< Sorafenib >> induced a cell cycle block and apoptosis in the acute myeloid leukemia cell lines MV4-11 and MOLM-13, both expressing [[ FLT3 ]] with an internal tandem duplication, whereas no effect was observed on four other acute myeloid leukemia cell lines.


INTERPRETATION AND CONCLUSIONS: These results warrant further clinical studies of << sorafenib >> for the treatment of myeloid malignancies expressing activated forms of [[ PDGFRbeta ]] and FLT3.


INTERPRETATION AND CONCLUSIONS: These results warrant further clinical studies of << sorafenib >> for the treatment of myeloid malignancies expressing activated forms of PDGFRbeta and [[ FLT3 ]].


Exposure to << mifepristone >> (a [[ glucocorticoid receptor ]] antagonist), but not spironolactone (a mineralocorticoid receptor antagonist), precluded both the corticosteroid-induced elevation in amiloride-sensitive I(sc) and the induced changes in beta- and gamma-ENaC mRNA.


Exposure to mifepristone (a glucocorticoid receptor antagonist), but not << spironolactone >> (a [[ mineralocorticoid receptor ]] antagonist), precluded both the corticosteroid-induced elevation in amiloride-sensitive I(sc) and the induced changes in beta- and gamma-ENaC mRNA.


Oral << aspirin >> (as a representative of the salicylate family) inhibited diabetes-induced increase in [[ NF-kappaB ]] DNA-binding affinity in electrophoretic mobility shift assay and transcription factor array in nuclear extract isolated from whole retina.


Oral aspirin (as a representative of the << salicylate >> family) inhibited diabetes-induced increase in [[ NF-kappaB ]] DNA-binding affinity in electrophoretic mobility shift assay and transcription factor array in nuclear extract isolated from whole retina.


All three << salicylates >> inhibited the diabetes-induced translocation of [[ p50 ]] (a subunit of NF-kappaB) into nuclei of retinal vascular endothelial cells of the isolated retinal vasculature, as well as of p50 and p65 into nuclei of cells in the ganglion cell layer and inner nuclear layer on whole-retinal sections.


All three << salicylates >> inhibited the diabetes-induced translocation of p50 (a subunit of NF-kappaB) into nuclei of retinal vascular endothelial cells of the isolated retinal vasculature, as well as of [[ p50 ]] and p65 into nuclei of cells in the ganglion cell layer and inner nuclear layer on whole-retinal sections.


All three << salicylates >> inhibited the diabetes-induced translocation of p50 (a subunit of NF-kappaB) into nuclei of retinal vascular endothelial cells of the isolated retinal vasculature, as well as of p50 and [[ p65 ]] into nuclei of cells in the ganglion cell layer and inner nuclear layer on whole-retinal sections.


All three << salicylates >> inhibited the diabetes-induced translocation of p50 (a subunit of [[ NF-kappaB ]]) into nuclei of retinal vascular endothelial cells of the isolated retinal vasculature, as well as of p50 and p65 into nuclei of cells in the ganglion cell layer and inner nuclear layer on whole-retinal sections.


<< Sulfasalazine >> (also as a representative of the salicylates) inhibited the diabetes-induced upregulation of several inflammatory gene products, which are regulated by [[ NF-kappaB ]], including vascular cell adhesion molecule, intracellular adhesion molecule-1, inducible nitric oxide synthase, and cyclooxygenase-2 in whole-retinal lysate.


<< Sulfasalazine >> (also as a representative of the salicylates) inhibited the diabetes-induced upregulation of several inflammatory gene products, which are regulated by NF-kappaB, including vascular cell adhesion molecule, [[ intracellular adhesion molecule-1 ]], inducible nitric oxide synthase, and cyclooxygenase-2 in whole-retinal lysate.


<< Sulfasalazine >> (also as a representative of the salicylates) inhibited the diabetes-induced upregulation of several inflammatory gene products, which are regulated by NF-kappaB, including vascular cell adhesion molecule, intracellular adhesion molecule-1, [[ inducible nitric oxide synthase ]], and cyclooxygenase-2 in whole-retinal lysate.


<< Sulfasalazine >> (also as a representative of the salicylates) inhibited the diabetes-induced upregulation of several inflammatory gene products, which are regulated by NF-kappaB, including vascular cell adhesion molecule, intracellular adhesion molecule-1, inducible nitric oxide synthase, and [[ cyclooxygenase-2 ]] in whole-retinal lysate.


Sulfasalazine (also as a representative of the << salicylates >>) inhibited the diabetes-induced upregulation of several inflammatory gene products, which are regulated by [[ NF-kappaB ]], including vascular cell adhesion molecule, intracellular adhesion molecule-1, inducible nitric oxide synthase, and cyclooxygenase-2 in whole-retinal lysate.


<< Salicylates >>, in doses administrated in our experiments, inhibited [[ NF-kappa ]]B and perhaps other transcription factors in the retina, were well tolerated, and offered new tools to investigate and inhibit the development of diabetic retinopathy.


Lymphocytes possess the essential components of a cholinergic system, including acetylcholine (<< ACh >>); [[ choline acetyltransferase ]] (ChAT), its synthesizing enzyme; and both muscarinic and nicotinic ACh receptors (mAChRs and nAChRs, respectively).


Lymphocytes possess the essential components of a cholinergic system, including acetylcholine (<< ACh >>); choline acetyltransferase ([[ ChAT ]]), its synthesizing enzyme; and both muscarinic and nicotinic ACh receptors (mAChRs and nAChRs, respectively).


Lymphocytes possess the essential components of a cholinergic system, including << acetylcholine >> (ACh); [[ choline acetyltransferase ]] (ChAT), its synthesizing enzyme; and both muscarinic and nicotinic ACh receptors (mAChRs and nAChRs, respectively).


Lymphocytes possess the essential components of a cholinergic system, including << acetylcholine >> (ACh); choline acetyltransferase ([[ ChAT ]]), its synthesizing enzyme; and both muscarinic and nicotinic ACh receptors (mAChRs and nAChRs, respectively).


In addition, activation of protein kinase C and increases in intracellular << cAMP >> also enhance cholinergic activity in T cells, and [[ lymphocyte function associated antigen-1 ]] (LFA-1; CD11a/CD18) is an important mediator of leukocyte migration and T cell activation.


In addition, activation of protein kinase C and increases in intracellular << cAMP >> also enhance cholinergic activity in T cells, and lymphocyte function associated antigen-1 ([[ LFA-1 ]]; CD11a/CD18) is an important mediator of leukocyte migration and T cell activation.


In addition, activation of protein kinase C and increases in intracellular << cAMP >> also enhance cholinergic activity in T cells, and lymphocyte function associated antigen-1 (LFA-1; [[ CD11a ]]/CD18) is an important mediator of leukocyte migration and T cell activation.


In addition, activation of protein kinase C and increases in intracellular << cAMP >> also enhance cholinergic activity in T cells, and lymphocyte function associated antigen-1 (LFA-1; CD11a/[[ CD18 ]]) is an important mediator of leukocyte migration and T cell activation.


We found that << simvastatin >> abolishes anti-[[ CD11a ]] mAb-induced increases in lymphocytic cholinergic activity in a manner independent of its cholesterol-lowering activity.


INTRODUCTION: Medroxyprogesterone acetate (<< MPA >>) induces estrogen receptor (ER)-positive and progesterone receptor ([[ PR ]])-positive ductal invasive mammary carcinomas in BALB/c mice.


INTRODUCTION: Medroxyprogesterone acetate (<< MPA >>) induces [[ estrogen receptor ]] (ER)-positive and progesterone receptor (PR)-positive ductal invasive mammary carcinomas in BALB/c mice.


INTRODUCTION: Medroxyprogesterone acetate (<< MPA >>) induces estrogen receptor ([[ ER ]])-positive and progesterone receptor (PR)-positive ductal invasive mammary carcinomas in BALB/c mice.


INTRODUCTION: << Medroxyprogesterone acetate >> (MPA) induces estrogen receptor (ER)-positive and progesterone receptor ([[ PR ]])-positive ductal invasive mammary carcinomas in BALB/c mice.


INTRODUCTION: << Medroxyprogesterone acetate >> (MPA) induces [[ estrogen receptor ]] (ER)-positive and progesterone receptor (PR)-positive ductal invasive mammary carcinomas in BALB/c mice.


INTRODUCTION: << Medroxyprogesterone acetate >> (MPA) induces estrogen receptor ([[ ER ]])-positive and progesterone receptor (PR)-positive ductal invasive mammary carcinomas in BALB/c mice.


INTRODUCTION: << Medroxyprogesterone acetate >> (MPA) induces estrogen receptor (ER)-positive and [[ progesterone receptor ]] (PR)-positive ductal invasive mammary carcinomas in BALB/c mice.


The expression of << ER-alpha >> and PR isoform A in virgin mice was surprisingly much higher in BALB/c than in C57BL/6 mammary glands, and both receptors were downregulated in [[ progestin ]]-treated BALB/c mice (P < 0.05).


The expression of ER-alpha and << PR isoform A >> in virgin mice was surprisingly much higher in BALB/c than in C57BL/6 mammary glands, and both receptors were downregulated in [[ progestin ]]-treated BALB/c mice (P < 0.05).


<< PR isoform B >> levels were low in virgin control mice and increased after [[ progestin ]] treatment in both strains.


Various genes controlled by << estrogen >>, including [[ X-inactive-specific transcript ]], anterior gradient-2, trefoil factor-1, CRP-ductin, ghrelin, and small proline-rich protein-2A, were dramatically over-expressed.


Various genes controlled by << estrogen >>, including X-inactive-specific transcript, [[ anterior gradient-2 ]], trefoil factor-1, CRP-ductin, ghrelin, and small proline-rich protein-2A, were dramatically over-expressed.


Various genes controlled by << estrogen >>, including X-inactive-specific transcript, anterior gradient-2, [[ trefoil factor-1 ]], CRP-ductin, ghrelin, and small proline-rich protein-2A, were dramatically over-expressed.


Various genes controlled by << estrogen >>, including X-inactive-specific transcript, anterior gradient-2, trefoil factor-1, [[ CRP-ductin ]], ghrelin, and small proline-rich protein-2A, were dramatically over-expressed.


Various genes controlled by << estrogen >>, including X-inactive-specific transcript, anterior gradient-2, trefoil factor-1, CRP-ductin, [[ ghrelin ]], and small proline-rich protein-2A, were dramatically over-expressed.


Various genes controlled by << estrogen >>, including X-inactive-specific transcript, anterior gradient-2, trefoil factor-1, CRP-ductin, ghrelin, and [[ small proline-rich protein-2A ]], were dramatically over-expressed.


<< Estrogen >>-regulated genes including cytokeratin 1-19 and [[ Cyp2a4 ]] were over-expressed, although Cyp3a25 was suppressed.


<< Estrogen >>-regulated genes including [[ cytokeratin 1-19 ]] and Cyp2a4 were over-expressed, although Cyp3a25 was suppressed.


<< Estrogen >>-regulated genes including cytokeratin 1-19 and Cyp2a4 were over-expressed, although [[ Cyp3a25 ]] was suppressed.


Several genes involved with steroid metabolism also showed remarkable expression changes, including increased expression of << 17beta-hydroxysteroid dehydrogenase-7 >> (HSD17beta7; involved in [[ estradiol ]] production) and decreased expression of HSD17beta5 (involved in testosterone production).


Several genes involved with steroid metabolism also showed remarkable expression changes, including increased expression of 17beta-hydroxysteroid dehydrogenase-7 (<< HSD17beta7 >>; involved in [[ estradiol ]] production) and decreased expression of HSD17beta5 (involved in testosterone production).


Several genes involved with steroid metabolism also showed remarkable expression changes, including increased expression of 17beta-hydroxysteroid dehydrogenase-7 (HSD17beta7; involved in estradiol production) and decreased expression of << HSD17beta5 >> (involved in [[ testosterone ]] production).


The expression of key genes important in << methionine >> metabolism, such as [[ methionine adenosyltransferase-1a ]], betaine-homocysteine methyltransferase and thioether S-methyltransferase, were suppressed.


The expression of key genes important in << methionine >> metabolism, such as methionine adenosyltransferase-1a, [[ betaine-homocysteine methyltransferase ]] and thioether S-methyltransferase, were suppressed.


The expression of key genes important in << methionine >> metabolism, such as methionine adenosyltransferase-1a, betaine-homocysteine methyltransferase and [[ thioether S-methyltransferase ]], were suppressed.


<< Monosodium urate >> crystals stimulate monocytes and macrophages to release [[ IL-1beta ]] through the NALP3 component of the inflammasome.


Structural basis of inhibition of the << human NAD+-dependent deacetylase SIRT5 >> by [[ suramin ]].


We identified << suramin >> as a compound that binds to human SIRT5 and showed that it inhibits [[ SIRT5 NAD(+)-dependent deacetylase ]] activity with an IC(50) value of 22 microM.


In humans, << methionine synthase >> deficiency results in the accumulation of [[ methyltetrahydrofolate ]] at the expense of folate derivatives required for purine and thymidylate biosynthesis.


<< Metformin >> and phenformin activate [[ AMP-activated protein kinase ]] in the heart by increasing cytosolic AMP concentration.


Metformin and << phenformin >> activate [[ AMP-activated protein kinase ]] in the heart by increasing cytosolic AMP concentration.


<< Metformin >> and phenformin, which are biguanides, have been reported to increase [[ AMPK ]] activity without increasing AMP/ATP.


Metformin and << phenformin >>, which are biguanides, have been reported to increase [[ AMPK ]] activity without increasing AMP/ATP.


Metformin and phenformin, which are << biguanides >>, have been reported to increase [[ AMPK ]] activity without increasing AMP/ATP.


In hearts treated with << phenformin >> for 18 min and then perfused for 20 min with Krebs-Henseleit buffer, [AMP] began to increase at 26 min and [[ AMPK ]] activity was elevated at 36 min.


In hearts treated with << metformin >>, [AMP] was increased at 50 min and [[ AMPK ]] activity, phosphorylated AMPK, and phosphorylated acetyl-CoA carboxylase were elevated at 61 min.


In hearts treated with << metformin >>, [AMP] was increased at 50 min and AMPK activity, phosphorylated [[ AMPK ]], and phosphorylated acetyl-CoA carboxylase were elevated at 61 min.


In hearts treated with << metformin >>, [AMP] was increased at 50 min and AMPK activity, phosphorylated AMPK, and [[ phosphorylated acetyl-CoA carboxylase ]] were elevated at 61 min.


In summary, << phenformin >> and metformin increase [[ AMPK ]] activity and phosphorylation in the isolated heart.


In summary, phenformin and << metformin >> increase [[ AMPK ]] activity and phosphorylation in the isolated heart.


Cytosolic [AMP] reported metabolically active << AMP >>, which triggered increased [[ AMPK ]] activity, but measures of total AMP did not.


<< Histamine H(1) >> blockade is one of the more prominent actions of the multi-receptor acting antipsychotic [[ clozapine ]].


It is currently not known how much this << H(1) >> antagonism of [[ clozapine ]] contributes to the therapeutic or adverse side effects of clozapine.


In the current project, we found that the selective << H(1) >> antagonist pyrilamine also reversed the [[ dizocilpine ]]-induced impairment in PPI of tactile startle with an auditory prepulse.


In the current project, we found that the selective << H(1) >> antagonist [[ pyrilamine ]] also reversed the dizocilpine-induced impairment in PPI of tactile startle with an auditory prepulse.


In summary, the therapeutic effect of << clozapine >> in reversing PPI impairment was mimicked by the [[ H(1) ]] antagonist pyrilamine, while pyrilamine had a mixed effect on cognition.


In summary, the therapeutic effect of clozapine in reversing PPI impairment was mimicked by the << H(1) >> antagonist [[ pyrilamine ]], while pyrilamine had a mixed effect on cognition.


In summary, the therapeutic effect of clozapine in reversing PPI impairment was mimicked by the << H(1) >> antagonist pyrilamine, while [[ pyrilamine ]] had a mixed effect on cognition.


Thus, << H(1) >> antagonism seems to play a role in part of the beneficial actions of antipsychotics, such as [[ clozapine ]].


Furthermore, the enzymatic activity of << alanine aminotransferase >> (ALT), which converts the critical gluconeogenic amino acid alanine into [[ pyruvate ]], is decreased (approximately 50%) in KLF15-/- hepatocytes.


Furthermore, the enzymatic activity of alanine aminotransferase (<< ALT >>), which converts the critical gluconeogenic amino acid alanine into [[ pyruvate ]], is decreased (approximately 50%) in KLF15-/- hepatocytes.


Furthermore, the enzymatic activity of << alanine aminotransferase >> (ALT), which converts the critical gluconeogenic [[ amino acid ]] alanine into pyruvate, is decreased (approximately 50%) in KLF15-/- hepatocytes.


Furthermore, the enzymatic activity of alanine aminotransferase (<< ALT >>), which converts the critical gluconeogenic [[ amino acid ]] alanine into pyruvate, is decreased (approximately 50%) in KLF15-/- hepatocytes.


Furthermore, the enzymatic activity of << alanine aminotransferase >> (ALT), which converts the critical gluconeogenic amino acid [[ alanine ]] into pyruvate, is decreased (approximately 50%) in KLF15-/- hepatocytes.


Furthermore, the enzymatic activity of alanine aminotransferase (<< ALT >>), which converts the critical gluconeogenic amino acid [[ alanine ]] into pyruvate, is decreased (approximately 50%) in KLF15-/- hepatocytes.


<< D-glucose >> stimulation of L-arginine transport and nitric oxide synthesis results from activation of mitogen-activated protein kinases p42/44 and [[ Smad2 ]] requiring functional type II TGF-beta receptors in human umbilical vein endothelium.


Elevated extracellular << D-glucose >> increases [[ transforming growth factor beta1 ]] (TGF-beta1) release from human umbilical vein endothelium (HUVEC).


Elevated extracellular << D-glucose >> increases transforming growth factor beta1 ([[ TGF-beta1 ]]) release from human umbilical vein endothelium (HUVEC).


<< TGF-beta1 >> release was higher ( approximately 1.6-fold) in 25 mM (high) compared with 5 mM (normal) [[ D-glucose ]].


TGF-beta1 and high << D-glucose >> increased [[ hCAT-1 ]] mRNA expression ( approximately 8-fold) and maximal transport velocity (V(max)), L-[(3)H]citrulline formation from L-[(3)H]arginine (index of NO synthesis) and endothelial NO synthase (eNOS) protein abundance, but did not alter eNOS phosphorylation.


TGF-beta1 and high D-glucose increased hCAT-1 mRNA expression ( approximately 8-fold) and maximal transport velocity (V(max)), L-[(3)H]citrulline formation from L-[(3)H]arginine (index of << NO >> synthesis) and [[ endothelial NO synthase ]] (eNOS) protein abundance, but did not alter eNOS phosphorylation.


TGF-beta1 and high D-glucose increased hCAT-1 mRNA expression ( approximately 8-fold) and maximal transport velocity (V(max)), L-[(3)H]citrulline formation from L-[(3)H]arginine (index of << NO >> synthesis) and endothelial NO synthase ([[ eNOS ]]) protein abundance, but did not alter eNOS phosphorylation.


TGF-beta1 and high << D-glucose >> increased p42/44(mapk) and [[ Smad2 ]] phosphorylation, an effect blocked by PD-98059 (MEK1/2 inhibitor).


TGF-beta1 and high D-glucose increased p42/44(mapk) and << Smad2 >> phosphorylation, an effect blocked by [[ PD-98059 ]] (MEK1/2 inhibitor).


High << D-glucose >> increases L-arginine transport and eNOS expression following [[ TbetaRII ]] activation by TGF-beta1 involving p42/44(mapk) and Smad2 in HUVEC.


High << D-glucose >> increases L-arginine transport and eNOS expression following TbetaRII activation by TGF-beta1 involving p42/44(mapk) and [[ Smad2 ]] in HUVEC.


High << D-glucose >> increases L-arginine transport and [[ eNOS ]] expression following TbetaRII activation by TGF-beta1 involving p42/44(mapk) and Smad2 in HUVEC.


<< n-3 and n-6 polyunsaturated fatty acids >> induce the expression of COX-2 via [[ PPARgamma ]] activation in human keratinocyte HaCaT cells.


<< n-3 and n-6 polyunsaturated fatty acids >> induce the expression of [[ COX-2 ]] via PPARgamma activation in human keratinocyte HaCaT cells.


We demonstrate that only treatment of HaCaT with << GLA >> and EPA or a PPARgamma ligand (roziglitazone), induced [[ COX-2 ]] expression (protein and mRNA).


We demonstrate that only treatment of HaCaT with GLA and << EPA >> or a PPARgamma ligand (roziglitazone), induced [[ COX-2 ]] expression (protein and mRNA).


We demonstrate that only treatment of HaCaT with GLA and EPA or a PPARgamma ligand (<< roziglitazone >>), induced [[ COX-2 ]] expression (protein and mRNA).


Moreover stimulation of << COX-2 promoter >> activity was increased by those [[ PUFAs ]] or rosiglitazone.


Moreover stimulation of << COX-2 promoter >> activity was increased by those PUFAs or [[ rosiglitazone ]].


The inhibitory effects of << GW9662 >> and T0070907 ([[ PPARgamma ]] antagonists), on COX-2 expression and on stimulation of COX-2 promoter activity by EPA and GLA suggest that PPARgamma is implicated in COX-2 induction.


The inhibitory effects of GW9662 and << T0070907 >> ([[ PPARgamma ]] antagonists), on COX-2 expression and on stimulation of COX-2 promoter activity by EPA and GLA suggest that PPARgamma is implicated in COX-2 induction.


Finally, PLA2 inhibitor methyl arachidonyl fluorophosphonate blocked the PUFA effects on COX-2 induction, promoter activity and arachidonic acid mobilization suggesting involvement of << AA >> metabolites in [[ PPAR ]] activation.


Finally, << PLA2 >> inhibitor methyl [[ arachidonyl fluorophosphonate ]] blocked the PUFA effects on COX-2 induction, promoter activity and arachidonic acid mobilization suggesting involvement of AA metabolites in PPAR activation.


Finally, PLA2 inhibitor methyl << arachidonyl fluorophosphonate >> blocked the PUFA effects on [[ COX-2 ]] induction, promoter activity and arachidonic acid mobilization suggesting involvement of AA metabolites in PPAR activation.


These findings demonstrate that << n-3 and n-6 PUFA >> increased [[ PPARgamma ]] activity is necessary for the COX-2 induction in HaCaT human keratinocyte cells.


These findings demonstrate that << n-3 and n-6 PUFA >> increased PPARgamma activity is necessary for the [[ COX-2 ]] induction in HaCaT human keratinocyte cells.


Given the anti-inflammatory properties of EPA, we suggest that induction of << COX-2 >> in keratinocytes may be important in the anti-inflammatory and protective mechanism of action of [[ PUFAs n-3 ]] or n-6.


OBJECTIVE: The aim of this study was to assess the efficacy and tolerability of nebulized arformoterol tartrate (a selective, long-acting << beta(2)-adrenergic >> agonist that is the [[ [R,R] isomer of formoterol ]]) and salmeterol xinafoate versus placebo in patients with chronic obstructive pulmonary disease (COPD).


OBJECTIVE: The aim of this study was to assess the efficacy and tolerability of nebulized << arformoterol tartrate >> (a selective, long-acting [[ beta(2)-adrenergic ]] agonist that is the [R,R] isomer of formoterol) and salmeterol xinafoate versus placebo in patients with chronic obstructive pulmonary disease (COPD).


<< Acetyl-coenzyme A carboxylase >> (ACC) enzymes exist as two isoforms, ACC1 and ACC2, which play critical roles in [[ fatty acid ]] biosynthesis and oxidation.


Acetyl-coenzyme A carboxylase (<< ACC >>) enzymes exist as two isoforms, ACC1 and ACC2, which play critical roles in [[ fatty acid ]] biosynthesis and oxidation.


Acetyl-coenzyme A carboxylase (ACC) enzymes exist as two isoforms, << ACC1 >> and ACC2, which play critical roles in [[ fatty acid ]] biosynthesis and oxidation.


Acetyl-coenzyme A carboxylase (ACC) enzymes exist as two isoforms, ACC1 and << ACC2 >>, which play critical roles in [[ fatty acid ]] biosynthesis and oxidation.


The cytosolic << ACC1 >> is expressed primarily in liver and adipose tissue, and uses malonyl-coenzyme A as a key building block in [[ fatty acid ]] biosynthesis.


The mitochondrial << ACC2 >> is primarily expressed in heart and skeletal muscle, where it is involved in the regulation of [[ fatty acid ]] oxidation.


In contrast, the << RA >> catabolising enzymes [[ Cyp26A1 ]] and Cyp26B1 which are known to be RA-responsive were not expressed at all in the developing eye.


In contrast, the << RA >> catabolising enzymes Cyp26A1 and [[ Cyp26B1 ]] which are known to be RA-responsive were not expressed at all in the developing eye.


Incretin-receptor activation leads to << glucose >>-dependent [[ insulin ]] secretion, induction of beta-cell proliferation, and enhanced resistance to apoptosis.


This report reviews published and unpublished data that suggest that << aripiprazole >> acts as a selective partial agonist at the [[ dopamine D(2) receptor ]] and does not affect 5-HT receptors at therapeutic doses.


<< Mifepriston'e >> blocks [[ glucocorticoid receptor ]] activation without modifying cortisol synthesis.


[N-(piperidin-1-yl)-5-(4-chlorophenyl)-4-methyl-1H-pyrazole-3-carboxyamide] (<< SR 141716A >>), a selective [[ cannabinoid CB1 receptor ]] antagonist, injected into the paraventricular nucleus of the hypothalamus (PVN) of male rats, induces penile erection.


[<< N-(piperidin-1-yl)-5-(4-chlorophenyl)-4-methyl-1H-pyrazole-3-carboxyamide >>] (SR 141716A), a selective [[ cannabinoid CB1 receptor ]] antagonist, injected into the paraventricular nucleus of the hypothalamus (PVN) of male rats, induces penile erection.


The present findings confirm that PVN CB1 receptors, localized mainly in GABAergic synapses that control in an inhibitory fashion excitatory synapses, exert an inhibitory control on penile erection, demonstrating for the first time that chronic blockade of << CB1 receptors >> by [[ SR 141716A ]] increases the density of these receptors in the PVN.


Modulation of the function of CD36 (CD36-/- mice), << p38 >>(MAPK) ([[ SB203580 ]]), COX-1 (indomethacin), and glycoprotein Ib alpha (Nk-protease, 6D1 antibody) induced approximately 50% inhibition.


Modulation of the function of CD36 (CD36-/- mice), p38(<< MAPK >>) ([[ SB203580 ]]), COX-1 (indomethacin), and glycoprotein Ib alpha (Nk-protease, 6D1 antibody) induced approximately 50% inhibition.


Modulation of the function of CD36 (CD36-/- mice), p38(MAPK) (SB203580), << COX-1 >> ([[ indomethacin ]]), and glycoprotein Ib alpha (Nk-protease, 6D1 antibody) induced approximately 50% inhibition.


We show that murine Rdh12 and human RDH13 do not reveal activity towards the checked steroids, but that << human type 12 RDH >> reduces dihydrotestosterone to [[ androstanediol ]], and is thus also involved in steroid metabolism.


The << sibutramine >> group showed significant retardation in gastric emptying of solids (P = .03), reduced maximum tolerated volume (P = .03), and increased postprandial [[ peptide YY ]] compared with the placebo group.


CONCLUSIONS: Weight reduction with << sibutramine >> is associated with altered gastric functions and increased [[ peptide YY ]] and is significantly associated with SLC6A4 genotype.


An investigation of the absolute configuration of the potent << histamine H3 receptor >> antagonist [[ GT-2331 ]] using vibrational circular dichroism.


In this study the neuromuscular blocking drug << vecuronium >> and the controls gallamine and pancuronium slowed the rate of atropine induced [(3)H]N-methylscopolamine dissociation from Chinese hamster ovary cells expressing recombinant [[ human muscarinic M2 receptors ]] K(off) values min(-1); vecuronium (125 nM), atropine 0.45+/-0.07+blocker 0.04+/-0.02; gallamine (21 nM), atropine 0.42+/-0.05+blocker 0.15+/-0.04; pancuronium(21 nM), atropine 0.36+/-0.03+blocker 0.03+/-0.01).


In this study the neuromuscular blocking drug vecuronium and the controls << gallamine >> and pancuronium slowed the rate of atropine induced [(3)H]N-methylscopolamine dissociation from Chinese hamster ovary cells expressing recombinant [[ human muscarinic M2 receptors ]] K(off) values min(-1); vecuronium (125 nM), atropine 0.45+/-0.07+blocker 0.04+/-0.02; gallamine (21 nM), atropine 0.42+/-0.05+blocker 0.15+/-0.04; pancuronium(21 nM), atropine 0.36+/-0.03+blocker 0.03+/-0.01).


In this study the neuromuscular blocking drug vecuronium and the controls gallamine and << pancuronium >> slowed the rate of atropine induced [(3)H]N-methylscopolamine dissociation from Chinese hamster ovary cells expressing recombinant [[ human muscarinic M2 receptors ]] K(off) values min(-1); vecuronium (125 nM), atropine 0.45+/-0.07+blocker 0.04+/-0.02; gallamine (21 nM), atropine 0.42+/-0.05+blocker 0.15+/-0.04; pancuronium(21 nM), atropine 0.36+/-0.03+blocker 0.03+/-0.01).


Patients with acute vitiligo have low epidermal << catalase >> expression/activities and accumulate 10(-3) M [[ H(2)O(2) ]].


<< Mammalian cysteine dioxygenase >> (CDO) is a non-heme iron metalloenzyme that catalyzes the first committed step in oxidative [[ cysteine ]] catabolism.


Mammalian cysteine dioxygenase (<< CDO >>) is a non-heme iron metalloenzyme that catalyzes the first committed step in oxidative [[ cysteine ]] catabolism.


However, upon addition of NO to << CDO >> in the presence of substrate [[ l-cysteine ]], a low-spin {FeNO}7 (S = 1/2) signal that accounts for approximately 85% of the iron within the enzyme develops.


The transcriptional activity of torafugu << PPARalpha1 >> was enhanced 4.5- and 11.5-fold by [[ Wy-14643 ]] and 5,8,11,14-eicosatetraynoic acid (ETYA) each at 10 microM, respectively, whereas that of PPARalpha2, 4.5- and 7.3-fold at the same concentration of the respective ligands, respectively.


The transcriptional activity of torafugu PPARalpha1 was enhanced 4.5- and 11.5-fold by << Wy-14643 >> and 5,8,11,14-eicosatetraynoic acid (ETYA) each at 10 microM, respectively, whereas that of [[ PPARalpha2 ]], 4.5- and 7.3-fold at the same concentration of the respective ligands, respectively.


The transcriptional activity of torafugu << PPARalpha1 >> was enhanced 4.5- and 11.5-fold by Wy-14643 and [[ 5,8,11,14-eicosatetraynoic acid ]] (ETYA) each at 10 microM, respectively, whereas that of PPARalpha2, 4.5- and 7.3-fold at the same concentration of the respective ligands, respectively.


The transcriptional activity of torafugu PPARalpha1 was enhanced 4.5- and 11.5-fold by Wy-14643 and << 5,8,11,14-eicosatetraynoic acid >> (ETYA) each at 10 microM, respectively, whereas that of [[ PPARalpha2 ]], 4.5- and 7.3-fold at the same concentration of the respective ligands, respectively.


The transcriptional activity of torafugu << PPARalpha1 >> was enhanced 4.5- and 11.5-fold by Wy-14643 and 5,8,11,14-eicosatetraynoic acid ([[ ETYA ]]) each at 10 microM, respectively, whereas that of PPARalpha2, 4.5- and 7.3-fold at the same concentration of the respective ligands, respectively.


The transcriptional activity of torafugu PPARalpha1 was enhanced 4.5- and 11.5-fold by Wy-14643 and 5,8,11,14-eicosatetraynoic acid (<< ETYA >>) each at 10 microM, respectively, whereas that of [[ PPARalpha2 ]], 4.5- and 7.3-fold at the same concentration of the respective ligands, respectively.


Furthermore, the activities of the two << torafugu PPARalphas >> were enhanced 4.3- and 7.6-fold by [[ arachidonic acid ]], 4.4- and 5.2-fold by docosahexaenoic acid, and 6.7- and 8.0-fold by eicosapentaenoic acid each at 50 microM, respectively.


Furthermore, the activities of the two << torafugu PPARalphas >> were enhanced 4.3- and 7.6-fold by arachidonic acid, 4.4- and 5.2-fold by [[ docosahexaenoic acid ]], and 6.7- and 8.0-fold by eicosapentaenoic acid each at 50 microM, respectively.


Furthermore, the activities of the two << torafugu PPARalphas >> were enhanced 4.3- and 7.6-fold by arachidonic acid, 4.4- and 5.2-fold by docosahexaenoic acid, and 6.7- and 8.0-fold by [[ eicosapentaenoic acid ]] each at 50 microM, respectively.


Combination chemotherapy with a << substance P receptor >> antagonist ([[ aprepitant ]]) and melarsoprol in a mouse model of human African trypanosomiasis.


Combination chemotherapy with a << substance P receptor >> antagonist (aprepitant) and [[ melarsoprol ]] in a mouse model of human African trypanosomiasis.


In this study we investigated the effects of combination chemotherapy with melarsoprol and a << humanised SP receptor >> antagonist [[ aprepitant ]] (EMEND) in this mouse model.


In this study we investigated the effects of combination chemotherapy with melarsoprol and a << humanised SP receptor >> antagonist aprepitant ([[ EMEND ]]) in this mouse model.


It is thought to play a critical role in the visual cycle by functioning as an acceptor of << 11-cis-retinol >> from the [[ isomerohydrolase ]] reaction.


<< Dimethylarginine dimethylaminohydrolase >> (DDAH) metabolizes asymmetric dimethylarginine to generate [[ L-citrulline ]] and is present in large quantities in the kidney.


Dimethylarginine dimethylaminohydrolase (<< DDAH >>) metabolizes asymmetric dimethylarginine to generate [[ L-citrulline ]] and is present in large quantities in the kidney.


<< Dimethylarginine dimethylaminohydrolase >> (DDAH) metabolizes asymmetric [[ dimethylarginine ]] to generate L-citrulline and is present in large quantities in the kidney.


Dimethylarginine dimethylaminohydrolase (<< DDAH >>) metabolizes asymmetric [[ dimethylarginine ]] to generate L-citrulline and is present in large quantities in the kidney.


We present a new study that optimizes the Prescott-Jones colorimetric assay to measure << DDAH >>-dependent [[ L-citrulline ]] generation in kidney homogenates.


We found that the removal of << urea >> with [[ urease ]] is necessary since urea also produces a positive reaction.


Our optimized << L-citrulline >> production assay to measure [[ DDAH ]] activity correlated closely with the direct measure of the rate of asymmetric dimethylarginine consumption.


Our optimized L-citrulline production assay to measure << DDAH >> activity correlated closely with the direct measure of the rate of asymmetric [[ dimethylarginine ]] consumption.


Using this assay, we found that both << superoxide >> and nitric oxide inhibit renal cortical [[ DDAH ]] activity in vitro.


Using this assay, we found that both superoxide and << nitric oxide >> inhibit renal cortical [[ DDAH ]] activity in vitro.


The next large phase III adjuvant trial for this subset of breast cancer is an international collaboration designed to evaluate the added or alternative benefit of an oral tyrosine kinase inhibitor targeting << HER2 >>/neu as well as the epidermal growth factor receptor (EGFR), [[ lapatinib ]].


The next large phase III adjuvant trial for this subset of breast cancer is an international collaboration designed to evaluate the added or alternative benefit of an oral tyrosine kinase inhibitor targeting HER2/<< neu >> as well as the epidermal growth factor receptor (EGFR), [[ lapatinib ]].


The next large phase III adjuvant trial for this subset of breast cancer is an international collaboration designed to evaluate the added or alternative benefit of an oral tyrosine kinase inhibitor targeting HER2/neu as well as the << epidermal growth factor receptor >> (EGFR), [[ lapatinib ]].


The next large phase III adjuvant trial for this subset of breast cancer is an international collaboration designed to evaluate the added or alternative benefit of an oral tyrosine kinase inhibitor targeting HER2/neu as well as the epidermal growth factor receptor (<< EGFR >>), [[ lapatinib ]].


Exposure of Jurkat cells to either << (5S,10R)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,b]cyclohepten-5,10-imine >> [(+)-MK 801] or D-(-)-2-amino-5-phosphonopentanoic acid (D-AP5), two selective [[ NMDA receptor ]] antagonists, limited cell growth by inhibiting cell cycle progression and inducing apoptosis, whereas l-glutamate (1 microM) and NMDA (10 microM) significantly increased (137.2+/-22.0%; P<0.01) Jurkat T cell adhesion to fibronectin.


Exposure of Jurkat cells to either (5S,10R)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,b]cyclohepten-5,10-imine [<< (+)-MK 801 >>] or D-(-)-2-amino-5-phosphonopentanoic acid (D-AP5), two selective [[ NMDA receptor ]] antagonists, limited cell growth by inhibiting cell cycle progression and inducing apoptosis, whereas l-glutamate (1 microM) and NMDA (10 microM) significantly increased (137.2+/-22.0%; P<0.01) Jurkat T cell adhesion to fibronectin.


Exposure of Jurkat cells to either (5S,10R)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,b]cyclohepten-5,10-imine [(+)-MK 801] or << D-(-)-2-amino-5-phosphonopentanoic acid >> (D-AP5), two selective [[ NMDA receptor ]] antagonists, limited cell growth by inhibiting cell cycle progression and inducing apoptosis, whereas l-glutamate (1 microM) and NMDA (10 microM) significantly increased (137.2+/-22.0%; P<0.01) Jurkat T cell adhesion to fibronectin.


Exposure of Jurkat cells to either (5S,10R)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,b]cyclohepten-5,10-imine [(+)-MK 801] or D-(-)-2-amino-5-phosphonopentanoic acid (<< D-AP5 >>), two selective [[ NMDA receptor ]] antagonists, limited cell growth by inhibiting cell cycle progression and inducing apoptosis, whereas l-glutamate (1 microM) and NMDA (10 microM) significantly increased (137.2+/-22.0%; P<0.01) Jurkat T cell adhesion to fibronectin.


<< Desvenlafaxine succinate >> identifies novel antagonist binding determinants in the [[ human norepinephrine transporter ]].


<< Desvenlafaxine succinate >> (DVS) is a recently introduced antagonist of the human norepinephrine and serotonin transporters ([[ hNET ]] and hSERT, respectively), currently in clinical development for use in the treatment of major depressive disorder and vasomotor symptoms associated with menopause.


<< Desvenlafaxine succinate >> (DVS) is a recently introduced antagonist of the human norepinephrine and serotonin transporters (hNET and [[ hSERT ]], respectively), currently in clinical development for use in the treatment of major depressive disorder and vasomotor symptoms associated with menopause.


Desvenlafaxine succinate (<< DVS >>) is a recently introduced antagonist of the human norepinephrine and serotonin transporters ([[ hNET ]] and hSERT, respectively), currently in clinical development for use in the treatment of major depressive disorder and vasomotor symptoms associated with menopause.


Desvenlafaxine succinate (<< DVS >>) is a recently introduced antagonist of the human norepinephrine and serotonin transporters (hNET and [[ hSERT ]], respectively), currently in clinical development for use in the treatment of major depressive disorder and vasomotor symptoms associated with menopause.


Using << hNET >> in transfected human embryonic kidney-293 cells, this difference in potency for DVS at sites labeled by [(3)H]NIS was found to distinguish DVS, the [[ DVS ]] analog rac-(1-[1-(3-chloro-phenyl)-2-(4-methylpiperazin-1-yl)-ethyl]cyclohexanol (WY-46824), methylphenidate, and the cocaine analog 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester (RTI-55) from other hNET antagonists, such as NIS, mazindol, tricyclic antidepressants, and cocaine.


Using << hNET >> in transfected human embryonic kidney-293 cells, this difference in potency for DVS at sites labeled by [(3)H]NIS was found to distinguish DVS, the DVS analog [[ rac-(1-[1-(3-chloro-phenyl)-2-(4-methylpiperazin-1-yl)-ethyl]cyclohexanol ]] (WY-46824), methylphenidate, and the cocaine analog 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester (RTI-55) from other hNET antagonists, such as NIS, mazindol, tricyclic antidepressants, and cocaine.


Using << hNET >> in transfected human embryonic kidney-293 cells, this difference in potency for DVS at sites labeled by [(3)H]NIS was found to distinguish DVS, the DVS analog rac-(1-[1-(3-chloro-phenyl)-2-(4-methylpiperazin-1-yl)-ethyl]cyclohexanol ([[ WY-46824 ]]), methylphenidate, and the cocaine analog 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester (RTI-55) from other hNET antagonists, such as NIS, mazindol, tricyclic antidepressants, and cocaine.


Using << hNET >> in transfected human embryonic kidney-293 cells, this difference in potency for DVS at sites labeled by [(3)H]NIS was found to distinguish DVS, the DVS analog rac-(1-[1-(3-chloro-phenyl)-2-(4-methylpiperazin-1-yl)-ethyl]cyclohexanol (WY-46824), [[ methylphenidate ]], and the cocaine analog 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester (RTI-55) from other hNET antagonists, such as NIS, mazindol, tricyclic antidepressants, and cocaine.


Using << hNET >> in transfected human embryonic kidney-293 cells, this difference in potency for DVS at sites labeled by [(3)H]NIS was found to distinguish DVS, the DVS analog rac-(1-[1-(3-chloro-phenyl)-2-(4-methylpiperazin-1-yl)-ethyl]cyclohexanol (WY-46824), methylphenidate, and the [[ cocaine ]] analog 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester (RTI-55) from other hNET antagonists, such as NIS, mazindol, tricyclic antidepressants, and cocaine.


Using << hNET >> in transfected human embryonic kidney-293 cells, this difference in potency for DVS at sites labeled by [(3)H]NIS was found to distinguish DVS, the DVS analog rac-(1-[1-(3-chloro-phenyl)-2-(4-methylpiperazin-1-yl)-ethyl]cyclohexanol (WY-46824), methylphenidate, and the cocaine analog [[ 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester ]] (RTI-55) from other hNET antagonists, such as NIS, mazindol, tricyclic antidepressants, and cocaine.


Using << hNET >> in transfected human embryonic kidney-293 cells, this difference in potency for DVS at sites labeled by [(3)H]NIS was found to distinguish DVS, the DVS analog rac-(1-[1-(3-chloro-phenyl)-2-(4-methylpiperazin-1-yl)-ethyl]cyclohexanol (WY-46824), methylphenidate, and the cocaine analog 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester ([[ RTI-55 ]]) from other hNET antagonists, such as NIS, mazindol, tricyclic antidepressants, and cocaine.


Using hNET in transfected human embryonic kidney-293 cells, this difference in potency for DVS at sites labeled by [(3)H]NIS was found to distinguish DVS, the DVS analog rac-(1-[1-(3-chloro-phenyl)-2-(4-methylpiperazin-1-yl)-ethyl]cyclohexanol (WY-46824), methylphenidate, and the cocaine analog 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester (RTI-55) from other << hNET >> antagonists, such as [[ NIS ]], mazindol, tricyclic antidepressants, and cocaine.


Using hNET in transfected human embryonic kidney-293 cells, this difference in potency for DVS at sites labeled by [(3)H]NIS was found to distinguish DVS, the DVS analog rac-(1-[1-(3-chloro-phenyl)-2-(4-methylpiperazin-1-yl)-ethyl]cyclohexanol (WY-46824), methylphenidate, and the cocaine analog 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester (RTI-55) from other << hNET >> antagonists, such as NIS, [[ mazindol ]], tricyclic antidepressants, and cocaine.


Using hNET in transfected human embryonic kidney-293 cells, this difference in potency for DVS at sites labeled by [(3)H]NIS was found to distinguish DVS, the DVS analog rac-(1-[1-(3-chloro-phenyl)-2-(4-methylpiperazin-1-yl)-ethyl]cyclohexanol (WY-46824), methylphenidate, and the cocaine analog 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester (RTI-55) from other << hNET >> antagonists, such as NIS, mazindol, [[ tricyclic ]] antidepressants, and cocaine.


Using hNET in transfected human embryonic kidney-293 cells, this difference in potency for DVS at sites labeled by [(3)H]NIS was found to distinguish DVS, the DVS analog rac-(1-[1-(3-chloro-phenyl)-2-(4-methylpiperazin-1-yl)-ethyl]cyclohexanol (WY-46824), methylphenidate, and the cocaine analog 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester (RTI-55) from other << hNET >> antagonists, such as NIS, mazindol, tricyclic antidepressants, and [[ cocaine ]].


Using << hNET >> in transfected human embryonic kidney-293 cells, this difference in potency for DVS at sites labeled by [(3)H]NIS was found to distinguish [[ DVS ]], the DVS analog rac-(1-[1-(3-chloro-phenyl)-2-(4-methylpiperazin-1-yl)-ethyl]cyclohexanol (WY-46824), methylphenidate, and the cocaine analog 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester (RTI-55) from other hNET antagonists, such as NIS, mazindol, tricyclic antidepressants, and cocaine.


<< Sorafenib >> and sunitinib are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 ([[ VEGFR-2 ]], VEGFR-3) and platelet-derived growth factor receptor beta (PDGFR-beta), while temsirolimus is an mTOR inhibitor.


<< Sorafenib >> and sunitinib are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 (VEGFR-2, [[ VEGFR-3 ]]) and platelet-derived growth factor receptor beta (PDGFR-beta), while temsirolimus is an mTOR inhibitor.


<< Sorafenib >> and sunitinib are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 (VEGFR-2, VEGFR-3) and [[ platelet-derived growth factor receptor beta ]] (PDGFR-beta), while temsirolimus is an mTOR inhibitor.


<< Sorafenib >> and sunitinib are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 (VEGFR-2, VEGFR-3) and platelet-derived growth factor receptor beta ([[ PDGFR-beta ]]), while temsirolimus is an mTOR inhibitor.


Sorafenib and << sunitinib >> are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 ([[ VEGFR-2 ]], VEGFR-3) and platelet-derived growth factor receptor beta (PDGFR-beta), while temsirolimus is an mTOR inhibitor.


Sorafenib and << sunitinib >> are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 (VEGFR-2, [[ VEGFR-3 ]]) and platelet-derived growth factor receptor beta (PDGFR-beta), while temsirolimus is an mTOR inhibitor.


Sorafenib and << sunitinib >> are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 (VEGFR-2, VEGFR-3) and [[ platelet-derived growth factor receptor beta ]] (PDGFR-beta), while temsirolimus is an mTOR inhibitor.


Sorafenib and << sunitinib >> are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 (VEGFR-2, VEGFR-3) and platelet-derived growth factor receptor beta ([[ PDGFR-beta ]]), while temsirolimus is an mTOR inhibitor.


Sorafenib and sunitinib are synthetic, orally active agents shown to directly inhibit vascular endothelial growth factor receptors -2 and -3 (VEGFR-2, VEGFR-3) and platelet-derived growth factor receptor beta (PDGFR-beta), while << temsirolimus >> is an [[ mTOR ]] inhibitor.


One is that the binding of retinoids to nuclear retinoic acid receptors (RARs) does not match their therapeutic efficacy: acitretin activates the three receptor subtypes, RAR-alpha, -beta and -gamma, without measurable receptor binding, whereas << tazarotene >> preferentially binds to and activates RAR-beta and -gamma in preference to [[ RAR-alpha ]].


Comprehensive review of << rasagiline >>, a second-generation [[ monoamine oxidase ]] inhibitor, for the treatment of Parkinson's disease.


Rasagiline [<< N-propargyl-l(R)-aminoindan >>] is a second-generation propargylamine pharmacophore that selectively and irreversibly inhibits brain [[ MAO-B ]] and is specifically designed for the treatment of Parkinson's disease (PD).


Rasagiline [N-propargyl-l(R)-aminoindan] is a second-generation << propargylamine >> pharmacophore that selectively and irreversibly inhibits brain [[ MAO-B ]] and is specifically designed for the treatment of Parkinson's disease (PD).


<< Rasagiline >> [N-propargyl-l(R)-aminoindan] is a second-generation propargylamine pharmacophore that selectively and irreversibly inhibits brain [[ MAO-B ]] and is specifically designed for the treatment of Parkinson's disease (PD).


Based on the results from those studies, we concluded that << rasagiline >> PO QD, at the therapeutic dosage range of 0.5 to 1 rag/d, is effective and well tolerated and completely, selectively, and specifically inhibited [[ MAO-B ]].


This overview focuses on the indirect antithrombin dependent pentasaccharide derivatives of idraparinux and on the most advanced oral direct inhibitors to << factor Xa >> ([[ rivaroxaban ]] and apixaban) and IIa (dabigatran).


This overview focuses on the indirect antithrombin dependent pentasaccharide derivatives of idraparinux and on the most advanced oral direct inhibitors to << factor Xa >> (rivaroxaban and [[ apixaban ]]) and IIa (dabigatran).


INTERVENTIONS: In the 8-week run-in period, all participants received the << ACE >> inhibitor [[ cilazapril ]] (5 mg), the ARB telmisartan (80 mg), and the diuretic hydrochlorothiazide (12.5 mg) as double RAAS blockade to achieve the target blood pressure of less than 130/80 mm Hg.


Porcine TLR8 and << TLR7 >> are both activated by a selective TLR7 ligand, [[ imiquimod ]].


Porcine << TLR8 >> and TLR7 are both activated by a selective TLR7 ligand, [[ imiquimod ]].


Two << imidazoquinoline >> molecules, imiquimod and gardiquimod, markedly activated both [[ porcine TLR7 ]] and TLR8 whereas only human TLR7, but not TLR8, was activated by the ligands.


Two << imidazoquinoline >> molecules, imiquimod and gardiquimod, markedly activated both porcine TLR7 and [[ TLR8 ]] whereas only human TLR7, but not TLR8, was activated by the ligands.


Two << imidazoquinoline >> molecules, imiquimod and gardiquimod, markedly activated both porcine TLR7 and TLR8 whereas only [[ human TLR7 ]], but not TLR8, was activated by the ligands.


Two imidazoquinoline molecules, << imiquimod >> and gardiquimod, markedly activated both [[ porcine TLR7 ]] and TLR8 whereas only human TLR7, but not TLR8, was activated by the ligands.


Two imidazoquinoline molecules, << imiquimod >> and gardiquimod, markedly activated both porcine TLR7 and [[ TLR8 ]] whereas only human TLR7, but not TLR8, was activated by the ligands.


Two imidazoquinoline molecules, << imiquimod >> and gardiquimod, markedly activated both porcine TLR7 and TLR8 whereas only [[ human TLR7 ]], but not TLR8, was activated by the ligands.


Two imidazoquinoline molecules, imiquimod and << gardiquimod >>, markedly activated both [[ porcine TLR7 ]] and TLR8 whereas only human TLR7, but not TLR8, was activated by the ligands.


Two imidazoquinoline molecules, imiquimod and << gardiquimod >>, markedly activated both porcine TLR7 and [[ TLR8 ]] whereas only human TLR7, but not TLR8, was activated by the ligands.


Two imidazoquinoline molecules, imiquimod and << gardiquimod >>, markedly activated both porcine TLR7 and TLR8 whereas only [[ human TLR7 ]], but not TLR8, was activated by the ligands.


Moreover, activation of transfected cells and porcine PBMC by << TLR7 >> ligands was inhibited by [[ bafilomycin A(1) ]] indicating the requirement of endosomal/lysosomal acidification for activation of the receptors.


High-affinity blockade of << voltage-operated skeletal muscle and neuronal sodium channels >> by [[ halogenated propofol ]] analogues.


The IC(50) for block of resting channels at -150 mV was 2.3, 3.9 and 11.3 microM in Na(V)1.4, respectively, and 29.2 microM for << 4-chloropropofol >> in [[ Na(V)1.2 ]].


Estimated affinities for the fast-inactivated channel state were 81 nM, 312 nM and 227 nM for << 4-iodopropofol >>, 4-bromopropofol and 4-chloropropofol in [[ Na(V)1.4 ]], and 450 nM for 4-chloropropofol in Na(V)1.2.


Estimated affinities for the fast-inactivated channel state were 81 nM, 312 nM and 227 nM for 4-iodopropofol, << 4-bromopropofol >> and 4-chloropropofol in [[ Na(V)1.4 ]], and 450 nM for 4-chloropropofol in Na(V)1.2.


Estimated affinities for the fast-inactivated channel state were 81 nM, 312 nM and 227 nM for 4-iodopropofol, 4-bromopropofol and << 4-chloropropofol >> in [[ Na(V)1.4 ]], and 450 nM for 4-chloropropofol in Na(V)1.2.


Estimated affinities for the fast-inactivated channel state were 81 nM, 312 nM and 227 nM for 4-iodopropofol, 4-bromopropofol and 4-chloropropofol in Na(V)1.4, and 450 nM for << 4-chloropropofol >> in [[ Na(V)1.2 ]].


CONCLUSIONS AND IMPLICATIONS: << Halogenated propofol >> analogues constitute a novel class of [[ sodium channel ]]-blocking drugs possessing almost 100-fold higher potency compared with the local anaesthetic and anti-arrhythmic drug lidocaine.


<< Irbesartan >> (Aprovel, Avapro, Irbetan, Karvea), an [[ angiotensin II receptor type 1 ]] antagonist, is approved in many countries worldwide for the treatment of hypertension.


Irbesartan (<< Aprovel >>, Avapro, Irbetan, Karvea), an [[ angiotensin II receptor type 1 ]] antagonist, is approved in many countries worldwide for the treatment of hypertension.


Irbesartan (Aprovel, << Avapro >>, Irbetan, Karvea), an [[ angiotensin II receptor type 1 ]] antagonist, is approved in many countries worldwide for the treatment of hypertension.


Irbesartan (Aprovel, Avapro, << Irbetan >>, Karvea), an [[ angiotensin II receptor type 1 ]] antagonist, is approved in many countries worldwide for the treatment of hypertension.


Irbesartan (Aprovel, Avapro, Irbetan, << Karvea >>), an [[ angiotensin II receptor type 1 ]] antagonist, is approved in many countries worldwide for the treatment of hypertension.


DNA damage is accepted as a consequence of << thymidylate >> deprivation induced by chemotherapeutic inhibitors of [[ thymidylate synthase ]] (TS), but the types of damage and signaling responses remain incompletely understood.


DNA damage is accepted as a consequence of << thymidylate >> deprivation induced by chemotherapeutic inhibitors of thymidylate synthase ([[ TS ]]), but the types of damage and signaling responses remain incompletely understood.


When RAD51, which is a central component of HR, was depleted by siRNA cells were sensitized to raltitrexed (<< RTX >>), which specifically inhibits [[ TS ]].


<< RTX >> treatment also induced foci of [[ RAD51 ]], gamma-H2AX, phospho-Chk1, and phospho-NBS1, although the extent of co-localization with RPA2 foci varied.


<< RTX >> treatment also induced foci of RAD51, [[ gamma-H2AX ]], phospho-Chk1, and phospho-NBS1, although the extent of co-localization with RPA2 foci varied.


<< RTX >> treatment also induced foci of RAD51, gamma-H2AX, [[ phospho-Chk1 ]], and phospho-NBS1, although the extent of co-localization with RPA2 foci varied.


<< RTX >> treatment also induced foci of RAD51, gamma-H2AX, phospho-Chk1, and [[ phospho-NBS1 ]], although the extent of co-localization with RPA2 foci varied.


<< Nicotinamide N-methyltransferase >> (NNMT) catalyses the conversion of nicotinamide to [[ 1-methylnicotinamide ]] and plays an important role in hepatic detoxification reactions.


Nicotinamide N-methyltransferase (<< NNMT >>) catalyses the conversion of nicotinamide to [[ 1-methylnicotinamide ]] and plays an important role in hepatic detoxification reactions.


<< Nicotinamide N-methyltransferase >> (NNMT) catalyses the conversion of [[ nicotinamide ]] to 1-methylnicotinamide and plays an important role in hepatic detoxification reactions.


Nicotinamide N-methyltransferase (<< NNMT >>) catalyses the conversion of [[ nicotinamide ]] to 1-methylnicotinamide and plays an important role in hepatic detoxification reactions.


<< Homocysteine >>, the atherogenic product of the [[ NNMT ]]-catalyzed reaction, was secreted from 3T3-L1 cells or adipose tissue cultures.


Homocysteine release increased during 3T3-L1 differentiation and was reduced when adipose tissue was treated with the << NNMT >> inhibitor [[ 1-methylnicotinamide ]].


Nicotinic acid (<< NA >>), a widely used drug to lower elevated plasma lipid levels, induced [[ NNMT ]] enzyme activity in white adipose tissue of mice.


<< Nicotinic acid >> (NA), a widely used drug to lower elevated plasma lipid levels, induced [[ NNMT ]] enzyme activity in white adipose tissue of mice.


These data support the concept that adipose tissue << NNMT >> contributes to the increased plasma [[ homocysteine ]] levels in patients treated with NA.


Global target profile of the << kinase >> inhibitor [[ bosutinib ]] in primary chronic myeloid leukemia cells.


Here, we characterized the target profile of the dual << SRC >>/ABL inhibitor [[ bosutinib ]] employing a two-tiered approach using chemical proteomics to identify natural binders in whole cell lysates of primary CML and K562 cells in parallel to in vitro kinase assays against a large recombinant kinase panel.


Here, we characterized the target profile of the dual SRC/<< ABL >> inhibitor [[ bosutinib ]] employing a two-tiered approach using chemical proteomics to identify natural binders in whole cell lysates of primary CML and K562 cells in parallel to in vitro kinase assays against a large recombinant kinase panel.


A comparison of bosutinib with << dasatinib >> across the whole [[ kinase ]] panel revealed overlapping, but distinct, inhibition profiles.


A comparison of << bosutinib >> with dasatinib across the whole [[ kinase ]] panel revealed overlapping, but distinct, inhibition profiles.


Finally, << bosutinib >> is the first [[ kinase ]] inhibitor shown to target CAMK2G, recently implicated in myeloid leukemia cell proliferation.


Finally, << bosutinib >> is the first kinase inhibitor shown to target [[ CAMK2G ]], recently implicated in myeloid leukemia cell proliferation.


Affinity alkylation with 2 alpha-bromoacetoxyprogesterone suggests that the << dehydrogenase >> and isomerase substrate [[ steroids ]] bind at different sites on the same protein.


The affinity labeling << nucleotide >> analog, 5'-[p-(fluorosulfonyl)benzoyl]adenosine (FSA), inactivates the [[ dehydrogenase ]] and isomerase activities at similar rates in an irreversible manner which follows first order kinetics with respect to both time and alkylator concentration (0.2-0.6 mM).


The affinity labeling nucleotide analog, << 5'-[p-(fluorosulfonyl)benzoyl]adenosine >> (FSA), inactivates the [[ dehydrogenase ]] and isomerase activities at similar rates in an irreversible manner which follows first order kinetics with respect to both time and alkylator concentration (0.2-0.6 mM).


The affinity labeling nucleotide analog, 5'-[p-(fluorosulfonyl)benzoyl]adenosine (<< FSA >>), inactivates the [[ dehydrogenase ]] and isomerase activities at similar rates in an irreversible manner which follows first order kinetics with respect to both time and alkylator concentration (0.2-0.6 mM).


The 3 beta-hydroxysteroid substrate, pregnenolone, protects isomerase as well as << dehydrogenase >> from inactivation by [[ FSA ]].


The most successful example of << kinase >> blockers is [[ Imatinib ]] (Imatinib mesylate, Gleevec, STI571), the inhibitor of Bcr/Abl oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.


The most successful example of kinase blockers is << Imatinib >> (Imatinib mesylate, Gleevec, STI571), the inhibitor of [[ Bcr ]]/Abl oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.


The most successful example of kinase blockers is << Imatinib >> (Imatinib mesylate, Gleevec, STI571), the inhibitor of Bcr/[[ Abl ]] oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.


The most successful example of << kinase >> blockers is Imatinib ([[ Imatinib mesylate ]], Gleevec, STI571), the inhibitor of Bcr/Abl oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.


The most successful example of kinase blockers is Imatinib (<< Imatinib mesylate >>, Gleevec, STI571), the inhibitor of [[ Bcr ]]/Abl oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.


The most successful example of kinase blockers is Imatinib (<< Imatinib mesylate >>, Gleevec, STI571), the inhibitor of Bcr/[[ Abl ]] oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.


The most successful example of << kinase >> blockers is Imatinib (Imatinib mesylate, [[ Gleevec ]], STI571), the inhibitor of Bcr/Abl oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.


The most successful example of kinase blockers is Imatinib (Imatinib mesylate, << Gleevec >>, STI571), the inhibitor of [[ Bcr ]]/Abl oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.


The most successful example of kinase blockers is Imatinib (Imatinib mesylate, << Gleevec >>, STI571), the inhibitor of Bcr/[[ Abl ]] oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.


The most successful example of << kinase >> blockers is Imatinib (Imatinib mesylate, Gleevec, [[ STI571 ]]), the inhibitor of Bcr/Abl oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.


The most successful example of kinase blockers is Imatinib (Imatinib mesylate, Gleevec, << STI571 >>), the inhibitor of [[ Bcr ]]/Abl oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.


The most successful example of kinase blockers is Imatinib (Imatinib mesylate, Gleevec, << STI571 >>), the inhibitor of Bcr/[[ Abl ]] oncoprotein, which has become a first-line therapy for chronic myelogenous leukemia.


Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (<< SU 11248 >>, Sutent) specific for [[ VEGF receptor ]] kinase, AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.


Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (<< SU 11248 >>, Sutent) specific for VEGF receptor [[ kinase ]], AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.


Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, << Sutent >>) specific for [[ VEGF receptor ]] kinase, AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.


Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, << Sutent >>) specific for VEGF receptor [[ kinase ]], AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.


Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for VEGF receptor kinase, << AMN107 >> (Nilotinib) and INNO-406 (NS-187) specific for [[ c-KIT ]] kinase.


Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for VEGF receptor kinase, AMN107 (<< Nilotinib >>) and INNO-406 (NS-187) specific for [[ c-KIT ]] kinase.


Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for VEGF receptor kinase, AMN107 (Nilotinib) and << INNO-406 >> (NS-187) specific for [[ c-KIT ]] kinase.


Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for VEGF receptor kinase, AMN107 (Nilotinib) and INNO-406 (<< NS-187 >>) specific for [[ c-KIT ]] kinase.


Others kinase inhibitors used recently in cancer therapy include << Dasatinib >> (BMS-354825) specific for [[ ABL ]] non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for VEGF receptor kinase, AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.


Others kinase inhibitors used recently in cancer therapy include << Dasatinib >> (BMS-354825) specific for ABL [[ non-receptor cytoplasmic kinase ]], Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for VEGF receptor kinase, AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.


Others kinase inhibitors used recently in cancer therapy include Dasatinib (<< BMS-354825 >>) specific for [[ ABL ]] non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for VEGF receptor kinase, AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.


Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, << Gefitinib >> (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for [[ VEGF receptor ]] kinase, AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.


Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, << Gefitinib >> (Iressa), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for VEGF receptor [[ kinase ]], AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.


Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (<< Iressa >>), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for [[ VEGF receptor ]] kinase, AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.


Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (<< Iressa >>), Erlotinib (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for VEGF receptor [[ kinase ]], AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.


Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), << Erlotinib >> (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for [[ VEGF receptor ]] kinase, AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.


Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), << Erlotinib >> (OSI-774, Tarceva) and Sunitinib (SU 11248, Sutent) specific for VEGF receptor [[ kinase ]], AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.


Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (<< OSI-774 >>, Tarceva) and Sunitinib (SU 11248, Sutent) specific for [[ VEGF receptor ]] kinase, AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.


Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (<< OSI-774 >>, Tarceva) and Sunitinib (SU 11248, Sutent) specific for VEGF receptor [[ kinase ]], AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.


Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, << Tarceva >>) and Sunitinib (SU 11248, Sutent) specific for [[ VEGF receptor ]] kinase, AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.


Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, << Tarceva >>) and Sunitinib (SU 11248, Sutent) specific for VEGF receptor [[ kinase ]], AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.


Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and << Sunitinib >> (SU 11248, Sutent) specific for [[ VEGF receptor ]] kinase, AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.


Others kinase inhibitors used recently in cancer therapy include Dasatinib (BMS-354825) specific for ABL non-receptor cytoplasmic kinase, Gefitinib (Iressa), Erlotinib (OSI-774, Tarceva) and << Sunitinib >> (SU 11248, Sutent) specific for VEGF receptor [[ kinase ]], AMN107 (Nilotinib) and INNO-406 (NS-187) specific for c-KIT kinase.


The following << TK >> blockers for treatment of various human tumors are in clinical development: [[ Lapatinib ]] (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib (CI-1033), Zactima (ZD6474), Vatalanib (PTK787/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide (SU101, Arava).


The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib ([[ Lapatinib ditosylate ]], Tykerb, GW-572016), Canertinib (CI-1033), Zactima (ZD6474), Vatalanib (PTK787/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide (SU101, Arava).


The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, [[ Tykerb ]], GW-572016), Canertinib (CI-1033), Zactima (ZD6474), Vatalanib (PTK787/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide (SU101, Arava).


The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, [[ GW-572016 ]]), Canertinib (CI-1033), Zactima (ZD6474), Vatalanib (PTK787/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide (SU101, Arava).


The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), [[ Canertinib ]] (CI-1033), Zactima (ZD6474), Vatalanib (PTK787/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide (SU101, Arava).


The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib ([[ CI-1033 ]]), Zactima (ZD6474), Vatalanib (PTK787/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide (SU101, Arava).


The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib (CI-1033), [[ Zactima ]] (ZD6474), Vatalanib (PTK787/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide (SU101, Arava).


The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib (CI-1033), Zactima ([[ ZD6474 ]]), Vatalanib (PTK787/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide (SU101, Arava).


The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib (CI-1033), Zactima (ZD6474), [[ Vatalanib ]] (PTK787/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide (SU101, Arava).


The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib (CI-1033), Zactima (ZD6474), Vatalanib ([[ PTK787 ]]/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide (SU101, Arava).


The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib (CI-1033), Zactima (ZD6474), Vatalanib (PTK787/[[ ZK 222584 ]]), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide (SU101, Arava).


The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib (CI-1033), Zactima (ZD6474), Vatalanib (PTK787/ZK 222584), [[ Sorafenib ]] (Bay 43-9006, Nexavar), and Leflunomide (SU101, Arava).


The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib (CI-1033), Zactima (ZD6474), Vatalanib (PTK787/ZK 222584), Sorafenib ([[ Bay 43-9006 ]], Nexavar), and Leflunomide (SU101, Arava).


The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib (CI-1033), Zactima (ZD6474), Vatalanib (PTK787/ZK 222584), Sorafenib (Bay 43-9006, [[ Nexavar ]]), and Leflunomide (SU101, Arava).


The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib (CI-1033), Zactima (ZD6474), Vatalanib (PTK787/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and [[ Leflunomide ]] (SU101, Arava).


The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib (CI-1033), Zactima (ZD6474), Vatalanib (PTK787/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide ([[ SU101 ]], Arava).


The following << TK >> blockers for treatment of various human tumors are in clinical development: Lapatinib (Lapatinib ditosylate, Tykerb, GW-572016), Canertinib (CI-1033), Zactima (ZD6474), Vatalanib (PTK787/ZK 222584), Sorafenib (Bay 43-9006, Nexavar), and Leflunomide (SU101, [[ Arava ]]).


Currently, the use of orally administered << MAO >> inhibitor antidepressants (eg, [[ phenelzine ]], tranylcypromine) is limited by the risk of tyramine-provoked events (eg, acute hypertension and headache, also known as the "cheese reaction") when combined with dietary tyramine.


Currently, the use of orally administered << MAO >> inhibitor antidepressants (eg, phenelzine, [[ tranylcypromine ]]) is limited by the risk of tyramine-provoked events (eg, acute hypertension and headache, also known as the "cheese reaction") when combined with dietary tyramine.


It undergoes extensive biotransformation, which is affected by poor metabolism by << cytochrome P450 (CYP) 2D6 >> in a small percentage of the population; these patients have greater exposure to and slower elimination of [[ atomoxetine ]] than extensive metabolizers.


<< CYP2D6 >> inhibitors, such as [[ paroxetine ]], are associated with changes in atomoxetine pharmacokinetics similar to those observed among poor CYP2D6 metabolizers.


CYP2D6 inhibitors, such as paroxetine, are associated with changes in << atomoxetine >> pharmacokinetics similar to those observed among poor [[ CYP2D6 ]] metabolizers.


<< Atomoxetine >> appeared better tolerated among extensive [[ CYP2D6 ]] metabolizers than among poor metabolizers.


<< Mammalian glutamate dehydrogenase >> (GDH) is a homohexameric enzyme that catalyzes the reversible oxidative deamination of l-glutamate to [[ 2-oxoglutarate ]] using NAD(P)(+) as coenzyme.


Mammalian glutamate dehydrogenase (<< GDH >>) is a homohexameric enzyme that catalyzes the reversible oxidative deamination of l-glutamate to [[ 2-oxoglutarate ]] using NAD(P)(+) as coenzyme.


<< Mammalian glutamate dehydrogenase >> (GDH) is a homohexameric enzyme that catalyzes the reversible oxidative deamination of [[ l-glutamate ]] to 2-oxoglutarate using NAD(P)(+) as coenzyme.


Mammalian glutamate dehydrogenase (<< GDH >>) is a homohexameric enzyme that catalyzes the reversible oxidative deamination of [[ l-glutamate ]] to 2-oxoglutarate using NAD(P)(+) as coenzyme.


The recently discovered hyperinsulinism/hyperammonemia disorder showed that the loss of allosteric inhibition of GDH by << GTP >> causes excessive secretion of [[ insulin ]].


Subsequent studies demonstrated that wild-type and hyperinsulinemia/hyperammonemia forms of << GDH >> are inhibited by the green tea polyphenols, [[ epigallocatechin gallate ]] and epicatechin gallate.


Subsequent studies demonstrated that wild-type and hyperinsulinemia/hyperammonemia forms of << GDH >> are inhibited by the green tea polyphenols, epigallocatechin gallate and [[ epicatechin gallate ]].


BACKGROUND: Peripheral inflammatory pain is associated with an upregulation of spinal cord << COX-2 >> (cyclooxygenase-2), with a subsequent increase in central [[ prostaglandin E2 ]] (PGE2) levels associated with the development of hyperalgesia.


BACKGROUND: Peripheral inflammatory pain is associated with an upregulation of spinal cord COX-2 (<< cyclooxygenase-2 >>), with a subsequent increase in central [[ prostaglandin E2 ]] (PGE2) levels associated with the development of hyperalgesia.


BACKGROUND: Peripheral inflammatory pain is associated with an upregulation of spinal cord << COX-2 >> (cyclooxygenase-2), with a subsequent increase in central prostaglandin E2 ([[ PGE2 ]]) levels associated with the development of hyperalgesia.


BACKGROUND: Peripheral inflammatory pain is associated with an upregulation of spinal cord COX-2 (<< cyclooxygenase-2 >>), with a subsequent increase in central prostaglandin E2 ([[ PGE2 ]]) levels associated with the development of hyperalgesia.


Using the << alpha 1-adrenoceptor >> subtype-selective antagonists chlorethylclonidine (CEC), WB4101, and [[ 5-methyl-urapidil ]], we have examined the possible heterogeneity in the alpha 1-adrenoceptor populations in rabbit aorta.


Using the << alpha 1-adrenoceptor >> subtype-selective antagonists [[ chlorethylclonidine ]] (CEC), WB4101, and 5-methyl-urapidil, we have examined the possible heterogeneity in the alpha 1-adrenoceptor populations in rabbit aorta.


Using the << alpha 1-adrenoceptor >> subtype-selective antagonists chlorethylclonidine ([[ CEC ]]), WB4101, and 5-methyl-urapidil, we have examined the possible heterogeneity in the alpha 1-adrenoceptor populations in rabbit aorta.


Using the << alpha 1-adrenoceptor >> subtype-selective antagonists chlorethylclonidine (CEC), [[ WB4101 ]], and 5-methyl-urapidil, we have examined the possible heterogeneity in the alpha 1-adrenoceptor populations in rabbit aorta.


Radioligand binding studies with the nonselective << alpha 1-adrenoceptor >> antagonist radioligand [[ 125I-BE2254 ]] showed that 73-87% of the binding sites in rabbit aorta are CEC sensitive and they are predominantly low affinity sites both for WB4101 (pKd = 8.1) and for 5-methylurapidil (pKd = 7.1).


The Schild plots for the competitive antagonists WB4101 and 5-methyl-urapidil against << alpha 1a-adrenoceptor >>-selective agonist [[ methoxamine ]]-induced contraction were linear and had slopes not significantly different from unity, with a pA2 of 9.07 +/- 0.07 (n = 5) for WB4101 and 9.09 +/- 0.05 (n = 3) for 5-methyl-urapidil.


The Schild plots for the competitive antagonists WB4101 and 5-methyl-urapidil against << alpha 1a-adrenoceptor >>-selective agonist methoxamine-induced contraction were linear and had slopes not significantly different from unity, with a pA2 of 9.07 +/- 0.07 (n = 5) for [[ WB4101 ]] and 9.09 +/- 0.05 (n = 3) for 5-methyl-urapidil.


The Schild plots for the competitive antagonists WB4101 and 5-methyl-urapidil against << alpha 1a-adrenoceptor >>-selective agonist methoxamine-induced contraction were linear and had slopes not significantly different from unity, with a pA2 of 9.07 +/- 0.07 (n = 5) for WB4101 and 9.09 +/- 0.05 (n = 3) for [[ 5-methyl-urapidil ]].


The Schild plots for the competitive antagonists << WB4101 >> and 5-methyl-urapidil against [[ alpha 1a-adrenoceptor ]]-selective agonist methoxamine-induced contraction were linear and had slopes not significantly different from unity, with a pA2 of 9.07 +/- 0.07 (n = 5) for WB4101 and 9.09 +/- 0.05 (n = 3) for 5-methyl-urapidil.


The Schild plots for the competitive antagonists WB4101 and << 5-methyl-urapidil >> against [[ alpha 1a-adrenoceptor ]]-selective agonist methoxamine-induced contraction were linear and had slopes not significantly different from unity, with a pA2 of 9.07 +/- 0.07 (n = 5) for WB4101 and 9.09 +/- 0.05 (n = 3) for 5-methyl-urapidil.


Computer-assisted analysis of these curvilinear Schild plots in a two-receptor system indicated that << alpha 1-adrenoceptor >> populations responsible for the constrictive response are predominantly (approximately 80-90%) low affinity sites for the two antagonists (pKd approximately 8.1 for [[ WB4101 ]] and pKd approximately 7.1 for 5-methyl-urapidil) and a small population (approximately 10-20%) are high affinity sites (pKd approximately 9.1 for both WB4101 and 5-methyl-urapidil), which was in good agreement with radioligand binding studies.(ABSTRACT TRUNCATED AT 400 WORDS)


Computer-assisted analysis of these curvilinear Schild plots in a two-receptor system indicated that << alpha 1-adrenoceptor >> populations responsible for the constrictive response are predominantly (approximately 80-90%) low affinity sites for the two antagonists (pKd approximately 8.1 for WB4101 and pKd approximately 7.1 for [[ 5-methyl-urapidil ]]) and a small population (approximately 10-20%) are high affinity sites (pKd approximately 9.1 for both WB4101 and 5-methyl-urapidil), which was in good agreement with radioligand binding studies.(ABSTRACT TRUNCATED AT 400 WORDS)


<< Ambrisentan >> is an [[ endothelin receptor ]] antagonist (ERA) that was recently approved for treatment of pulmonary arterial hypertension (PAH).


<< Ambrisentan >> is the first [[ ET(A) ]] selective ERA approved for use in the US.


As discussed in this review, various progestogens including dydrogesterone and its 20alpha-dihydro-derivative, medrogestone, << promegestone >>, nomegestrol acetate and norelgestromin can reduce intratissular levels of estradiol in breast cancer by blocking [[ sulfatase ]] and 17beta-hydroxysteroid-dehydrogenase type 1 activities.


As discussed in this review, various progestogens including dydrogesterone and its 20alpha-dihydro-derivative, medrogestone, << promegestone >>, nomegestrol acetate and norelgestromin can reduce intratissular levels of estradiol in breast cancer by blocking sulfatase and [[ 17beta-hydroxysteroid-dehydrogenase type 1 ]] activities.


As discussed in this review, various progestogens including dydrogesterone and its 20alpha-dihydro-derivative, medrogestone, promegestone, << nomegestrol acetate >> and norelgestromin can reduce intratissular levels of estradiol in breast cancer by blocking [[ sulfatase ]] and 17beta-hydroxysteroid-dehydrogenase type 1 activities.


As discussed in this review, various progestogens including dydrogesterone and its 20alpha-dihydro-derivative, medrogestone, promegestone, << nomegestrol acetate >> and norelgestromin can reduce intratissular levels of estradiol in breast cancer by blocking sulfatase and [[ 17beta-hydroxysteroid-dehydrogenase type 1 ]] activities.


As discussed in this review, various progestogens including dydrogesterone and its 20alpha-dihydro-derivative, medrogestone, promegestone, nomegestrol acetate and << norelgestromin >> can reduce intratissular levels of estradiol in breast cancer by blocking [[ sulfatase ]] and 17beta-hydroxysteroid-dehydrogenase type 1 activities.


As discussed in this review, various progestogens including dydrogesterone and its 20alpha-dihydro-derivative, medrogestone, promegestone, nomegestrol acetate and << norelgestromin >> can reduce intratissular levels of estradiol in breast cancer by blocking sulfatase and [[ 17beta-hydroxysteroid-dehydrogenase type 1 ]] activities.


As discussed in this review, various << progestogens >> including dydrogesterone and its 20alpha-dihydro-derivative, medrogestone, promegestone, nomegestrol acetate and norelgestromin can reduce intratissular levels of estradiol in breast cancer by blocking [[ sulfatase ]] and 17beta-hydroxysteroid-dehydrogenase type 1 activities.


As discussed in this review, various << progestogens >> including dydrogesterone and its 20alpha-dihydro-derivative, medrogestone, promegestone, nomegestrol acetate and norelgestromin can reduce intratissular levels of estradiol in breast cancer by blocking sulfatase and [[ 17beta-hydroxysteroid-dehydrogenase type 1 ]] activities.


As discussed in this review, various progestogens including << dydrogesterone >> and its 20alpha-dihydro-derivative, medrogestone, promegestone, nomegestrol acetate and norelgestromin can reduce intratissular levels of estradiol in breast cancer by blocking [[ sulfatase ]] and 17beta-hydroxysteroid-dehydrogenase type 1 activities.


As discussed in this review, various progestogens including << dydrogesterone >> and its 20alpha-dihydro-derivative, medrogestone, promegestone, nomegestrol acetate and norelgestromin can reduce intratissular levels of estradiol in breast cancer by blocking sulfatase and [[ 17beta-hydroxysteroid-dehydrogenase type 1 ]] activities.


As discussed in this review, various progestogens including dydrogesterone and its 20alpha-dihydro-derivative, << medrogestone >>, promegestone, nomegestrol acetate and norelgestromin can reduce intratissular levels of estradiol in breast cancer by blocking [[ sulfatase ]] and 17beta-hydroxysteroid-dehydrogenase type 1 activities.


As discussed in this review, various progestogens including dydrogesterone and its 20alpha-dihydro-derivative, << medrogestone >>, promegestone, nomegestrol acetate and norelgestromin can reduce intratissular levels of estradiol in breast cancer by blocking sulfatase and [[ 17beta-hydroxysteroid-dehydrogenase type 1 ]] activities.


As discussed in this review, various progestogens including dydrogesterone and its 20alpha-dihydro-derivative, medrogestone, promegestone, nomegestrol acetate and norelgestromin can reduce intratissular levels of << estradiol >> in breast cancer by blocking [[ sulfatase ]] and 17beta-hydroxysteroid-dehydrogenase type 1 activities.


As discussed in this review, various progestogens including dydrogesterone and its 20alpha-dihydro-derivative, medrogestone, promegestone, nomegestrol acetate and norelgestromin can reduce intratissular levels of << estradiol >> in breast cancer by blocking sulfatase and [[ 17beta-hydroxysteroid-dehydrogenase type 1 ]] activities.


<< Mitiglinide >> reduced fasting plasma glucose and [[ GA ]] levels after 4 weeks and Hb(A1c) levels after 8 weeks.


<< Mitiglinide >> reduced fasting plasma glucose and GA levels after 4 weeks and [[ Hb(A1c) ]] levels after 8 weeks.


A molecular mechanism for << ibuprofen >>-mediated [[ RhoA ]] inhibition in neurons.


<< Ibuprofen >> is a nonsteroidal anti-inflammatory drug widely used to relieve pain and inflammation in many disorders via inhibition of [[ cyclooxygenases ]].


Recently, we have demonstrated that << ibuprofen >> inhibits intracellular signaling of [[ RhoA ]] and promotes significant axonal growth and functional recovery following spinal cord lesions in rodents.


In addition, another study suggests that << ibuprofen >> reduces generation of amyloid-beta42 peptide via inactivation of RhoA signaling, although it may also regulate [[ amyloid-beta42 ]] formation by direct inhibition of the gamma-secretase complex.


In addition, another study suggests that << ibuprofen >> reduces generation of [[ amyloid-beta42 ]] peptide via inactivation of RhoA signaling, although it may also regulate amyloid-beta42 formation by direct inhibition of the gamma-secretase complex.


In addition, another study suggests that << ibuprofen >> reduces generation of amyloid-beta42 peptide via inactivation of [[ RhoA ]] signaling, although it may also regulate amyloid-beta42 formation by direct inhibition of the gamma-secretase complex.


In addition, another study suggests that << ibuprofen >> reduces generation of amyloid-beta42 peptide via inactivation of RhoA signaling, although it may also regulate amyloid-beta42 formation by direct inhibition of the [[ gamma-secretase complex ]].


The molecular mechanisms by which << ibuprofen >> inhibits the [[ RhoA ]] signal in neurons, however, remain unclear.


Here, we report that the transcription factor peroxisome proliferator-activated receptor gamma (PPARgamma) is essential for coupling << ibuprofen >> to [[ RhoA ]] inhibition and subsequent neurite growth promotion in neurons.


<< Ibuprofen >> activates [[ PPARgamma ]] in neuron-like PC12 and B104 cells.


Activation of PPARgamma with traditional agonists mimics the << RhoA >>-inhibiting properties of [[ ibuprofen ]] in PC12 cells and, like ibuprofen, promotes neurite elongation in primary cultured neurons exposed to axonal growth inhibitors.


These findings support that PPARgamma plays an essential role in mediating the << RhoA >>-inhibiting effect of [[ ibuprofen ]].


Elucidation of the novel molecular mechanisms linking << ibuprofen >> to [[ RhoA ]] inhibition may provide additional therapeutic targets to the disorders characterized by RhoA activation, including spinal cord injuries and Alzheimer's disease.


Of these, the << thrombin >> inhibitor [[ dabigatran ]] and factor Xa inhibitor rivaroxaban have recently been licensed for thromboprophylaxis after orthopaedic surgery mainly in Europe.


Of these, the thrombin inhibitor dabigatran and << factor Xa >> inhibitor [[ rivaroxaban ]] have recently been licensed for thromboprophylaxis after orthopaedic surgery mainly in Europe.


In addition, the << factor Xa >> inhibitor [[ apixaban ]] is in late-stage clinical development.


<< Captopril >> directly inhibits [[ matrix metalloproteinase-2 ]] activity in continuous ambulatory peritoneal dialysis therapy.


We determined whether an << angiotensin-converting enzyme >> (ACE) inhibitor, [[ captopril ]], inhibits MMP-2 activity in peritoneal effluents from patients on CAPD, and simulated molecular models of the MMP-2-captopril complex.


We determined whether an angiotensin-converting enzyme (<< ACE >>) inhibitor, [[ captopril ]], inhibits MMP-2 activity in peritoneal effluents from patients on CAPD, and simulated molecular models of the MMP-2-captopril complex.


METHODS: The inhibitory effect of << captopril >> on [[ MMP-2 ]] activity was measured in peritoneal effluents from 17 patients on CAPD.


RESULTS: << Captopril >> directly inhibited [[ MMP-2 ]] activity in peritoneal effluents from patients on CAPD (IC50; 48 micromol/l), and that captopril binding to the MMP-2 active site could be formed in each complex model without molecular distortion.


CONCLUSION: ACE inhibitors, such as << captopril >>, may be applied as important compounds for [[ MMP-2 ]] inhibition in inflammation caused by CAPD.


CONCLUSION: << ACE >> inhibitors, such as [[ captopril ]], may be applied as important compounds for MMP-2 inhibition in inflammation caused by CAPD.


<< Phenformin >> has a direct inhibitory effect on the [[ ATP-sensitive potassium channel ]].


<< Phenformin >> but not metformin inhibits a number of variants of [[ K(ATP) ]] including the cloned equivalents of currents present in vascular and non-vascular smooth muscle (Kir6.1/SUR2B and Kir6.2/SUR2B) and pancreatic beta-cells (Kir6.2/SUR1).


<< Phenformin >> but not metformin inhibits a number of variants of K(ATP) including the cloned equivalents of currents present in vascular and non-vascular smooth muscle ([[ Kir6.1 ]]/SUR2B and Kir6.2/SUR2B) and pancreatic beta-cells (Kir6.2/SUR1).


<< Phenformin >> but not metformin inhibits a number of variants of K(ATP) including the cloned equivalents of currents present in vascular and non-vascular smooth muscle (Kir6.1/[[ SUR2B ]] and Kir6.2/SUR2B) and pancreatic beta-cells (Kir6.2/SUR1).


<< Phenformin >> but not metformin inhibits a number of variants of K(ATP) including the cloned equivalents of currents present in vascular and non-vascular smooth muscle (Kir6.1/SUR2B and [[ Kir6.2 ]]/SUR2B) and pancreatic beta-cells (Kir6.2/SUR1).


<< Phenformin >> but not metformin inhibits a number of variants of K(ATP) including the cloned equivalents of currents present in vascular and non-vascular smooth muscle (Kir6.1/SUR2B and Kir6.2/[[ SUR2B ]]) and pancreatic beta-cells (Kir6.2/SUR1).


<< Phenformin >> but not metformin inhibits a number of variants of K(ATP) including the cloned equivalents of currents present in vascular and non-vascular smooth muscle (Kir6.1/SUR2B and Kir6.2/SUR2B) and pancreatic beta-cells ([[ Kir6.2 ]]/SUR1).


<< Phenformin >> but not metformin inhibits a number of variants of K(ATP) including the cloned equivalents of currents present in vascular and non-vascular smooth muscle (Kir6.1/SUR2B and Kir6.2/SUR2B) and pancreatic beta-cells (Kir6.2/[[ SUR1 ]]).