Fumarate reductase (<< FRD >>) is the key enzyme in [[ fumarate ]] respiration induced by anaerobic growth of bacteria.


<< Fumarate reductase >> (FRD) is the key enzyme in [[ fumarate ]] respiration induced by anaerobic growth of bacteria.


The frdA gene coding for subunit A of FRD, and two control genes, << copA >> and copP associated with the export of [[ copper ]] out of H. pylori, were inactivated by insertion of the chloramphenicol acetyltransferase cassette into these individual genes.


The frdA gene coding for subunit A of FRD, and two control genes, copA and << copP >> associated with the export of [[ copper ]] out of H. pylori, were inactivated by insertion of the chloramphenicol acetyltransferase cassette into these individual genes.


Given that << FRD >>, present in all H. pylori strains, is immunogenic in H. pylori -infected patients and H. pylori growth in vitro can be inhibited by three anthelmintics ([[ morantel ]], oxantel and thiabendazole), this enzyme could potentially be used both as a novel drug target as well as in the development of vaccines for H. pylori prevention and eradication.


Given that << FRD >>, present in all H. pylori strains, is immunogenic in H. pylori -infected patients and H. pylori growth in vitro can be inhibited by three anthelmintics (morantel, [[ oxantel ]] and thiabendazole), this enzyme could potentially be used both as a novel drug target as well as in the development of vaccines for H. pylori prevention and eradication.


Given that << FRD >>, present in all H. pylori strains, is immunogenic in H. pylori -infected patients and H. pylori growth in vitro can be inhibited by three anthelmintics (morantel, oxantel and [[ thiabendazole ]]), this enzyme could potentially be used both as a novel drug target as well as in the development of vaccines for H. pylori prevention and eradication.


To begin to examine whether these changes are mediated by alterations in gene expression for << tryptophan hydroxylase >> (TPH), the rate-limiting enzyme in [[ 5-HT ]] biosynthesis, we quantitated its mRNA levels by competitive reverse transcription-polymerase chain reaction (RT-PCR).


To begin to examine whether these changes are mediated by alterations in gene expression for tryptophan hydroxylase (<< TPH >>), the rate-limiting enzyme in [[ 5-HT ]] biosynthesis, we quantitated its mRNA levels by competitive reverse transcription-polymerase chain reaction (RT-PCR).


In contrast, there was little change in mRNA levels for << GTP cyclohydrolase I >> (GTPCH), the rate limiting enzyme in synthesis of the [[ tetrahydrobiopterin ]] (BH4), the obligate cofactor for TPH.


In contrast, there was little change in mRNA levels for GTP cyclohydrolase I (<< GTPCH >>), the rate limiting enzyme in synthesis of the [[ tetrahydrobiopterin ]] (BH4), the obligate cofactor for TPH.


In contrast, there was little change in mRNA levels for << GTP cyclohydrolase I >> (GTPCH), the rate limiting enzyme in synthesis of the tetrahydrobiopterin ([[ BH4 ]]), the obligate cofactor for TPH.


In contrast, there was little change in mRNA levels for GTP cyclohydrolase I (<< GTPCH >>), the rate limiting enzyme in synthesis of the tetrahydrobiopterin ([[ BH4 ]]), the obligate cofactor for TPH.


In relation to zinc bioavailability, << α-CPPs >>, β-CPPs, α(s1)-CN(64-74)4P and β-CN(1-25)4P increased [[ zinc ]] uptake.


In relation to zinc bioavailability, α-CPPs, << β-CPPs >>, α(s1)-CN(64-74)4P and β-CN(1-25)4P increased [[ zinc ]] uptake.


In relation to zinc bioavailability, α-CPPs, β-CPPs, << α(s1)-CN >>(64-74)4P and β-CN(1-25)4P increased [[ zinc ]] uptake.


In relation to zinc bioavailability, α-CPPs, β-CPPs, α(s1)-CN(64-74)4P and << β-CN >>(1-25)4P increased [[ zinc ]] uptake.


In contrast to parenteral delivery of rBChE, which currently requires posttranslational modification for good plasma stability, an unmodified aer-rBChE pretreatment given 1-40h prior to >1 LD50 of aer-<< paraoxon >> (Px) was able to prevent inhibition of circulating [[ cholinesterase ]] in a dose-dependent manner.


Next to << Glut-4 >>, the predominant protein influencing [[ glucose ]] metabolism is PPARα and γ whose expressions were also positively modulated.


Both the << 5 alpha-reductase >> inhibitor [[ finasteride ]] and alpha 1-adrenoceptor antagonists (e.g. alfuzosin, doxazosin, prazosin, tamsulosin and terazosin) have been recommended as appropriate treatment options for patients with lower urinary tract symptoms (LUTS) associated with benign prostatic obstruction (BPO), and their efficacy has been proven in several placebo-controlled trials.


Both the 5 alpha-reductase inhibitor finasteride and << alpha 1-adrenoceptor >> antagonists (e.g. [[ alfuzosin ]], doxazosin, prazosin, tamsulosin and terazosin) have been recommended as appropriate treatment options for patients with lower urinary tract symptoms (LUTS) associated with benign prostatic obstruction (BPO), and their efficacy has been proven in several placebo-controlled trials.


Both the 5 alpha-reductase inhibitor finasteride and << alpha 1-adrenoceptor >> antagonists (e.g. alfuzosin, [[ doxazosin ]], prazosin, tamsulosin and terazosin) have been recommended as appropriate treatment options for patients with lower urinary tract symptoms (LUTS) associated with benign prostatic obstruction (BPO), and their efficacy has been proven in several placebo-controlled trials.


Both the 5 alpha-reductase inhibitor finasteride and << alpha 1-adrenoceptor >> antagonists (e.g. alfuzosin, doxazosin, [[ prazosin ]], tamsulosin and terazosin) have been recommended as appropriate treatment options for patients with lower urinary tract symptoms (LUTS) associated with benign prostatic obstruction (BPO), and their efficacy has been proven in several placebo-controlled trials.


Both the 5 alpha-reductase inhibitor finasteride and << alpha 1-adrenoceptor >> antagonists (e.g. alfuzosin, doxazosin, prazosin, [[ tamsulosin ]] and terazosin) have been recommended as appropriate treatment options for patients with lower urinary tract symptoms (LUTS) associated with benign prostatic obstruction (BPO), and their efficacy has been proven in several placebo-controlled trials.


Both the 5 alpha-reductase inhibitor finasteride and << alpha 1-adrenoceptor >> antagonists (e.g. alfuzosin, doxazosin, prazosin, tamsulosin and [[ terazosin ]]) have been recommended as appropriate treatment options for patients with lower urinary tract symptoms (LUTS) associated with benign prostatic obstruction (BPO), and their efficacy has been proven in several placebo-controlled trials.


Central << 5-HT3 >> receptor stimulation by [[ m-CPBG ]] increases blood glucose in rats.


Injections of << m-CPBG >>, a selective [[ 5-HT3 ]] receptor agonist, induced a significant increase in blood glucose in non-stressed rats in both fasted and in fed states.


The hyperglycemic effect of << m-CPBG >> central administration was blocked by pretreatment with ondansetron, a specific [[ 5-HT3 ]] receptor antagonist, indicating that the effects here obtained with m-CPBG were a result of its interaction with 5-HT3 receptors.


<< 3'-R/S-Hydroxyvoacamine >>, a potent [[ acetylcholinesterase ]] inhibitor from Tabernaemontana divaricata.


Guided by the << acetylcholinesterase >> inhibiting activity, the [[ bisindole alkaloid ]] 3'-R/S-hydroxyvoacamine was isolated from a stem extract of Tabernaemontana divaricata, a plant used in Thailand in traditional rejuvenation remedies for improving the memory.


Guided by the << acetylcholinesterase >> inhibiting activity, the bisindole alkaloid [[ 3'-R/S-hydroxyvoacamine ]] was isolated from a stem extract of Tabernaemontana divaricata, a plant used in Thailand in traditional rejuvenation remedies for improving the memory.


<< α-Amino-α´-Halomethylketones >>: Synthetic Methodologies and Pharmaceutical Applications as [[ Serine and Cysteine Protease ]] Inhibitors.


Introduction: 5-Lipoxygenase (<< 5-LO >>) is a crucial enzyme of the [[ arachidonic acid ]] (AA) cascade and catalyzes the formation of bioactive leukotrienes (LTs) with the help of FLAP, the 5-LO-activating protein.


Introduction: << 5-Lipoxygenase >> (5-LO) is a crucial enzyme of the [[ arachidonic acid ]] (AA) cascade and catalyzes the formation of bioactive leukotrienes (LTs) with the help of FLAP, the 5-LO-activating protein.


Using a transient heterologous cell expression system, we find that the transport activities of the << short OATP2B1 >> variant towards substrates [[ estrone sulfate ]] and rosuvastatin are similar to the well-characterized full length variant.


Using a transient heterologous cell expression system, we find that the transport activities of the << short OATP2B1 >> variant towards substrates estrone sulfate and [[ rosuvastatin ]] are similar to the well-characterized full length variant.


<< Memantine >> is an uncompetitive (channel blocking) [[ NMDA receptor ]] antagonist.


Like other << NMDA receptor >> antagonists, [[ memantine ]] at high concentrations can inhibit mechanisms of synaptic plasticity that are believed to underlie learning and memory.


Blockade of << NMDA receptors >> by [[ memantine ]] could theoretically confer disease-modifying activity in AD by inhibiting the "weak" NMDA receptor-dependent excitotoxicity that has been hypothesized to play a role in the progressive neuronal loss that underlies the evolving dementia.


Blockade of NMDA receptors by << memantine >> could theoretically confer disease-modifying activity in AD by inhibiting the "weak" [[ NMDA receptor ]]-dependent excitotoxicity that has been hypothesized to play a role in the progressive neuronal loss that underlies the evolving dementia.


Moreover, recent in vitro studies suggest that << memantine >> abrogates [[ beta-amyloid ]] (Abeta) toxicity and possibly inhibits Abeta production.


Moreover, recent in vitro studies suggest that << memantine >> abrogates beta-amyloid ([[ Abeta ]]) toxicity and possibly inhibits Abeta production.


Moreover, recent in vitro studies suggest that << memantine >> abrogates beta-amyloid (Abeta) toxicity and possibly inhibits [[ Abeta ]] production.


Considerable attention has focused on the investigation of theories to explain the better tolerability of << memantine >> over other [[ NMDA receptor ]] antagonists, particularly those that act by a similar channel blocking mechanism such as dissociative anesthetic-like agents (phencyclidine, ketamine, MK-801).


The concomitantly administered effects of << rifampicin >> on other drugs can result in their altered metabolism or transportation that are metabolised by cytochromes P450 or transported by [[ p-glycoprotein ]] in the gastrointestinal tract and liver.


The concomitantly administered effects of << rifampicin >> on other drugs can result in their altered metabolism or transportation that are metabolised by [[ cytochromes P450 ]] or transported by p-glycoprotein in the gastrointestinal tract and liver.


In general, rifampicin can act on a pattern: << rifampicin >> activates the [[ nuclear pregnane X receptor ]] that in turn affects cytochromes P450, glucuronosyltransferases and p-glycoprotein activities.


In general, << rifampicin >> can act on a pattern: rifampicin activates the [[ nuclear pregnane X receptor ]] that in turn affects cytochromes P450, glucuronosyltransferases and p-glycoprotein activities.


We describe here the isolation and biochemical characterization of the marine natural << sesquiterpene >> palinurin as a [[ GSK-3β ]] inhibitor.


We describe here the isolation and biochemical characterization of the marine natural sesquiterpene << palinurin >> as a [[ GSK-3β ]] inhibitor.


Experimental studies performed for characterizing the inhibitory mechanism indicate that << GSK-3β >> inhibition by [[ palinurin ]] cannot be competed out by ATP nor peptide substrate.


Moreover, molecular dynamics simulations have identified an allosteric mechanism by which binding of << palinurin >> leads to [[ GSK-3β ]] inhibition.


<< Cyclooxygenase(COX)-2 >>-derived [[ prostanoids ]] can influence several processes that are linked to carcinogenesis.


Platelet-induced COX-2-dependent PGE2 synthesis in HT29 cells was involved in downregulation of << p21 >>(WAF1/CIP1) and upregulation of cyclinB1, since these effects were prevented by [[ rofecoxib ]](a selective COX-2 inhibitor) and rescued by exogenous PGE2.


Platelet-induced COX-2-dependent PGE2 synthesis in HT29 cells was involved in downregulation of p21(<< WAF1 >>/CIP1) and upregulation of cyclinB1, since these effects were prevented by [[ rofecoxib ]](a selective COX-2 inhibitor) and rescued by exogenous PGE2.


Platelet-induced COX-2-dependent PGE2 synthesis in HT29 cells was involved in downregulation of p21(WAF1/<< CIP1 >>) and upregulation of cyclinB1, since these effects were prevented by [[ rofecoxib ]](a selective COX-2 inhibitor) and rescued by exogenous PGE2.


Platelet-induced COX-2-dependent PGE2 synthesis in HT29 cells was involved in downregulation of p21(WAF1/CIP1) and upregulation of << cyclinB1 >>, since these effects were prevented by [[ rofecoxib ]](a selective COX-2 inhibitor) and rescued by exogenous PGE2.


Platelet-induced COX-2-dependent PGE2 synthesis in HT29 cells was involved in downregulation of p21(WAF1/CIP1) and upregulation of cyclinB1, since these effects were prevented by << rofecoxib >>(a selective [[ COX-2 ]] inhibitor) and rescued by exogenous PGE2.


Platelet-induced << COX-2 >>-dependent [[ PGE2 ]] synthesis in HT29 cells was involved in downregulation of p21(WAF1/CIP1) and upregulation of cyclinB1, since these effects were prevented by rofecoxib(a selective COX-2 inhibitor) and rescued by exogenous PGE2.


Previous studies demonstrated that the << Group III mGlu receptor >>-selective orthosteric agonist, [[ LSP1-2111 ]] produced anxiolytic- but not antidepressant-like effects upon peripheral administration.


The anti-hyperthermic effect of Lu AF21934 (5 mg/kg) in the SIH test was inhibited by the benzodiazepine receptor antagonist flumazenil (10 mg/kg) and was not serotonin-dependent, as it persisted in serotonin-deficient mice and upon blockade of either << 5-HT(1A) >> receptors by [[ WAY100635 ]], or 5-HT(2A/2C) receptors by ritanserin.


The anti-hyperthermic effect of Lu AF21934 (5 mg/kg) in the SIH test was inhibited by the benzodiazepine receptor antagonist flumazenil (10 mg/kg) and was not serotonin-dependent, as it persisted in serotonin-deficient mice and upon blockade of either 5-HT(1A) receptors by WAY100635, or << 5-HT(2A/2C) >> receptors by [[ ritanserin ]].


The anti-hyperthermic effect of Lu AF21934 (5 mg/kg) in the SIH test was inhibited by the << benzodiazepine receptor >> antagonist [[ flumazenil ]] (10 mg/kg) and was not serotonin-dependent, as it persisted in serotonin-deficient mice and upon blockade of either 5-HT(1A) receptors by WAY100635, or 5-HT(2A/2C) receptors by ritanserin.


Catalytic-site affinities for cGMP, vardenafil, sildenafil, << tadalafil >>, or 3-isobutyl-1-methylxanthine (IBMX) were respectively weakened 14-, 123-, 30-, 51-, and 43-fold for Y612A; 63-, 511-, 43-, 95- and 61-fold for [[ Q817A ]]; and 59-, 448-, 71-, 137-, and 93-fold for F820A.


<< Allicin >> treatment showed reduced production of pro-inflammatory cytokines and NO and increased [[ HO-1 ]] activity.


<< Allicin >> treatment showed reduced production of pro-inflammatory [[ cytokines ]] and NO and increased HO-1 activity.


Recently, it has been shown that the activation of particular << T2R >> bitter taste receptors is partially involved with the bitter aftertaste sensation of [[ saccharin ]] and acesulfame-K.


Recently, it has been shown that the activation of particular << T2R >> bitter taste receptors is partially involved with the bitter aftertaste sensation of saccharin and [[ acesulfame-K ]].


We also found that << TRPV1 >> receptors are activated by [[ CuSO(4) ]], ZnSO(4), and FeSO(4), three salts known to produce a metallic taste sensation.


We also found that << TRPV1 >> receptors are activated by CuSO(4), [[ ZnSO(4) ]], and FeSO(4), three salts known to produce a metallic taste sensation.


We also found that << TRPV1 >> receptors are activated by CuSO(4), ZnSO(4), and [[ FeSO(4) ]], three salts known to produce a metallic taste sensation.


<< 2-Arylpropionic >> CXC chemokine receptor 1 (CXCR1) ligands as novel noncompetitive [[ CXCL8 ]] inhibitors.


<< (R)-Ketoprofen >> (1) was previously reported to be a potent and specific noncompetitive inhibitor of [[ CXCL8 ]]-induced human PMNs chemotaxis.


Role of organic cation/carnitine transporter 1 in uptake of << phenformin >> and inhibitory effect on [[ complex I ]] respiration in mitochondria.


Role of << organic cation/carnitine transporter 1 >> in uptake of [[ phenformin ]] and inhibitory effect on complex I respiration in mitochondria.


<< Phenformin >> causes lactic acidosis in clinical situations due to inhibition of [[ mitochondrial respiratory chain complex I ]].


In this study, uptake of phenformin and [(14)C]tetraethylammonium (TEA) and << complex I >> inhibition by [[ phenformin ]] were examined in isolated liver and heart mitochondria.


Inhibition by << phenformin >> of oxygen consumption via [[ complex I ]] respiration in isolated rat liver mitochondria was greater than that in heart mitochondria, whereas inhibitory effect of phenformin on complex I respiration was similar in inside-out structured submitochondrial particles prepared from rat livers and hearts.


Inhibition by phenformin of oxygen consumption via complex I respiration in isolated rat liver mitochondria was greater than that in heart mitochondria, whereas inhibitory effect of << phenformin >> on [[ complex I ]] respiration was similar in inside-out structured submitochondrial particles prepared from rat livers and hearts.


These observations suggest that uptake of << phenformin >> into liver mitochondria is at least partly mediated by OCTN1 and functionally relevant to its inhibition potential of [[ complex I ]] respiration.


These observations suggest that uptake of << phenformin >> into liver mitochondria is at least partly mediated by [[ OCTN1 ]] and functionally relevant to its inhibition potential of complex I respiration.


A series of << xanthine >> derivatives in which a methylene was inserted at position 8 of xanthine scaffold was synthesized and evaluated as inhibitors of [[ dipeptidyl peptidase 4 ]] (DPP-4) for the treatment of type 2 diabetes.


A series of << xanthine >> derivatives in which a methylene was inserted at position 8 of xanthine scaffold was synthesized and evaluated as inhibitors of dipeptidyl peptidase 4 ([[ DPP-4 ]]) for the treatment of type 2 diabetes.


A series of xanthine derivatives in which a methylene was inserted at position 8 of << xanthine >> scaffold was synthesized and evaluated as inhibitors of [[ dipeptidyl peptidase 4 ]] (DPP-4) for the treatment of type 2 diabetes.


A series of xanthine derivatives in which a methylene was inserted at position 8 of << xanthine >> scaffold was synthesized and evaluated as inhibitors of dipeptidyl peptidase 4 ([[ DPP-4 ]]) for the treatment of type 2 diabetes.


The animals were divided into thirteen groups (n=4 each) receiving an i.v. bolus injection of, either physiological saline (0.3 ml/kg; control), or the antagonists << SB224289 >> (300 microg/kg; [[ 5-HT1B ]]), BRL15572 (300 microg/kg; 5-HT1D), rauwolscine (300 microg/kg; alpha2), SB224289 + BRL15572 (300 microg/kg each), SB224289 + rauwolscine (300 microg/kg each), BRL15572 + rauwolscine (300 microg/kg each), rauwolscine (300 microg/kg) + prazosin (100 microg/kg; alpha1), SB224289 (300 microg/kg) + prazosin (100 microg/kg), SB224289 (300 microg/kg) + rauwolscine (300 microg/kg) + prazosin (100 microg/kg), SB224289 (300 microg/kg) + prazosin (100 microg/kg) + BRL44408 (1,000 microg/kg; alpha2A), SB224289 (300 microg/kg) + prazosin (100 microg/kg)+ imiloxan (1,000 microg/kg; alpha2B), or SB224289 (300 microg/kg) + prazosin (100 microg/kg) + MK912 (300 microg/kg; alpha2C).


The animals were divided into thirteen groups (n=4 each) receiving an i.v. bolus injection of, either physiological saline (0.3 ml/kg; control), or the antagonists SB224289 (300 microg/kg; 5-HT1B), << BRL15572 >> (300 microg/kg; [[ 5-HT1D ]]), rauwolscine (300 microg/kg; alpha2), SB224289 + BRL15572 (300 microg/kg each), SB224289 + rauwolscine (300 microg/kg each), BRL15572 + rauwolscine (300 microg/kg each), rauwolscine (300 microg/kg) + prazosin (100 microg/kg; alpha1), SB224289 (300 microg/kg) + prazosin (100 microg/kg), SB224289 (300 microg/kg) + rauwolscine (300 microg/kg) + prazosin (100 microg/kg), SB224289 (300 microg/kg) + prazosin (100 microg/kg) + BRL44408 (1,000 microg/kg; alpha2A), SB224289 (300 microg/kg) + prazosin (100 microg/kg)+ imiloxan (1,000 microg/kg; alpha2B), or SB224289 (300 microg/kg) + prazosin (100 microg/kg) + MK912 (300 microg/kg; alpha2C).


In an earlier report, DRD2 E8 A/A genotype was associated with reduced responsiveness to the << dopamine D2 >> agonist [[ apomorphine ]]; however, it is not clear whether both findings share the same biological basis.


As predicted, TES enhanced the production of both peroxynitrite precursors (i.e., superoxide and nitic oxide), and << xanthine oxidase >> was identified as the likely source of [[ TES ]]-stimulated superoxide production.


As predicted, TES enhanced the production of both peroxynitrite precursors (i.e., superoxide and nitic oxide), and << xanthine oxidase >> was identified as the likely source of TES-stimulated [[ superoxide ]] production.


Functional and biochemical studies indicated that << TES >> signaling involved activity of the phosphoinositide 3 (PI3) kinase-protein kinase B (Akt) cascade initiated by activation of the [[ androgen receptor ]] and culminated in enhanced production of cGMP and microvascular vasodilation.


These findings, derived from a variety of analytical and functional approaches, provide evidence for a novel nongenomic signaling mechanism for androgen action in the microvasculature: TES-stimulated vasodilation mediated primarily by << peroxynitrite >> formed from [[ xanthine oxidase ]]-generated superoxide and NO.


These findings, derived from a variety of analytical and functional approaches, provide evidence for a novel nongenomic signaling mechanism for androgen action in the microvasculature: TES-stimulated vasodilation mediated primarily by peroxynitrite formed from << xanthine oxidase >>-generated [[ superoxide ]] and NO.


These findings, derived from a variety of analytical and functional approaches, provide evidence for a novel nongenomic signaling mechanism for androgen action in the microvasculature: TES-stimulated vasodilation mediated primarily by peroxynitrite formed from << xanthine oxidase >>-generated superoxide and [[ NO ]].


<< Mouse brain serine racemase >> catalyzes specific elimination of L-serine to [[ pyruvate ]].


<< Mouse brain serine racemase >> catalyzes specific elimination of [[ L-serine ]] to pyruvate.


<< D-Serine >> was previously identified in mammalian brain and was shown to be a co-agonist at the 'glycine' site of the [[ N-methyl-D-aspartate (NMDA)-type receptors ]].


Racemization of << serine >> is catalyzed by [[ serine racemase ]], a pyridoxal 5'-phosphate-dependent enzyme expressed mainly in brain and liver.


Pharmacogenetic analysis of two genes, the << warfarin >> metabolic enzyme [[ CYP2C9 ]] and warfarin target enzyme, vitamin K epoxide reductase complex 1 VKORC1, confirmed their influence on warfarin maintenance dose.


Possession of << CYP2C9 >>*2 or CYP2C9*3 variant alleles, which result in decreased enzyme activity, is associated with a significant decrease in the mean [[ warfarin ]] dose.


Possession of CYP2C9*2 or << CYP2C9 >>*3 variant alleles, which result in decreased enzyme activity, is associated with a significant decrease in the mean [[ warfarin ]] dose.


<< Pseudoephedrine >> inhibits T-cell activation by targeting [[ NF-kappaB ]], NFAT and AP-1 signaling pathways.


<< Pseudoephedrine >> inhibits T-cell activation by targeting NF-kappaB, [[ NFAT ]] and AP-1 signaling pathways.


<< Pseudoephedrine >> inhibits T-cell activation by targeting NF-kappaB, NFAT and [[ AP-1 ]] signaling pathways.


We found that << PSE >> inhibits interleukin-2 (IL-2) and [[ tumor necrosis factor (TNF) alpha ]]-gene transcription in stimulated Jurkat cells, a human T-cell leukemia cell line.


We found that << PSE >> inhibits [[ interleukin-2 ]] (IL-2) and tumor necrosis factor (TNF) alpha-gene transcription in stimulated Jurkat cells, a human T-cell leukemia cell line.


We found that << PSE >> inhibits interleukin-2 ([[ IL-2 ]]) and tumor necrosis factor (TNF) alpha-gene transcription in stimulated Jurkat cells, a human T-cell leukemia cell line.


To further characterize the inhibitory mechanisms of PSE at the transcriptional level, we examined the transcriptional activities of nuclear factor kappa B (NF-kappaB), nuclear factor of activated T cells (NFAT), and activator protein-1 (AP-1) transcription factors and found that << PSE >> inhibited [[ NF-kappaB ]]-dependent transcriptional activity without affecting either the phosphorylation, the degradation of the cytoplasmic NF-kappaB inhibitory protein, IkappaBalpha or the DNA-binding activity.


However, phosphorylation of the << p65 >>/RelA subunit was clearly inhibited by [[ PSE ]] in stimulated cells.


However, phosphorylation of the p65/<< RelA >> subunit was clearly inhibited by [[ PSE ]] in stimulated cells.


In addition, PSE inhibited the transcriptional activity of NFAT without interfering with the << calcium >>-induced [[ NFAT ]] dephosphorylation event, which represents the major signaling pathway for its activation.


In addition, << PSE >> inhibited the transcriptional activity of [[ NFAT ]] without interfering with the calcium-induced NFAT dephosphorylation event, which represents the major signaling pathway for its activation.


NFAT cooperates with c-Jun, a compound of the AP-1 complex, to activate target genes, and we also found that << PSE >> inhibited both [[ JNK ]] activation and AP-1 transcriptional activity.


NFAT cooperates with c-Jun, a compound of the AP-1 complex, to activate target genes, and we also found that << PSE >> inhibited both JNK activation and [[ AP-1 ]] transcriptional activity.


Furthermore, experiments showed that treatment with << DEC >> results in a reduction in the amount of [[ COX-1 ]] protein in peritoneal exudate cells.


Micromolar Ntp dose-dependently increased the mean open channel probability in ligand-free solution (P(O(max))) and attenuated the << ATP >> inhibition of [[ K(IR)6.2 ]]/SUR1, but had no effect on homomeric K(IR)6.2 channels.


Micromolar Ntp dose-dependently increased the mean open channel probability in ligand-free solution (P(O(max))) and attenuated the << ATP >> inhibition of K(IR)6.2/[[ SUR1 ]], but had no effect on homomeric K(IR)6.2 channels.


These effects resemble those seen with N-terminal deletions (DeltaN) of K(IR)6.0, and application of Ntp to << DeltaNK(ATP) channels >> decreased their P(O(max)) and apparent IC(50) for [[ ATP ]] in the absence of Mg(2+).


<< Monocarboxylate transporters >> (MCTs) are proton-linked membrane carriers involved in the transport of [[ monocarboxylates ]] such as lactate, pyruvate, as well as ketone bodies.


Monocarboxylate transporters (<< MCTs >>) are proton-linked membrane carriers involved in the transport of [[ monocarboxylates ]] such as lactate, pyruvate, as well as ketone bodies.


<< Monocarboxylate transporters >> (MCTs) are proton-linked membrane carriers involved in the transport of monocarboxylates such as [[ lactate ]], pyruvate, as well as ketone bodies.


Monocarboxylate transporters (<< MCTs >>) are proton-linked membrane carriers involved in the transport of monocarboxylates such as [[ lactate ]], pyruvate, as well as ketone bodies.


<< Monocarboxylate transporters >> (MCTs) are proton-linked membrane carriers involved in the transport of monocarboxylates such as lactate, [[ pyruvate ]], as well as ketone bodies.


Monocarboxylate transporters (<< MCTs >>) are proton-linked membrane carriers involved in the transport of monocarboxylates such as lactate, [[ pyruvate ]], as well as ketone bodies.


<< Monocarboxylate transporters >> (MCTs) are proton-linked membrane carriers involved in the transport of monocarboxylates such as lactate, pyruvate, as well as [[ ketone ]] bodies.


Monocarboxylate transporters (<< MCTs >>) are proton-linked membrane carriers involved in the transport of monocarboxylates such as lactate, pyruvate, as well as [[ ketone ]] bodies.


Interestingly, part of << MCT2 >> immunoreactivity is located at postsynaptic sites, suggesting a particular role of [[ monocarboxylates ]] and their transporters in synaptic transmission.


Differentiating the roles of mGlu2 and mGlu3 receptors using << LY541850 >>, an [[ mGlu2 ]] agonist/mGlu3 antagonist.


Differentiating the roles of mGlu2 and mGlu3 receptors using << LY541850 >>, an mGlu2 agonist/[[ mGlu3 ]] antagonist.


<< LY541850 >> was claimed from human mGlu receptors expressed in non-neuronal cells to be a selective orthosteric [[ mGlu2 ]] agonist and mGlu3 antagonist.


<< LY541850 >> was claimed from human mGlu receptors expressed in non-neuronal cells to be a selective orthosteric mGlu2 agonist and [[ mGlu3 ]] antagonist.


These results confirm the selective << mGlu2 >> agonist and mGlu3 antagonist actions of [[ LY541850 ]].


These results confirm the selective mGlu2 agonist and << mGlu3 >> antagonist actions of [[ LY541850 ]].


Selective precipitation of cytosol receptors with 36% << (NH4)2SO4 >> reduced [[ CBG ]] concentrations to negligible levels.


The activity of the human nasal mucosa microsomes was inhibited by << 8-methoxypsoralen >>, a known [[ CYP2A ]] inhibitor.


Effects of some mono- and bisquaternary ammonium compounds on the reactivatability of << soman >>-inhibited [[ human acetylcholinesterase ]] in vitro.


<< Acetylcholinesterase >> (AChE) inhibited by the organophosphate soman (1,2,2-trimethyl-propylmethylphosphonofluoridate) rapidly becomes resistant to reactivation by [[ oximes ]] due to dealkylation of the soman-enzyme complex.


Acetylcholinesterase (<< AChE >>) inhibited by the organophosphate soman (1,2,2-trimethyl-propylmethylphosphonofluoridate) rapidly becomes resistant to reactivation by [[ oximes ]] due to dealkylation of the soman-enzyme complex.


<< Acetylcholinesterase >> (AChE) inhibited by the [[ organophosphate ]] soman (1,2,2-trimethyl-propylmethylphosphonofluoridate) rapidly becomes resistant to reactivation by oximes due to dealkylation of the soman-enzyme complex.


Acetylcholinesterase (<< AChE >>) inhibited by the [[ organophosphate ]] soman (1,2,2-trimethyl-propylmethylphosphonofluoridate) rapidly becomes resistant to reactivation by oximes due to dealkylation of the soman-enzyme complex.


<< Acetylcholinesterase >> (AChE) inhibited by the organophosphate [[ soman ]] (1,2,2-trimethyl-propylmethylphosphonofluoridate) rapidly becomes resistant to reactivation by oximes due to dealkylation of the soman-enzyme complex.


Acetylcholinesterase (<< AChE >>) inhibited by the organophosphate [[ soman ]] (1,2,2-trimethyl-propylmethylphosphonofluoridate) rapidly becomes resistant to reactivation by oximes due to dealkylation of the soman-enzyme complex.


<< Acetylcholinesterase >> (AChE) inhibited by the organophosphate soman ([[ 1,2,2-trimethyl-propylmethylphosphonofluoridate ]]) rapidly becomes resistant to reactivation by oximes due to dealkylation of the soman-enzyme complex.


Acetylcholinesterase (<< AChE >>) inhibited by the organophosphate soman ([[ 1,2,2-trimethyl-propylmethylphosphonofluoridate ]]) rapidly becomes resistant to reactivation by oximes due to dealkylation of the soman-enzyme complex.


The effect of the four mono- and bisquaternary ammonium compounds tetramethylammonium (TMA), hexamethonium, decamethonium and suxamethonium on the reactivatability of << soman >>-inhibited, solubilized [[ AChE ]] from human erythrocytes was investigated in vitro.


If the effectors were added after 5 min of aging they increased the activity of << soman >>-inhibited [[ AChE ]], but to a considerably smaller extent than HI 6.


First, in the presence of 1 mm ATP or the nonhydrolyzable analog adenosine 5'-(beta,gamma-imino)triphosphate, << TOP2 >>-mediated DNA cleavage induced by ATP-sensitive TOP2 poisons (e.g. [[ doxorubicin ]], etoposide, mitoxantrone, and 4'-(9-acridinylamino)methanesulfon-m-anisidide) was 30-100-fold stimulated, whereas DNA cleavage induced by ATP-insensitive TOP2 poisons (e.g. amonafide, batracylin, and menadione) was only slightly (less than 3-fold) affected.


First, in the presence of 1 mm ATP or the nonhydrolyzable analog adenosine 5'-(beta,gamma-imino)triphosphate, TOP2-mediated DNA cleavage induced by ATP-sensitive << TOP2 >> poisons (e.g. [[ doxorubicin ]], etoposide, mitoxantrone, and 4'-(9-acridinylamino)methanesulfon-m-anisidide) was 30-100-fold stimulated, whereas DNA cleavage induced by ATP-insensitive TOP2 poisons (e.g. amonafide, batracylin, and menadione) was only slightly (less than 3-fold) affected.


First, in the presence of 1 mm ATP or the nonhydrolyzable analog adenosine 5'-(beta,gamma-imino)triphosphate, << TOP2 >>-mediated DNA cleavage induced by ATP-sensitive TOP2 poisons (e.g. doxorubicin, [[ etoposide ]], mitoxantrone, and 4'-(9-acridinylamino)methanesulfon-m-anisidide) was 30-100-fold stimulated, whereas DNA cleavage induced by ATP-insensitive TOP2 poisons (e.g. amonafide, batracylin, and menadione) was only slightly (less than 3-fold) affected.


First, in the presence of 1 mm ATP or the nonhydrolyzable analog adenosine 5'-(beta,gamma-imino)triphosphate, TOP2-mediated DNA cleavage induced by ATP-sensitive << TOP2 >> poisons (e.g. doxorubicin, [[ etoposide ]], mitoxantrone, and 4'-(9-acridinylamino)methanesulfon-m-anisidide) was 30-100-fold stimulated, whereas DNA cleavage induced by ATP-insensitive TOP2 poisons (e.g. amonafide, batracylin, and menadione) was only slightly (less than 3-fold) affected.


First, in the presence of 1 mm ATP or the nonhydrolyzable analog adenosine 5'-(beta,gamma-imino)triphosphate, << TOP2 >>-mediated DNA cleavage induced by ATP-sensitive TOP2 poisons (e.g. doxorubicin, etoposide, [[ mitoxantrone ]], and 4'-(9-acridinylamino)methanesulfon-m-anisidide) was 30-100-fold stimulated, whereas DNA cleavage induced by ATP-insensitive TOP2 poisons (e.g. amonafide, batracylin, and menadione) was only slightly (less than 3-fold) affected.


First, in the presence of 1 mm ATP or the nonhydrolyzable analog adenosine 5'-(beta,gamma-imino)triphosphate, TOP2-mediated DNA cleavage induced by ATP-sensitive << TOP2 >> poisons (e.g. doxorubicin, etoposide, [[ mitoxantrone ]], and 4'-(9-acridinylamino)methanesulfon-m-anisidide) was 30-100-fold stimulated, whereas DNA cleavage induced by ATP-insensitive TOP2 poisons (e.g. amonafide, batracylin, and menadione) was only slightly (less than 3-fold) affected.


First, in the presence of 1 mm ATP or the nonhydrolyzable analog adenosine 5'-(beta,gamma-imino)triphosphate, << TOP2 >>-mediated DNA cleavage induced by ATP-sensitive TOP2 poisons (e.g. doxorubicin, etoposide, mitoxantrone, and [[ 4'-(9-acridinylamino)methanesulfon-m-anisidide ]]) was 30-100-fold stimulated, whereas DNA cleavage induced by ATP-insensitive TOP2 poisons (e.g. amonafide, batracylin, and menadione) was only slightly (less than 3-fold) affected.


First, in the presence of 1 mm ATP or the nonhydrolyzable analog adenosine 5'-(beta,gamma-imino)triphosphate, TOP2-mediated DNA cleavage induced by ATP-sensitive << TOP2 >> poisons (e.g. doxorubicin, etoposide, mitoxantrone, and [[ 4'-(9-acridinylamino)methanesulfon-m-anisidide ]]) was 30-100-fold stimulated, whereas DNA cleavage induced by ATP-insensitive TOP2 poisons (e.g. amonafide, batracylin, and menadione) was only slightly (less than 3-fold) affected.


First, in the presence of 1 mm ATP or the nonhydrolyzable analog adenosine 5'-(beta,gamma-imino)triphosphate, TOP2-mediated DNA cleavage induced by ATP-sensitive TOP2 poisons (e.g. doxorubicin, etoposide, mitoxantrone, and 4'-(9-acridinylamino)methanesulfon-m-anisidide) was 30-100-fold stimulated, whereas DNA cleavage induced by ATP-insensitive << TOP2 >> poisons (e.g. [[ amonafide ]], batracylin, and menadione) was only slightly (less than 3-fold) affected.


First, in the presence of 1 mm ATP or the nonhydrolyzable analog adenosine 5'-(beta,gamma-imino)triphosphate, TOP2-mediated DNA cleavage induced by ATP-sensitive TOP2 poisons (e.g. doxorubicin, etoposide, mitoxantrone, and 4'-(9-acridinylamino)methanesulfon-m-anisidide) was 30-100-fold stimulated, whereas DNA cleavage induced by ATP-insensitive << TOP2 >> poisons (e.g. amonafide, [[ batracylin ]], and menadione) was only slightly (less than 3-fold) affected.


First, in the presence of 1 mm ATP or the nonhydrolyzable analog adenosine 5'-(beta,gamma-imino)triphosphate, TOP2-mediated DNA cleavage induced by ATP-sensitive TOP2 poisons (e.g. doxorubicin, etoposide, mitoxantrone, and 4'-(9-acridinylamino)methanesulfon-m-anisidide) was 30-100-fold stimulated, whereas DNA cleavage induced by ATP-insensitive << TOP2 >> poisons (e.g. amonafide, batracylin, and [[ menadione ]]) was only slightly (less than 3-fold) affected.


In addition, ADP was shown to strongly antagonize << TOP2 >>-mediated DNA cleavage induced by [[ ATP ]]-sensitive but not ATP-insensitive TOP2 poisons.


Second, C427A mutant human TOP2alpha, which exhibits reduced << ATPase >> activity, was shown to exhibit cross-resistance to all ATP-sensitive but not [[ ATP ]]-insensitive TOP2 poisons.


Activation of << ALDH2 >> with [[ ethanol ]] attenuates diabetes induced myocardial injury in rats.


This study assessed changes in myocardial ALDH2 expression in the diabetic rat, in particular the diabetic rat pretreated with << ALDH2 >> activator [[ ethanol ]] (EtOH).


This study assessed changes in myocardial ALDH2 expression in the diabetic rat, in particular the diabetic rat pretreated with << ALDH2 >> activator ethanol ([[ EtOH ]]).


HbA1c level in DM12W group was higher than in DM4W group, << HbA1c >> level in [[ EtOH ]]+DM8W group was lower than in DM8W group.


Compared with DM8W group, << SOD >> and ALDH2 in [[ EtOH ]]+DM8W group was increased, MDA was decreased.


Compared with DM8W group, SOD and << ALDH2 >> in [[ EtOH ]]+DM8W group was increased, MDA was decreased.


Kinetic mechanism of << quinone oxidoreductase 2 >> and its inhibition by the antimalarial [[ quinolines ]].


<< QR2 >> catalyzes the two-electron reduction of menadione via the oxidation of N-alkylated or [[ N-ribosylated nicotinamides ]].


<< QR2 >> catalyzes the two-electron reduction of [[ menadione ]] via the oxidation of N-alkylated or N-ribosylated nicotinamides.


<< QR2 >> catalyzes the two-electron reduction of menadione via the oxidation of [[ N-alkylated ]] or N-ribosylated nicotinamides.


To investigate the mechanism and consequences of inhibition of << QR2 >> by the [[ quinolines ]] further, we have used steady-state and transient-state kinetics to define the mechanism of QR2.


To investigate the mechanism and consequences of inhibition of QR2 by the << quinolines >> further, we have used steady-state and transient-state kinetics to define the mechanism of [[ QR2 ]].


Our studies shed light on the possible in vivo potency of the << quinolines >> and provide a foundation for future studies aimed at creating more potent [[ QR2 ]] inhibitors and at understanding the physiological significance of QR2.


Methods: Stabilized anaplastic thyroid cancer cell lines (BHT-101 and CAL-62) and primary cultures from patients who underwent thyroidectomy for anaplastic thyroid cancer were treated with the << histone deacetylase >> inhibitor [[ LBH589 ]].


Results: Our results demonstrate that treatment with << LBH589 >> leads to [[ NIS ]] RNA expression as shown by RT-PCR and luciferase assay, and to protein expression as determined by immunofluorescence in vitro and by immunohistochemistry in xenograft tumors.


Pharmacokinetic Interactions between << Monoamine Oxidase A >> Inhibitor [[ Harmaline ]] and 5-Methoxy-N,N-Dimethyltryptamine, and the Impact of CYP2D6 Status.


Our recent study has demonstrated that coadministration of << monoamine oxidase A >> (MAO-A) inhibitor [[ harmaline ]] (5 mg/kg) increases systemic exposure to 5-MeO-DMT (2 mg/kg) and active metabolite bufotenine.


Our recent study has demonstrated that coadministration of monoamine oxidase A (<< MAO-A >>) inhibitor [[ harmaline ]] (5 mg/kg) increases systemic exposure to 5-MeO-DMT (2 mg/kg) and active metabolite bufotenine.


Our data revealed that inhibition of << MAO-A >>-mediated metabolic elimination by [[ harmaline ]] (2, 5, and 15 mg/kg) led to a sharp increase in systemic and cerebral exposure to 5-MeO-DMT (2 and 10 mg/kg) at all dose combinations.


The in vivo inhibitory effect of << harmaline >> on CYP2D6-catalyzed bufotenine formation was confirmed by in vitro study using purified [[ CYP2D6 ]].


The in vivo inhibitory effect of << harmaline >> on [[ CYP2D6 ]]-catalyzed bufotenine formation was confirmed by in vitro study using purified CYP2D6.


The in vivo inhibitory effect of harmaline on CYP2D6-catalyzed << bufotenine >> formation was confirmed by in vitro study using purified [[ CYP2D6 ]].


The in vivo inhibitory effect of harmaline on << CYP2D6 >>-catalyzed [[ bufotenine ]] formation was confirmed by in vitro study using purified CYP2D6.


Given these findings, a unified PK model including the inhibition of << MAO-A >>- and CYP2D6-catalyzed 5-MeO-DMT metabolism by harmaline was developed to describe blood [[ harmaline ]], 5-MeO-DMT, and bufotenine PK profiles in both wild-type and Tg-CYP2D6 mouse models.


Given these findings, a unified PK model including the inhibition of MAO-A- and << CYP2D6 >>-catalyzed 5-MeO-DMT metabolism by harmaline was developed to describe blood [[ harmaline ]], 5-MeO-DMT, and bufotenine PK profiles in both wild-type and Tg-CYP2D6 mouse models.


Given these findings, a unified PK model including the inhibition of MAO-A- and CYP2D6-catalyzed 5-MeO-DMT metabolism by harmaline was developed to describe blood << harmaline >>, 5-MeO-DMT, and bufotenine PK profiles in both wild-type and Tg-[[ CYP2D6 ]] mouse models.


Given these findings, a unified PK model including the inhibition of << MAO-A >>- and CYP2D6-catalyzed 5-MeO-DMT metabolism by [[ harmaline ]] was developed to describe blood harmaline, 5-MeO-DMT, and bufotenine PK profiles in both wild-type and Tg-CYP2D6 mouse models.


Given these findings, a unified PK model including the inhibition of MAO-A- and << CYP2D6 >>-catalyzed 5-MeO-DMT metabolism by [[ harmaline ]] was developed to describe blood harmaline, 5-MeO-DMT, and bufotenine PK profiles in both wild-type and Tg-CYP2D6 mouse models.


Given these findings, a unified PK model including the inhibition of MAO-A- and CYP2D6-catalyzed 5-MeO-DMT metabolism by << harmaline >> was developed to describe blood harmaline, 5-MeO-DMT, and bufotenine PK profiles in both wild-type and Tg-[[ CYP2D6 ]] mouse models.


Given these findings, a unified PK model including the inhibition of << MAO-A >>- and CYP2D6-catalyzed 5-MeO-DMT metabolism by harmaline was developed to describe blood harmaline, [[ 5-MeO-DMT ]], and bufotenine PK profiles in both wild-type and Tg-CYP2D6 mouse models.


Given these findings, a unified PK model including the inhibition of MAO-A- and << CYP2D6 >>-catalyzed 5-MeO-DMT metabolism by harmaline was developed to describe blood harmaline, [[ 5-MeO-DMT ]], and bufotenine PK profiles in both wild-type and Tg-CYP2D6 mouse models.


Given these findings, a unified PK model including the inhibition of MAO-A- and CYP2D6-catalyzed 5-MeO-DMT metabolism by harmaline was developed to describe blood harmaline, << 5-MeO-DMT >>, and bufotenine PK profiles in both wild-type and Tg-[[ CYP2D6 ]] mouse models.


Given these findings, a unified PK model including the inhibition of << MAO-A >>- and CYP2D6-catalyzed [[ 5-MeO-DMT ]] metabolism by harmaline was developed to describe blood harmaline, 5-MeO-DMT, and bufotenine PK profiles in both wild-type and Tg-CYP2D6 mouse models.


Given these findings, a unified PK model including the inhibition of MAO-A- and << CYP2D6 >>-catalyzed [[ 5-MeO-DMT ]] metabolism by harmaline was developed to describe blood harmaline, 5-MeO-DMT, and bufotenine PK profiles in both wild-type and Tg-CYP2D6 mouse models.


Given these findings, a unified PK model including the inhibition of MAO-A- and CYP2D6-catalyzed << 5-MeO-DMT >> metabolism by harmaline was developed to describe blood harmaline, 5-MeO-DMT, and bufotenine PK profiles in both wild-type and Tg-[[ CYP2D6 ]] mouse models.


Compared pharmacological characteristics in humans of racemic << cetirizine >> and levocetirizine, two [[ histamine H1-receptor ]] antagonists.


Compared pharmacological characteristics in humans of racemic cetirizine and << levocetirizine >>, two [[ histamine H1-receptor ]] antagonists.


The potent << histamine H(1)-receptor >> antagonist [[ cetirizine ]] (Zyrtec) is a racemic mixture of levocetirizine (now available under the trademark Xyzal and dextrocetirizine.


The potent << histamine H(1)-receptor >> antagonist cetirizine ([[ Zyrtec ]]) is a racemic mixture of levocetirizine (now available under the trademark Xyzal and dextrocetirizine.


The potent << histamine H(1)-receptor >> antagonist cetirizine (Zyrtec) is a racemic mixture of [[ levocetirizine ]] (now available under the trademark Xyzal and dextrocetirizine.


The potent << histamine H(1)-receptor >> antagonist cetirizine (Zyrtec) is a racemic mixture of levocetirizine (now available under the trademark [[ Xyzal ]] and dextrocetirizine.


The potent << histamine H(1)-receptor >> antagonist cetirizine (Zyrtec) is a racemic mixture of levocetirizine (now available under the trademark Xyzal and [[ dextrocetirizine ]].


<< Vegfrecine >>, an Inhibitor of [[ VEGF Receptor Tyrosine Kinases ]] Isolated from the Culture Broth of Streptomyces sp.


A new inhibitor of << VEGF receptor tyrosine kinases >>, [[ vegfrecine ]] (1), was isolated from the culture broth of Streptomyces sp.


As opposed to the rat and flounder orthologs, << hNaDC-3 >> was hardly inhibited by [[ lithium ]] concentrations up to 5 mM.


Effects of inhibition of << urokinase-type plasminogen activator >> (u-PA) by [[ amiloride ]] in the cornea and tear fluid of eyes irradiated with UVB.


Effects of inhibition of urokinase-type plasminogen activator (<< u-PA >>) by [[ amiloride ]] in the cornea and tear fluid of eyes irradiated with UVB.


The purpose of the present study was to test our hypothesis that << amiloride >>, a specific [[ u-PA ]] inhibitor, effectively decreases u-PA activity in cornea as well as in tear fluid and favourably affects corneal healing.


The purpose of the present study was to test our hypothesis that << amiloride >>, a specific u-PA inhibitor, effectively decreases [[ u-PA ]] activity in cornea as well as in tear fluid and favourably affects corneal healing.


Therefore, comparative histochemical and biochemical studies of << u-PA >> and the effects of amiloride were performed on rabbit corneas and tear fluid using the sensitive fluorogenic substrate [[ Z-Gly-Gly-Arg-7-amino-4-trifluoromethylcoumarin ]].


When << amiloride >> was dropped on the eye surface on the first day of irradiation and subsequently daily until the end of the experiment, [[ u-PA ]] activity in both cornea and tear fluid was strongly inhibited.


In conclusion, early application of << amiloride >> inhibited [[ u-PA ]] activity in UVB-irradiated corneas as well as in tear fluid and diminished the development of corneal pathology.


<< Prednisolone >> also inhibited ACTH and cortisol secretion in response to exogenous [[ CRH ]] stimulation, inferring rapid feedback inhibition at the anterior pituitary.


Prednisolone also inhibited ACTH and << cortisol >> secretion in response to exogenous [[ CRH ]] stimulation, inferring rapid feedback inhibition at the anterior pituitary.


Pharmacophore identification of << c-Myc >> inhibitor [[ 10074-G5 ]].


A structure-activity relationship (SAR) study of the << c-Myc >> (Myc) inhibitor [[ 10074-G5 ]] (N-([1,1'-biphenyl]-2-yl)-7-nitrobenzo[c][1,2,5]oxadiazol-4-amine, 1) - which targets a hydrophobic domain of the Myc oncoprotein that is flanked by arginine residues - was executed in order to determine its pharmacophore.


A structure-activity relationship (SAR) study of the c-Myc (<< Myc >>) inhibitor [[ 10074-G5 ]] (N-([1,1'-biphenyl]-2-yl)-7-nitrobenzo[c][1,2,5]oxadiazol-4-amine, 1) - which targets a hydrophobic domain of the Myc oncoprotein that is flanked by arginine residues - was executed in order to determine its pharmacophore.


A structure-activity relationship (SAR) study of the << c-Myc >> (Myc) inhibitor 10074-G5 ([[ N-([1,1'-biphenyl]-2-yl)-7-nitrobenzo[c][1,2,5]oxadiazol-4-amine ]], 1) - which targets a hydrophobic domain of the Myc oncoprotein that is flanked by arginine residues - was executed in order to determine its pharmacophore.


A structure-activity relationship (SAR) study of the c-Myc (<< Myc >>) inhibitor 10074-G5 ([[ N-([1,1'-biphenyl]-2-yl)-7-nitrobenzo[c][1,2,5]oxadiazol-4-amine ]], 1) - which targets a hydrophobic domain of the Myc oncoprotein that is flanked by arginine residues - was executed in order to determine its pharmacophore.


Importantly, the carboxylic acid of << JY-3-094 >> improves the physicochemical properties of the lead compound, which will facilitate the incorporation of additional hydrophobicity that might enhance [[ Myc ]] inhibitory activity further still.


<< Miglustat >>, a small iminosugar molecule approved for the treatment of Gaucher disease, reversibly inhibits [[ glucosylceramide synthase ]], which catalyses the first committed step in glycosphingolipid synthesis.


Furthermore, compared with control groups, the plaque endothelium level of << p75(NTR) >> was 3-fold increased and the liver level of p75(NTR) was 17.4-fold increased by [[ SFO ]]-HD.


Furthermore, compared with control groups, the plaque endothelium level of p75(NTR) was 3-fold increased and the liver level of << p75(NTR) >> was 17.4-fold increased by [[ SFO ]]-HD.


Meanwhile, the serum level of KC (a functional homolog of << IL-8 >> and the main proinflammatory alpha chemokine in mice) in apoE(-/-) mice was up to 357pg/ml in [[ SFO ]]-HD treated group.


Meanwhile, the serum level of KC (a functional homolog of IL-8 and the main proinflammatory << alpha chemokine >> in mice) in apoE(-/-) mice was up to 357pg/ml in [[ SFO ]]-HD treated group.


Thus, << SFO >> contributes to the instability of atherosclerotic plaque in apoE(-/-) mice through activating [[ p75(NTR) ]] and IL-8 and cell apoptosis in plaque.


Thus, << SFO >> contributes to the instability of atherosclerotic plaque in apoE(-/-) mice through activating p75(NTR) and [[ IL-8 ]] and cell apoptosis in plaque.


<< Levodopa >> is absorbed in the small bowel and is rapidly catabolized by [[ aromatic-L-amino-acid decarboxylase ]] (AADC) and catechol-O-methyltransferase (COMT).


<< Levodopa >> is absorbed in the small bowel and is rapidly catabolized by aromatic-L-amino-acid decarboxylase ([[ AADC ]]) and catechol-O-methyltransferase (COMT).


<< Levodopa >> is absorbed in the small bowel and is rapidly catabolized by aromatic-L-amino-acid decarboxylase (AADC) and [[ catechol-O-methyltransferase ]] (COMT).


<< Levodopa >> is absorbed in the small bowel and is rapidly catabolized by aromatic-L-amino-acid decarboxylase (AADC) and catechol-O-methyltransferase ([[ COMT ]]).


Because gastric AADC and COMT degrade levodopa, the drug is given with inhibitors of << AADC >> (carbidopa or [[ benserazide ]]), and inhibitors of COMT will also enter clinical use.


Because gastric AADC and COMT degrade levodopa, the drug is given with inhibitors of << AADC >> ([[ carbidopa ]] or benserazide), and inhibitors of COMT will also enter clinical use.


Because gastric << AADC >> and COMT degrade [[ levodopa ]], the drug is given with inhibitors of AADC (carbidopa or benserazide), and inhibitors of COMT will also enter clinical use.


Because gastric AADC and << COMT >> degrade [[ levodopa ]], the drug is given with inhibitors of AADC (carbidopa or benserazide), and inhibitors of COMT will also enter clinical use.


Rats were fed experimental diets containing SPI or << casein >> as a [[ nitrogen ]] source.


Different substrates were used as the relative specific substrates for the determination of aminopeptidase enzymatic activity: 4-methoxy-2-naphthylamide of L-alanine for aminopeptidase N, 4-methoxy-2-naphthylamide of L-leucine for leucine aminopeptidase, 4-methoxy-2-naphthylamide of L-glutamic acid for aminopeptidase A and 4-methoxy-2-naphthylamide of << L-arginine >> for [[ aminopeptidase B ]].


Different substrates were used as the relative specific substrates for the determination of aminopeptidase enzymatic activity: << 4-methoxy-2-naphthylamide >> of L-alanine for [[ aminopeptidase N ]], 4-methoxy-2-naphthylamide of L-leucine for leucine aminopeptidase, 4-methoxy-2-naphthylamide of L-glutamic acid for aminopeptidase A and 4-methoxy-2-naphthylamide of L-arginine for aminopeptidase B.


Different substrates were used as the relative specific substrates for the determination of aminopeptidase enzymatic activity: 4-methoxy-2-naphthylamide of << L-alanine >> for [[ aminopeptidase N ]], 4-methoxy-2-naphthylamide of L-leucine for leucine aminopeptidase, 4-methoxy-2-naphthylamide of L-glutamic acid for aminopeptidase A and 4-methoxy-2-naphthylamide of L-arginine for aminopeptidase B.


Different substrates were used as the relative specific substrates for the determination of aminopeptidase enzymatic activity: 4-methoxy-2-naphthylamide of L-alanine for aminopeptidase N, << 4-methoxy-2-naphthylamide >> of L-leucine for [[ leucine aminopeptidase ]], 4-methoxy-2-naphthylamide of L-glutamic acid for aminopeptidase A and 4-methoxy-2-naphthylamide of L-arginine for aminopeptidase B.


Different substrates were used as the relative specific substrates for the determination of aminopeptidase enzymatic activity: 4-methoxy-2-naphthylamide of L-alanine for aminopeptidase N, 4-methoxy-2-naphthylamide of << L-leucine >> for [[ leucine aminopeptidase ]], 4-methoxy-2-naphthylamide of L-glutamic acid for aminopeptidase A and 4-methoxy-2-naphthylamide of L-arginine for aminopeptidase B.


Different substrates were used as the relative specific substrates for the determination of aminopeptidase enzymatic activity: 4-methoxy-2-naphthylamide of L-alanine for aminopeptidase N, 4-methoxy-2-naphthylamide of L-leucine for leucine aminopeptidase, << 4-methoxy-2-naphthylamide >> of L-glutamic acid for [[ aminopeptidase A ]] and 4-methoxy-2-naphthylamide of L-arginine for aminopeptidase B.


Different substrates were used as the relative specific substrates for the determination of aminopeptidase enzymatic activity: 4-methoxy-2-naphthylamide of L-alanine for aminopeptidase N, 4-methoxy-2-naphthylamide of L-leucine for leucine aminopeptidase, 4-methoxy-2-naphthylamide of << L-glutamic acid >> for [[ aminopeptidase A ]] and 4-methoxy-2-naphthylamide of L-arginine for aminopeptidase B.


Different substrates were used as the relative specific substrates for the determination of aminopeptidase enzymatic activity: 4-methoxy-2-naphthylamide of L-alanine for aminopeptidase N, 4-methoxy-2-naphthylamide of L-leucine for leucine aminopeptidase, 4-methoxy-2-naphthylamide of L-glutamic acid for aminopeptidase A and << 4-methoxy-2-naphthylamide >> of L-arginine for [[ aminopeptidase B ]].


The inhibition of << aminopeptidase >> activity in the presence of [[ bestatin ]] and puromycin inhibitors was also investigated.


The inhibition of << aminopeptidase >> activity in the presence of bestatin and [[ puromycin ]] inhibitors was also investigated.


Here, we demonstrate that << peptidyl-prolyl cis/trans-isomerase A1 >> (Pin1), an enzyme that catalyzes the conversion of the peptide bond of [[ pSer ]]/pThr-Pro moieties in signaling proteins from cis to trans, is highly susceptible to HNE modification.


Here, we demonstrate that peptidyl-prolyl cis/trans-isomerase A1 (<< Pin1 >>), an enzyme that catalyzes the conversion of the peptide bond of [[ pSer ]]/pThr-Pro moieties in signaling proteins from cis to trans, is highly susceptible to HNE modification.


Here, we demonstrate that << peptidyl-prolyl cis/trans-isomerase A1 >> (Pin1), an enzyme that catalyzes the conversion of the peptide bond of pSer/[[ pThr ]]-Pro moieties in signaling proteins from cis to trans, is highly susceptible to HNE modification.


Here, we demonstrate that peptidyl-prolyl cis/trans-isomerase A1 (<< Pin1 >>), an enzyme that catalyzes the conversion of the peptide bond of pSer/[[ pThr ]]-Pro moieties in signaling proteins from cis to trans, is highly susceptible to HNE modification.


Here, we demonstrate that << peptidyl-prolyl cis/trans-isomerase A1 >> (Pin1), an enzyme that catalyzes the conversion of the peptide bond of pSer/pThr-[[ Pro ]] moieties in signaling proteins from cis to trans, is highly susceptible to HNE modification.


Here, we demonstrate that peptidyl-prolyl cis/trans-isomerase A1 (<< Pin1 >>), an enzyme that catalyzes the conversion of the peptide bond of pSer/pThr-[[ Pro ]] moieties in signaling proteins from cis to trans, is highly susceptible to HNE modification.


Withdrawal from free-choice << ethanol >> consumption results in increased packing density of [[ glutamine synthetase ]]-immunoreactive astrocytes in the prelimbic cortex of alcohol-preferring rats.


Astrocytes may play a role in these manifestations because astrocytes are essential in the regulation of released glutamate and its conversion to << glutamine >> through the enzyme [[ glutamine synthetase ]] (GS).


Astrocytes may play a role in these manifestations because astrocytes are essential in the regulation of released glutamate and its conversion to << glutamine >> through the enzyme glutamine synthetase ([[ GS ]]).


Astrocytes may play a role in these manifestations because astrocytes are essential in the regulation of released << glutamate >> and its conversion to glutamine through the enzyme [[ glutamine synthetase ]] (GS).


Astrocytes may play a role in these manifestations because astrocytes are essential in the regulation of released << glutamate >> and its conversion to glutamine through the enzyme glutamine synthetase ([[ GS ]]).


<< All-trans retinoic acid >> protects hepatocellular carcinoma cells against serum-starvation-induced cell death by upregulating [[ collagen 8A2 ]].


The protein exhibited modest << H(2)O(2) >>-dependent [[ peroxidase ]] activities with guaiacol, potassium iodide, and 2,2(')-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid (ABTS).


The protein exhibited modest H(2)O(2)-dependent << peroxidase >> activities with [[ guaiacol ]], potassium iodide, and 2,2(')-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid (ABTS).


The protein exhibited modest H(2)O(2)-dependent << peroxidase >> activities with guaiacol, [[ potassium iodide ]], and 2,2(')-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid (ABTS).


The protein exhibited modest H(2)O(2)-dependent << peroxidase >> activities with guaiacol, potassium iodide, and [[ 2,2(')-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid ]] (ABTS).


The protein exhibited modest H(2)O(2)-dependent << peroxidase >> activities with guaiacol, potassium iodide, and 2,2(')-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid ([[ ABTS ]]).


Ferredoxin 1 (<< FDX1 >>; adrenodoxin) is an iron-sulfur protein that is involved in various metabolic processes, including [[ steroid ]] hormone synthesis in mammalian tissues.


Ferredoxin 1 (FDX1; << adrenodoxin >>) is an iron-sulfur protein that is involved in various metabolic processes, including [[ steroid ]] hormone synthesis in mammalian tissues.


<< Ferredoxin 1 >> (FDX1; adrenodoxin) is an iron-sulfur protein that is involved in various metabolic processes, including [[ steroid ]] hormone synthesis in mammalian tissues.


Ferredoxin 1 (<< FDX1 >>; adrenodoxin) is an iron-sulfur protein that is involved in various metabolic processes, including [[ steroid hormone ]] synthesis in mammalian tissues.


Ferredoxin 1 (FDX1; << adrenodoxin >>) is an iron-sulfur protein that is involved in various metabolic processes, including [[ steroid hormone ]] synthesis in mammalian tissues.


<< Ferredoxin 1 >> (FDX1; adrenodoxin) is an iron-sulfur protein that is involved in various metabolic processes, including [[ steroid hormone ]] synthesis in mammalian tissues.


Luciferase reporter assays showed that transcription of << FDX1 >> was synergistically activated by the NR5A family and [[ 8Br-cAMP ]] treatment through two SF-1 binding sites and a CRE-like sequence in a human ovarian granulosa cell line, KGN.


These results indicate transcription of << FDX1 >> is regulated by the NR5A family and [[ cAMP ]] signaling, and participates in steroid hormone production in ovarian granulosa cells.


These results indicate transcription of << FDX1 >> is regulated by the NR5A family and cAMP signaling, and participates in [[ steroid ]] hormone production in ovarian granulosa cells.


<< Flutamide >>, an effective competitive inhibitor of the [[ androgen receptor ]] used orally for palliative treatment of prostatic carcinoma and regulation of prostatic hyperplasia was evaluated for its genotoxic effects in the intact rat and in primary cultures of human hepatocytes.


In the liver of rats given << flutamide >> as initiating agent at the dose of 500 mg/kg/week for 6 successive weeks, [[ gamma-glutamyltraspeptidase ]]-positive foci were detected only in 3 of 10 rats.


<< Cycloxygenase-2 >> (COX-2)-derived [[ prostaglandin E2 ]] (PGE2) has been shown to be important in esophageal tumorigenesis.


Cycloxygenase-2 (<< COX-2 >>)-derived [[ prostaglandin E2 ]] (PGE2) has been shown to be important in esophageal tumorigenesis.


<< Cycloxygenase-2 >> (COX-2)-derived prostaglandin E2 ([[ PGE2 ]]) has been shown to be important in esophageal tumorigenesis.


Cycloxygenase-2 (<< COX-2 >>)-derived prostaglandin E2 ([[ PGE2 ]]) has been shown to be important in esophageal tumorigenesis.


We have shown that << COX-2 >> mediates acid-induced [[ PGE2 ]] production.


We conclude that << mPGES1 >> mediates acid-induced increase in [[ PGE2 ]] production and cell proliferation.


<< Butein >> also increased [[ heme oxygenase-1 ]] (HO-1) protein expression and HO activity.


<< Butein >> also increased heme oxygenase-1 ([[ HO-1 ]]) protein expression and HO activity.


<< Butein >> also increased heme oxygenase-1 (HO-1) protein expression and [[ HO ]] activity.


Furthermore, << butein >> treatment caused nuclear accumulation of nuclear factor-E2-related factor 2 (Nrf2) and increased the promoter activity of [[ antioxidant response elements ]] (AREs).


Furthermore, << butein >> treatment caused nuclear accumulation of nuclear factor-E2-related factor 2 (Nrf2) and increased the promoter activity of antioxidant response elements ([[ AREs ]]).


Furthermore, << butein >> treatment caused nuclear accumulation of [[ nuclear factor-E2-related factor 2 ]] (Nrf2) and increased the promoter activity of antioxidant response elements (AREs).


Furthermore, << butein >> treatment caused nuclear accumulation of nuclear factor-E2-related factor 2 ([[ Nrf2 ]]) and increased the promoter activity of antioxidant response elements (AREs).


Treatment of HDP cells with a c-Jun NH2-terminal kinase (JNK) inhibitor also reduced butein-induced HO-1 expression, and << butein >> treatment led to increased [[ JNK ]] phosphorylation.


Treatment of HDP cells with a c-Jun NH2-terminal kinase (JNK) inhibitor also reduced << butein >>-induced [[ HO-1 ]] expression, and butein treatment led to increased JNK phosphorylation.


The refolding kinetics of guanidine-denatured disulfide-intact bovine pancreatic ribonuclease A (RNase A) and its << proline-42-to-alanine >> mutant (Pro42Ala) have been studied by monitoring tyrosine burial and [[ 2'-cytidine monophosphate ]] (2'CMP) inhibitor binding.


The refolding kinetics of guanidine-denatured disulfide-intact bovine pancreatic ribonuclease A (RNase A) and its proline-42-to-alanine mutant (<< Pro42Ala >>) have been studied by monitoring tyrosine burial and [[ 2'-cytidine monophosphate ]] (2'CMP) inhibitor binding.


The refolding kinetics of guanidine-denatured disulfide-intact << bovine pancreatic ribonuclease A >> (RNase A) and its proline-42-to-alanine mutant (Pro42Ala) have been studied by monitoring tyrosine burial and [[ 2'-cytidine monophosphate ]] (2'CMP) inhibitor binding.


The refolding kinetics of guanidine-denatured disulfide-intact bovine pancreatic ribonuclease A (<< RNase A >>) and its proline-42-to-alanine mutant (Pro42Ala) have been studied by monitoring tyrosine burial and [[ 2'-cytidine monophosphate ]] (2'CMP) inhibitor binding.


The refolding kinetics of guanidine-denatured disulfide-intact bovine pancreatic ribonuclease A (RNase A) and its << proline-42-to-alanine >> mutant (Pro42Ala) have been studied by monitoring tyrosine burial and 2'-cytidine monophosphate ([[ 2'CMP ]]) inhibitor binding.


The refolding kinetics of guanidine-denatured disulfide-intact bovine pancreatic ribonuclease A (RNase A) and its proline-42-to-alanine mutant (<< Pro42Ala >>) have been studied by monitoring tyrosine burial and 2'-cytidine monophosphate ([[ 2'CMP ]]) inhibitor binding.


The refolding kinetics of guanidine-denatured disulfide-intact << bovine pancreatic ribonuclease A >> (RNase A) and its proline-42-to-alanine mutant (Pro42Ala) have been studied by monitoring tyrosine burial and 2'-cytidine monophosphate ([[ 2'CMP ]]) inhibitor binding.


The refolding kinetics of guanidine-denatured disulfide-intact bovine pancreatic ribonuclease A (<< RNase A >>) and its proline-42-to-alanine mutant (Pro42Ala) have been studied by monitoring tyrosine burial and 2'-cytidine monophosphate ([[ 2'CMP ]]) inhibitor binding.


The folding rate for wild-type << RNase A >> is faster in the presence of the inhibitor [[ 2'CMP ]] than in its absence, indicating that the transition-state structure in the rate-determining step is stabilized by 2'CMP.


During early pregnancy in sheep, the elongating conceptus secretes interferon-τ (IFNT) and the conceptus as well as endometrial epithelia produce << prostaglandins >> (PG) via [[ PG synthase 2 ]] (PTGS2) and cortisol via hydroxysteroid (11-β) dehydrogenase 1 (HSD11B1).


During early pregnancy in sheep, the elongating conceptus secretes interferon-τ (IFNT) and the conceptus as well as endometrial epithelia produce << prostaglandins >> (PG) via PG synthase 2 ([[ PTGS2 ]]) and cortisol via hydroxysteroid (11-β) dehydrogenase 1 (HSD11B1).


During early pregnancy in sheep, the elongating conceptus secretes interferon-τ (IFNT) and the conceptus as well as endometrial epithelia produce prostaglandins (PG) via PG synthase 2 (PTGS2) and << cortisol >> via [[ hydroxysteroid (11-β) dehydrogenase 1 ]] (HSD11B1).


During early pregnancy in sheep, the elongating conceptus secretes interferon-τ (IFNT) and the conceptus as well as endometrial epithelia produce prostaglandins (PG) via PG synthase 2 (PTGS2) and << cortisol >> via hydroxysteroid (11-β) dehydrogenase 1 ([[ HSD11B1 ]]).


The primary aim of these studies was to test the hypothesis that << HSD11B1 >>-derived [[ cortisol ]] has a biological role in endometrial function and conceptus development during early pregnancy in sheep.


In study 1, cyclic ewes received vehicle, cortisol, << PF 915275 >> (PF; a selective inhibitor of [[ HSD11B1 ]]), cortisol and PF, meloxicam (a selective inhibitor of PTGS2), cortisol and meloxicam, recombinant ovine IFNT, or IFNT and PF into the uterus from day 10 to day14 after estrus.


In study 1, cyclic ewes received vehicle, cortisol, PF 915275 (PF; a selective inhibitor of HSD11B1), cortisol and PF, << meloxicam >> (a selective inhibitor of [[ PTGS2 ]]), cortisol and meloxicam, recombinant ovine IFNT, or IFNT and PF into the uterus from day 10 to day14 after estrus.


<< Cortisol >> and IFNT stimulated endometrial [[ HSD11B1 ]] expression and activity, increased endometrial PTGS2 activity and the amount of PG in the uterine lumen, and up-regulated many conceptus elongation-related genes in the endometrium.


<< Cortisol >> and IFNT stimulated endometrial HSD11B1 expression and activity, increased endometrial [[ PTGS2 ]] activity and the amount of PG in the uterine lumen, and up-regulated many conceptus elongation-related genes in the endometrium.


These results suggest that << HSD11B1 >>-derived [[ cortisol ]] mediates, in part, actions of ovarian progesterone and the conceptus on endometrial function and support the hypothesis that IFNT, PG, and cortisol coordinately regulate endometrial functions important for conceptus elongation and implantation during early pregnancy in sheep.


<< 2-(2-Aminoethyl)-quinoline >> (D-1997): a novel agonist at [[ 5-hydroxytryptamine1-like receptors ]] in the canine basilar artery.


2-(2-Aminoethyl)-quinoline (<< D-1997 >>): a novel agonist at [[ 5-hydroxytryptamine1-like receptors ]] in the canine basilar artery.


The effects of D-1997 in the basilar artery were not modified by incubation with either the 5-HT2 receptor antagonist ketanserin (0.01-1 microM), the 5-HT3 and 5-HT4 receptor antagonist ICS205930 (tropisetron; 0.1-10 microM), the 5-HT1A receptor antagonist spiroxatrine (0.01-1 microM), the << beta-adrenoceptor >> blocker with high affinity for 5-HT1A and 5-HT1B binding sites [[ (+/-)-pindolol ]] (0.01-1 microM), or the alpha 1-adrenoceptor antagonist prazosin (0.01-1 microM).


The effects of D-1997 in the basilar artery were not modified by incubation with either the << 5-HT2 receptor >> antagonist [[ ketanserin ]] (0.01-1 microM), the 5-HT3 and 5-HT4 receptor antagonist ICS205930 (tropisetron; 0.1-10 microM), the 5-HT1A receptor antagonist spiroxatrine (0.01-1 microM), the beta-adrenoceptor blocker with high affinity for 5-HT1A and 5-HT1B binding sites (+/-)-pindolol (0.01-1 microM), or the alpha 1-adrenoceptor antagonist prazosin (0.01-1 microM).


The effects of D-1997 in the basilar artery were not modified by incubation with either the 5-HT2 receptor antagonist ketanserin (0.01-1 microM), the << 5-HT3 >> and 5-HT4 receptor antagonist ICS205930 ([[ tropisetron ]]; 0.1-10 microM), the 5-HT1A receptor antagonist spiroxatrine (0.01-1 microM), the beta-adrenoceptor blocker with high affinity for 5-HT1A and 5-HT1B binding sites (+/-)-pindolol (0.01-1 microM), or the alpha 1-adrenoceptor antagonist prazosin (0.01-1 microM).


The effects of D-1997 in the basilar artery were not modified by incubation with either the 5-HT2 receptor antagonist ketanserin (0.01-1 microM), the 5-HT3 and << 5-HT4 >> receptor antagonist ICS205930 ([[ tropisetron ]]; 0.1-10 microM), the 5-HT1A receptor antagonist spiroxatrine (0.01-1 microM), the beta-adrenoceptor blocker with high affinity for 5-HT1A and 5-HT1B binding sites (+/-)-pindolol (0.01-1 microM), or the alpha 1-adrenoceptor antagonist prazosin (0.01-1 microM).


The effects of D-1997 in the basilar artery were not modified by incubation with either the 5-HT2 receptor antagonist ketanserin (0.01-1 microM), the 5-HT3 and 5-HT4 receptor antagonist ICS205930 (tropisetron; 0.1-10 microM), the << 5-HT1A >> receptor antagonist [[ spiroxatrine ]] (0.01-1 microM), the beta-adrenoceptor blocker with high affinity for 5-HT1A and 5-HT1B binding sites (+/-)-pindolol (0.01-1 microM), or the alpha 1-adrenoceptor antagonist prazosin (0.01-1 microM).


The effects of D-1997 in the basilar artery were not modified by incubation with either the 5-HT2 receptor antagonist ketanserin (0.01-1 microM), the 5-HT3 and 5-HT4 receptor antagonist ICS205930 (tropisetron; 0.1-10 microM), the 5-HT1A receptor antagonist spiroxatrine (0.01-1 microM), the beta-adrenoceptor blocker with high affinity for 5-HT1A and 5-HT1B binding sites (+/-)-pindolol (0.01-1 microM), or the << alpha 1-adrenoceptor >> antagonist [[ prazosin ]] (0.01-1 microM).


In contrast, the << D-1997 >>-induced responses were potently and concentration-dependently antagonized by the mixed [[ 5-HT1-like ]] and 5-HT2 receptor antagonist methiothepin (0.01-1 microM).


In contrast, the << D-1997 >>-induced responses were potently and concentration-dependently antagonized by the mixed 5-HT1-like and [[ 5-HT2 receptor ]] antagonist methiothepin (0.01-1 microM).


In contrast, the D-1997-induced responses were potently and concentration-dependently antagonized by the mixed << 5-HT1-like >> and 5-HT2 receptor antagonist [[ methiothepin ]] (0.01-1 microM).


In contrast, the D-1997-induced responses were potently and concentration-dependently antagonized by the mixed 5-HT1-like and << 5-HT2 receptor >> antagonist [[ methiothepin ]] (0.01-1 microM).


It is concluded that << D-1997 >> contracts the canine basilar artery by stimulating [[ 5-HT1-like receptors ]] unrelated to either the 5-HT1A or 5-HT1B receptor subtypes.


It is concluded that << D-1997 >> contracts the canine basilar artery by stimulating 5-HT1-like receptors unrelated to either the [[ 5-HT1A ]] or 5-HT1B receptor subtypes.


It is concluded that << D-1997 >> contracts the canine basilar artery by stimulating 5-HT1-like receptors unrelated to either the 5-HT1A or [[ 5-HT1B ]] receptor subtypes.


Although Bak and Bcl-2-associated X protein (Bax), another member of the Bcl-2 family, are generally thought to be functionally redundant, only Bak is necessary and sufficient for << VK2 >>-induced [[ cytochrome c ]] (cyt c) release and cell death.


Although Bak and Bcl-2-associated X protein (Bax), another member of the Bcl-2 family, are generally thought to be functionally redundant, only Bak is necessary and sufficient for << VK2 >>-induced cytochrome c ([[ cyt c ]]) release and cell death.


In muscle and liver, << TCDD >> (10 ng/kg/day) induced increases in methylation and decreases in mRNA expression of [[ Igf2r ]].


<< Rasagiline >> is a propargylamine and irreversible [[ monoamine oxidase (MAO) B ]] inhibitor used for the treatment of Parkinson's disease (PD).


Rasagiline is a << propargylamine >> and irreversible [[ monoamine oxidase (MAO) B ]] inhibitor used for the treatment of Parkinson's disease (PD).


<< Tolvaptan >> is a selective [[ arginine vasopressin (AVP) V(2) receptor ]] blocker used to induce free water diuresis in the treatment of euvolemic or hypervolemic hyponatremia.


Prolonged use of << tolvaptan >> leads to increased endogenous levels of AVP and perhaps over-stimulation of [[ V(1A) receptors ]].


Prolonged use of << tolvaptan >> leads to increased endogenous levels of [[ AVP ]] and perhaps over-stimulation of V(1A) receptors.


In addition, << tolvaptan >> is metabolized by the [[ CYP3A4 ]] system; thus physicians should be aware of the potential for increased interactions with other medications.


<< Fisetin >> treatment showed a significant decline in the levels of blood glucose, glycosylated hemoglobin (HbA1c), NF-kB p65 unit (in pancreas) and IL-1β (plasma), serum nitric oxide (NO) with an elevation in plasma [[ insulin ]].


<< Fisetin >> treatment showed a significant decline in the levels of blood glucose, [[ glycosylated hemoglobin ]] (HbA1c), NF-kB p65 unit (in pancreas) and IL-1β (plasma), serum nitric oxide (NO) with an elevation in plasma insulin.


<< Fisetin >> treatment showed a significant decline in the levels of blood glucose, glycosylated hemoglobin ([[ HbA1c ]]), NF-kB p65 unit (in pancreas) and IL-1β (plasma), serum nitric oxide (NO) with an elevation in plasma insulin.


<< Fisetin >> treatment showed a significant decline in the levels of blood glucose, glycosylated hemoglobin (HbA1c), [[ NF-kB ]] p65 unit (in pancreas) and IL-1β (plasma), serum nitric oxide (NO) with an elevation in plasma insulin.


<< Fisetin >> treatment showed a significant decline in the levels of blood glucose, glycosylated hemoglobin (HbA1c), NF-kB [[ p65 ]] unit (in pancreas) and IL-1β (plasma), serum nitric oxide (NO) with an elevation in plasma insulin.


<< Fisetin >> treatment showed a significant decline in the levels of blood glucose, glycosylated hemoglobin (HbA1c), NF-kB p65 unit (in pancreas) and [[ IL-1β ]] (plasma), serum nitric oxide (NO) with an elevation in plasma insulin.


High-<< glucose >> environment enhanced oxidative stress and increased [[ interleukin-8 ]] secretion from keratinocytes: New insights on impaired diabetic wound healing.


Using cultured human keratinocytes and diabetic rat model, the current study showed that high-<< glucose >> environment enhanced [[ IL-8 ]] production via epidermal growth factor receptor (EGFR) -extracelluar signal-regulated kinase (ERK) pathway in a reactive oxygen species (ROS)-dependent manner in keratinocytes.


In conclusion, << IL-8 >> production and neutrophil infiltration are increased in high-[[ glucose ]] environment due to elevated ROS level and contributed to impaired wound healing in diabetic skin.


The results showed that (1) 15mg/kg body weight PhIP induced obvious histopathological changes in gastric mucosa; (2) << PhIP >> (10 and/or 15mg/kg) significantly decreased superoxide dismutase (SOD) and glutathioneperoxidase (GPx) activities, while increased [[ catalase ]] (CAT) activity compared with the control.


The results showed that (1) 15mg/kg body weight PhIP induced obvious histopathological changes in gastric mucosa; (2) << PhIP >> (10 and/or 15mg/kg) significantly decreased superoxide dismutase (SOD) and glutathioneperoxidase (GPx) activities, while increased catalase ([[ CAT ]]) activity compared with the control.


The results showed that (1) 15mg/kg body weight PhIP induced obvious histopathological changes in gastric mucosa; (2) << PhIP >> (10 and/or 15mg/kg) significantly decreased [[ superoxide dismutase ]] (SOD) and glutathioneperoxidase (GPx) activities, while increased catalase (CAT) activity compared with the control.


The results showed that (1) 15mg/kg body weight PhIP induced obvious histopathological changes in gastric mucosa; (2) << PhIP >> (10 and/or 15mg/kg) significantly decreased superoxide dismutase ([[ SOD ]]) and glutathioneperoxidase (GPx) activities, while increased catalase (CAT) activity compared with the control.


The results showed that (1) 15mg/kg body weight PhIP induced obvious histopathological changes in gastric mucosa; (2) << PhIP >> (10 and/or 15mg/kg) significantly decreased superoxide dismutase (SOD) and [[ glutathioneperoxidase ]] (GPx) activities, while increased catalase (CAT) activity compared with the control.


The results showed that (1) 15mg/kg body weight PhIP induced obvious histopathological changes in gastric mucosa; (2) << PhIP >> (10 and/or 15mg/kg) significantly decreased superoxide dismutase (SOD) and glutathioneperoxidase ([[ GPx ]]) activities, while increased catalase (CAT) activity compared with the control.


With the elevated doses of PhIP, malondialdehyde (MDA) contents, protein carbonyl (PCO) contents and DNA-protein crosslinks (DPC) coefficients were significantly raised in a dose-dependent manner; (3) << PhIP >> at the doses of 10mg/kg and/or 15mg/kg significantly inhibited p16 mRNA and protein expression, whereas enhanced c-fos and [[ c-jun ]] expression relative to control.


With the elevated doses of PhIP, malondialdehyde (MDA) contents, protein carbonyl (PCO) contents and DNA-protein crosslinks (DPC) coefficients were significantly raised in a dose-dependent manner; (3) << PhIP >> at the doses of 10mg/kg and/or 15mg/kg significantly inhibited p16 mRNA and protein expression, whereas enhanced [[ c-fos ]] and c-jun expression relative to control.


With the elevated doses of PhIP, malondialdehyde (MDA) contents, protein carbonyl (PCO) contents and DNA-protein crosslinks (DPC) coefficients were significantly raised in a dose-dependent manner; (3) << PhIP >> at the doses of 10mg/kg and/or 15mg/kg significantly inhibited [[ p16 ]] mRNA and protein expression, whereas enhanced c-fos and c-jun expression relative to control.


The data indicated that << PhIP >> could cause stomach injury, oxidative stress in rat stomachs as well as the activation of [[ c-fos ]] and c-jun and inactivation of p16, which may play a role in the pathogenesis of PhIP-associated stomach cancer.


The data indicated that << PhIP >> could cause stomach injury, oxidative stress in rat stomachs as well as the activation of c-fos and [[ c-jun ]] and inactivation of p16, which may play a role in the pathogenesis of PhIP-associated stomach cancer.


The data indicated that << PhIP >> could cause stomach injury, oxidative stress in rat stomachs as well as the activation of c-fos and c-jun and inactivation of [[ p16 ]], which may play a role in the pathogenesis of PhIP-associated stomach cancer.


We also shortly discuss the ongoing debate on whether << NO >> is the actual reaction product of [[ NOS ]] catalysis, as well as the phenomenon of NO-mediated autoinhibition.


<< Prostacyclin >> analogues inhibit [[ tissue factor ]] expression in the human monocytic cell line THP-1 via a cyclic AMP-dependent mechanism.


The present studies were undertaken to determine whether stable analogues of << prostacyclin >>, a potent endothelium-derived platelet inhibitor and vasodilator, could inhibit [[ tissue factor ]] expression by human monocytic cells.


Preincubation for 30 minutes with << iloprost >>, ciprostene, and carbacyclin led to a dose-dependent inhibition of [[ tissue factor ]] expression induced by all three challenging agents.


Preincubation for 30 minutes with iloprost, << ciprostene >>, and carbacyclin led to a dose-dependent inhibition of [[ tissue factor ]] expression induced by all three challenging agents.


Preincubation for 30 minutes with iloprost, ciprostene, and << carbacyclin >> led to a dose-dependent inhibition of [[ tissue factor ]] expression induced by all three challenging agents.


This effect was potentiated by << isobutylmethylxanthine >>, an inhibitor of [[ phosphodiesterase ]].


The inhibitory effects of iloprost on << tissue factor >> expression were also potentiated by [[ isobutylmethylxanthine ]] and mimicked by forskolin and dibutyryl cyclic AMP but not dibutyryl cyclic GMP.


The inhibitory effects of iloprost on << tissue factor >> expression were also potentiated by isobutylmethylxanthine and mimicked by [[ forskolin ]] and dibutyryl cyclic AMP but not dibutyryl cyclic GMP.


The inhibitory effects of iloprost on << tissue factor >> expression were also potentiated by isobutylmethylxanthine and mimicked by forskolin and d[[ ibutyryl cyclic AMP ]] but not dibutyryl cyclic GMP.


These results suggest that prostacyclin may play a role in downregulating << tissue factor >> expression in monocytes, at least in part via elevation of intracellular levels of [[ cyclic AMP ]].


These results suggest that << prostacyclin >> may play a role in downregulating [[ tissue factor ]] expression in monocytes, at least in part via elevation of intracellular levels of cyclic AMP.


PURPOSE: The fluoropyrimidine carbamate (capecitabine) is converted to << 5-fluorouracil >> (5-FU) by thymidine phosphorylase ([[ TP ]]) inside target tissues.


PURPOSE: The fluoropyrimidine carbamate (capecitabine) is converted to << 5-fluorouracil >> (5-FU) by [[ thymidine phosphorylase ]] (TP) inside target tissues.


PURPOSE: The fluoropyrimidine carbamate (capecitabine) is converted to 5-fluorouracil (<< 5-FU >>) by thymidine phosphorylase ([[ TP ]]) inside target tissues.


PURPOSE: The fluoropyrimidine carbamate (capecitabine) is converted to 5-fluorouracil (<< 5-FU >>) by [[ thymidine phosphorylase ]] (TP) inside target tissues.


PURPOSE: The << fluoropyrimidine carbamate >> (capecitabine) is converted to 5-fluorouracil (5-FU) by thymidine phosphorylase ([[ TP ]]) inside target tissues.


PURPOSE: The << fluoropyrimidine carbamate >> (capecitabine) is converted to 5-fluorouracil (5-FU) by [[ thymidine phosphorylase ]] (TP) inside target tissues.


PURPOSE: The fluoropyrimidine carbamate (<< capecitabine >>) is converted to 5-fluorouracil (5-FU) by thymidine phosphorylase ([[ TP ]]) inside target tissues.


PURPOSE: The fluoropyrimidine carbamate (<< capecitabine >>) is converted to 5-fluorouracil (5-FU) by [[ thymidine phosphorylase ]] (TP) inside target tissues.


<< 5-FU >> interferes with DNA synthesis by blocking [[ thymidylate synthase ]] (TS) but is inactivated by dihydropyrimidine dehydrogenase (DPD).


<< 5-FU >> interferes with DNA synthesis by blocking thymidylate synthase ([[ TS ]]) but is inactivated by dihydropyrimidine dehydrogenase (DPD).


Favorable enzyme profiles (high << TP >> and low DPD) generate high intratumor levels of [[ 5-FU ]] that are effective against many tumors, especially those with low TS.


Favorable enzyme profiles (high TP and low << DPD >>) generate high intratumor levels of [[ 5-FU ]] that are effective against many tumors, especially those with low TS.


Previous studies by this research team proved that vasodilating << prostaglandins >> (PGs) E1, E2 and I2 inhibit [[ carbonic anhydrase ]] (CA) in vitro and in vivo, which suggested involvement of CA in gastric acid secretion inhibition and the increase of gastric mucosa blood flow produced by this group of PGs.


Previous studies by this research team proved that vasodilating << prostaglandins >> (PGs) E1, E2 and I2 inhibit carbonic anhydrase ([[ CA ]]) in vitro and in vivo, which suggested involvement of CA in gastric acid secretion inhibition and the increase of gastric mucosa blood flow produced by this group of PGs.


Previous studies by this research team proved that vasodilating prostaglandins (<< PGs >>) E1, E2 and I2 inhibit [[ carbonic anhydrase ]] (CA) in vitro and in vivo, which suggested involvement of CA in gastric acid secretion inhibition and the increase of gastric mucosa blood flow produced by this group of PGs.


Previous studies by this research team proved that vasodilating prostaglandins (<< PGs >>) E1, E2 and I2 inhibit carbonic anhydrase ([[ CA ]]) in vitro and in vivo, which suggested involvement of CA in gastric acid secretion inhibition and the increase of gastric mucosa blood flow produced by this group of PGs.


Histamine and << Ca >> added to NSAIDs amplified the activating effect of the latter on [[ CA II ]].


Association of PGE2 or << acetazolamide >> to NSAIDs reduced NSAID-induced activation of [[ CA I ]] and CA II.


Association of PGE2 or << acetazolamide >> to NSAIDs reduced NSAID-induced activation of CA I and [[ CA II ]].


<< Indomethacin >> abolished the inhibitory effect of acetazolamide on [[ CA I ]] and CA II.


<< Indomethacin >> abolished the inhibitory effect of acetazolamide on CA I and [[ CA II ]].


Indomethacin abolished the inhibitory effect of << acetazolamide >> on [[ CA I ]] and CA II.


Indomethacin abolished the inhibitory effect of << acetazolamide >> on CA I and [[ CA II ]].


<< COX-1 >> inhibition was measured as percentage inhibition of serum [[ TXB2 ]] generation in clotting whole blood, and as closure time with use of the platelet function analyser PFA-100.


CONCLUSIONS: In the maximum registered dosage, << nabumetone >> inhibits thromboxane production much more than meloxicam, signifying less [[ COX-2 ]] selectivity of the former.


Treatment with << diclofenac >> resulted in nuclear condensation (a morphological change due to apoptosis of NSCs) 24hr after the treatment and activated [[ caspase-3 ]] after 6 hr, indicating that diclofenac may cause apoptosis of neuronal cells via activation of the caspase cascade.


Treatment with diclofenac resulted in nuclear condensation (a morphological change due to apoptosis of NSCs) 24hr after the treatment and activated caspase-3 after 6 hr, indicating that << diclofenac >> may cause apoptosis of neuronal cells via activation of the [[ caspase ]] cascade.


Correlation between activation of << PPARγ >> and resistin downregulation in a mouse adipocyte cell line by a series of [[ thiazolidinediones ]].


Correlation between activation of PPARγ and << resistin >> downregulation in a mouse adipocyte cell line by a series of [[ thiazolidinediones ]].


Firstly, in the normal human renal epithelial HK-2 cells, the measurement of the expression of 30 previously reported << NRF2 >> target genes in response to NRF2 inducers ([[ sulforaphane ]], tert-butylhydroquinone, cinnamic aldehyde, and hydrogen peroxide) showed that the aldo-keto reductase (AKR) 1C1 is highly inducible by all treatments.


Firstly, in the normal human renal epithelial HK-2 cells, the measurement of the expression of 30 previously reported NRF2 target genes in response to << NRF2 >> inducers ([[ sulforaphane ]], tert-butylhydroquinone, cinnamic aldehyde, and hydrogen peroxide) showed that the aldo-keto reductase (AKR) 1C1 is highly inducible by all treatments.


Firstly, in the normal human renal epithelial HK-2 cells, the measurement of the expression of 30 previously reported << NRF2 >> target genes in response to NRF2 inducers (sulforaphane, [[ tert-butylhydroquinone ]], cinnamic aldehyde, and hydrogen peroxide) showed that the aldo-keto reductase (AKR) 1C1 is highly inducible by all treatments.


Firstly, in the normal human renal epithelial HK-2 cells, the measurement of the expression of 30 previously reported NRF2 target genes in response to << NRF2 >> inducers (sulforaphane, [[ tert-butylhydroquinone ]], cinnamic aldehyde, and hydrogen peroxide) showed that the aldo-keto reductase (AKR) 1C1 is highly inducible by all treatments.


Firstly, in the normal human renal epithelial HK-2 cells, the measurement of the expression of 30 previously reported << NRF2 >> target genes in response to NRF2 inducers (sulforaphane, tert-butylhydroquinone, [[ cinnamic aldehyde ]], and hydrogen peroxide) showed that the aldo-keto reductase (AKR) 1C1 is highly inducible by all treatments.


Firstly, in the normal human renal epithelial HK-2 cells, the measurement of the expression of 30 previously reported NRF2 target genes in response to << NRF2 >> inducers (sulforaphane, tert-butylhydroquinone, [[ cinnamic aldehyde ]], and hydrogen peroxide) showed that the aldo-keto reductase (AKR) 1C1 is highly inducible by all treatments.


Firstly, in the normal human renal epithelial HK-2 cells, the measurement of the expression of 30 previously reported << NRF2 >> target genes in response to NRF2 inducers (sulforaphane, tert-butylhydroquinone, cinnamic aldehyde, and [[ hydrogen peroxide ]]) showed that the aldo-keto reductase (AKR) 1C1 is highly inducible by all treatments.


Firstly, in the normal human renal epithelial HK-2 cells, the measurement of the expression of 30 previously reported NRF2 target genes in response to << NRF2 >> inducers (sulforaphane, tert-butylhydroquinone, cinnamic aldehyde, and [[ hydrogen peroxide ]]) showed that the aldo-keto reductase (AKR) 1C1 is highly inducible by all treatments.


Firstly, in the normal human renal epithelial HK-2 cells, the measurement of the expression of 30 previously reported NRF2 target genes in response to NRF2 inducers (<< sulforaphane >>, tert-butylhydroquinone, cinnamic aldehyde, and hydrogen peroxide) showed that the [[ aldo-keto reductase (AKR) 1C1 ]] is highly inducible by all treatments.


Firstly, in the normal human renal epithelial HK-2 cells, the measurement of the expression of 30 previously reported NRF2 target genes in response to NRF2 inducers (sulforaphane, << tert-butylhydroquinone >>, cinnamic aldehyde, and hydrogen peroxide) showed that the [[ aldo-keto reductase (AKR) 1C1 ]] is highly inducible by all treatments.


Firstly, in the normal human renal epithelial HK-2 cells, the measurement of the expression of 30 previously reported NRF2 target genes in response to NRF2 inducers (sulforaphane, tert-butylhydroquinone, << cinnamic aldehyde >>, and hydrogen peroxide) showed that the [[ aldo-keto reductase (AKR) 1C1 ]] is highly inducible by all treatments.


Firstly, in the normal human renal epithelial HK-2 cells, the measurement of the expression of 30 previously reported NRF2 target genes in response to NRF2 inducers (sulforaphane, tert-butylhydroquinone, cinnamic aldehyde, and << hydrogen peroxide >>) showed that the [[ aldo-keto reductase (AKR) 1C1 ]] is highly inducible by all treatments.


The treatment of U937 cells with << NRF2 >> inducers including [[ sulforaphane ]] effectively elevated the expression of AKR1B1, 1B10, 1C1, 1C2, and 1C3.


The treatment of U937 cells with NRF2 inducers including << sulforaphane >> effectively elevated the expression of [[ AKR1B1, 1B10, 1C1, 1C2, and 1C3 ]].


Whereas, the levels of both the basal and << sulforaphane >>-inducible expression of [[ AKR1C1 ]] were significantly reduced in NRF2-silenced stable U937 cells compared to the control cells.


<< Human and rat renin >> and angiotensinogen genes were downregulated in dTGR and were increased by [[ losartan ]] and cilazapril treatments, whereas no changes in the expression of rat ACE and AT1A receptor genes were observed.


Human and rat renin and << angiotensinogen >> genes were downregulated in dTGR and were increased by [[ losartan ]] and cilazapril treatments, whereas no changes in the expression of rat ACE and AT1A receptor genes were observed.


<< Human and rat renin >> and angiotensinogen genes were downregulated in dTGR and were increased by losartan and [[ cilazapril ]] treatments, whereas no changes in the expression of rat ACE and AT1A receptor genes were observed.


Human and rat renin and << angiotensinogen >> genes were downregulated in dTGR and were increased by losartan and [[ cilazapril ]] treatments, whereas no changes in the expression of rat ACE and AT1A receptor genes were observed.


<< Endothelial NO synthase >> expression was increased by [[ cilazapril ]] but not by losartan.


In addition to this pronounced loss of function, << M1766L >> also showed a 10-fold increase in the persistent late [[ sodium ]] current.


Western blot analysis revealed that << OMT >> decreased the expression of [[ Bax ]] and repaired the balance of pro- and anti-apoptotic proteins.


Furthermore, << OMT >> significantly reversed the up-regulation of [[ NR2B ]] and inhibited the calcium overload in the cultured neurons after challenging the NMDA.


<< OMT >> showed partial protection in the cortical neurons via down-regulation of NR2B containing NMDA receptors and up-regulation of [[ Bcl-2 ]] family.


<< OMT >> showed partial protection in the cortical neurons via down-regulation of NR2B containing [[ NMDA receptors ]] and up-regulation of Bcl-2 family.


<< OMT >> showed partial protection in the cortical neurons via down-regulation of [[ NR2B ]] containing NMDA receptors and up-regulation of Bcl-2 family.


<< Emodin-6-O-β-D-glucoside >> inhibits [[ HMGB1 ]]-induced inflammatory responses in vitro and in vivo.


Pharmacology of << ramelteon >>, a selective [[ MT1 ]]/MT2 receptor agonist: a novel therapeutic drug for sleep disorders.


Pharmacology of << ramelteon >>, a selective MT1/[[ MT2 ]] receptor agonist: a novel therapeutic drug for sleep disorders.


<< Ramelteon >> (Rozerem; Takeda Pharmaceutical Company Limited, Osaka, Japan) is an orally active, highly selective melatonin [[ MT(1) ]]/MT(2) receptor agonist.


<< Ramelteon >> (Rozerem; Takeda Pharmaceutical Company Limited, Osaka, Japan) is an orally active, highly selective melatonin MT(1)/[[ MT(2) ]] receptor agonist.


Unlike the sedative hypnotics that target GABA(A) receptor complexes, << ramelteon >> is a chronohypnotic that acts on the melatonin [[ MT(1) ]] and MT(2) receptors, which are primarily located in the suprachiasmatic nucleus, the body's "master clock." As such, ramelteon possesses the first new therapeutic mechanism of action for a prescription insomnia medication in over three decades.


Unlike the sedative hypnotics that target GABA(A) receptor complexes, << ramelteon >> is a chronohypnotic that acts on the melatonin MT(1) and [[ MT(2) ]] receptors, which are primarily located in the suprachiasmatic nucleus, the body's "master clock." As such, ramelteon possesses the first new therapeutic mechanism of action for a prescription insomnia medication in over three decades.


<< Am80 >> slightly inhibited the growth of both myeloma cells and HUVECs, and remarkably inhibited the growth of HUVECs stimulated by [[ VEGF ]].


<< Am80 >> inhibited VEGF-induced phosphorylation of [[ VEGF receptor ]].


<< Am80 >> inhibited [[ VEGF ]]-induced phosphorylation of VEGF receptor.


In addition, << VEGF >>-induced formation of tube-like structures in vitro and neovascularization in mouse corneas were significantly inhibited by [[ Am80 ]].


We have examined the effect of dihydropyridine << Ca2+-channel >> blockers [[ felodipine ]] and nicardipine on CaMPDE.


We have examined the effect of dihydropyridine << Ca2+-channel >> blockers felodipine and [[ nicardipine ]] on CaMPDE.


We have examined the effect of << dihydropyridine >> [[ Ca2+-channel ]] blockers felodipine and nicardipine on CaMPDE.


The results suggest that the 63-kDa (<< PDE 1B1 >>) and 60-kDa (PDE 1A2) CaMPDE isozymes are inhibited by [[ felodipine ]] and nicardipine by partial competitive inhibition and that these two Ca2+ antagonists appear to counteract each other.


The results suggest that the 63-kDa (PDE 1B1) and 60-kDa (<< PDE 1A2 >>) CaMPDE isozymes are inhibited by [[ felodipine ]] and nicardipine by partial competitive inhibition and that these two Ca2+ antagonists appear to counteract each other.


The results suggest that the 63-kDa (PDE 1B1) and 60-kDa (PDE 1A2) << CaMPDE >> isozymes are inhibited by [[ felodipine ]] and nicardipine by partial competitive inhibition and that these two Ca2+ antagonists appear to counteract each other.


The results suggest that the 63-kDa (<< PDE 1B1 >>) and 60-kDa (PDE 1A2) CaMPDE isozymes are inhibited by felodipine and [[ nicardipine ]] by partial competitive inhibition and that these two Ca2+ antagonists appear to counteract each other.


The results suggest that the 63-kDa (PDE 1B1) and 60-kDa (<< PDE 1A2 >>) CaMPDE isozymes are inhibited by felodipine and [[ nicardipine ]] by partial competitive inhibition and that these two Ca2+ antagonists appear to counteract each other.


The results suggest that the 63-kDa (PDE 1B1) and 60-kDa (PDE 1A2) << CaMPDE >> isozymes are inhibited by felodipine and [[ nicardipine ]] by partial competitive inhibition and that these two Ca2+ antagonists appear to counteract each other.


Felodipine and nicardipine have similar affinities for 60-kDa << CaMPDE >> isozymes but bring about different levels of enzyme inhibition, suggesting the possibility of designing specific drugs that can protect the enzyme from inhibition by [[ dihydropyridine ]] Ca2+-channel blockers.


Felodipine and nicardipine have similar affinities for 60-kDa CaMPDE isozymes but bring about different levels of enzyme inhibition, suggesting the possibility of designing specific drugs that can protect the enzyme from inhibition by << dihydropyridine >> [[ Ca2+-channel ]] blockers.


Several inhibitors of << Lp-PLA(2) >> have been described, including [[ darapladib ]], which is currently in phase 3 clinical development for the treatment of atherosclerosis.