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<< Cetrorelix >> completely blocked the rise of levels of the two most abundant species, 5.0 kb and 4.5 kb, of the [[ GnRH-R ]] mRNA, during both the infantile and the juvenile periods.

<< Cetrorelix >> also abolished the developmental rise of the [[ gonadotropin beta ]] subunit mRNAs during the two periods of the study.

The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosages of the nonsedating << histamine H1-receptor >> antagonists [[ terfenadine ]], astemizole, loratadine, and acrivastine are reviewed.

The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosages of the nonsedating << histamine H1-receptor >> antagonists terfenadine, [[ astemizole ]], loratadine, and acrivastine are reviewed.

The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosages of the nonsedating << histamine H1-receptor >> antagonists terfenadine, astemizole, [[ loratadine ]], and acrivastine are reviewed.

The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosages of the nonsedating << histamine H1-receptor >> antagonists terfenadine, astemizole, loratadine, and [[ acrivastine ]] are reviewed.

<< Terfenadine >> and astemizole are chemically unrelated to [[ histamine H1-receptor ]] antagonists such as diphenhydramine and chlorpheniramine.

Terfenadine and << astemizole >> are chemically unrelated to [[ histamine H1-receptor ]] antagonists such as diphenhydramine and chlorpheniramine.

Terfenadine and astemizole are chemically unrelated to << histamine H1-receptor >> antagonists such as [[ diphenhydramine ]] and chlorpheniramine.

Terfenadine and astemizole are chemically unrelated to << histamine H1-receptor >> antagonists such as diphenhydramine and [[ chlorpheniramine ]].

Anti-inflammatory effect of << prunetin >> via the suppression of [[ NF-κB ]] pathway.

Promoter assay revealed that << prunetin >> inhibits LPS-induced nitric oxide and prostaglandin E2 production through the suppression of [[ iNOS ]] and COX-2 at the transcriptional level.

Promoter assay revealed that << prunetin >> inhibits LPS-induced nitric oxide and prostaglandin E2 production through the suppression of iNOS and [[ COX-2 ]] at the transcriptional level.

In addition, << prunetin >> inhibits [[ NF-κB ]]-dependent inflammatory responses by modulating IκB kinase (IKK)-inhibitor κBα (IκBα)-NF-κB signaling.

Consistent with these results, << prunetin >> significantly reduced serum levels of inflammatory [[ cytokines ]] and mortality in mice challenged with lipopolysaccharide.

G6PC2: A Negative Regulator of Basal << Glucose >>-Stimulated [[ Insulin ]] Secretion.

G6pc2 deletion resulted in a leftward shift in the dose-response curve for << glucose >>-stimulated [[ insulin ]] secretion (GSIS).

These data suggest that << G6pc2 >> represents a novel, negative regulator of basal GSIS that acts by hydrolyzing [[ glucose-6-phosphate ]], thereby reducing glycolytic flux.

Using the << mTOR >> inhibitor [[ PP242, ]] we found that TGFβ-induced both early and sustained activation of TORC1 and TORC2 was necessary for deptor suppression.

<< PP242 >>-induced reversal of [[ deptor ]] suppression by TGFβ was associated with a significant inhibition of TGFβ-stimulated protein synthesis and hypertrophy.

METHODS: (+/-)-Modafinil and its R-(-)- and S-(+)-enantiomers were synthesized and tested for inhibition of << [(3)H] dopamine >> (DA) uptake and [(3)H]WIN 35428 binding in [[ human dopamine transporter ]] (DAT) wild-type and mutants with altered conformational equilibria.

METHODS: (+/-)-Modafinil and its R-(-)- and S-(+)-enantiomers were synthesized and tested for inhibition of << [(3)H] dopamine >> (DA) uptake and [(3)H]WIN 35428 binding in human dopamine transporter ([[ DAT ]]) wild-type and mutants with altered conformational equilibria.

METHODS: (+/-)-Modafinil and its R-(-)- and S-(+)-enantiomers were synthesized and tested for inhibition of [(3)H] dopamine (<< DA >>) uptake and [(3)H]WIN 35428 binding in [[ human dopamine transporter ]] (DAT) wild-type and mutants with altered conformational equilibria.

METHODS: (+/-)-Modafinil and its R-(-)- and S-(+)-enantiomers were synthesized and tested for inhibition of [(3)H] dopamine (<< DA >>) uptake and [(3)H]WIN 35428 binding in human dopamine transporter ([[ DAT ]]) wild-type and mutants with altered conformational equilibria.

RESULTS: (+/-)-, R-, and S-modafinil bind to the << DAT >> and inhibit [[ DA ]] uptake less potently than cocaine, with R-modafinil having approximately threefold higher affinity than its S-enantiomer.

Apple << polyphenols >> suppress antigen presentation of [[ ovalbumin ]] by THP-1-derived dendritic cells.

A significant decrease in << HLA-DR >> expression was observed in the AP and fractionated [[ procyanidin ]]-treated cells in the presence of ovalbumin (OVA), but no effect on CD86 expression was observed.

Furthermore, the up-regulation of << IL-12 >> and TNF-α was found in the [[ procyanidin ]] trimers-treated cells in the presence of OVA.

Furthermore, the up-regulation of IL-12 and << TNF-α >> was found in the [[ procyanidin ]] trimers-treated cells in the presence of OVA.

The acute toxicity of << organophosphorus >> (OP) compounds in mammals is due to their irreversible inhibition of [[ acetylcholinesterase ]] (AChE) in the nervous system, which leads to increased synaptic acetylcholine levels.

The acute toxicity of << organophosphorus >> (OP) compounds in mammals is due to their irreversible inhibition of acetylcholinesterase ([[ AChE ]]) in the nervous system, which leads to increased synaptic acetylcholine levels.

The acute toxicity of organophosphorus (OP) compounds in mammals is due to their irreversible inhibition of << acetylcholinesterase >> (AChE) in the nervous system, which leads to increased synaptic [[ acetylcholine ]] levels.

The acute toxicity of organophosphorus (OP) compounds in mammals is due to their irreversible inhibition of acetylcholinesterase (<< AChE >>) in the nervous system, which leads to increased synaptic [[ acetylcholine ]] levels.

In phosphotriesterase and physostigmine-treated mice, a 4- and 2-fold higher << sarin >> dose, respectively, was needed to cause a 50% inhibition of brain [[ AChE ]] activity.

The << CYP3A4 >> activity could be induced 2-fold by [[ rifampicin ]], whereas CYP2C9 activity remained equally high.

The CYP3A4 activity could be induced 2-fold by << rifampicin >>, whereas [[ CYP2C9 ]] activity remained equally high.

<< PF-04859989 >> as a template for structure-based drug design: identification of new pyrazole series of irreversible [[ KAT II ]] inhibitors with improved lipophilic efficiency.

PF-04859989 as a template for structure-based drug design: identification of new << pyrazole >> series of irreversible [[ KAT II ]] inhibitors with improved lipophilic efficiency.

The structure-based design, synthesis, and biological evaluation of a new << pyrazole >> series of irreversible [[ KAT II ]] inhibitors are described herein.

The modification of the inhibitor scaffold of 1 and 2 from a << dihydroquinolinone >> core to a tetrahydropyrazolopyridinone core led to discovery of a new series of potent [[ KAT II ]] inhibitors with excellent physicochemical properties.

The modification of the inhibitor scaffold of 1 and 2 from a dihydroquinolinone core to a << tetrahydropyrazolopyridinone >> core led to discovery of a new series of potent [[ KAT II ]] inhibitors with excellent physicochemical properties.

The capacity of << acetylcholinesterase >> inhibitors, with the exception of [[ tacrine ]] and ambenonium, to displace bound [3H]-oxotremorine-M in preference to [3H]quinuclinidyl benzilate predicts that the former compounds could act as potential agonists at muscarinic receptors.

The capacity of << acetylcholinesterase >> inhibitors, with the exception of tacrine and [[ ambenonium ]], to displace bound [3H]-oxotremorine-M in preference to [3H]quinuclinidyl benzilate predicts that the former compounds could act as potential agonists at muscarinic receptors.

Moreover, the rank order for potency in inhibiting << acetylcholinesterase >> (ambenonium>neostigmine=physostigmine =tacrine>[[ pyridostigmine ]]=edrophonium=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of acetylcholinesterase also displaced [3H]-oxotremorine-M to the greatest extent.

Moreover, the rank order for potency in inhibiting acetylcholinesterase (ambenonium>neostigmine=physostigmine =tacrine><< pyridostigmine >>=edrophonium=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of [[ acetylcholinesterase ]] also displaced [3H]-oxotremorine-M to the greatest extent.

Moreover, the rank order for potency in inhibiting << acetylcholinesterase >> (ambenonium>neostigmine=physostigmine =tacrine>pyridostigmine=[[ edrophonium ]]=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of acetylcholinesterase also displaced [3H]-oxotremorine-M to the greatest extent.

Moreover, the rank order for potency in inhibiting acetylcholinesterase (ambenonium>neostigmine=physostigmine =tacrine>pyridostigmine=<< edrophonium >>=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of [[ acetylcholinesterase ]] also displaced [3H]-oxotremorine-M to the greatest extent.

Moreover, the rank order for potency in inhibiting << acetylcholinesterase >> (ambenonium>neostigmine=physostigmine =tacrine>pyridostigmine=edrophonium=[[ galanthamine ]] >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of acetylcholinesterase also displaced [3H]-oxotremorine-M to the greatest extent.

Moreover, the rank order for potency in inhibiting acetylcholinesterase (ambenonium>neostigmine=physostigmine =tacrine>pyridostigmine=edrophonium=<< galanthamine >> >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of [[ acetylcholinesterase ]] also displaced [3H]-oxotremorine-M to the greatest extent.

Moreover, the rank order for potency in inhibiting << acetylcholinesterase >> (ambenonium>neostigmine=physostigmine =tacrine>pyridostigmine=edrophonium=galanthamine >[[ desoxypeganine ]]>parathion>gramine) indicated that the most effective inhibitors of acetylcholinesterase also displaced [3H]-oxotremorine-M to the greatest extent.

Moreover, the rank order for potency in inhibiting acetylcholinesterase (ambenonium>neostigmine=physostigmine =tacrine>pyridostigmine=edrophonium=galanthamine ><< desoxypeganine >>>parathion>gramine) indicated that the most effective inhibitors of [[ acetylcholinesterase ]] also displaced [3H]-oxotremorine-M to the greatest extent.

Moreover, the rank order for potency in inhibiting << acetylcholinesterase >> (ambenonium>neostigmine=physostigmine =tacrine>pyridostigmine=edrophonium=galanthamine >desoxypeganine>[[ parathion ]]>gramine) indicated that the most effective inhibitors of acetylcholinesterase also displaced [3H]-oxotremorine-M to the greatest extent.

Moreover, the rank order for potency in inhibiting acetylcholinesterase (ambenonium>neostigmine=physostigmine =tacrine>pyridostigmine=edrophonium=galanthamine >desoxypeganine><< parathion >>>gramine) indicated that the most effective inhibitors of [[ acetylcholinesterase ]] also displaced [3H]-oxotremorine-M to the greatest extent.

Moreover, the rank order for potency in inhibiting << acetylcholinesterase >> (ambenonium>neostigmine=physostigmine =tacrine>pyridostigmine=edrophonium=galanthamine >desoxypeganine>parathion>[[ gramine ]]) indicated that the most effective inhibitors of acetylcholinesterase also displaced [3H]-oxotremorine-M to the greatest extent.

Moreover, the rank order for potency in inhibiting acetylcholinesterase (ambenonium>neostigmine=physostigmine =tacrine>pyridostigmine=edrophonium=galanthamine >desoxypeganine>parathion><< gramine >>) indicated that the most effective inhibitors of [[ acetylcholinesterase ]] also displaced [3H]-oxotremorine-M to the greatest extent.

Moreover, the rank order for potency in inhibiting << acetylcholinesterase >> ([[ ambenonium ]]>neostigmine=physostigmine =tacrine>pyridostigmine=edrophonium=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of acetylcholinesterase also displaced [3H]-oxotremorine-M to the greatest extent.

Moreover, the rank order for potency in inhibiting acetylcholinesterase (<< ambenonium >>>neostigmine=physostigmine =tacrine>pyridostigmine=edrophonium=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of [[ acetylcholinesterase ]] also displaced [3H]-oxotremorine-M to the greatest extent.

Moreover, the rank order for potency in inhibiting << acetylcholinesterase >> (ambenonium>[[ neostigmine ]]=physostigmine =tacrine>pyridostigmine=edrophonium=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of acetylcholinesterase also displaced [3H]-oxotremorine-M to the greatest extent.

Moreover, the rank order for potency in inhibiting acetylcholinesterase (ambenonium><< neostigmine >>=physostigmine =tacrine>pyridostigmine=edrophonium=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of [[ acetylcholinesterase ]] also displaced [3H]-oxotremorine-M to the greatest extent.

Moreover, the rank order for potency in inhibiting << acetylcholinesterase >> (ambenonium>neostigmine=[[ physostigmine ]] =tacrine>pyridostigmine=edrophonium=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of acetylcholinesterase also displaced [3H]-oxotremorine-M to the greatest extent.

Moreover, the rank order for potency in inhibiting acetylcholinesterase (ambenonium>neostigmine=<< physostigmine >> =tacrine>pyridostigmine=edrophonium=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of [[ acetylcholinesterase ]] also displaced [3H]-oxotremorine-M to the greatest extent.

Moreover, the rank order for potency in inhibiting << acetylcholinesterase >> (ambenonium>neostigmine=physostigmine =[[ tacrine ]]>pyridostigmine=edrophonium=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of acetylcholinesterase also displaced [3H]-oxotremorine-M to the greatest extent.

Moreover, the rank order for potency in inhibiting acetylcholinesterase (ambenonium>neostigmine=physostigmine =<< tacrine >>>pyridostigmine=edrophonium=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of [[ acetylcholinesterase ]] also displaced [3H]-oxotremorine-M to the greatest extent.

CONCLUSIONS: Total vitamin B6 is abnormally high in autism, consistent with previous reports of an impaired << pyridoxal kinase >> for the conversion of pyridoxine and pyridoxal to [[ PLP ]].

CONCLUSIONS: Total vitamin B6 is abnormally high in autism, consistent with previous reports of an impaired << pyridoxal kinase >> for the conversion of [[ pyridoxine ]] and pyridoxal to PLP.

CONCLUSIONS: Total vitamin B6 is abnormally high in autism, consistent with previous reports of an impaired << pyridoxal kinase >> for the conversion of pyridoxine and [[ pyridoxal ]] to PLP.

Synthesis, molecular modeling and evaluation of novel << N'-2-(4-benzylpiperidin-/piperazin-1-yl)acylhydrazone >> derivatives as dual inhibitors for [[ cholinesterases ]] and Aβ aggregation.

Synthesis, molecular modeling and evaluation of novel << N'-2-(4-benzylpiperidin-/piperazin-1-yl)acylhydrazone >> derivatives as dual inhibitors for cholinesterases and [[ Aβ ]] aggregation.

To develop new drugs for treatment of Alzheimer's disease, a group of << N'-2-(4-Benzylpiperidin-/piperazin-1-yl)acylhydrazones >> was designed, synthesized and tested for their ability to inhibit [[ acetylcholinesterase ]], butyrylcholinesterase and aggregation of amyloid beta peptides (1-40, 1-42 and 1-40_1-42).

To develop new drugs for treatment of Alzheimer's disease, a group of << N'-2-(4-Benzylpiperidin-/piperazin-1-yl)acylhydrazones >> was designed, synthesized and tested for their ability to inhibit acetylcholinesterase, [[ butyrylcholinesterase ]] and aggregation of amyloid beta peptides (1-40, 1-42 and 1-40_1-42).

β-Amyloid aggregation results showed that all compounds exhibited remarkable << Aβ >> fibril aggregation inhibition activity with a nearly similar potential as the reference compound [[ rifampicin ]], which makes them promising anti-Alzheimer drug candidates.

Here, translocation studies using the human androgen receptor (hAR) and the human glucocorticoid receptor (hGR) were performed to aid in identifying the mechanism by which anabolic-androgenic << steroids >> (AAS) were activating [[ hAR ]] and potentially interacting with hGR and how glucocorticoid ligands were interacting with the hGR and hAR.

<< Licofelone >>, a balanced inhibitor of [[ cyclooxygenase ]] and 5-lipoxygenase, reduces inflammation in a rabbit model of atherosclerosis.

<< Licofelone >>, a balanced inhibitor of cyclooxygenase and [[ 5-lipoxygenase ]], reduces inflammation in a rabbit model of atherosclerosis.

<< Licofelone >>, a dual anti-inflammatory drug that inhibits 5-lipoxygenase (LOX) and cyclooxygenase (COX) enzymes, may have a better cardiovascular profile that cycloxygenase-2 inhibitors due to [[ cycloxygenase-1 ]] blockade-mediated antithrombotic effect and a better gastrointestinal tolerability.

<< Licofelone >>, a dual anti-inflammatory drug that inhibits [[ 5-lipoxygenase ]] (LOX) and cyclooxygenase (COX) enzymes, may have a better cardiovascular profile that cycloxygenase-2 inhibitors due to cycloxygenase-1 blockade-mediated antithrombotic effect and a better gastrointestinal tolerability.

<< Licofelone >>, a dual anti-inflammatory drug that inhibits 5-lipoxygenase ([[ LOX ]]) and cyclooxygenase (COX) enzymes, may have a better cardiovascular profile that cycloxygenase-2 inhibitors due to cycloxygenase-1 blockade-mediated antithrombotic effect and a better gastrointestinal tolerability.

<< Licofelone >>, a dual anti-inflammatory drug that inhibits 5-lipoxygenase (LOX) and [[ cyclooxygenase ]] (COX) enzymes, may have a better cardiovascular profile that cycloxygenase-2 inhibitors due to cycloxygenase-1 blockade-mediated antithrombotic effect and a better gastrointestinal tolerability.

<< Licofelone >>, a dual anti-inflammatory drug that inhibits 5-lipoxygenase (LOX) and cyclooxygenase ([[ COX ]]) enzymes, may have a better cardiovascular profile that cycloxygenase-2 inhibitors due to cycloxygenase-1 blockade-mediated antithrombotic effect and a better gastrointestinal tolerability.

We examined the anti-inflammatory effect of licofelone on atherosclerotic lesions as well as in isolated neutrophils from whole blood of rabbits compared with a selective inhibitor of << COX-2 >>, [[ rofecoxib ]].

<< Licofelone >> reduced intima/media ratio in injured arteries, the macrophages infiltration in the neointimal area, [[ monocyte chemoattractant protein-1 ]] (MCP-1) gene expression, and the activation of nuclear factor-kappaB in rabbit atheroma.

<< Licofelone >> reduced intima/media ratio in injured arteries, the macrophages infiltration in the neointimal area, monocyte chemoattractant protein-1 ([[ MCP-1 ]]) gene expression, and the activation of nuclear factor-kappaB in rabbit atheroma.

<< Licofelone >> reduced intima/media ratio in injured arteries, the macrophages infiltration in the neointimal area, monocyte chemoattractant protein-1 (MCP-1) gene expression, and the activation of [[ nuclear factor-kappaB ]] in rabbit atheroma.

Moreover, << licofelone >> inhibited [[ COX-2 ]] and 5-LOX protein expression in vascular lesions.

Moreover, << licofelone >> inhibited COX-2 and [[ 5-LOX ]] protein expression in vascular lesions.

<< Rofecoxib >> only diminished [[ COX-2 ]] protein expression and MCP-1 gene expression in vascular atheroma.

<< Rofecoxib >> only diminished COX-2 protein expression and [[ MCP-1 ]] gene expression in vascular atheroma.

<< Licofelone >> almost abolished [[ 5-LOX ]] activity by inhibiting leukotriene B4 generation in rabbit neutrophils and prevented platelet thromboxane B2 production from whole blood.

Licofelone almost abolished << 5-LOX >> activity by inhibiting [[ leukotriene B4 ]] generation in rabbit neutrophils and prevented platelet thromboxane B2 production from whole blood.

Licofelone almost abolished << 5-LOX >> activity by inhibiting leukotriene B4 generation in rabbit neutrophils and prevented platelet [[ thromboxane B2 ]] production from whole blood.

No influence of moderate hepatic impairment on the pharmacokinetics of << lumiracoxib >>, an oral [[ COX-2 ]] selective inhibitor.

The aim of this study was to evaluate the influence of hepatic impairment on the pharmacokinetics (PK) of the novel << cyclooxygenase-2 >> (COX-2) selective inhibitor [[ lumiracoxib ]] (Prexige), so that dose recommendations for clinical use can be provided.

The aim of this study was to evaluate the influence of hepatic impairment on the pharmacokinetics (PK) of the novel cyclooxygenase-2 (<< COX-2 >>) selective inhibitor [[ lumiracoxib ]] (Prexige), so that dose recommendations for clinical use can be provided.

The aim of this study was to evaluate the influence of hepatic impairment on the pharmacokinetics (PK) of the novel << cyclooxygenase-2 >> (COX-2) selective inhibitor lumiracoxib ([[ Prexige ]]), so that dose recommendations for clinical use can be provided.

The aim of this study was to evaluate the influence of hepatic impairment on the pharmacokinetics (PK) of the novel cyclooxygenase-2 (<< COX-2 >>) selective inhibitor lumiracoxib ([[ Prexige ]]), so that dose recommendations for clinical use can be provided.

In addition, << ethanol >> induced degradation of [[ DNA methyltransferases ]] (DNMT-1, DNMT-3a, and DNMT-3b), as well as the methyl CpG-binding proteins (MeCP-2, MBD-2 and MBD-3), in MEF cells by the proteasomal pathway.

In addition, << ethanol >> induced degradation of DNA methyltransferases ([[ DNMT- ]]1, DNMT-3a, and DNMT-3b), as well as the methyl CpG-binding proteins (MeCP-2, MBD-2 and MBD-3), in MEF cells by the proteasomal pathway.

In addition, << ethanol >> induced degradation of DNA methyltransferases (DNMT-1, [[ DNMT-3a ]], and DNMT-3b), as well as the methyl CpG-binding proteins (MeCP-2, MBD-2 and MBD-3), in MEF cells by the proteasomal pathway.

In addition, << ethanol >> induced degradation of DNA methyltransferases (DNMT-1, DNMT-3a, and [[ DNMT-3b ]]), as well as the methyl CpG-binding proteins (MeCP-2, MBD-2 and MBD-3), in MEF cells by the proteasomal pathway.

In addition, << ethanol >> induced degradation of DNA methyltransferases (DNMT-1, DNMT-3a, and DNMT-3b), as well as the [[ methyl CpG-binding proteins ]] (MeCP-2, MBD-2 and MBD-3), in MEF cells by the proteasomal pathway.