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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.