RESULTS: Pretreatment of ucOC (30ng/ml) prevented LA-induced apoptosis in insulin-stimulated endothelial cells; effects were abolished by pretreatment with the phosphatidylinositol 3-kinase (<< PI3-kinase >>) inhibitor, [[ wortmannin ]].


In addition, during acute exposure tests performed at the end of the chronic exposure, biofilms chronically exposed to 75 and 150μgL(-1) << oxyfluorfen >> showed a higher [[ CAT ]] activity than controls.


The involvement of the various DA receptor subtypes in the motor effects of N/OFQ and NOP receptor antagonists was evaluated pharmacologically, using << D1 >>/D5 ([[ SCH23390 ]]), D2/D3 (raclopride, amisulpride) and D3 (S33084) receptor antagonists, and by using D2 receptor knockout mice.


The involvement of the various DA receptor subtypes in the motor effects of N/OFQ and NOP receptor antagonists was evaluated pharmacologically, using D1/<< D5 >> ([[ SCH23390 ]]), D2/D3 (raclopride, amisulpride) and D3 (S33084) receptor antagonists, and by using D2 receptor knockout mice.


The involvement of the various DA receptor subtypes in the motor effects of N/OFQ and NOP receptor antagonists was evaluated pharmacologically, using D1/D5 (SCH23390), << D2 >>/D3 ([[ raclopride ]], amisulpride) and D3 (S33084) receptor antagonists, and by using D2 receptor knockout mice.


The involvement of the various DA receptor subtypes in the motor effects of N/OFQ and NOP receptor antagonists was evaluated pharmacologically, using D1/D5 (SCH23390), D2/<< D3 >> ([[ raclopride ]], amisulpride) and D3 (S33084) receptor antagonists, and by using D2 receptor knockout mice.


The involvement of the various DA receptor subtypes in the motor effects of N/OFQ and NOP receptor antagonists was evaluated pharmacologically, using D1/D5 (SCH23390), << D2 >>/D3 (raclopride, [[ amisulpride ]]) and D3 (S33084) receptor antagonists, and by using D2 receptor knockout mice.


The involvement of the various DA receptor subtypes in the motor effects of N/OFQ and NOP receptor antagonists was evaluated pharmacologically, using D1/D5 (SCH23390), D2/<< D3 >> (raclopride, [[ amisulpride ]]) and D3 (S33084) receptor antagonists, and by using D2 receptor knockout mice.


The involvement of the various DA receptor subtypes in the motor effects of N/OFQ and NOP receptor antagonists was evaluated pharmacologically, using D1/D5 (SCH23390), D2/D3 (raclopride, amisulpride) and << D3 >> ([[ S33084 ]]) receptor antagonists, and by using D2 receptor knockout mice.


<< Haloperidol >> promotes mTORC1-dependent phosphorylation of [[ ribosomal protein S6 ]] via dopamine- and cAMP-regulated phosphoprotein of 32 kDa and inhibition of protein phosphatase-1.


<< Haloperidol >> promotes mTORC1-dependent phosphorylation of ribosomal protein S6 via dopamine- and cAMP-regulated phosphoprotein of 32 kDa and inhibition of [[ protein phosphatase-1 ]].


This effect was prevented by << rapamycin >>, an inhibitor of the [[ mammalian target of rapamycin complex 1 ]] (mTORC1), or by PF470867, a selective inhibitor of the p70 ribosomal S6 kinase 1 (S6K1).


This effect was prevented by << rapamycin >>, an inhibitor of the mammalian target of rapamycin complex 1 ([[ mTORC1 ]]), or by PF470867, a selective inhibitor of the p70 ribosomal S6 kinase 1 (S6K1).


This effect was prevented by rapamycin, an inhibitor of the mammalian target of rapamycin complex 1 (mTORC1), or by << PF470867 >>, a selective inhibitor of the [[ p70 ribosomal S6 kinase 1 ]] (S6K1).


This effect was prevented by rapamycin, an inhibitor of the mammalian target of rapamycin complex 1 (mTORC1), or by << PF470867 >>, a selective inhibitor of the p70 ribosomal S6 kinase 1 ([[ S6K1 ]]).


In line with this observation, incubation of striatal slices with << okadaic acid >> and calyculin A, two inhibitors of [[ PP-1 ]], increased Ser240/244 phosphorylation.


In line with this observation, incubation of striatal slices with okadaic acid and << calyculin A >>, two inhibitors of [[ PP-1 ]], increased Ser240/244 phosphorylation.


These results show that << haloperidol >> promotes mTORC1- and S6K1-dependent phosphorylation of [[ rpS6 ]] at Ser240/244, in a subpopulation of striatal MSNs expressing D2Rs.


These compounds resulted from our efforts to merge the pharmacophores of selective << factor Xa >> inhibitor [[ rivaroxaban ]] with a mimic of the Arg-Gly-Asp (RGD) sequence of fibrinogen to obtain designed multiple ligands with potential antithrombotic activity.


Resulting from this study, a structurally novel class of submicromolar fibrinogen << GPIIb/IIIa >> binding inhibitor bearing [[ 1,2,4-oxadiazol-5(4H)-one ]] moiety is also described.


Rats intoxicated with << Cd >> for 30 days, significantly increased tissue malondialdehyde (MDA) levels and significantly decreased enzymatic antioxidants [[ superoxide dismutase ]], glutathione peroxidase and catalase in the frontal cortex tissue.


Rats intoxicated with << Cd >> for 30 days, significantly increased tissue malondialdehyde (MDA) levels and significantly decreased enzymatic antioxidants superoxide dismutase, [[ glutathione peroxidase ]] and catalase in the frontal cortex tissue.


Rats intoxicated with << Cd >> for 30 days, significantly increased tissue malondialdehyde (MDA) levels and significantly decreased enzymatic antioxidants superoxide dismutase, glutathione peroxidase and [[ catalase ]] in the frontal cortex tissue.


The << caspase-3 >> immunopositivity was increased in degenerating neurons of the [[ Cd ]] group.


In contrast, TSH-induced differentiation of progenitor cells, in particular the expression of the << sodium iodide symporter >>, was significantly inhibited by [[ 17beta-oestradiol ]].In conclusion, oestrogen stimulated growth and simultaneously inhibited differentiation of thyroid nodules derived stem/progenitor cells.


Drug-drug interactions are dependent on statins' pharmacokinetic profile: << simvastatin >>, lovastatin and atorvastatin are metabolized through [[ cytochrome P450 (CYP) 3A ]], while the metabolism of the other statins is independent of this CYP.


Drug-drug interactions are dependent on statins' pharmacokinetic profile: simvastatin, << lovastatin >> and atorvastatin are metabolized through [[ cytochrome P450 (CYP) 3A ]], while the metabolism of the other statins is independent of this CYP.


Drug-drug interactions are dependent on statins' pharmacokinetic profile: simvastatin, lovastatin and << atorvastatin >> are metabolized through [[ cytochrome P450 (CYP) 3A ]], while the metabolism of the other statins is independent of this CYP.


All HIV PIs except nelfinavir are coadministered with a low dose of << ritonavir >>, a potent [[ CYP3A ]] inhibitor to improve their pharmacokinetic properties.


The HCV-PIs << boceprevir >> and telaprevir are both, to different extents, inhibitors of [[ CYP3A ]].


The HCV-PIs boceprevir and << telaprevir >> are both, to different extents, inhibitors of [[ CYP3A ]].


Simvastatin and lovastatin metabolized through CYP3A have the highest potency for drug-drug interaction with potent << CYP3A >> inhibitors such as ritonavir- or cobicistat-boosted HIV-PI or the hepatitis C virus (HCV) PI, telaprevir or [[ boceprevir ]], and therefore their coadministration is contraindicated.


Simvastatin and lovastatin metabolized through CYP3A have the highest potency for drug-drug interaction with potent << CYP3A >> inhibitors such as [[ ritonavir ]]- or cobicistat-boosted HIV-PI or the hepatitis C virus (HCV) PI, telaprevir or boceprevir, and therefore their coadministration is contraindicated.


Simvastatin and lovastatin metabolized through CYP3A have the highest potency for drug-drug interaction with potent << CYP3A >> inhibitors such as ritonavir- or [[ cobicistat ]]-boosted HIV-PI or the hepatitis C virus (HCV) PI, telaprevir or boceprevir, and therefore their coadministration is contraindicated.


Simvastatin and lovastatin metabolized through CYP3A have the highest potency for drug-drug interaction with potent << CYP3A >> inhibitors such as ritonavir- or cobicistat-boosted HIV-PI or the hepatitis C virus (HCV) PI, [[ telaprevir ]] or boceprevir, and therefore their coadministration is contraindicated.


<< Simvastatin >> and lovastatin metabolized through [[ CYP3A ]] have the highest potency for drug-drug interaction with potent CYP3A inhibitors such as ritonavir- or cobicistat-boosted HIV-PI or the hepatitis C virus (HCV) PI, telaprevir or boceprevir, and therefore their coadministration is contraindicated.


Simvastatin and << lovastatin >> metabolized through [[ CYP3A ]] have the highest potency for drug-drug interaction with potent CYP3A inhibitors such as ritonavir- or cobicistat-boosted HIV-PI or the hepatitis C virus (HCV) PI, telaprevir or boceprevir, and therefore their coadministration is contraindicated.


<< Atorvastatin >> is also a [[ CYP3A ]] substrate, but less potent drug-drug interactions have been reported with CYP3A inhibitors.


The synthesis, preclinical profile, and in vivo efficacy in rat xenograft models of the novel and selective << anaplastic lymphoma kinase >> inhibitor 15b ([[ LDK378 ]]) are described.


In this initial report, preliminary structure-activity relationships (SARs) are described as well as the rational design strategy employed to overcome the development deficiencies of the first generation << ALK >> inhibitor 4 ([[ TAE684 ]]).


Limitation of SRF was produced by the anticonvulsant BDZs (diazepam, clonazepam, nitrazepam and lorazepam) at low to mid nanomolar concentrations, by a convulsant BDZ which does not bind to high affinity BDZ receptors (Ro 5-4864) at high nanomolar concentrations and by a << BDZ receptor >> weak partial agonist ([[ Ro 15-1788 ]]) at micromolar concentrations.


The limitation of SRF by diazepam was not prevented by inverse or partial agonists at the << BDZ receptor >>, including [[ Ro 15-1788 ]] and the beta CCs.


The limitation of SRF by diazepam was not prevented by inverse or partial agonists at the << BDZ receptor >>, including Ro 15-1788 and the [[ beta CCs ]].


These findings suggest that limitation of SRF was produced by binding of BDZs, but not beta CCs, to voltage-dependent sodium channels and not to high affinity central BDZ receptors, and that << BDZs >> limit SRF by slowing recovery of [[ sodium channels ]] from inactivation.


In addition to effects on cell proliferation, << DHT >> increased the percentage of [[ alkaline phosphatase ]] (ALP) positive cells in all three bone cell systems tested, and this effect was inhibited by antiandrogens.


In addition to effects on cell proliferation, << DHT >> increased the percentage of alkaline phosphatase ([[ ALP ]]) positive cells in all three bone cell systems tested, and this effect was inhibited by antiandrogens.


We conclude that << androgens >> can stimulate human and murine osteoblastic cell proliferation in vitro, and induce expression of the [[ osteoblast-line differentiation marker ]] ALP, presumably by an androgen receptor mediated mechanism.


We conclude that << androgens >> can stimulate human and murine osteoblastic cell proliferation in vitro, and induce expression of the osteoblast-line differentiation marker [[ ALP ]], presumably by an androgen receptor mediated mechanism.


The effect of << histamine-H1 receptor >> antagonism with [[ terfenadine ]] on concentration-related AMP-induced bronchoconstriction in asthma.


<< Ibrutinib >> (Imbruvica(R)) is a first-in-class, potent, orally administered, covalent inhibitor of Bruton's tyrosine kinase (BTK) that inhibits [[ B-cell antigen receptor ]] signalling downstream of BTK.


Ibrutinib (<< Imbruvica(R) >>) is a first-in-class, potent, orally administered, covalent inhibitor of Bruton's tyrosine kinase (BTK) that inhibits [[ B-cell antigen receptor ]] signalling downstream of BTK.


<< Ibrutinib >> (Imbruvica(R)) is a first-in-class, potent, orally administered, covalent inhibitor of Bruton's tyrosine kinase ([[ BTK ]]) that inhibits B-cell antigen receptor signalling downstream of BTK.


<< Ibrutinib >> (Imbruvica(R)) is a first-in-class, potent, orally administered, covalent inhibitor of Bruton's tyrosine kinase (BTK) that inhibits B-cell antigen receptor signalling downstream of [[ BTK ]].


<< Ibrutinib >> (Imbruvica(R)) is a first-in-class, potent, orally administered, covalent inhibitor of [[ Bruton's tyrosine kinase ]] (BTK) that inhibits B-cell antigen receptor signalling downstream of BTK.


Ibrutinib (<< Imbruvica(R) >>) is a first-in-class, potent, orally administered, covalent inhibitor of Bruton's tyrosine kinase ([[ BTK ]]) that inhibits B-cell antigen receptor signalling downstream of BTK.


Ibrutinib (<< Imbruvica(R) >>) is a first-in-class, potent, orally administered, covalent inhibitor of [[ Bruton's tyrosine kinase ]] (BTK) that inhibits B-cell antigen receptor signalling downstream of BTK.


To study the mechanism underlying this phenomenon, the effects of the nonselective << beta-adrenoceptor >> antagonists [[ propranolol ]] [no intrinsic sympathomimetic activity (ISA)], alprenolol (weak ISA) and mepindolol (strong ISA) on lymphocyte beta 2-adrenoceptor density--assessed by (+/-)-[125I]-iodocyanopindolol (ICYP) binding--and plasma renin activity (PRA) were investigated in male healthy volunteers aged 23-35 years.


To study the mechanism underlying this phenomenon, the effects of the nonselective << beta-adrenoceptor >> antagonists propranolol [no intrinsic sympathomimetic activity (ISA)], [[ alprenolol ]] (weak ISA) and mepindolol (strong ISA) on lymphocyte beta 2-adrenoceptor density--assessed by (+/-)-[125I]-iodocyanopindolol (ICYP) binding--and plasma renin activity (PRA) were investigated in male healthy volunteers aged 23-35 years.


To study the mechanism underlying this phenomenon, the effects of the nonselective << beta-adrenoceptor >> antagonists propranolol [no intrinsic sympathomimetic activity (ISA)], alprenolol (weak ISA) and [[ mepindolol ]] (strong ISA) on lymphocyte beta 2-adrenoceptor density--assessed by (+/-)-[125I]-iodocyanopindolol (ICYP) binding--and plasma renin activity (PRA) were investigated in male healthy volunteers aged 23-35 years.


<< Propranolol >> treatment (4 X 40 mg/day) increased the density of [[ beta 2-adrenoceptors ]] by 25% after 2 days; concomitantly PRA and heart rate were reduced.


<< Mepindolol >> treatment (2 X 5 mg/day) caused a 30% decrease of [[ beta 2-adrenoceptor ]] density and PRA after 2 days; both parameters remained reduced during treatment.


Inhibition of << 5-lipoxygenase >> pathway of arachidonic acid metabolism in human neutrophils by sulfasalazine and [[ 5-aminosalicylic acid ]].


Inhibition of << 5-lipoxygenase >> pathway of arachidonic acid metabolism in human neutrophils by [[ sulfasalazine ]] and 5-aminosalicylic acid.


Inhibition of << 5-lipoxygenase >> pathway of [[ arachidonic acid ]] metabolism in human neutrophils by sulfasalazine and 5-aminosalicylic acid.


Interference with << lipoxygenase >> enzymes, rather than a [[ steroid ]]-like inhibition of arachidonic acid release from intracellular phospholipids, seems to be the mode of action.


Interference with << lipoxygenase >> enzymes, rather than a steroid-like inhibition of [[ arachidonic acid ]] release from intracellular phospholipids, seems to be the mode of action.


<< Bevantolol >>: a [[ beta-1 adrenoceptor ]] antagonist with unique additional actions.


UNLABELLED: << Bevantolol >> is a [[ beta-1 adrenoceptor ]] antagonist that has been shown to be as effective as other beta blockers for the treatment of angina pectoris and hypertension.


It is suggested that all the additional actions of << bevantolol >> can be attributed to a partial agonist action on [[ alpha-adrenoceptors ]].


The apparent affinity of << benzodiazepine receptors >> for clonazepam in mice receiving alprazolam (0.05 mg/kg) was unchanged from that in untreated control mice, an observation suggesting that low doses of [[ alprazolam ]] increased receptor number.(ABSTRACT TRUNCATED AT 250 WORDS)


When menadione was omitted from the diet, however, << 4HPR >>-dosed animals had elevated [[ prothrombin ]] times.


In the high-dose << ROAc >> group, there was a twofold increase in [[ prothrombin ]] times but only after prolonged dosing.


The order of effect was << 4HPR >> greater than ROAc greater than 13cisRA, with increases in [[ prothrombin ]] times correlating with increases in hemorrhagic deaths.


The order of effect was 4HPR greater than << ROAc >> greater than 13cisRA, with increases in [[ prothrombin ]] times correlating with increases in hemorrhagic deaths.


The order of effect was 4HPR greater than ROAc greater than << 13cisRA >>, with increases in [[ prothrombin ]] times correlating with increases in hemorrhagic deaths.


<< 13cisRA >> and ROAc, but not 4HPR, caused a dose-dependent reduction in plasma [[ osteocalcin ]], an effect that correlated with retinoid-induced bone effects.


13cisRA and << ROAc >>, but not 4HPR, caused a dose-dependent reduction in plasma [[ osteocalcin ]], an effect that correlated with retinoid-induced bone effects.


13cisRA and ROAc, but not << 4HPR >>, caused a dose-dependent reduction in plasma [[ osteocalcin ]], an effect that correlated with retinoid-induced bone effects.


In contrast, serum << alkaline phosphatase >> was elevated in animals dosed with [[ 13cisRA ]] or 4HPR but not in those dose with ROAc.


In contrast, serum << alkaline phosphatase >> was elevated in animals dosed with 13cisRA or [[ 4HPR ]] but not in those dose with ROAc.


However, in the presence of 100 mM << Na+ >>, which is required for opiate inhibition of [[ adenylate cyclase ]] activity, analysis of competition binding data revealed three sites: the first, consisting of 17.5% of total receptor population has a Kd = 0.38 +/- 0.18 nM; the second, 50.6% of the population, has a Kd = 6.8 +/- 2.2 nM; and the third, 31.9% of the population, has a Kd of 410 +/- 110 nM.


Inhibition of the leukotriene synthetase of rat basophil leukemia cells by diethylcarbamazine, and synergism between << diethylcarbamazine >> and piriprost, a [[ 5-lipoxygenase ]] inhibitor.


Inhibition of the leukotriene synthetase of rat basophil leukemia cells by diethylcarbamazine, and synergism between diethylcarbamazine and << piriprost >>, a [[ 5-lipoxygenase ]] inhibitor.


Inhibition of the << leukotriene synthetase >> of rat basophil leukemia cells by [[ diethylcarbamazine ]], and synergism between diethylcarbamazine and piriprost, a 5-lipoxygenase inhibitor.


Similar concentrations also inhibited the formation of << leukotriene C4 >> (LTC4) by [[ LTC synthetase ]], a detergent-solubilized cell free particulate enzyme from RBL cells which is capable of coupling LTA4 to glutathione.


Similar concentrations also inhibited the formation of leukotriene C4 (<< LTC4 >>) by [[ LTC synthetase ]], a detergent-solubilized cell free particulate enzyme from RBL cells which is capable of coupling LTA4 to glutathione.


Similar concentrations also inhibited the formation of leukotriene C4 (LTC4) by << LTC synthetase >>, a detergent-solubilized cell free particulate enzyme from RBL cells which is capable of coupling [[ LTA4 ]] to glutathione.


The EC50 for inhibition of the << leukotriene C synthetase >> of RBL cells was directly proportional to the [[ LTA4 ]] concentration in the incubations, ranging from 1.5 mM at 10 microM LTA4 to over 40 mM at 500 microM LTA4.


Kinetic analysis revealed that the inhibition of the << leukotriene C synthetase >> reaction by [[ diethylcarbamazine ]] was competitive with respect to LTA4.


In contrast to << diethylcarbamazine >>, piriprost (U-60,257; 6,9-deepoxy-6,9-(phenylimino)-delta 6,8-prostaglandin I1), which inhibits the formation of sulfidopeptide leuktrienes in RBL cells at the [[ 5-lipoxygenase ]] step (EC50 5 microM), did not inhibit the leukotriene synthetase of these cells.


In contrast to << diethylcarbamazine >>, piriprost (U-60,257; 6,9-deepoxy-6,9-(phenylimino)-delta 6,8-prostaglandin I1), which inhibits the formation of sulfidopeptide leuktrienes in RBL cells at the 5-lipoxygenase step (EC50 5 microM), did not inhibit the [[ leukotriene synthetase ]] of these cells.


In contrast to diethylcarbamazine, << piriprost >> (U-60,257; 6,9-deepoxy-6,9-(phenylimino)-delta 6,8-prostaglandin I1), which inhibits the formation of sulfidopeptide leuktrienes in RBL cells at the [[ 5-lipoxygenase ]] step (EC50 5 microM), did not inhibit the leukotriene synthetase of these cells.


In contrast to diethylcarbamazine, piriprost (<< U-60,257 >>; 6,9-deepoxy-6,9-(phenylimino)-delta 6,8-prostaglandin I1), which inhibits the formation of sulfidopeptide leuktrienes in RBL cells at the [[ 5-lipoxygenase ]] step (EC50 5 microM), did not inhibit the leukotriene synthetase of these cells.


In contrast to diethylcarbamazine, piriprost (U-60,257; << 6,9-deepoxy-6,9-(phenylimino)-delta 6,8-prostaglandin I1 >>), which inhibits the formation of sulfidopeptide leuktrienes in RBL cells at the [[ 5-lipoxygenase ]] step (EC50 5 microM), did not inhibit the leukotriene synthetase of these cells.


In contrast to diethylcarbamazine, piriprost (U-60,257; 6,9-deepoxy-6,9-(phenylimino)-delta 6,8-prostaglandin I1), which inhibits the formation of << sulfidopeptide leuktrienes >> in RBL cells at the [[ 5-lipoxygenase ]] step (EC50 5 microM), did not inhibit the leukotriene synthetase of these cells.


These results are consistent with the interpretation that both piriprost and diethylcarbamazine inhibit leukotriene formation but that they act on sequential steps in the biosynthetic pathway in such a manner as to synergistically interfere with the availability or utilization of << LTA4 >> in the [[ leukotriene C synthetase ]] reaction.


The test procedure was verified with respect to intestinal << lactose >> hydrolysis by demonstrating a linear relationship between lactose/lactulose excretion and log jejunal mucosal [[ lactase ]] activity by in vitro assay (R2 = 0.95) in a further group of subjects.


The test procedure was verified with respect to intestinal lactose hydrolysis by demonstrating a linear relationship between << lactose >>/lactulose excretion and log jejunal mucosal [[ lactase ]] activity by in vitro assay (R2 = 0.95) in a further group of subjects.


The test procedure was verified with respect to intestinal lactose hydrolysis by demonstrating a linear relationship between lactose/<< lactulose >> excretion and log jejunal mucosal [[ lactase ]] activity by in vitro assay (R2 = 0.95) in a further group of subjects.


Differential << lactose >>/lactulose/L-rhamnose absorption provides a non-invasive and sensitive index of small intestinal integrity of value for the interpretation of prolonged or otherwise complicated enteritis and the distinction of primary secondary intestinal [[ lactase ]] deficiency.


Differential lactose/<< lactulose >>/L-rhamnose absorption provides a non-invasive and sensitive index of small intestinal integrity of value for the interpretation of prolonged or otherwise complicated enteritis and the distinction of primary secondary intestinal [[ lactase ]] deficiency.


Differential lactose/lactulose/<< L-rhamnose >> absorption provides a non-invasive and sensitive index of small intestinal integrity of value for the interpretation of prolonged or otherwise complicated enteritis and the distinction of primary secondary intestinal [[ lactase ]] deficiency.


The irreversible complex between << phenoxybenzamine >> and calmodulin may be useful for inhibiting certain [[ calmodulin ]]-dependent reactions and for studying the various biological functions of calmodulin.


<< Xanthines >> are classical antagonists for adenosine receptors for many of their pharmacological actions may be due to blockade of [[ adenosine receptors ]].


<< Xanthines >> are classical antagonists for [[ adenosine receptors ]] for many of their pharmacological actions may be due to blockade of adenosine receptors.


Inhibition of testicular << LDH-X >> from laboratory animals and man by [[ gossypol ]] and its isomers.


The inhibitory effect of << (+)-, (-)-, (+/-)-gossypol >> and (+/-)-gossypol acetic acid upon testicular cytosolic [[ LDH-X ]] was measured in vitro.


The inhibitory effect of (+)-, (-)-, (+/-)-gossypol and << (+/-)-gossypol acetic acid >> upon testicular cytosolic [[ LDH-X ]] was measured in vitro.


<< Gossypol acetic acid >> (0-100 mumol/l) inhibited [[ LDH-X ]] prepared from the testes of the mouse greater than rabbit greater than human greater than rat greater than hamster.


<< Gossypol >> and its isomers were non-competitive inhibitors of [[ human and hamster LDH-X ]] with respect to the coenzyme NADH, competitive inhibitors of human LDH-X and noncompetitive-competitive inhibitors of hamster LDH-X with respect to the substrate alpha-ketobutyrate.


Gossypol and its isomers were non-competitive inhibitors of human and hamster LDH-X with respect to the coenzyme << NADH >>, competitive inhibitors of [[ human LDH-X ]] and noncompetitive-competitive inhibitors of hamster LDH-X with respect to the substrate alpha-ketobutyrate.


Gossypol and its isomers were non-competitive inhibitors of human and hamster LDH-X with respect to the coenzyme NADH, competitive inhibitors of human LDH-X and noncompetitive-competitive inhibitors of << hamster LDH-X >> with respect to the substrate [[ alpha-ketobutyrate ]].


Inactivation of << prostaglandin H synthase >> and prostacyclin synthase by [[ phenylbutazone ]].


Inactivation of prostaglandin H synthase and << prostacyclin synthase >> by [[ phenylbutazone ]].


Most reducing cofactors for the peroxidase protect << PHS >> and prostacyclin synthase from inactivation by [[ hydroperoxides ]].


Most reducing cofactors for the peroxidase protect PHS and << prostacyclin synthase >> from inactivation by [[ hydroperoxides ]].


Chromatographic analysis of the metabolism of 14C-labeled arachidonic acid in this system revealed that PB-dependent inactivation of << PHS >> is markedly increased in the presence of 100 microM [[ H2O2 ]].


Chromatographic analysis of the metabolism of << 14C-labeled arachidonic acid >> in this system revealed that PB-dependent inactivation of [[ PHS ]] is markedly increased in the presence of 100 microM H2O2.


In plasma membranes prepared from these isolated brown fat cells by << borate >> extraction there was a similar enrichment of activity of [[ SSAO ]] and of the plasma membrane marker enzyme, phosphodiesterase I.


Positive staining of mitochondria was achieved in the presence of the << MAO >> substrate, [[ tryptamine ]].


Staining around the edges of the brown fat cells was observed with the << SSAO >> substrates, [[ tyramine ]] and benzylamine.


Staining around the edges of the brown fat cells was observed with the << SSAO >> substrates, tyramine and [[ benzylamine ]].


Staining was largely absent when substrate was omitted or after pretreatment with the irreversible << SSAO >> inhibitor, [[ hydralazine ]] and the slowly reversible inhibitor, semicarbazide.


Staining was largely absent when substrate was omitted or after pretreatment with the irreversible << SSAO >> inhibitor, hydralazine and the slowly reversible inhibitor, [[ semicarbazide ]].


This agent acts synergistically with many << penicillins >>, such as ampicillin, carbenicillin, and the like, and with cephalosporins, cefazolin, cefamandole, or cefoxitin to inhibit gram-negative bacilli, probably on the basis of binding to different proteins needed for the production of the [[ peptidoglycan ]] of the bacterial cell wall.


This agent acts synergistically with many penicillins, such as << ampicillin >>, carbenicillin, and the like, and with cephalosporins, cefazolin, cefamandole, or cefoxitin to inhibit gram-negative bacilli, probably on the basis of binding to different proteins needed for the production of the [[ peptidoglycan ]] of the bacterial cell wall.


This agent acts synergistically with many penicillins, such as ampicillin, << carbenicillin >>, and the like, and with cephalosporins, cefazolin, cefamandole, or cefoxitin to inhibit gram-negative bacilli, probably on the basis of binding to different proteins needed for the production of the [[ peptidoglycan ]] of the bacterial cell wall.


This agent acts synergistically with many penicillins, such as ampicillin, carbenicillin, and the like, and with << cephalosporins >>, cefazolin, cefamandole, or cefoxitin to inhibit gram-negative bacilli, probably on the basis of binding to different proteins needed for the production of the [[ peptidoglycan ]] of the bacterial cell wall.


This agent acts synergistically with many penicillins, such as ampicillin, carbenicillin, and the like, and with cephalosporins, << cefazolin >>, cefamandole, or cefoxitin to inhibit gram-negative bacilli, probably on the basis of binding to different proteins needed for the production of the [[ peptidoglycan ]] of the bacterial cell wall.


This agent acts synergistically with many penicillins, such as ampicillin, carbenicillin, and the like, and with cephalosporins, cefazolin, << cefamandole >>, or cefoxitin to inhibit gram-negative bacilli, probably on the basis of binding to different proteins needed for the production of the [[ peptidoglycan ]] of the bacterial cell wall.


This agent acts synergistically with many penicillins, such as ampicillin, carbenicillin, and the like, and with cephalosporins, cefazolin, cefamandole, or << cefoxitin >> to inhibit gram-negative bacilli, probably on the basis of binding to different proteins needed for the production of the [[ peptidoglycan ]] of the bacterial cell wall.


Since both << TFP >> and W-7 are potent inhibitors of [[ calmodulin ]], we investigated the possibility that inhibition of calmodulin was responsible for the loss of receptors.


Since both TFP and << W-7 >> are potent inhibitors of [[ calmodulin ]], we investigated the possibility that inhibition of calmodulin was responsible for the loss of receptors.


Three lines of evidence suggest that calmodulin inhibition is not responsible for the inhibition of binding and endocytosis: 1) << Promethazine >>, a phenothiazine that is a poor inhibitor of calmodulin, is nearly as effective as TFP at inhibiting endocytosis; calmidazolium, a potent inhibitor of several [[ calmodulin ]] functions, did not cause a loss of binding; 2) the microinjection of calmodulin into cells did not reverse the effects of W-7; using pressure microinjection, we introduced up to a 100-fold excess of calmodulin over native levels into individual gerbil fibroma cells; using rhodamine-labeled alpha 2-macroglobulin, we saw that the W-7 induced inhibition of receptor-mediated endocytosis was the same in injected and uninjected cells; 3) we injected calcineurin, a calmodulin-binding protein, into cells (1-3 pg/cell) and observed no effect on the receptor-mediated endocytosis of rhodamine-labeled alpha 2-macroglobulin.


Three lines of evidence suggest that calmodulin inhibition is not responsible for the inhibition of binding and endocytosis: 1) Promethazine, a << phenothiazine >> that is a poor inhibitor of calmodulin, is nearly as effective as TFP at inhibiting endocytosis; calmidazolium, a potent inhibitor of several [[ calmodulin ]] functions, did not cause a loss of binding; 2) the microinjection of calmodulin into cells did not reverse the effects of W-7; using pressure microinjection, we introduced up to a 100-fold excess of calmodulin over native levels into individual gerbil fibroma cells; using rhodamine-labeled alpha 2-macroglobulin, we saw that the W-7 induced inhibition of receptor-mediated endocytosis was the same in injected and uninjected cells; 3) we injected calcineurin, a calmodulin-binding protein, into cells (1-3 pg/cell) and observed no effect on the receptor-mediated endocytosis of rhodamine-labeled alpha 2-macroglobulin.


Three lines of evidence suggest that calmodulin inhibition is not responsible for the inhibition of binding and endocytosis: 1) Promethazine, a phenothiazine that is a poor inhibitor of calmodulin, is nearly as effective as << TFP >> at inhibiting endocytosis; calmidazolium, a potent inhibitor of several [[ calmodulin ]] functions, did not cause a loss of binding; 2) the microinjection of calmodulin into cells did not reverse the effects of W-7; using pressure microinjection, we introduced up to a 100-fold excess of calmodulin over native levels into individual gerbil fibroma cells; using rhodamine-labeled alpha 2-macroglobulin, we saw that the W-7 induced inhibition of receptor-mediated endocytosis was the same in injected and uninjected cells; 3) we injected calcineurin, a calmodulin-binding protein, into cells (1-3 pg/cell) and observed no effect on the receptor-mediated endocytosis of rhodamine-labeled alpha 2-macroglobulin.


From these results, it is proposed that << tyrosine hydroxylase >> activity determines p-HPAA concentrations by regulating [[ p-tyrosine ]] availability.


The binding of << FHA >>-HIS was inhibited on 35-79% of the platelets by the histamine H1 receptor antagonists [[ diphenhydramine ]] and clemastine.


The binding of << FHA >>-HIS was inhibited on 35-79% of the platelets by the histamine H1 receptor antagonists diphenhydramine and [[ clemastine ]].


The binding of FHA-HIS was inhibited on 35-79% of the platelets by the << histamine H1 receptor >> antagonists [[ diphenhydramine ]] and clemastine.


The binding of FHA-HIS was inhibited on 35-79% of the platelets by the << histamine H1 receptor >> antagonists diphenhydramine and [[ clemastine ]].


The histamine H2 receptor antagonist << cimetidine >> blocked the [[ FHA ]]-HIS binding on 14-37% of the platelets.


The << histamine H2 receptor >> antagonist [[ cimetidine ]] blocked the FHA-HIS binding on 14-37% of the platelets.


<< Alanine:glyoxylate aminotransferase >> (AGT) in the liver catalyzes most of the [[ glyoxylate ]] transamination in mammalian tissues (E. V. Rowsell, K. Snell, J. A. Carnie, and K. V. Rowsell (1972) Biochem. J. 127, 155-165).


Alanine:glyoxylate aminotransferase (<< AGT >>) in the liver catalyzes most of the [[ glyoxylate ]] transamination in mammalian tissues (E. V. Rowsell, K. Snell, J. A. Carnie, and K. V. Rowsell (1972) Biochem. J. 127, 155-165).


The holo activity of combined peroxisomal and mitochondrial << AGT 1 >> with a low Km for [[ L-alanine ]] rapidly decreased after a lag time of about 2 days during feeding of the vitamin B6-deficient diet (by 50% in 5 days, by 86% in 14 days).


The holo activity of AGT 2 with a high Km for << L-alanine >> decreased more slowly than [[ AGT 1 ]] (by 33% in 14 days, by 60% in 28 days).


The holo activity of << AGT 2 >> with a high Km for [[ L-alanine ]] decreased more slowly than AGT 1 (by 33% in 14 days, by 60% in 28 days).


<< Triclosan >> inhibited both [[ cyclooxygenase 1 ]] and cyclo-oxygenase 2 with IC-50 values of 43 microM and 227 microM, respectively.


<< Triclosan >> inhibited both cyclooxygenase 1 and [[ cyclo-oxygenase 2 ]] with IC-50 values of 43 microM and 227 microM, respectively.


<< Triclosan >> also inhibited [[ 5-lipoxygenase ]] with an IC-50 of 43 microM.


The << 15-lipoxygenase >> was similarly inhibited by [[ triclosan ]] with an IC-50 of 61 microM.


Hence, << triclosan >> has the ability to inhibit both the [[ cyclo-oxygenase ]] and lipoxygenase pathways of arachidonic acid metabolism with similar efficacy.


Hence, << triclosan >> has the ability to inhibit both the cyclo-oxygenase and [[ lipoxygenase ]] pathways of arachidonic acid metabolism with similar efficacy.


Hence, triclosan has the ability to inhibit both the << cyclo-oxygenase >> and lipoxygenase pathways of [[ arachidonic acid ]] metabolism with similar efficacy.


Hence, triclosan has the ability to inhibit both the cyclo-oxygenase and << lipoxygenase >> pathways of [[ arachidonic acid ]] metabolism with similar efficacy.


In cell culture experiments, it was found that << triclosan >> inhibited [[ IL-1 beta ]] induced prostaglandin E2 production by human gingival fibroblasts in a concentration dependent manner, and at relatively low concentrations.


In cell culture experiments, it was found that triclosan inhibited << IL-1 beta >> induced [[ prostaglandin E2 ]] production by human gingival fibroblasts in a concentration dependent manner, and at relatively low concentrations.


Cells propagated in medium containing << N5-methyltetrahydrofolate >> and homocysteine showed a substantial increase in [[ MS ]] activity which paralleled the increase in the intracellular concentration of Me-Cbl and the Cbl bound to the enzyme.


Cells propagated in medium containing N5-methyltetrahydrofolate and << homocysteine >> showed a substantial increase in [[ MS ]] activity which paralleled the increase in the intracellular concentration of Me-Cbl and the Cbl bound to the enzyme.


<< Ergovaline >> binding and activation of [[ D2 dopamine receptors ]] in GH4ZR7 cells.


Ergovaline inhibition of radioligand binding to the D2 dopamine receptor and << ergot alkaloid >> inhibition of [[ vasoactive intestinal peptide ]] (VIP)-stimulated cyclic AMP production in GH4ZR7 cells, stably transfected with a rat D2 dopamine receptor, were evaluated.


Ergovaline inhibition of radioligand binding to the D2 dopamine receptor and << ergot alkaloid >> inhibition of vasoactive intestinal peptide ([[ VIP ]])-stimulated cyclic AMP production in GH4ZR7 cells, stably transfected with a rat D2 dopamine receptor, were evaluated.


Ergovaline inhibition of radioligand binding to the D2 dopamine receptor and ergot alkaloid inhibition of << vasoactive intestinal peptide >> (VIP)-stimulated [[ cyclic AMP ]] production in GH4ZR7 cells, stably transfected with a rat D2 dopamine receptor, were evaluated.


Ergovaline inhibition of radioligand binding to the D2 dopamine receptor and ergot alkaloid inhibition of vasoactive intestinal peptide (<< VIP >>)-stimulated [[ cyclic AMP ]] production in GH4ZR7 cells, stably transfected with a rat D2 dopamine receptor, were evaluated.


<< Ergot alkaloids >> were also effective in inhibiting [[ VIP ]]-stimulated cyclic AMP production, with EC50 values for ergovaline, ergonovine, alpha-ergocryptine, ergotamine, and dopamine of 8 +/- 2, 47 +/- 2, 28 +/- 2, 2 +/- 1, and 8 +/- 1 nM, respectively.


Ergot alkaloids were also effective in inhibiting << VIP >>-stimulated cyclic AMP production, with EC50 values for [[ ergovaline ]], ergonovine, alpha-ergocryptine, ergotamine, and dopamine of 8 +/- 2, 47 +/- 2, 28 +/- 2, 2 +/- 1, and 8 +/- 1 nM, respectively.


Ergot alkaloids were also effective in inhibiting << VIP >>-stimulated cyclic AMP production, with EC50 values for ergovaline, [[ ergonovine ]], alpha-ergocryptine, ergotamine, and dopamine of 8 +/- 2, 47 +/- 2, 28 +/- 2, 2 +/- 1, and 8 +/- 1 nM, respectively.


Ergot alkaloids were also effective in inhibiting << VIP >>-stimulated cyclic AMP production, with EC50 values for ergovaline, ergonovine, [[ alpha-ergocryptine ]], ergotamine, and dopamine of 8 +/- 2, 47 +/- 2, 28 +/- 2, 2 +/- 1, and 8 +/- 1 nM, respectively.


Ergot alkaloids were also effective in inhibiting << VIP >>-stimulated cyclic AMP production, with EC50 values for ergovaline, ergonovine, alpha-ergocryptine, [[ ergotamine ]], and dopamine of 8 +/- 2, 47 +/- 2, 28 +/- 2, 2 +/- 1, and 8 +/- 1 nM, respectively.


Ergot alkaloids were also effective in inhibiting << VIP >>-stimulated cyclic AMP production, with EC50 values for ergovaline, ergonovine, alpha-ergocryptine, ergotamine, and [[ dopamine ]] of 8 +/- 2, 47 +/- 2, 28 +/- 2, 2 +/- 1, and 8 +/- 1 nM, respectively.


Ergot alkaloids were also effective in inhibiting << VIP >>-stimulated [[ cyclic AMP ]] production, with EC50 values for ergovaline, ergonovine, alpha-ergocryptine, ergotamine, and dopamine of 8 +/- 2, 47 +/- 2, 28 +/- 2, 2 +/- 1, and 8 +/- 1 nM, respectively.


Inhibition of cyclic AMP production by ergovaline was blocked by the << dopamine receptor >> antagonist, [[ (-)-sulpiride ]] (IC50, 300 +/- 150 nM).


These findings suggest that some of the deleterious effects of consumption of endophyte-infected tall fescue, which contains several << ergot alkaloids >> including ergovaline, may be due to [[ D2 dopamine receptor ]] activation.


These findings suggest that some of the deleterious effects of consumption of endophyte-infected tall fescue, which contains several ergot alkaloids including << ergovaline >>, may be due to [[ D2 dopamine receptor ]] activation.


Incubation of rat aortic membranes with the irreversible << alpha 1B-adrenoceptor >> antagonist, [[ chloroethylclonidine ]] (CEC: 10 microM) did not change the KD of [3H]-prazosin binding in comparison to untreated membranes, but reduced by 88% the total number of binding sites (Bmax).


Incubation of rat aortic membranes with the irreversible << alpha 1B-adrenoceptor >> antagonist, chloroethylclonidine ([[ CEC ]]: 10 microM) did not change the KD of [3H]-prazosin binding in comparison to untreated membranes, but reduced by 88% the total number of binding sites (Bmax).


Intraperitoneal administration of << (+/- )propranolol HCl >> (2.5-10 mg/kg), a nonselective [[ beta-adrenoceptor ]] antagonist, dose dependently attenuated the desipramine-induced enhancement of aggressive behavior without significantly affecting the basal aggressive responses.


<< ICI118,551 HCl >> (1.25-5 mg/kg, IP), a selective [[ beta 2-adrenoceptor ]] antagonist, also blocked the desipramine-induced enhancement of aggressive behavior in a dose-dependent manner, whereas metoprolol tartrate (5-20 mg/kg, IP), a selective beta 1-adrenoceptor antagonist, did not affect it.


ICI118,551 HCl (1.25-5 mg/kg, IP), a selective beta 2-adrenoceptor antagonist, also blocked the desipramine-induced enhancement of aggressive behavior in a dose-dependent manner, whereas << metoprolol tartrate >> (5-20 mg/kg, IP), a selective [[ beta 1-adrenoceptor ]] antagonist, did not affect it.


Moreover, << clenbuterol HCl >> (0.1-0.5 mg/kg, IP), a lipophilic [[ beta 2-adrenoceptor ]] agonist, significantly increased the duration of basal aggressive behavior.


Taken together with our previous finding that the desipramine-induced enhancement of aggressive behavior can be blocked by << yohimbine >>, an [[ alpha 2-adrenoceptor ]] antagonist, the present results indicate that not only alpha 2- but also beta 2-adrenoceptor stimulation plays important roles in modulation of aggressive behavior in long-term isolated mice.


In beta-escin-skinned strips of chloroethylclonidine-pretreated smooth muscle, the enhancement of Ca2+ contraction produced by norepinephrine was significantly decreased, whereas the amplitude was the same as that produced by methoxamine or clonidine; this enhancement was inhibited by the selective << alpha 1A-adrenoceptor >> antagonist [[ WB 4101 ]] (100 nM).


Furthermore, the phosphorylation of << myosin light chain >> produced by [[ norepinephrine ]] was greater than that produced by clonidine.


Furthermore, the phosphorylation of << myosin light chain >> produced by norepinephrine was greater than that produced by [[ clonidine ]].


The drug had a potent cytotoxic effect on RIN cells expressing << GLUT2 >>, but had no effect on cells lacking GLUT2 expression, as indicated by histological analysis and measurement of the blood [[ glucose ]] levels of treated animals.


Consistent with these data, only << GLUT2 >>-expressing RIN or AtT-20ins cells transported [[ STZ ]] efficiently.


We conclude that expression of << GLUT2 >> is required for efficient killing of neuroendocrine cells by [[ STZ ]], and this effect is related to specific recognition of the drug as a transported substrate by GLUT2 but not GLUT1.


We conclude that expression of GLUT2 is required for efficient killing of neuroendocrine cells by << STZ >>, and this effect is related to specific recognition of the drug as a transported substrate by [[ GLUT2 ]] but not GLUT1.


Inhibitory effects of << lysine >> analogues on [[ t-PA ]] induced whole blood clot lysis.


The present study utilized blood from normal volunteers and 125I-fibrinogen in a dilute whole blood clot assay to determine the relative concentrations of << lysine >> analogues required for inhibition of clot lysis induced by exogenous [[ t-PA ]].


<< AMCA >> (0.06 mM) and EACA (0.6 mM) were effective in prolonging clot lysis if (1) whole blood clots were formed and then exposed to a lysine analogue and exogenous [[ t-PA ]] or if (2) whole blood clots were formed in the presence of exogenous t-PA and a lysine analogue.


<< AMCA >> (0.06 mM) and EACA (0.6 mM) were effective in prolonging clot lysis if (1) whole blood clots were formed and then exposed to a lysine analogue and exogenous t-PA or if (2) whole blood clots were formed in the presence of exogenous [[ t-PA ]] and a lysine analogue.


AMCA (0.06 mM) and << EACA >> (0.6 mM) were effective in prolonging clot lysis if (1) whole blood clots were formed and then exposed to a lysine analogue and exogenous [[ t-PA ]] or if (2) whole blood clots were formed in the presence of exogenous t-PA and a lysine analogue.


AMCA (0.06 mM) and << EACA >> (0.6 mM) were effective in prolonging clot lysis if (1) whole blood clots were formed and then exposed to a lysine analogue and exogenous t-PA or if (2) whole blood clots were formed in the presence of exogenous [[ t-PA ]] and a lysine analogue.


However, their inhibitory effect was markedly reduced if clots were formed in the presence of << t-PA >> and then exposed to either of the [[ lysine ]] analogues.


The data suggest that << lysine >> analogues, even at low concentrations, reduce the rate of [[ t-PA ]] induced whole blood clot lysis by several mechanisms.


<< Histamine >> enhances the depolarizing afterpotential of immunohistochemically identified vasopressin neurons in the rat supraoptic nucleus via [[ H1-receptor ]] activation.


The enhancement of the depolarizing afterpotential by histamine was mimicked by the << histamine H1-receptor >> agonist [[ 2-thiazolylethylamine ]] and was reduced or blocked by the H1-receptor antagonist promethazine, but was not blocked or reduced in the presence of the histamine H2-receptor antagonist, cimetidine.


The enhancement of the depolarizing afterpotential by histamine was mimicked by the histamine H1-receptor agonist 2-thiazolylethylamine and was reduced or blocked by the << H1-receptor >> antagonist [[ promethazine ]], but was not blocked or reduced in the presence of the histamine H2-receptor antagonist, cimetidine.


The enhancement of the depolarizing afterpotential by histamine was mimicked by the histamine H1-receptor agonist 2-thiazolylethylamine and was reduced or blocked by the H1-receptor antagonist promethazine, but was not blocked or reduced in the presence of the << histamine H2-receptor >> antagonist, [[ cimetidine ]].


In summary, these results show that the excitatory effect of << histamine >> on immunohistochemically identified vasopressin neurons in the supraoptic nucleus is due in part to the [[ H1-receptor ]]-mediated enhancement of the depolarizing afterpotential independent of any change in the afterhyperpolarizing potential or membrane potential.


The goal of the present study was to compare the effects of three potent reference << renin >> inhibitors ([[ remikiren ]], CGP 38560A, and enalkiren) in sodium-depleted normotensive squirrel monkeys.


The goal of the present study was to compare the effects of three potent reference << renin >> inhibitors (remikiren, [[ CGP 38560A ]], and enalkiren) in sodium-depleted normotensive squirrel monkeys.


The goal of the present study was to compare the effects of three potent reference << renin >> inhibitors (remikiren, CGP 38560A, and [[ enalkiren ]]) in sodium-depleted normotensive squirrel monkeys.


Finally, the three drugs were compared with the << angiotensin converting enzyme >> inhibitor [[ cilazapril ]].


One possible explanation is that, in our model, << remikiren >> in contrast to CGP 38560A and enalkiren is able to inhibit [[ renin ]] in a functionally important extraplasmatic compartment.


One possible explanation is that, in our model, remikiren in contrast to << CGP 38560A >> and enalkiren is able to inhibit [[ renin ]] in a functionally important extraplasmatic compartment.


One possible explanation is that, in our model, remikiren in contrast to CGP 38560A and << enalkiren >> is able to inhibit [[ renin ]] in a functionally important extraplasmatic compartment.


Inhibition of << cytokine >>-primed eosinophil chemotaxis by [[ nedocromil sodium ]].


RESULTS: << Nedocromil sodium >> inhibited the chemotactic response toward FMLP and NAF/IL-8 of [[ GM-CSF ]] primed eosinophils approximately 60% (inhibitory concentration of 50% [IC50] approximately 1 to 10 nmol/L), whereas these responses of IL-3 primed eosinophils was completely inhibited (IC50 approximately 1 nmol/L).


RESULTS: << Nedocromil sodium >> inhibited the chemotactic response toward FMLP and NAF/IL-8 of GM-CSF primed eosinophils approximately 60% (inhibitory concentration of 50% [IC50] approximately 1 to 10 nmol/L), whereas these responses of [[ IL-3 ]] primed eosinophils was completely inhibited (IC50 approximately 1 nmol/L).


RESULTS: << Nedocromil sodium >> inhibited the chemotactic response toward FMLP and [[ NAF ]]/IL-8 of GM-CSF primed eosinophils approximately 60% (inhibitory concentration of 50% [IC50] approximately 1 to 10 nmol/L), whereas these responses of IL-3 primed eosinophils was completely inhibited (IC50 approximately 1 nmol/L).


RESULTS: << Nedocromil sodium >> inhibited the chemotactic response toward FMLP and NAF/[[ IL-8 ]] of GM-CSF primed eosinophils approximately 60% (inhibitory concentration of 50% [IC50] approximately 1 to 10 nmol/L), whereas these responses of IL-3 primed eosinophils was completely inhibited (IC50 approximately 1 nmol/L).


CONCLUSIONS: The chemotactic responses toward << C5a >> were inhibited by [[ nedocromil sodium ]] at higher concentrations than were required in the priming studies (IC50 approximately 10 to 100 nmol/L).


Glutathione-independent prostaglandin D synthase [<< prostaglandin-H2 D-isomerase >>; (5Z,13E)-(15S)-9 alpha,11 alpha-epidioxy-15-hydroxyprosta-5,13-dienoate D-isomerase, EC 5.3.99.2] is an enzyme responsible for biosynthesis of [[ prostaglandin D2 ]] in the central nervous system.


Glutathione-independent prostaglandin D synthase [prostaglandin-H2 D-isomerase; << (5Z,13E)-(15S)-9 alpha,11 alpha-epidioxy-15-hydroxyprosta-5,13-dienoate D-isomerase >>, EC 5.3.99.2] is an enzyme responsible for biosynthesis of [[ prostaglandin D2 ]] in the central nervous system.


Glutathione-independent prostaglandin D synthase [prostaglandin-H2 D-isomerase; (5Z,13E)-(15S)-9 alpha,11 alpha-epidioxy-15-hydroxyprosta-5,13-dienoate D-isomerase, << EC 5.3.99.2 >>] is an enzyme responsible for biosynthesis of [[ prostaglandin D2 ]] in the central nervous system.


Glutathione-independent << prostaglandin D synthase >> [prostaglandin-H2 D-isomerase; (5Z,13E)-(15S)-9 alpha,11 alpha-epidioxy-15-hydroxyprosta-5,13-dienoate D-isomerase, EC 5.3.99.2] is an enzyme responsible for biosynthesis of [[ prostaglandin D2 ]] in the central nervous system.


Kainate-evoked currents showed partial desensitization that was reduced on incubation with concanavalin A (conA) but not cyclothiazide and were attenuated by the non-<< N-methyl-D-aspartate (NMDA) receptor >> antagonist [[ CNQX ]] (6-cyano-7-nitro-quinoxalinedione).


Kainate-evoked currents showed partial desensitization that was reduced on incubation with concanavalin A (conA) but not cyclothiazide and were attenuated by the non-<< N-methyl-D-aspartate (NMDA) receptor >> antagonist CNQX ([[ 6-cyano-7-nitro-quinoxalinedione ]]).


One group of experimental animals was treated with << 5-lipoxygenase >> (5-LO) inhibitor, [[ diethylcarbamazine ]] (DEC, Sigma, St. Louis, Missouri) (50 mg/kg, i.v.), immediately before blast.


One group of experimental animals was treated with 5-lipoxygenase (<< 5-LO >>) inhibitor, [[ diethylcarbamazine ]] (DEC, Sigma, St. Louis, Missouri) (50 mg/kg, i.v.), immediately before blast.


One group of experimental animals was treated with << 5-lipoxygenase >> (5-LO) inhibitor, diethylcarbamazine ([[ DEC ]], Sigma, St. Louis, Missouri) (50 mg/kg, i.v.), immediately before blast.


One group of experimental animals was treated with 5-lipoxygenase (<< 5-LO >>) inhibitor, diethylcarbamazine ([[ DEC ]], Sigma, St. Louis, Missouri) (50 mg/kg, i.v.), immediately before blast.


Although << DEC >> exerts local antioxidant activity with beneficial effects on lung tissue, this [[ 5-LO ]] inhibitor intensifies the blast overpressure caused hemodynamic insufficiency.


<< Tamsulosin >>, the first prostate-selective [[ alpha 1A-adrenoceptor ]] antagonist.


Expressions of << insulin >> and PC3, but not PC2, are coordinately regulated by [[ glucose ]], consistent with the important role of PC3 in regulating proinsulin processing.


Expressions of insulin and << PC3 >>, but not PC2, are coordinately regulated by [[ glucose ]], consistent with the important role of PC3 in regulating proinsulin processing.


After 7 days of << DMI >> administration the number of [[ beta-adrenoceptors ]] was lower in frontal and occipital cortex and hippocampus.


The << DMI >> induced reduction in [[ beta-adrenoceptors ]] did not differ in OB and sham-operated control rats.


<< DMI >> administration for up to 21 days produced a progressive reduction in the number of [[ 5-HT2A ]] receptors in frontal cortex, without significant alterations in occipital cortex.


The time course of the reduction in the number of << 5-HT2A >> receptors was similar to that of the [[ DMI ]]-induced behavioural changes whereas that for the reduction in beta-adrenoceptors was clearly different.


The time course of the reduction in the number of 5-HT2A receptors was similar to that of the << DMI >>-induced behavioural changes whereas that for the reduction in [[ beta-adrenoceptors ]] was clearly different.


The present results suggest that the action of << DMI >> in this animal model is unlikely to be directly related to a reduction in [[ beta-adrenoceptors ]] but may be related to a reduction in frontal cortical 5-HT2A receptors.


The present results suggest that the action of << DMI >> in this animal model is unlikely to be directly related to a reduction in beta-adrenoceptors but may be related to a reduction in frontal cortical [[ 5-HT2A ]] receptors.


Binding of << thalidomide >> to alpha1-acid glycoprotein may be involved in its inhibition of [[ tumor necrosis factor alpha ]] production.


The immunomodulatory activity of << thalidomide >> has been ascribed to the selective inhibition of [[ tumor necrosis factor alpha ]] from monocytes.


We show that the binding of thalidomide photoaffinity label to authentic human AGP is competed with both << thalidomide >> and the nonradioactive photoaffinity label at concentrations comparable to those required for inhibition of production of [[ tumor necrosis factor alpha ]] from human monocytes, suggesting that AGP may be involved in the immunomodulatory activity of thalidomide.


In conclusion, our data suggest that chronic << cocaine >> use is associated with modestly reduced levels of striatal DA and the [[ DA transporter ]] in some subjects and that these changes might contribute to the neurological and psychiatric effects of the drug.


It appears likely that the << histamine H2 receptor >> blocked by [[ cimetidine ]] obviated the pulmonary vasodilator effect of tolazoline therapy.


<< GYKI 52466 >> decreased the peak amplitude of hippocampal area CA1 [[ AMPA receptor ]]-mediated excitatory postsynaptic currents (e.p.s.cs) (IC50 10.8 +/- 0.8 microM) with no apparent effect on response kinetics.


<< Cyclothiazide >> prolonged the decay time constant of [[ AMPA receptor ]]-mediated e.p.s.cs (EC50 35.7 +/- 6.5 microM) with less pronounced effects in slowing e.p.s.c. onset kinetics and increasing e.p.s.c. amplitude.


Activation of cytoprotective << prostaglandin synthase-1 >> by [[ minoxidil ]] as a possible explanation for its hair growth-stimulating effect.


We thus speculated that activation of << PGHS-1 >> might be a mechanism by which [[ minoxidil ]] (2,4-diamino-6-piperidinopyrimidine-3-oxyde) stimulates hair growth in vivo.


We thus speculated that activation of << PGHS-1 >> might be a mechanism by which minoxidil ([[ 2,4-diamino-6-piperidinopyrimidine-3-oxyde ]]) stimulates hair growth in vivo.


We demonstrate here that << minoxidil >> is a potent activator of purified [[ PGHS-1 ]] (AC50 = 80 microM), as assayed by oxygen consumption and PGE2 production.


This study was designed to determine the gastroprotective properties of << cinitapride >> (CNT), a novel prokinetic benzamide derivative agonist of [[ 5-HT4 ]] and 5-HT1 receptors and 5-HT2 antagonist, on mucosal injury produced by 50% (v/v) ethanol.


This study was designed to determine the gastroprotective properties of << cinitapride >> (CNT), a novel prokinetic benzamide derivative agonist of 5-HT4 and [[ 5-HT1 ]] receptors and 5-HT2 antagonist, on mucosal injury produced by 50% (v/v) ethanol.


This study was designed to determine the gastroprotective properties of cinitapride (CNT), a novel prokinetic << benzamide >> derivative agonist of [[ 5-HT4 ]] and 5-HT1 receptors and 5-HT2 antagonist, on mucosal injury produced by 50% (v/v) ethanol.


This study was designed to determine the gastroprotective properties of cinitapride (CNT), a novel prokinetic << benzamide >> derivative agonist of 5-HT4 and [[ 5-HT1 ]] receptors and 5-HT2 antagonist, on mucosal injury produced by 50% (v/v) ethanol.


This study was designed to determine the gastroprotective properties of cinitapride (<< CNT >>), a novel prokinetic benzamide derivative agonist of [[ 5-HT4 ]] and 5-HT1 receptors and 5-HT2 antagonist, on mucosal injury produced by 50% (v/v) ethanol.


This study was designed to determine the gastroprotective properties of cinitapride (<< CNT >>), a novel prokinetic benzamide derivative agonist of 5-HT4 and [[ 5-HT1 ]] receptors and 5-HT2 antagonist, on mucosal injury produced by 50% (v/v) ethanol.


This study was designed to determine the gastroprotective properties of << cinitapride >> (CNT), a novel prokinetic benzamide derivative agonist of 5-HT4 and 5-HT1 receptors and [[ 5-HT2 ]] antagonist, on mucosal injury produced by 50% (v/v) ethanol.


This study was designed to determine the gastroprotective properties of cinitapride (CNT), a novel prokinetic << benzamide >> derivative agonist of 5-HT4 and 5-HT1 receptors and [[ 5-HT2 ]] antagonist, on mucosal injury produced by 50% (v/v) ethanol.


This study was designed to determine the gastroprotective properties of cinitapride (<< CNT >>), a novel prokinetic benzamide derivative agonist of 5-HT4 and 5-HT1 receptors and [[ 5-HT2 ]] antagonist, on mucosal injury produced by 50% (v/v) ethanol.


We have identified << adenosine deaminase >>, an enzyme involved in [[ purine ]] metabolism whose deficiency is associated with severe combined immunodeficiency, as a Grb3-3 binding protein that is not able to bind to Grb2.


<< Alendronate >> inhibition of [[ protein-tyrosine-phosphatase-meg1 ]].


Here we report that << alendronate >> is a potent inhibitor of the [[ protein-tyrosine-phosphatase-meg1 ]] (PTPmeg1).


Here we report that << alendronate >> is a potent inhibitor of the protein-tyrosine-phosphatase-meg1 ([[ PTPmeg1 ]]).


With either substrate, << alendronate >> was a slow binding inhibitor of [[ PTPmeg1 ]].


Among the other << bisphosphonates >> studied, alendronate was more potent and selective for [[ PTPmeg1 ]].


Among the other bisphosphonates studied, << alendronate >> was more potent and selective for [[ PTPmeg1 ]].


The hydrolysis of fluorescein diphosphate by PTP epsilon and PTPmeg1 was sensitive to alendronate, with IC50 values of less than 1 microM; << PTPsigma >>, however, under the same conditions, was inhibited by only 50% with 141 microM [[ alendronate ]].


The hydrolysis of fluorescein << diphosphate >> by [[ PTP epsilon ]] and PTPmeg1 was sensitive to alendronate, with IC50 values of less than 1 microM; PTPsigma, however, under the same conditions, was inhibited by only 50% with 141 microM alendronate.


The hydrolysis of fluorescein << diphosphate >> by PTP epsilon and [[ PTPmeg1 ]] was sensitive to alendronate, with IC50 values of less than 1 microM; PTPsigma, however, under the same conditions, was inhibited by only 50% with 141 microM alendronate.


<< Alendronate >> inhibited [[ PTPmeg1 ]] with an IC50 value of 23 microM, PTPsigma with an IC50 value of 2 microM, and did not inhibit PTP epsilon at concentrations up to 1 mM.


<< Alendronate >> inhibited PTPmeg1 with an IC50 value of 23 microM, [[ PTPsigma ]] with an IC50 value of 2 microM, and did not inhibit PTP epsilon at concentrations up to 1 mM.


The << alendronate >> inhibition of these three [[ PTPs ]] and two substrates is consistent with the formation of a ternary complex comprised of enzyme, substrate, and inhibitor.


<< PTP >> inhibition by [[ hisphosphonates ]] or vanadate was diminished by the metal chelating agent EDTA, or by the reducing agent dithiothreitol, suggesting that a metal ion and the oxidation of a cysteine residue are required for full inhibition.


<< PTP >> inhibition by hisphosphonates or [[ vanadate ]] was diminished by the metal chelating agent EDTA, or by the reducing agent dithiothreitol, suggesting that a metal ion and the oxidation of a cysteine residue are required for full inhibition.


These observations show substrate- and enzyme-specific << PTP >> inhibition by [[ alendronate ]] and support the possibility that a certain PTP(s) may be the molecular target for alendronate action.


16,16-dimethyl-PGE2 and two putative << EP1 >> antagonists, [[ AH6809 ]] and SC-19220, did not show any significant binding to this receptor.


16,16-dimethyl-PGE2 and two putative << EP1 >> antagonists, AH6809 and [[ SC-19220 ]], did not show any significant binding to this receptor.


<< M&B-28767 >>, a putative [[ EP3 ]] agonist, and misoprostol, a putative EP2/EP3 agonist, also bound to this receptor with Ki values of 120 nM.


M&B-28767, a putative EP3 agonist, and << misoprostol >>, a putative [[ EP2 ]]/EP3 agonist, also bound to this receptor with Ki values of 120 nM.


M&B-28767, a putative EP3 agonist, and << misoprostol >>, a putative EP2/[[ EP3 ]] agonist, also bound to this receptor with Ki values of 120 nM.


Blockage of the << HERG human cardiac K+ channel >> by the gastrointestinal prokinetic agent [[ cisapride ]].


We tested the hypothesis that << cisapride >> blocks [[ HERG ]].


Under voltage-clamp conditions, << cisapride >> block of [[ HERG ]] is dose dependent with a half-maximal inhibitory concentration of 6.5 nM at 22 degrees C (n = 25 cells).


Block of << HERG >> with [[ cisapride ]] after channel activation was voltage dependent.


At -20 mV, 10 nM << cisapride >> reduced [[ HERG ]] tail-current amplitude by 5%, whereas, at + 20 mV, the tail-current amplitude was reduced by 45% (n = 4 cells).


We conclude that << cisapride >> is a potent blocker of [[ HERG ]] channels expressed in HEK293 cells.


Intravenous (I.V.) cocaine (0.03-3 mg/kg) produced dose-dependent, rapid, and brief increases in blood pressure (BP) in conscious rats pretreated with the << dopamine receptor >> antagonist, [[ SCH 23390 ]].


Monoamine uptake inhibitors structurally analogous to cocaine (cocaethylene, CFT, betaCIT, CPT, (+)-cocaine, norcocaine, and benztropine) also produced this rapid pressor response, whereas structurally unrelated uptake inhibitors with diverse << monoamine transporter >> selectivities ([[ BTCP ]], indatraline, GBR 12935, mazindol, nomifensine, and zimeldine) either did not produce a rapid pressor response or produced only a small pressor response.


Monoamine uptake inhibitors structurally analogous to cocaine (cocaethylene, CFT, betaCIT, CPT, (+)-cocaine, norcocaine, and benztropine) also produced this rapid pressor response, whereas structurally unrelated uptake inhibitors with diverse << monoamine transporter >> selectivities (BTCP, [[ indatraline ]], GBR 12935, mazindol, nomifensine, and zimeldine) either did not produce a rapid pressor response or produced only a small pressor response.


Monoamine uptake inhibitors structurally analogous to cocaine (cocaethylene, CFT, betaCIT, CPT, (+)-cocaine, norcocaine, and benztropine) also produced this rapid pressor response, whereas structurally unrelated uptake inhibitors with diverse << monoamine transporter >> selectivities (BTCP, indatraline, [[ GBR 12935 ]], mazindol, nomifensine, and zimeldine) either did not produce a rapid pressor response or produced only a small pressor response.


Monoamine uptake inhibitors structurally analogous to cocaine (cocaethylene, CFT, betaCIT, CPT, (+)-cocaine, norcocaine, and benztropine) also produced this rapid pressor response, whereas structurally unrelated uptake inhibitors with diverse << monoamine transporter >> selectivities (BTCP, indatraline, GBR 12935, [[ mazindol ]], nomifensine, and zimeldine) either did not produce a rapid pressor response or produced only a small pressor response.


Monoamine uptake inhibitors structurally analogous to cocaine (cocaethylene, CFT, betaCIT, CPT, (+)-cocaine, norcocaine, and benztropine) also produced this rapid pressor response, whereas structurally unrelated uptake inhibitors with diverse << monoamine transporter >> selectivities (BTCP, indatraline, GBR 12935, mazindol, [[ nomifensine ]], and zimeldine) either did not produce a rapid pressor response or produced only a small pressor response.


Monoamine uptake inhibitors structurally analogous to cocaine (cocaethylene, CFT, betaCIT, CPT, (+)-cocaine, norcocaine, and benztropine) also produced this rapid pressor response, whereas structurally unrelated uptake inhibitors with diverse << monoamine transporter >> selectivities (BTCP, indatraline, GBR 12935, mazindol, nomifensine, and [[ zimeldine ]]) either did not produce a rapid pressor response or produced only a small pressor response.


At nonconvulsant doses, the << sodium channel >> blockers [[ acetylprocainamide ]], dibucaine, dyclonine, prilocaine, proparacaine, quinidine, and tetracaine produced a small pressor response or no increase in BP.


At nonconvulsant doses, the << sodium channel >> blockers acetylprocainamide, [[ dibucaine ]], dyclonine, prilocaine, proparacaine, quinidine, and tetracaine produced a small pressor response or no increase in BP.


At nonconvulsant doses, the << sodium channel >> blockers acetylprocainamide, dibucaine, [[ dyclonine ]], prilocaine, proparacaine, quinidine, and tetracaine produced a small pressor response or no increase in BP.


At nonconvulsant doses, the << sodium channel >> blockers acetylprocainamide, dibucaine, dyclonine, [[ prilocaine ]], proparacaine, quinidine, and tetracaine produced a small pressor response or no increase in BP.


At nonconvulsant doses, the << sodium channel >> blockers acetylprocainamide, dibucaine, dyclonine, prilocaine, [[ proparacaine ]], quinidine, and tetracaine produced a small pressor response or no increase in BP.


At nonconvulsant doses, the << sodium channel >> blockers acetylprocainamide, dibucaine, dyclonine, prilocaine, proparacaine, [[ quinidine ]], and tetracaine produced a small pressor response or no increase in BP.


At nonconvulsant doses, the << sodium channel >> blockers acetylprocainamide, dibucaine, dyclonine, prilocaine, proparacaine, quinidine, and [[ tetracaine ]] produced a small pressor response or no increase in BP.


The << sodium channel >>-blocking action of [[ cocaine ]] per se does not appear to be involved in the rapid pressor response to cocaine.


Characterization of binding sites of a new << neurotensin receptor >> antagonist, [[ [3H]SR 142948A ]], in the rat brain.


The present study describes the characterization of the binding properties and autoradiographic distribution of a new nonpeptide antagonist of << neurotensin receptors >>, [[ [3H]SR 142948A ]] (2-[[5-(2,6-dimethoxyphenyl)-1-(4-(N-(3-dimethylaminopropyl)-N-methyl carbamoyl)-2-isopropylphenyl)-1H-pyrazole-3-carbonyl]-amino]-ad amantane-2-carboxylic acid, hydrochloride), in the rat brain.


The present study describes the characterization of the binding properties and autoradiographic distribution of a new nonpeptide antagonist of << neurotensin receptors >>, [3H]SR 142948A ([[ 2-[[5-(2,6-dimethoxyphenyl)-1-(4-(N-(3-dimethylaminopropyl)-N-methyl carbamoyl)-2-isopropylphenyl)-1H-pyrazole-3-carbonyl]-amino]-ad amantane-2-carboxylic acid, hydrochloride ]]), in the rat brain.


Saturation and competition studies in the presence or absence of the << histamine H1 receptor >> antagonist, [[ levocabastine ]], revealed that [3H]SR 142948A bound with similar affinities to both the levocabastine-insensitive neurotensin NT1 receptors (20% of the total binding population) and the recently cloned levocabastine-sensitive neurotensin NT2 receptors (80% of the receptors) (Kd = 6.8 and 4.8 nM, respectively).


In conclusion, these findings indicate that << [3H]SR 142948A >> is a new potent antagonist radioligand which recognizes with high affinity both [[ neurotensin NT1 ]] and NT2 receptors and represents thus an excellent tool to study neurotensin receptors in the rat brain.


In conclusion, these findings indicate that << [3H]SR 142948A >> is a new potent antagonist radioligand which recognizes with high affinity both neurotensin NT1 and [[ NT2 receptors ]] and represents thus an excellent tool to study neurotensin receptors in the rat brain.


Isoform-specific inhibition of << L-type calcium channels >> by [[ dihydropyridines ]] is independent of isoform-specific gating properties.


<< Dihydropyridines >> (DHPs) block [[ L-type Ca2+ channels ]] more potently at depolarized membrane potentials, consistent with high affinity binding to the inactivated state.


Dihydropyridines (<< DHPs >>) block [[ L-type Ca2+ channels ]] more potently at depolarized membrane potentials, consistent with high affinity binding to the inactivated state.


<< Nisoldipine >> (a DHP antagonist) blocks the [[ smooth muscle channel ]] more potently than the cardiac one, a phenomenon observed not only in native channels but also in expressed channels.


Nisoldipine (a << DHP >> antagonist) blocks the [[ smooth muscle channel ]] more potently than the cardiac one, a phenomenon observed not only in native channels but also in expressed channels.


We thus conclude that the more potent << nisoldipine >> inhibition of smooth muscle versus [[ cardiac L-type Ca2+ channels ]] is not attributable to differences in channel inactivation or activation.


<< Methylenetetrahydrofolate reductase >> deficiency impairs [[ methyltetrahydrofolate ]] synthesis, defects in cytosolic reduction of hydroxocobalamin (CblC/D) impair the synthesis of both methyl- and adenosyl cobalamin and deficiencies of methionine synthase (CblE/G) are associated with defective methyl cobalamin synthesis.


Methylenetetrahydrofolate reductase deficiency impairs methyltetrahydrofolate synthesis, defects in cytosolic reduction of hydroxocobalamin (CblC/D) impair the synthesis of both methyl- and adenosyl cobalamin and deficiencies of << methionine synthase >> (CblE/G) are associated with defective [[ methyl cobalamin ]] synthesis.


Increased << Cat3 >>-mediated cationic [[ amino acid ]] transport functionally compensates in Cat1 knockout cell lines.


The majority of << L-Arg >> transport is mediated by [[ System y+ ]], although several other carriers have been kinetically defined.


<< System y+ >> cationic [[ amino acid ]] transport is mediated by proteins encoded by a family of genes, Cat1, Cat2, and Cat3.


System y+ cationic << amino acid >> transport is mediated by proteins encoded by a family of genes, [[ Cat1 ]], Cat2, and Cat3.


System y+ cationic << amino acid >> transport is mediated by proteins encoded by a family of genes, Cat1, [[ Cat2 ]], and Cat3.


System y+ cationic << amino acid >> transport is mediated by proteins encoded by a family of genes, Cat1, Cat2, and [[ Cat3 ]].


However, the apparent affinity for << lysine >> transport was 2.4 times lower in Cat1(-/-) cells when compared with wild type cells, a property characteristic of [[ Cat3 ]]-mediated transport.


These results suggest that << Cat3 >> compensates for the loss of functional Cat1 in cells derived from Cat1 knockout mice and mediates the majority of high affinity [[ arginine ]] transport.


Effect of << lintitript >>, a new [[ CCK-A receptor ]] antagonist, on gastric emptying of a solid-liquid meal in humans.


We studied the role of endogenous CCK in the emptying of a solid/liquid meal administering the new, highly specific and potent << CCK-A receptor >> antagonist [[ lintitript ]].


<< Lintitript >> markedly increased postprandial plasma [[ CCK ]] release (P<0.001) while distinctly reducing postprandial PP levels (P<0.01) as compared to placebo.


<< Lintitript >> markedly increased postprandial plasma CCK release (P<0.001) while distinctly reducing postprandial [[ PP ]] levels (P<0.01) as compared to placebo.


The study demonstrates for the first time the marked gastrokinetic properties of the new << CCK-A receptor >> antagonist [[ lintitript ]] in humans.


Concanavalin A (Con A)-induced << IFN-gamma >>, GM-CSF, and IL-3 mRNAs are dose-dependently inhibited by the nonselective betaAR agonist [[ isoproterenol ]] and by the selective beta2AR agonist fenoterol.


Concanavalin A (Con A)-induced IFN-gamma, << GM-CSF >>, and IL-3 mRNAs are dose-dependently inhibited by the nonselective betaAR agonist [[ isoproterenol ]] and by the selective beta2AR agonist fenoterol.


Concanavalin A (Con A)-induced IFN-gamma, GM-CSF, and << IL-3 >> mRNAs are dose-dependently inhibited by the nonselective betaAR agonist [[ isoproterenol ]] and by the selective beta2AR agonist fenoterol.


Concanavalin A (Con A)-induced << IFN-gamma >>, GM-CSF, and IL-3 mRNAs are dose-dependently inhibited by the nonselective betaAR agonist isoproterenol and by the selective beta2AR agonist [[ fenoterol ]].


Concanavalin A (Con A)-induced IFN-gamma, << GM-CSF >>, and IL-3 mRNAs are dose-dependently inhibited by the nonselective betaAR agonist isoproterenol and by the selective beta2AR agonist [[ fenoterol ]].


Concanavalin A (Con A)-induced IFN-gamma, GM-CSF, and << IL-3 >> mRNAs are dose-dependently inhibited by the nonselective betaAR agonist isoproterenol and by the selective beta2AR agonist [[ fenoterol ]].


Concanavalin A (Con A)-induced IFN-gamma, GM-CSF, and IL-3 mRNAs are dose-dependently inhibited by the nonselective << betaAR >> agonist [[ isoproterenol ]] and by the selective beta2AR agonist fenoterol.


Concanavalin A (Con A)-induced IFN-gamma, GM-CSF, and IL-3 mRNAs are dose-dependently inhibited by the nonselective betaAR agonist isoproterenol and by the selective << beta2AR >> agonist [[ fenoterol ]].


The observed inhibition on << IFN-gamma >>, GM-CSF, and IL-3 mRNA was blocked by the selective beta2AR antagonist [[ ICI 118,551 ]] (10(-6) M) and by timolol (10(-6) M), a nonselective antagonist.


The observed inhibition on IFN-gamma, << GM-CSF >>, and IL-3 mRNA was blocked by the selective beta2AR antagonist [[ ICI 118,551 ]] (10(-6) M) and by timolol (10(-6) M), a nonselective antagonist.


The observed inhibition on IFN-gamma, GM-CSF, and << IL-3 >> mRNA was blocked by the selective beta2AR antagonist [[ ICI 118,551 ]] (10(-6) M) and by timolol (10(-6) M), a nonselective antagonist.


The observed inhibition on << IFN-gamma >>, GM-CSF, and IL-3 mRNA was blocked by the selective beta2AR antagonist ICI 118,551 (10(-6) M) and by [[ timolol ]] (10(-6) M), a nonselective antagonist.


The observed inhibition on IFN-gamma, << GM-CSF >>, and IL-3 mRNA was blocked by the selective beta2AR antagonist ICI 118,551 (10(-6) M) and by [[ timolol ]] (10(-6) M), a nonselective antagonist.


The observed inhibition on IFN-gamma, GM-CSF, and << IL-3 >> mRNA was blocked by the selective beta2AR antagonist ICI 118,551 (10(-6) M) and by [[ timolol ]] (10(-6) M), a nonselective antagonist.


The observed inhibition on IFN-gamma, GM-CSF, and IL-3 mRNA was blocked by the selective << beta2AR >> antagonist [[ ICI 118,551 ]] (10(-6) M) and by timolol (10(-6) M), a nonselective antagonist.


The observed inhibition on IFN-gamma, GM-CSF, and IL-3 mRNA was blocked by the selective << beta2AR >> antagonist ICI 118,551 (10(-6) M) and by [[ timolol ]] (10(-6) M), a nonselective antagonist.


The selective << beta1AR >> antagonist [[ atenolol ]] (0.3 x 10(-6) M) did not have any effect.


Secretion of << GM-CSF >> protein in the presence of increasing concentrations of [[ isoproterenol ]] followed a similar pattern as observed for GM-CSF mRNA.


Secretion of GM-CSF protein in the presence of increasing concentrations of << isoproterenol >> followed a similar pattern as observed for [[ GM-CSF ]] mRNA.


Although beta3AR mRNA was detectable in Con A-activated T lymphocytes, we could not demonstrate a functional activity in the regulation of cytokine expression: the << beta3AR >> agonist [[ BRL 37344 ]] had no effect on the accumulation of the studied cytokine mRNAs, and did not significantly affect cellular cAMP levels.


All three compounds displayed antagonistic properties against << oxytocin >> in vitro, with [[ carbetocin ]] being the strongest inhibitor (pA2 = 8.21) and carbetocin metabolite II (pA2 = 8.01) being stronger than carbetocin metabolite I (pA2 = 7.81).


All three compounds displayed antagonistic properties against << oxytocin >> in vitro, with carbetocin being the strongest inhibitor (pA2 = 8.21) and [[ carbetocin ]] metabolite II (pA2 = 8.01) being stronger than carbetocin metabolite I (pA2 = 7.81).


All three compounds displayed antagonistic properties against << oxytocin >> in vitro, with carbetocin being the strongest inhibitor (pA2 = 8.21) and carbetocin metabolite II (pA2 = 8.01) being stronger than [[ carbetocin ]] metabolite I (pA2 = 7.81).


These results indicate that << carbetocin >> is a partial agonist/antagonist to the [[ oxytocin receptor ]] while the two metabolites carbetocin metabolite I and carbetocin metabolite II are pure antagonists.


These results indicate that carbetocin is a partial agonist/antagonist to the << oxytocin receptor >> while the two metabolites [[ carbetocin ]] metabolite I and carbetocin metabolite II are pure antagonists.


These results indicate that carbetocin is a partial agonist/antagonist to the << oxytocin receptor >> while the two metabolites carbetocin metabolite I and [[ carbetocin ]] metabolite II are pure antagonists.


Crystallographic analysis of the << human phenylalanine hydroxylase catalytic domain >> with bound [[ catechol ]] inhibitors at 2.0 A resolution.


The << aromatic amino acid hydroxylases >> represent a superfamily of structurally and functionally closely related enzymes, one of those functions being reversible inhibition by [[ catechol ]] derivatives.


Here we present the crystal structure of the dimeric catalytic domain (residues 117-424) of << human phenylalanine hydroxylase >> (hPheOH), cocrystallized with various potent and well-known [[ catechol ]] inhibitors and refined at a resolution of 2.0 A.


Here we present the crystal structure of the dimeric catalytic domain (residues 117-424) of human phenylalanine hydroxylase (<< hPheOH >>), cocrystallized with various potent and well-known [[ catechol ]] inhibitors and refined at a resolution of 2.0 A.


Crystallographic comparison with the structurally related << rat tyrosine hydroxylase >> binary complex with the oxidized cofactor 7,8-dihydrobiopterin revealed overlapping binding sites for the catechols and the cofactor, compatible with a competitive type of inhibition of the [[ catechols ]] versus BH4.


All GCs including the antagonistic compound << RU486 >> efficiently reduced [[ NF-kappaB ]]-mediated transactivation to comparable extents, suggesting that ligand-induced nuclear localization of the GR is sufficient for transrepression.


The ATP-sensitive potassium (KATP) channels in pancreatic beta cells are critical in the regulation of << glucose >>-induced [[ insulin ]] secretion.


These results suggest that SUR1 binds 8-azido-ATP strongly at NBF1 and that MgADP, either by direct binding to NBF2 or by hydrolysis of bound << MgATP >> at [[ NBF2 ]], stabilizes prebound 8-azido-ATP binding at NBF1.