However, desipramine at a low concentration essentially blocked the radioactive outflow induced by all of these substances with the exception of << MPP+ >>, indicating the [[ NAT ]] and not an OCT as their primary site of action.


Our observations indicate an << OCT >>-mediated transmembrane transport of [[ [3H]-MPP+ ]].


Amongst the three << OCTs >> expressed in the SCG, OCT3 best fits the profile of substrates and antagonists that cause trans-stimulation and trans-inhibition, respectively, of [[ [3H]-MPP+ ]] release.


Amongst the three OCTs expressed in the SCG, << OCT3 >> best fits the profile of substrates and antagonists that cause trans-stimulation and trans-inhibition, respectively, of [[ [3H]-MPP+ ]] release.


An inhibitor of << type B monoamine oxidase >> (MAO-B), [[ (-)deprenyl ]] (selegiline), was reported to have neuroprotective activity, but clinical trials failed to confirm it.


An inhibitor of type B monoamine oxidase (<< MAO-B >>), [[ (-)deprenyl ]] (selegiline), was reported to have neuroprotective activity, but clinical trials failed to confirm it.


An inhibitor of << type B monoamine oxidase >> (MAO-B), (-)deprenyl ([[ selegiline ]]), was reported to have neuroprotective activity, but clinical trials failed to confirm it.


An inhibitor of type B monoamine oxidase (<< MAO-B >>), (-)deprenyl ([[ selegiline ]]), was reported to have neuroprotective activity, but clinical trials failed to confirm it.


<< Rasagiline >> prevented the PT in mitochondria directly and also indirectly through induction of antiapoptotic [[ Bcl-2 ]] and a neurotrophic factor, glial cell line-derived neurotrophic factor (GDNF).


<< Rasagiline >> prevented the PT in mitochondria directly and also indirectly through induction of antiapoptotic Bcl-2 and a [[ neurotrophic factor ]], glial cell line-derived neurotrophic factor (GDNF).


<< Rasagiline >> prevented the PT in mitochondria directly and also indirectly through induction of antiapoptotic Bcl-2 and a neurotrophic factor, [[ glial cell line-derived neurotrophic factor ]] (GDNF).


<< Rasagiline >> prevented the PT in mitochondria directly and also indirectly through induction of antiapoptotic Bcl-2 and a neurotrophic factor, glial cell line-derived neurotrophic factor ([[ GDNF ]]).


Long-term administration of << propargylamines >> to rats increased the activities of antioxidative enzymes [[ superoxide dismutase ]] (SOD) and catalase in the brain regions containing dopamine neurons.


Long-term administration of << propargylamines >> to rats increased the activities of antioxidative enzymes superoxide dismutase ([[ SOD ]]) and catalase in the brain regions containing dopamine neurons.


Long-term administration of << propargylamines >> to rats increased the activities of antioxidative enzymes superoxide dismutase (SOD) and [[ catalase ]] in the brain regions containing dopamine neurons.


Practical asymmetric synthesis of << aprepitant >>, a potent human [[ NK-1 receptor ]] antagonist, via a stereoselective Lewis acid-catalyzed trans acetalization reaction.


A streamlined and high-yielding synthesis of << aprepitant >> (1), a potent [[ substance P (SP) receptor ]] antagonist, is described.


Pentosan polysulfate << sodium >> (PPS) has been shown to exert antitumor activity by antagonizing the binding of [[ bFGF ]] to cell surface receptors.


These findings suggest that << RhBG >> and RhCG may play important and cell-specific roles in [[ ammonium ]] transport and signaling in these regions of the kidney.


These findings suggest that RhBG and << RhCG >> may play important and cell-specific roles in [[ ammonium ]] transport and signaling in these regions of the kidney.


<< PDE5 >> is the predominant PDE in the corpus cavernosum, and [[ cGMP ]] is its primary substrate.


PDE5 is the predominant << PDE >> in the corpus cavernosum, and [[ cGMP ]] is its primary substrate.


Therefore, in men with ED, elevation of cGMP in corpus cavernosal tissue via selective inhibition of << cGMP >>-specific [[ PDE5 ]] is a means of improving erectile function at minimal risk of adverse events.


This approach is validated by the clinical efficacy and safety of << sildenafil >>, the pioneering drug for selective [[ PDE5 ]] inhibitor therapy for ED.


<< Sildenafil >> exhibits inhibitory potency against PDE5 and a 10-fold lower dose-related inhibitory potency against rod outer segment PDE6, the predominant [[ PDE ]] in the phototransduction cascade in rods.


<< Sildenafil >> exhibits inhibitory potency against [[ PDE5 ]] and a 10-fold lower dose-related inhibitory potency against rod outer segment PDE6, the predominant PDE in the phototransduction cascade in rods.


<< Sildenafil >> exhibits inhibitory potency against PDE5 and a 10-fold lower dose-related inhibitory potency against rod outer segment [[ PDE6 ]], the predominant PDE in the phototransduction cascade in rods.


As free << sildenafil >> plasma concentrations approach concentrations sufficient to inhibit retinal [[ PDE6 ]], usually at higher therapeutic doses, transient, reversible visual adverse events can occur, albeit infrequently.


Selective inhibition of << PDE5 >> is a rational therapeutic approach in ED, as proved by the clinical success of [[ sildenafil ]].


However, when coapplied with 10 micro m GABA, << ivermectin >> potentiated the GABA-evoked current of the [[ GAB-1 ]]/HG1A receptor, but attenuated the GABA response of the GAB-1/HG1E receptor.


However, when coapplied with 10 micro m GABA, << ivermectin >> potentiated the GABA-evoked current of the GAB-1/[[ HG1A ]] receptor, but attenuated the GABA response of the GAB-1/HG1E receptor.


However, when coapplied with 10 micro m GABA, << ivermectin >> potentiated the GABA-evoked current of the GAB-1/HG1A receptor, but attenuated the GABA response of the [[ GAB-1 ]]/HG1E receptor.


However, when coapplied with 10 micro m GABA, << ivermectin >> potentiated the GABA-evoked current of the GAB-1/HG1A receptor, but attenuated the GABA response of the GAB-1/[[ HG1E ]] receptor.


<< Yohimbine >> is a potent and selective [[ alpha2- versus alpha1-adrenoceptor ]] antagonist.


Plasmacytoid dendritic cells produce cytokines and mature in response to the << TLR7 >> agonists, imiquimod and [[ resiquimod ]].


Plasmacytoid dendritic cells produce cytokines and mature in response to the << TLR7 >> agonists, [[ imiquimod ]] and resiquimod.


The immune response modifiers, << imiquimod >> and resiquimod, are TLR7 agonists that induce [[ type I interferon ]] in numerous species, including humans.


The immune response modifiers, imiquimod and << resiquimod >>, are TLR7 agonists that induce [[ type I interferon ]] in numerous species, including humans.


The immune response modifiers, << imiquimod >> and resiquimod, are [[ TLR7 ]] agonists that induce type I interferon in numerous species, including humans.


The immune response modifiers, imiquimod and << resiquimod >>, are [[ TLR7 ]] agonists that induce type I interferon in numerous species, including humans.


Here, we characterize the activation of human pDC with the << TLR7 >> agonists [[ imiquimod ]] and resiquimod.


Here, we characterize the activation of human pDC with the << TLR7 >> agonists imiquimod and [[ resiquimod ]].


Results indicate that << imiquimod >> and resiquimod induce [[ IFN-alpha ]] and IFN-omega from purified pDC, and pDC are the principle IFN-producing cells in the blood.


Results indicate that << imiquimod >> and resiquimod induce IFN-alpha and [[ IFN-omega ]] from purified pDC, and pDC are the principle IFN-producing cells in the blood.


<< Resiquimod >>-stimulated pDC also produce a number of other [[ cytokines ]] including TNF-alpha and IP-10.


<< Resiquimod >>-stimulated pDC also produce a number of other cytokines including [[ TNF-alpha ]] and IP-10.


<< Resiquimod >>-stimulated pDC also produce a number of other cytokines including TNF-alpha and [[ IP-10 ]].


<< Resiquimod >> enhances co-stimulatory marker expression, [[ CCR7 ]] expression, and pDC viability.


These results demonstrate that << imidazoquinoline >> molecules directly induce pDC maturation as determined by [[ cytokine ]] induction, CCR7 and co-stimulatory marker expression and prolonging viability.


Induction of << heat shock proteins >> (HSPs) by [[ sodium arsenite ]] in cultured astrocytes and reduction of hydrogen peroxide-induced cell death.


Induction of heat shock proteins (<< HSPs >>) by [[ sodium arsenite ]] in cultured astrocytes and reduction of hydrogen peroxide-induced cell death.


<< Arsenite >> triggered strong induction of [[ HSPs ]], which was prevented by 1 micro g/mL cycloheximide (CXH).


Arsenite triggered strong induction of << HSPs >>, which was prevented by 1 micro g/mL [[ cycloheximide ]] (CXH).


Arsenite triggered strong induction of << HSPs >>, which was prevented by 1 micro g/mL cycloheximide ([[ CXH ]]).


<< H2O2 >> caused cell loss and increased cell death with features of apoptosis, i.e. TdT-mediated dUTP nick-end labelling (TUNEL) reaction and [[ caspase-3 ]] activation.


Pre-treatment with arsenite increased << protein kinase B >> (Akt) and extracellular signal regulated kinase 1/2 (ERK1/2) phosphorylation after [[ H2O2 ]].


Pre-treatment with arsenite increased protein kinase B (<< Akt >>) and extracellular signal regulated kinase 1/2 (ERK1/2) phosphorylation after [[ H2O2 ]].


However, while << Akt >> phosphorylation was prevented by CHX, Erk1/2 phosphorylation was further enhanced by [[ CHX ]].


The results show that transient << arsenite >> pre-treatment induces Hsp72, HO-1 and, to a lesser extent, Hsp27; it reduces H2O2-induced astrocyte death; and it causes selective activation of [[ Akt ]] following H2O2.


The results show that transient arsenite pre-treatment induces Hsp72, HO-1 and, to a lesser extent, Hsp27; it reduces H2O2-induced astrocyte death; and it causes selective activation of << Akt >> following [[ H2O2 ]].


The results show that transient << arsenite >> pre-treatment induces [[ Hsp72 ]], HO-1 and, to a lesser extent, Hsp27; it reduces H2O2-induced astrocyte death; and it causes selective activation of Akt following H2O2.


The results show that transient << arsenite >> pre-treatment induces Hsp72, [[ HO-1 ]] and, to a lesser extent, Hsp27; it reduces H2O2-induced astrocyte death; and it causes selective activation of Akt following H2O2.


The results show that transient << arsenite >> pre-treatment induces Hsp72, HO-1 and, to a lesser extent, [[ Hsp27 ]]; it reduces H2O2-induced astrocyte death; and it causes selective activation of Akt following H2O2.


Investigation of bradykinin metabolism in human and rat plasma in the presence of the dual << ACE >>/NEP inhibitors [[ GW660511X ]] and omapatrilat.


Investigation of bradykinin metabolism in human and rat plasma in the presence of the dual ACE/<< NEP >> inhibitors [[ GW660511X ]] and omapatrilat.


Investigation of bradykinin metabolism in human and rat plasma in the presence of the dual << ACE >>/NEP inhibitors GW660511X and [[ omapatrilat ]].


Investigation of bradykinin metabolism in human and rat plasma in the presence of the dual ACE/<< NEP >> inhibitors GW660511X and [[ omapatrilat ]].


In this work a novel approach combining HPLC-UV on-line with oaTOF-MS and ICPMS was applied to investigate in human and rat plasma the metabolism of labelled BK (79/81 Br-Phe5) BrBK in the presence of two new dual << ACE >>/NEP inhibitors ([[ GW660511X ]] and omapatrilat) currently under clinical trial.


In this work a novel approach combining HPLC-UV on-line with oaTOF-MS and ICPMS was applied to investigate in human and rat plasma the metabolism of labelled BK (79/81 Br-Phe5) BrBK in the presence of two new dual ACE/<< NEP >> inhibitors ([[ GW660511X ]] and omapatrilat) currently under clinical trial.


In this work a novel approach combining HPLC-UV on-line with oaTOF-MS and ICPMS was applied to investigate in human and rat plasma the metabolism of labelled BK (79/81 Br-Phe5) BrBK in the presence of two new dual << ACE >>/NEP inhibitors (GW660511X and [[ omapatrilat ]]) currently under clinical trial.


In this work a novel approach combining HPLC-UV on-line with oaTOF-MS and ICPMS was applied to investigate in human and rat plasma the metabolism of labelled BK (79/81 Br-Phe5) BrBK in the presence of two new dual ACE/<< NEP >> inhibitors (GW660511X and [[ omapatrilat ]]) currently under clinical trial.


Unlike GW660511X, << omapatrilat >> abolished the production of [[ BrBK1-5 ]] and BrBK1-7, suggesting a better ACE inhibition effect over GW660511X as no NEP activity was found.


Unlike GW660511X, << omapatrilat >> abolished the production of BrBK1-5 and [[ BrBK1-7 ]], suggesting a better ACE inhibition effect over GW660511X as no NEP activity was found.


Unlike GW660511X, << omapatrilat >> abolished the production of BrBK1-5 and BrBK1-7, suggesting a better [[ ACE ]] inhibition effect over GW660511X as no NEP activity was found.


Unlike GW660511X, omapatrilat abolished the production of BrBK1-5 and BrBK1-7, suggesting a better << ACE >> inhibition effect over [[ GW660511X ]] as no NEP activity was found.


In addition the production of << BrBK1-8 >> was enhanced in the presence of these inhibitors with a greater accumulation being observed with [[ omapatrilat ]].


The production of << Br-Phe5 >> was reduced with [[ GW660511X ]] while no significant change was observed with omapatrilat after 4 h of incubation.


<< GW660511X >> and omapatrilat reduced the production of [[ BrBK1-5 ]] and BrBK1-7 with more effect being observed with omapatrilat.


<< GW660511X >> and omapatrilat reduced the production of BrBK1-5 and [[ BrBK1-7 ]] with more effect being observed with omapatrilat.


GW660511X and << omapatrilat >> reduced the production of [[ BrBK1-5 ]] and BrBK1-7 with more effect being observed with omapatrilat.


GW660511X and << omapatrilat >> reduced the production of BrBK1-5 and [[ BrBK1-7 ]] with more effect being observed with omapatrilat.


GW660511X and omapatrilat reduced the production of << BrBK1-5 >> and BrBK1-7 with more effect being observed with [[ omapatrilat ]].


GW660511X and omapatrilat reduced the production of BrBK1-5 and << BrBK1-7 >> with more effect being observed with [[ omapatrilat ]].


<< GW660511X >> and omapatrilat increased the production of both [[ BrBK1-8 ]] and Br-Phe5 but not that of BrBK4-8 and BrBK2-8.


<< GW660511X >> and omapatrilat increased the production of both BrBK1-8 and [[ Br-Phe5 ]] but not that of BrBK4-8 and BrBK2-8.


GW660511X and << omapatrilat >> increased the production of both [[ BrBK1-8 ]] and Br-Phe5 but not that of BrBK4-8 and BrBK2-8.


GW660511X and << omapatrilat >> increased the production of both BrBK1-8 and [[ Br-Phe5 ]] but not that of BrBK4-8 and BrBK2-8.


This study shows that the potency of << GW660511X >> in comparison with omapatrilat is more than 100-fold lower in human, but less than 10-fold lower in rat plasma, suggesting that rat may not be a suitable in vivo model for the evaluation of [[ ACE ]]/NEP inhibition in relation to effects in humans.


This study shows that the potency of << GW660511X >> in comparison with omapatrilat is more than 100-fold lower in human, but less than 10-fold lower in rat plasma, suggesting that rat may not be a suitable in vivo model for the evaluation of ACE/[[ NEP ]] inhibition in relation to effects in humans.


This study shows that the potency of GW660511X in comparison with << omapatrilat >> is more than 100-fold lower in human, but less than 10-fold lower in rat plasma, suggesting that rat may not be a suitable in vivo model for the evaluation of ACE/[[ NEP ]] inhibition in relation to effects in humans.


Acetylcholinesterase (<< AChE >>) predominates in the healthy brain, with butyrylcholinesterase (BuChE) considered to play a minor role in regulating brain [[ acetylcholine ]] (ACh) levels.


Acetylcholinesterase (AChE) predominates in the healthy brain, with << butyrylcholinesterase >> (BuChE) considered to play a minor role in regulating brain [[ acetylcholine ]] (ACh) levels.


Acetylcholinesterase (AChE) predominates in the healthy brain, with butyrylcholinesterase (<< BuChE >>) considered to play a minor role in regulating brain [[ acetylcholine ]] (ACh) levels.


<< Acetylcholinesterase >> (AChE) predominates in the healthy brain, with butyrylcholinesterase (BuChE) considered to play a minor role in regulating brain [[ acetylcholine ]] (ACh) levels.


Acetylcholinesterase (<< AChE >>) predominates in the healthy brain, with butyrylcholinesterase (BuChE) considered to play a minor role in regulating brain acetylcholine ([[ ACh ]]) levels.


Acetylcholinesterase (AChE) predominates in the healthy brain, with << butyrylcholinesterase >> (BuChE) considered to play a minor role in regulating brain acetylcholine ([[ ACh ]]) levels.


Acetylcholinesterase (AChE) predominates in the healthy brain, with butyrylcholinesterase (<< BuChE >>) considered to play a minor role in regulating brain acetylcholine ([[ ACh ]]) levels.


<< Acetylcholinesterase >> (AChE) predominates in the healthy brain, with butyrylcholinesterase (BuChE) considered to play a minor role in regulating brain acetylcholine ([[ ACh ]]) levels.


Experimental evidence from the use of agents with enhanced selectivity for BuChE (cymserine analogues, MF-8622) and the dual inhibitor of both << AChE >> and BuChE, [[ rivastigmine ]], indicates potential therapeutic benefits of inhibiting both AChE and BuChE in AD and related dementias.


Experimental evidence from the use of agents with enhanced selectivity for BuChE (cymserine analogues, MF-8622) and the dual inhibitor of both AChE and << BuChE >>, [[ rivastigmine ]], indicates potential therapeutic benefits of inhibiting both AChE and BuChE in AD and related dementias.


Experimental evidence from the use of agents with enhanced selectivity for BuChE (cymserine analogues, MF-8622) and the dual inhibitor of both AChE and BuChE, << rivastigmine >>, indicates potential therapeutic benefits of inhibiting both [[ AChE ]] and BuChE in AD and related dementias.


Experimental evidence from the use of agents with enhanced selectivity for BuChE (cymserine analogues, MF-8622) and the dual inhibitor of both AChE and BuChE, << rivastigmine >>, indicates potential therapeutic benefits of inhibiting both AChE and [[ BuChE ]] in AD and related dementias.


The development of specific << BuChE >> inhibitors and further experience with the dual enzyme inhibitor [[ rivastigmine ]] will improve understanding of the aetiology of AD and should lead to a wider variety of potent treatment options.


Agents which have recently been shown to block << cyclin D1 >> translation by regulating calcium levels are the [[ unsaturated essential fatty acid ]], eicosapentaenoic acid (EPA), the antidiabetic thiazolidinediones, and the antifungal agent, clotrimazole.


Agents which have recently been shown to block << cyclin D1 >> translation by regulating calcium levels are the unsaturated essential fatty acid, [[ eicosapentaenoic acid ]] (EPA), the antidiabetic thiazolidinediones, and the antifungal agent, clotrimazole.


Agents which have recently been shown to block << cyclin D1 >> translation by regulating calcium levels are the unsaturated essential fatty acid, eicosapentaenoic acid ([[ EPA ]]), the antidiabetic thiazolidinediones, and the antifungal agent, clotrimazole.


Agents which have recently been shown to block << cyclin D1 >> translation by regulating calcium levels are the unsaturated essential fatty acid, eicosapentaenoic acid (EPA), the antidiabetic [[ thiazolidinediones ]], and the antifungal agent, clotrimazole.


Agents which have recently been shown to block << cyclin D1 >> translation by regulating calcium levels are the unsaturated essential fatty acid, eicosapentaenoic acid (EPA), the antidiabetic thiazolidinediones, and the antifungal agent, [[ clotrimazole ]].


<< Angiotensin AT1 receptor >> antagonist [[ losartan ]] and the defence reaction in the anaesthetised rat.


We investigated the effect of << AT1 receptor >> blockade in the NTS on the response to stimulation of HDA in anaesthetised rats treated with the neuromuscular blocking agent [[ pancuronium bromide ]].


Blockade of << LTC4 >> synthesis caused by additive inhibition of [[ gIV-PLA2 ]] phosphorylation: Effect of salmeterol and PDE4 inhibition in human eosinophils.


OBJECTIVE: To determine (a) whether << PDE4 >> inhibition alone with [[ rolipram ]] blocked secretions of arachidonic acid (AA) and leukotriene C(4) (LTC(4)) caused by activation of eosinophils with formyl-met-leu-phe plus cytochalasin B (FMLP/B), (b) to determine if PDE4 inhibition plus beta(2)-adrenoceptor agonist act additively to augment endogenous cAMP concentration, and (c) to determine the mechanism by which additive inhibition of AA and LTC(4) synthesis is regulated by cAMP.


RESULTS: Rolipram unmasked the inhibitory effect of << beta(2)-adrenoceptor >> stimulation with [[ salmeterol ]] and significantly attenuated the stimulated release of AA and subsequent LTC(4).


Inhibition corresponded to increased cAMP production caused by rolipram alone or << rolipram >> plus salmeterol and blocked proportionately the phosphorylation and activation of [[ gIV-PLA(2) ]] in FMLP/B-activated eosinophils.


Inhibition corresponded to increased cAMP production caused by rolipram alone or rolipram plus << salmeterol >> and blocked proportionately the phosphorylation and activation of [[ gIV-PLA(2) ]] in FMLP/B-activated eosinophils.


CONCLUSIONS: Inhibition of << PDE4 >> by [[ rolipram ]] unmasks beta(2)-adrenergic blockade of LTC(4) synthesis caused by FMLP/B.


Anabolic effects of << clenbuterol >> on skeletal muscle are mediated by [[ beta 2-adrenoceptor ]] activation.


The potent anabolic effects of the << beta 2-adrenoceptor >> agonist [[ clenbuterol ]] on skeletal muscle have been reported to be independent of actions on beta-adrenoceptors.


These effects were not mimicked by oral administration of the << beta 2-adrenoceptor >> agonist [[ salbutamol ]] even at high dose (52 mg/kg diet), and the effects of clenbuterol were not inhibited by addition of DL-propranolol (200 mg/kg diet).


These effects were not mimicked by oral administration of the << beta 2-adrenoceptor >> agonist salbutamol even at high dose (52 mg/kg diet), and the effects of [[ clenbuterol ]] were not inhibited by addition of DL-propranolol (200 mg/kg diet).


In the hot-plate test in mice, the antinociceptive action of the << alpha 2-adrenoceptor >> agonist, [[ UK 14,304 ]], was abolished by the alpha 2-adrenoceptor antagonist, idazoxan, the potent alpha 2A-adrenoceptor antagonist, RX 821002 and the preferential alpha 2A-adrenoceptor antagonist, BRL 44408.


In the hot-plate test in mice, the antinociceptive action of the alpha 2-adrenoceptor agonist, UK 14,304, was abolished by the << alpha 2-adrenoceptor >> antagonist, [[ idazoxan ]], the potent alpha 2A-adrenoceptor antagonist, RX 821002 and the preferential alpha 2A-adrenoceptor antagonist, BRL 44408.


In the hot-plate test in mice, the antinociceptive action of the alpha 2-adrenoceptor agonist, UK 14,304, was abolished by the alpha 2-adrenoceptor antagonist, idazoxan, the potent << alpha 2A-adrenoceptor >> antagonist, [[ RX 821002 ]] and the preferential alpha 2A-adrenoceptor antagonist, BRL 44408.


In the hot-plate test in mice, the antinociceptive action of the alpha 2-adrenoceptor agonist, UK 14,304, was abolished by the alpha 2-adrenoceptor antagonist, idazoxan, the potent alpha 2A-adrenoceptor antagonist, RX 821002 and the preferential << alpha 2A-adrenoceptor >> antagonist, [[ BRL 44408 ]].


The preferential << alpha 2A-adrenoceptor >> partial agonist, [[ guanfacine ]], partially inhibited UK 14,304-induced antinociception.


The preferential << alpha 2A-adrenoceptor >> partial agonist, guanfacine, partially inhibited [[ UK 14,304 ]]-induced antinociception.


<< SDH >> (L-serine dehydratase, EC 4.3.1.17) catalyzes the pyridoxal 5'-phosphate (PLP)-dependent dehydration of L-serine to yield [[ pyruvate ]] and ammonia.


SDH (L-serine dehydratase, << EC 4.3.1.17 >>) catalyzes the pyridoxal 5'-phosphate (PLP)-dependent dehydration of L-serine to yield [[ pyruvate ]] and ammonia.


SDH << (L-serine dehydratase >>, EC 4.3.1.17) catalyzes the pyridoxal 5'-phosphate (PLP)-dependent dehydration of L-serine to yield [[ pyruvate ]] and ammonia.


<< SDH >> (L-serine dehydratase, EC 4.3.1.17) catalyzes the pyridoxal 5'-phosphate (PLP)-dependent dehydration of L-serine to yield pyruvate and [[ ammonia ]].


SDH (L-serine dehydratase, << EC 4.3.1.17 >>) catalyzes the pyridoxal 5'-phosphate (PLP)-dependent dehydration of L-serine to yield pyruvate and [[ ammonia ]].


SDH << (L-serine dehydratase >>, EC 4.3.1.17) catalyzes the pyridoxal 5'-phosphate (PLP)-dependent dehydration of L-serine to yield pyruvate and [[ ammonia ]].


<< SDH >> (L-serine dehydratase, EC 4.3.1.17) catalyzes the pyridoxal 5'-phosphate (PLP)-dependent dehydration of [[ L-serine ]] to yield pyruvate and ammonia.


SDH (L-serine dehydratase, << EC 4.3.1.17 >>) catalyzes the pyridoxal 5'-phosphate (PLP)-dependent dehydration of [[ L-serine ]] to yield pyruvate and ammonia.


SDH << (L-serine dehydratase >>, EC 4.3.1.17) catalyzes the pyridoxal 5'-phosphate (PLP)-dependent dehydration of [[ L-serine ]] to yield pyruvate and ammonia.


Formation of << pyruvate >> by [[ SDH ]] is a two-step reaction in which the hydroxyl group of serine is cleaved to produce aminoacrylate, and then the aminoacrylate is deaminated by nonenzymatic hydrolysis to produce pyruvate.


Formation of pyruvate by << SDH >> is a two-step reaction in which the hydroxyl group of serine is cleaved to produce aminoacrylate, and then the aminoacrylate is deaminated by nonenzymatic hydrolysis to produce [[ pyruvate ]].


Formation of pyruvate by << SDH >> is a two-step reaction in which the hydroxyl group of serine is cleaved to produce [[ aminoacrylate ]], and then the aminoacrylate is deaminated by nonenzymatic hydrolysis to produce pyruvate.


Blocking EGFR signaling with the EGFR/HER-2 kinase inhibitor (KI) << GW572016 >> decreased the postradiation survival of irradiated [[ Ras ]]-transformed cells and normal cells but had no effect on the survival of unirradiated cells.


Blocking << EGFR >> signaling with the EGFR/HER-2 kinase inhibitor (KI) [[ GW572016 ]] decreased the postradiation survival of irradiated Ras-transformed cells and normal cells but had no effect on the survival of unirradiated cells.


Blocking EGFR signaling with the << EGFR >>/HER-2 kinase inhibitor (KI) [[ GW572016 ]] decreased the postradiation survival of irradiated Ras-transformed cells and normal cells but had no effect on the survival of unirradiated cells.


Blocking EGFR signaling with the EGFR/<< HER-2 >> kinase inhibitor (KI) [[ GW572016 ]] decreased the postradiation survival of irradiated Ras-transformed cells and normal cells but had no effect on the survival of unirradiated cells.


Ras-CM and TGF-alpha also increase << PI3-K >> activity downstream of the EGFR and increase postradiation survival, both of which are abrogated by [[ GW572016 ]].


Ras-CM and TGF-alpha also increase PI3-K activity downstream of the << EGFR >> and increase postradiation survival, both of which are abrogated by [[ GW572016 ]].


Thus, << Ras >> utilizes autocrine signaling through EGFR to increase radioresistance, and the EGFR KI [[ GW572016 ]] acts as a radiosensitizer.


Thus, Ras utilizes autocrine signaling through EGFR to increase radioresistance, and the << EGFR >> KI [[ GW572016 ]] acts as a radiosensitizer.


The observation that << Ras >>-transformed cells can be sensitized to killing by ionizing radiation with [[ GW572016 ]] demonstrates that EGFR KIs could potentially be used to radiosensitize tumors in which radioresistance is dependent on Ras-driven autocrine signaling through EGFR.


The observation that Ras-transformed cells can be sensitized to killing by ionizing radiation with << GW572016 >> demonstrates that [[ EGFR ]] KIs could potentially be used to radiosensitize tumors in which radioresistance is dependent on Ras-driven autocrine signaling through EGFR.


(-)-Isoprenaline and a nonconventional << beta(3)-adrenoceptor >> agonist, [[ (+/-)-[4-[3-[(1,1-dimethylethyl)amino]-2-hydroxypropoxy]-1,3-dihydro-2H-benzimida zol-2-one] hydrochloride ]] ((+/-)-CGP12177A), induced concentration-dependent relaxation of (-)-phenylephrine (0.3 microM) preconstricted spiral preparations.


(-)-Isoprenaline and a nonconventional << beta(3)-adrenoceptor >> agonist, (+/-)-[4-[3-[(1,1-dimethylethyl)amino]-2-hydroxypropoxy]-1,3-dihydro-2H-benzimida zol-2-one] hydrochloride ([[ (+/-)-CGP12177A ]]), induced concentration-dependent relaxation of (-)-phenylephrine (0.3 microM) preconstricted spiral preparations.


Pretreatment with a combination of << (+/-)-2-hydroxy-5-[2-[[2-hydroxy-3-[4-[1-methyl-4-(trifluoromethyl)-1H-imidazol-2 -yl]phenoxy]propyl]amino]ethoxy]-benzamide methanesulfonate >> (CGP20712A, a selective [[ beta(1)-adrenoceptor ]] antagonist) and (+/-)-1-[2,3-(dihydro-7-methyl-1H-inden-4-yl)oxy]-3-[(1-methylethyl)amino]-2-buta nol hydrochloride (ICI-118,5511, a selective beta(2)-adrenoceptor antagonist) (0.1 microM for each) produced a 14-fold rightward shift of the concentration-response curve for (-)-isoprenaline; however, the relaxation in response to (+/-)-CGP12177A was unaffected by the blockade of beta(1)- and beta(2)-adrenoceptors.


Pretreatment with a combination of (+/-)-2-hydroxy-5-[2-[[2-hydroxy-3-[4-[1-methyl-4-(trifluoromethyl)-1H-imidazol-2 -yl]phenoxy]propyl]amino]ethoxy]-benzamide methanesulfonate (<< CGP20712A >>, a selective [[ beta(1)-adrenoceptor ]] antagonist) and (+/-)-1-[2,3-(dihydro-7-methyl-1H-inden-4-yl)oxy]-3-[(1-methylethyl)amino]-2-buta nol hydrochloride (ICI-118,5511, a selective beta(2)-adrenoceptor antagonist) (0.1 microM for each) produced a 14-fold rightward shift of the concentration-response curve for (-)-isoprenaline; however, the relaxation in response to (+/-)-CGP12177A was unaffected by the blockade of beta(1)- and beta(2)-adrenoceptors.


Pretreatment with a combination of (+/-)-2-hydroxy-5-[2-[[2-hydroxy-3-[4-[1-methyl-4-(trifluoromethyl)-1H-imidazol-2 -yl]phenoxy]propyl]amino]ethoxy]-benzamide methanesulfonate (CGP20712A, a selective beta(1)-adrenoceptor antagonist) and << (+/-)-1-[2,3-(dihydro-7-methyl-1H-inden-4-yl)oxy]-3-[(1-methylethyl)amino]-2-buta nol hydrochloride >> (ICI-118,5511, a selective [[ beta(2)-adrenoceptor ]] antagonist) (0.1 microM for each) produced a 14-fold rightward shift of the concentration-response curve for (-)-isoprenaline; however, the relaxation in response to (+/-)-CGP12177A was unaffected by the blockade of beta(1)- and beta(2)-adrenoceptors.


Pretreatment with a combination of (+/-)-2-hydroxy-5-[2-[[2-hydroxy-3-[4-[1-methyl-4-(trifluoromethyl)-1H-imidazol-2 -yl]phenoxy]propyl]amino]ethoxy]-benzamide methanesulfonate (CGP20712A, a selective beta(1)-adrenoceptor antagonist) and (+/-)-1-[2,3-(dihydro-7-methyl-1H-inden-4-yl)oxy]-3-[(1-methylethyl)amino]-2-buta nol hydrochloride (<< ICI-118,5511 >>, a selective [[ beta(2)-adrenoceptor ]] antagonist) (0.1 microM for each) produced a 14-fold rightward shift of the concentration-response curve for (-)-isoprenaline; however, the relaxation in response to (+/-)-CGP12177A was unaffected by the blockade of beta(1)- and beta(2)-adrenoceptors.


The specificity of tracer uptake was determined by adding the << NET >> inhibitor [[ imipramine ]].


<< [(131)I]MIBG >> uptake in PC12 cells, which express the [[ NET ]] endogenously, was 20- to 28-fold lower than in transduced cells.


In vivo, A431<< NET >> tumors demonstrated a 33-fold higher [[ [(123)I]MIBG ]] uptake than parental tumors.


The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, << formoterol >>, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.


The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, << broxaterol >>) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.


The aim of this study was, therefore, to provide comparative binding characteristics of agonists (<< epinephrine >>, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.


The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, << norepinephrine >>, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.


The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, << isoproterenol >>, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.


The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, << fenoterol >>, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.


The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, << salbutamol >>, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.


The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, << salmeterol >>, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.


The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, << terbutalin >>, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.


The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (<< propranolol >>, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.


The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, << alprenolol >>, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.


The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, << atenolol >>, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.


The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, << metoprolol >>, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.


The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, << bisoprolol >>, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.


The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, << carvedilol >>, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.


The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, << pindolol >>, BRL 37344, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.


The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, << BRL 37344 >>, CGP 20712, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.


The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, << CGP 20712 >>, SR 59230A, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.


The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, << SR 59230A >>, CGP 12177, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.


The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, << CGP 12177 >>, ICI 118551) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.


The aim of this study was, therefore, to provide comparative binding characteristics of agonists (epinephrine, norepinephrine, isoproterenol, fenoterol, salbutamol, salmeterol, terbutalin, formoterol, broxaterol) and antagonists (propranolol, alprenolol, atenolol, metoprolol, bisoprolol, carvedilol, pindolol, BRL 37344, CGP 20712, SR 59230A, CGP 12177, << ICI 118551 >>) at all three subtypes of [[ human beta-adrenergic receptors ]] in an identical cellular background.


Manipulation of kinetic profiles in << 2-aryl propionic acid >> [[ cyclooxygenase ]] inhibitors.


Effects of the << EGFR >>/HER2 kinase inhibitor [[ GW572016 ]] on EGFR- and HER2-overexpressing breast cancer cell line proliferation, radiosensitization, and resistance.


Effects of the EGFR/<< HER2 >> kinase inhibitor [[ GW572016 ]] on EGFR- and HER2-overexpressing breast cancer cell line proliferation, radiosensitization, and resistance.


Effects of the EGFR/HER2 << kinase >> inhibitor [[ GW572016 ]] on EGFR- and HER2-overexpressing breast cancer cell line proliferation, radiosensitization, and resistance.


To gauge the potential clinical utility of targeting both EGFR and HER2 to control growth and radiosensitize human breast cancers, we examined the effect of a dual << EGFR >>/HER2 inhibitor, [[ GW572016 ]], on the proliferation and radiation response of either EGFR- or HER2-overexpressing human breast cancer cell lines.


To gauge the potential clinical utility of targeting both EGFR and HER2 to control growth and radiosensitize human breast cancers, we examined the effect of a dual EGFR/<< HER2 >> inhibitor, [[ GW572016 ]], on the proliferation and radiation response of either EGFR- or HER2-overexpressing human breast cancer cell lines.


RESULTS: << GW572016 >> inhibited constitutive and/or ligand-induced [[ EGFR ]] or HER2 tyrosine phosphorylation of all five cell lines, which correlated with the antiproliferative response in all but one cell line.


RESULTS: << GW572016 >> inhibited constitutive and/or ligand-induced EGFR or [[ HER2 ]] tyrosine phosphorylation of all five cell lines, which correlated with the antiproliferative response in all but one cell line.


Exploration of potential mechanisms of resistance in SUM185 cells revealed failure of << GW572016 >> to inhibit downstream ERK and Akt activation, despite inhibition of [[ HER2 ]] phosphorylation.


CONCLUSION: << GW572016 >> potently inhibits receptor phosphorylation in either [[ EGFR ]]- or HER2-overexpressing cell lines and has both antiproliferative and radiosensitizing effects.


CONCLUSION: << GW572016 >> potently inhibits receptor phosphorylation in either EGFR- or [[ HER2 ]]-overexpressing cell lines and has both antiproliferative and radiosensitizing effects.


Metformin, but not leptin, regulates AMP-activated protein kinase in pancreatic islets: impact on << glucose >>-stimulated [[ insulin ]] secretion.


<< Metformin >>, a drug widely used in the treatment of type 2 diabetes, has recently been shown to act on skeletal muscle and liver in part through the activation of [[ AMP-activated protein kinase ]] (AMPK).


<< Metformin >>, a drug widely used in the treatment of type 2 diabetes, has recently been shown to act on skeletal muscle and liver in part through the activation of AMP-activated protein kinase ([[ AMPK ]]).


Whether << metformin >> or the satiety factor leptin, which also stimulates [[ AMPK ]] in muscle, regulates this enzyme in pancreatic islets is unknown.


Increases in << glucose >> concentration from 0 to 3 and from 3 to 17 mM inhibited [[ AMPK ]] activity in primary islets from mouse, rat, and human, confirming previous findings in insulinoma cells.


Incubation with << metformin >> (0.2-1 mM) activated [[ AMPK ]] in both human islets and MIN6 beta-cells in parallel with an inhibition of insulin secretion, whereas leptin (10-100 nM) was without effect in MIN6 cells.


Incubation with << metformin >> (0.2-1 mM) activated AMPK in both human islets and MIN6 beta-cells in parallel with an inhibition of [[ insulin ]] secretion, whereas leptin (10-100 nM) was without effect in MIN6 cells.


The inhibitory effects of << metformin >> on [[ insulin ]] secretion may therefore need to be considered with respect to the use of this drug for the treatment of type 2 diabetes.


A novel retinoic acid-responsive element regulates << retinoic acid >>-induced [[ BLR1 ]] expression.


RA is known to induce expression of the Burkitt's lymphoma receptor 1 (BLR1) gene which propels RA-induced cell cycle arrest and differentiation of HL-60 human myeloblastic leukemia cells, motivating the present analysis of transcriptional regulation of << blr1 >> expression by [[ RA ]].


<< RA >> is known to induce expression of the [[ Burkitt's lymphoma receptor 1 ]] (BLR1) gene which propels RA-induced cell cycle arrest and differentiation of HL-60 human myeloblastic leukemia cells, motivating the present analysis of transcriptional regulation of blr1 expression by RA.


<< RA >> is known to induce expression of the Burkitt's lymphoma receptor 1 ([[ BLR1 ]]) gene which propels RA-induced cell cycle arrest and differentiation of HL-60 human myeloblastic leukemia cells, motivating the present analysis of transcriptional regulation of blr1 expression by RA.


A 5'-flanking region capable of supporting << RA >>-induced [[ blr1 ]] activation in HL-60 cells was found to contain a 205-bp sequence in the distal portion that was necessary for transcriptional activation by RA.


The ability of this cis-acting RAR-RXR binding element to activate transcription in response to << RA >> also depended on downstream sequences where an octamer transcription factor 1 (Oct1) site and a [[ nuclear factor of activated T cells ]] (NFATc) site between this element and the transcriptional start, as well as a cyclic AMP response element binding factor (CREB) site between the transcriptional start and first exon of the blr1 gene, were necessary.


In sum the results of the present study indicate that << RA >>-induced expression of [[ blr1 ]] expression depends on a novel RA response element.


The persistent membrane retention of << desipramine >> causes lasting inhibition of [[ norepinephrine transporter ]] function.


[3H]DMI trapped in membranes was displaceable by the structurally unrelated << NET >> inhibitor, [[ nisoxetine ]], in a concentration-dependent manner, implying interaction of retained [3H]DMI with the NET.


<< Irbesartan >> is a long-acting [[ angiotensin II ]] antagonist acting specifically at the level of the Type 1-receptor subtype (AT1-receptor).


<< Irbesartan >> may have antiatherosclerotic properties beyond those expected from blood pressure lowering per se: this AT1-blocker decreases the vascular oxidative stress and prevents the procoagulant as well as the pro-inflammatory effects of [[ angiotensin II ]].


<< Irbesartan >> may have antiatherosclerotic properties beyond those expected from blood pressure lowering per se: this [[ AT1 ]]-blocker decreases the vascular oxidative stress and prevents the procoagulant as well as the pro-inflammatory effects of angiotensin II.


To verify the hypothesis that the non-conventional partial agonist << (-)-CGP12177 >> binds at two beta(1)-adrenoceptor sites, [[ human beta(1)-adrenoceptors ]], expressed in CHO cells, were labelled with (-)-[(3)H]-CGP12177.


To verify the hypothesis that the non-conventional partial agonist << (-)-CGP12177 >> binds at two [[ beta(1)-adrenoceptor ]] sites, human beta(1)-adrenoceptors, expressed in CHO cells, were labelled with (-)-[(3)H]-CGP12177.


<< Imiquimod >>, a Toll-like receptor-7 agonist, induces [[ perforin ]] in cytotoxic T lymphocytes in vitro.


<< Imiquimod >>, a [[ Toll-like receptor-7 ]] agonist, induces perforin in cytotoxic T lymphocytes in vitro.


<< Imiquimod >> (IMQ), an activator of [[ Toll-like receptor-7 ]] (TLR-7), induces by several routes a profound anti-viral and anti-tumor effect in vivo.


<< Imiquimod >> (IMQ), an activator of Toll-like receptor-7 ([[ TLR-7 ]]), induces by several routes a profound anti-viral and anti-tumor effect in vivo.


Imiquimod (<< IMQ >>), an activator of [[ Toll-like receptor-7 ]] (TLR-7), induces by several routes a profound anti-viral and anti-tumor effect in vivo.


Imiquimod (<< IMQ >>), an activator of Toll-like receptor-7 ([[ TLR-7 ]]), induces by several routes a profound anti-viral and anti-tumor effect in vivo.


In peripheral lymphocytes of healthy and diseased subjects, << IMQ >> induced a significant increase of [[ perforin ]](+) CTLs within 12h in all experiments performed.


This effect was most pronounced in CTLs of patients suffering from atopic dermatitis, a model disorder for subnormal perforin expression: as compared to perforin(+) CTLs detected at time point zero (100%), up to 270% of << perforin >>(+) CTLs were induced by 2.5 microg/ml [corrected] [[ IMQ ]].


Thus, the biological activity of << IMQ >> appears to exceed its previously known functions, inasmuch as it boosts up significantly the [[ perforin ]]-granule system.


<< Ang II >> level in plasma and mesenteric arteries in SHR group was the same or lower than that in WKY group, and was higher in [[ irbesartan ]] group and lower in imidapril group.


<< Ang II >> level in plasma and mesenteric arteries in SHR group was the same or lower than that in WKY group, and was higher in irbesartan group and lower in [[ imidapril ]] group.


The ratio of << TGF-beta1 >> absorbed light value to GAPDH absorbed light value in the SHR group was 0.887+/-0.019, which was significantly higher than that in WKY group, [[ imidapril ]] group, and irbesartan group with the ratios of 0.780+/-0.018, 0.803+/-0.005, and 0.847+/-0.017, respectively (P<0.01).


The ratio of TGF-beta1 absorbed light value to << GAPDH >> absorbed light value in the SHR group was 0.887+/-0.019, which was significantly higher than that in WKY group, [[ imidapril ]] group, and irbesartan group with the ratios of 0.780+/-0.018, 0.803+/-0.005, and 0.847+/-0.017, respectively (P<0.01).


The ratio of << TGF-beta1 >> absorbed light value to GAPDH absorbed light value in the SHR group was 0.887+/-0.019, which was significantly higher than that in WKY group, imidapril group, and [[ irbesartan ]] group with the ratios of 0.780+/-0.018, 0.803+/-0.005, and 0.847+/-0.017, respectively (P<0.01).


The ratio of TGF-beta1 absorbed light value to << GAPDH >> absorbed light value in the SHR group was 0.887+/-0.019, which was significantly higher than that in WKY group, imidapril group, and [[ irbesartan ]] group with the ratios of 0.780+/-0.018, 0.803+/-0.005, and 0.847+/-0.017, respectively (P<0.01).


<< Ang II >> level in plasma and mesenteric arteries in imidapril group was significantly lower than that in [[ irbesartan ]] group (P<0.05).


<< Ang II >> level in plasma and mesenteric arteries in [[ imidapril ]] group was significantly lower than that in irbesartan group (P<0.05).


The << c-Jun >> absorbed light value/GAPDH absorbed light value of mesenteric arteries in the SHR group was 0.850+/-0.015, which was significantly higher than that in the WKY, [[ imidapril ]], and irbesartan groups (0.582+/-0.013, 0.743+/-0.012, and 0.789+/-0.013, respectively, P<0.01), and was significantly lower in imidapril group than in irbesartan group (P<0.05).


The c-Jun absorbed light value/<< GAPDH >> absorbed light value of mesenteric arteries in the SHR group was 0.850+/-0.015, which was significantly higher than that in the WKY, [[ imidapril ]], and irbesartan groups (0.582+/-0.013, 0.743+/-0.012, and 0.789+/-0.013, respectively, P<0.01), and was significantly lower in imidapril group than in irbesartan group (P<0.05).


The << c-Jun >> absorbed light value/GAPDH absorbed light value of mesenteric arteries in the SHR group was 0.850+/-0.015, which was significantly higher than that in the WKY, imidapril, and [[ irbesartan ]] groups (0.582+/-0.013, 0.743+/-0.012, and 0.789+/-0.013, respectively, P<0.01), and was significantly lower in imidapril group than in irbesartan group (P<0.05).


The c-Jun absorbed light value/<< GAPDH >> absorbed light value of mesenteric arteries in the SHR group was 0.850+/-0.015, which was significantly higher than that in the WKY, imidapril, and [[ irbesartan ]] groups (0.582+/-0.013, 0.743+/-0.012, and 0.789+/-0.013, respectively, P<0.01), and was significantly lower in imidapril group than in irbesartan group (P<0.05).


CONCLUSION: << Imidapril >> and irbesartan can not only control blood pressure but also inhibit mesenteric arteries remodeling and mRNA expression of [[ TGF-beta1 ]], c-Jun in SHR.


CONCLUSION: << Imidapril >> and irbesartan can not only control blood pressure but also inhibit mesenteric arteries remodeling and mRNA expression of TGF-beta1, [[ c-Jun ]] in SHR.


CONCLUSION: Imidapril and << irbesartan >> can not only control blood pressure but also inhibit mesenteric arteries remodeling and mRNA expression of [[ TGF-beta1 ]], c-Jun in SHR.


CONCLUSION: Imidapril and << irbesartan >> can not only control blood pressure but also inhibit mesenteric arteries remodeling and mRNA expression of TGF-beta1, [[ c-Jun ]] in SHR.


BACKGROUND: To assess the sensitivity of biochemical, physiological, and pharmacological markers of peripheral norepinephrine (NE) transporter (NET) function, we chronically antagonized << NET >> by a range of doses of [[ duloxetine ]] [(+)-N-methyl-3-(1-naphthalenyloxy)-2 thiophenepropanamine], which blocks the NE reuptake process.


BACKGROUND: To assess the sensitivity of biochemical, physiological, and pharmacological markers of peripheral norepinephrine (NE) transporter (NET) function, we chronically antagonized << NET >> by a range of doses of duloxetine [[[ (+)-N-methyl-3-(1-naphthalenyloxy)-2 thiophenepropanamine ]]], which blocks the NE reuptake process.


BACKGROUND: To assess the sensitivity of biochemical, physiological, and pharmacological markers of peripheral norepinephrine (NE) transporter (NET) function, we chronically antagonized << NET >> by a range of doses of duloxetine [(+)-N-methyl-3-(1-naphthalenyloxy)-2 thiophenepropanamine], which blocks the [[ NE ]] reuptake process.


<< Auranofin >>, an antirheumatic gold compound, is an inhibitor of selenocysteine enzymes, such as thioredoxin reductase and [[ glutathione peroxidase ]].


<< Auranofin >>, an antirheumatic gold compound, is an inhibitor of [[ selenocysteine enzymes ]], such as thioredoxin reductase and glutathione peroxidase.


<< Auranofin >>, an antirheumatic gold compound, is an inhibitor of selenocysteine enzymes, such as [[ thioredoxin reductase ]] and glutathione peroxidase.


There was significantly less << thioredoxin reductase >> activity in rat liver extracts, whereas the level of glutathione activity remained unchanged, demonstrating that the dose of [[ auranofin ]] used was able to selectively inhibit one of these enzyme systems.


Furthermore, << gallium >> also seems to affect intracellular availability of iron already taken up via this pathway, probably due to its inhibitory activity on [[ vacuolar-type H(+)-ATPases ]].


However, some experimental findings raise the question whether these effects resulting from the << iron >>-mimicking properties of gallium are solely responsible for its antineoplastic activity or whether additional mechanisms are involved, such as antimitotic effects which result from its capability of inhibiting [[ tubulin ]] polymerization.


However, some experimental findings raise the question whether these effects resulting from the iron-mimicking properties of << gallium >> are solely responsible for its antineoplastic activity or whether additional mechanisms are involved, such as antimitotic effects which result from its capability of inhibiting [[ tubulin ]] polymerization.


GABA-evoked currents were completely and reversibly blocked by the competitive << GABAA receptor >> antagonist [[ bicuculline ]] (IC50 = 1.7 microM), indicating expression of GABAA but not GABAC receptors.


<< Histamine H1-receptor >> (H1R) antagonists, or [[ antihistamines ]], often induce sedative side effects when used for the treatment of allergic disorders.


Histamine H1-receptor (<< H1R >>) antagonists, or [[ antihistamines ]], often induce sedative side effects when used for the treatment of allergic disorders.


A novel membrane sensor for << histamine H1-receptor >> antagonist "[[ fexofenadine ]]".


<< Thymidylate synthase >> (TS) continues to be a critical target for 5-fluorouracil (5-FU) and its prodrugs, UFT/LV (Orzel), capecitabine (Xeloda), and S-1, primarily because this enzyme is essential for the synthesis of [[ 2-deoxythymidine-5-monophosphate ]], a precursor for DNA synthesis.


Thymidylate synthase (<< TS >>) continues to be a critical target for 5-fluorouracil (5-FU) and its prodrugs, UFT/LV (Orzel), capecitabine (Xeloda), and S-1, primarily because this enzyme is essential for the synthesis of [[ 2-deoxythymidine-5-monophosphate ]], a precursor for DNA synthesis.


While fluoropyrimidine antimetabolites have other sites of action, antifolates << ZD1694 >> (raltitrexed, Tomudex) and AG337 (Thymitag) are more specific and potent [[ TS ]] inhibitors.


While fluoropyrimidine antimetabolites have other sites of action, antifolates ZD1694 (<< raltitrexed >>, Tomudex) and AG337 (Thymitag) are more specific and potent [[ TS ]] inhibitors.


While fluoropyrimidine antimetabolites have other sites of action, antifolates ZD1694 (raltitrexed, << Tomudex >>) and AG337 (Thymitag) are more specific and potent [[ TS ]] inhibitors.


While fluoropyrimidine antimetabolites have other sites of action, antifolates ZD1694 (raltitrexed, Tomudex) and << AG337 >> (Thymitag) are more specific and potent [[ TS ]] inhibitors.


While fluoropyrimidine antimetabolites have other sites of action, antifolates ZD1694 (raltitrexed, Tomudex) and AG337 (<< Thymitag >>) are more specific and potent [[ TS ]] inhibitors.


The availability of the 5-FU prodrugs offers the possibility of greater therapeutic selectivity based on the demonstration that << thymidine phosphorylase >>, the activating enzyme for [[ 5-FU ]], is expressed at a higher level in tumor tissue compared with normal tissue counterparts.


<< Orlistat >> is an inhibitor of [[ pancreatic lipase ]] which is able to block the absorption of 30% of ingested fat.


<< Troglitazone >>, bosentan and glibenclamide inhibit the [[ bile salt export pump ]] (Bsep) which transports taurocholate into bile.


<< Troglitazone >>, bosentan and glibenclamide inhibit the bile salt export pump ([[ Bsep ]]) which transports taurocholate into bile.


Troglitazone, << bosentan >> and glibenclamide inhibit the [[ bile salt export pump ]] (Bsep) which transports taurocholate into bile.


Troglitazone, << bosentan >> and glibenclamide inhibit the bile salt export pump ([[ Bsep ]]) which transports taurocholate into bile.


Troglitazone, bosentan and << glibenclamide >> inhibit the [[ bile salt export pump ]] (Bsep) which transports taurocholate into bile.


Troglitazone, bosentan and << glibenclamide >> inhibit the bile salt export pump ([[ Bsep ]]) which transports taurocholate into bile.


Troglitazone, bosentan and glibenclamide inhibit the << bile salt export pump >> (Bsep) which transports [[ taurocholate ]] into bile.


Troglitazone, bosentan and glibenclamide inhibit the bile salt export pump (<< Bsep >>) which transports [[ taurocholate ]] into bile.


The discovery of a second isoform of cyclooxygenase (COX) led to the search for compounds that could selectively inhibit COX-2 in humans while sparing << prostaglandin >> formation from [[ COX-1 ]].


We report here the pharmacological properties of a third selective << COX-2 >> inhibitor, [[ valdecoxib ]], which is the most potent and in vitro selective of the marketed COX-2 inhibitors that we have studied.


We report here the pharmacological properties of a third selective COX-2 inhibitor, << valdecoxib >>, which is the most potent and in vitro selective of the marketed [[ COX-2 ]] inhibitors that we have studied.


<< Valdecoxib >> potently inhibits recombinant [[ COX-2 ]], with an IC(50) of 0.005 microM; this compares with IC values of 0.05 microM for celecoxib, 0.5 microM for rofecoxib, and 5 microM for etoricoxib.


Valdecoxib potently inhibits recombinant << COX-2 >>, with an IC(50) of 0.005 microM; this compares with IC values of 0.05 microM for [[ celecoxib ]], 0.5 microM for rofecoxib, and 5 microM for etoricoxib.


Valdecoxib potently inhibits recombinant << COX-2 >>, with an IC(50) of 0.005 microM; this compares with IC values of 0.05 microM for celecoxib, 0.5 microM for [[ rofecoxib ]], and 5 microM for etoricoxib.


Valdecoxib potently inhibits recombinant << COX-2 >>, with an IC(50) of 0.005 microM; this compares with IC values of 0.05 microM for celecoxib, 0.5 microM for rofecoxib, and 5 microM for [[ etoricoxib ]].


Unique binding interactions of << valdecoxib >> with COX-2 translate into a fast rate of inactivation of [[ COX-2 ]] (110,000 M/s compared with 7000 M/s for rofecoxib and 80 M/s for etoricoxib).


<< Valdecoxib >> inhibits [[ COX-1 ]] in a competitive fashion only at very high concentrations (IC(50) = 150 microM).


<< Valdecoxib >> showed similar activity in the [[ human whole-blood COX ]] assay (COX-2 IC(50) = 0.24 microM; COX-1 IC(50) = 21.9 microM).


<< Valdecoxib >> showed similar activity in the human whole-blood COX assay ([[ COX-2 ]] IC(50) = 0.24 microM; COX-1 IC(50) = 21.9 microM).


<< Valdecoxib >> showed similar activity in the human whole-blood COX assay (COX-2 IC(50) = 0.24 microM; [[ COX-1 ]] IC(50) = 21.9 microM).


An angiotensin II AT1 receptor antagonist, << telmisartan >> augments glucose uptake and [[ GLUT4 ]] protein expression in 3T3-L1 adipocytes.


An << angiotensin II AT1 receptor >> antagonist, [[ telmisartan ]] augments glucose uptake and GLUT4 protein expression in 3T3-L1 adipocytes.


An angiotensin II AT1 receptor antagonist, telmisartan augments << glucose >> uptake and [[ GLUT4 ]] protein expression in 3T3-L1 adipocytes.


Treatment of both differentiating adipocytes and fully differentiated adipocytes with << telmisartan >> caused a dose-dependent increase in mRNA levels for [[ PPARgamma ]] target genes such as aP2 and adiponectin.


Treatment of both differentiating adipocytes and fully differentiated adipocytes with << telmisartan >> caused a dose-dependent increase in mRNA levels for PPARgamma target genes such as [[ aP2 ]] and adiponectin.


Treatment of both differentiating adipocytes and fully differentiated adipocytes with << telmisartan >> caused a dose-dependent increase in mRNA levels for PPARgamma target genes such as aP2 and [[ adiponectin ]].


By contrast, << telmisartan >> attenuated [[ 11beta-hydroxysteroid dehydrogenase type 1 ]] mRNA level in differentiated adipocytes.


Of note, we demonstrated for the first time that << telmisartan >> augmented [[ GLUT4 ]] protein expression and 2-deoxy glucose uptake both in basal and insulin-stimulated state of adipocytes, which may contribute, at least partly, to its insulin-sensitizing ability.


Of note, we demonstrated for the first time that telmisartan augmented << GLUT4 >> protein expression and [[ 2-deoxy glucose ]] uptake both in basal and insulin-stimulated state of adipocytes, which may contribute, at least partly, to its insulin-sensitizing ability.


Especially, the compound 1 showed strong inhibition (IC50=1.33 microM) against the enzyme << tyrosinase >>, as compared to the standard tyrosinase inhibitors [[ kojic acid ]] (IC50=16.67 microM) and L-mimosine (IC50=3.68 microM), indicating its potential used for the treatment of hyperpigmentation associated with the high production of melanocytes.


Especially, the compound 1 showed strong inhibition (IC50=1.33 microM) against the enzyme << tyrosinase >>, as compared to the standard tyrosinase inhibitors kojic acid (IC50=16.67 microM) and [[ L-mimosine ]] (IC50=3.68 microM), indicating its potential used for the treatment of hyperpigmentation associated with the high production of melanocytes.


Oxytocin antagonist (OTA), << TT-235 >>, was developed by our group and shown to inhibit either spontaneous or [[ oxytocin ]]-induced uterine contractions in primates.


<< Oxytocin >> antagonist (OTA), [[ TT-235 ]], was developed by our group and shown to inhibit either spontaneous or oxytocin-induced uterine contractions in primates.


The purpose of the present study was to confirm the duration of << TT-235 >> to block [[ oxytocin ]]-induced uterine contractions in estrous rats.


In Experiment 1, << Antag I >>, Antag II and TT-235 inhibited the integrated uterine response to [[ oxytocin ]] at 5 minutes by 76%, 77% and 80%, respectively, compared to controls (p<0.05).


In Experiment 1, Antag I, << Antag II >> and TT-235 inhibited the integrated uterine response to [[ oxytocin ]] at 5 minutes by 76%, 77% and 80%, respectively, compared to controls (p<0.05).


In Experiment 1, Antag I, Antag II and << TT-235 >> inhibited the integrated uterine response to [[ oxytocin ]] at 5 minutes by 76%, 77% and 80%, respectively, compared to controls (p<0.05).


In Experiment 2, << TT-235 >> induced a significant decrease (p<0.05) in [[ oxytocin receptor ]] number and binding affinity at both 0.5 and 4 hours compared with controls.


In conclusion, << TT-235 >> may inhibit the uterine response to oxytocin by decreasing [[ oxytocin receptor ]] numbers and oxytocin binding affinity, which might explain the prolonged oxytocin antagonist activity of TT-235.


In conclusion, << TT-235 >> may inhibit the uterine response to [[ oxytocin ]] by decreasing oxytocin receptor numbers and oxytocin binding affinity, which might explain the prolonged oxytocin antagonist activity of TT-235.


In conclusion, TT-235 may inhibit the uterine response to oxytocin by decreasing oxytocin receptor numbers and oxytocin binding affinity, which might explain the prolonged << oxytocin >> antagonist activity of [[ TT-235 ]].


Preclinical pharmacology of << lumiracoxib >>: a novel selective inhibitor of [[ cyclooxygenase-2 ]].


This manuscript presents the preclinical profile of << lumiracoxib >>, a novel [[ cyclooxygenase-2 ]] (COX-2) selective inhibitor.


This manuscript presents the preclinical profile of << lumiracoxib >>, a novel cyclooxygenase-2 ([[ COX-2 ]]) selective inhibitor.


<< Lumiracoxib >> inhibited purified [[ COX-1 ]] and COX-2 with K(i) values of 3 and 0.06 microM, respectively.


<< Lumiracoxib >> inhibited purified COX-1 and [[ COX-2 ]] with K(i) values of 3 and 0.06 microM, respectively.


In cellular assays, << lumiracoxib >> had an IC(50) of 0.14 microM in [[ COX-2 ]]-expressing dermal fibroblasts, but caused no inhibition of COX-1 at concentrations up to 30 microM (HEK 293 cells transfected with human COX-1).


In a human whole blood assay, IC(50) values for << lumiracoxib >> were 0.13 microM for [[ COX-2 ]] and 67 microM for COX-1 (COX-1/COX-2 selectivity ratio 515).


In a human whole blood assay, IC(50) values for << lumiracoxib >> were 0.13 microM for COX-2 and 67 microM for [[ COX-1 ]] (COX-1/COX-2 selectivity ratio 515).


In a human whole blood assay, IC(50) values for << lumiracoxib >> were 0.13 microM for COX-2 and 67 microM for COX-1 ([[ COX-1 ]]/COX-2 selectivity ratio 515).


In a human whole blood assay, IC(50) values for << lumiracoxib >> were 0.13 microM for COX-2 and 67 microM for COX-1 (COX-1/[[ COX-2 ]] selectivity ratio 515).


Ex vivo, << lumiracoxib >> inhibited [[ COX-1 ]]-derived thromboxane B(2) (TxB(2)) generation with an ID(50) of 33 mg kg(-1), whereas COX-2-derived production of prostaglandin E(2) (PGE(2)) in the lipopolysaccharide-stimulated rat air pouch was inhibited with an ID(50) value of 0.24 mg kg(-1).


Ex vivo, lumiracoxib inhibited << COX-1 >>-derived [[ thromboxane B(2) ]] (TxB(2)) generation with an ID(50) of 33 mg kg(-1), whereas COX-2-derived production of prostaglandin E(2) (PGE(2)) in the lipopolysaccharide-stimulated rat air pouch was inhibited with an ID(50) value of 0.24 mg kg(-1).


Ex vivo, lumiracoxib inhibited << COX-1 >>-derived thromboxane B(2) ([[ TxB(2) ]]) generation with an ID(50) of 33 mg kg(-1), whereas COX-2-derived production of prostaglandin E(2) (PGE(2)) in the lipopolysaccharide-stimulated rat air pouch was inhibited with an ID(50) value of 0.24 mg kg(-1).


Ex vivo, lumiracoxib inhibited COX-1-derived thromboxane B(2) (TxB(2)) generation with an ID(50) of 33 mg kg(-1), whereas << COX-2 >>-derived production of [[ prostaglandin E(2) ]] (PGE(2)) in the lipopolysaccharide-stimulated rat air pouch was inhibited with an ID(50) value of 0.24 mg kg(-1).


Ex vivo, lumiracoxib inhibited COX-1-derived thromboxane B(2) (TxB(2)) generation with an ID(50) of 33 mg kg(-1), whereas << COX-2 >>-derived production of prostaglandin E(2) ([[ PGE(2) ]]) in the lipopolysaccharide-stimulated rat air pouch was inhibited with an ID(50) value of 0.24 mg kg(-1).


However, consistent with its low << COX-1 >> inhibitory activity, [[ lumiracoxib ]] at a dose of 100 mg kg(-1) orally caused no ulcers and was significantly less ulcerogenic than diclofenac (P<0.05).


However, consistent with its low << COX-1 >> inhibitory activity, lumiracoxib at a dose of 100 mg kg(-1) orally caused no ulcers and was significantly less ulcerogenic than [[ diclofenac ]] (P<0.05).


<< Lumiracoxib >> is a highly selective [[ COX-2 ]] inhibitor with anti-inflammatory, analgesic and antipyretic activities comparable with diclofenac, the reference NSAID, but with much improved gastrointestinal safety.


Lumiracoxib is a highly selective << COX-2 >> inhibitor with anti-inflammatory, analgesic and antipyretic activities comparable with [[ diclofenac ]], the reference NSAID, but with much improved gastrointestinal safety.


As << thiamine >> metabolism deficiencies have been seen in placental infarcts previously, these indicate that [[ PP20 ]]/hTPK may have a role in placental diseases.


As << thiamine >> metabolism deficiencies have been seen in placental infarcts previously, these indicate that PP20/[[ hTPK ]] may have a role in placental diseases.


Safety and tolerability of << denufosol tetrasodium >> inhalation solution, a novel [[ P2Y2 receptor ]] agonist: results of a phase 1/phase 2 multicenter study in mild to moderate cystic fibrosis.


<< Denufosol tetrasodium >> (INS37217) is a selective [[ P2Y(2) ]] agonist that stimulates ciliary beat frequency and Cl(-) secretion in normal and cystic fibrosis (CF) airway epithelia, and is being investigated as an inhaled treatment for CF.


Denufosol tetrasodium (<< INS37217 >>) is a selective [[ P2Y(2) ]] agonist that stimulates ciliary beat frequency and Cl(-) secretion in normal and cystic fibrosis (CF) airway epithelia, and is being investigated as an inhaled treatment for CF.


The << Cl(-) >> secretory response is mediated via a non-[[ CFTR ]] pathway, and the driving force for Cl(-) secretion is enhanced by the effect of P2Y(2) activation to also inhibit epithelial Na(+) transport.


<< Denufosol >> is metabolically more stable and better tolerated, and may enhance mucociliary clearance for a longer period of time than previously investigated [[ P2Y(2) ]] agonists.


The dextromethorphan analog << dimemorfan >> attenuates kainate-induced seizures via [[ sigma1 receptor ]] activation: comparison with the effects of dextromethorphan.


The << dextromethorphan >> analog dimemorfan attenuates kainate-induced seizures via [[ sigma1 receptor ]] activation: comparison with the effects of dextromethorphan.


Dimemorfan pre-treatment also attenuated the << KA >>-induced increases in c-fos/c-jun expression, [[ activator protein (AP)-1 ]] DNA-binding activity, and loss of cells in the CA1 and CA3 fields of the hippocampus.


Dimemorfan pre-treatment also attenuated the << KA >>-induced increases in [[ c-fos ]]/c-jun expression, activator protein (AP)-1 DNA-binding activity, and loss of cells in the CA1 and CA3 fields of the hippocampus.


Dimemorfan pre-treatment also attenuated the << KA >>-induced increases in c-fos/[[ c-jun ]] expression, activator protein (AP)-1 DNA-binding activity, and loss of cells in the CA1 and CA3 fields of the hippocampus.


<< Dimemorfan >> pre-treatment also attenuated the KA-induced increases in [[ c-fos ]]/c-jun expression, activator protein (AP)-1 DNA-binding activity, and loss of cells in the CA1 and CA3 fields of the hippocampus.


<< Dimemorfan >> pre-treatment also attenuated the KA-induced increases in c-fos/[[ c-jun ]] expression, activator protein (AP)-1 DNA-binding activity, and loss of cells in the CA1 and CA3 fields of the hippocampus.


<< Dimemorfan >> pre-treatment also attenuated the KA-induced increases in c-fos/c-jun expression, [[ activator protein (AP)-1 ]] DNA-binding activity, and loss of cells in the CA1 and CA3 fields of the hippocampus.


The anticonvulsant action of dextromethorphan or dimemorfan was significantly counteracted by a selective << sigma1 receptor >> antagonist [[ BD 1047 ]], suggesting that the anticonvulsant action of dextromethorphan or dimemorfan is, at least in part, related to sigma1 receptor-activated modulation of AP-1 transcription factors.


Binding domains of the oxytocin receptor for the selective << oxytocin receptor >> antagonist barusiban in comparison to the agonists [[ oxytocin ]] and carbetocin.


Binding domains of the oxytocin receptor for the selective << oxytocin receptor >> antagonist barusiban in comparison to the agonists oxytocin and [[ carbetocin ]].


Binding domains of the oxytocin receptor for the selective << oxytocin receptor >> antagonist [[ barusiban ]] in comparison to the agonists oxytocin and carbetocin.


We have analyzed binding domains of the oxytocin receptor for barusiban, a highly selective oxytocin receptor antagonist, in comparison to the combined << vasopressin V1A/oxytocin receptor >> antagonist atosiban and the agonists [[ oxytocin ]] and carbetocin.


We have analyzed binding domains of the oxytocin receptor for barusiban, a highly selective oxytocin receptor antagonist, in comparison to the combined << vasopressin V1A/oxytocin receptor >> antagonist atosiban and the agonists oxytocin and [[ carbetocin ]].


We have analyzed binding domains of the oxytocin receptor for barusiban, a highly selective oxytocin receptor antagonist, in comparison to the combined << vasopressin V1A/oxytocin receptor >> antagonist [[ atosiban ]] and the agonists oxytocin and carbetocin.


We have analyzed binding domains of the oxytocin receptor for << barusiban >>, a highly selective [[ oxytocin receptor ]] antagonist, in comparison to the combined vasopressin V1A/oxytocin receptor antagonist atosiban and the agonists oxytocin and carbetocin.


For the << vasopressin V1A/oxytocin receptor >> antagonist [[ atosiban ]], none of the receptor constructs were able to provide a binding with higher affinity than the starting vasopressin V2 receptor.


The binding domain of barusiban differs from the binding domain of the agonists and the nonselective << oxytocin receptor >> antagonist [[ d(CH2)5[Tyr-(Me)2,Thr4,Orn8,Tyr9]vasotocin ]] that has been used in previous studies.


The compounds << 5'-azacytidine >> (AZC) and procainamide (PCA) belong to inhibitors of [[ DNMT1 ]], whose low activity correlates with increase in transcription of various genes.


The compounds 5'-azacytidine (<< AZC >>) and procainamide (PCA) belong to inhibitors of [[ DNMT1 ]], whose low activity correlates with increase in transcription of various genes.


The compounds 5'-azacytidine (AZC) and << procainamide >> (PCA) belong to inhibitors of [[ DNMT1 ]], whose low activity correlates with increase in transcription of various genes.


The compounds 5'-azacytidine (AZC) and procainamide (<< PCA >>) belong to inhibitors of [[ DNMT1 ]], whose low activity correlates with increase in transcription of various genes.


However, the flowcytometric analysis revealed that << AZC >> and PCA decreased intracellular contents of [[ CD3-zeta chain ]] in these cells in dose dependent manner.


However, the flowcytometric analysis revealed that AZC and << PCA >> decreased intracellular contents of [[ CD3-zeta chain ]] in these cells in dose dependent manner.


Clinical studies in cancer patients treated with the new << fluoropyrimidine >> analogue capecitabine (N4-pentoxycarbonyl-5'-5-fluorocytidine) have shown that plasma 2'-deoxyuridine was significantly elevated after 1 week of treatment, consistent with inhibition of [[ thymidylate synthase ]] (TS).


Clinical studies in cancer patients treated with the new << fluoropyrimidine >> analogue capecitabine (N4-pentoxycarbonyl-5'-5-fluorocytidine) have shown that plasma 2'-deoxyuridine was significantly elevated after 1 week of treatment, consistent with inhibition of thymidylate synthase ([[ TS ]]).


Clinical studies in cancer patients treated with the new fluoropyrimidine analogue << capecitabine >> (N4-pentoxycarbonyl-5'-5-fluorocytidine) have shown that plasma 2'-deoxyuridine was significantly elevated after 1 week of treatment, consistent with inhibition of [[ thymidylate synthase ]] (TS).


Clinical studies in cancer patients treated with the new fluoropyrimidine analogue << capecitabine >> (N4-pentoxycarbonyl-5'-5-fluorocytidine) have shown that plasma 2'-deoxyuridine was significantly elevated after 1 week of treatment, consistent with inhibition of thymidylate synthase ([[ TS ]]).


Clinical studies in cancer patients treated with the new fluoropyrimidine analogue capecitabine (<< N4-pentoxycarbonyl-5'-5-fluorocytidine >>) have shown that plasma 2'-deoxyuridine was significantly elevated after 1 week of treatment, consistent with inhibition of [[ thymidylate synthase ]] (TS).


Clinical studies in cancer patients treated with the new fluoropyrimidine analogue capecitabine (<< N4-pentoxycarbonyl-5'-5-fluorocytidine >>) have shown that plasma 2'-deoxyuridine was significantly elevated after 1 week of treatment, consistent with inhibition of thymidylate synthase ([[ TS ]]).


Clinical studies in cancer patients treated with the new fluoropyrimidine analogue capecitabine (N4-pentoxycarbonyl-5'-5-fluorocytidine) have shown that plasma << 2'-deoxyuridine >> was significantly elevated after 1 week of treatment, consistent with inhibition of [[ thymidylate synthase ]] (TS).


Clinical studies in cancer patients treated with the new fluoropyrimidine analogue capecitabine (N4-pentoxycarbonyl-5'-5-fluorocytidine) have shown that plasma << 2'-deoxyuridine >> was significantly elevated after 1 week of treatment, consistent with inhibition of thymidylate synthase ([[ TS ]]).


These findings suggest that the mechanism of antiproliferative toxicity of capecitabine is at least partly due to << TS >> inhibitory activity of its active metabolite 5-fluoro-2'-deoxyuridine monophosphate ([[ FdUMP ]]).


These findings suggest that the mechanism of antiproliferative toxicity of << capecitabine >> is at least partly due to [[ TS ]] inhibitory activity of its active metabolite 5-fluoro-2'-deoxyuridine monophosphate (FdUMP).


These findings suggest that the mechanism of antiproliferative toxicity of capecitabine is at least partly due to << TS >> inhibitory activity of its active metabolite [[ 5-fluoro-2'-deoxyuridine monophosphate ]] (FdUMP).


Induction of heparin-binding EGF-like growth factor and activation of << EGF receptor >> in [[ imatinib mesylate ]]-treated squamous carcinoma cells.


<< Imatinib mesylate >> is a tyrosine kinase inhibitor of the ABL, platelet-derived growth factor receptor ([[ PDGFR ]]), and c-kit kinases.


<< Imatinib mesylate >> is a tyrosine kinase inhibitor of the ABL, platelet-derived growth factor receptor (PDGFR), and [[ c-kit ]] kinases.


<< Imatinib mesylate >> is a tyrosine kinase inhibitor of the ABL, platelet-derived growth factor receptor (PDGFR), and c-kit [[ kinases ]].


<< Imatinib mesylate >> is a [[ tyrosine kinase ]] inhibitor of the ABL, platelet-derived growth factor receptor (PDGFR), and c-kit kinases.


<< Imatinib mesylate >> is a tyrosine kinase inhibitor of the [[ ABL ]], platelet-derived growth factor receptor (PDGFR), and c-kit kinases.


<< Imatinib mesylate >> is a tyrosine kinase inhibitor of the ABL, [[ platelet-derived growth factor receptor ]] (PDGFR), and c-kit kinases.


Treatment of head and neck squamous carcinoma cells with clinically relevant concentrations of << imatinib >>-induced changes in cell morphology and growth similar to changes associated with [[ epidermal growth factor receptor ]] (EGFR) activation.


Treatment of head and neck squamous carcinoma cells with clinically relevant concentrations of << imatinib >>-induced changes in cell morphology and growth similar to changes associated with epidermal growth factor receptor ([[ EGFR ]]) activation.


<< Imatinib >>-induced changes were blocked with the EGFR antagonist cetuximab, which suggested direct involvement of [[ EGFR ]] in this process.


Western blot analysis of cells incubated with << imatinib >> demonstrated activation of [[ EGFR ]] and downstream signaling that was reduced by inhibition of mitogen-activated protein/extracellular signal-regulated kinase kinase 1 (MEK1) and EGFR, but not Her2/ErbB2.


Inhibitors and neutralizing antibodies against heparin-binding epidermal growth factor-like growth factor (HB-EGF), and to a lesser extent transforming growth factor-alpha, reduced << imatinib >>-mediated [[ mitogen activated protein kinase ]] (MAPK) activation.


Inhibitors and neutralizing antibodies against heparin-binding epidermal growth factor-like growth factor (HB-EGF), and to a lesser extent transforming growth factor-alpha, reduced << imatinib >>-mediated mitogen activated protein kinase ([[ MAPK ]]) activation.


<< Imatinib >> stimulated the rapid release of soluble HB-EGF and the subsequent induction of membrane-bound HB-EGF, which correlated with biphasic [[ MAPK ]] activation.


<< Imatinib >> stimulated the rapid release of soluble [[ HB-EGF ]] and the subsequent induction of membrane-bound HB-EGF, which correlated with biphasic MAPK activation.


<< Imatinib >> stimulated the rapid release of soluble HB-EGF and the subsequent induction of membrane-bound [[ HB-EGF ]], which correlated with biphasic MAPK activation.


Together, these results suggested that << imatinib >> affects EGFR activation and signaling pathways through rapid release and increased expression of endogenous [[ EGFR ]]-activating ligands.


Although, << imatinib >> primarily inhibits tyrosine kinases, it also stimulates the activity of [[ EGFR ]] tyrosine kinase in head and neck squamous tumors.


Although, << imatinib >> primarily inhibits tyrosine kinases, it also stimulates the activity of EGFR [[ tyrosine kinase ]] in head and neck squamous tumors.


Although, << imatinib >> primarily inhibits [[ tyrosine kinases ]], it also stimulates the activity of EGFR tyrosine kinase in head and neck squamous tumors.


The identity of the lung << beta-ADHs >> was further demonstrated by their characteristic pH-activity profiles for ethanol oxidation, Km values for NAD and ethanol, and inhibition by [[ 4-methylpyrazole ]] or 1,10-phenanthroline.


The identity of the lung << beta-ADHs >> was further demonstrated by their characteristic pH-activity profiles for ethanol oxidation, Km values for NAD and ethanol, and inhibition by 4-methylpyrazole or [[ 1,10-phenanthroline ]].


The identity of the lung << beta-ADHs >> was further demonstrated by their characteristic pH-activity profiles for [[ ethanol ]] oxidation, Km values for NAD and ethanol, and inhibition by 4-methylpyrazole or 1,10-phenanthroline.


The identity of the lung << beta-ADHs >> was further demonstrated by their characteristic pH-activity profiles for ethanol oxidation, Km values for NAD and [[ ethanol ]], and inhibition by 4-methylpyrazole or 1,10-phenanthroline.


These findings indicate that human pulmonary << ethanol >>-metabolizing activities differ significantly with respect to genetic polymorphism at both the [[ ADH2 ]] and the ALDH2 loci.


These findings indicate that human pulmonary << ethanol >>-metabolizing activities differ significantly with respect to genetic polymorphism at both the ADH2 and the [[ ALDH2 ]] loci.


The results suggest that individuals with high Vmax << beta 2-ADH >> and deficient in low-Km mitochondrial ALDH2, accounting for approximately 45% of the Chinese population, may end up with [[ acetaldehyde ]] accumulation during alcohol consumption, rendering them vulnerable to tissue injury caused by this highly reactive and toxic metabolite.


The results suggest that individuals with high Vmax beta 2-ADH and deficient in low-Km mitochondrial << ALDH2 >>, accounting for approximately 45% of the Chinese population, may end up with [[ acetaldehyde ]] accumulation during alcohol consumption, rendering them vulnerable to tissue injury caused by this highly reactive and toxic metabolite.


The results suggest that individuals with high Vmax << beta 2-ADH >> and deficient in low-Km mitochondrial ALDH2, accounting for approximately 45% of the Chinese population, may end up with acetaldehyde accumulation during [[ alcohol ]] consumption, rendering them vulnerable to tissue injury caused by this highly reactive and toxic metabolite.


The results suggest that individuals with high Vmax beta 2-ADH and deficient in low-Km mitochondrial << ALDH2 >>, accounting for approximately 45% of the Chinese population, may end up with acetaldehyde accumulation during [[ alcohol ]] consumption, rendering them vulnerable to tissue injury caused by this highly reactive and toxic metabolite.


<< Simvastatin >> induces [[ interleukin-18 ]] production in human peripheral blood mononuclear cells.


<< Simvastatin >>, an HMG-CoA reductase inhibitor with mild inhibition of LFA-1, induced the production of [[ interleukin (IL)-18 ]], tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma in human peripheral blood mononuclear cells (PBMC).


<< Simvastatin >>, an HMG-CoA reductase inhibitor with mild inhibition of LFA-1, induced the production of interleukin (IL)-18, [[ tumor necrosis factor (TNF)-alpha ]] and interferon (IFN)-gamma in human peripheral blood mononuclear cells (PBMC).


<< Simvastatin >>, an HMG-CoA reductase inhibitor with mild inhibition of LFA-1, induced the production of interleukin (IL)-18, tumor necrosis factor (TNF)-alpha and [[ interferon (IFN)-gamma ]] in human peripheral blood mononuclear cells (PBMC).


<< Simvastatin >>, an [[ HMG-CoA reductase ]] inhibitor with mild inhibition of LFA-1, induced the production of interleukin (IL)-18, tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma in human peripheral blood mononuclear cells (PBMC).


<< Simvastatin >>, an HMG-CoA reductase inhibitor with mild inhibition of [[ LFA-1 ]], induced the production of interleukin (IL)-18, tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma in human peripheral blood mononuclear cells (PBMC).


The IL-18 production is located upstream of the << cytokine >> cascade activated by [[ simvastatin ]].


The << IL-18 >> production is located upstream of the cytokine cascade activated by [[ simvastatin ]].


Moreover, << simvastatin >> concentration-dependently inhibited the expression of ICAM-1 and induced the expression of [[ CD40 ]] on monocytes.


Moreover, << simvastatin >> concentration-dependently inhibited the expression of [[ ICAM-1 ]] and induced the expression of CD40 on monocytes.


In the presence of IL-18, << simvastatin >> suppressed the expression of ICAM-1 and CD40 as well as the production of [[ IL-12 ]], TNF-alpha and IFN-gamma in PBMC, contributing to the anti-inflammatory effect of simvastatin.


In the presence of IL-18, << simvastatin >> suppressed the expression of ICAM-1 and CD40 as well as the production of IL-12, [[ TNF-alpha ]] and IFN-gamma in PBMC, contributing to the anti-inflammatory effect of simvastatin.


In the presence of IL-18, << simvastatin >> suppressed the expression of ICAM-1 and CD40 as well as the production of IL-12, TNF-alpha and [[ IFN-gamma ]] in PBMC, contributing to the anti-inflammatory effect of simvastatin.


In the presence of IL-18, << simvastatin >> suppressed the expression of [[ ICAM-1 ]] and CD40 as well as the production of IL-12, TNF-alpha and IFN-gamma in PBMC, contributing to the anti-inflammatory effect of simvastatin.


In the presence of IL-18, << simvastatin >> suppressed the expression of ICAM-1 and [[ CD40 ]] as well as the production of IL-12, TNF-alpha and IFN-gamma in PBMC, contributing to the anti-inflammatory effect of simvastatin.


The effects of simvastatin were abolished by the addition of the product of the << HMG-CoA reductase >>, [[ mevalonate ]], indicating the involvement of HMG-CoA reductase in the action of simvastatin.


<< COX-1 >> and COX-2 inhibition in horse blood by [[ phenylbutazone ]], flunixin, carprofen and meloxicam: an in vitro analysis.


COX-1 and << COX-2 >> inhibition in horse blood by [[ phenylbutazone ]], flunixin, carprofen and meloxicam: an in vitro analysis.


<< COX-1 >> and COX-2 inhibition in horse blood by phenylbutazone, [[ flunixin ]], carprofen and meloxicam: an in vitro analysis.


COX-1 and << COX-2 >> inhibition in horse blood by phenylbutazone, [[ flunixin ]], carprofen and meloxicam: an in vitro analysis.


<< COX-1 >> and COX-2 inhibition in horse blood by phenylbutazone, flunixin, [[ carprofen ]] and meloxicam: an in vitro analysis.


COX-1 and << COX-2 >> inhibition in horse blood by phenylbutazone, flunixin, [[ carprofen ]] and meloxicam: an in vitro analysis.


<< COX-1 >> and COX-2 inhibition in horse blood by phenylbutazone, flunixin, carprofen and [[ meloxicam ]]: an in vitro analysis.


COX-1 and << COX-2 >> inhibition in horse blood by phenylbutazone, flunixin, carprofen and [[ meloxicam ]]: an in vitro analysis.


We report on the inhibitory activity of the NSAIDs meloxicam, << carprofen >>, phenylbutazone and flunixin, on blood [[ cyclooxygenases ]] in the horse using in vitro enzyme-linked assays.


We report on the inhibitory activity of the NSAIDs meloxicam, carprofen, << phenylbutazone >> and flunixin, on blood [[ cyclooxygenases ]] in the horse using in vitro enzyme-linked assays.


We report on the inhibitory activity of the NSAIDs meloxicam, carprofen, phenylbutazone and << flunixin >>, on blood [[ cyclooxygenases ]] in the horse using in vitro enzyme-linked assays.


We report on the inhibitory activity of the NSAIDs << meloxicam >>, carprofen, phenylbutazone and flunixin, on blood [[ cyclooxygenases ]] in the horse using in vitro enzyme-linked assays.


As expected, comparison of IC50 indicated that << meloxicam >> and carprofen are more selective inhibitors of [[ COX-2 ]] than phenylbutazone and flunixin; meloxicam was the most advantageous for horses of four NSAIDs examined.


As expected, comparison of IC50 indicated that meloxicam and << carprofen >> are more selective inhibitors of [[ COX-2 ]] than phenylbutazone and flunixin; meloxicam was the most advantageous for horses of four NSAIDs examined.


As expected, comparison of IC50 indicated that meloxicam and carprofen are more selective inhibitors of << COX-2 >> than [[ phenylbutazone ]] and flunixin; meloxicam was the most advantageous for horses of four NSAIDs examined.


As expected, comparison of IC50 indicated that meloxicam and carprofen are more selective inhibitors of << COX-2 >> than phenylbutazone and [[ flunixin ]]; meloxicam was the most advantageous for horses of four NSAIDs examined.


However at IC80, phenylbutazone (+134.4%) and flunixin (+29.7%) had greater COX-2 selectivity than at IC50, and meloxicam (-41.2%) and << carprofen >> (-12.9%) had lower [[ COX-2 ]] selectivity than at IC50.


However at IC80, << phenylbutazone >> (+134.4%) and flunixin (+29.7%) had greater [[ COX-2 ]] selectivity than at IC50, and meloxicam (-41.2%) and carprofen (-12.9%) had lower COX-2 selectivity than at IC50.


However at IC80, phenylbutazone (+134.4%) and << flunixin >> (+29.7%) had greater [[ COX-2 ]] selectivity than at IC50, and meloxicam (-41.2%) and carprofen (-12.9%) had lower COX-2 selectivity than at IC50.


However at IC80, phenylbutazone (+134.4%) and flunixin (+29.7%) had greater COX-2 selectivity than at IC50, and << meloxicam >> (-41.2%) and carprofen (-12.9%) had lower [[ COX-2 ]] selectivity than at IC50.


<< Carvedilol >> prevents cardiac hypertrophy and overexpression of [[ hypoxia-inducible factor-1alpha ]] and vascular endothelial growth factor in pressure-overloaded rat heart.


<< Carvedilol >> prevents cardiac hypertrophy and overexpression of hypoxia-inducible factor-1alpha and [[ vascular endothelial growth factor ]] in pressure-overloaded rat heart.


Treatment with << carvedilol >> reversed both protein and mRNA of HIF-1alpha, VEGF, BNP, and [[ NGF-beta ]] to the baseline values.


Treatment with << carvedilol >> reversed both protein and mRNA of [[ HIF-1alpha ]], VEGF, BNP, and NGF-beta to the baseline values.


Treatment with << carvedilol >> reversed both protein and mRNA of HIF-1alpha, [[ VEGF ]], BNP, and NGF-beta to the baseline values.


Treatment with << carvedilol >> reversed both protein and mRNA of HIF-1alpha, VEGF, [[ BNP ]], and NGF-beta to the baseline values.


Increased immunohistochemical labeling of << HIF-1alpha >>, VEGF, and BNP in the ventricular myocardium was observed in the banding group and [[ carvedilol ]] again normalized the labeling.


Increased immunohistochemical labeling of HIF-1alpha, << VEGF >>, and BNP in the ventricular myocardium was observed in the banding group and [[ carvedilol ]] again normalized the labeling.


Increased immunohistochemical labeling of HIF-1alpha, VEGF, and << BNP >> in the ventricular myocardium was observed in the banding group and [[ carvedilol ]] again normalized the labeling.


Treatment with << carvedilol >> is associated with a reversal of abnormal regulation of [[ HIF-1alpha ]], VEGF, BNP, and NGF-beta in the hypertrophic myocardium.


Treatment with << carvedilol >> is associated with a reversal of abnormal regulation of HIF-1alpha, [[ VEGF ]], BNP, and NGF-beta in the hypertrophic myocardium.


Treatment with << carvedilol >> is associated with a reversal of abnormal regulation of HIF-1alpha, VEGF, [[ BNP ]], and NGF-beta in the hypertrophic myocardium.


<< Imatinib >> (STI571, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of [[ KIT ]], ABL, BCR-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.


<< Imatinib >> (STI571, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, [[ ABL ]], BCR-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.


<< Imatinib >> (STI571, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, [[ BCR ]]-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.


<< Imatinib >> (STI571, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-[[ ABL ]], PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.


<< Imatinib >> (STI571, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-ABL, [[ PDGFRA ]], and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.


<< Imatinib >> (STI571, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-ABL, PDGFRA, and [[ PDGFRB, ]] represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.


Imatinib (<< STI571 >>, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of [[ KIT ]], ABL, BCR-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.


Imatinib (<< STI571 >>, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, [[ ABL ]], BCR-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.


Imatinib (<< STI571 >>, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, [[ BCR ]]-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.


Imatinib (<< STI571 >>, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-[[ ABL ]], PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.


Imatinib (<< STI571 >>, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-ABL, [[ PDGFRA ]], and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.


Imatinib (<< STI571 >>, Gleevec, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-ABL, PDGFRA, and [[ PDGFRB, ]] represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.


Imatinib (STI571, << Gleevec >>, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of [[ KIT ]], ABL, BCR-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.