2007
VEGF‐induced heme oxygenase‐1 confers cytoprotection from lethal hyperoxia in vivo
Siner JM, Jiang G, Cohen ZI, Shan P, Zhang X, Lee CG, Elias JA, Lee PJ. VEGF‐induced heme oxygenase‐1 confers cytoprotection from lethal hyperoxia in vivo. The FASEB Journal 2007, 21: 1422-1432. PMID: 17264168, DOI: 10.1096/fj.06-6661com.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBase SequenceBronchoalveolar Lavage FluidCytoprotectionDisease Models, AnimalDNA PrimersEnzyme InductionHeme Oxygenase (Decyclizing)HumansHyperoxiaIn Situ Nick-End LabelingLipid PeroxidationLungMiceMice, TransgenicRespiratory Distress SyndromeReverse Transcriptase Polymerase Chain ReactionRNA, Small InterferingVascular Endothelial Growth Factor AConceptsHyperoxic acute lung injuryVascular endothelial growth factorAcute lung injuryHeme oxygenase-1Lung injuryTransgenic miceVivo modelLung lavage protein concentrationVEGF transgenic miceLavage protein concentrationEndothelial growth factorHO-1 mRNAHO-1 functionEffect of inhibitionShort hairpin RNAProlong survivalDry ratioProtective effectLethal hyperoxiaHyperoxia resultsOxygenase-1Mouse lungTUNEL stainingCytoprotective effectsInjury
2006
A Role for MAP Kinase Signaling in Behavioral Models of Depression and Antidepressant Treatment
Duman CH, Schlesinger L, Kodama M, Russell DS, Duman RS. A Role for MAP Kinase Signaling in Behavioral Models of Depression and Antidepressant Treatment. Biological Psychiatry 2006, 61: 661-670. PMID: 16945347, DOI: 10.1016/j.biopsych.2006.05.047.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAniline CompoundsAnimalsAntidepressive AgentsBehavior, AnimalBenzamidesBrain-Derived Neurotrophic FactorDepressionDisease Models, AnimalDose-Response Relationship, DrugDrug InteractionsEnzyme InhibitorsHelplessness, LearnedHindlimb SuspensionMaleMiceMice, Inbred C57BLMice, KnockoutMitogen-Activated Protein Kinase KinasesMotor ActivitySignal TransductionSwimmingConceptsBrain-derived neurotrophic factorAntidepressant-like effectsAntidepressant treatmentSwim testBDNF heterozygous knockout miceDepressive-like behaviorDepressive-like phenotypeTail suspension testEffects of desipramineHeterozygous knockout miceDepressive behavioral phenotypeEffect of inhibitionRodent behavioral modelsMouse behavioral modelsHeterozygous gene deletionAntidepressant mechanismAcute administrationAcute blockadeNeurotrophic factorAntidepressant drugsSuspension testDepressive phenotypeKnockout miceMEK inhibitionMEK inhibitors
2005
Regression of Existing Glomerulosclerosis by Inhibition of Aldosterone
Aldigier JC, Kanjanbuch T, Ma LJ, Brown NJ, Fogo AB. Regression of Existing Glomerulosclerosis by Inhibition of Aldosterone. Journal Of The American Society Of Nephrology 2005, 16: 3306-3314. PMID: 16192423, DOI: 10.1681/asn.2004090804.Peer-Reviewed Original ResearchConceptsInhibition of aldosteroneAngiotensin type 1 receptor antagonistType 1 receptor antagonistAdult male Sprague-DawleySeverity of glomerulosclerosisDevelopment of glomerulosclerosisMale Sprague-DawleyEffect of inhibitionCONT ratsGlomerulosclerosis indexSerum creatinineSystolic BPAntihypertensive drugsReceptor antagonistSprague-DawleySP ratsGlomerulosclerosisSpironolactoneSame ratsRatsSP groupAldosteroneFurther treatmentWkInhibition
2001
Ca2+ mediates the effect of inhibition of Na+-K+-ATPase on the basolateral K+ channels in the rat CCD
Wei Y, Lu M, Wang W. Ca2+ mediates the effect of inhibition of Na+-K+-ATPase on the basolateral K+ channels in the rat CCD. American Journal Of Physiology - Cell Physiology 2001, 280: c920-c928. PMID: 11245609, DOI: 10.1152/ajpcell.2001.280.4.c920.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBenzylaminesBiological TransportCalciumCalcium-Calmodulin-Dependent Protein KinasesDose-Response Relationship, DrugEnzyme InhibitorsFemaleIon Channel GatingIonomycinIonophoresKidney Tubules, CollectingMaleMembrane PotentialsNaphthalenesNG-Nitroarginine Methyl EsterNitratesPotassium ChannelsProtein Kinase CRatsRats, Sprague-DawleySodium-Potassium-Exchanging ATPaseSpecific Pathogen-Free OrganismsStrophanthidinSulfonamidesSuperoxidesConceptsNitro-L-arginine methyl esterIntracellular Ca2Inhibitory effectNM Ca2Nitric oxideChannel activityEffects of strophanthidinKN-93KN-62Protein kinase CCalphostin CEffect of inhibitionCalmodulin-dependent kinase IICell-attached patchesExtracellular Ca2Rat CCDKinase CMicroM ionomycinRat kidneyMechanism of Ca2High concentrationsStrophanthidinCa2Methyl esterKinase II
1999
Effects of Hypoxia-Ischemia and Inhibition of Nitric Oxide Synthase on Cerebral Energy Metabolism in Newborn Piglets
Groenendaal F, De Graaf R, Van Vliet G, Nicolay K. Effects of Hypoxia-Ischemia and Inhibition of Nitric Oxide Synthase on Cerebral Energy Metabolism in Newborn Piglets. Pediatric Research 1999, 45: 827-833. PMID: 10367773, DOI: 10.1203/00006450-199906000-00008.Peer-Reviewed Original ResearchConceptsNitric oxide synthaseCerebral energy metabolismHypoxia-ischemiaCerebral hypoxia-ischemiaN-acetylaspartate ratiosOxide synthaseBaseline valuesNewborn pigletsInorganic phosphate ratioHypoxia groupCerebral energy statusEnergy metabolismSaline 1 hEffect of inhibitionBilateral occlusionNω-nitroCarotid arteryAcetylaspartate ratioL-arginineOld pigletsPhosphate ratioBaseline periodReperfusionNNLAPiglets
1993
Mechanism of apical K+ channel modulation in principal renal tubule cells. Effect of inhibition of basolateral Na(+)-K(+)-ATPase.
Wang W, Geibel J, Giebisch G. Mechanism of apical K+ channel modulation in principal renal tubule cells. Effect of inhibition of basolateral Na(+)-K(+)-ATPase. Journal Of General Physiology 1993, 101: 673-694. PMID: 8393065, PMCID: PMC2216783, DOI: 10.1085/jgp.101.5.673.Peer-Reviewed Original ResearchConceptsEffect of inhibitionPump inhibitionInhibitory effectChannel activityProtein kinase CPump activityAddition of strophanthidinPatch-clamp techniqueRenal tubule cellsBath solutionCell-attached patchesExtracellular Ca2Removal of Ca2Intracellular Ca2MicroM ionomycinTubule cellsControl valuesLow-conductance K channelsPrincipal cellsChannel modulationK channelsInhibitionNM staurosporineDependent protein kinase CPotent inhibitor
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