2014
Apolipoprotein E Induction in Syrian Hamster Testis Following Tributyltin Exposure: A Potential Mechanism of Male Infertility
Kanimozhi V, Palanivel K, Kadalmani B, Krikun G, Taylor HS. Apolipoprotein E Induction in Syrian Hamster Testis Following Tributyltin Exposure: A Potential Mechanism of Male Infertility. Reproductive Sciences 2014, 21: 1006-1014. PMID: 24516040, DOI: 10.1177/1933719114522519.Peer-Reviewed Original ResearchFollicle-stimulating hormone receptorMale Syrian hamstersSyrian hamstersSteroid hormone receptor expressionApoE messenger RNAAdult male Syrian hamstersSerum lipid profileHormone receptor expressionVehicle-treated controlsEstrogen receptor βDays of treatmentEstrogen receptor αSex steroid biosynthesisSex hormone synthesisReverse transcriptase-polymerase chain reaction analysisReal-time reverse transcriptase-polymerase chain reaction analysisPolymerase chain reaction analysisLipid profileAndrogen receptorReceptor expressionApoE expressionTestosterone levelsUntoward effectsApolipoprotein ESyrian hamster testis
2013
Tissue Selective Estrogen Complexes (TSECs) Differentially Modulate Markers of Proliferation and Differentiation in Endometrial Cells
Kulak J, Ferriani RA, Komm BS, Taylor HS. Tissue Selective Estrogen Complexes (TSECs) Differentially Modulate Markers of Proliferation and Differentiation in Endometrial Cells. Reproductive Sciences 2013, 20: 129-137. PMID: 23171676, PMCID: PMC3826278, DOI: 10.1177/1933719112463251.Peer-Reviewed Original ResearchConceptsTissue selective estrogen complexSelective estrogen receptor modulatorsLeukemia inhibitory factorProgesterone receptorBazedoxifene acetateEndometrial effectsEndometrial proliferationEstrogen complexEffects of raloxifeneRisk of estrogenVehicle-treated controlsEndometrial cell proliferationEstrogen receptor modulatorsEndometrial gene expressionMessenger RNA expressionDifferential effectsEndometrial safetyEstrogen-responsive genesEndometrial hyperplasiaLIF expressionPR expressionEndometrial cellsReceptor modulatorsMore estrogenIshikawa cells
2011
Macrophages Promote Cyst Growth in Polycystic Kidney Disease
Karihaloo A, Koraishy F, Huen SC, Lee Y, Merrick D, Caplan MJ, Somlo S, Cantley LG. Macrophages Promote Cyst Growth in Polycystic Kidney Disease. Journal Of The American Society Of Nephrology 2011, 22: 1809-1814. PMID: 21921140, PMCID: PMC3187181, DOI: 10.1681/asn.2011010084.Peer-Reviewed Original ResearchConceptsPolycystic kidney diseaseCyst-lining cellsKidney diseaseCyst growthPkd1-deficient cellsContribution of inflammationMacrophage-depleted miceVehicle-treated controlsPostnatal day 10Renal functionInflammatory componentIschemic injuryOrthologous modelCre miceCystic areasLiposomal clodronateCyst progressionRenal parenchymaCystic indexTubular cellsDay 10Therapeutic potentialDay 24Macrophage migrationMacrophagesReduced CGP12177 binding to cardiac β-adrenoceptors in hyperglycemic high-fat-diet-fed, streptozotocin-induced diabetic rats
Thackeray JT, Parsa-Nezhad M, Kenk M, Thorn SL, Kolajova M, Beanlands RS, DaSilva JN. Reduced CGP12177 binding to cardiac β-adrenoceptors in hyperglycemic high-fat-diet-fed, streptozotocin-induced diabetic rats. Nuclear Medicine And Biology 2011, 38: 1059-1066. PMID: 21831645, DOI: 10.1016/j.nucmedbio.2011.04.002.Peer-Reviewed Original ResearchMeSH KeywordsAdrenergic beta-AntagonistsAnimalsBiomarkersBlotting, WesternDiabetes Mellitus, ExperimentalDiet, High-FatGene Expression RegulationHyperglycemiaMaleMyocardiumPositron-Emission TomographyPropanolaminesProtein BindingRatsRats, Sprague-DawleyReceptors, Adrenergic, beta-1Receptors, Adrenergic, beta-2Substrate SpecificityConceptsAbnormal sympathetic nervous systemΒ-AR expressionSympathetic nervous systemDiabetic rat heartsSingle intraperitoneal injectionVehicle-treated controlsInfusion of isoproterenolCardiac β-adrenoceptorsΒ-AR subtypesΒ-AR antagonistsSpecific bindingHalf of ratsNormal Sprague-DawleyΒ-AR stimulationPositron emission tomographyΒ-adrenoceptor signalingCardiac bindingAR expressionCardiac dysfunctionDiabetic ratsInsulin resistanceSustained hyperglycemiaIntraperitoneal injectionΒ-adrenoceptorsDiet feeding
2001
9-cis-Retinoic acid represses transcription of the gonadotropin-releasing hormone (GnRH) gene via proximal promoter region that is distinct from all-trans-retinoic acid response element
Cho S, Chung J, Han J, Lee B, Kim H, Rhee K, Kim K. 9-cis-Retinoic acid represses transcription of the gonadotropin-releasing hormone (GnRH) gene via proximal promoter region that is distinct from all-trans-retinoic acid response element. Brain Research 2001, 87: 214-222. PMID: 11245924, DOI: 10.1016/s0169-328x(01)00020-1.Peer-Reviewed Original ResearchMeSH KeywordsAlitretinoinAnimalsAntineoplastic AgentsCells, CulturedDose-Response Relationship, DrugGene Expression RegulationGonadotropin-Releasing HormoneLigandsPromoter Regions, GeneticRatsReceptors, Retinoic AcidRetinoid X ReceptorsRNA, MessengerTranscription FactorsTranscription, GeneticTransfectionTretinoinConceptsGT1-1 cellsRat GnRH promoterPromoter-driven luciferase activityRetinoid X receptorTrans-RAGnRH expressionGnRH transcriptionLuciferase activityImmortalized GnRH neuronsRXR beta expressionGnRH promoterVehicle-treated controlsGnRH mRNA levelsGonadotropin-releasing hormone gene transcriptionGnRH gene expressionGonadotropin-releasing hormone (GnRH) geneTime-related mannerGnRH promoter activityTrans retinoic acidGnRH gene transcriptionTime-dependent mannerGnRH neuronsPresent studyBeta expressionResponse element
2000
Insulin-Like Growth Factor-1 Fails to Enhance Central Nervous System Myelin Repair during Autoimmune Demyelination
Cannella B, Pitt D, Capello E, Raine C. Insulin-Like Growth Factor-1 Fails to Enhance Central Nervous System Myelin Repair during Autoimmune Demyelination. American Journal Of Pathology 2000, 157: 933-943. PMID: 10980132, PMCID: PMC1885703, DOI: 10.1016/s0002-9440(10)64606-8.Peer-Reviewed Original ResearchConceptsInsulin-like growth factor-1Experimental autoimmune encephalomyelitisCentral nervous system tissueGrowth factor-1Nervous system tissueAcute phaseChronic phaseChronic time pointsTime pointsVehicle-treated groupIGF-1 administrationVehicle-treated controlsFactor 1Oligodendrocyte progenitor populationClinical ameliorationAutoimmune encephalomyelitisCytokine levelsDifferent time pointsTreatment regimenAutoimmune demyelinationMultiple sclerosisSJL miceMyelin regenerationMyelin repairTGF-beta2
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