简介：ＴＨＥＳＴＵＤＹＯＦＥＳＴＲＯＧＥＮＡＮＤＰＲＯＧＥＳＴＥＲＯＮＥＲＥＣＥＰＴＯＲＩＮＮＡＳＯＰＨＡＲＹＮＧＥＡＬＣＡＲＣＩＮＯＭＡＺｈｅｎｇＴｉａｎｒｏｎｇ郑天荣；ＬｉＪｉａｎｃｈｅｎｇ李建成；ＬｉｕＸｉｕｙｉｎｇ刘秀英；（Ｄｅｐａｒｔｍｅｎｔｏｆ...

简介：ObjectivesToinvestigatetheeffectsoftestosteroneenanthate(TE)onserumlipidsandlipoproteinsmetabolismandtheexpressionofandrogenreceptor(AR),estrogenreceptorbeta(ER-β)andplateletderivedgrowthfactorbeta(PDGFR-β)inaorticvascularsmoothmuscletissues(VSMTs).MethodsFortyagedmaleratswererandomlydividedinto4groups,groupA(placebogroup),groupB(2.5mg/kgintramuscularinjectionofTEonceaweek),groupC(5.0mg/kgintramuscularinjectionofTEonceaweek),groupD(10.0mg,/kgintramuscularinjectionofTEonceaweek).Allanimalswerefedfreelyduring16-weektreatmentperiods.TheexpressionofAR,ER-βandPDGFR-βwerestudiedbyWesternbolt.ResultsAverageserumLDL-CwasloweringroupDthanthatingroupA(p＜0.01).Comparedwiththeothergroups,averageserumTCwasalsoloweringroupD(p＜0.05).ARexpressioninaorticvascularsmoothmuscletissuescouldberegulatedbyTE:99.50±21.74,125.38±28.68and101.98±15.42forTEconcentrationsat2.5mg/kg,5.0mg/kgand10.0mg/kg,respectively,theexpressionofER-βcouldberegulatedbyTE:92.34±18.68,47.72±18.12,82.13±23.50,andtheexpressionofPDGFR-βcouldberegulatedaswellbyTE:219.70±45.59,50.16±9.72,125.36±15.74(DataforAR,ER-βandPDGFR-βproteinbandintensitywereexpressedwithx±s,withcontrolgrouptakenas100).ConclusionsThisstudyindicatesthatandrogenshavesignificanteffectsonserumlipidsandlipoproteinmetabolism.Testosteroneenanthateat5.0mg/kgcanstimulatetheexpressionofAR,butinhibitetheexpressionofPDGFR.Testosteroneenanthateattheconcentrationsof5.0mg/kgand10.0mg/kgcaninhibitetheexpressionofER-β.

简介：Objective:Despiteevidencethatestrogensandinsulinareinvolvedinthedevelopmentandprogressionofmanycancers,theirsynergisticroleinendometrialcarcinoma(EC)hasnotbeenanalyzedyet.Methods:Here,weinvestigatedhowestrogensactsynergisticallywithinsulintopromoteECprogression.Cellgrowthinvitroandinvivo,effectsofestradiolandinsulinonapoptosisandcellcycledistribution,andexpressionandactivationofestrogenreceptor(ER),insulinreceptor(InsR),andkeyproteinsinthePI3KandMAPKpathwayswereexaminedaftercombinedstimulationwithestradiolandinsulin.Results:ComparedtoECcellstreatedwithestradiolorinsulinalone,thosetreatedwithbothestradiolandinsulinexhibitedstrongerstimulation.EstradiolsignificantlyinducedphosphorylationofInsR-βandIRS-1,whereasinsulinsignificantlyinducedphosphorylationofER-α.Inaddition,treatmentwithbothinsulinandestradioltogethersignificantlyincreasedtheexpressionandphosphorylationofAkt,MAPK,andERK.Notably,InsR-βinhibitionhadalimitedeffectonestradiol-dependentproliferation,cellcycle,andapoptosis,whereasER-αinhibitionhadalimitedinsulin-dependenteffect,inECcelllines.InsulinandestradiolindividuallyandsynergisticallypromotedECxenograftgrowthinmice.Conclusions:EstrogenandinsulinplaysynergisticrolesinECcarcinogenesisandprogressionbyactivatingInsR-βandER-α,promotingacrosstalkbetweenthem,andtherebyresultingintheactivationofdownstreamPI3K/AktandMAPK/ERKsignalingpathways.

简介：AbstractObjective:Despite the fact that adenomyosis is a fairly common gynecological disorder, its pathogenesis remains elusive. Several theories on the pathogenesis of adenomyosis have been proposed, but none of them has been proven experimentally. So far, the most used one is the neonatal feeding of tamoxifen (TAM) in Institute of Cancer Research/cryopreserved (ICR/CD-1) mouse. However, its underlying mechanism of action is unknown. To further delineate the mechanism of TAM-induced adenomyosis in ICR/CD-1 mouse with regard to specific estrogen receptor (ER), we conducted an experiment that neonatal mice were fed with either TAM, or 4,4′,4″-(4-propyl-[1H]-pyrazole-1,3,5-triyl) trisphenol (PPT; an ERα agonist), or 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN; an ERβ agonist), or G-1 (a G-protein coupled receptor 30 agonist), or just vehicle, in an attempt to tease out which specific receptor plays a dominant role in the genesis of adenomyosis induced by neonatal feeding of TAM.Methods:Forty female neonatal mice were randomly divided into 5 equal-sized groups: CTL (control), TAM, PPT, DPN, and G-1. Three months later, all mice were sacrificed and their uterine horns were harvested, weighed, and processed for histological evaluation.Results:All mice in the TAM group developed adenomyosis, so did 4 mice (50%) in the DPN group, a result that should be considered significant given that mice in the CTL group would not develop adenomyosis. No mouse in the PPT or G-1 group developed adenomyosis. Remarkably, all lesions in the DPN group were seen exclusively near the uterine serosa, which are dramatically different from that of TAM mice and reminiscent of extrinsic or external adenomyosis in humans.Conclusions:Neonatal feeding of DPN induces adenomyosis, but the adenomyotic lesions appear to be different from those induced by TAM. Thus, the cause of TAM-induced adenomyosis in ICR/CD-1 mouse cannot be attributable to one specific ER alone. This suggests that the extrinsic/external adenomyosis may have a pathogenesis that is different from other sub-types of adenomyosis.

简介：Inthepresentstudyexpressionofestrogenreceptorsubtype-α(ERα)and-β(ERβ)inthecerebralcortex,cerebellum,andolfactorybulbwasinvestigatedandcomparedbetweenneonatal(1～3-days-old)andadult(250～350g)rats,usingreversetranscription-polymerasechainreaction(RT-PCR).NoERαtranscriptsweredetectableintheadultcerebellumandolfactorybulb,whereasveryweakexpressionofERαwaspresentintheadultcerebralcortex.NosignificantdifferenceinERβtranscriptswasdetectablebetweentheneonatalandadultrats.WhiletranscriptsforbothERsubtypeswereco-expressedinthesebrainareasofneonatalrats,althoughERαexpressionwassignificantlyweakerthanERβ.EveninthecerebralcortexknowntocontainbothERsubtypesinadultrats,ERαtranscriptsinneonatalratsweremuchhigherthaninadult.TheseobservationsprovideevidencefortheexistenceofdifferentexpressionpatternsofERα/ERβtranscriptsinthesethreebrainareasbetweentheneonatalandadultrats,suggestingthateachERsubtypemayplayadistinctroleintheregulationofdifferentiation,development,andfunctionsofthebrainbyestrogen.

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简介：Themonoclonalantibodyagainstbovinerotavirus(BRV)receptor(BRV-R-mAb)wasusedtoexplorethesimilaritybetweenthereceptorsofBRVandhumanrotavirus(HRV).ELISA,dotimmunobindingassay,cellprotectionassay,solid-phaseassayandimmunohistochemistrymethodwereapplied.BRV-R-mAbboundbothanti-BRVIgGandanti-HRVIgGrespectivelyandcouldprotectMA104cellsagainstBRVandHRVchallenges.Immunohistochemistrytestshowedthattherewererotavirusreceptorsonthesurfacesoffoetalintestinal,trachealmucosaandMA104cellsmembrane.WepurifiedtherotavirusreceptorsonMA104ceils,whichcouldbindbothBRVandHRVinvitro.ItisconcludedthatBRVreceptorandHRVreceptorarehomogenousproteinsandcanberecognizedbybothBRVandHRV.

简介：AbstractNormal pregnancy is associated with dramatically increased estrogen biosynthesis whose role is believed to raise uterine blood flow to facilitate the bi-directional maternal-fetal exchanges of gases (O2 and CO2), to deliver nutrients, and exhaust wastes to support fetal development and survival. Constrained uterine blood flow in pregnancy is a leading cause of preeclampsia with fetal growth restriction, rendering investigations of uterine hemodynamics to hold a high promise to inform pathways as targets for therapeutic interventions for preeclampsia. The mechanisms of estrogen-induced uterine vasodilation in pregnancy have long been attributed to enhanced endothelium production of nitric oxide, but clinical trials targeting this pathway that dominates uterine hemodynamics have achieved no to little success. Emerging evidence has recently shown a novel proangiogenic vasodilatory role of hydrogen sulfide in regulating uterine hemodynamics in pregnancy and preeclampsia, provoking a new field of perinatal research in searching for alternative pathways for pregnancy disorders especially preeclampsia and intrauterine growth restriction. This minireview is intended to summarize the nitric oxide pathway and to discuss the emerging hydrogen sulfide pathway in modulating estrogen-induced uterine vasodilation in pregnancy and preeclampsia.

简介：AbstractObjective:This study aimed at investigating the expression of nuclear factor kappa B (NF-κB) and mammalian target of rapamycin (mTOR) related signal pathways in liver tissues of intrahepatic cholestasis of pregnancy animal models.Methods:Estrogen (EE)-induced cholestasis and a placental ischemia-reperfusion (IR) model were established in pregnant rats. All pregnant rats were divided into four groups by random number table: EE-IR group (n= 6), EE-sham group (n = 6), control-IR group (n= 6) and control-sham group (n= 6). Liver expression of mTOR, its upstream regulator DNA damage response-1 (REDD1), and downstream factor glucose transporter type-1 (GLUT1), accompanied by NF-κB (p65 is the most important component), its activator toll-like receptor 4 (TLR4), and inhibitor IκBα, were detected by western blot analysis and real-time polymerase chain reaction. The intergroup comparisons were performed with a one-way analysis of variance, the comparisons among groups were analyzed with the nonparametric Kruskal-Wallis test.Results:Giving pregnant rats EE alone reduced the hepatic expression of IκBα (0.72 ± 0.20 vs. 1.01 ± 0.07, P= 0.008). Meanwhile, giving pregnant rats placental IR alone increased liver levels of REDD1 (3.24 ± 0.98 vs. 1.06 ± 0.24, P= 0.025), GLUT1 (2.37 ± 0.82 vs. 1.09 ± 0.10, P= 0.039), TLR4 (2.12 ± 0.29 vs. 1.20 ± 0.28, P= 0.010), and p65 (2.09 ± 0.85 vs. 1.04 ± 0.06, P= 0.023), and decreased hepatic mTOR (0.50 ± 0.07 vs. 1.01 ± 0.03, P= 0.001) and IκBα (0.61 ± 0.08 vs. 1.01 ± 0.07, P= 0.014) expression. Subjecting EE-treated rats to placental IR did not further alter liver levels of GLUT1 (2.02 ± 0.45 vs. 1.79 ± 0.39, P= 0.240), TLR4 (2.10 ± 0.74 vs. 1.60 ± 0.36, P= 0.129), or p65 (2.41 ± 0.83 vs. 1.65 ± 0.46, P= 0.145), whereas it did decrease hepatic mTOR (0.42 ± 0.09 vs. 0.90 ± 0.14, P= 0.008) and IκBα (0.43 ± 0.09 vs. 0.72 ± 0.20, P= 0.004) expression and enhance REDD1 expression (4.46 ± 0.65 vs. 2.05 ± 0.47, P= 0.009). Placental IR stress did impact the hepatic expression of REDD1-mTOR-GLUT1 and TLR4/NF-κB/IκBα in pregnant rats.Conclusion:Placental IR-induced hepatic GLUT1, TLR4, and p65 alternation, which responded efficiently in control rats, were impaired in EE-induced ICP rats.

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简介：2013年10月12—13日中国生理学会张锡钧基金会第十二届全国青年优秀生理学学术论文交流会在湖南长沙顺利召开。由各省生理学会推荐的37名参赛选手的论文参与评选，会议展示了选手们近3年来在生理学研究方面所取得的最新研究成果。经过专家对参评者论文和现场报告的综合评判，评出一等奖、二等奖、三等奖、特别奖、最佳表达奖、最佳答辩奖和最佳图标奖共11名。从2013年第6期开始，《生理通讯》将陆续转载获奖者的参评论文各一篇，以飨读者。

简介：客观：为了与M-CSFR验证MAF-J6-1受体的抗原协会并且进一步学习M-CSF和它的受体的角色，调停了在支持白血病的房间增长的juxtacrine。方法：MAF-J6-1RRE2的Monoclonal抗体(McAb)和rhM-CSFR的polyclonal抗体(PolyAb)被准备。到M-CSFR的McAbRE2的特性被ELISA被间接ELISA，有J6-1房间殖民地形成的跨neutralizing试金和中立化测试证实。结果：到M-CSFR的净化的RE2的反应活动是超过1：16000。M-CSFR和MAF-J6-1R的禁止的活动能被RE2和anti-M-CSFR抗体堵住。到M-CSFR的RE2的反应能被M-CSFR减少。结论：到M-CSFR的RE2的特性被证实，有M-CSFR的MAF-J6-1R的抗原协会被证明。它建议M-CSF和它的受体调停了auto-juxtacrine刺激能是在白血病或nonhematological恶意的起作用的机制。

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简介：客观：在glucocorticoid之中调查关系受体(GCR)水平，免疫学的分类和在尖锐成淋巴细胞的白血病(所有)的化疗的临床的功效孩子。方法：静脉的血淋巴细胞的GCR水平被受体radioligand绑定试金与童年在50种情况中测量所有和41个正常孩子。有所有的32个孩子的免疫学的分类被ABCimmunoenzymatic方法分析。结果：在正常孩子的静脉的血淋巴细胞的GCR数字是4651

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简介：Estrogendeficiencyhasbeenproposedasariskfactorforalveolarboneloss,butwhetherornotestrogenwillinflucencethebonerebuiltingprocessduringorthodontictoothmovementandwhatthemechanismsinvolvedremainunclear.Thepaperaimstoprovidenewinformationthatmayelucidatethemodulatoryeffectofestrogenonthebone-resorbingcytokinesRANKLanditsanti-resorptivefactorOPGsecrectedbyHPLFswhicharealreadyforce-stimulated.TheexpressionofOPGmRNAisrisingaftermechanicalloadingeitherwithorwithoutstimulatedbyestrogenbefore.ButHPDLcellsexposuredtoestrogenfor24hbeforeloadedtendtoexpressmoreOPGmRNA.Comparedwiththeno-estrogengroup,theinhibittrendofRANKLmRNAismuchmoreapparentinwith-estrogengroup.Moreover,estrogenandmechanicforcetime-dependentlyincreasedOPGexpressionandattenuatedtheRANKLexpression.

简介：Objective:Theelevatedincidenceofobesityhasbeenparalleledwithhigherrisksofbreastcancer.Highadiposityincreasesleptinsecretionfromadiposetissue,whichinturnincreasescancercellproliferation.Theinterplaybetweenleptinandestrogenisoneofthemechanismsthroughwhichleptininfluencesbreastcarcinogenesis.Anunbalancedestrogenmetabolismincreasestheformationsofcatecholestrogenquinones,DNAadducts,andcancermutations.ThisstudyaimstoinvestigatetheeffectofleptinonsomeestrogenmetabolicenzymesandDNAadductioninbreastcancercells.Methods:Highperformanceliquidchromatography(HPLC)wasperformedtoanalyzetheDNAadducts4-OHE1[E2]-1-N3adenineand4-OHE1[E2]-1-N7guanine.Reportergeneassay,realtimereversetranscriptionpolymerasechainreaction(realtimeRT-PCR),andWesternblotwereusedtoassesstheexpressionofestrogenmetabolizinggenesandenzymes:CytochromeP-4501B1(CYP1B1),Nicotinamideadeninedinucleotidephosphate-quinoneoxidoreductase1(NQO1),andCatechol-O-methyltransferase(COMT).Results:LeptinsignificantlyincreasedtheDNAadducts4-OHE1[E2]-1-N3adenineand4-OHE1[E2]-1-N7guanine.Furthermore,leptinsignificantlyupregulatedCYP1B1promoteractivityandproteinexpression.TheluciferasepromoteractivitiesofNQO1andmRNAlevelsweresignificantlyreduced.Moreover,leptingreatlyreducedthereporteractivitiesoftheCOMT-P1andCOMT-P2promotersanddiminishedtheproteinexpressionofCOMT.Conclusions:LeptinincreasesDNAadductlevelsinbreastcancercellspartlybyaffectingkeygenesandenzymesinvolvedinestrogenmetabolism.Thus,increasedfocusshouldbedirectedtowardleptinanditseffectsontheestrogenmetabolicpathwayasaneffectiveapproachagainstbreastcancer.

简介：现在的学习试图定义postsynaptic的角色在多巴胺(DA)的规定的密度(PSD)-95受体功能。我们发现PSD-95身体上在co-transfectedHEK-293房间与D1或D2DA受体联系。DA受体的刺激以一种时间依赖者方式改变了在D1受体和PSD-95之间的协会。功能的试金显示PSD-95合作表示没影响D1刺激受体的营地生产，Gs蛋白质激活或受体不敏感性。然而，PSD-95由支持受体再循环加速了使内在化的膜受体的恢复，因此导致使内在化的D1受体的提高的促进感受性。我们的结果提供新奇机制因为调整再循环那的DA受体可以在postsynapticDA功能的调整和synapticneuroplasticity起一个重要作用。

简介：Receptor-ligandinteractionsinbloodflowarecrucialtoinitiatesuchbiologicalprocessesasinflammatorycascade,plateletthrombosis,aswellastumormetastasis.Tomediatecelladhesion,theinteractingreceptorsandligandsmustbeanchoredontotwoapposingsurfacesoftwocellsoracellandasubstratum,i.e.,two-dimensional(2D)binding,whichisdifferentfromthebindingofasolubleligandinfluidphasetoareceptor,i.e.,three-dimensional(3D)binding.Whilenumerousworkshavebeenfocusedon3Dkineticsofreceptor-ligandinteractionsintheimmunesystem,2Dkineticsanditsregulationshavebeenlessunderstood,sincenotheoreticalframeworkorexperimentalassayswereestablisheduntil1993.Notonlydoesthemolecularstructuredominate2Dbindingkinetics,buttheshearforceinbloodflowalsoregulatescelladhesionmediatedbyinteractingreceptorsandligands.Here,weprovideanoverviewofcurrentprogressin2Dbindingandregulations,mainlyfromourgroup.Relevantissuesoftheoreticalframeworks,experimentalmeasurements,kineticratesandbindingaffinities,andforceregulationsarediscussed.

简介：在血流动的Receptor-ligand相互作用是关键的作为煽动性的串联，血小板血栓，以及肿瘤转移开始生物过程。为了调停，房间粘附，交往的受体和ligands必须被抛锚到二个房间或一个房间和一个基础的二apposing表面上，即，二维(2D)绑定，与在到受体的液体阶段的可溶的ligand的绑定不同，三维(3D)有约束力。当众多的工作在免疫系统集中于receptor-ligand相互作用的3D动力学时，2D动力学和它的规定少些被理解，自从没有理论框架和试验性的试金被建立了直到1993。不仅分子的结构统治在血流动的力量也调整的2D绑定动力学，而是shear房间粘附由交往的受体和ligands调停了。这里，我们在2D绑定和规定提供了当前的进步的概述。理论框架，试验性的大小，运动的率和有约束力的亲密关系的相关问题，和力量规定，被讨论。