RH dysfunction 什么意思_百度知道
RH dysfunction 什么意思
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出门在外也不愁erectile dysfunction
[i'rektail d?s'f??k??n]
[?'r?kt?l d?s'f??k??n]
勃起功能障碍
勃起功能障碍；
勃起障碍；
性功能障碍
大家都在背：
1. Erectile dysfunction, metabolic risk factors and cardiovascular disease - What is the link?
代谢危险因素、心血管疾病及勃起功能障碍之间的关系.
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2. Methods: 20 patients with erectile dysfunction were examined twice about NPT after AVSS.
方法: 对有勃起功能障碍主诉的20名被鉴定人,进行视听觉性刺激后的阴茎夜间勃起检测自身对照.
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3. Objective : To evaluate the sex therapy for erectile dysfunction ( ED ).
目的: 探讨 ED 性治疗的临床应用.
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4. Sex therapy is one of the early therapies for erectile dysfunction ( ED ).
性治疗是最早使用的治疗 勃 起功能障碍的方法之一.
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5. Patients were interviewed about components relative to erectile dysfunction and hypogonadal - related symptoms.
采访患者对于勃起功能障碍和性腺功能低减相关症状.
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1. impotence resulting from a man's inability to have or maintain an erection of his penis
1. 勃起功能障碍
勃起功能障碍（Erectile Dysfunction）的英文缩写，阳痿即勃起功能障碍是指在企图性交时，阴茎勃起硬度不足于插入阴道，或阴茎勃 …
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2. 勃起障碍
勃起障碍(erectile dysfunction),也称为阳痿或简称-ed-,是指一个男子不能达到充分的阴茎勃起而完成性交。 当一个男子身体不适或焦虑.
- 基于135个网页
阳痿（英语是Erectile Dysfunction）是指在有性欲要求时，阴茎不能勃起或勃起不坚，或者虽然有勃起且有一定程度的硬度，但不能保 …
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4. 性功能障碍
医学词汇之吸烟导致的病症_外语教育网 ... Emphysema 肺气肿 Erectile Dysfunction 性功能障碍 Esophageal Cancer 食管癌.
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1. 勃起功能障碍药物
erectile... ... erectile dysfunction medicine ： 勃起功能障碍药物 fixing erectile dysfunction ： 确定勃起功能障碍.
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1. 阳萎性机能障碍治疗
固精补髓Stimulates male virility阳萎性机能障碍治疗reats erectile dysfunction成分: 原支风乾海豹鞭 Seal penis
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1. 勃起机能障碍
drug 毒品ED erectile dysfunction 勃起机能障碍first aid 急救
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1. 男性勃起功能障碍
...，预计2008 年完成临床前研究。TPN519 有望成为具有自主知识产权的，用于男性勃起功能障碍（male erectile dysfunction）的一 …
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方便的话，请您留下一种联系方式，便于问题的解决：北京生命科学研究所研究生导师简介-邵峰 博士
邵峰博士北京生命科学研究所资深研究员FengShao,Ph.D.Investigator,NIBS,Beijing,ChinaPhone：010-0Fax：010-E-mail：shaofeng@教育经历Education1996年北京大学技术系应用专业学士B.S.AppliedChemistry,PekingUniversity,Beijing,China1999年中国科学院所分子学硕士M.S.MolecularBiology,InstituteofBiophysics,ChineseAcademyofSciences,Beijing,China2003年美国密西根大学院博士Ph.D.BiologicalChemistry,UniversityofMichiganMedicalSchool,AnnArbor,MI,USA工作经历ProfessionalExperience2012-present北京生命科学研究所资深研究员Investigator,NationalInstituteofBiologicalSciences,Beijing,China年北京生命科学研究所高级研究员AssociateInvestigator,NationalInstituteofBiologicalSciences,Beijing,China年北京生命科学研究所研究员AssistantInvestigator,NationalInstituteofBiologicalSciences,Beijing,China年哈佛大学院博士后DamonRunyonPostdoctoralResearchFellow,HarvardMedicalSchool,Boston,USA年美国加洲大学圣地亚哥分校院博士后PostdoctoralResearchFellow,SchoolofMedicine,UniversityofCalifornia,SanDiego,USA研究概述ResearchDescription我们实验室的研究兴趣集中在病原细菌感染宿主和宿主先天性免疫防御的分子机制。对于细菌感染来说，通过特殊的分泌系统向宿主细胞中注入毒素效应蛋白是病原细菌普遍采用的重要致病机制。这些效应蛋白往往以非常有效的方式作用于宿主信号转导中的关键分子，使其发生功能紊乱。效应蛋白的作用有利于细菌在宿主中的生存和进一步感染。我们的研究以多种临床上常见的病原菌（Shigella,Salmonella,EnteropathogenicE.coli,Legionella以及Burkholderia）为模式，着眼于发现并揭示效应蛋白在抑制真核细胞重要信号转导通路中的一些新的、较为普遍的机制。实验室最近的研究工作在这方面取得了一系列的突破和发现。1)来源于Shigella，Salmonella和植物假单胞杆菌的OspF家族三型分泌系统效应蛋白通过一种崭新的磷酸化苏氨酸裂合酶的活性，特异性地、不可逆地“去磷酸化”宿主MAPK激酶并使其失活,从而抑制宿主细胞因子的表达。2)Legionella的四型分泌系统效应蛋白LegK1能模拟宿主中的IKK激酶而磷酸化IκBa蛋白，并诱导其被泛素化和降解，进而激活NF-κB通路并对巨噬细胞凋亡产生抑制作用。3)三型分泌系统效应蛋白CHBP（Burkholderia）和Cif（EnteropathogenicE.coli）特异性地修饰（脱氨）泛素和泛素样蛋白NEDD8中Gln-40。这种修饰能有效地阻断宿主泛素-蛋白酶体通路并导致诸如细胞周期等重要细胞生理过程发生功能紊乱。我们认为，这些研究不仅对理解感染和致病的分子机理有极大的促进作用，更为重要的是，由于病原细菌和宿主(人类)长期共同进化，其分泌的毒素效应蛋白也为我们研究真核细胞本身的信号转导机制提供了独特的、前所未有的视角和研究工具。同时，我们也对宿主巨噬细胞如何通过其先天性免疫系统来拮抗病原微感染的机制感兴趣。在受到感染后，巨噬细胞能感受到多种来自病原菌或其它病原微的一些模式分子，从而激活一类被称为炎症小体的蛋白复合物，同时发生炎症性细胞坏死和分泌白介素1b。炎症小体利用一类叫作NOD-like的受体分子感受来自病原菌的信号，但除此之外人们对炎症小体的组装和其上游的信号转导机制了解甚少。我们将结合、细胞学以及小鼠遗传学等多种手段来研究和阐明炎症小体被激活的生化机制。Dr.FengShao’slaboratoryisinterestedinstudyingmolecularmechanismsofbacterialinfectionandhostinnateimmunitydefense.BacterialpathogensusespecializedsecretionsystemssuchastypeIII/IVsecretionsystemtoinjecteffectorproteinsintohostcells,servingasakeyanduniversalvirulencemechanism.Theeffectorsusuallyharborauniqueandpotentactivitythatmodulatesthefunctionofkeysignalingmoleculesinthehost,andthisplaysacriticalroleinbacterialsurvivalandsystemicinfections.UsingpathogenssuchasShigella,Salmonella,EnteropathogenicE.coli(EPEC),LegionellaandBurkholderiaasthemodel,weareworkingtodiscoverandrevealsomenovelandcommonbiochemicalmechanismsutilizedbybacterialeffectorsinmodulatinghostsignaltransductionpathways.Ourrecentworkhasledtoseveralinterestingdiscoveries.1)TheOspFfamilyoftypeIIIeffectors,conservedinShigella,SalmonellaandtheplantpathogenP.syringae,harborsanovelphosphothreoninelyaseactivitythatspecificallyandirreversibly“dephosphorylates”hostMAPKs,leadingtokinaseinactivationandinhibitedcytokineproduction.2)TheLegionellatypeIVeffectorLegK1mimicshostIKKtophosphorylateIkBa,whichresultsinubiquitinationanddegradationofIkBaandconsequentactivationofhostanti-apoptoticNF-kBsignaling.3)TypeIIIeffectorsCHBP(Burkholderia)andCif(EPEC)useapapain-likecatalyticactivitytodeamidateubiquitinandubiquitin-likeproteinNEDD8.Thisleadstodysfunctioningofhostubiquitin-proteasomesystem,andthereforemanyimportantcellularprocessessuchascellcycleprogressionbecomeabnormal.Webelievethatsuchkindofresearchanddiscoveryisnotonlyrevealinginbacterialpathogenesis,butalsoprovidesanunprecedenteduniqueangleforstudyingthemechanismofeukaryoticsignaltransduction.Meanwhile,wearealsointerestedinhowthehostusesitsinnateimmunitysystemtocounteractbacterialinfection,particularlytheinflammasomepathwayinmacrophages.Macrophagesensesmanykindsofpathogen-derivedmolecularpatternsandtherebyactivatesthecytoplasmicinflammasomecomplex,andthisleadstoIl-1bproductionandinflammatorycelldeathofthemacrophage.TheNOD-likereceptorininflammasomeisrequiredforsensingbacteria-derivedsignals.However,littleisknownabouthowtheinflammasomeisassembled/activated,andthesignalingcascadeupstreamoftheinflammasomeremainsobscure.Wearecombiningmultipleapproachesincludingbiochemicalreconstitution,cellbiologyandmousegeneticstoidentifynewcomponentsinpathogen-inducedinflammasomeactivationandtofurtherrevealtheunderlyingbiochemicalmechanism.发表文章PublicationsResearcharticles:1.DongN,ZhuY,LuQ,HuL,ZhengY,ShaoF.(2012)StructurallyDistinctBacterialTBC-likeGAPsLinkArfGTPasetoRab1InactivationtoCounteractHostDefenses.Cell,150,.GeJ,GongYN,XuY,ShaoF.(2012)PreventingbacterialDNAreleaseandabsentinmelanoma2inflammasomeactivationbyaLegionellaeffectorfunctioninginmembranetrafficking.Proc.Natl.Acad.Sci.,109,.ZhangL,DingX,CuiJ,XuH,ChenJ,GongYN,HuL,ZhouY,GeJ,LuQ,LiuL,ChenS,ShaoF.(2012)Cysteinemethylationdisruptsubiquitin-chainsensinginNF-kBactivation.Nature,481,204-8.4.ZhaoY,YangJ,ShiJ,GongYN,LuQ,XuH,LiuL,ShaoF.(2011)TheNLRC4inflammasomereceptorsforbacterialflagellinandtypeIIIsecretionapparatus.Nature,477,596C600.5.CuiJ,YaoQ,LiS,DingX,LuQ,MaoH,LiuL,ZhengN,ChenS,ShaoF.(2010)Glutaminedeamidationanddysfunctionofubiquitin/NEDD8inducedbyabacterialeffectorfamily.Science,329,.GongYN,WangX,WangJ,YangZ,LiS,YangJ,LiuL,LeiX,ShaoF.(2010)Chemicalprobingrevealsinsightsintothesignalingmechanismofinflammasomeactivation.CellResearch,20,.DongN,LiuL,ShaoF.(2010)AbacterialeffectortargetshostDH-PHdomainRhoGEFsandantagonizesmacrophagephagocytosis.EMBOJ.,29,.ZhuY,HuL,ZhouY,YaoQ,LiuL,ShaoF.(2010)StructuralmechanismofhostRab1activationbythebifunctionalLegionellatypeIVeffectorSidM/DrrA.Proc.Natl.Acad.Sci.,107,.GeJ,XuH,LiT,ZhouY,ZhangZ,LiS,LiuL,ShaoF.(2009)ALegionellatypeIVeffectoractivatestheNF-κBpathwaybyphosphorylatingtheIκBfamilyofinhibitors.Proc.Natl.Acad.Sci.,106,.ChenY,YangZ,MengM,ZhaoY,DongN,YanH,LiuL,DingM,Peng,HB,ShaoF.(2009)CullinmediatesdegradationofRhoAthroughevolutionarilyconservedBTBadaptorstocontrolactincytoskeletonstructureandcellmovement.Mol.Cell,35,841-55.11.YaoQ,CuiJ,ZhuY,WangG,HuL,LongC,Cao,R,LiuX,HuangN,ChenS,LiuL,ShaoF.(2009)AbacterialtypeIIIeffectorfamilyusesthepapain-likehydrolyticactivitytoarrestthehostcellcycle.Proc.Natl.Acad.Sci.,106,.ZhuY.,LiH.,HuL.,Wang,J.,ZhouY.,PangZ.,LiuL.,ShaoF.(2008)StructureofaShigellaeffectorrevealsanewclassofubiquitinligases.NatureStructural&MolecularBiology,15,.ZhuY,LiH,LongC,HuL,XuH,LiuL,ChenS,WangDC,ShaoF.(2007)StructuralinsightsintotheenzymaticmechanismofthepathogenicMAPKphosphothreoninelyase.Mol.Cell,28,899-913.14.ZhangJ,ShaoF,LiY,CuiH,ChenL,LiH,ZouY,LongC,LanL,ChaiJ,ChenS,TangX,ZhouJM.(2007)APseudomonassyringaeeffectorinactivatesMAPKstosuppressPAMP-inducedimmunity.CellHost&Microbe,1,175-85.15.LiH,XuH,ZhouY,ZhangJ,LongC,LiS,ChenS,ZhouJM,ShaoF.(2007)ThephosphothreoninelyaseactivityofabacterialtypeIIIeffectorfamily.Science,315,.AltoNM,ShaoF,LazarCS,BrostRL,ChuaG,Mattoo,SM,McMahonSA,GhoshP,HughesTR,BooneC,DixonJE.(2006)IdentificationofabacterialtypeIIIeffectorfamilywithG-proteinmimicryfunctions.Cell,124,133-45.17.ZhuM,ShaoF,InnesRW,DixonJE,XuZ.(2004)ThecrystalstructureofPseudomonasavirulenceproteinAvrPphB:apapain-likefoldwithadistinctsubstrate-bindingsite.Proc.Natl.Acad.Sci.,101,302-7.18.ShaoF,Golstein,C,AdeJ,StoutemyerM.,DixonJE,InnesRW.(2003)CleavageofArabidopsisPBS1byabacterialtypeIIIeffector.Science,301,.ShaoF,VacratsisPO,BaoZ,BowersKE,FierkeCA,DixonJE.(2003)BiochemicalcharacterizationoftheYersiniaYopTprotease:cleavagesiteandrecognitionelementsinRhoGTPases.Proc.Natl.Acad.Sci.,100,904-9.20.ShaoF,MerrittPM,BaoZ,InnesRW,DixonJE.(2002)AYersiniaeffectorandaPseudomonasavirulenceproteindefineafamilyofcysteineproteasesfunctioninginbacterialpathogenesis.Cell,109,575-88.21.ShaoF,BaderMW,JakobU,BardwellJC.(2000)DsbG,aproteindisulfideisomerasewithchaperoneactivity.J.Biol.Chem.,275,.ShaoF,HuZ,XiongYM,HuangQZ,WangCG,ZhuRH,WangDC.(1999)AnewantifungalpeptidefromtheseedsofPhytolaccaamericana:characterization,aminoacidsequenceandcDNAcloning.Biochim.Biophys.Acta,.23.ShaoF,XiongYM,ZhuRH,LingM,ChiCW,WangDC.(1999)ExpressionandpurificationoftheBmKM1neurotoxinfromthescorpionButhusmartensiiKarsch.ProteinExpr.Purif.,17,358-65.Invitedreviewarticles:24.ZhaoY,ShaoF.(2012)NLRC5:aNOD-likereceptorproteinwithmanyfacesinimmuneregulation.CellResearch,22,.GongYN,ShaoF.(2012)SensingbacterialinfectionsbyNAIPreceptorsinNLRC4inflammasomeactivation.Protein&Cell,3,98-105.26.GeJ,ShaoF.(2011)ManipulationofhostvesiculartraffickingandinnateimmunedefensebyLegionellaDot/Icmeffectors.Cell.Microbiol.,13,.CuiJ,ShaoF.(2011)Biochemistryandcellsignalingtaughtbybacterialeffectors.TrendsinBiochemicalSciences,36,532-40.28.ShaoF.(2008)BiochemicalfunctionsofYersiniatypeIIIeffectors.CurrentOpinioninMicrobiology,11,21-9.29.JurisSJ,ShaoF,DixonJE.(2002)Yersiniaeffectorstargetmammaliansignalingpathways.Cell.Microbiol.,4:201-11(Co-firstauthor).
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