医学英文文献阅读 高殿帅

文献（学术论文）阅读医学学术论文综述徐州医学院生物学教研室

高殿帅综述发展的轨迹（线索）现状的总结（归纳）指出存在的问题提出解决问题的策略不是今天要的内容！有机会再讲。学术论文是某一学术课题在实验性、理论性或观测性上具有新的科学研究成果或创新见解的知识和科学记录；或是某种已知原理应用于实际中取得新进展的科学总结，用以提供学术会议上宣读、交流或讨论；或在学术刊物上发表；或作其他用途的书面文件。

学术论文具有四大特点：①学术性②科学性③创造性④理论性医学学术论文

学术论文（科研文章）学术论文的形态结构（格式）传递学术论文信息的语言单位理解学术论文的三层境界学术论文的形态结构（格式）题名作者摘要关键词引言材料与方法结果讨论致谢参考文献一以贯之Thestructureofanarticle文章的结构Authors作者Title题目Abstract摘要Keywords关键词Maintext正文References参考文献Supplementarymaterial补充资料Introduction引言Methods方法Results结果Acknowledgments致谢Discussion讨论Clearlydescribescontents

Ensuresrecognitionforthewriter/s

Describessuccinctlywhatwasdone

Providessupplementarydatafortheexpertreader

Ensurespreviouslypublishedworkisrecognized

EnsuresthearticleiscorrectlyidentifiedinabstractingandindexingservicesExplainsthehypothesis

Explainshowthedatawerecollected

Describeswhatwasdiscovered

Discussestheimplicationsofthefindings

Ensuresthosewhohelpedintheresearcharerecognized

Howtowriteascientificarticle如何写科学文章题名题名是以最恰当、最简洁的词语反映学术论文中最重要的特定内容的逻辑组合。题名应该具有吸引力。题名举例Neuralstemandprogenitorcellsretaintheirpotentialforproliferationanddifferentiationintofunctionalneuronsdespitelowernumberinagedbrain.Radialglia-likecellspersistintheadultratbrain.Nogginexpandsneuralstemcellsintheadulthippocampus.UpregulationofchemokinereceptorexpressionbyIL-10/IL-4inadultneuralstemcells.题名注意句法结构：完整的句子？

特定的词组？注意内容结构：处理因素

实验对象

实验效应（观察指标）DeathreceptorsandcaspasesbutnotmitochondriaareactivatedintheGDNF-orBDNF-depriveddopaminergicneurons题名分析摘要20世纪60年代国外首先提出科技论文应附摘要，《中华医学杂志》英文版1972年也提出要求附摘要。20世纪80年代加拿大温哥华一个研究小组进一步提出结构式摘要，即要求摘要写法分成四部分，分别冠以标题，使读者无需查阅正文即可基本了解实质性内容。摘要具有独立性和自含性，即不阅读全文，就能获得必要的信息。

摘要一般应说明研究工作目的、材料与方法、结果、结论等，而重点是结果和结论。

摘要DeathReceptorsandCaspasesButNotMitochondriaAreActivatedintheGDNF-orBDNF-DeprivedDopaminergicNeurons

Neurotrophicfactors,includingglialcellline-derivedneurotrophicfactor(GDNF)andbrain-derivedneurotrophicfactor(BDNF),promotesurvivalofmidbraindopaminergicneurons,butthedeathpathwaysactivatedinthedopaminergicneuronsbydeprivationofthesefactorsarepoorlystudied.WeshowherethatdeprivationofGDNForBDNFtriggersanovelmitochondria-independentdeathpathwayintheculturedembryonicdopaminergicneurons:cytochromecwasnotreleasedfromthemitochondriatocytosol,proapoptoticproteinBaxwasnotactivated,andoverexpressedBcl-xLdidnotblockthedeath.Caspaseswerecriticallyrequired,becausethedeathwascompletelyblockedbycaspaseinhibitorBAF[boc-aspartyl(OMe)-fluoromethylketone]andoverexpressionofdominant-negativemutantsofcaspase-9,-3,and-7significantlyblockedthedeath.Also,thedeathreceptorpathwaywasinvolved,becauseblockageofcaspase-8orFADD(Fas-associatedproteinwithdeathdomain),anadapterrequiredforcaspase-8activation,inhibiteddeathinducedbyGDNForBDNFdeprivation.LigationofFasbyagonisticanti-FasantibodyinducedapoptosisintheGDNF-orBDNF-maintainedneurons,andinhibitionofFasbyFas-FcchimerablockedthedeathofGDNF-orBDNF-deprivedneurons,whereasFAIML(longisoformofFasapoptosisinhibitorymolecule)couldcontroltheactivityofFasinthedopaminergicneurons.Neurotrophicfactors,includingglialcellline-derivedneurotrophicfactor(GDNF)andbrain-derivedneurotrophicfactor(BDNF),promotesurvivalofmidbraindopaminergicneurons,butthedeathpathwaysactivatedinthedopaminergicneuronsbydeprivationofthesefactorsarepoorlystudied.

包括GDNF和BDNF在内的神经营养因子能促进中脑DA能神经元的存活，但很少有人研究，在这些DA能神经元内，由于剥夺这些营养因子而激活的细胞死亡信号通路是什么。请翻译！WeshowherethatdeprivationofGDNForBDNFtriggersanovelmitochondria-independentdeathpathwayintheculturedembryonicdopaminergicneurons:cytochromecwasnotreleasedfromthemitochondriatocytosol,proapoptoticproteinBaxwasnotactivated,andoverexpressedBcl-xLdidnotblockthedeath.这里，我们的结果显示：在体外培养的胚胎源DA能神经细胞，剥夺GDNF或BDNF，激活了这些细胞内一条新的非线粒体依赖性死亡信号通路。因为，没有细胞色素C从线粒体释放到胞浆、前凋亡蛋白Bax也没有被激活，且过表达Bcl-xL也不能阻止细胞的死亡。Caspaseswerecriticallyrequired,becausethedeathwascompletelyblockedbycaspaseinhibitorBAF[boc-aspartyl(OMe)-fluoromethylketone]andoverexpressionofdominant-negativemutantsofcaspase-9,-3,and-7significantlyblockedthedeath.Also,thedeathreceptorpathwaywasinvolved,becauseblockageofcaspase-8orFADD(Fas-associatedproteinwithdeathdomain),anadapterrequiredforcaspase-8activation,inhibiteddeathinducedbyGDNForBDNFdeprivation.但是，Caspases是必需的，因为，细胞死亡能被caspase抑制剂BAF（boc-aspartyl(OMe)-fluoromethylketone）完全阻断；caspase-9、-3、和-7的显性负突变体的过表达也能显著地阻滞细胞死亡。此外，死亡受体通路也参与了细胞死亡过程，因为，caspase-8或FADD（Fas相关蛋白细胞死亡结构域），一种caspase-8激活的必需接头蛋白，同样能抑制因GDNF或BDNF剥夺而致的细胞死亡。LigationofFasbyagonisticanti-FasantibodyinducedapoptosisintheGDNF-orBDNF-maintainedneurons,andinhibitionofFasbyFas-FcchimerablockedthedeathofGDNF-orBDNF-deprivedneurons,whereasFAIM(L)(longisoformofFasapoptosisinhibitorymolecule)couldcontroltheactivityofFasinthedopaminergicneurons.由具有激动剂性质的抗Fas抗体与Fas结合可引发在GDNF或BDNF维持存活下的神经元的凋亡，由Fas-Fc嵌合体抑制Fas的作用则能阻滞由GDNF或BDNF剥夺引起的神经元死亡，相反，FAIM(L)（Fas

凋亡抑制分子的长异构体？）能控制DA能神经元中的Fas活性。

请说出该摘要中下列几部分是怎样表达的？目的材料和方法结果结论DeathreceptorsandcaspasesbutnotmitochondriaareactivatedintheGDNF-orBDNF-depriveddopaminergicneurons

Neurotrophicfactors,includingglialcellline-derivedneurotrophicfactor(GDNF)andbrain-derivedneurotrophicfactor(BDNF),promotesurvivalofmidbraindopaminergicneurons,butthedeathpathwaysactivatedinthedopaminergicneuronsbydeprivationofthesefactorsarepoorlystudied.

WeshowherethatdeprivationofGDNForBDNFtriggersanovelmitochondria-independentdeathpathwayintheculturedembryonicdopaminergicneurons:cytochromecwasnotreleasedfromthemitochondriatocytosol,proapoptoticproteinBaxwasnotactivated,andoverexpressedBcl-xLdidnotblockthedeath.Caspaseswerecriticallyrequired,becausethedeathwascompletelyblockedbycaspaseinhibitorBAF[boc-aspartyl(OMe)-fluoromethylketone]andoverexpressionofdominant-negativemutantsofcaspase-9,-3,and-7significantlyblockedthedeath.Also,thedeathreceptorpathwaywasinvolved,becauseblockageofcaspase-8orFADD(Fas-associatedproteinwithdeathdomain),anadapterrequiredforcaspase-8activation,inhibiteddeathinducedbyGDNForBDNFdeprivation.LigationofFasbyagonisticanti-FasantibodyinducedapoptosisintheGDNF-orBDNF-maintainedneurons,andinhibitionofFasbyFas-FcchimerablockedthedeathofGDNF-orBDNF-deprivedneurons,whereasFAIM(L)(longisoformofFasapoptosisinhibitorymolecule)couldcontroltheactivityofFasinthedopaminergicneurons.引言引言又称前言，属于整篇论文的引论部分。其写作内容包括：研究的背景、现状，存在的问题，提出解决问题的策略（自己的创新点），阐述所提策略的理论依据和实验基础，主要研究内容。

引言的文字不可冗长，内容选择不必过于分散、琐碎，措词要精炼，要吸引读者读下去。言简意赅，不要与摘要雷同，不要成为摘要的注释。一般教科书中有的知识，在引言中不必赘述。Mostneuronalpopulationsundergoaperiodofontogeneticdeathduringwhichtheinitiallyoverproducedneuronsarereducedtothefinalnumberbytarget-derivedneurotrophicfactors(Barde,1989;Oppenheim,1991).Theintrinsicdeathprogramoftheneuronsissuppressedbyneurotrophicfactorsor,conversely,releasedintheirabsence(JohnsonandDeckwerth,1993;Changetal.,2002).Themolecularnatureofthisprogramis,however,poorlydescribedfordifferentneuronaltypes.Deathreceptorsandcaspasesbutnotmitochondriaare

activatedintheGDNF-orBDNF-depriveddopaminergicneuronsSurvivalofthemidbraindopaminergic(DA)neuronsthatdegenerateinParkinson’sdiseaseispotentlypromotedbyglialcellline-derivedneurotrophicfactor(GDNF)invitro(Linetal.,1993;Burkeetal.,1998),invivo(Ooetal.,2003,2005),andinseveralmodelsofParkinson’sdisease(AiraksinenandSaarma,2002;BespalovandSaarma,2007;Lindholmetal.,2007).GDNFbindstocoreceptorGFRα1,andthiscomplexactivatesreceptortyrosinekinaseRet(BespalovandSaarma,2007).GeneticmanipulationsofRetintheDAneurons(Granholmetal.,2000;Jainetal.,2006;Krameretal.,2007;Mijatovicetal.,2007)havegivencontroversialresultswhetherand/orwhenRetphysiologicallyregulatessurvival/deathofDAneurons.TreatmentofParkinson’spatientswithGDNFhasalsobeencontradictory,becausesomestudiesreportedconsiderableimprovement(Gilletal.,2003;Slevinetal.,2005),whereasothersdidnot(Langetal.,2006).Thesecontradictionsrequirefurtherstudies.Deathreceptorsandcaspasesbutnotmitochondriaare

activatedintheGDNF-orBDNF-depriveddopaminergicneuronsBrain-derivedneurotrophicfactor(BDNF),amemberoftheneurotrophinfamily,alsopromotessurvivalofDAneurons(Krieglsteinetal.,1996;Baquetetal.,2005)butviaadifferentreceptortyrosinekinase,TrkB.ThephysiologicalroleofBDNFintheontogenetic(Krameretal.,2007)orpathological(Baquetetal.,2005;Sunetal.,2005)death/survivalofDAneuronsispoorlyunderstood.Deathreceptorsandcaspasesbutnotmitochondriaare

activatedintheGDNF-orBDNF-depriveddopaminergicneuronsClassically,apoptosisoccursviaeitherdeathreceptorormitochondrialpathway(DanialandKorsmeyer,2004;Thorburn,2004;RiedlandSalvesen,2007).Ligateddeathreceptorsrecruitandactivateapicalprocaspase-8viaadaptersasFas-associatedproteinwithdeathdomain(FADD)(PeterandKrammer,2003;Peteretal.,2007).Inthemitochondrialpathway,activatedproapoptoticproteins(e.g.,Bax)releaseproteins(includingcytochromec)fromthemitochondriatothecytosol,leadingtotheassemblyofanapoptosomeandactivationofapicalcaspase-9.Apicalcaspasescleaveandactivateexecutionarycaspase-3,-6,and-7,whichultimatelydemolishthecell(ShackaandRoth,2006;RiedlandSalvesen,2007).Somecaspases(e.g.,caspase-2)areactivatedviaadifferentbutpoorlycharacterizedmechanism(Troyetal.,2000;Baligaetal.,2004).Also,somenonclassicalcaspase-dependentapoptoticpathwayshavebeendescribed(Mehlenetal.,1998;Bredesenetal.,2006).Deathreceptorsandcaspasesbutnotmitochondriaare

activatedintheGDNF-orBDNF-depriveddopaminergicneuronsWerecentlyshowedthatintheGDNF-deprivedsympatheticneurons,caspase-2and-7areactivatedviaanovelpathwaywithoutmitochondriaanddeathreceptors:Baxisnottranslocatedtothe

mitochondria;cytochromecisnotreleasedtothecytosolandcaspase-9and-3,butalsocaspase-8andFADDarenotinvolved(Yuetal.,2003).Here,weaddressedthedeathpathwaysinGDNF-andBDNF-deprivedDAneurons.Inbothcases,theneuronsdiedviaanonclassicalapoptoticpathwayinwhichdeathreceptorsandcaspases,butnotmitochondria,wereactivated.Deathreceptorsandcaspasesbutnotmitochondriaare

activatedintheGDNF-orBDNF-depriveddopaminergicneurons材料和方法Culturesof13-d-oldmouseventralmesencephalonandsurvivalassays.Transfections.Immunocytochemistry.Reversetranscription-PCR.Immunoblotandcoimmunoprecipitation.结果为假说提供证据！这篇文章的假说是什么？Here,weaddressedthedeathpathwaysinGDNF-andBDNF-deprivedDAneurons.Inbothcases,theneuronsdiedviaanonclassicalapoptoticpathwayinwhichdeathreceptorsandcaspases,butnotmitochondria,wereactivated.结果（研究内容）EmbryonicdopaminergicneuronsdieinculturebecauseofGDNForBDNFdeprivationMitochondrialdeathpathwayisnotactivatedinGDNF-andBDNF-depriveddopaminergicneuronsCaspasesarerequiredforthedeathofGDNF-orBDNF-depriveddopaminergicneuronsThedeathreceptorpathwayisactivatedinGDNF-andBDNF-depriveddopaminergicneuronsDeathreceptorsandcaspasesbutnotmitochondriaare

activatedintheGDNF-orBDNF-depriveddopaminergicneurons讨论：从结果到结论的过程！

具有以下几个主要特征：①只对“结果”进行论述，而不应进行重述。论述其是怎样支持“结论”的。②要能指出你的结果和解释与以前发表的著作相一致或不一致的地方。③要论述你的研究工作的理论含义以及实际应用的各种可能性。④要能指出任何的例外情况或相互关系中有问题的地方，并且应明确提出尚未解决的问题及解决的方向。讨论WehavepreviouslyshownthatGDNF-deprivedsympatheticneuronsactivatecaspasesviaanovelmitochondria-independentdeathpathway(Yuetal.,2003).HereweshowthatalsotheembryonicDAneuronsdonotactivatemitochondrialdeathpathwaybydeprivationofGDNF(butalsoBDNF):BaxisnottranslocatedtothemitochondriaandBaxinhibitiondoesnotblockthedeath,cytochromecisnotreleasedtothecytosol,andantiapoptoticmitochondrialproteinBcl-xLdoesnotblockthedeath.Intheimmunostainingexperiments,wehadtopreventcelldeathbycaspaseinhibition,becausethechangesinthelocalizationofBaxandcytochromecoccuronlybrieflybeforedeathandwerealmostimpossibletodetect.Theapoptoticmitochondrialchangesarebelievedtooccurwithoutcaspaseinvolvement(Changetal.,2002;Gogvadzeetal.,2006),butcaspase-2isreportedtobeactivatedupstreamofmitochondria(Guoetal.,2002;Lassusetal.,2002;Robertsonetal.,2004).WecannotexcludethatcaspaseinhibitionaffectedthemovementofBaxandcytochromecinourfactor-deprivedneurons.However,caspase-2wasnotcriticalforthedeathofDAneurons.Moreover,experimentswithKu70orBcl-xLwereperformedwithoutcaspaseinhibitors.Wethereforeconcludethatmitochondriawerenotactivatedintheneurotrophicfactor-deprivedDAneurons.CaspaseswerestillabsolutelyrequiredforthedeathofGDNF-andBDNF-deprivedDAneurons.WhencomparedwiththeGDNF-deprivedsympatheticneurons,theinvolvedcaspaseswerecompletelydifferent:caspase-2wascriticalforthedeathofGDNF-deprivedsympatheticneuronsbutnotGDNF-deprivedDAneurons.Instead,theDAneuronsdiedviacaspase-9,-3,and-7,whichwerenotessentialinthesympatheticneurons.Howcaspase-9isactivatedwithoutcytosoliccytochromecremainsanopenquestion.Caspase-9isactivatedattheapoptosomebydimerization(Boatrightetal.,2003;Popetal.,2006),butitisalsocleavedintheapoptoticcells,whichenhancesitscatalyticactivity(BaoandShi,2007;RiedlandSalvesen,2007).Wespeculatethatcaspase-8,activatedatthedeathreceptors,couldcleaveandactivatecaspase-9inourneurons,asrecentlyshowninothersystems(McDonnelletal.,2003;Gyrd-Hansenetal.,2006).Indeed,blockageofcaspase-8preventedthedeathoftheneurons,suggestingthatcaspase-9isactivateddownstreamofcaspase-8.OurattemptstovisualizecleavageproductsofthecaspasesbyWesternblottingfailed,mostprobablybecauseofthesmallamountofthematerialavailable.Immunostainingofthecultureswithantibodiestoactivatedcaspasesalsodidnotgiveconsistentresultsinourhands.Thus,furtherstudiesarerequiredtounderstandcaspase-9activationinourmodel.DeathreceptorswereactivatedintheGDNF-andBDNF-deprivedDAneurons,becausethedeathwassignificantlyblockedbyinhibitionofcaspase-8orFADD,butalsowithoverexpressionofFasinhibitorFAIML.FasagonistsandantagonistsaswellasthePCRresultsstronglysuggesttheexistenceoffunctionalFas-likereceptoronthesurfaceoftheDAneurons,anditsactivationbyGDNForBDNFdeprivation.MostprobablytheFasandFasLinteractvianeuriticcontactsthatareextensiveinourdensecultures,asalsosuggestedfortrophicfactor-deprivedmotoneurons(Raouletal.,1999;Ugolinietal.,2003;Raouletal.,2006).FasandFasLwereconstitutivelypresentinthemidbraincultures,suggestingthataninhibitorysystemshouldpreventtheunwantedactivationofFas.Indeed,wefoundthataneuronspecificinhibitoryproteinFAIML(Seguraetal.,2007)wasexpressedinthemidbraincultures.FAIMLinteractswithFas,bothphysically,asrevealedbycoimmunoprecipitation,andfunctionally,asrevealedbytransfectionofDAneurons.Thus,thefindingsofSeguraetal.(2007)wererepeatedinourmodel.ItistemptingtospeculatethatinthehealthyDAneurons,Fascouldperformsomenonapoptoticfunctions(Peteretal.,2007)withitsapoptoticactivityblockedbyFAIML,whereasFAIMLcouldbedegradedorremovedfromFasbyapoptoticstimulussuchasneurotrophicfactordeprivation.Wefoundthatde-ligationofRetactivatesdifferentdeathpathwaysinsympatheticandDAneurons,whereasthesamepathwayswereactivatedintheDAneuronsbyde-ligationofRetandTrkB.WeincludedBDNFforcomparisontoGDNFexpectingdifferentdeathpathways,becauseitwasinthesympatheticneuronsdeprivedofNGF(de-ligationofTrkAthatishomologousto