怎样在国际权威杂志上发表科学论文.ppt

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1、怎样在国际权威杂志上发表科学论文 Still waters run deep.流静水深流静水深,人静心深人静心深 Where there is life,there is hope。有生命必有希望。有生命必有希望新视野系列研究生课程：科技论文的构思、撰写和发表 生物医学世纪讲坛How to Publish Your Papers in the Top Scientific Journals 鲁白 教授鲁白教授1957年12月生于上海市。1982年获上海华东师范大学学士学位。1990年获康乃尔大学博士学位后，在洛克菲勒大学和哥伦比亚大学从事博士后研究,导师为Paul Greengard和蒲慕明教

2、授。1993年加入罗氏分子生物学研究所，并任哥伦比亚大学助理教授。1996年加入NIH儿童健康和人类发育研究所，任突触发育和可塑性研究室主任。主要研究神经营养因子在突触发育和可塑性中的作用。他的研究室是最早提出并发现神经营养因子对神经系统突触传递、突触发育可塑性有调控作用的实验室之一，与几个著名实验室一起开创了神经营养因子的突触调控这一新领域。Bai Lu 怎怎 样样 在在 国国 际际 权权 威威 杂杂 志志 上上 发发 表表 科科 学学 论论 文文 鲁鲁 白白鲁鲁 迅迅 Lu Xun(1881-1936)The father of modern Chinese literaturesThe

3、most influential poet in Chinese history李李 白白 Li Bai(701-762)1.M.F.Egan,M.Kojima,J.H.Callicott,T.E.Goldberg,B.S.Kolachana,E.Zaistev,A.Bertolino,B.Gold,D.Goldman,M.Dean,B.Lu,(co-corresponding author)andD.R.Weinberger.(2003)TheBDNFval66metpolymorphismaffectsactivity-dependentsecretionofBDNFandhumanmem

4、oryandhippocampalfunction.Cell112,257-269.2.L.Ma,Y.-Z.Huang,J.Valtschanoff,L.Feng,B.Lu,W.Xiong,R.Weinberg,L.Mei.(2003)Ligand-dependentrecruitmentoftheneuregulinsignalingcomplexintoneuronallipidrafts.J.Neurosci.23,3164-3175.3.J.Wang,C.-Q.Chen,B.Lu,andC.-P.Wu.(2003)GDNFacutelypotentiatesCa2+channelsan

5、dexcitatorysynaptictransmissioninmidbraindopaminergicneurons.NeuroSignals12,78-88.4.M.Miura,S.Gronthos,M.Zhao,B.Lu,L.W.Fisher,P.G.Robey,andS.Shi(2003)SHED:Stemcellsfromhumanexfoliateddeciduousteeth.Proc.Natl.Acad.Sci.USA100,5807-5812.5.Y.X.Zhou,M.Zhao,K.Shimazu,K.Sakata,D.Li,C.-X.Deng,B.Lu.(2003)Imp

6、airmentsincerebellumPurkinjecellsandmotorfunctioninmicelackingSmad4inthecentralnervoussystem.J.Biol.Chem.278,42313-42320.6.J.Du,L.Feng,E.Zaitsev,H.S.Je,X.Liu,andB.Lu.(2003)Activity-andtyrosinekinase-dependentfacilitationofTrkBreceptorinternalizationinhippocampalneurons.JCellBiol.Inpress.7.Z.G.Luo,H.

7、-S.Je,F.Yang,W.C.Xiong,B.Lu,andL.Mei(2003)ActivationofgeranylgenanyltransferaseisessentialforAgrin-inducedAChRclustering.NeuronInpress.8.S.X.Bamji,K.Shimazu,N.Kimes,J.Huelsken,W.Birchmeier,B.Lu,L.F.Reichardt.(2003)Regulationofpresynapticassemblyandmaintenanceby-catenin.NeuronInPress.9.F.Yang,X.He,J.

8、Russell,andB.Lu.(2003)Ca2+influxindependenttransmitterreleasemediatedbymitochondrialNa+-Ca2+exchangerandproteinkinaseC.J.CellBiol.Inpress.2003 research articlesWhat Is the Purpose of Doing Research?It is not about the number of papersIt is not about the number of papers It is not about the impact fa

9、ctor of the papers It is not about the impact factor of the papers It is not about the Nobel Prize It is not about the Nobel Prize Publish or perishPublish or perish1 Nature=10 JBC1 Nature=10 JBCBasic Elements for Basic ResearchPassionPassion6 6 SigmaSigmaSilver bullet testSilver bullet testGood Res

10、earch Is the KeyGood Research Is the Keyn n My English is not goodMy English is not goodn n They are biased against Chinese(foreigners)They are biased against Chinese(foreigners)n n 人家没做过人家没做过人家没做过人家没做过 你就要做你就要做你就要做你就要做n n 这是新的这是新的这是新的这是新的=这是好的这是好的这是好的这是好的What Is a First-Class Paper/Research?n n Maj

11、or advance in a classic fieldMajor advance in a classic field干细胞是如何分化成特定组织细胞的，胆固醇在人体的正常功用干细胞是如何分化成特定组织细胞的，胆固醇在人体的正常功用干细胞是如何分化成特定组织细胞的，胆固醇在人体的正常功用干细胞是如何分化成特定组织细胞的，胆固醇在人体的正常功用n n New techniques and methods that can be widely usedNew techniques and methods that can be widely used人类基因组研究中的自动测序技术人类基因组研究中

12、的自动测序技术人类基因组研究中的自动测序技术人类基因组研究中的自动测序技术,PCR,Patch clamp,Ca2+PCR,Patch clamp,Ca2+Imaging,GFPImaging,GFPn n Discoveries with obvious practical implications Discoveries with obvious practical implicationsAIDS virus receptor AIDS virus receptor AIDS virus receptor AIDS virus receptor 的发现的发现的发现的发现,老年痴呆症基因的

13、发现老年痴呆症基因的发现老年痴呆症基因的发现老年痴呆症基因的发现 n n Conceptual breakthrough,novel ideasConceptual breakthrough,novel ideas神经营养因子可以促进学习记忆神经营养因子可以促进学习记忆神经营养因子可以促进学习记忆神经营养因子可以促进学习记忆,RNARNARNARNA干干干干扰现扰现扰现扰现象象象象 n n Challenge to traditional views,break dogmaChallenge to traditional views,break dogma脑内有可分裂的神经干细胞，打破了传统观

14、念脑内有可分裂的神经干细胞，打破了传统观念脑内有可分裂的神经干细胞，打破了传统观念脑内有可分裂的神经干细胞，打破了传统观念 n n Opening up new area,cross boardOpening up new area,cross board“细胞凋亡细胞凋亡细胞凋亡细胞凋亡”现象的发现现象的发现现象的发现现象的发现,开辟了新的科研领域开辟了新的科研领域开辟了新的科研领域开辟了新的科研领域 What Is a Mediocre Paper/Research?Horizontal growthI made the discovery in rats,you find the sam

15、e in cat.Filling gapsEGF activates JNK which is known to induce c-Jun expression.You show that EFG enhances c-Jun expression.Working out detailsI found NO induces the production of cGMP,you work out dose response and time course.Support existing idea,“me too”EGF-R endocytosis requires dynamin,PDGF-R

16、 too.Follow up CREB binds to CRE.Working out CRE sequence.Incomplete study,preliminaryHow to Read Scientific Papers?The Gilbert way Keep these in mind when you read What is the major question addressed in this paper?Is this question important and why?What are the approaches used in this paper,and wh

17、ether they are adequate for the questions?What are the novel idea or using innovative approaches?What is the concept coming out of this paper?Do the results presented support this new concept?Weekly reading of CNS titles Critical,appreciativeWhat Makes Good Science?Important and significant Original

18、 and innovative Solid and rigorous Unique and unusual Novelty is essential语不惊人誓不休语不惊人誓不休The evaluation processThe evaluation processEditorial staff Board of Reviewing Editors20-30%REJECTREVIEWREJECT70%ACCEPT(10%)rejected before in-depth reviewrejected after in-depth reviewpublished(biological)publis

19、hed(physical sci)70%20%6%4%Should your paper go to CNS?n n Is it your best ever?Is it your best ever?n n Will it have a big impact?Will it have a big impact?n n Does it interest scientists in other fields?Does it interest scientists in other fields?n n Does it overturn conventional wisdom?Does it ov

20、erturn conventional wisdom?n n Work that represents a large step forward Work that represents a large step forward solution to long-standing problemsolution to long-standing problem different way of thinkingdifferent way of thinking broad implicationsbroad implicationsWhat helps:n nConvincing dataCo

21、nvincing datan nAppropriate controlsAppropriate controlsn nCareful presentationCareful presentationn nConsideration of all viable alternativesConsideration of all viable alternativesWhat doesnt helpn nThe minimal publishable unit.The minimal publishable unit.n nExcessive or unfounded speculationExce

22、ssive or unfounded speculationn nRepeat examples of a known phenomenonRepeat examples of a known phenomenonn nInsufficient advance over previously published Insufficient advance over previously published workworkEditorial Policies of Different Journals Cell/Neuron/ImmunityEditorial board does a lot

23、of reviews.Editors discuss and decide Nature sister journalsEditors discuss and decide ScienceSpace meeting,board of review editors PNASCommunicate,contribute,Track C OthersProcedures for High Profile Journals Pre-submission inquiry Submit/cover letter Initial screen Send out for reviews Reject/soft

24、 reject/revise Rebuttal Revise again Accept significance/importance general interests unusual/surpriseInitial screening suggest reviewers,may take one friends may not always support you“not to review”always honored“soft”and“harsh”reviewersSelection of reviewersYouEditorsCover Letters main findings s

25、ignificance suggested reviewers “not to review”list who have readDearEditor,WewouldliketosubmittheenclosedmanuscriptentitledGDNFAcutelyModulatesNeuronalExcitabilityandA-typePotassiumChannelsinMidbrainDopaminergicNeurons,whichwewishtobeconsideredforpublicationinNature Neuroscience.GDNFhaslongbeenthou

26、ghttobeapotentneurotrophicfactorforthesurvivalofmidbraindopaminergicneurons,whicharedegeneratedinParkinsonsdisease.Inthispaper,wereportanunexpected,acuteeffectofGDNFonA-typepotassiumchannels,leadingtoapotentiationofneuronalexcitability,inthedopaminergicneuronsincultureaswellasinadultbrainslices.Furt

27、her,weshowthatGDNFregulatestheK+channelsthroughamechanismthatinvolvesactivationofMAPkinase.Thus,thisstudyhasrevealed,forthefirsttime,anacutemodulationofionchannelsbyGDNF.OurfindingschallengetheclassicviewofGDNFasalong-termsurvivalfactorformidbraindopaminergicneurons,andsuggestthatthenormalfunctionof

28、GDNFistoregulateneuronalexcitability,andconsequentlydopaminerelease.TheseresultsmayalsohaveimplicationsinthetreatmentofParkinsonsdisease.Duetoadirectcompetitionandconflictofinterest,werequestthatDrs.XXXofHarvardUniv.,andYYofYaleUniv.notbeconsideredasreviewers.Withthanksforyourconsideration,IamSincer

29、elyyours,DearEditor,WewouldliketosubmittheenclosedmanuscriptentitledCa2+-bindingproteinfrequeninmediatesGDNF-inducedpotentiationofCa2+channelsandtransmitterrelease,whichwewishtobeconsideredforpublication in Neuron.WebelievethattwoaspectsofthismanuscriptwillmakeitinterestingtogeneralreadersofNeuron.F

30、irst,wereportthatGDNFhasalong-termregulatoryeffectonneurotransmitterreleaseattheneuromuscularsynapses.Thisprovidesthefirstphysiologicalevidencefora roleofthisnewfamilyofneurotrophicfactorsinfunctionalsynaptictransmission.Second,weshowthattheGDNFeffectismediatedbyenhancingtheexpressionoftheCa2+-bindi

31、ngproteinfrequenin.Further,GDNFandfrequeninfacilitatesynaptictransmissionbyenhancingCa2+channelactivity,leadingtoanenhancementofCa2+influx.Thus,thisstudyhasidentified,forthefirsttime,amoleculartargetthatmediatesthelong-term,synapticactionofaneurotrophicfactor.Ourfindingsmayalsohavegeneralimplication

32、sinthecellbiologyofneurotransmitterrelease.DearEditor:Enclosed are copies ofamanuscript entitled BDNFandNT-4/5Promote theDevelopment ofLong-TermPotentiationintheHippocampus,whichwewishtobeconsideredforpublicationinNature.Asyouknow,thereisagreatdealofinterestandexcitementrecentlyinunderstandingtherol

33、eofneurotrophinsinsynapsedevelopmentandplasticity.Ourmanuscriptprovides,forthefirsttime,thephysiological evidencethatneurotrophinsregulatelong-term potentiation(LTP).ThemainpointofthepaperisthattheneurotrophinsBDNFandNT-4induceanearlierappearanceofLTPindevelopinghippocampus.IncontrasttorecentScience

34、articlebyXXsgroup,we(andseveralotherLTPgroups)didnotseethatBDNFenhancebasalsynaptictransmissioninadullthippocampus.However,wefoundthatinadulthippocampus,inhibitionofBDNF/TrkBactivityattenuatedLTP,andweaktetanusthatnormallycannotinduceLTPproducedenduringLTP.Thesefindingsmayhaveimplicationsinthebasicm

35、echanismforregulationofsynapsedevelopmentandlong-termmodulationofsynapticefficacy.Becauseoftherathercompetitivenatureofthefieldandtheimportantimplicationofourfindings,wehavenotyetpresentedthisworkinanypublicforum.However,confidentialdiscussionwithseveral prominent neuroscientists such as 111 and 222

36、 have generated tremendous excitement.Thus,wefeelthatthisworkisofgeneralinterestandissuitableforpublicationinNature.WewouldliketosuggestDrs.aaaofYaleUniv.,bbbofHarvardMedicalSchool,andcccofUniv.ofCalifornia-Berkeley,asreviewersforthismanuscript.Duetoadirectcompetitionandconflictofinterest,werequestt

37、hatDr.XXandYY.notbeconsideredasreviewers.Thankyouverymuchforyourconsideration.Titles Important/significant Unexpected/unusual Function Mechanisms Simple Straight forward SpecificSynCAM,a synaptic adhesion molecule that drives synapse assemblyInhibition of Retroviral RNA production by ZAP,a CCCH-type

38、 Zinc finger proteinProtein phosphatase 1 is a molecular constraint on learning and memoryE3 ubiquitin ligase that recognizes sugar chainMolecular evolution of FOXP2,a gene involved in speech and languageSingle cell gene profilingStructure,mechanism,an regulation of the Neurospora plasma membrane H+

39、Modulation of postendocytic sorting of G-protein-coupled receptorsDistinct molecular mechanism for initiating TRAF6 signalingIdentification of;Role of;Involvement ofSequence of writing Abstract Figure layout Figure legend Material and methods Results Introduction DiscussionAbstract Rationale“remain

40、unknown”;“To determine”Summary statement“Here we show”Body Dont go into details;dont use many special terms Significance Must point out,but dont claim too muchFormation of the normal mammalian cerebral cortex requires the migration of GABAergic inhibitory interneurons from an extracortical origin,th

41、e lateral ganglionic eminence(LGE).Mechanisms guiding the migratory direction of these neurons,or other neurons in the neocortex,are not well understood.We have used an explant assay to study GABAergic neuronal migration and found that the ventricular zone(VZ)of the LGE is repulsive to GABAergic neu

42、rons.Furthermore,the secreted protein Slit is a chemorepellent guiding the migratory direction of GABAergic neurons,and blockade of endogenous Slit signaling inhibits the repulsive activity in the VZ.These results have revealed a cellular source of guidance for GABAergic neurons,demonstrated a molec

43、ular cue important for cortical development,and suggested a guidance mechanism for the migration of extracortical neurons into the neocortex.It has not escaped our notice that the specific pairing we have postulated immediately suggests a possible copying mechanism for the genetic material.-J.D.Wats

44、on and F.H.C.CrickNeuronal responses to brain-derived neurotrophic factor(BDNF)are initiated by the activation of the receptor TrkB tyrosine kinase(1).In this study we examined whether cholesterol-and glycolipid-rich microdomains,lipid rafts,provide a functional platform for BDNF-dependent signal tr

45、ansduction(2).Using primary culture of cortical neurons,we demonstrated that TrkB was dramatically translocated into lipid rafts in BDNF-dependent manner(3).This translocation was blocked by the pharmacological effect of general Trk inhibitors,indicating that TrkB activation is required for the tran

46、slocation mechanism.We also showed that BDNF and TrkB-FL were both concentrated in lipid rafts during development of cerebral cortex,concomitant with that of synaptic vesicle proteins,including soluble N-ethylmaleimide-sensitive factor attachment protein receptor(SNARE)proteins and synaptophysin(4).

47、This result,together with the findings that BDNF stimulation caused translocation of synaptophysin into lipid rafts(5)and that BDNF-enhanced glutamate release and exocytosis were both attenuated by depletion of cholesterol from the cell surface with methyl-beta-cyclodextrin(MCD),indicates that lipid

48、 rafts are essential for BDNF regulation of neurotransmitter release(6).Brain-derived neurotrophic factor(BDNF)plays an important role in synaptic plasticity but the underlying signaling mechanisms remain unknown.Here we show that BDNF rapidly recruits full-length TrkB(TrkB-FL)receptor into choleste

49、rol-rich lipid rafts from non-raft regions of neuronal plasma membranes.Truncated TrkB lacking the intracellular kinase domain was not translocated,and the translocation of TrkB-FL was blocked by Trk inhibitors,suggesting a role for TrkB tyrosine kinase in the translocation.Disruption of lipid rafts

50、 by depleting cholesterol from the cell surface blocked BDNF-dependent TrkB translocation.Disruption of rafts also prevented the potentiating effect of BDNF on transmitter release in cultured neurons,as well as that on synaptic response to tetanus in hippocampal slices.In contrast,lipid rafts are no