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生物醫(yī)學(xué)世紀(jì)講壇特邀報告：HowtoPublishYourPapersintheTopScientificJournals魯白教授WhatIsaFirst-ClassPaper?Majoradvanceinaclassicfield干細(xì)胞是如何分化成特定組織細(xì)胞的，膽固醇在人體的正常功用Newtechniquesandmethodsthatcanbewidelyused人類基因組研究中的自動測序技術(shù),PCR,PatchclampDiscoverieswithobviouspracticalimplicationsAIDSvirusreceptor的發(fā)現(xiàn),老年癡呆癥基因的發(fā)現(xiàn)

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Whatisthemajorquestionaddressedinthispaper?Isthisquestionimportantandwhy?Whataretheapproachesusedinthispaper,andwhethertheyareadequateforthequestions?Whatarethenovelideaorusinginnovativeapproaches?Whatistheconceptcomingoutofthispaper?Dotheresultspresentedsupportthisnewconcept?WeeklyreadingofCNStitlesCritical,appreciativeArticles

AnRNAThermosensorControlsExpressionofVirulenceGenesinListeriamonocytogenes

J?rgenJohansson,PierreMandin,AdrianaRenzoni,ClaudeChiaruttini,MathiasSpringer,andPascaleCossart

Single-StrandedAntisensesiRNAsGuideTargetRNACleavageinRNAi

JavierMartinez,AgnieszkaPatkaniowska,HenningUrlaub,ReinhardLührmann,andThomasTuschlOcaBIsRequiredforNormalTranscriptionandV(D)JRecombinationofaSubsetofImmunoglobulin

geneRafaelCasellas,MilaJankovic,GesaMeyer,AnnaGazumyan,YanLuo,RobertG.Roeder,andMichelC.NussenzweigCellSeptember6,2002:110(5)

Pages551–561

563–574575–585587–597AStructuralMechanismofIntegrin

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''Inside-Out''ActivationasRegulatedbyItsCytoplasmicFaceOlgaVinogradova,AlgirdasVelyvis,AstaVelyviene,BinHu,ThomasA.Haas,EdwardF.Plow,andJunQin

GlobalConformationalRearrangementsinIntegrinExtracellularDomainsinOutside-InandInside-OutSignaling

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whohavereadDearEditor,Wewouldliketosubmittheenclosedmanuscriptentitled"GDNFAcutelyModulatesNeuronalExcitabilityandA-typePotassiumChannelsinMidbrainDopaminergicNeurons",whichwewishtobeconsideredforpublicationinNatureNeuroscience.GDNFhaslongbeenthoughttobeapotentneurotrophicfactorforthesurvivalofmidbraindopaminergicneurons,whicharedegeneratedinParkinson’sdisease.Inthispaper,wereportanunexpected,acuteeffectofGDNFonA-typepotassiumchannels,leadingtoapotentiationofneuronalexcitability,inthedopaminergicneuronsincultureaswellasinadultbrainslices.Further,weshowthatGDNFregulatestheK+channelsthroughamechanismthatinvolvesactivationofMAPkinase.Thus,thisstudyhasrevealed,forthefirsttime,anacutemodulationofionchannelsbyGDNF.OurfindingschallengetheclassicviewofGDNFasalong-termsurvivalfactorformidbraindopaminergicneurons,andsuggestthatthenormalfunctionofGDNFistoregulateneuronalexcitability,andconsequentlydopaminerelease.TheseresultsmayalsohaveimplicationsinthetreatmentofParkinson’sdisease.

Duetoadirectcompetitionandconflictofinterest,werequestthatDrs.XXXofHarvardUniv.,andYYofYaleUniv.notbeconsideredasreviewers.Withthanksforyourconsideration,Iam

Sincerelyyours,DearEditor,Wewouldliketosubmittheenclosedmanuscriptentitled"Ca2+-bindingproteinfrequeninmediatesGDNF-inducedpotentiationofCa2+channelsandtransmitterrelease",whichwewishtobeconsideredforpublication

in

Neuron.WebelievethattwoaspectsofthismanuscriptwillmakeitinterestingtogeneralreadersofNeuron.First,wereportthatGDNFhasalong-termregulatoryeffectonneurotransmitterreleaseatthe

neuromuscularsynapses.

Thisprovidesthefirstphysiologicalevidencefora

roleofthisnewfamilyofneurotrophicfactorsinfunctionalsynaptictransmission.

Second,weshowthattheGDNFeffectismediatedbyenhancingtheexpressionoftheCa2+-bindingproteinfrequenin.Further,GDNFandfrequeninfacilitatesynaptictransmissionbyenhancingCa2+channelactivity,leadingtoanenhancementofCa2+influx.Thus,thisstudyhasidentified,forthefirsttime,amoleculartargetthatmediatesthelong-term,synapticactionofaneurotrophicfactor.Ourfindingsmayalsohavegeneralimplicationsinthecellbiologyofneurotransmitterrelease.

DearEditor:

Enclosedarecopiesofamanuscriptentitled"BDNFandNT-4/5PromotetheDevelopmentofLong-TermPotentiationintheHippocampus",whichwewishtobeconsideredforpublicationinNature.

Asyouknow,thereisagreatdealofinterestandexcitementrecentlyinunderstandingtheroleofneurotrophinsinsynapsedevelopmentandplasticity.Ourmanuscriptprovides,forthefirsttime,thephysiologicalevidencethatneurotrophinsregulatelong-termpotentiation(LTP).ThemainpointofthepaperisthattheneurotrophinsBDNFandNT-4induceanearlierappearanceofLTPindevelopinghippocampus.IncontrasttorecentSciencearticlebyErinSchuman'sgroup,we(andseveralotherLTPgroups)didnotseethatBDNFenhancebasalsynaptictransmissioninadullthippocampus.However,wefoundthatinadulthippocampus,inhibitionofBDNF/TrkBactivityattenuatedLTP,andweaktetanusthatnormallycannotinduceLTPproducedenduringLTP.Thesefindingsmayhaveimplicationsinthebasicmechanismforregulationofsynapsedevelopmentandlong-termmodulationofsynapticefficacy.

Becauseoftherathercompetitivenatureofthefieldandtheimportantimplicationofourfindings,wehavenotyetpresentedthisworkinanypublicforum.However,confidentialdiscussionwithseveralprominentneuroscientistssuchas111and222havegeneratedtremendousexcitement.Thus,wefeelthatthisworkisofgeneralinterestandissuitableforpublicationinNature.WewouldliketosuggestDrs.aaaofYaleUniv.,bbbofHarvardMedicalSchool,andcccofUniv.ofCalifornia-Berkeley,asreviewersforthismanuscript.Duet