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文獻(xiàn)(學(xué)術(shù)論文)閱讀醫(yī)學(xué)學(xué)術(shù)論文綜述徐州醫(yī)學(xué)院生物學(xué)教研室
高殿帥綜述發(fā)展的軌跡(線索)現(xiàn)狀的總結(jié)(歸納)指出存在的問(wèn)題提出解決問(wèn)題的策略不是今天要的內(nèi)容!有機(jī)會(huì)再講。學(xué)術(shù)論文是某一學(xué)術(shù)課題在實(shí)驗(yàn)性、理論性或觀測(cè)性上具有新的科學(xué)研究成果或創(chuàng)新見(jiàn)解的知識(shí)和科學(xué)記錄;或是某種已知原理應(yīng)用于實(shí)際中取得新進(jìn)展的科學(xué)總結(jié),用以提供學(xué)術(shù)會(huì)議上宣讀、交流或討論;或在學(xué)術(shù)刊物上發(fā)表;或作其他用途的書面文件。
學(xué)術(shù)論文具有四大特點(diǎn):①學(xué)術(shù)性②科學(xué)性③創(chuàng)造性④理論性醫(yī)學(xué)學(xué)術(shù)論文
學(xué)術(shù)論文(科研文章)學(xué)術(shù)論文的形態(tài)結(jié)構(gòu)(格式)傳遞學(xué)術(shù)論文信息的語(yǔ)言單位理解學(xué)術(shù)論文的三層境界學(xué)術(shù)論文的形態(tài)結(jié)構(gòu)(格式)題名作者摘要關(guān)鍵詞引言材料與方法結(jié)果討論致謝參考文獻(xiàn)一以貫之Thestructureofanarticle文章的結(jié)構(gòu)Authors作者Title題目Abstract摘要Keywords關(guān)鍵詞Maintext正文References參考文獻(xiàn)Supplementarymaterial補(bǔ)充資料Introduction引言Methods方法Results結(jié)果Acknowledgments致謝Discussion討論Clearlydescribescontents
Ensuresrecognitionforthewriter/s
Describessuccinctlywhatwasdone
Providessupplementarydatafortheexpertreader
Ensurespreviouslypublishedworkisrecognized
EnsuresthearticleiscorrectlyidentifiedinabstractingandindexingservicesExplainsthehypothesis
Explainshowthedatawerecollected
Describeswhatwasdiscovered
Discussestheimplicationsofthefindings
Ensuresthosewhohelpedintheresearcharerecognized
Howtowriteascientificarticle如何寫科學(xué)文章題名題名是以最恰當(dāng)、最簡(jiǎn)潔的詞語(yǔ)反映學(xué)術(shù)論文中最重要的特定內(nèi)容的邏輯組合。題名應(yīng)該具有吸引力。題名舉例Neuralstemandprogenitorcellsretaintheirpotentialforproliferationanddifferentiationintofunctionalneuronsdespitelowernumberinagedbrain.Radialglia-likecellspersistintheadultratbrain.Nogginexpandsneuralstemcellsintheadulthippocampus.UpregulationofchemokinereceptorexpressionbyIL-10/IL-4inadultneuralstemcells.題名注意句法結(jié)構(gòu):完整的句子?
特定的詞組?注意內(nèi)容結(jié)構(gòu):處理因素
實(shí)驗(yàn)對(duì)象
實(shí)驗(yàn)效應(yīng)(觀察指標(biāo))DeathreceptorsandcaspasesbutnotmitochondriaareactivatedintheGDNF-orBDNF-depriveddopaminergicneurons題名分析摘要20世紀(jì)60年代國(guó)外首先提出科技論文應(yīng)附摘要,《中華醫(yī)學(xué)雜志》英文版1972年也提出要求附摘要。20世紀(jì)80年代加拿大溫哥華一個(gè)研究小組進(jìn)一步提出結(jié)構(gòu)式摘要,即要求摘要寫法分成四部分,分別冠以標(biāo)題,使讀者無(wú)需查閱正文即可基本了解實(shí)質(zhì)性內(nèi)容。摘要具有獨(dú)立性和自含性,即不閱讀全文,就能獲得必要的信息。
摘要一般應(yīng)說(shuō)明研究工作目的、材料與方法、結(jié)果、結(jié)論等,而重點(diǎn)是結(jié)果和結(jié)論。
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在內(nèi)的神經(jīng)營(yíng)養(yǎng)因子能促進(jìn)中腦DA能神經(jīng)元的存活,但很少有人研究,在這些DA能神經(jīng)元內(nèi),由于剝奪這些營(yíng)養(yǎng)因子而激活的細(xì)胞死亡信號(hào)通路是什么。請(qǐng)翻譯!WeshowherethatdeprivationofGDNForBDNFtriggersanovelmitochondria-independentdeathpathwayintheculturedembryonicdopaminergicneurons:cytochromecwasnotreleasedfromthemitochondriatocytosol,proapoptoticproteinBaxwasnotactivated,andoverexpressedBcl-xLdidnotblockthedeath.這里,我們的結(jié)果顯示:在體外培養(yǎng)的胚胎源DA能神經(jīng)細(xì)胞,剝奪GDNF或BDNF,激活了這些細(xì)胞內(nèi)一條新的非線粒體依賴性死亡信號(hào)通路。因?yàn)?,沒(méi)有細(xì)胞色素C從線粒體釋放到胞漿、前凋亡蛋白Bax也沒(méi)有被激活,且過(guò)表達(dá)Bcl-xL也不能阻止細(xì)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?yàn)?,?xì)胞死亡能被caspase抑制劑BAF(boc-aspartyl(OMe)-fluoromethylketone)完全阻斷;caspase-9、-3、和-7的顯性負(fù)突變體的過(guò)表達(dá)也能顯著地阻滯細(xì)胞死亡。此外,死亡受體通路也參與了細(xì)胞死亡過(guò)程,因?yàn)?,caspase-8或FADD(Fas相關(guān)蛋白細(xì)胞死亡結(jié)構(gòu)域),一種caspase-8激活的必需接頭蛋白,同樣能抑制因GDNF或BDNF剝奪而致的細(xì)胞死亡。LigationofFasbyagonisticanti-FasantibodyinducedapoptosisintheGDNF-orBDNF-maintainedneurons,andinhibitionofFasbyFas-FcchimerablockedthedeathofGDNF-orBDNF-deprivedneurons,whereasFAIM(L)(longisoformofFasapoptosisinhibitorymolecule)couldcontroltheactivityofFasinthedopaminergicneurons.由具有激動(dòng)劑性質(zhì)的抗Fas抗體與Fas結(jié)合可引發(fā)在GDNF或BDNF維持存活下的神經(jīng)元的凋亡,由Fas-Fc嵌合體抑制Fas的作用則能阻滯由GDNF或BDNF剝奪引起的神經(jīng)元死亡,相反,F(xiàn)AIM(L)(Fas
凋亡抑制分子的長(zhǎng)異構(gòu)體?)能控制DA能神經(jīng)元中的Fas活性。
請(qǐng)說(shuō)出該摘要中下列幾部分是怎樣表達(dá)的?目的材料和方法結(jié)果結(jié)論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.引言引言又稱前言,屬于整篇論文的引論部分。其寫作內(nèi)容包括:研究的背景、現(xiàn)狀,存在的問(wèn)題,提出解決問(wèn)題的策略(自己的創(chuàng)新點(diǎn)),闡述所提策略的理論依據(jù)和實(shí)驗(yàn)基礎(chǔ),主要研究?jī)?nèi)容。
引言的文字不可冗長(zhǎng),內(nèi)容選擇不必過(guò)于分散、瑣碎,措詞要精煉,要吸引讀者讀下去。言簡(jiǎn)意賅,不要與摘要雷同,不要成為摘要的注釋。一般教科書中有的知識(shí),在引言中不必贅述。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.結(jié)果為假說(shuō)提供證據(jù)!這篇文章的假說(shuō)是什么?Here,weaddressedthedeathpathwaysinGDNF-andBDNF-deprivedDAneurons.Inbothcases,theneuronsdiedviaanonclassicalapoptoticpathwayinwhichdeathreceptorsandcaspases,butnotmitochondria,wereactivated.結(jié)果(研究?jī)?nèi)容)EmbryonicdopaminergicneuronsdieinculturebecauseofGDNForBDNFdeprivationMitochondrialdeathpathwayisnotactivatedinGDNF-andBDNF-depriveddopaminergicneuronsCaspasesarerequiredforthedeathofGDNF-orBDNF-depriveddopaminergicneuronsThedeathreceptorpathwayisactivatedinGDNF-andBDNF-depriveddopaminergicneuronsDeathreceptorsandcaspasesbutnotmitochondriaare
activatedintheGDNF-orBDNF-depriveddopaminergicneurons討論:從結(jié)果到結(jié)論的過(guò)程!
具有以下幾個(gè)主要特征:①只對(duì)“結(jié)果”進(jìn)行論述,而不應(yīng)進(jìn)行重述。論述其是怎樣支持“結(jié)論”的。②要能指出你的結(jié)果和解釋與以前發(fā)表的著作相一致或不一致的地方。③要論述你的研究工作的理論含義以及實(shí)際應(yīng)用的各種可能性。④要能指出任何的例外情況或相互關(guān)系中有問(wèn)題的地方,并且應(yīng)明確提出尚未解決的問(wèn)題及解決的方向。討論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
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