正式生物医学写作英文小论文1

浙江大学姓名：杨霞学号：21118228年级：2011级TheprotectiveeffectofTNF-MAbonacutepancreatitisAbsractBackground:Acutepancreatitisisaninflammatorydiseasecharacterizedbytissueedema,acinarnecrosis,hemorrhageandfatnecrosisaswellasinflammationandperivascularinfiltrationinthepancreas.Althoughtheexactetiologyofacutepancreatitisisstillunclear,somestudieshaveshownthattumornecrosisfactor(TNF-α)involvesinthepathogenesisofacutepancreatitis.ItremainsunknownwhetherMonoclonalTumorNecrosisFactorAntibody(TNF-MAb)hasprotectiveeffectonacutepancreatitisornot.TheaimofthisresearchistoinvestigatetheprotectiveeffectofTNF-MAbonacutepancreatitis.Method:Atotalof48healthySpragueDawleyratsweredividedintothreegroups,experimentalgroup,controlgroupandtreatmentgroup.ThelevelofTNF-αinserumofratsweremeasuredatintervalsof24and48hoursoftreatmentwithsurgery,andthepanthologicalalterationswereobservedwithlightmicroscopyandelectromicroscopy.Results:TheexperimentalgroupshowedahigherlevelofTNF-αinserumthanthecontrolgroup.ThelevelofTNF-αinserumofthetreatmentgroupshowedasignificantdecrease.Theexperimentalgroupexhibitedmuchseverepanthologicalalterations,withthetreatmentgrouplessserioussymptomsandthecontrolgroupnoapparentsymptoms.Conclusion:Astheresultsofthepresentreseachshown,itcouldconcludethatTNF-αinterferswiththepathogenesisofacutepancreatitis,andTNF-MAbhasaprotectionagainstacutepancreatitisandcanreducethelevelofTNF-αinserumofratssufferingfromacutepancreatitis.Keywords:acutepancreatitis,panthologicalalterations,TNF-α,rats1.Introduction:Acutepancreatitisisaninflammatorydiseasecharacterizedbytissueedema,acinarnecrosis,hemorrhageandfatnecrosisaswellasinflammationandperivascularinfiltrationinthepancreas.Althoughtheexactetiologyofacutepancreatitisisstillunclear,somestudyshowsthattumornecrosisfactor(TNF-α)involvesinthepathogenesisofacutepancreatitis.ItremainsunknownwhetherMonoclonalTumorNecrosisFactorAntibody(TNF-MAb)hasprotectiveeffectonacutepancreatitisornot.InordertoinvestigatetheprotectiveeffectofMonoclonalTumorNecrosisFactorAntibody(TNF-MAb)onacutepancreatitis,wemakethemodelofacutepancreatitisbysurgeryanddrug,anddivideintothreegroupstodoourresearch.TheaimofourstudyistoinvestigatetheprotectiveeffectofTNF-MAbonacutepancreatitis.MaterialsandMethods2.1AnimalsandtreatmentAtotalof48healthySpragueDawleyratsweighing250～300g,regardlessofgender,werepurchasedfromShanXitraditionalChinsemedicineAcademy.Animalswerehousedinstainlesssteelcagesinaventilatedanimalroom.Roomtemperaturewasmaintainedat20±2◦C,relativehumidityat60±10%,anda12-hlight/darkcycle.Distilledwaterandsterilizedfoodforratswereavailableadlibitum.Theywereacclimatedtothisenvironmentfor5dayspriortodosing.Allproceduresusedinanimalexperimentswereincompliancewiththeethicscommittee.Animalswererandomlydividedintothreegroups:experimentalgroup,controlgroupandtreatmentgroup.Animalswerefastedovernightbeforetheexperiment,buthadfreeaccesstowater.Anesthesiawasinducedwithintraperitonealinjectionof1%pentobarbital.Afteranesthesiaalltheratswerecutinabdomenatthecenteroftheepigastriumandweredealtwithligtationofthepancreaticduct.Theexperimentalgroupandcontrolgroupwererespectivelyinjected5%sodiumtaurocholateandphysiologicalsalineonmulti-locusofpancreascapsule.ThetreatmentgroupwereaddtionallyinjectedTNF-MAbincaudalvein,comparedwiththeexperimentalgroup.1mlserumofeachratatintervalsof24and48hoursoftreatmentwithsurgerywereobtainedfromcaudalveinandthelevelofTNF-αinserumwasmeasuredbythemethodofenzymelinkedimmunosorbentassay(ELISA).2.2ChemicalsandinstrumentsPentobarbitalandsodiumtaurocholatewerepurchasedfromSigmaofAmerica.ThelightmicroscopywaspurchasedfromShanghaiopticalinstrumentfactoryandtheelectromicroscopyfromHITACHICo.,Japan.2.3.MicroscopyPancreatictissueofeachratwascutrapidlyafter48h.Onepartofthetissuewasfixedwith10%formaldehyde,andthendehydrated,withgradesofethanol(70,80,90,95and100%).Dehydrationwasthenfollowedbyparaffineimbeddingandblockingout.Paraffinsectionsweregeneratedandthenobservedwithlightmicroscopy.AnotherpartofpancreatictissuefromeachratwasLiverwasfixedby2.5%glutaraldehydein0.1mol/dm3cacody-latebufferfor2h,washedthreetimeswith0.1mol/dm3cacodylatebuffer(pH7.2–7.4)andpostfixedfor1hin1%osmiumtetraoxide.Thespecimensweredehydratedbyagradedseriesofethanol(75%,85%,95%,and100%)andembeddedinEpon812.Ultrathinsectionsweregenerated,contrastedwithuranylacetateandleadcitrateandobservedwithaJEOL1010TEM.2.4.StatisticalanalysisStatisticalanalyseswereconductedwithSPSS11.7software.Datawereexpressedasmeans±SE.One-wayanalysisofvariance(ANOVA)wascarriedouttocomparethedifferencesofmeansamongmulti-groupdata.Dunnett’stestwascarriedoutwheneachgroupofexperimentaldatawascomparedwithsolvent-controldata.Statisticalsignificanceforalltestswasjudgedataprobabilitylevelof0.05.Results3.1ThelevelofTNF-αinserumofratsatintervalsof24and48hoursaftertreatmentwithsurgeryTheexperimentalgroupshowsahigherlevelofTNF-αinserumthanthecontrolgroup.ThelevelofTNF-αinserumofthetreatmentgroupshowsaremarkabledecrease.Thesedifferencesaresignificant(P＜0.05).TheresultscanbeshowninthefollowinggraphGraph1.thelevelofTNF-αinserumofratsatintervalsof24and48hoursaftertreatmentwithsurgery3.2.PancreaticpanthologicalevaluationComparedwiththecontrolgroup,thefollowingpanthologicalalterationsweredetectedinsideandoutsidethepancreaticintheexperimentalandtreatmentgroups.Thesepanthologicalalterationsoftheexperimentalgroupwereobservedinfigures1.Insideandoutsidethepancreaticlobleoftheexperimentalgroup,patchynecrosis,alargenumberofinflammatorycellsinfiltrated,heavymitochrondrialswelling,partialmitochrondrialcristaobliteration,endoplamicreticulumderangementandavacuole-likestructureincytoplasmcanbeobserved.Thetreatmentgroupshowpetechialhemorrihage,aslightmitochrondrialswelling,asmallnumberofinflammatorycellsinfiltrated,endoplamicreticulumderangementandexpansion,comparedwiththeexperimentalgroup.Noapparentpanthologicalalterationscanbeobservedinsideandoutsidethepancreaticlobleofthecontrolgroup.xiFig1.Therearemanginflammatorycellsinfiltratedcanbeobservedinpancreatictissue.(640*415)4.DiscussionTheresultsofthisstudyindicatethatthelevelofTNF-αinserumshowsasignificantdecreaseaftertreatmentwithTNF-MAb.Besidessomestudieshaveshownthattumornecrosisfactor(TNF-α)involvesinthepathogenesisofacutepancreatitis.Tumornecrosisfactor(TNF)-alphaisapleiotropiccytokinethatexertshost-damagingeffectsindifferentautoimmuneandinflammatorydiseases.Itisakeyregulatorofotherproinflammatorycytokinesandofleukocyteadhesionmolecules,anditisaprimingactivatorofimmunecells.Inrecentyears,severalresearchlines-mostlyderivedfromanimalmodelsandinvitrostudies-suggestedthatTNF-alphaplaysapivotalroleinthepathogenesisofacutepancreatitis.Inparticular,itcontributestothesystemicprogressionoftheinflammatoryresponseandtotheend-organdysfunctionoftenobservedinseveredisease.MonoclonalTumorNecrosisFactorAntibody(TNF-MAb)istheantibodyofTNFandcancombinewithTNFtoremovetheeffectofTNFintheprocessofacutepancreatitis.SowethinkthatMonoclonalTumorNecrosisFactorAntibody(TNF-MAb)hasprotectiveeffectonacutepancreatitis.Conclusion:ThelevelofTNF-αinserumofratsfromtheexperimentalgroupishigherthanthatofthecontrolgroupandrisescontinuouslyduringthe48hofnotreatment.Thepanthologicalalterationsoftheexperimentalgroupdegeneratewiththetimeofnotreatment,andtheextentofdamageofpanthologicalalterationsofpancreascorrelatescloselywiththelevelofTNF-αinserum.Incomparisonwiththeexperimentalgroup,thelevelofTNF-αinserumofratsfromthetreatmentgroupdroppedapparently,andthestateofpanthologicalalterationsimprovedsignificantly.Astheresultsofthepresentreseachshown,someconclusionscanbedrawnasfollowing.Firstly,TNF-αinterferswiththepathogenesisofacutepancreatitis.Secondly,TNF-MAbhasaprotectiveonacutepancreatitis.Thirdly,TNF-MAbcanreducethecontentofTNF-αinserumofratssufferingfromacutepancreatitis.References1.SchwarzM,ThomsonJ,MeyerH,BüchlerMW,BegerHG:Frequencyandtimecourseofpancreaticandextrapancreaticbacterialinfectioninexperimentalpancreatitisinrats.Surgery2000;127:427–432.2.SteerML:Etiologyandpathophysiologyofacutepancreatitis;inGoVLV,DiamagnoEP,GardnerJD,LebenthalE,ReberA,ScheeleGA(eds):ThePancreas:Biology,Pathophys-iology,andDisease.NewYork