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简介：客观：在在人的创伤的奔流和正常透镜的上皮的房间之间的原子factor-KB(NF-κB)的表示学习差别。方法：全部的RNAof前面的囊标本从受不了创伤的奔流做半量的RT-PCR并且在在他们之间的NF-κB的表示进行差别的分析的正常cadaveric眼睛施主和那些在显微镜下面被拿。结果：作为与在正常控制组的0.8337的平均数相比，NF-κB的表示等价物为在创伤的奔流患者的透镜的上皮的房间是0.9074，并且差别具有显著意义(t=2.447，P<0.05)因此。结论：NF-κB是可能的对必要的一种抄写因素维持正常透镜的上皮的房间的新陈代谢。在创伤的奔流患者可得到的更高的NF-κB“透镜的上皮的房间工具NF-κB具有到创伤的奔流的出现和开发的可能的关联的s。

简介：RecentstudiessuggestthatMHCclassⅡgenetransfercouldstimulateprotectiveantitumorimmunity.WhetherxenogeneicMHCⅡtransfectedtumorcellshavetheseeffectisunknown.Inthisstudy,HLA-DR3αandβchaincDNAwereclonedbyRT-PCRfromhumanBlymphomaRajicelllineandconfirmedbyDNAsequencing.TherecombinantexpressingvectorswereconstructedbyinsertingtheαandβchaincDNAintoPCEP4/pLXSNvectorsrespectively.AftertransfectingbylipofectamineandselectingwithG418andHyg,theHLA-DR3transfectedmousemelanomaB16recombinantcloneswereobtained.Approximately59%ofthe

简介：ObjectiveTo观察激活p21的kinase6(PAK6)在在成年rat.MethodsSprague-Dawley老鼠的针的绳索损害(SCI)以后的表示和它的可能的角色受到针的绳索损害。为了探索PAK6，表示模式和PAK6的分发的病理学、生理的意义，没被西方的污点观察，免疫组织化学和immunofluorescence.ResultsWestern污点分析证明PAK6蛋白质水平在白天2和白天4上是显著地起来调整的，然后减少了并且有到白天14为止的起来规定。免疫组织化学分析证明PAK6的表示显著地在与控制组相比的白天4上被增加。而且，染色的两倍immunofluorescence证明PAK6首先在控制组在神经原和星形细胞被表示。当时在损害以后，PAK6的表示在星形细胞显著地被增加，神经原，和星形细胞大部分被增殖。我们也检验了增殖的房间的表示原子抗原(PCNA)并且发现它的变化与PAK6的表示被相关。重要地，在在受伤针的绳索的PAK6的injury.ConclusionThe起来规定可以与glial增长被联系以后，染色的两倍immunofluorescence表明PCNA评估的房间增长在白天4上出现在许多PAK6-express-ing房间。

简介：Objective:Tostudytheeffectofdecoy-oligodeoxynucleotides(decoy-ODNs)indumbbellshapewiththeoligodeoxynucleotidesequencesimilartonuclearfactorkappaB(NF-κB)cis-elementsonexpressionofinflammationmediatorsinpMΦcellsfromrats.Methods:Withcarriersofcationicliposomes,decoy-ODNsweretransfectedintopMΦcellsofrats.Thentheinhibitingeffectsofthedecoy-ODNsontumornecrosisfactorα(TNFα),interleukin-6(IL-6)andIL-10wereanalyzed.Results:Decoy-ODNscoulddecreasetheexpressionofTNFαandIL-6indose-dependentfashionbuthadweakerinhibitingeffectonIL-10.Conclusions:Decoy-ODNstargetingNF-κBcandecreasetheexpressionofinflammatorymediatorsinpMΦcellsfromrats.

简介：Objective:Tomonitorthesystemicgeneexpressionprofileinamurinemodeloflipopolysaccharide-inducedacutelunginjury.Methods:Acutelunginjurywasinducedbyintratrachealinjectionoflipopolysaccharidein3mice.Another3normalmicereceivingsamevolumeofnormalsalineweretakenasthecontrols.Thecomprehensivegeneexpressionprofilewasmonitoredbytherecentlymodifiedlongserialanalysisofgeneexpression.Results:Atotalof24670tagsrepresenting12168transcriptsinthecontrolmiceand26378tagsrepresenting13397transcriptsinthemicewithlunginjurywereidentifiedrespectively.Therewere11transcriptsincreasingand7transcriptsdecreasingmorethan10foldsinthelipopolysaccharide-treatedmice.ThemostoverexpressedgenesinthemicewithlunginjuryincludedserumamyloidA3,metallothionein2,lipocalin2,cyclin-dependentkinaseinhibitor1A,lactatedehydrogenase1,melatoninreceptor,S100calcium-bindingproteinA9,natriureticpeptideprecursor,etc.Mitogenactivatedproteinkinase3,serumalbumin,complementcomponent1inhibitor,andATPsynthasewereunderexpressedinthelunginjurymice.Conclusions:Serialanalysisofgeneexpressionprovidesamolecularcharacteristicofacutelunginjury.

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简介：Objective:Toobservetheexpressionoflamininandfibronectininalkali-burnedcorneasinrats.Methods:Atotalof18normalWistarratswererandomlydividedinto6groups(n=3ineachgroup).Foreachrat,oneeyewasinjuredbyalkaliburn,theotheronewastakenasthenormalcontrol.Thenallthecorneasweresurgicallyremovedandtheexpressionoflamininandfibronectinwasobservedwithimmunohistochemistryrespectivelyat7hours,1day,3days,7days,14daysand28daysafteralkaliburn.Results:Comparedwiththatofthenormalcontrols,theexpressionoflamininandfibronectinoftheburnedeyeswasdramaticallyhigherat7hours,reachedpeakat14daysanddecreasedtothenormallevelat28daysafteralkaliburn.Conclusions:Intheprocessofwoundhealingafteralkaliburn,theexpressionoflamininandfibronectinincreasesdramatically,whichsuggeststhatlamininandfibronectinmayparticipateintheprocessofcornealwoundhealing.

简介：Objective:ToexploretheexpressionofmRNAanditsproteininburnedratsandtheireffectsofburnwoundhealing.Methods:Apartial-thicknessburnof30%totalbodysurfaceareawascreatedonthebackof40Wistarrats.Insituhybridizationandimmunohistochemicalmethodswereusedtoexaluatethelocationandtheamountofthec-fosmRNAanditsproteininnormalskinandtheburnedskin,respectively,at3h,6h,1d,3d,7dand14dafterburn.Results:Underalightmicroscope,boththeexpressionofc-formRNAanditsproteincouldbefoundinthenormalskin,buttheirinductionlevelsweremuchhigherintheburnedskin.Thelevelofforproteinexpressionreachedpeakat3hafterburnwhilethatofc-formRNAreachedpeakat6hafterburn.Conclusions:Theexpressionofc-foscanbeinducedbyburns.Andthepeaklevelexpressionofc-formRNAcomeslaterthanthatofc-fosprotein.Itindicatesthattheactionoffosproteinisinducedbypost-translationalmodificationofpre-existingfosmolecules.

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简介：Objective:ToinvestigateCaspase-3expressionanditsroleinneuronalapoptosis.Methods:TheT13-L2spinalcordofratswasinjuredbytractionaftertheamplitudeofP1-N1wave,monitoredbyacorticalsomatosensoryevokedpotential(CSEP)monitor,decreasedtoseventypercentofthatbeforeoperation.Thenratswerekilledin6h,1d,4d,7d,14dand21drespectivelyafteroperation.Flowcytometerterminaldeoxynucleotldyltransferease-mediatedbiotinylateddeoxynuridinetriphosphatenickendlabeling(TUNEL),Caspase-3activityassayandimmunohistochemicalmethodwereappliedtoinvestigateCaspase-3expressioninthespinalcordtissueandtostudyneuronalapoptosisinrats.Results:Afterspinalcordinjury,apoptoticcellsdetectedbyflowcytometryandTUNEL-positivecellsweresignificantlymore,andpositiveimmunohistochemicalstainingofCaspase-3andCaspase-3activityweresignificantlyhigherinGroupinjurythaninGroupscontrolandlaminectomy,respectively(P>0.05,P>0.01).Similartrendofchangeswasnoticedinapoptoticcells,TUNEL-positivecellsandpositiveimmunohistochemicalstainingofCaspase-3,allofwhichreachedtheirrespectivepeak7daysafteroperation.Caspase-3activityreacheditspeak,however,4dayspostoperatively.Conclusions:IncreasedexpressionandactivityofCaspase-3proteininneuronsaftertractivespinalcordinjuryisthebiochemicalsignalofearlyspinalcellapoptosis.Itisofgreatsignificanceforunderstandingthemechanismofspinalcordinjury.

简介：Objective:TostudythechangesofthegeneexpressionpatternofspinalcordtissuesintheearlystageafterinjurybyDNAmicroarray(genechip).Methods:ThecontusionmodelofratspinalcordwasestablishedaccordingtoAllen'sfallingstrikemethodandthegeneexpressionpatternsofnormalandinjuredspinalcordtissueswerestudiedbygenechip.Results:Theexpressionof45geneswassignificantlychangedintheearlystageafterspinalcordinjury,inwhich22genesup-regulatedand23genesdown-regulated.Conclusions:Theexpressionofsomegeneschangessignificantlyintheearlystageafterspinalcordinjury,whichindicatesthecomplexityofsecondaryspinalcordinjury.

简介：Objective:Toinvestigatetheexpressionofneurotrophin-3(NT-3)geneinSchwanncellsofratsciaticnerveintroducedbyanadenovirusvectorinvivo.Methods:ArecombinantadenovirusvectorforNT-3(Ad-NT-3)waspropagatedin293packagingcellsandtiteredwithtissuecultureinfectiousdose50(TCID50).Ad-NT-3wasinjecteddirectlyintotheratsciaticnerveaftertransectionandimmediaterepair.ImmunohistochemicalstainingwasemployedtodeterminetheexpressionofNT-3inSchwanncellsinratsciaticnerveandtheexpressiveintensityofthetissueslicesofthesciaticnervewasmeasuredwithLEICAM550imageanalysissystem.Results:Onthe2nddayafterinjectionofAd-NT-3,positivestainintheSchwanncellswasapparentinthevicinityofanastomosis.NT-3expressionincreasedsignificantlyonthe7thday(P<0.01)andthendecreased14-28daysafterinjection(P<0.01).TherewasnosignificantdifferenceofNT-3expressionbetweenthe14thand28thdaygroups(P>0.05).Comparedwiththe2nddaygroup,the14thand28thdaygroupsstillmaintainedarelativelyhighlevelofNT-3(P<0.01).Intactandrepairednerves,whichwereinjectedwithadenovirusencodingLacZgenes(Ad-LacZ)orphysiologicalsalineservedascontrols,showednoNT-3-positiveSchwanncells.Conclusions:AnadenovirusvectorcanbeusedtoinduceefficientlytheexpressionofNT-3geneinSchwanncellsofratperipheralnervesfollowingnerveinjuryandrepair,whichsuggeststhatneurotrophicfactorscanbeintroducedintoSchwanncellswithanadenovirusvectortopromoteperipheralnerveregeneration.

简介：Objective:ToinvestigatetheeffectofsubstanceP(SP)ongeneexpressionoftransforminggrowthfactorβ-1(TGFβ-1),transforminggrowthfactorreceptor-1(TGFR-1)andtransforminggrowthfactorreceptor-2(TGFR-2)infibroblastsculturedinvitrofromrat'sgranulationtissues.Methods:Thefibroblastsfromthegranulationtissuesintheskeletalmuscleofrat'shindlimbsinjuredbyformaldehydewereculturedinvitro.Whendifferentconcentrations(10-9-10-5mol/L)ofSPwereaddedintotheculturemedium,thechangesofgeneexpressionofTGFβ-1,TGFR-1andTGFR-2intheculturedfibroblastswereobservedwithreversetranscriptionpolymerasechainreactionatdifferentintervals(0,3,6,12and24hoursafterincubation).Results:ThegeneexpressionofTGFβ-1,TGFR-1andTGFR-2inthefibroblastsculturedfromrat'sgranulationtissueswasup-regulatedbySP.ThepeaklevelofthemRNAexpressionwasfoundat10-8mol/LSPandtheup-regulationeffectwasnotfoundat10-5mol/Land10-6mol/L.ThepeaklevelsofgeneexpressionofTGFβ-1,TGFR-1andTGFR-2inthefibroblaststreatedwithSPwereachievedat6and12hours,respectively.Conclusions:SPhasup-regulationeffectonthegeneexpressionofTGFβ-1,TGFR-1andTGFR-2infibroblastsfromrat'sgranulationtissuesinvitro,andtheeffectisrelatedtodifferentstimulatingconcentrationsofSP.Itmaybeconcernedwithproliferationanddifferentiationoffibroblastsandformationofscartissuesduringwoundhealing.

简介：Objective:TostudytherelationshipbetweentheexpressionofBax,Bcl-2proteins,andapoptosisinradiationcompoundwoundhealingofrats.Methods:Apoptosis,BaxandBcl-2proteinswereestimatedbyinsituterminallabeling(TUNEL)andimmunohistochemicalmethods.Results:(1)Changesoftheapoptosisinwoundhealingshowedthreetypicalcharacteristics:earlyoccurrence,highfrequencyanddelayeddisappearanceafterradiationtoratswhencomparedwiththoseofsimplewoundgroup,whichmightbeanimportantreasonforradiation-induceddelayedwoundhealing.(2)TheexpressionofBaxproteinincreasedevidentlywiththeincrementofapoptosisandshowedagoodcorrespondingrelationshipwiththeapoptoticfrequencyintheprocessofwoundhealing.WhiletheexpressionofBcl-2proteindecreasedobviouslyastheapoptosisreachedamaximumandshowedincreasingtendencyuptonormallevelwhentheapoptosisdecreaseddistinctively.Conclusions:BaxandBcl-2proteinsplayanimportantroleintheapoptoticregulationofradiationcompoundwoundhealinginrats.

简介：Objective:Toexploretheeffectsofhyperbaricoxygen(HBO)treatmentontheneuronalapoptosisatanearlierstageandtheexpressionsofCytochromeC(CytC),Bcl-2(B-celllymphoma-2family)andBax(Bcl-2associatedXprotein)inratbraintissuesaftertraumaticbraininjury(TBI).Methods:Fortyadultratsweredividedintotwogroups,i.e.,GroupA(theratswithuntreatedTBI)andGroupB(ratswithHBOtreatmentafterTBI).Sectionsofbraintissuesofthesetwogroupswerethendetectedat3,6,12,24,72hoursafterTBIbyimmunohistochemistryandelectronmicroscope,respectively.Results:HBOtreatmentcouldup-regulatetheexpressionofBcl-2within72hours,reducethereleaseofCytCfrommitochondria,attenuatetheformationofdimericBaxandalleviatethemitochondrialedemawithin24hoursafterTBI.Conclusions:HBOtreatmentcanalleviateneuronalapoptosisafterTBIbyreducingthereleaseofCytCandthedimersofBaxandup-regulatingtheexpressionofBcl-2.

简介：Objective:ToinvestigatetheeffectofRadixPaeoniaeRubra(RPR)ontheexpressionofhemeoxygenase(HO-1)andinducednitricoxidesynthase(iNOS)inendotoxin-inducedacutelunginjuryinratsanditsprotectivemechanism.Methods:FortyWistarratsweredividedrandomlyinto5groupswith8ratsineachgroup:salinecontrolgroup(NSgroup),lipopolysaccharidegroup(LPSgroup),RPR-treatmentgroup,RPR-preventiongroupandHemingroup.TheeffectofRPRonproteincontent,theratioofneutrophilesinbronchoalveolarlavagefluid,malondialdehyde(MDA)contentinthelungandtheactivityofserumNOwereobserved.Arterialbloodwasdrawnforblood-gasanalysis.TheexpressionofHO-1andiNOSinlungtissueswasdetectedbyimmunohistochemitryandmorphometrycomputerimageanalysis.Thehistologicalchangesofthelungwereobservedunderlightmicroscope.Results:ComparedwiththatinNSgroup,theexpressionofHO-1andiNOSwasmarkedlyincreasedinLPSgroup(P<0.01).InRPR-treatment,RPR-prevention,andHemingroups,theexpressionofiNOSwassignificantlylower,whiletheexpressionofHO-1washigherthanthatinLPSgroup(P<0.05).Theproteincontent,theratioofneutrophilesinbronchoalveolarlavagefluid,thecontentofMDAandtheactivityofserumNOinLPSgroupweresignificantlyhigherthanthoseinNSgroup(P<0.01).TherewasasignificantdecreaseinthelevelofarterialbicarbonateandpartialpressureofoxygenintheLPSgroup(P<0.01);theseparametersoflunginjuryhowever,weresignificantlylowerinRPR-treatment.RPR-prevention,andHemingroupsthanLPSgroup(P<0.05orP<0.01).ThepathologicchangesoflungtissuesweresubstantiallyattenuatedinRPR-treatment,RPR-prevention,andHemingroupsthanLPSgroup.Conclusions:ThehighexpressionofHO-1reflectsanimportantprotectivefunctionofthebodyduringlipopolysaccharide-inducedacutelunginjury.TheprotectiveeffectofRPRonlipopolysaccharide-inducedacutelunginjuryisrelatedtotheinhibi

简介：ToexploretherelationshipbetweensubstanceP(SP)releasedfromperipheralnerveendingsandtheexpressionofepidermalgrowthfactor(EGF)andepidermalgrowthfactorreceptor(EGFR)duringwoundhealing.Methods:FiftyWistarratswererandomlydividedinto2groups,injurygroupandcapsaicingroup.Intheinjurygroup,afull-thicknessskinwoundonthebackoftheratwastaken.Thewoundedgeandgranulationtissuesweretakenonthe1st,3rd,6th,9th,12thdaysafterinjury,respectively.Inthecapsaicingroup,capsaicinwasinjectedsubcutaneouslyonthebackoftheratstodestroythesensorynervetopreventthesecretionofSP,thenawoundandsamplewasmadeinthesameway.ImmunohistochemistryandinsituhybridizationwereemployedtodetecttheexpressionofSP,EGF/EGFR,andEGFmRNA/EGFRmRNAinthegranulationtissues.Results:Intheinjurygroup,immunohistochemicalstainofSPandEGF/EGFRwaslocatedonthehairfolliclesandsebaceousglandsatthe1stday.AndthestainofSPwasobviousatthe3rddayinthegranulationtissues,thendecreasedgradually.EGF/EGFRwasatlowlevelatthe3rdday,thenincreasedgraduallyandreachedthepeakatthe9thday,thendeclined.Inthecapsaicingroup,theimmunohistochemicalstainofSPandEGF/EGFRwasfaintandwithoutobviouschangeduringthewoundhealingprocess.ThetendencyoftheEGFmRNA/EGFRmRNAexpressionwassimilartothatofEGF/EGFR.Conclusions:Duringwoundhealing,SPmaypromotethehealingprocessbyaffectingtheexpressionofEGF/EGFRinthegranuationtissues.

简介：Objective:Toinvestigatetheneointimaformationandtheexpressionofmonocytechemoattractantprotein-1(MCP-1)andtumornecrosisfactor-α(TNF-α)incuff-inducedvascularinjuryinmousemodel,andtoexaminetheeffectofangiotensinIItype1receptor(AT1)blocker,olmesartan,onMCP-1andTNF-αexpressionandconsequentlyvascularremodeling.Methods:Vascularinjurywasinducedbypolyethylenecuff-placementaroundthemousefemoralartery.SomemiceweretreatedwithAT1receptorblocker,olmesartan,atthedoseof3mg*kg-1*day-1withanosmoticminipump.Neointimaformationandtheproliferationofvascularsmoothmusclecells(VSMCs)weremeasuredbymorphometricanalysisandbromodeoxyuridine(BrdU)incorporation.MCP-1andTNF-αexpressionwasdetectedbyWesternblotandimmunohistochemicalstaining.Results:Weobservedneointimaformation14daysaftercuffplacementaswellasVSMCsproliferationinthemediaandneointima.CuffplacementalsoinducedMCP-1andTNF-αexpressioninthemediaandneointimathattheVSMCsspecificallyexisted.Treatmentofmicewitholmesartanatadoseof3mg*kg-1*day-1,whichdidnotinfluencesystolicbloodpressure,significantlydecreasedneointimaformationandtheproliferationofVSMCs.OlmesartanalsoinhibitedMCP-1andTNF-αexpressionintheinjuredarteries.Conclusions:OurresultsdemonstratethatblockadeofAT1receptorinhibitsMCP-1andTNF-αexpressionandtherebyimprovesvascularremodeling.

简介：Objective:Toinvestigatethebiologicalfunctionofplatelet-derivedgrowthfactorB(PDGF-B)onthesurvivalandproliferationofcatcornealendothelialcellssoastoprovidebasesforfurtherstudiesofitsroleinwoundrepairanditsclinicalapplication.Methods:TotalRNAwasextractedfromtheplacentatissuesofhealthypregnantwomenundergoinghysterotokotomyandPDGFeDNAwasobtainedwithre-versetranscription-polymerasechainreaction(RT-PCR).TheprokaryoticexpressionvectorpET-PDGF-BwasconstructedandexpressedtherecombinantPDGF-BinEscherichiacoli(E.coli)BL21(DE3).AfterpurificationandrefoldingonNi2+-chelationaffinitychromatography(NTA)column,itwasusedtoculturecatcornealendothelialcells.Cellproliferationwastestedbymodifiedtertrazoliumsalt(MTT)andflowcytometer.Andthemorphologicchangeandtheultrastructurewereob-servedunderaninvertedphasecontrastmicroscope,ascan-ningelectronmicroscopeandatransmissionelectonmicroscope,respectively.Results:PDGF-Bchainpeptide(PDGF-BB)genewassuccessfullyinsertedintotheprokaryoticexpressionvector,pET-28a(+).ThepurifiedrecombinedproteinpET-PDGF-Bshowedasinglebandonsodiumdodecylsulfatepolyacry-lamidegelelectropheresis(SDS-PAGE)withthemolecularweightofabout27u,whichwasinagreementwiththede-ducedvalue.MTTandflowcytometryshowedthatPDGF-BBpromotedthesurvivalandproliferationofcatcornealen-dothelialcells.Conclusions:Theconstructionofrecombinantprokary-oticexpressionvectorpET-PDGF-BandthepreparationofPDGF-BBproteinprovideafoundationforfurtherstudyofthefunctionofPDGF-BBandproducingbiologicalPDGF-BBprotein.TheexpressedPDGF-BBpromotestheprolif-erationofculturedcatcornealendothelialcells.