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.

简介：Objective:Todetecttheconcentrationofmonocytechemoattractantprotein-1(MCP-1)intheserumofpatientswithincompletespinalcordinjuryandevaluateitsrelationwiththepathologicclassificationofthespinalcordinjury.Methods:MCP-1concentrationintheserumofpatientswithincompletespinalcordinjury(iSCI),singlespinecompressionandhealthysubjectsweredetectedbyELISA,respectivelyinthepresentstudyandthemagneticresonanceimagingdataofthesepatientswerestudiedatthesametimeonablindbase.Results:SerumlevelofMCP-1iniSCIpatientswas428pg/ml±11pg/mlbyELISA,whichwashigherthanboththatofthepatientswithsinglespinecompressionandofcontrols,withtheconcentrationof184pg/ml±21pg/mland124pg/ml±15pg/ml,respectively.Therewassignificantdifferencebetweenanytwogroups(P<0.01).iSCIpatientswithnormalMRIshowedalowerserumlevelofMCP-1as312pg/ml±30pg/ml.Pathologicalclassificationofspinalcordedemaandhematomacorrespondedto390pg/ml±16pg/mland508pg/ml±24pg/mlintheconcentrationofMCP-1.Conclusions:MCP-1mayinducesecondaryinflammatoryresponsebyrecruitinginflammatorycellstotheinjurysiteandthusaffecttheprognosisofspinalcordinjury.

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简介：Objective:Toexplorethecontentchangeofneurofilament(NF)proteinsubunitsintheexperimentalbraindiffuseaxonalinjury(DAI)bylateralheadrotation.Methods:Twenty-fourSpragueDawley(SD)ratswereequallydividedintothreeinjurygroups(2h,12h,and24hpostinjury)andonecontrolgroup.ThemodelsofDAIweremadeintheinjurygroupsbylateralheadrotation.westernblottingtechniquewasusedtomeasuretheconteneofNF68(akindofNFproteinsubunit)inthebrainstemtissuesamongalltheinjuredandcontrolrats.TheNF68immunohistochemicalstainingwasusedinanothersixSDratsinordertoobservethemorphologicalchangesinDAI.Results:TheNF68contentinthebrainstemtendedtodecreaseat2hpostinjury,decreasedsignificantlyat12handcontinueditsdecreaseat24h.NF56andNF52,asthebreakdownproductsofNF68,hadatendencytoincreaseat2-12haftertheinjury,andamountedtoasignificantlyhigherlevelat24h.Microscopically,therewerealotofswellingneuronalaxonsintheventralpartofthemedullaroblongateat2haftertheinjury.someaxonsweredisconnected,andaxonalretractionballsformedontheirproximalend.Conclusions:ThereisandoccurrenceofphosphorolysiswithinthebrainsteminDAIbylateralheadrotation.ThesereactionscausethebreakdownofNF68,whichresultsinthedecreaseofNF68incontent.ItsuggeststhatthebreakdownofneurofilamentproteinsubunitsisanimportantreasonforstructuraldestroyofneurofilamentsinDAI.

简介：Objective:Toexploretheeffectofdexamethasonebylocaltreatmentofcerebraledemaandbraindamageafterbraininjury.Methods:Twenty-tworabbitswereclassifiedinto2groups,GroupA(thecontrolgroup,n=11)andGroupB(thetreatedgroup,n=11).Anrabbitbraincontusionmodelwasmadebybonewindowplastybyextraduralhitting.Groupbwastreatedbylocalinfiltratingandsprayingofdexamethasoneatequidistancetolesions.GroupAwasgivennormalsalineinthesamewayasGroupB.Thechangesofmoistureinbraintissuesandserummyelinbasicprotein(MBP)wereobserved.Results:ThepercentageofwatercontentindamagedhemisphereinGroupAandGroupbwas81.7%±0.56%and79.45%±0.52%respectively.Therewasasignificantdifferencebetweenthe2groups(P<0.05).ThenormallevelofMBPwas1.66μg/L±0.71μg/L,whilethevalueofMBPinGroupAandGroupbwere5.98μg/L±2.08μg/Land3.15μg/L±1.09μg/Lseparately.ThelevelofMBPinGroupAandGroupBwerehigherthannormallevelandtherewasalsoasignificantdifferencebetweenGroupAandGroupB(P<0.05).Conclusions:TheresultsofourstudyshowedthatthebrainmoistureandMBPinserumwereincreasedafterbraininjurywhilereducedaftertreatmentwithdexamethasone.ItisdemonstratedthatlocaltreatmentofbraininjurywithdexamethasonehasanobvioustherapeuticeffectoncerebraledemaandserumMBP.

简介：Objective:ToanalyzethedynamicchangeofserumproteinS100binpatientswithtraumaticbraininjuryanditsclinicalvalueinassessingbraindamage.Methods:AccordingtoGlasgowcomascale(GCS),102casesoftraumaticbraininjuryweredividedintomildbraininjurygroup(GCS≥13,n=31,GroupA),moderatebraininjurygroup(8

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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:Toevaluatetheosteogenicpotentialofbonemorphogeneticprotein(BMP)-2genetransfectedgoatbonemarrow-derivedmesenchymalstemcells(MSCs).Methods:Goatbonemarrow-derivedMSCsweretransfectedbyAdv-humanbonemorphogeneticprotein(hBMP)-2gene(Group1),Adv-betagaltransfectedMSCs(Group2)anduninfectedMSCs(Group3).Westernblotanalysis,alkalinephosphatasestaining,VonKossastainingandtransmissionelectronmicroscopywereadoptedtodeterminethephenotypeofMSCs.Thenthecellswereinjectedintothighmusclesofthenudemice.Radiographicalandhistologicalevaluationswereperformedatdifferentintervals.Results:OnlyAdv-hBMP-2transfectedMSCsproducedhBMP-2.Thesecellswerepositiveforalkalinephosphatasestainingatthe12thdayandwerepositiveforVonKossastainingatthe16thdayaftergenetransfer.Electronmicroscopicobservationshowedthatthereweremoreroughendoplasmicreticulum,mitochondriaandlysosomesinAdv-hBMP-2transfectedMSCscomparedtoMSCsofothertwogroups.Atthe3rdand6thweeksaftercellinjection,ectopicboneswereobservedinmusclesofnudemiceofGroup1.Onlyfibroustissueoralittlebonewasfoundinothertwogroups.Conclusions:BMP-2genetransfectedMSCscandifferentiateintoosteoblastsinvitroandinduceboneformationinvivo.