简介：Themoditicationoftumorcellsoreffcorcellsusingcytokinegenesasastrategytoenhancehostantitumorimmunityhasbeenstudiedintensivelyoverthe

简介：Aim:Toinvestigateglycoconjugatechangesonthecellsurfaceofproliferativelesionsandneoplasmsofmicelungsatvariousstagesoftumorigenesis,therelationbetweenprogressivedevelopmentofmousepulmonarytumorsandexpressionofcellsurfacesaccharide.Materialsandmethods:Thirty-onemaleA/Jstrainmiceat5weeksofageweretreatedintraperitoneallywithasingleinjectionof20-methylcholanthrene(20-MC),292pulmonarylesionsincluding31hyperplasias,145alveolaradenomas,61papillaryadenomas,55papillaryadenocarcinomasandtheircombinedtypewereobtained.Thebindingaffinitiesofcellsinnormalrespiratoryepitheliaandinproliferativelesionstofourperoxidases-conjugatedlectins,Maclurapomiferaagglutinin(MPA),Arachishypogeaagglutinin(PNA),Ricinuscommunisagglutinin(RCA),andwheatgermagglutinin(WGA)wereexamined.Results:Cellsofhyperplasiaandalveolaradenomashowedfairlystrongaffinitytoallthefourlectins.However,partofpapillaryadenomacellsandgreaterpartofpapillaryadenocarcinomacellslosttheirbindingaffinitytoMPA,PNA,andRCA,butnottoWGA.ThebindingsofMPA,PNAandRNAweredetectedpredominentlyontheluminalsurfacesofbenigntumorsbutnotontheluminalsurfacesofmalignanttumors.WGAmightbindtovariedtypesofbenignandmalignanttumors.Pretreatedwithneuraminidase,thelesionsenhancedthestainingintensityforthefourlectins,thebindingsitesofWGAtomalignanttumorcellswerenumerous.Adistinctdifferenceinlectinbindingaffinitybetweenhyperplasia/alveolaradenoma/papillaryadenomaandpapillaryadenocarcinomawasclearlyshown(x2=46.89,P＜0.01,x2=36.77,P＜0.01andx2=52.87,P＜0.01)inthisexperiment.Thecomplexglycoconjugatesonthecellsurfaceofmalignantandbenignlesionsduringthedevelopmentofpulmonarytumorwerechanged,malignanttumorcellsdifferedfromthesurfaceofbenigntumorcells,thelevelsoftotalsialicacidwerehigherinmalignanttumorce

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简介：Objective:　Tocomparethedynamicchangesofinterleukin-1(IL-1),interleukin-6(IL-6),andtumornecrosisfactor(TNF)inintermingledskingraftwiththoseinothertypesofskingraftsinrats.　　Methods:　A10%-15%third-degreeburnwascreatedin180Spregue-Dawley(SD)rats.Afterremovingthescar,skingraftswereperformedontheopenwoundsimmediatelywithautoskin(aus,n=54),alloskin(als,n=54)andintermingledskin(n=36).Thatistosay,intheintermingledskingraft,abigpieceofalloskin(mals)wasgraftedfirst,and3dayslater,smallpiecesofautoskin(maus)wereembeddedinthealloskin.Therest36ratsweretakenasthecontrols.AndthebiologicalactivitiesofIL-1,IL-6andTNFingraftsheetsineachgroupweredetectedafterskingraft.　　Results:　ThelevelsofIL-1,IL-6andTNFintheausgroupdecreasedsteadilyaftertheirinitialelevations,whereasinthealsgrouptheyincreasedsignificantlyandkeptonthepeaklevelinthelaterphases.Intheintermingledgroup,thereappearedalowestIL-1levelinthemalsandahighestoneinthemaussimultaneouslyat7(4)days(Thenumberoutofparenthesisisthedaysaftertransplantingwithalloskinsheets,andthenumberinparenthesisisthedaysafterembeddingautoskinsheetsintheintermingledskingraft.Similarlyhereinafter.)afterskingraft(P<0.01),andthehighlevelinthemausabruptlydecreasedat14(11)daysafterskingraft.Atexactlythesamephaseonday7(4),aprominentpeakedIL-6inthemalsoccurred.Inthelaterphases,thelevelsofTNFremainedrelativelylowbothinthemalsandinthemaus.Fromday7(4)on,eachcytokinefluctuationinthemalssynchronizedwiththatinthemaus.Thelongertheposttransplantationperiodlasted,themorethepositivecytokinecorrelatedbetweenthemalsandthemaus.　　Conclusions:　ThelowlevelsofIL-1andTNFmaybeimportantfactorstolightentheintensityoflocalrejectionintheintermingledskingraft.Thetempo

简介：GenemodificationoftumorcellstoexpressavarietyofcytokinessuchasIL-2ortheco-stimulatorymoleculeB7.1ledtoincreasedimmunogenicityandreducedtumorigenicityoftumorshasseveralmodelsandthisprocessinvolvesTcells.WehavepreviouslyreporteddecreasedtumorigenicityofthemurineplasmacytomaJ558L(MHCclassⅠ~+andclassⅡ~-)expressingIL-2orB7.l.Whensystemicimmunitywasanalyzed,

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：Ithasbeendemonstratedthattbecriticalroleofbonemarrowstromalcells(HMSCs)istosustaintheselfrenewalofpluripotenthematopoieticstemcellsandmaintainthehomeostasisofbonemarrowhematopoiesismicroenvironment.BMSCprogenitorcandifferentiateintoseveralclementsincludingmacrophages,endothelialcells,fibroblastsandsomeothercells.Almostall