简介：Previousstudiessuggestthatreductionanddysfunctionofcirculatingendothelialprogenitorcells(EPCs),anddysregulationinstromalcellderivedfactor-1/CXC-chemokinereceptor4(SDF-1/CXCR4)axisindiabetescouldbetherapeutictargetsfordiabeticischemicstroke.ThisstudyinvestigatedtheefficacyofCXCR4-primingEPCsoncerebralrepairfollowingischemicstrokeindb/dbdiabeticmice.BonemarrowderivedEPCsfromdb/+controlmiceweretransfectedwithadenovirus(1×10~7IU)carryingCXCR4(Ad-CXCR4-EPCs)ornull(Ad-null-EPCs).Thedb/dbmiceweredividedintothreegroupsforEPCsinjection(2×10~5cells/100μl):Ad-CXCR4-EPCs,Ad-null-EPCsorsaline(vehicle),viatailvein2hrsaftermiddlecerebralarteryocclusion(MCAO)surgery.Cerebralbloodflow(CBF)wasmeasuredwithlaserDopplerflowmeter.Miceweresacrificedat2or7daysthereafter.LevelofcirculatingEPCswasmeasuredbyflowcytometry.Ischemicdamage,cerebralmicrovasculardensity(MVD),angiogenesisandneurogenesisweredeterminedbyhistologicalstainingwithFluoro-J,CD31,CD31+BrdU,NeuN+BrdU,GFAP+BrdU,respectively.Results(table)showed:1)LevelsofCXCR4expressionwerereducedinthebrainandEPCsofdb/dbmiceasmeasuredbyreal-timeRT-PCRandwesternblotanalyses(datanotshown);2)ThelevelofcirculatingEPCswasmoreinthemicetreatedwithAd-CXCR4-EPCs;3)EPCtransfusionimprovedCBF,increasedMVD,angiogenesisandneurogenesisinperi-infarctarea,anddecreasedischemicdamage.TheefficacieswerebetterinAd-CXCR4-EPCsgroup.DatasuggestthattransfusionofAd-CXCR4-EPCscouldbeatherapeuticavenueforischemiastrokeindiabetes.

简介：原发性扩张型心肌病临床表现复杂,缺乏特异性诊断手段,误诊、漏诊率较高.我院1990～2000年间临床诊断的原发性扩张型心肌病95例,误诊31例,占326%.现就误诊原因分析如下.

简介：Intherecentpast,bonemarrow(BM)-derivedcellshavebeenusedtoregeneratedamagedcardiovasculartissuespostmyocardialinfarction(MI).Recentclinicaltrialshaveshowncontroversialresultsinrecoveringdamagedcardiactissue.Newprogresshasshownthattheunderlyingmechanismsofcell-basedtherapyreliesmoreheavilyonhumoralandparacrineeffectsratherthanonnewtissuegeneration.However,studieshavealsoreportedthepotentialofnewendothelialcellgenerationfromBMcells.Thus,effortshavebeenmadetoidentifycellshavinghigherhumoralortherapeuticeffectsaswellastheirsurfacemarkers.Specifically,BM-derivedCD31~+cellswereisolatedbyasurfacemarkeranddemonstratedhighangio-vasculogeniceffects.IwillpresentrecentadvancesinthetherapeuticuseofBM-derivedcellsandtheusefulnessofCD31~+cellsasanextgenerationcelltherapy.