简介：IntroductionRecently,bonemarrowmesenchymalstemcells(MSCs)havebeenreportedtorepairchronicallyinfractedmyocardiumwithdirectinjection.However,itisverydifficulttolocalizetheinjectedcellsontotheischemicareatoregeneratesufficientcardiacmassinthethinnedscararea.Toovercometheproblem,wehaveutilizedourcellsheettechnologybasedontemperature-responsiveculturedishes.Whentheculturetemperatureisreducedfrom37℃to20℃,allcellsconnectedviacell-celljunctionproteinsareharvestedasasinglesheetwithoutusingproteolyticenzymes.Thistechnologyallowsustotransplantstemcellsinvivofortreatmentheartdiseasewithouttheproblemsmentionintheprevious.MethodsMaleClawnminipigswereusedinthisstudy.Bonemarrow(5-7mL)wascollectedundergeneralanesthesia.Histopaqe-1077(15mL),wereaddedtobonemarrowandcentrifuged.Thecellswerecollectedandculturedfor7days.Weseededthebonemarrow-derivedMSCsattheconcentrationof(6×10~5/ml)on60mmdiametertemperature-responsivedishesfor7days.Astheculturetemperaturedecreasedfrom37℃to20℃,MSCsheetdetacheditselfspon-taneouslyandfloatedupintotheculturemedium.Triplelayerswerestackedtogetherrepeatedlyformingspecialmultiplayer.Myocardialinfarctionwascreatedbytheligationoftheleftanteriordescendingbranchoftheleftcoronaryartery.Acellsheetswastransplantedontotheischemiaarea.Theechocardiographywasperformedtwoandfourweeksaftertransplantation.Thehearttissuewithcellsheetswereremovedandfixedwith10%formalinforhistologicalanalysisonemonthafterthetransplantationofcellsheets.ResultsMostMSCsarepositiveforCD29,CD90,CD146andCD73.ThesemeantheculturecellsheetswerecomposedofundifferentiatedMSCsandremainedmultipotent.Monolayers(20-30μm)andmultilayer(120μm)cellsheetswereproduced,whichretainedallcell-to-cellcontaction.Histologicalanalysesshowthecellsheetsbecomecloselycontactedwiththehearttiss

简介：ObjectivesToinvestigatetheprotectiveeffectofthrombopoietin(TPO)onmyocardialcellsinvitro.MethodsH9C2celllinewasmaintainedinIscove’smodifiedDulbecco’smedium(IMDM)supplementedwith10%calfserum.Beatingcellsfromheartventriclesofneonatalheartwereculturedataninvitrosystem.Apoptosisofthecelllineabovewasinducedbytreatmentofdoxorubicin(DOX)andwasblockedbyTPO.CellsurvivalrateofH9C2cellwasmeasuredbytheMTTassay.Changesofbeatingrateofneonatalmyocardialcellswerecapturedbydigitalcameraandbeatingratewascalculated.Flowcytometrywasemployedtostudyanti-apoptoticeffectofTPObystainingJC-1proteintoH9C2cell.ResultsMTTassaydemonstratedthatdoxorubicinreducedcellsurvivalrateby73.8%±1.1%,50ng·mL-1and100ng·mL-1TPOincreasedcellsurvivalrateby84.6%±3.6%(P<0.05),86%±4%(P<0.01)atadose-dependentmanner.Beatingrateofprimaryneonatalmyocardialcellsalsodecreasedto15%±8%at48h,100ng·mL-1TPOimprovedbeatingrateto48%±11%(P<0.01).TPOdecreasedapoptoticratefrom19%±9%to11%±6%(P<0.05).ConclusionsTPOhasprotectiveeffectonmyocardialcellsinvitro.Anti-apoptosisisoneofthemechanismsbywhichTPOprotectsinjuredheart.

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

简介：Itiswellestablishedthatstemcellscandifferentiateintocelltypesoftheorganinwhichthesearetransplanted.However,theprocessisveryslowduetolackofunderstandingofsignalsimportantfortheirsurvivalanddifferentiation,mostoptimalstemcellsandtheirplasticity.Limitationsandadvantagesofvariouscellsubtypeswillbedescribed.Therateofstemcellsmobilizationandtheirsurvivalintheischemicenvironmentaremajorobstaclesinengraftmentanddifferentiationofstemcellsformeaningfulrepairoftheinfarctedmyocardium.Manipulationofstemcellswithischemicpreconditioning,combinedgeneandcelltherapytogetherwithsimultaneousactivationofdiversesignalingpathwaysformassivestemcellmobilization®enerationhassignificantimpactontherepairprocessbystemcells.Theseandotherdifficultiesencounteredinefficientuseofvariousstemcellshaveresultedininventionofinducedpluripotentstemcellswhichcouldrevolutionizethestemcellbasedtherapyandtheirapplicationsforunderstandingofhumandiseaseanddrugscreeninginthenearfuture.ReprogrammingofadultcellsintoiPScellswithouttheuseofviralvectorsisamajorchallengetowardsgettingiPScellswithoutviralintegrationintocells.Tomeetthischallengewehaverepro-grammedskeletalmyoblastsintoiPScellswithhighefficiencyusingepigeneticmodifiers.TransplantationofiPScellsderivedpurecardiacprogenitorsintoinfarctedmyocardiumledtoextensiverepopulationofscarareawithfullydevelopedmyocyteswithouttumorformationandresultinginmarkedimprovementincardiacfunction.Reprogrammingwithpurechemicalmeanswillmaketherapeuticuseofthesecellsmoresafer.Targetingtheinducedpluripotentstemcellstowardscardiacprogenitorsandtheirapplicationtowardstransplantationisamajorstepforwardinenhancingthemyocardialrepaircapacitybythesecells.

简介：Objective:Toassessthecardiovascularabnormalitiesinpatientswithspontaneoussubarachnoidhemorrhage(SAH).Methods:AllpatientsadmittedtoourinstitutionwithaprimarydiagnosisofspontaneousSAHandhadatransthoracicechocardiogram(TTE)performedfrom1stofJuly2011until30thofMay2014wereenrolled.Results:Outof2058patientsadmittedtoourinstitutionwithadiagnosisofSAH,overathreeyearperiod,only244patients(12%)hadTTEperformedduringtheindexhospitalization.Inthisselectedcohort,themeanagewas59yearsand66%ofpatientswerefemale.ElevatedtroponinTwasnoticedin37%ofpatientsandQTcprolongationwasthecommonestECGabnormalityoccurringin49%ofthepatients.Thirtyninepatients(16%)hadarestingsegmentalwallmotionabnormalityontheTTE,includingfivepatientswithapicalballooning.In-hospitalmortalitywas15.6%(38patients).Conclusion:CardiovascularabnormalitiesinselectedpatientswithSAHwhohadcardiacultrasoundarerelativelycommon;howevertheincidenceofventricularballooningislow.InordertoattainthecorrectincidenceofcardiovascularabnormalitiesinSAHpatients,allpatientsadmittedwithSAHshouldundergoTTEandhaveECGandcardiacmarkerscheckedduringtheirhospitalization.

简介：动脉粥样硬化是各种损伤刺激作用于动脉管壁引起的,涉及多细胞、多因素、多环节的全身性疾病,其发病机制至今未完全阐明。微小RNA（miRNA）是一类在进化上高度保守的非编码小分子单链RNA（约22个碱基）,在转录后水平负性调控基因表达。

简介：BackgroundPreviousstudieshavesuggestedthatpatientswithlowendothelialprogenitorcell(EPC)countsandimpairedendothelialcolonyformingactivityhaveahigherincidenceforcardiovasculareventscomparedtopatientswithhighEPCcountsandfavorablecolonyformingactivity.ThepathophysiologicalbasisforthisfindingmaybeaninsufficientendothelialcellrepairbyEPC.TheobjectiveofthisstudywastodeterminewhetherthenumberofEPCsinperipheralbloodwasassociatedwiththepresenceandseverityofangiographicstenosisinpatientsofthelatephaseafteracutemyocardialinfarction(AMI).MethodsOnehundredandonepatientsundergoingcardiaccatheterizationinourhospitalwereenrolledinthestudy.ThenumberofcirculatingEPCswasmeasuredbyafluorescent-activatedcellsorter(FACS).Patientswithacutecoronarysyndromeswereexcluded.ResultsComparedwithpatientswithnormalcoronaryartery,thenumberofcirculatingEPCswassignificantlyreducedamongpatientsinthelatephaseafterAMI(P<0.01).Wealsofoundthatcomparedwiththecontrolgroup,thenumberofEPCsofsingle-vesselstenosisgroupandmulti-vesselstenosisgroupweresignificantlyreduced(P=0.005;P=0.001).ConclusionsThenumberofEPCsintheperipheralbloodisdecreasedinpatientsofthelatephaseafterAMI.TheEPCsnumbercorrelatedwithangiographicstenosisseverity,whichsuggeststhatendothelialinjuryinthedeficientcirculatingEPCsmayaffecttheseverityoftheheartdisorderandtheclinicalpresentations.

简介：

简介：backgroundBonemarrowmesenchymalstemcells(BMSCs)canbeisolatedandculturedtomanypassages.However,StemcellsincludingBMSCsquicklyundergosenescenceinculture.Thecellsenescenceandmulti-directionaldifferentiationhavehamperedproducingBMSCsinquantitywiththeirundifferentiatedstate.Inthisstudywereportanaturalcompound,vitaminC(Vc),maintainsBMSCsstemproperty.MethodsHumanBMSCswereisolatedfrombonemarrowandpurifiedby1.073g/mLdensitygradientcentrifugation.50ng/mLVcwereaddedtoBMSCsfordifferenttimepoint.FlowcytometrywasusedtodetectcellsurfacemarkersofBMSCswithorwithoutVctreatment.BMSCsproliferationwasanalyzedbyMTTassay.PCR(polymerasechainreaction)andreal-timePCRwereusedfordetectingc-kit,nanog,andOct-4genesexpressionlevels.DNAmethyltransferase(Dnmt)1andDnmt3blevelswerealsodetectedbyreal-timePCR.ResultsFlowcytometryshowedthatafterVctreatmentfor6h,thesurfacemarkersofBMSCswerealmostunchanged.VcincreasedtheproliferationactivityofBMSCsfrom6hto24h.PCRshowedtheexpressionofc-kit,nanog,andoct-4geneswereobviouslyincreasedinVctreatedgroupthancontrolgroupat12h.Real-timePCRshowedthatthelevelofc-kit,nanog,andoct-4geneswereunregulatedfrom6hto12hcomparedwithcontrolgroup.VcalsoincreasedDnmt3bbutnotDnmt1geneexpression.ConclusionsOurresultsshowedVcactsatleastacceleratesBMSCsproliferationandmaintainsstemcellproperty.Inourstudy,wehighlightedamethodofimprovingthespeedofBMSCsgenerationandprovidedadditionalinsightsintothemechanisticbasisofpreventingBMSCssenescence.

简介：ObjectivesTodetectionofchlamydiapneumoniae(Cpn)DNAinthecirculatingmononuclearcellfractionsofcoronaryheartdiseaseandtoinvestigatetheassociationbetweeninfectionwithchlamydiapneumoniaeandcoronaryheartdisease(CHD)andprospectivelywhetherblood-basednestedpolymerasechainreaction(nPCR)isusefulinidentifyingCpninfection.MethodsTheperipheralbloodmononuclearcell(PBMC)CpnDNAwasexaminedusingnPCRtechniqueandconfirmedbyelectrophoresisin150patientswithCHD.Select55patientswithclinicalsuspectedCHDbutangiographyresultarenormalascontrolgroup(CG).Thenweconductedaprospective,randomized,double-blind,placebo-controlledstudyof6monthsofazithromycinandplacebotreatmentinCHDgroup.PatientswithCpnDNApositivewerethenrandomizedtoreceiveazithromycinorplacebo.Aftertreatmentbloodsamplewerecollectedforrepeatedmeasurement.ResultsChlamydiapneumoniaeDNAwasdetectedin49(32.7%)of150personswithCHDandin1(1.8%)of55personswithcontrolgroup,oddsratio26.2,95%confidenceinterva13.52-194.98.ThepositivityratesofnPCRinCHDgroupswerehigherthanthoseincontrolgroup.16cases(29.1%)inlatentcoronaryheartdiseases(LCHD)group,19cases(39.6%)inunstableangina(UAP)group,and14cases(29.9%)inacutemyocardialinfarction(AMI)groupwereCpnpositivebynPCR.TherewerenosignificantdifferenceamonginAMIUAPandLCHDgroup.ThereweresignificiantdifferenceinCpnDNAnegativeratesaftertheazithromycinandtheplacebotreatment.ConclusionsChlamydiapneumoniaeispresentinPBMCofasignificantproportionofpersonswithCHD.Thepotentialroleofchlamydiapneumoniaeincoronaryatherosclerosismaythereforebemorerelatedtoaccelerationofdiseaseorsystemiceffectsbypersistentinfectionthantosuddeninitiationofprogressivecoronaryarterydiseasebyacuteinfection.ThedetectionofCpnDNAinPBMCwithnPCRmaybeofgreatvalueforidentifyingCpncarriersandfo

简介：BackgroundTheeffectofselectiveradiofrequencyablationfortreatingparoxysmalsupraventriculartachycardia(PSVT)anditsassociatedparoxysmalatrialfibrillation(PAF)wasassessed.MethodsDatawerecollectedretrospectivelyfrompatientsdiagnosedofPSVTandsubsequentlytreatedwithradiofrequencyablation.Regularmonthlyfollow-upbydynamicelectrocardiography(ECG)wasperformed.Incidentratesofatrialfibrillationbeforeandafterablationwerecompared.Results382PSVTpatientswith58havingatrialfibrillationwereenrolled.TheorderofcomplicatedPAFfromhightolowinthesepatientswasdisplayedas:atrialtachycardia(AT),atrioventricularreentranttachycardia(AVRT)andatrioventricularnodalreentranttachycardia(AVNRT).AmongAVRTpatients,PAFwasmorefrequentinpatientshavingaccessorypathways.AVNRTpatientshadsignificantlylowerPAFratecomparingtootherpatients.PAFincidentratewassignificantlyreducedbyradiofrequencyablationtherapy.ConclusionWeadviseregulardynamicECGforPSVTpatients,especiallythosewithatrialflutter,ATorpre-excitationsyndrome.SelectiveradiofrequencyablationisafeasibleapproachfortreatingAFcomplicatedPSVTpatients.

简介：最新研究证明长链非编码RNA（IncRNA）可调节脂质及糖代谢，调控血管壁功能，参与血管内皮细胞和平滑肌细胞的增殖、迁移、老化、凋亡以及血管炎症及免疫应答，从而影响动脉粥样硬化的发生发展。本文就lncRNA与动脉粥样硬化关系研究的进展作一综述。

简介：冠状动脉粥样硬化（atherosclerosis,AS）性心脏病简称冠心病,指冠状动脉发生粥样硬化引起的管腔狭窄或闭塞,导致心肌缺血缺氧或者坏死而引起的心脏病。冠心病是AS导致器官病变的最常见的类型,也是严重危害人类健康的常见病。

简介：ObjectivesToinvestigateeffectofAngll,captoprilonsingleguineamyocytesonL-typecalciumcurrentandsodiumcurrent.MethodsMembranepatchclampwholecellrecordingtechniquewasusedtoinvestigateeffectofangll,captoprilonL-Camaximumcurrentdensityandsodiummaximumcurrentdensity.ResutlsAngllincreasedthemaximumcurrentdensitycomparedwithcontrolafterperfused5min,357.7±219.7Vs279.5±240.5PA/PF,increaserateis27.9%,theshapeofcurrent-voltagerelationshipcurvewasunchanged,peakedat+10mv,indicatedthatangllincreasedL-Cacurrentdensityinvoltage-dependent.Afterperfusedwithcaptopril,captopril+angll3,5min,L-Cacurrentwasrecorded,resultssuggestL-Camaximumcurrentdensitydecreasedsignificantlycomparedwithcontrol,incaptoprilgroup,128.4±92.6Vs286.2±89.7,66.7±68.3Vs286.2±89.7,respectively,rateofinhibitionis55.1%,76.6%,respectively.L-Cacurrentfurtherdecreasedincaptoprilpe

简介：目的探讨非瓣膜病心房颤动（房颤）患者血清小分子RNA（miRNA）全基因组表达差异及其可能的调控作用和早期预警价值.方法15例房颤患者,分为阵发性、持续性和永久性房颤组,每组5例,对照组5例健康人.射频消融术前和术中分别取外周血和冠状窦血,提取血浆总RNA,使用microRNA芯片（microRNAv18.0）进行全基因组miRNA表达谱微阵列分析,VolcanoPlot法获得差异表达niRNAs,并用tMEV软件进行聚类分析,以及通过mirbase、miranda、targetscan数据库进行靶基因分析,并进行RT-PCR的差异表达验证.结果房颤组冠状窦血与外周血比较有14个miRNAs表达差异显著,其中6个表达上调：即miR-1266、miR-4279、miR-4787-5p、miR-4666a-3p、kshv-miR-K12-6-3p和miR-3150a-5p,8个表达下调：即miR-892a、miR-3149、miR-3171、miR-3664-5p、miR-3591-3p、miR-4423-5p、miR-4473和miR-574-3p.其中,miR-1266在阵发性、持续性和永久性房颤组均明显升高,而miR-3171则显著降低.房颤组与对照组外周血及冠状窦血比较miRNAs表达也有明显差异.结论房颤患者冠状窦血与外周血比较miRNAs表达均有显著差异,而冠状窦血miRNAs更能反映心脏的代谢与调控状况;血清miR-3171、miR-892a、miR-3149在房颤发生发展早期出现且持续表达差异,有可能成为早期预警诊断的标志物;miR-1266、miR-4279、miR-4666a-3p有可能成为未来治疗房颤的干预靶点。

简介：ObjectivesToob-servetheeffectofdifferentestrogenlevelsonthesecretoryfunctionofvascularendothelialcellsoffemalerats,andstudytheeffectofmodulationofestrogenlevelontheexpressionofvascularcelladhesionmolecule-1andtheconcentrationofestrogenreceptorinvascularendothelialcells.MethodsRadioim-munologywasusedtomeasuretheserumconcentrationofendothelinandPGI2,andcopper-cadmiumreductionwasemployedtomeasuretheserumcontentofnitrogenmonoxide.Radioligandbindingandflowcy-tometrywereusedtomeasuretheexpressionofestrogenreceptorandvascularcelladhesionmolecule(VCAM-1)ofvascularendothelialcellsrespectively.Results1.TheserumconcentrationofnitricoxideandPGI2decreasedwhentheovariesoffemaleratswereremoved.Inovariectomizedrats,givenestrogen,theconcentrationrose(P<0.05),buttheplasmaconcentrationofendothelinwasadversetoit.2.Theconcentrationofestrogenreceptorofvascularendothelialcel

简介：BackgroundValvularheartdisease(VHD)isdefinedasastructuralorfunctionalabnormalityincardiacvalvewhichencompassesanumberofcommoncardiovascularconditions.ThisstudywasaimedtoanalyzetheepidemiologicalchangesofVHDinasinglecardiovascularcenterofSouthernChina.MethodsAtotalof13,138VHDpatientsofGuangdonggeneralhospitalfromJanuary2011toDecember2013werescreenedbytransthoracicechocardiography(TTE)ortransesophagealechocardiography(TEE)andenrolledforthisstudy.Themorbidity,etiologicalspectrumandmanagementofthesepatientswereanalyzed.Continuousvariableswereexpressedasmean±standarddeviation.Categoricalvariableswereexpressedasratioorpercentage.ResultsPatientsinthisstudyweredividedintodifferentgroupsandwereanalyzedthroughoutchangesinmorbidity,etiologicalspectrumandmanagement.ConclusionsTheprevalenceofVHDremainshighinSouthernChinaandRHDisstilltheleadingetiologyofVHD.Butmorbidityrateisreducedandsurgeryisstillthemaintreatmentoption.

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简介：心房颤动（atrialfibrillation,简称房颤）是临床上最常见的心律失常之一.近来一项关于心房颤动危险因素的回顾性研究指出,高龄、吸烟、肥胖、高血压、左心房扩大、左室射血分数减低等容易促进房颤的发生[1].中国的房颤流行病学调查显示,我国目前房颤患病率为0.77％,根据我国标准人口构成校正后为0.61％,若按目前我国13亿人口计算,我国房颤人数接近800万[2].房颤可以造成心排血量减少、心室率过快或过慢,可加重心肌缺血及恶化心功能,此外房颤所致附壁血栓脱落还可引起体循环栓塞等严重心脑血管事件发生.

简介：目的观察微小RNA(microRNA,miR)-142-3p对血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)诱导的心肌肥厚中线粒体功能的影响。方法我们使用Sprague-Dawley(SD)大鼠的乳鼠心肌细胞,细胞培养后分成4组:空白组;AngII组;miRnc+AngII组;miR-142-3pmimic+AngII组。分别往细胞中转染相同浓度的miR-142-3p和miRnc质粒6h,实时定量聚合酶链反应(real-timepolymerasechainreaction,rt-PCR)检测实验组miR-142-3pmRNA表达增多,提示细胞质粒转染成功,再用10-6mol/L浓度的AngII诱导细胞48h,使用线粒体Mito-RedTracker处理细胞30min,共聚焦显微镜观察细胞中线粒体密度的变化;使用流式细胞仪检测线粒体膜电位变化。结果与空白组相比,AngII组的线粒体膜电位减低(n=3,P<0.01);与AngⅡ+miRnc组相比,AngⅡ+miR-142-3p组的线粒体膜电位增加(n=3,P<0.01)。与空白组相比,AngⅡ组的线粒体荧光数量减低(n=3,P<0.01);与AngⅡ+miRnc组相比,AngⅡ+miR-142-3p组的线粒体荧光数量增加(n=3,P<0.01)。结论在AngⅡ诱导心肌肥大过程中miR-142-3p对心肌线粒体具有保护作用。