简介:BackgroundOurpreviousstudyshowedthe150mg/mLfetalcardiacsupernatant(FCS)couldinducedifferentiationofBMSCsintocardiomyocye-likecellswithoutcardiomyocytetouch,butdifferentiationefficiencyisnothighenough.Inhibitionofglycogensynthasekinase-3enhancedtheproliferationandsurvivesofstemcells.Wetestedif6-bromoindirubin-3-oxime(BIO,glycogensynthasekinase-3inhibitor)enhancestheeffectsofFCSondifferentiationofBMSCsandexplorethegrowthfactorsinFCS.MethodsBMSCswereisolatedfromthefemurandtibiaoffour-week-oldmaleSprague-Dawleyratsandco-culturedwithFCS(150mg/mL)thatwasmadefromfetalheartsfromnineteen-daypregnantWistarrats.BIOwithdifferentconcentration(0,1,10,and100nM)wasintroducedinculturedishes.Transforminggrowthfactorbeta1(TGF-β1),bonemorphogeneticprotein2(BMP-2)andAktincardiacsupernatantandculturemediumwereassayedwithELISAmethods.ResultsAfterco-culturingwithFCS,beatingmyotubeswereobservedin25.9%BMSCsdishesafter1to2weeks’culture.ThelevelsofTGF-β1andBMP-2inFCSconcentrationswerenomorethanthatinyoungandadultcardiacsupernatant.AllBIOgroupssignificantlyenhancedtheeffectsofFCSondifferentiationofBMSCsintothecardiomyocyte-likecells(1nM,83%;10nM,73%;100nM,100%).AktlevelswerehigherinBMSCsculturalmediumwithFCS.ConclusionsFCScouldinducethedifferentiationofBMSCsintothecardiomyocyte-likecells.TGF-β1andBMP-2mightnotplayaroleinthedifferentiationofBMSCsinducedbyFCS.BIOenhancedtheeffectsofFCSonthedifferentiationofBMSCsintocardiomyocyte-likecells,whichmightinvolvetheAktpathway.
简介:目的观察急性心肌梗死(AMI)患者血清高敏肌钙蛋白T(hs-TnT)及线粒体偶联因子-6(CF6)含量在冠状动脉循环中的变化。方法纳入2009年4月到2011年3月期间我院收诊的AMI患者60例,同期选取冠脉造影结果无狭窄或狭窄程度〈50%的患者30例作为对照组。取两组受试者冠状静脉窦、冠状动脉与外周血清,分别采用发光免疫法和放射免疫法测定hs-TnT及CF6浓度。结果AMI患者冠状静脉窦、冠状动脉与外周静脉血清中hs-TnT、CF6浓度与对照组相比,差异均有统计学意义(P〈0.01);AMI患者冠状静脉窦血清hs-TnT、CF6较冠状动脉血清hs-TnT、CF6均值升高,差异有统计学意义(P〈0.01)。结论AMI可导致冠脉循环hs-TnT和CF6浓度升高,二者可在一定程度上预测心肌梗死面积。
简介:BackgroundThefactorsinfluencingtheq-wavechangesinV5andV6duringanterioracutemyocardialinfarction(AMI)havenotbeenthoroughlydescribed.MethodsWestudied70patientswithafirstanteriorAMI,inwhomtheelectrocardiogram(ECG)showedeitherdisappearanceofthenormalseptalqwave(n=24)orpresenceofpathologicalQwaveinV5andV6(n=46)duringfollow-up.TheECGandcoronaryangiographyfindingswerecorrelated.ResultsTherewasnodifferencebetweenthe2groupsintheculpritsiteproximaltoS1(46%vs.36%,P=0.405),buttheculpritsitewasmorefrequentlylocatedproximaltoD1inthegroupwithabnormalQwave(21%vs.67%,P=0.001).Patientswithdisappearanceoftheseptalqwavemoreoftenhadalargeobtusemarginalbranch(46%vs.22%,P=0.037)anddisappearanceoftherwaveinV1(88%vs.7%,P=0.001).PatientswithabnormalQ-wavemoreoftenhadalargeLAD(42%vs.71%),smallrwaveortallorwideRwaveinV1(0%vs.89%,P=0.001)andabnormalQwavesintheinferiorleads(33%vs.59%,P=0.044).ConclusionsInpatientswithfirstanteriorAMI,qwavechangesinV5andV6correlatedwiththemorphologyinV1.EmergingabnormalQwaveinV5/V6predictedtheculpritlesioninalargeLADproximaltoD1,butdisappearanceoftheseptalqwavecouldnotpredicttheculpritlesionproximaltoS1.