简介:目的中国汉族人群中SCN5A基因A1673G多态与孤立阵发房颤的相关性。方法选取汉族孤立阵发房颤患者120例为观察组,以健康汉族人群120例为对照组,采用限制性片段长度多态性分析(RFLP),对SCN5A基因A1673G的多态位点进行基因型鉴定,并随机挑选样本进行测序,检验其可靠性。结果SCN5A基因A1673G多态位点在中国汉族人群孤立阵发房颤患者和正常组比较,基因型频率符合Hardy-Weinberg平衡定律;A1673G多态的基因型频率在两组间差异有统计学意义(P〈0.05),房颤患者G等位基因高于正常组;GG基因型对房颤患者有明显影响(P〈0.05)。结论SCN5A基因变异可能与中国汉族人群孤立阵发性房颤相关。
简介:Tostudytherelationshipbetweenmyeloperoxidase(MPO)-463G/Apolymorphismsandsusceptibilitytocoronaryarterydisease(CAD)inHanpeopleofnorthAnhuiprovince.MethodsThecasegroupconsistedof79patientswhohadallangiographicallyprovenCADwereretrospectivelystudied.Usedpolymerasechainreaction-restrictionfragmentlengthpolymorphism(PCR-RFLP)methodstodecidethegenotypeofallthepatients.ResultsThefrequencyofAAhomozygotictypeinHanpeopleofAnhuiprovincewas1.4%.TheriskofCADforpersoncarryingatleastoneAallelegenotype(GAandAA)was0.37timesofGGgenotype.TheseverityofcoronaryarterystenosisinCADpatientscarryingatleastoneAallelegenotypewas0.197timesofGGgenotype(P<0.05).ConclusionsThefrequencyofAAhomozygotictypeandMPO-463G/ApolymorphisminHanpeopleofAnhuiprovinceinfluencedtheriskofCAD.AallelehadprotectivefunctioninCAD.
简介:The5thChina-JapanJointHypertensionSymposiumwasheldonNovember6th,2002inGuangdongCardiovascularInstitute,GuangdongProvincialPeople’sHospital,Guangzhou,China.Therewereatotalof96paperspublished(includedspeciallectures,oralpresentations,posters).Almost200cardiologists,whocamefromJapanandChina,attendedthesymposium.
简介:The5thAnnualScientificSessionofCardiologyinSouthChinawasheldfromApril3—7.2003inGuangzhou.Aseminar——“TheFrontlineProblemsandNewViewpointsinCardiologyinRecentTimes”washeldatthesametime.MorethanonethousandcardiologyspecialistscamefromsouthandmiddleChinatoparticipateinthemeetingand135paperswere
简介:ObjectivesPhenotypicoverlapofBrugadasyndromewithtype3longQTsyndromeisobservedinsomecarriersofmutationsintheNachannelSCN5A.Concomitant-Brugadasyndromeand3typelongQTsyndromeassociatedwithsodiumchannelmutationwasreportedbefore,however,nodatashowedconcomitant-BrugadatypeandshortQTintervalelectrocardiogram(ECG)andrevealedtheassociated-genemutation.MethodsThedirectDNAsequencewasconducedtofindthemutation.Themutationwasreproducedinvitrousingsite-directedmutagenesisandcharacterizedusingthepatchclamptechniqueinthewhole-cellconfiguration.ResultsThepatientwiththefamilyhistoryofsuddendeathshowedBrugadaandshortQTintervalECG.SequenceofSCN5Aidentifiedamissensemutation,R689H,previouslyassociatedwithalongQTsyndrome.BiophysicalstudyshowedthattheR689Hfailedtogenerateanycurrentwhenheterolo-gouslyexpressedinHEKcells.ConclusionsOurfindingsindicateforthefirsttimethatcoexisted-BrugadatypeandshortQTintervalECGlinkedtothelossoffunctioninSCN5Amutation.
简介:ObjectivesToinvestigatetheeffectofGαq/11signalingpathwayandATP-sensitivepotassiumchannel(KATPchannel)onischemicpreconditioning(IPC)protectioninrathearts.MethodsTwoseriesofexperimentswereperformedinWistarrathearts.Inthefirstseriesofexperiment,ischemicpreconditioningwasinducedbyleftanteriordescendingocclusion(three,5minepisodesseparatedby5minofreperfusion),ischemia-reperfusioninjurywasinducedby30mincoronaryarteryocclusionfollowedby90minreperfusion.Hemodynamics,infarctsizeandscoresofventriculararrhythmiasweremeasured.TheexpressionofGαq/11proteinintheheartwasmeasuredbyWesternblotanalysisinthesecondseries.ResultsIschemicpreconditioningratsshoweddecreasedinfarctsizeandscoresofventriculararrhythmiavsnon-IPcontrolrats.TheeffectofIPCwassignificantlyattenuatedbyglibenclamide(1mg/kg,ip),anonselectiveKATPchannelinhibitor.IPCcausedasignificantincreaseintheexpressionofGαq/11protein.ConclusionsActivationsofGαq/11signalpathwayandKATPchannelplayedsignificantrolesintheclassicalcardioprotectionofischemicprecon-ditioningratheartandmightbeanimportantmechanismofsignaltransductionpathwayduringtheischemicpreconditioning.
简介:The5thSCCSS&IICwillbeheldonApril4th-7th,2003intheGuangdongHotel,GuangzhouCity,About800specialistsandclinicalphysiciansincardiologywillattendtheconlerences.TheywillcomefromGuandong.Hunan,Hainanandotherprovincesinmedial-southChina.ManyworldfamouscardiologistsfromAmerica,Canada,Germany,theU.K.andHongkong,Beijing,Shanghai,etc.,willbe
简介:BackgroundApolipoprotein(apo)A-Visanovelmemberoftheapolipoproteinclusterinvolvedintriacylglycerol(TG)homeostasis.IthasreportedthatAPOA5genepolymorphismsiscorrelatedwitharterioscleroticdiseases.However,ThisassociationisunknownonChinesepatientswithatheroscleroticcerebralinfarction.ThepresentstudyaimedtoelucidatetherelationshipofAPOA5-1131T>Candarterioscleroticcerebralinfarction(ACI)aswellasthelevelsofserumlipids.MethodsPolymerasechainreaction-restrictionfragmentslengthpolymorphisms(PCR-RFLP)analysis,enzymaticandimmunoturbidimetrymethodswereusedtomeasure-1131T>Cgenotype,allelefrequencyaswellasplasmalipidlevelof90ACIpatientsand221healthysubjectsofHanChinese.ResultsInACIgroup,thelevelofTGinalleleCcarrierswashigherthanthatofnon-Ccarriers(P<0.05).ThefrequencyofalleleCinACIgroupwashigherthaninhealthygroup(χ~2=5.568,P=0.018).Exceptsex,ageandBMI,thelevelsoftotalcholesterol(TC),triglycerides(TG),highdensitylipoproteincholesterol(HDL-C),low-densitylipoproteincholesterol(LDL-C),APOA1andAPOBinACIgroupdistinctivelywerehigherthanthoseinhealthygroup.ConclusionTheAPOA5-1131alleleCisassociatedwiththehighlevelofTGinACIpatients,whichisprobablylinkedwithACIdangerofChineseHan.
简介:1病例报告患者男性,79岁.主因发作性心前区闷痛2竽,活动后气短5年余,拟诊为冠心病,陈旧性前间壁心肌梗死,频发室性早搏,间歇性完全性右束支传导阻滞,心功能4级入院.患者1995年10月8日心电图出现间歇性完全性右束支传导阻滞(图1),之前为正常心电图(图2).1995年10月9日始表现为持续性完全性右束支传导阻滞,其后共行心电图检查12次,均表现为完全性右束支传导阻滞(图3),并于1996年10月9日行动态心电图检查,亦表现为持续性完全性右束支传导阻滞.