简介:目的:探讨血红素加氧酶-1(HO-1)基因启动子区域的GT重复序列(GTn)决定的等位基因多态性与冠心病(CHD)发病风险之间的关系。方法:采用聚合酶链式反应(PCR)扩增技术和聚丙烯酰胺凝胶电泳方法分析57例CHD患者和44例健康体检者(健康对照组)HO-1基因启动子区域GTn的分布是否存在差异。结果:与健康对照组比较,CHD组中H0—1基因启动子区S型等位基因(56.8%比38.6%)及sS基因型频率(36.4%比15.8%)显著降低,L型等位基因(43.2%比61.4%)及LL基因型频率(22.7%比38.6%)显著升高(P均〈0.05)。结论:血红素加氧酶-1基因启动子区GTn多态性可能增加冠心病的发病风险。
简介:目的研究血小板内皮细胞黏附分子1(PECAM1)、平滑肌蛋白1(LMOD1)基因多态性位点与缺血性卒中患者颈动脉斑块易损风险的关系。方法前瞻性纳入自2014年5月至2017年10月于北京天坛医院就诊的具有颈动脉斑块的缺血性卒中患者,采集人口统计学资料及相关临床信息,采用颈动脉高分辨MRI区分易损及稳定斑块,依次纳入易损斑块组与稳定斑块组。利用实时聚合酶链反应方法,使用TaqMan探针对易损斑块组及稳定斑块组患者PECAM1、LMOD1基因多态性位点rs1867624、rs2820315进行基因分型并进行统计学分析。采用二分类Logistic回归分析探讨影响颈动脉粥样硬化斑块易损性的危险因素。结果共纳入具有颈动脉斑块的缺血性卒中患者270例,其中189例具有易损斑块,81例具有稳定斑块。对两组患者PECAM1基因rs1867624位点的多态性分析显示,等位基因T是易损性斑块风险基因,其基因频率在易损斑块组、稳定斑块组中分别为87.3%(330/378)、79.6%(129/162;OR=1.759,95%CI:1.080~2.864,P=0.022)。对LMOD1基因SNP位点rs2820315的分析显示,等位基因C是易损性斑块的危险基因,其基因频率在易损斑块组、稳定斑块组中分别中为87.6%(331/378)、80.9%(131/162;OR=1.667,95%CI:1.014~2.738,P=0.042)。Logistic回归分析结果显示,年龄(OR=1.069,95%CI:1.022~1.118,P=0.004)、PECAM1基因rs1867624位点T/T基因型(OR=2.202,95%CI:1.035~4.688,P=0.041)和LMOD1基因rs2820315位点C/C基因型(OR=2.199,95%CI:1.005~4.809,P=0.048)是形成易损性斑块的风险因素。结论PECAM1基因单核苷酸多态性位点rs1867624、LMOD1基因单核苷酸多态性位点rs2820315与颈动脉斑块易损性相关。
简介:目的探讨甲型H1N1流感患者心脏损害的特点。方法回顾性研究分析2009年7月至2010年1月期间确诊为甲型H1N1流感患者172例的临床资料,所有患者根据病情分为轻症组,重症组,危重症组,并收集非甲型H1N1流感患者21例作为对照。大部分患者接受分子生物学检测磷酸肌酸激酶,磷酸肌酸激酶同工酶,高敏C反应蛋白,并接受胸部X线摄片检查,计算心胸比。结果甲型H1N1流感多发生于青壮年患者,轻症患者较重症患者更年轻(P<0.05)。在危重症患者中,磷酸肌酸激酶,磷酸肌酸激酶同工酶,高敏C反应蛋白和心胸比均较其他组高(P<0.05或P<0.01)。1例死于心肌损害。结论与既往研究相符,2009甲型H1N1流感可以导致心肌损害,特别是在危重症患者中心肌损害较显著,从而将导致心脏扩大等损害,导致死亡率升高。
简介:目的探讨抑制Twf1基因表达对高糖诱导的心肌细胞增殖、凋亡及NF-κB信号的影响。方法高糖刺激H9c2细胞,将H9c2细胞分为对照组(5.5mmol/L的葡萄糖处理细胞)、NC组(瞬时转染无干扰作用的siRNA后用5.5mmol/L的葡萄糖刺激细胞)、高糖组(瞬时转染无干扰作用的siRNA后用25mmol/L的葡萄糖刺激细胞)和Twf1-siRNA组(瞬时转染干扰Twf1表达的siRNA后用25mmol/L的葡萄糖刺激细胞)。Westernblotting检测蛋白表达,CCK8检测细胞活力,流式细胞仪检测细胞凋亡率及ROS含量。结果高糖可引起H9c2细胞Twf1表达升高,转染Twf1-siRNA后H9c2细胞Twf1的表达明显降低;高糖组细胞活力低于NC组,细胞凋亡率、ROS含量及p-IκBα、Bax和TNF-α的表达均高于NC组,差异均有统计学意义(P<0.05);Twf1-siRNA组的细胞活力高于高糖组,细胞凋亡率、ROS含量及p-IκBα、Bax和TNF-α的表达均低于高糖组,差异均有统计学意义(P<0.05)。结论抑制H9c2细胞Twf1基因表达可逆转高糖诱导的细胞活力降低及凋亡的增加,其机制可能与细胞内ROS含量降低及NF-κB信号下调有关。
简介:ObjectivesToexploretheprotectiveeffectofirbesartan(Irb)undertheinterferencewithangiotensinⅡ(AngⅡ)onABCA1.MethodsElectronmicroscopywasusedtodetectthemorphousoffoamcells.TheexpressionofABCA1mRNAanditsproteinweredeterminedbyRT-PCRandWesternblotting,respectively.Thevarianceofcellularcholesterolcontentwasmeasuredbyzymochemistryvia-fluorospectrophotometer.ResultsApositivefacilitativeeffectofAngⅡontheformationoffoamcellswasobserved.TotalcholesterolwasincreasedsignificantlybyAngⅡ,theexpressionofABCA1wasdown-regulatedobviouslybyAngⅡ;IrbcouldprotectABCA1againstthelesionofAngⅡ;TotalcellularcholesterolcontentwasreducedsignificantlyinIrb+AngⅡgroup;However,considerablealterationaboutthecholesterolcontentandtheexpressionofABCA1werenotobservedinIrbgroupwithoutincubationwithAngⅡ.ConclusionsIrbcouldprotectABCA1againstthelesionofAngⅡ,whichmaycontributetoitsanti-atheroscleroticproperties.
简介:目的探讨中国汉族人群谷胱甘肽硫转移酶(glutathioneS-transferases.GST)M1及T1基因(GSTMI/GSTFl)多态性与先天性心脏病(先心病)发病风险的关系。方法采用病例一对照研究(病例组365例,对照组372例),运用多重聚合酶链反应检测先心病患者及健康对照GSTM1/GSTT1基因型:并利用多因素非条件logistic回归模型,进行先心病发病风险影响因素关联强度及交互作用分析。结果GSTM1/GSTI'I基因多态性及研究对象母亲围孕期吸烟、饮酒、化学物质接触、孕前体质量指数、教育程度、定期产检以及怀孕知情时间在病例组和对照组之间分布存在明显差异(P〈O.05)。GSTM1/GSTT1基因缺失与先心病发病风险显著正相关(OR=1.56,P=0.049;OR=1.73,P=0.036)。经logistic回归分析,GSTM1(-)/GSTT1(-)基因型和研究对象母亲围孕期吸烟、饮酒、化学物质接触以及孕前高体质量指数是先心病发病的高危因素,研究对象母亲围孕期定期产检以及摄人充足的叶酸是先心病的保护因素。研究对象母亲围孕期吸烟与GSTM1(-)/GSTFl(-)基因型之间具有正相加交互作用。与母亲围孕期不吸烟且GSTM1/T1基因未缺失的研究对象相比,其母亲围孕期吸烟且携带GSTM1(-)和(或)GSqTl(-)基因型的先心病发病风险显著上升(OR=9.01,3.87,3.01;95%CI:1.73—39.69,1.21~19.57,1.13—9.69)。结论GSTM1/GSTY1基因缺失是先心病发病风险的独立危险因素;GSTM1(-)/GSTY1(-)基因型与孕母围孕期吸烟在先心病的发生中具有协同作用。
简介:T1mappingusingcardiovascularmagneticresonance(CMR)introducesnoveltechniquesformyocardialtissuecharacterizationtodetectandquantifydiseaseprocessesoccurringatthemicroscopiclevel.EventhoughT1mappinghaslimitedspatialresolution,cellularandmolecularchangesoccurringwithineachvoxelcanaffecttheaggregateT1signalrenderingthemquantifiable.TheestimatedT1-basedparametersquantifiedona“map”demonstratethespatiallocalizationofthesechangeswherebyeachpixelexpressesthequantitativevalueofthatparameter.Thisquantificationpermitsdetectionofdiffusediseaseevenifitisnotdirectlyvisible.Ratherthanrelyingonnonspecificfunctionalmeasures,T1mappingfocusesonintrinsicchangesofmyocardialcompositionthatadvancesunderstandingaboutspecificdiseasepathways.Thesechangesinmyocardialtissuecompositioninformdiagnosisandprognosis.T1mappingencompassestwokeyparameters:native(i.e.,precontrast)T1andextracellularvolumefraction(ECV)derivedfromadditionalpostcontrastT1andbloodT1measurements.Theseadvancesintroducenewtoolstodetectfocalanddiffusemyocardialderangementsoccurringincardiacdiseasethatcanbeotherwisedifficulttodetect.T1andECVmappingfosterprecisionmedicineandpersonalizedcare,promisingtoimprovepatientoutcomesthroughtargetedtherapy.CapitalizingontheopportunitiesintroducedbyT1mappingandECVrequiresfurtherinvestigation.
简介:BackgroundCoronarymicroembolization(CME)ischaracterizedbydistalmicrovascularocclusion.However,theinflammatorymechanismsandtherapeutictargetsofCMEarelargelyunknown.MethodsAtotalof11GuangxiBamaminiatureswinesweredividedintotwogroups:sham(n=5)andCME(n=6).MicrosphereswereinjectedintotheleftanteriordescendingarteryoftheCMEgrouptomakeananimalmodelofCME.TheexpressionsofmicroRNA-146a(miR-146a)andIRAK1,TRAF6,andAUF1inthemyocardiumweredetectedbyqPCR.ResultsIntheCMEgroup,microspheres,microinfarction,andinflammatorycellinfiltrationwerefoundunderanopticalmicroscope.TheexpressionlevelsofmiR-146awerelowinbothgroups.AfterCME,theexpressionlevelsofIRAK1,TRAF6,andAUF1intheCMEgroupwereupregulatedcomparedwiththoseintheshamgroup(P<0.01;P<0.05;P<0.05,respectively).ConclusionsAUF1,IRAK1andTRAF6,butnotmiR-146a,couldbeinvolved,inmyocardiuminflammationfollowingCME.
简介:BackgroundEssentialhypertension(EH)hasbecomethemostcommonchronicnon-infectiousepidemicandisoneofthemostcommonriskfactorsforthedamagetoheart,brain,kidneyandotherorgans.TheserumlevelsofICAM-1,IGF-1andIL-8playimportantrolesinthepathogenesisofEH.MethodsInthemedicalcheck-upcenteroftheAffiliatedHospitalofQingdaoUniversityMedicalCollege,sixtynormaloffspringwithafamilyhistoryofEHwererandomlyrecruitedintotwogroups:30offspringwithafatherormothersufferingfromEHassingle-parentgroup,and30offspringwithbothparentssufferingfromEHasdouble-parentgroup,andanother30normaloffspringwhoseparentsdidnotsufferfromEHascontrolgroup.TheserumlevelsofICAM-1,IGF-1andIL-8weredeterminedbyenzyme-linkedimmunosorbentassay(ELISA).ResultTheserumlevelsofICAM-1,IGF-1andIL-8weresignificantlyhigherinbothsingle-parentgroupanddouble-parentgroupthaninthecontrolgroup(P<0.05),andtheserumlevelsofICAM-1,IGF-1andIL-8werehigherinthedouble-parentgroupthaninthesingle-parentgroup(P<0.05).TheserumlevelsofICAM-1,IGF-1andIL-8werepositivelycorrelatedwiththeseverityofbloodpressureelevation(r=0.375,r=0.465,r=0.326,P<0.05,P<0.01,P<0.05respectively).ConclusionsDuetotheinfluenceofheredity,theseruminflammatoryfactorcontentsinnormaloffspringwithEHfamilyhistorymayincreasebeforebloodpressurerise.DetectionofseruminflammatoryfactorsinhealthyoffspringwithafamilyhistoryofEHcouldpredictoccurrenceofhypertension,andprovideamorereliablebasisfortheprimarypreventionofhypertension.
简介:目的探讨血管紧张素转换酶(ACE)基因插入/缺失多态性和血管紧张素Ⅱ受体1(AT1R)A1166C基因多态性与脑出血的关系,并分析两者是否有协同致脑出血的效应。方法应用聚合酶链反应及限制性片段长度多态性技术,检测80例脑出血患者(脑出血组)和90名健康对照者(健康对照组)的ACE和AT1R基因型和等位基因,并运用Logistic回归分析不同基因型致脑出血的效应。结果脑出血组ACEDD基因型频率为35.0%,D等位基因频率为51.9%,明显高于健康对照组的15.6%和38.9%,均P〈0.05;AT1RAC基因型频率为32.5%,C等位基因频率为16.2%,明显高于健康对照组的11.1%和5.6%,均P〈0.05;Logistic回归显示,170例入组者中,携带AT1RAC基因型(OR:3.852,95%CI:1.719~8.632;P〈0.01)、ACE基因DD型(OR:2.923;95%CI:1.406~6.079;P〈0.01)及同时携带有AT1RAC基因型和ACEDD基因型(OR:4.250;95%CI:1.479~12.209;P〈0.01)是脑出血的独立危险因素。结论ACE基因插入/缺失多态性和AT1RA1166C基因多态性可能是脑出血发病的独立遗传因素;且两者间具有协同致脑出血的作用。
简介:目的:探讨血清转化生长因子(TGF-β1)和胰岛素样生长因子(IGF-1)水平对冠心病患者心功能的影响.方法:选择因胸痛住院患者88例分为急性心肌梗死(AMI)组、心绞痛(AP)组和对照组,填调查表,入院择日行选择性冠状动脉造影术,术前采股动脉血,以ABC双抗体夹心ELISA法检测血清TGF-β1和IGF-1浓度,入院2周内完成超声心动图,所有资料用SPSS10.0软件处理.结果:AMI患者与AP患者相比,血清TGF-β1浓度较低(P<0.05),IGF-1血清浓度较低(P<0.001);冠心病患者血清IGF-1水平与EF(P<0.05)和FS(P<0.02)正相关.结论:TGF-β1和IGF-1对冠心病患者具有某种保护作用,其中IGF-1能保护冠心病患者的心功能.