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: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:ObjectivesToevaluatetheeffectsofn-3fattyacidsonthecoronaryheartdiseasepatients.MethodsFromSeptember2007toMarch2008,60patientswithcoronaryheartdiseasewererandomlyassignedton-3fattyacidsgroup(groupN)andcontrolgroup(groupC).BothgroupsreceivedstandardcoronaryarterydiseasesecondarypreventiontreatmentandgroupNalsoreceivedeicosapentaenoicacid(EPA)1.8gplusdocosahexaenoicacid(DHA)1.2gperdayfor12weeks.Plasmatriacylglycerols,totalcholesterol,low-densitylipoproteincholesterol(LDL-C),high-densitylipoproteincholesterol(HDL-C)andbloodpressureweremeasuredbeforeandafterthestudy.ResultsPlasmatriacylglycerols,bloodpressureandLDL-ClevelwereloweringroupNaftern-3fattyacidstreatmentwhilenochangewasfoundingroupC(P<0.05).HDL-Clevelslightlyincreasedandtotalcholesterollevelslightlydecreasedaftern-3fattyacidsbutbothchangewerenotsignificant(P>0.05).ConclusionsN-3fattyacidshavebeneficialeffectsonthecoronaryarterydiseasepatients.
简介:INTRODUCTIONWiththedevelopmentofeconomyandimprovementoflifequality,theincidencesofhypertension,hyper-cholesterolemia,diabetes,obesityandsmokinghavebeenincreasedinChina,whichhasledtoasignificantincreaseinthemorbidityandmortalityofcoronaryarterydisease(CAD)~1.SinceitwasintroducedintoChinain1984,coronaryintervention(PCI)hasdevelopedrapidlyandhasbecomethemajortreatmentofCADbecauseofitsuniquecharacteristicsofminimalinvasiveand
简介:目的比较CT薄层增强扫描与3D-DSA数据源在颅内动静脉畸形(AVM)3D打印数据重组中的效果。方法前瞻性选取5例AVM患者,Spetzler-Martin分级Ⅱ级3例,Ⅲ级2例。对其中2例采用256层螺旋CT薄层增强扫描,3例采用3D-DSA旋转成像,提取检查结果的DICOM原始数据,通过Mimics14.0软件进行数字化处理,并按1∶1比例进行3D打印,获得实体模型并进行效果比较。结果基于256层螺旋CT薄层增强扫描数据源的3D打印可获取颅骨及血管的图像信息,能显示最细直径0.9mm的血管,但AVM内部细支结构难于分辨;基于3D-DSA数据的3D打印,数字减影无颅骨数据信息,但血管分支情况显示更丰富,可显示最细直径0.5mm的血管。结论应用CT薄层增强扫描或3D-DSA数据源均可获得AVM畸形团3D重组图像,而3D-DSA显示AVM畸形团空间构造效果更佳,有助于术前治疗方案的设计及相应辅助工具的开发。
简介:ObjectivesToinvestigatethechangesofβ3-adrenoceptor(β3-AR)mRNAexpressionintheratswithchronicheartfailure(CHF),andtoexploretheeffectofβblockers(βBs)onβ3mRNAexpression.MethodsThirty-fourratswererandomlydividedintoShamgroup(n=10)andheartfailuregroup(n=24).Ratmodelwasestablishedbyaorticconstriction.Thesurvivalratsinheartfailuregroupweredividedintoheartfailurecontrolgroup(HFgroup,n=6),metoprololgroup(METgroup,n=8)andcarvedilolgroup(CARgroup,n=8)threemonthsafteroperation.Metoprololtartartewasstartedorallywith12mg·kg-1·d-1,carvedilolwith6mg·kg-1·d-1,isometricsalinewasstartedinHFgroup.Afterthreemonthsofdrugtherapy,measurementofhemodynamics,indexofventricularmass,thelevelofβ3-ARmRNAexpressionwereperformed.ResultsComparedwithShamgroup,leftventricularendsystolicpressure(LVESP),andtheabsolutevaluesofmaximalrateofriseandfall(±dp/dtmax)ofleftventricularpressurewereallsignificantlydecreased(P<0.01),leftventricularenddiastolicpressure(LVEDP)wassignificantlyincreasedinHFgroup(P<0.01).ThehemodynamicparameterswereimprovedbyβBs,andcarvedilolwasmoreeffectivethanmetoprolol(P<0.01).TheindexofventricularmasswashigherinHFgroupthanMETgroup,CARgroupandShamgroup(P<0.01).βBssignificantlydecreasedtheindexofleftventricularmass(LVMI),andCarvedilolwasmoreeffectivethanmetoprolol(P<0.01).Theindexofrightventricularmass(RVMI)didnotchangeinMETgroup(P>0.05),butsignificantdecreasecouldbeseeninCARgroup(P<0.01).Thelevelofβ3-ARexpressioninleftventriclewasgreaterthanthatinrightventriclewhetherinthefailingheartorinthenon-failingheart.ComparedwithShamgroup,thelevelofβ3-ARmRNAexpressionwassignificantlyincreasedinHFgroup(P<0.01).Thelevelsofβ3-ARmRNAexpressionshowedaremarkabledecreaseinCARgroup(P<
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。