简介:Hypertensionisaleadingriskfactorforcardiovasculardisease,theleadingcauseofdeathandmorbidityinoursocietyandonaglobalscale.Majorcomponentsofcardiovasculardiseaseincludestroke,coronaryarterydisease,heartfailure,andchronickidneydisease,inallofwhichhypertensionplaysamajorrole.Theriskofthesecomplicationsincreasesdirectlyandlinearlywithsystolicbloodpressurestartingat115mmHg.Althoughusuallyasymptomatic,hypertensionisreadilydetectableonphysicalexaminationandisamenabletobothlifestylemodificationandpharmacologictreatmentinmostpatients.However,largeproportionsofthehypertensivepopulationremainundetectedandundertreated.Numerousguidelineshavebeenissuedduringthepastfewdecadestopromotedetectionandoptimaltherapy.Despitetheincreaseinriskwithsystolicbloodpressuregreaterthan115mmHg,thegenerallyacceptedthresholdfordiagnosisandtreatmenthasbeensystolicbloodpressuregreaterthan139mmHganddiastolicbloodpressuregreaterthan80mmHgbecauseuntilrecentlytreatmenttolowerlevelshasbeenassociatedwithanunfavorablerelationbetweenclinicalbenefitandharm.Inthepastseveralyears,newguidelines,advisories,commentaries,andclinicaltrialshaveprovidedevidenceforapotentialchangeincurrentrecommendationsforthemanagementofhypertension.Inthisregard,thelong-awaitedeighthreportoftheJointNationalCommitteeonthePrevention,Detection,Evaluation,andTreatmentofHighBloodPressurerecommendedpatientsolderthan60yearsbetreatedtoasystolicbloodpressureoflessthan150mmHg,whichhasgeneratedconsiderablecontroversyandcaution.ThestrikingfindingsoftheSystolicBloodPressureInterventionTrial(SPRINT)havereceivedconsiderableattentionbecauseofthedemonstrationthatintensivetherapytoatargetsystolicbloodpressurebelow120mmHgdecreasescardiovascularmortalityandmorbiditymorethanlessintensivetreatmenttoatargetsystolicbloodpressurebelow140mmHg
简介:ObjectivesToelucidatethepotentialroleofcytokinesinthepathogenesisofcoronaryheartdisease(CHD).MethodsTNF-αandIFN-γactivity,IL-8levelsofplasmaandsupernatantsweremeasuredin62patientswithCHDand30healthcontrolsbymethodsofdirectcytotoxicityassay,cytopathiceffectinhibitiontestandELISArespectively.ResultsBothTNF-αactivityandIL-8levelsofplasmainCHDpatientswerehigherandIFN-γactivityofsupernatantsinCHDpatientswerelowerthanthoseofhealthycontrols(P<0.001),TherehavesignificantdifferencesbetweenhealthycontrolsandthesubgroupsofCHD(P<0.01).IL-8levelsofplasmaincreasedwiththeadvancingofthediseaseandtherehaveobviousdifferencesamongsubgroupsoftheillness(P<0.05).TNF-αactivityofplasmainstableanginapectoris(SAP)subgroupwaslowerthanthoseofunstableanginapectoris(UAP)andacutemyocardialinfarction(AMI)subgroups,thedifferencesbetweenSAPandUAPorAMIweresignificant(P<0.05),ButtherehavenosignificantdifferencesbetweenUAPandAMI(P>0.05).However,IFN-γactivityofsupernatantsshowednodifferenceamonganysubgroups.ConclusionstherehavecloserelationsbetweenTNF-α,IFN-γ,IL-8andCHD.
简介:Thepanaxnotoginsengsaponin(PNS)hadbeenclinicallyusedforthetreatmentofcardiovasculardiseasesandstrokeinChina.IthadbeendemonstratedthatPNScouldprotectcardiomyocytesfrominjuryinducedbyischemi-a,buttheunderlyingmolecularmechanismsofthisprotectiveeffectwerestillunclear.ThisstudywasaimedtoinvestigatetheprotectiveeffectandmolecularmechanismsofPNSonapoptosisinH9c2cellsinvitroandratmyocardialischemiainjurymodelinvivo.Annexin-V/PIassayshewthatPNScouldprotectH9c2cellsfromapoptosisinducedbyserum,glucoseandoxygendeprivation(SGOD)inadose-dependentmanner.However,theanti-apoptoticeffectofPNSwasreversedbyLY294002,aspecificPI3Kinhibitor.ThisantiapoptoticeffectofPNSwasconfirmedbyJC-1,aspecificprobeofmitochondrialmembranepotentialstaining.PNScouldsignificantlyincreasephos-AktinH9c2cellsbyWesternblotassaysanditseffectcouldbeinhibitedbyLY294002.Furthermore,PNScouldimproveischemic-inducedleftventricularfunctionasreflectedbyEF,LVDdandLVDs.PNScouldalsoinhibitedcellularapoptosisinmyocardialtissuesinischemicratsbyTUNELassay.PNSadministrationalsoincreasedtheexpressionofphos-Aktinratischemicmyocardialtissues.TheseresultssuggestedthatPNScouldprotectmyocardialcellsfromapoptosisinducedbyischemiainvitromodelandinvivomodelthroughactivating-PI3K/AktsignalpathwaywhichmaybemeaningfulforfurtherunderstandingthemolecularmechanismsofcardiacprotectionofPNS.Andtheresultsmightbeusefulintreatmentofmyocardialischemiainfuture.
简介:我院自1998年6月以来,采用“沈大牌”膀胱碎石镜直视下钳夹碎石治疗膀胱结石8例,效果满意,报告如下。
简介:目的:观察热应激诱导心肌热休克蛋白(HSP)70表达上调,对兔快速心房起搏致房颤心肌钙激活钾通道(KCa)3.1表达的影响。方法:将24只新西兰大白兔随机分为假手术组(n=8,仅植入电极而不起博)、起搏组(n=8,以600次/min快速起搏右心房6h)和热应激起搏组(热应激组,n=8,先行热应激预处理,再行与起搏组一样的快速起搏)。结果:与假手术组和起搏组比较,热应激组心脏各部位HSP70mRNA和蛋白表达显著上调[HSP70蛋白,左房:(39.00±3.21)比(39.75±2.82)比(69.75±3.45),右房:(38.38±2.92)比(39.50±3.89)比(69.00±2.93),左心耳:(37.75±3.28)比(39.00±3.89)比(68.63±3.23),右心耳:(37.00±3.85)比(38.38±3.74)比(68.75±2.82)],P均〈0.01,而起搏组和假手术组间无显著性差异(P〉0.05);与起搏组KCa3.1mRNA和蛋白表达量显著下调比较,热应激组心脏各部位KCa3.1mRNA和蛋白表达量显著上调[KCa3.1蛋白,左房:(21.25±1.67)比(24.00±2.62),右房:(21.13±1.96)比(23.75±1.83),左心耳:(21.00±2.07)比(23.75±1.67),右心耳:(20.88±2.03)比(23.50±2.45)],P均〈0.05,且热应激组与假手术组间无显著差异(P〉0.05)。结论:热应激可诱导心房起搏心肌热休克蛋白(HSP)70表达上调,抑制KCa3.1mRNA和蛋白表达量显著下降。
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:Objectives:Apoptosisisrecognizedasanimportantmechanismincontrast-inducednephropathy(CIN).Cordycepssinensis(CS),atime-honoredtonicfoodandherbalmedicineinChina,canimprovethemicrocirculation,increasethetolerancetoischemiainpatientswithmicrocirculatorydisorders.AsCShasbeenfoundtoberenoprotectiveandanti-apoptoticinmultiplekidneyinjuries,wehypothesizedthatCSwouldpreventCIN.TheobjectiveofthisresearchistostudythemechanismofCSontubularepithelialcellapoptosisindiabeticCINrats.
简介:目的探讨冠心病患者血清炎症因子白介素-6(IL-6)、白介素-8(L-8)和肿瘤坏死因子(TNF)含量在冠心病发展过程中的意义。方法测定81例冠心病患者血清炎症因子IL-6、IL-8和TNF含量,观察冠心病患者冠脉狭窄程度与血清IL-6、IL-8及TNF含量变化的关系。结果40例冠脉重度狭窄者血清炎症因子IL-6、IL-8和TNF分别为(163.41±64.18)pg/ml、(0.41±0.11)ng/ml、(2.54±0.63)ng/ral,41例冠脉轻中度狭窄者血清炎症因子IL-6、IL-8和TNF分别为(97.05±27.29)pg/ml、(0.34±0.16)ng/ml、(1.86±0.33)ng/ml,两组间差异存在统计学意义(P〈0.05)。结论血清炎症因子IL-6、IL-8和TNF与冠心病的严重程度有关。冠脉狭窄越明显,炎症因子IL-6、IL-8及TNF含量越高。