简介：ObjectivesLittleisknownaboutthemechanismofexercise-indueedangiogenieresponseinisehemicmyoeardium.Thisstudywasdesignedtoinvestigatetheeffeetsofexercisetrainingonexpressionofvaseularendothelialgrowthfaetorandangiogenesisininfarctedheart.MethodsFiftymaleFVBmiceweredividedintothreesubgroupstotestvariousresponsestoexercise,includingtimedependentresponseofangiogenicfactorstoexercisetraininginintactheart(n=10)andinfarctedheart(n=10),aswellasexercise-inducedangiogenieresponseinheartwithmyocardialinfarction(MI)(n=30).Themiceintheexercise-traininggroupswereallowedtoexercisedailyat1hourperdayfor7days.ResultsVEGFproteinexpressionwasup-regulatedbyexercisetrainingintimedependentfashioninmicewithMI.AngiogenesiswasevidentbyincreasedmyocardialmicrovesselsobservedbyPECAM-1immunohistoc-hemicalstaininginpost-MIexercisegroup(16.5±3.4)/0.4mm^2versuspost-MIsedentarymice(10±2.1)/0.4mm^2(P<0.05).Cellproliferationassessmentshowedsignificantlyhigher(P<0.05)numberofBrdUpositivecellsinpostMImiceinexerciseerouoasopposedtosedentarypostMImice.2%TTCstainingdisclosedaprofounddifferenceinthesizeofMI(18.25±2.93)%inexercisegroupvssedentarygroup(29.26±7.64)%(P<0.05).ConclusionsActivationandup-regulationofVEGFininfarctedmiceheartmaycontributestheangiogenicresponsetoexercisetrainingattheearlystageofmyocardialinfarction.Thisunderscorestheimpactofexerciseonangiogenesisinpostmyocardialinfarctionsetting.

简介：BackgroundStudieshaveshownthattheapo(a)gene(LPA)rs3798220polymorphismisassociatedwiththelevelsoflipidsandthecurativeeffectofstatintherapyforcarotidatherosclerosis(CAS).Whethercarriersofanapo(a)variantbenefitmorefromstatinremainsunclear.MethodsOnehundredandthreepatientswithCASwererecruitedfromApril2012toApril2013intheShundeFirstPeoplesHospitalAffiliatedtoSouthernMedicalUniversityinFoshan.Allpatientswereadministeredatorvastatin20mg/dandwerefollowed-upfor2years.withthelevelsofplasmaLp(a),totalcholesterol(TC),triglyceride(TG),highdensitylipoprotein(HDL),lowdensitylipoprotein(LDL).LPArs3798220genotypesofallpatientswereanalyzed.ResultsStatintreatmentsignificantlyreducedthelevelsofIMT,TC,TG,LDLandincreasedthelevelofHDL,butstatintreatmentdidnotreducethelevelofLp(a).AccordingtothecurativeeffectofstatintherapyinpatientswithCAS,rs3798220polymorphismhadacertaininfluenceonLDLandTClevels,butnotontheimprovementoftheIMT,TG,HDLandLp(a).ConclusionRs3798220polymorphismhasacertainimpactonthecurativeeffectsofstatin,onLDLandTClevels.

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.