简介：ObjectivesToobservetheeffectsoftelmisartanandrosiglitazoneandexplorethemechanismonearlyatherogenesisinmaleratswithtype2diabetesmellitus.MethodsFortymaleSDratswererandomlyandequallydividedintofourgroups:controlgroup,type2diabetesmellitusgroup,telmisartangroupandrosiglitazonegroup.HighlipidandhighglucosewereusedforinducingDMinSDrats.Theratswereraisedforsixteenweeks.TC,TG,LDL-CandBG,PGIweremeasured.Theaortaewerecollectedforhistopathlogicalandimmunohistochemicalstudies.Immunohisto-chemistrywasusedtoanalyzetheexpressionofPPAR-γ,VCAM-1andICAM-1inthearterialvesselwall.ResultsComparedwiththecontrolgroup,thelevelofTC,TG,LDL-C,andBGinbloodwereincreasedsignificantly(P<0.01)intype2Diabeticgroup.ThetelmisartanandrosiglitazonetreatmentdecreasedbloodTC,TG,LDL-CandBG.TheexpressionofPPAR-γintype2diabeticgroup,telmisartanandrosiglitazonegroupshadsignificantdifferencescomparedwiththecontrolgroup,buttherewasn'tanysignificantdifferences(P>0.05)amongthosethreegroups.ExpressionofVCAM-1,ICAM-1andthemonocytesinfilitratingintotheintimaoftheaortastelmisartanandrosiglitazoregroupwassignificantlylowerthanthoseindiabeticgroup(P<0.01).Theendothelialdamageoftheaortaeintehnisartanandrosiglitazonegroupwaslessseverethanthatindiabetesmellitusgroup.ConclusionTelmisartanandrosiglitazonecanpreventearlyatherogenesisthroughalleviatingthedamagetothearterialwallbyincreasingtheactivationofPPAR-γandinhibitingtheVCAM-1,ICAM-1expressionandthemonocytesinfilitratingintothearterialwall.

简介：BackgroundHeartfailureisoneofthemaincausesofdeathduetoprogressivemusculardystrophyofDuchennemusculardystrophy(DMD)inthemajorityofthecases.ThereishighincidenceofarterialthromboembolisminDMDpatientswithsevereheartfailure.However,ithasbeenreceivinglittleattentionwhetheranticoagulativetherapyinDMDpatientswithsevereheartfailureinsinusrhythmshouldbeperformed.HereinwepresentacaseofDMDpatients,withsevereheartfailureinsinusrhythm,whopresentsalargemuralthrombusformationatleftventricularanteriorwall.