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：BackgroundCurrentlyusedheartvalveprosthesesareassociatedwithanticoagulationcomplicationsorlimiteddurability.Theadvancementofstemcellstudyandtissue-engineeredheartvalveresearchmayofferarelativelyidealsolutiontotheseproblems.MethodsBonemarrowwasaspiratedfromsternumoflambgoatstoisolateBMCs.Cellswereidentifiedbyflowcytometryanditscapacityofdifferentiation.CellularviabilitywasassessedwithRhdomine123staining.1×107cellswereseededonapatchofPGAsheet.Aftertwo-dayinvitroculture,theautologouscell/scaffoldsheetswereusedtoreplacetherightposteriorpulmonaryvalveleafletsundercardiopulmonarybypass.Theleafletswereexplantedat2days,2,6,8and10weeksafterimplantation.Thesampleswereexaminedmacroscopically,histologically,immunohistochemically,andbyScanningElectronMicroscope(SEM).Twogoatswereimplantedwithacellularsheetsandestablishedasacontrolgroup.ResultsBMCsexhibitedfibroblastoidmorphologywithgoodviability.FlowcytometryshowednegativeCD14andCD45expression.InvitroculturedBMCsdemonstratedthepotentialtodifferentiateintoadipocytes.Theexplantedleafletsresembledthecharacteristicsofnativeleafletsmacroscopicallyinthecellulargroup.Histologyshowedextracellularmatrixwassynthesizedandcellsweredistributedinthesingle-layeredleaflets.ImmunohistochemistryrevealedpositivestainingforvonWillebrandfactor,α-SMA,vimentin.AconfluentcellsurfacewasformedontheexplantedTEHLs.Nocalciumdepositedontheleaflets.Incontrolgroup,theacellularscaffoldswerecompletelydegraded,withoutleafletremainedat8weeks.ConclusionsItispossibletocreatetissue-engineeredheartvalvesinvivousingautologousbonemarrow-derivedcells.

简介：ObjectivesTodevelopasimple,accurateandreproduciblemethod,whichcombinesmacroandhistopathologicaltechniquesfordeterminingthedegreeoflipiddepositioningeneticallymodifiedmice.MethodTheentireaortasfromC57BL/6,ldlr-/-andapoE-/-micewerestainedwithSudanⅣusingeitherinvivoperfusionortraditionalinvitroenfacestainingtechniques.Histologicalsectionsofaorticrootandheartswereembeddedintissuefreezingmediumandcutwithacryostat,thenstainedwithOilRedO.Thecalculatedaorticrootareabasedontheaorticrootcircumferencewasusedtoreducemeasurementerrors.ResultsTheinvitroenfacestainingcanstainallfat,whichincludetheadventitialtissuearoundaorta.Howevertheinvivoperfusionstainingcanspecificallystainthefattydepositioninsideofaorta.Bothentireaortaandaorticrootsectionstainingshowedthattherewasahighlysignificantincreaseinfattydepositionintheaortasofthegeneticmodifiedmice.Althoughallmicegeneticbackgroundwassame,theapoE-/-micehadlargeratheroscleroticlesionsthanldlr-/-mice.ConclusionsThenewinvivoperfusionmethodismoreaccuratethantheinvitroenfacemethod.Thecombinationofthesemacroandmicroscopictechniquesovercomestheshortcomingsoftheearlierpublishedmethodswhicharegenerallylimitedtothemeasurementoffattyredstainingareasonly,neglectingnon-specificadventitialfatstainingaroundaortaandaorticrootsectiontissuedistortion.