【摘要】Objective-Atherosclerosisisaninflammatorydiseaseinwhichmacrophageactivationandlipidloadingplayacrucialrole.Inthisstudy,weinvestigatedexpressionandfunctionoftheNR4Anuclearreceptorfamily,comprisingNur77(NR4A1,TR3),Nurr1(NR4A2),andNOR-1(NR4A3)inhumanmacrophages.MethodsandResults-Nur77,Nurr1...
参考资料医源资料库；在线期刊；动脉硬化血栓血管生物学杂志；2006年第26卷第10期【摘要】Objective—Endothelin-1(ET-1)andangiotensinII(AngII)activatecommonsignalingpathwaystopromotechangesinvascularreactivity,remodeling,inflammation,andoxidativestress.Herewesoughttodeterminewhetherupstreamregulatorsofmitogen-activatedproteinkinases(MAPKs)aredifferentiallyregulatedbyET-1...
参考资料医源资料库；在线期刊；动脉硬化血栓血管生物学杂志；2007年第27卷第9期【摘要】Objective-Monocytesurvivalisanimportantdeterminantinthedevelopmentofatheroscleroticlesions.WeinvestigatedtheinfluenceofphospholipaseA2-modifiedLDL(PLA-LDL),apro-atherogenicfactor,onactivationofthepro-survivalkinaseAktandcelldeathinmonocyticcells.MethodsandResults-PLA-LDLinducedrobustphos...
参考资料医源资料库；在线期刊；动脉硬化血栓血管生物学杂志；2006年第26卷第11期【摘要】Objective—ApolipoproteinA5(APOA5)isakeydeterminantofplasmatriglyceride(TG)concentrations.GeneticvariationattheAPOA5locuscouldberesponsibleforsomeoftheobserveddifferencesinresponsetofenofibratetherapy.MethodsandResults—WeexaminedtheassociationbetweenG)atAPOA5andTGandHDL-Crespo...
参考资料医源资料库；在线期刊；动脉硬化血栓血管生物学杂志；2007年第27卷第6期KarenS.Meir;EranLeitersdorfFromtheDepartmentofPathology(K.S.M.),theCenterforResearch,Prevention,andTreatmentofAtherosclerosis(K.S.M.,E.L.),andtheDepartmentofInternalMedicineB(E.L.),HadassahUniversityHospital,Jerusalem,Israel.ABSTRACTArguablythemostcriticaladvancementintheelucidationoffactorsaffectin...
参考资料医源资料库；在线期刊；动脉硬化血栓血管生物学杂志；2004年第24卷第6期【摘要】Bylocation,betweenthebloodandtissuesandthemultiplefunctions,theendothelialcells(ECs)playamajorroleinsecuringbodyhomeostasis.TheECssenseallvariationsoccurringintheplasmaandinterstitialfluid,andrespond(functionofintensity),initiallybymodulationoftheirconstitutivefunctions,thenbydysfunction...
参考资料医源资料库；在线期刊；动脉硬化血栓血管生物学杂志；2007年第27卷第2期【摘要】Afterreceptor-mediatedendocytosis,theintracellularfateoftriglyceride-richlipoproteins(TRLs)isfarmorecomplexthantheclassicaldegradationpathwayoflow-densitylipoproteins.Onceinternalized,TRLsdisintegrateinperipheralendosomes,followedbyadifferentialsortingofTRLcomponents.Althoughcorelipidsan...
参考资料医源资料库；在线期刊；动脉硬化血栓血管生物学杂志；2006年第26卷第3期FromDépartementd’Athérosclérose(A.G.,H.D.,A.H-C.,C.D.,B.S.,J.F-N,J-C.F.),U.545INSERM,InstitutPasteurdeLilleandFacultédePharmaciedeLille,LilleCedex,France;GenfitSA(D.W.H.,G.M.),Loos,France;GenomicsDivision(L.A.P.),LawrenceBerkeleyNationalLaboratory,Berkeley,Calif.CorrespondencetoJamilaFruchart-...
参考资料医源资料库；在线期刊；动脉硬化血栓血管生物学杂志；2005年第25卷第6期SharonC.Tai;G.BrettRobb;PhilipA.MarsdenFromtheRenalDivisionandDepartmentofMedicine,St.Michael’sHospitalandUniversityofToronto,Ontario,Canada.CorrespondencetoPhilipA.Marsden,Room7358,MedicalSciencesBuilding,UniversityofToronto,1KingsCollegeCircle,Toronto,OntarioM5S1A8Canada.E-mailp.marsden@utoronto...
参考资料医源资料库；在线期刊；动脉硬化血栓血管生物学杂志；2004年第24卷第3期【摘要】Objective-Heparin-inducedthrombocytopenia(HIT)isaprothromboticdrugreactioncausedbyantibodiesthatrecognizepositivelychargedplateletfactor4(PF4),boundtothepolyanion,heparin.Theresultingimmunecomplexesactivateplatelets.Unfractionatedheparin(UFH)causesHITmorefrequentlythanlow-molecular-weigh...
参考资料医源资料库；在线期刊；动脉硬化血栓血管生物学杂志；2006年第26卷第10期