简介：RecentstudiesrevealingtheimportantrolesofmicroRNAs（miRNAs）inregulatingexpressionofionchannelgeneshaveopeneduparesearchfieldforextendinganddeepeningourinvesti-gationintothecardiacexcitabilityandtheassociatedarrhythmogenesis.Cardiacexcitability,thefundamentalpropertyofthecardiacmyocytes,definesthecardiacconduction,repolarization,automaticity,intracellularcalciumhandling,andtheirregionalheterogeneity.OurpreviousandongoingstudiesandtheworkfromotherlaboratorieshavedemonstratedthesignificantinvolvementofmiRNAsinregulatingeveryaspectsofcardiacexcitability.Wehavefoundearlierthatthemuscle-specificmiRNAmiR-1boostsupthearrhythmogenicpotentialthroughtargetinggapjunctionchannelconnexin43inmyocardialinfarction.AsubsequentstudyrevealedthatmiR-1canalsocausearrhythmiasbyimpairingCa2+handlingbytargetingphosphatase.Wethenidentifiedanothermuscle-specificmiRNAmiR-133promotesabnormalQTprolongationbyrepressingHERGK+channelexpressionindiabeticcardiomyopathy.Subsequently,wediscoveredthatbothmiR-1andmiR-133areinvolvedinthereexpressionofpacemakerchannelsHCN2/HCN4toenhanceabnormalautomaticityincardiachypertrophy.Recently,wefurtheridentifiedmiR-328asanimportantdeterminantforatrialfibrillation（AF）andtheassociatedadverseatrialelectricalremodelingviatargetingL-typeCa2+channels.Whilealltheabove-mentionedmiRNAsareproarrhythmic,wehavenewlyidentifiedforthefirsttimeanaturalantiarrhythmicmiRNAmiR-26.WefoundthatallthreemembersofthemiR-26familyisdownregulatedintheirexpressioninAFtissuesandthisdownregulationincreasesAFvulnerabilityasaresultofremovalofanendogenousantiarrhythmicfactor.miR-26downregulationshortensatrialactionpotentialfavoringAFbyincreasinginwardrectifierK+current（IK1）density.ThisiscausedbyanupregulationofKir2.1K+channelsu

简介：Theriskofmyocardialinfarctionincreasesinpatientswithdiabetesmellitus.Theincidenceofmyocardialinfarctionissimilarinpatientswithtype2diabeteswithouthistoryofmyocardialinfarctionandinnon-diabeticpatientswithhistoryofmyocardialinfarction.DiabetesmellituswasconsideredasacoronarydiseaseequivalentbytheNationalCholesterolEducationProgram.Strictglycemiccontrolcanimprovethelong-termoutcomeofbothtype1andtype2diabetesmellitus.Whateverwithdiabeticornon-diabetic,strictglycemiccontrolwithintensiveinsulintherapycanreducethemortalityofcriticallyillpatientsinhospital.Aftermyocardialinfarction,therewouldbeaworseoutcomeforpatientswithpoorglycemiccontrol,whateverindiabeticornon-diabeticpatientswithstresshyperglycemia.Meanwhile,strictglycemiccontrolcanimprovetheoutcome.TheguidelineofAmericanCollegeofCardiology/AmericanHeartAssociationin2004onST-elevatedmyocardialinfarctionrecommendedinsulininfusionmaintainingtheeuglycemiaforpatientswithacutemyocardialinfarctionandcomplicatedconditions,whetherwithdiabetesmellitusornot,anditwasconsideredreasonabletoinfuseinsulinforallpatientswithhyperglycemiaduringtheperiodofacutemyocardialinfarction.Thispaperproposedaneffectiveandsafemethodforintravenousinsulininfusiontherapyfordiabeticpatientswithacutemyocardialinfarction.

简介：ObjectivesToinvestigateserumconcentrationofprocollagentypeIcarboxyterminalpeptide(PIP),typeⅢaminopeptide(PⅢP)andtypeIcollagentelopeptide(ICTP)inessentialhypertension(EH).MethodsSerumlevelsofPIP,PⅢPandICTPin42EHpatientsand30healthycontrolweremeasuredbyradioimmunoassays.ResultsInEHpatients,serumconcentrationofPIP,PⅢPwassignificantlyhigherthanthatin30healthycontrol.AlthoughEHpatientsdidtendtoexhibitahigherserumICTPconcentrationthannormalcontrolsubjects,thedifferencewasnotstatisticallysignificant.EHpatientswithleftventricularhypertrophyexhibitedhighervaluesofPIP(P<0.05)andlowervaluesofICTP(P<0.05)thanEHpatientswithoutleftventricularhypertrophy.NosignificantdifferencewasnotedbetweentheserumPⅢPoftheEHpatientswithandwithoutleftventricularhypertrophy(P>0.05).ConclusionsTheresultssuggestthatPIPandPⅢParesensitiveserummarkersofmyocardialcollagensynthesis.Myocardialfibrosismaybeduetotheexcessivesynthesisandinsufficientdegradationofcollagen.PIP,PⅢPandICTPmaybeindirectmarkersofmyocardialfibrosis.

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