简介:Strokeisaleadingcauseoflong-termdisability.Moststrokepatientsregaintheirfunctionpartiallyorfullyduringthefirst3–6monthsdependingonlocationandsizeofthelesion.Duringthisfunctionalrecoveryphase,corticalreorganizationorplasticityoccurs,andphysiologicalresponsivenessorneuronalexcitabilityisalteredintheipsilesionalandcontralesionalareas.However,howtodrivesuccessfulplasticchangesorsuccessfulstrokerecoveryarenotfullyelucidatedyet.
简介:Strokeisaleadingcauseofdeathanddisabilityinadultsworldwide.Fordecades,theprimaryapproachandgoaloftherapyforstrokehasfocusedonneuroprotection,namelytreatingtheinjuredtissue,withinterventionsdesignedtoreducethevolumeofcerebralinfarction.Enormouseffortinthelaboratoryhasbeendevotedtothedevelopmentof
简介:Oxidativestressiscloselyassociatedwithsecondarycelldeathinmanydisordersofthecentralnervoussystemincludingstroke,Parkinson’sdisease,Alzheimer’sdisease.Amongmanyaberrantoxidativestress-associatedproteins,DJ-1hasbeenassociatedwiththeoxidativestresscelldeathcascadeprimarilyinParkinson’sdisease.Althoughprincipallyexpressedinthecytoplasmandnucleus,DJ-1canbesecretedintotheserumunderpathologicalcondition.Recently,aclosepathologicalassociationbetweenDJ-1andoxidativestressinstrokehasbeenimplicated.Tothisend,weandothershavedemonstratedtheimportantroleofmitochondriainneuroprotectionforstrokebydemonstratingthatthetranslocationofDJ-1inthemitochondriacouldpotentiallymitigatemitochondrialinjury.Here,wediscussourrecentfindingstestingthehypothesisthatDJ-1notonlyfunctionsasaformofintracellularprotectionfromoxidativestress,butthatitalsoutilizesparacrineand/orautocrinecuesinordertoaccomplishextracellularsignalingbetweenneighboringneuronalcells,resultinginneuroprotection.ThisarticlehighlightsrecentevidencesupportingthestatusofDJ-1askeyanti-oxidativestresstherapeutictargetforstroke.
简介:BackgroundTheclinicalcharacteristicsofstrokepatientstreatedwithdoubleanti-platelettherapy(DAPT)afterpercutaneouscoronaryintervention(PCI)isnotclear.MethodsIntotal,2675patientsunderwentPCIandDAPTinGuangdongGeneralHospital,and68outofthemwerehospitalizedduetosuspectedstroke,ofwhom23werediagnosedashavingstroke.Dataofthe23strokepatientswerecollectedandtraditionalriskfactorsassociatedwithstrokewereanalyzedretrospectively.ResultsThemeanageofthesepatientswas75.6±8.7years,and20(87.0%)weremales.Notably,19patientswerecomplicatedwithhypertension,7withdiabetesmellitus,7withprevioushistoryofstroke,nonewithatrialfibrillation(AF)orpatentforamenovale(PFO).Specifically,22patientswerediagnosedwithischemicstroke,and1patientwithhemorrhagicstroke.ConclusionStrokeinpatientstreatedwithDAPTafterPCIwascorrelatedwithadvancedage,gender,hypertension,diabetesmellitus,strokehistory.Longtermelectrocardiography(ECG)maybeneededforthediagnosisofAF,whiletrans-esophagealechocardiography(TEE)maybeneededforPFO.
简介:Moststudiesaddressingthespecificityofmeridiansandacupuncturepointshavefocusedmainlyonthedifferentneuraleffectsofacupunctureatdifferentpointsinhealthyindividuals.Thisstudyexaminedtheeffectsofacupunctureonbrainfunctioninapathologicalcontext.Sixteenpatientswithischemicstrokewererandomlyassignedtotruepointgroup(trueacupunctureatrightWaiguan(SJ5))andshampointgroup(shamacupuncture).Resultsoffunctionalmagneticresonanceimagingrevealedactivationinrightparietallobe(Brodmannareas7and19),therighttemporallobe(Brodmannarea39),therightlimbiclobe(Brodmannarea23)andbilateraloccipitallobes(Brodmannarea18).Furthermore,inhibitionofbilateralfrontallobes(Brodmannarea4,6,and45),rightparietallobe(Brodmannareas1and5)andlefttemporallobe(Brodmannarea21)wereobservedinthetruepointgroup.Activationintheprecuneusofrightparietallobe(Brodmannarea7)andinhibitionoftheleftsuperiorfrontalgyrus(Brodmannarea10)wasobservedintheshamgroup.Comparedwithshamacupuncture,acupunctureatWaiguaninstrokepatientsinhibitedBrodmannarea5onthehealthyside.Resultsindicatedthatthealteredspecificityofsensation-associatedcortex(Brodmannarea5)ispossiblyassociatedwithacentralmechanismofacupunctureatWaiguanforstrokepatients.
简介:Basementmembranedegradationandblood-brainbarrierdamageappearaftercerebralinfarction,severelyimpactingneuronalandbrainfunctioning;however,theunderlyingpathogeneticmechanismsremainpoorlyunderstood.Inthisstudy,weinducedcerebralinfarctioninstrokepronespontaneouslyhypertensiveratsbyintragastricadministrationofhigh-sodiumwater(1.3%NaCl)for7consecutiveweeks.Immunohistochemicalandimmunofluorescenceassaysdemonstratedthat,comparedwiththenon-infarctedcontralateralhemisphere,stroke-pronespontaneouslyhypertensiveratsonnormalsodiumintakeandWistar-Kyotorats,matrixmetalloproteinase-9expression,thenumberofbloodvesselswithdiscontinuouscollagenIVexpressionandmicrovesseldensityweresignificantlyhigher,andthenumberofcontinuouscollagenIV-positivebloodvesselswaslowerintheinfarctborderzonesofstroke-pronespontaneouslyhypertensiveratsgivenhigh-sodiumwater.Linearcorrelationanalysisshowedmatrixmetalloproteinase-9expressionwaspositivelycorrelatedwiththenumberofdiscontinuouslycollagenIV-labeledbloodvesselsandmicrovesseldensityincerebralinfarctsofstroke-pronespontaneouslyhypertensiverats.Theseresultssuggestthatmatrixmetalloproteinase-9upregulationisassociatedwithincreasedregionalangiogenesisanddegradationofcollagenIV,themajorcomponentofthebasallamina,instroke-pronespontaneouslyhypertensiveratswithhigh-sodiumwater-inducedfocalcerebralinfarction.