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8 个结果
  • 简介:BACKGROUND:Previousstudiesreportedthatfrontal-temporal-parietal-occipitalpathologicalchangesanddiseasedrangeintherightcerbralhemispherewerecorrelatedwithneglect.Butstudiesonthecorrelationofneglectwithdiseasedregionandareainpatientswhosufferfrominitialattackofsinglefocusofcerebralinfarction(CI)inleftandrightcerebralhemispheresarefew.OBJECTIVE:ToobservethestatusofneglectinpatientswhosufferfromsinglefocusofCIincerebralhemisphereandanalyzethecorrelationofneglectwithdiseasedregionandareaofCI.DESIGN:CaseanalysisSETTING:TreatmentCenterforCardiocerebrovascularDisease,SecondHospitalofXiamencity;DepartmentofNeurology,FirstHospitalAffiliatedtoBaotouMedicalCollege.PARTICIPANTS:AlltheCIpatientshospitalizedintheDepartmentofNeurology.FirstHospitalAffiliatedtoBaotouMedicalCollegefromJune1998toMay2001wereretrieved.Inclusivecriteria:①PatientswhosufferedfrominitialattackofCI.whichwasconfirmedbyskullCTorMRIwithin24hoursafteronsetandpresentedsinglefocusincerebralhemisphere.②beconsciousandcouldcooperateintheexamination.③didnotreceiveformaleducation,butcoulddoaccountsandsomesimplewritingandreading.④Patientswithhomonymoushemianopiawereexcludedthroughtheexaminationofperimeter.⑤Informedconsentswereobtainedfromallthepatients.Among67patientswhomettheinclusivecriteria.33sufferedfromCIintheleftcerebralhemisphereand34intherightcerebralhemisphere.METHODS:①PatientsreceivedneglectsupplementexaminationandChineseaphasiaexaminationwithin2.5to3monthsaftertheattackofCI.Thediagnosticcriteriaofneglectinthetestsoflinecancellation.1inebisectionandcopyingthefigureswereasfollows:InthelinecancellationtestbasedonthemethodofAlbert.patientswhocouldnotcanceloneormorelineswereregardedasabnormal.InthelinebisectiontestbasedonthemethodofPeter.patientswholeftdeviated1.16%

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  • 简介:Thehippocampalregionofthebrainisimportantforencodingenvironmentinputsandmemoryformation.However,theunderlyingmechanismsareunclear.ToinvestigatethebehaviorofindividualneuronsinresponsetosomatosensoryinputsinthehippocampalCA1region,werecordedandanalyzedchangesinlocalfieldpotentialsandthefiringratesofindividualpyramidalcellsandinterneuronsduringtailclampinginurethane-anesthetizedrats.Wealsoexploredthemechanismsunderlyingtheneuronalresponses.Somatosensorystimulation,intheformoftailclamping,changedlocalfieldpotentialsintothetarhythm-dominatedwaveforms,decreasedthespikefiringofpyramidalcells,andincreasedinterneuronfiring.Inaddition,somatosensorystimulationattenuatedorthodromic-evokedpopulationspikes.TheseresultssuggestthatsomatosensorystimulationsuppressestheexcitabilityofpyramidalcellsinthehippocampalCA1region.Increasedinhibitionbylocalinterneuronsmightunderliethiseffect.Thesefindingsprovideinsightintothemechanismsofsignalprocessinginthehippocampusandsuggestthatsensorystimulationmighthavetherapeuticpotentialforbraindisordersassociatedwithneuronalhyperexcitability.

  • 标签: 海马CA1区 锥体细胞 兴奋性 大鼠 神经元 脑部疾病
  • 简介:BACKGROUND:Matrixmetalloproteinase-9(MMP-9)expressionincreaseswithintracerebralhemorrhage,andparticipatesinthepathophysiologicalprocessesofsecondarybraininjuryafterintracerebralhemorrhage.OBJECTIVE:ToinvestigatetheeffectsofmildhypothermiaonMMP-9expressionandbrainedemaintheperihematomalregionofexperimentalintracerebralhemorrhagerats.DESIGN,TIMEANDSETTING:Therandomized,controlledexperimentwasperformedattheCentralLaboratoryofShandongProvincialHospitalbetweenMayandSeptember2007.MATERIALS:Seventy-two,Wistar,malerats,12-weeksold,wereusedforthisstudy.Rabbitanti-MMP-9primaryantibodywaspurchasedfromBoster,China.METHODS:Wistarratswereequallyandrandomlydividedintonormothermiaandmildhypothermiagroups.Thetwogroupseachcomprisedcontrol,6-hourintracerebralhemorrhage,24-hourintracerebralhemorrhage,48-hourintracerebralhemorrhage,72-hourintracerebralhemorrhage,and1-weekintracerebralhemorrhagesubgroups,withsixratsineachsubgroup.Ratmodelsofintracerebralhemorrhagewereestablishedbyinjecting100μLofautologousbloodintotheratcaudatenucleus.Ratsinthemildhypothermiagroupreceivedfourhoursoflocalmildhypothermiaimmediatelyfollowingtheinjection.Intracerebraltemperaturewasmaintainedat(33±0.5)℃.Subsequently,intracerebraltemperaturewasspontaneouslyrecoveredat25℃.Ratsinthecontrolsubgroupwerenotinjectedwithautologousbloodandreceivedonlywithintracerebralhemorrhage.MAINOUTCOMEMEASURES:BrainwatercontentandMMP-9expressionsurroundingthehematomaregion.RESULTS:MMP-9expressionincreasedat6hours,andbrainedemareachedapeakat48hoursafterintracerebralhemorrhage.MMP-9expressionwassignificantlydecreasedinthemildhypothermiagroupcomparedwiththenormothermiagroupateachtimepoint(P<0.05).CONCLUSION:MildhypothermiacansignificantlyinhibitMMP-9overexpressionandrelievebrainedemafollowingintracerebralhemo

  • 标签: 大脑内出血 降低体温作用 MMP-9表达 脑损伤
  • 简介:BACKGROUND:Previousstudieshaveshownthatthemitochondrialstructureandfunctionaredamagedinanimalmodelsofepilepsy.Inaddition,theBcl-2proteiniscapableofregulatingmitochondrialstability.OBJECTIVE:ToobserveandvalidatechangesinmitochondrialstructureandBcl-2expression,andtoanalyzethesecharacteristicsinthehippocampalCA3regionofratmodelsofepilepsy.DESIGN,TIMEANDSETTING:Thisrandomized,controlled,animalexperimentwasperformedattheLaboratoryofElectronMicroscopyandDepartmentofHistologyandEmbryology,LuzhouMedicalCollegebetween2007and2008.MATERIALS:CoriamyrtinwasprovidedbythePharmacyFactoryofWestChinaUniversityofMedicalSciences.TheprimaryandsecondaryantibodieswereprovidedbyZhongshanGoldenbridgeBiotechnology,Beijing.METHODS:Atotalof44adult,male,SpragueDawleyratswererandomlydividedintocontrol(n=11)andepilepsy(n=33)groups.Ratsintheepilepsygroupwereinducedbycoriamyrtin(50μg/kg),whichwasinjectedintothelateralventricles.Theratswerethenobservedat3,6,and24hoursafterepilepsyinduction,with11ratsateachtimepoint.Epilepsywasnotinducedinratsfromthecontrolgroup.MAINOUTCOMEMEASURES:PathologicalchangesinthehippocampalCA3regionwereobservedbylightmicroscopy;Bcl-2expressionwasanalyzedbyimmunohistochemistry;andmitochondrialchangesinthehippocampuswereobservedundertransmissionelectronmicroscopy.RESULTS:(1)ThecontrolgroupdisplayedverylittleBcl-2proteinexpressioninthehippocampalCA3region.However,after3hoursofepilepsy,expressionwasvisible.By6hours,expressionpeakedandthensubsequentlydecreasedafter24hours,butremainedhigherthanthecontrolgroup(P<0.05).(2)Mitochondriaweredamagedtovaryingdegreesintheepilepsygroups.Forexample,mitochondriaedema,cristaespaceincrease,anddisappearanceofmitochondriawereapparent.Moreover,mitochondrialdamageoccurredpriortopathologicalchangesintheneuronsandnucleolus.CONCLUSION:

  • 标签: 海马CA3区 线粒体损伤 急性癫痫 大鼠模型 Bcl 透射电子显微镜
  • 简介:BACKGROUND:Animalexperimentshaveconfirmedthatbonemarrowstromalcell(BMSC)transplantationcanserveasatreatmentforepilepsy.OBJECTIVE:BMSCsderivedfromgreenfluorescentprotein(GFP)miceweretransplantedintothehippocampalCA1regionofepilepticrats.Theaimofthestudywastorecordelectroencephalogram(EEG),analyzesurvivalandmigrationofBMSCs,andvalidatetheeffectofBMSCtransplantationforthetreatmentofepilepsy.DESIGN,TIMEANDSETTING:ArandomizedblockdesignexperimentwasperformedattheInstituteofNeuroscience,KunmingMedicalCollegefromMarch2005toFebruary2006.MATERIALS:HomozygousC57BL/6CrSlcTgN(acr-EGFP)OsbC14-Y01-FM131mice,8-12weeksofage,wereselectedforpreparationofcellsuspension.SpragueDawleyratswereselectedforestablishingepilepsymodels.METHODS:Ratswererandomlydividedinto4groups:control(n=8),model(n=8),normalsaline(n=24),andBMSC(n=24).Inthemodel,normalsaline,andBMSCgroups,epilepsywasestablishedwithpenicillin(3×107U/kgi.p.×7days).RatsintheBMSCgroupreceivedaBMSCsuspensionderivedfromgreenfluorescentproteinmiceintotherighthippocampalCA1region.RatsinthevehiclecontrolgroupwereinjectedwiththesamevolumeofnormalsalineintothehippocampalCA1region.MAINOUTCOMEMEASURES:Theelectroencephalogramwasusedtomonitorbrainactivity.SurvivalandmigrationofthetransplantedBMSCswasobservedusingfluorescencemicroscopyat1,2,and4weeksaftertransplantation.RESULTS:InBMSCgroup,fluorescentcellswereobservedatthetransplantationsiteandintheadjacenttissue,aswellasinthetissuesurroundingtheneedletract,indicatingthemigrationofimplantedcells.Fluorescentcellswerenotdetectedinthevehiclecontrolgroup.Theelectroencephalogramofthecontrolanimalsexhibited7-9Hzαwaves,withawaveamplitude<50μV.Inthemodelandvehiclecontrolgroups,randomspike-and-wavedischargesofthesharpspike-sharplowwavetyp

  • 标签: 骨髓间质细胞 脑电图 癫痫 荧光蛋白 移植手术
  • 简介:OurpreliminarystudiesconfirmedthatanactiveprincipleregionofBuyangHuanwudecoction,comprisingalkaloid,polysaccharide,aglycon,glucosideandvolatileoil,caninducebonemarrowmesenchymalstemcelldifferentiationintoneurons.Mitogen-activatedproteinkinasesignalingwasidentifiedasoneofthekeypathwaysunderlyingthisdifferentiationprocess.Thepresentstudyshowsphosphorylatedextracellularsignal-regulatedproteinkinaseandphosphorylatedp38proteinexpressionwasincreasedafterdifferentiation.Cellularsignalingpathwayblockingagents,PD98059andSB203580,inhibitedextracellularsignal-regulatedproteinkinaseandp38inmitogen-activatedproteinkinasesignalingpathwaysrespectively.mRNAandproteinexpressionoftheneuronalmarker,neuronspecificenolase,andneuralstemcellmarker,nestin,weredecreasedinbonemarrowmesenchymalstemcellsaftertreatmentwiththeactiveprincipleregionofBuyangHuanwudecoction.Experimentalfindingsindicatethat,extracellularsignal-regulatedproteinkinaseandp38inmitogen-activatedproteinkinasesignalingpathwaysparticipateinbonemarrowmesenchymalstemcelldifferentiationintoneuron-likecells,inducedbytheactiveprincipleregionofBuyangHuanwudecoction.

  • 标签: P38丝裂原活化蛋白激酶 补阳还五汤 细胞分化 信号通路 骨髓基质 神经元特异性烯醇化酶
  • 简介:Thepresentstudywasdesignedtodeterminemicrotubule-associatedprotein-2andsynaptophysinexpressioninthehippocampalCA3regioninaratmodelofmiddlecerebralarteryocclusion.TheratsweretreatedwithacupunctureatBaihui(GV20),Qubin(GB7),andQianding(GV21)points,inadditiontoexercisetraining.Resultswerecomparedwithratsundergoingexercisetrainingonly.TheY-mazemethodandimmunohistochemistryrevealeddecreasederrorfrequencyofpassingthroughY-maze,aswellassignificantlyincreasedmicrotubule-associatedprotein-2andsynaptophysinexpression,intheacupuncturewithexercisetraininggroupcomparedwiththemodelandexercisetraininggroupsafter5weeks.Microtubule-associatedprotein-2andsynaptophysinexpressionsnegativelycorrelatedwitherrorfrequencyofpassingthroughtheY-maze.Theseresultssuggestedthatacupuncturecombinedwithexercisetrainingimprovedlearningandmemoryfunctionsinaratmodelofcerebralinfarction.ThemechanismsofactionwerehypothesizedtobeassociatedwithdendriticorsynapticplasticityintheipsilateralhippocampalCA3region.

  • 标签: 微管相关蛋白 海马CA3区 运动训练 大鼠模型 记忆功能 突触素
  • 简介:BACKGROUND:Intracerebralhemorrhage(ICH)andcoronaryheartdisease(CHD)havethesamepathologicalbase,atherosclerosis,andthesimilarriskfactors,suchassmoking,drinking,hypertension,hyperlipemia,diabetesmellitus,etc;butthedistributionsoftwodiseasesareverydifferentinthepopulations.Thismayberelatedtotheexposureofriskfactorsanddifferenteffectsofriskfactorsontwodiseases.OBJECTIVE:ToanalyzethedistributiondifferenceofriskfactorsforICHandCHDinthepopulationsofTongliaocityofNeiMonggolAutonomousRegion.DESIGN:Retrospectiveanalysis.SETTING:SchoolofRadiationMedicineandPublicHealth,SoochowUniversity;TongliaoHospital,NeiMonggolAutonomousRegion.PARTICIPANTS:Randomsamplingwasusedtoselect6hospitalsfrom10hospitalsaffiliatedtoTongliaoCityofNeiMonggolAutonomousRegion.Totally1672medicalrecordsofpatientswithICHand2195medicalrecordsofpatientswithCHDadmittedtoDepartmentofNeurologyandDepartmentofCardiovascularInternalMedicineofabove-mentioned6hospitalsbetweenJanuary2003andDecember2005werecollectedaccordingtotheinvestigationneed.METHODS:Thesubjects,whosemedicalrecordswereinvolved,wereperformedretrospectiveanalysiswithpre-preparedquestionnaire'StrokeandCoronaryHeartDiseaseEpidemiologicQuestionnaire'.Themaincontentsincluded:①Socialdemographycondition:Thedistributionsofgender,age,nationality,etc.②Previoushistoryofdisease:hypertension,diabetesmellitus,etc.③Relatedriskfactors:systolicbloodpressure,diastolicbloodpressure,totalcholesterol,triglyceride,high-densitylipoproteincholesterol,low-densitylipoproteincholesterol,smoking,drinkingandglucose(GLU).ThedatabaseofEpidatawastransformedtoSPSSdatabase.Single-andmultiple-factornon-conditionalLogisticregressionanalysiswereperformedonthedata,andORvalueand95%CIwerecalculated.Thedistributiondifferencesofriskfactorsfortwodiseaseswerecompared

  • 标签: 脑出血 冠心病 风险因素 病理基础