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简介:Three-RiverProjectProceedsSmoothly¥//SOINAMDAGYIThecentraldrainagesectionoftheYarlungZangboRiveranditstwotributaries,theNyang...
简介:Traumaticbraininjury(TBI)istheleadingcauseofdeathanddisabilityofpersonsunder45yearsoldintheUnitedStates,affectingover1.5millionindividualseachyear.Ithadbeenthoughtthatrecoveryfromsuchinjuriesisseverelylimitedduetotheinabilityoftheadultbraintoreplacedamagedneurons.However,recentstudiesindicatethatthematuremammaliancentralnervoussystem(CNS)hasthepotentialtoreplenishdamagedneuronsbyproliferationandneuronaldifferentiationofadultneuralstem/progenitorcellsresidingintheneurogenicregionsinthebrain.Furthermore,increasingevidenceindicatesthattheseendogenousstem/progenitorcellsmayplayregenerativeandreparativerolesinresponsetoCNSinjuriesordiseases.Insupportofthisnotion,heightenedlevelsofcellproliferationandneurogenesishavebeenobservedinresponsetobraintraumaorinsultssuggestingthatthebrainhastheinherentpotentialtorestorepopulationsofdamagedordestroyedneurons.Thisreviewwilldiscussthepotentialfunctionsofadultneurogenesisandrecentdevelopmentofstrategiesaimingatharnessingthisneurogeniccapacityinordertorepopulateandrepairtheinjuredbrain.
简介:Objective:Tostudythecorrelationbetweenbrainedema,elevatedintracranialpressure(ICP)andcellapoptosisintraumaticbraininjury(TBI).Methods:Inthisstudy,totally42rabbitsin7groupswerestudied.Sixoftheanimalswereidentifiedasacontrolgroup,andtheremaining36animalswereequallydividedinto6TBIgroups.TBImodelswereproducedbythemodifiedmethodofFeeney.Aftertheimpact,ICPofeachsubjectwasrecordedcontinuouslybyanICPmonitoruntiltheanimalwassacrificedatscheduledtime.Theapoptoticbraincellsweredetectedbyanterminaldeoxynucleotide-transferase-mediateddUTP-digoxigeninnickendlabeling(TUNEL)assay.Cerebralwatercontent(CWC)wasmeasuredwithadryingmethodandcalculatedaccordingtotheElliottformula.Then,ananalysiswasconductedtodeterminethecorrelationbetweenthecountofapoptoticcellsandtheclinicalpathologicalchangesofthebrain.Results:Apoptoticcellcountbegantoincrease2haftertheimpact,andreacheditsmaximumabout3daysaftertheimpact.ThepeakvalueofCWCandICPappeared1dayand3daysaftertheimpact,respectively.ApoptoticcellcounthadapositivecorrelationwithCWCandICP.Conclusions:InTBI,occurrenceofbrainedemaandICPincreasemightleadtoapoptosisofbraincells.Anytherapywhichcanrelievebrainedemaand/ordecreaseICPwouldbeabletoreduceneuronapoptosis,therebytoattenuatethesecondarybraindamage.
简介:Objective:Tostudytheeffectsofmagnesiumsulfateonbrainmitochondrialrespiratoryfunctioninratsafterexperimentaltraumaticbraininjuryandthepossiblemechanism.Methods:ThemiddledegreebraininjuryinratswasmadebyBIM-IIImulti-functionimpactingmachine.Thebrainmitochondrialrespiratoryfunctionwasmeasuredwithoxygenelectrodeandtheultra-structuralchangeswereobservedwithtransmissionelectronmicroscope(TEM).Results:1.ThebrainmitochondrialrespiratorystageIIIandrespirationcontrolratereducedsignificantlyintheuntreatedgroupswithin24and72hours.ButtreatedGroupAshowedcertaindegreeofrecoveryofrespiratoryfunction;treatedGroupBshowedfurtherimprovement.2.UntreatedGroup,treatedGroupsAandBhaddifferentdegreesofmitochondrialultra-structuraldamagerespectively,whichcouldbeattenuatedafterthetreatmentwithmagnesiumsulfate.Conclusions:Themitochondrialrespiratoryfunctiondecreasessignificantlyaftertraumaticbraininjury.ButitcanbeapparentlyimprovedaftermagnesiumsulfatemanagementalongwiththeattenuateddamageofmitochondriadiscoveredbyTEM.Thelongercourseoftreatmentcanobtainabetterimprovementofmitochondrialrespiratoryfunction.
简介:Objective:Tostudytheeffectofmildhypothermiaonglucosemetabolismandglycerolofbraintissueinpatientswithseveretraumaticbraininjury(STBI)usingclinicalmicrodialysis.Methods:Thirty-onepatientswithSTBI(GCS≤8)wererandomlydividedintohypothermicgroup(GroupA)andcontrolgroup(GroupB).Microdialysiscatheterswereinsertedintothecerebralcortexofperilesionalandnormalbraintissue.AllsampleswereanalyzedusingCMAmicrodialysisanalyzer.Results:Incomparisonwiththecontrolgroup,lactate/glucoseratio(L/G),lactate/pyruvateratio(L/P)andglycerol(Gly)inperilensionaltissueweresignificantlydecreased;L/Pinnormalbraintissuewassignificantlydecreased.Incontrolgroup,L/G,L/PandGlyinperilensionaltissuewerehigherthanthatinnormalbraintissue.Inthehypothermicgroup.L/Pinperilensionaltissuewashigherthanthatinrelativenormalbrain.Conclusions:MildhypothermiaprotectsbraintissuesbydecreasingL/G,L/PandGlyinperilensionaltissueandL/Pin'normalbrain'tissues.Theenergycrisisandmembranephospholipiddegradationinperilensionaitissueareeasiertohappenaftertraumaticbraininjury,andmildhypothermiaprotectsbrainbetterinperilensionaltissuethaninnormalbraintissue.