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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.

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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.

简介：Thebrainasasystemwithgraduallydecreasingresourcesmaximizesitschancesbyreorganizingneuralnetworkstoensureefficientperformance.Auditoryevent-relatedpotentialswererecordedin28healthyvolunteerscomprising14youngand14elderlysubjectsinauditorydiscriminationmotortask(lowfrequencytone-righthandmovementandhighfrequencytone-lefthandmovement).Theamplitudesofthesensoryevent-relatedpotentialcomponents(N1,P2)weremorepronouncedwithincreasingageforeithertoneandthiseffectforP2amplitudewasmorepronouncedinthefrontalregion.ThelatencyrelationshipofN1betweenthegroupswastone-dependent,whilethatofP2wastone-independentwithaprominentdelayintheelderlygroupoverallbrainregions.Theamplitudesofthecognitivecomponents(N2,P3)diminishedwithincreasingageandthehemisphericasymmetryofN2(butnotforP3)reducedwithincreasingage.ProlongedN2latencywithincreasingagewaswidespreadforeithertonewhilebetween-groupdifferenceinP3latencywastone-dependent.HighfrequencytonestimulationandmovementrequirementsleadtoP3delayintheelderlygroup.Theamplitudedifferenceofthesensorycomponentsbetweentheagegroupscouldbeduetoageneralgreateralertness,lessexpressedhabituation,ordeclineintheabilitytoretreatattentionalresourcesfromthestimuliintheelderlygroup.Withaging,aneuralcircuitreorganizationofthebrainactivityaffectsthecognitiveprocesses.Theapproachusedinthisstudyisusefulforanearlydiscriminationbetweennormalandpathologicalbrainagingforearlytreatmentofcognitivealterationsanddementia.

简介：TelomeraseisanenzymethatmaintainstelomeresindividingcellsusingatemplateonitsinherentRNAcomponent.Additionally,theproteinpartTERT(TelomeraseReverseTranscriptase)hasvariousnon-canonicalfunctions.Forexample,itcanlocalizetomitochondriaunderincreasedstressandprotectcellsinvitrofromoxidativestress,DNAdamageandapoptosis.RecentlyithasbeendemonstratedthatTERTproteinpersistsinadultneuronsinthebrainanddataemergesuggestingthatitmighthaveaprotectivefunctioninthesepost-mitoticcellsaswell.WehaverecentlypublishedthatTERTproteinaccumulatedinmitochondriafrombraintissueofmicethathaveundergoneshort-termdietaryrestriction(DR)andrapamycintreatment.Thislocalizationcorrelatedtolowerlevelsofoxidativestressinthesebrainmitochondria.SincerapamycintreatmentdecreasesmTORsignalingwhichisalsothoughttoplayanimportantroleforthebeneficialeffectsofDR,weconcludethatthemTORpathwaymightbeinvolvedintheTERTlocalizationanditseffectsinbrainmitochondriainvivo.ThesedataareinlinewithpreviousfindingsfromourgroupaboutincreasedmitochondriallocalizationofTERTinAlzheimer'sdisease(AD)brainsandaprotectivefunctionofTERTproteininneuronsinvitroagainstpathologicaltau.

简介：OnDecember18,AnnualConferenceofCCOIC,sponsoredbyCCPITwassuccessfullyheldinBeijing.Thethemeofthisconferencewas'todrivetheglobalizationoftheenterprises&improvetheirinternationalcompetitiveness'.About600peopleincludinghigh-levelgovernmentofficials,famouseconomistsandexpertsaswellasentrepreneursattendedtheannualconference.Businesswisdomsparkedtheconference.Andthefollowingissomeinspiringandsplendidthoughtfromthoseintelligent.

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简介：Differentmodalitiesinbiomedicalimages,likeCT,MRIandPETscanners,providedetailedcross-sectionalviewsofhumananatomy.Thispaperintroducesthree-dimensionalbrainreconstructionbasedonCTslices.Itcontainsfiltering,fuzzysegmentation,matchingmethodofcontours,cellarraystructureandimageanimation.Experimentalresultshaveshownitsvalidity.TheinnovationismatchingmethodofcontoursandfuzzysegmentationalgorithmofCTslices.

简介：Thebrainishighlyplasticafterstrokeorepilepsy;however,thereisapaucityofbrainplasticityinvestigationaftertraumaticbraininjury(TBI).ThisminireviewsummarizesthemostrecentevidenceofbrainplasticityinhumanTBIpatientsfromtheperspectiveofadvancedmagneticresonanceimaging.Similartootherformsofacquiredbraininjury,TBIpatientsalsodemonstratedbothstructuralreorganizationaswellasfunctionalcompensationbytherecruitmentofotherbrainregions.However,thelargescalebrainnetworkalterationsafterTBIarestillunknown,andthefieldisstillshortofpropermeansonhowtoguidethechoiceofTBIrehabilitationortreatmentplantopromotebrainplasticity.Theauthorsalsopointoutthenewdirectionofbrainplasticityinvestigation.

简介：Objective:ToobservetheeffectsofgangliosideGM1onreductionofbrainedemaandameliorationofcerebralmetabolismaftertraumaticbraininjury(TBI).Methods:AnacuteexperimentalclosedTBImodelinratswasinducedbyafluid-percussionbraininjurymodel.AtfiveandsixtyminutesafterTBI,theanimalswereintraperitoneallyinjectedbygangliosideGM1(30mg/kg)orthesamevolumeofsaline.Atthe6thhourafterTBI,effectsofgangliosideGM1orsalineonchangesofmeanarterialpressure(MAP),contentsofwater,lacticacid(LA)andlipipperoxidation(LPO)intheinjuredcerebraltissueswereobserved.Results:AfterTBI,MAPdecreasedandcontentsofwater,LAandLPOincreasedinbraininjurygroup;however,MAPwasbacktonormallevelsandcontentsofwater,LAandLPOdecreasedingangliosideGM1treatedgroup,comparedwiththoseinbraininjurygroup(P<0.05).Nosignificantdifferencebetweenthesalinetreatedgroupandthebraininjurygroup(P>0.05)wasobserved.Conclusions:GangliosideGM1doeshaveobviousneuroprotectiveeffectonearlyTBI.