简介：Gastrodin,anactivecomponentoftallgastrodiatuber,iswidelyusedinthetreatmentofdizziness,paralysis,epilepsy,strokeanddementia,andexhibitsaneuroprotectiveeffect.AratmodelofspinalcordinjurywasestablishedusingAllen’smethod,andgastrodinwasadministeredviathesubarachnoidcavityandbyintraperitonealinjectionfor7days.Resultsshowthatgastrodinpromotedthesecretionofbrain-derivedneurotrophicfactorinratswithspinalcordinjury.Aftergastrodintreatment,themaximumangleoftheinclinedplanetest,andtheBasso,BeattieandBresnahanscoresincreased.Moreover,gastrodinimprovedneuraltissuerecoveryintheinjuredspinalcord.Theseresultsdemonstratethatgastrodinpromotesthesecretionofbrain-derivedneurotrophicfactor,contributestotherecoveryofneurologicalfunction,andprotectsneuralcellsagainstinjury.

简介：Theliteratureshowsthatimprovementsincognitiveperformancemaybeobservedfollowinganacuteboutofexercise.However,evidenceinsupportofthebiologicalmechanismsofthiseffectisstilllimited.Findingsfrombothrodentandhumanstudiessuggestbrain-derivedneurotrophicfactor(BDNF)asapotentialmechanismoftheeffectofacuteexerciseonmemory.ThemolecularpropertiesofBDNFallowthisproteintobeassessedintheperiphery(pBDNF)(i.e.,bloodserum,bloodplasma),makingmeasurementsofacuteexercise-inducedchangesinBDNFconcentrationrelativelyaccessible.StudiesexploringtheacuteexerciseepBDNFecognitiveperformancerelationshiphavehadmixedfindings,butthismaybemorereflectiveofmethodologicaldifferencesbetweenstudiesthanitisastatementabouttheroleofBDNF.Forexample,significantassociationshavebeenobservedbetweenacuteexercise-inducedchangesinpBDNFconcentrationandcognitiveperformanceinstudiesassessingmemory,andnon-significantassociationshavebeenfoundinstudiesassessingnon-memorycognitivedomains.ThreesuggestionsaremadeforfutureresearchaimedatunderstandingtheroleofBDNFasabiologicalmechanismofthisrelationship:1)Assessmentsofcognitiveperformancemaybenefitfromafocusonvarioustypesofmemory(e.g.,relational,spatial,long-term);2)MorefinegrainedmeasurementsofpBDNFwillallowfortheassessmentofconcentrationsofspecificisoformsoftheBDNFprotein(i.e.,immature,mature);3)StatisticaltechniquesdesignedtotestthemediatingroleofpBDNFintheacuteexercise-cognitiveperformancerelationshipshouldbeutilizedinordertomakecausalinferences.

简介：BACKGROUND:Studieshavedemonstratedthatbrain-derivedneurotrophicfactor(BDNF)hasadualeffectonepilepsy.However,therelationshipbetweenepilepsy-inducedbraininjuryandBDNFremainspoorlyunderstood.OBJECTIVE:Accordingtoultrastructuralandmolecularparameters,todetectthedegreeofneuronalinjuryandBDNFexpressionchangesatdifferentbrainregionsanddifferentkindlingtimestodeterminetheeffectsofBDNFonepilepsy-inducedbraininjury.DESIGN,TIMEANDSETTING:Arandomized,controlled,animalexperimentbasedonneuropathologyandmolecularbiologywasperformedattheDepartmentofPhysiologyandDepartmentofPathology,BasicMedicalCollegeofJilinUniversityin2003.MATERIALS:UltraSensitiveSPkitforimmunohistochemistry(FuzhouMaximBiotechnology,China),BDNFantibody(concentratedtype,WuhanBosterBiologicalTechnology,China),JEM-1000SXtransmissionelectronmicroscopy(JEOL,Japan),andBH-2lightmicroscope(Olympus,Japan)wereusedinthepresentstudy.METHODS:Wistarratswererandomlyassignedtocontrol(n=6),sham-surgery(n=6),andmodel(n=60)groups.Thecontrolgroupratswerenottreated;anelectrodewasembeddedintotheamygdalainratsfromthesham-surgeryandmodelgroups;anamygdalakindlingepilepsymodelwasestablishedinthemodelgroup.MAINOUTCOMEMEASURES:Pathologicalchangesinthetemporallobeandhippocampuswereobservedbylightandelectronmicroscopyat1,3,7,14,and21daysfollowingkindling,andBDNFexpressioninthevariousbrainregionswasdeterminedbyimmunohistochemistry.RESULTS:Inthemodelgroup,temporallobecorticalandhippocampalneuronswereswollenandthenucleiwerelaterallydeviated.Therewerealsosomeapoptoticneurons3daysafterkindling.Thenucleolidisappearedandthenucleiappearedbrokenorlysed,aswellasslightmicrogliahyperplasia,at7days.Electronmicroscopicobservationdisplayedchromatinaggregationinthenucleiandslightmitochondrionswelling3daysafterkindling.Injurychangeswereaggravatedat7days,characteriz

简介：无

简介：

简介：BACKGROUND:Ithasbeenshownthatginsenoside,theeffectivecomponentofginseng,canenhanceexpressionofcholineacetyltransferase,aswellasbrain-derivedneurotrophicfactor(BDNF)anditsreceptortyrosinekinaseB(TrkB),incholinergicneuronsofthebasalforebrain.OBJECTIVE:ToqualitativelyandquantitativelyverifytheinfluenceofginsenosideonexpressionofBDNFanditsreceptor,TrkB,inthemedialseptumofagedrats,andtoprovideamolecularbasisforclinicalapplication.DESIGN,TIMEANDSETTING:Acontraststudy,whichwasperformedintheDepartmentofAnatomy,ChinaMedicalUniversity,andtheDepartmentofAnatomy,ShenyangMedicalCollegebetweenDecember2005andMay2007.MATERIALS:Thirty-five,healthy,female,SpragueDawleyratswereselectedforthisstudy.Ginsenoside(81%purity)wasprovidedbyJilinJi’anWantaiChineseMedicineFactory;anti-BDNFantibody,anti-TrkBantibody,andtheirkitswereprovidedbyWuhanBosterCompany.METHODS:Atotalof35ratsweredividedintothreegroups:young(fourmonthsold),aging(26monthsold),andginsenoside.Ratsintheginsenosidegroupwereadministeredginsenoside(25mg/kg/d)between17monthsand26months.MAINOUTCOMEMEASURES:ImmunohistochemistryandinsituhybridizationwereusedtomeasureexpressionofBDNFandTrkBinthemedialseptumofagedrats,andthedetectedresultswereexpressedasgrayvalues.RESULTS:①Qualitativedetection:usingmicroscopy,degenerativeneuronswerevisibleinthemedialseptumintheaginggroup.However,neuronalmorphologyintheginsenosidegroupwassimilartoneuronsintheyounggroup.②Quantitativedetection:themeangrayvalueofBDNF-positiveandTrkB-positiveproductsintheaginggroupweresignificantlyhigherthanintheyounggroup(t=3.346,4.169,P<0.01);however,themeangrayvalueintheginsenosidegroupwassignificantlylowerthanintheaginggroup(t=2.432,2.651,P<0.01).CONCLUSION:GinsenosidecanincreaseexpressionofBDNFandTrkBinth

简介：Thedevelopmentandplasticityofcentralauditorysystemcanbeinfluencedbythechangeofperipheralneuronalactivity.However,themolecularmechanismparticipatingintheprocessremainselusive.Brain-derivedneurotrophicfactor(BDNF)bindingwithitsfunctionalreceptortropomyosinreceptorkinaseB(TrkB)hasmultipleeffectsonneurons.Hereweusedaratmodelofauditorydeprivationbybilateralcochlearablation,toinvestigatethechangesinexpressionofBDNFandTrkBintheauditorycortexafterauditorydeprivationthatoccurredduringthecriticalperiodforthedevelopmentofcentralauditorysystem.Reversetranscription-quantitativepolymerasechainreaction(RTqPCR)andimmunohistochemistrymethodswereadoptedtodetectthemRNAandproteinexpressionlevelsofBDNFandTrkBintheauditorycortexat2,4,6and8weeksaftersurgery,respectively.ThechangeintheexpressionofBDNFandTrkBmRNAsandproteinsfollowedsimilartrend.Inthebilateralcochlearablationgroups,theBDNF-TrkBexpressionlevelinitiallydecreasedat2weeksbutincreasedat4weeksfollowedbythereductionat6and8weeksaftercochlearremoval,ascomparedtotheage-matchedshamcontrolgroups.Inconclusion,theBDNF-TrkBsignalingisinvolvedintheplasticityofauditorycortexinanactivity-dependentmanner.

简介：Objective:Toexaminetheeffectsofratmarrowstromalcells(rMSCs)ongeneexpressionoflocalbrain-derivedneurotrophicfactor(BDNF)andnervegrowthfactor(NGF)afterinjectionofrMSCsintoCisternMagnumofadultratssubjectedtotraumaticbraininjury(TBI).Results:GroupcelltransplantationhadhigherBDNFandNGFgeneexpressionsthanGroupsalinecontrolduringaperiodoflessthan3weeks(P<0.05).Conclusions:rMSCstransplantationviaCisternMagnuminratssubjectedtotraumaticbraininjurycanenhanceexpressionsoflocalbrainNGFandBDNFtoacertainextent.

简介：BACKGROUND:Ithasbeendemonstratedthattransforminggrowthfactor-β(TGF-β)andbrain-derivedneurotrophicfactor(BDNF)caninducestemcelldifferentiationintoneuron-likecells.OBJECTIVE:ToinvestigatetheefficacyofTGF-βandBDNFatinducingthedifferentiationofadultratbonemarrowstromalcells(BMSCs)intoneuron-likecells,bothincombinationoralone.DESIGN,TIMEANDSETTING:AcomparativeobservationexperimentwasperformedattheDepartmentofOrthopedics,FirstAffiliatedHospitalofLiaoningMedicalUniversitybetweenOctober2007andJanuary2008.MATERIALS:TGF-βandBDNFwerepurchasedfromSigma,USA;mouseanti-ratneuronspecificenolase,neurofilamentandglialfibrillaryacidicproteinwerepurchasedfromBeijingHMHLBiochemLtd.,China.METHODS:BMSCswereisolatedfromratsaged4weeksandincubatedwithTGF-β(1μg/L)and/orBDNF(50μg/mL).MAINOUTCOMEMEASURES:Expressionofneuron-specificenolase,neurofilamentandglialfibrillaryacidicproteinweredeterminedbyimmunocytochemistry.RESULTS:BMSCsdifferentiatedintoneuron-likecellsfollowinginductionofTGF-βandBDNF,andexpressedbothneuron-specificenolaseandneurofilament.ThepercentofpositivecellswassignificantlygreaterinthecombinationgroupthanthoseinducedwithTGF-βorBDNFalone(P<0.01).CONCLUSION:TreatmentofBMSCswithacombinationofTGF-βandBDNFinduceddifferentiationintoneuron-likecells,withtheinductionbeingsignificantlygreaterthanwithTGF-βorBDNFalone.

简介：无

简介：摘要BackgroundDelayed encephalopathy (DE) is the most severe complication after acute carbon monoxide (CO) poisoning, which seriously affects the outcome of patients and leads to a high disability rate. Prior studies have shown that hyperbaric oxygen (HBO2) therapy is therapeutic for DE due to reducing immune-mediated neuropathology and thus improving cognitive performance.MethodsIn our present perspective study, five DE patients were treated regularly with HBO2 therapy. The mini-mental state examination (MMSE) and Barthel index (BI) were intermittently collected during their hospitalization for mental and physical status evaluation, the peripheral bloods were serially sampled to determine the concentration changes of circulating stem cells, as well as corresponding BDNF and neural markers.ResultsMMSE and BI showed series of improvements after multiple HBO2 therapies. The CD34+/CD90+ and CD34+/CD133+ dual positive cells, which were categorized as circulating stem cells, were observed an overall up-regulation since the beginning of the DE onset upon the application of HBO2 therapy. Characteristic neurotrophin BDNF, neural markers such as nestin and synaptophysin (SYP) were also up-regulated after exposure of HBO2. Conclusion The application of HBO2 therapy is of significance in improving the cognition of DE patients, along with mobilized circulating stem cells.ConclusionWe primarily infer that the CD34+/CD90+ and CD34+/CD133+ cells were mobilized by HBO2 exposure and have played a positive role in cognition improvement on DE patients by up-regulation of BDNF, nestin and SYP. The altering amount of circulating stem cells mobilized in peripheral blood could be a potential marker on predicting the outcome of DE.

简介：AbstractBrain metastasis (BM) is the leading cause of mortality in lung cancer patients. The process of BM (from initial primary tumor development, migration and intravasation, dissemination and survival in the bloodstream, extravasation, to colonization and growth to metastases) is a complex process for which few tumor cells complete the entire process. Recent research on BM of lung cancer has recently stressed the essential role of tumor microenvironment (TME) in assisting tumor cells in the completion of each BM step. This review summarizes recent studies regarding the effects of TME on tumor cells in the entire process of BM derived from lung cancer. The identification of vulnerable targets in the TME and their prospects to provide novel therapeutic opportunities are also discussed.

简介：

简介：

简介：

简介：

简介：

简介：

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.