简介：Withtheadventofmoderntechniques,drugs,andmonitoring,generalanesthesiahascometobeconsideredanunlikelycauseofharm,particularlyforhealthypatients.Whilethisislargelytrue,newlyemergingclinicalandlaboratorystudieshavesuggestedthatexposuretoanestheticagentsduringearlychildhoodmayhavelong-lastingadverseeffectsoncognitivefunction.Thisconcernhasbeenthefocusofintensestudyinthefieldof

简介：Inthisstudy,ratswereputintotraumaticbraininjury-inducedcomaandtreatedwithmediannerveelectricalstimulation.Weexploredthewake-promotingeffect,andpossiblemechanisms,ofmediannerveelectricalstimulation.Electricalstimulationupregulatedtheexpressionlevelsoforexin-AanditsreceptorOX1Rintheratprefrontalcortex.Orexin-Aexpressiongraduallyincreasedwithincreasingstimulation,whileOX1Rexpressionreachedapeakat12hoursandthendecreased.Inaddition,aftertheOX1Rantagonist,SB334867,wasinjectedintothebrainofratsaftertraumaticbraininjury,fewerratswererestoredtoconsciousness,andorexin-AandOXIRexpressionintheprefrontalcortexwasdownregulated.Ourfindingsindicatethatmediannerveelectricalstimulationinducedanup-regulationoforexin-AandOX1Rexpressionintheprefrontalcortexoftraumaticbraininjury-inducedcomarats,whichmaybeapotentialmechanisminvolvedinthewake-promotingeffectsofmediannerveelectricalstimulation.

简介：BACKGROUND:Microgliaareverysensitivetoenvironmentalchanges,oftenbecomingactivatedbypathologicalconditions.Activatedmicrogliacanexertadualroleininjuryandrepairinvariousdiseasesofthecentralnervoussystem,includingcerebralischemia,Parkinson’sdisease,andAlzheimer’sdisease.OBJECTIVE:Animmortalmicroglialcellline,BV2,wastreatedwithvaryingconcentrationsoflipopolysaccharide(LPS)toinduceapathologicalsituation.Supernatantwasharvestedandincubatedwithbonemarrowmesenchymalstemcellsand,concomitantly,bonemarrowmesenchymalstemcelldifferentiationwasobserved.DESIGN:Acontrolledobservation,invitroexperiment.SETTING:DepartmentofNeurology,FirstAffiliatedHospitalofChinaMedicalUniversity.MATERIALS:Fivemale2–3-week-oldSpragueDawleyratswerepurchasedfromAnimalLaboratoryCenterofChinaMedicalUniversityandincludedinthisstudy.Theprotocolwasperformedinaccordancewithethicalguidelinesfortheuseandcareofanimals.ThemicroglialcelllineBV2wasproducedbyCellResearchInstituteofChineseAcademyofSciences.LPSwasproducedbySigmaCompany,USA.METHODS:ThisstudywasperformedintheCentralLaboratoryofChinaMedicalUniversityfromSeptember2006toMarch2007.Ratfemoralandtibialbonemarrowwascollectedforseparationandprimarycultureofbonemarrowmesenchymalstemcells.Bonemarrowmesenchymalstemcellculturesweredividedinto5groups:controlgroup,non-activatedgroup,aswellaslow-,medium-,andhigh-doseLPSgroups.Inthecontrolgroup,bonemarrowmesenchymalstemcellswereculturedwithDulbecco’smodifiedEagle’smedium(DMEM)supplementedwithfetalbovineserum(volumefraction0.1).Inthenon-activatedgroup,bonemarrowmesenchymalstemcellswereincubatedwithnon-activatedBV2supernatant.Inthelow-,medium-,andhigh-doseLPSgroups,bonemarrowmesenchymalstemcellswereincubatedwithLPS(0.01,0.1and1μg/L,respectively)-activatedBV2supernatant.MAIN

简介：Alzheimer’sdisease(AD)isthemostcommontypeofdementiainelderlypopulation.WithagrowingagingpopulationnotonlyintheUnitedStatesbutalsointheworldwide,ADconstitutesanemergentpublichealthproblem.Overdecades,theprevailinghypothesiswasthatneurodegenerationmightresultfromoneortwoofthespecificlesions

简介：Freeradicalsinducedbytraumaticbraininjuryhavedeleteriouseffectsonthefunctionandantioxidantvitaminlevelsofseveralorgansystemsincludingthebrain.Melatoninpossessesantioxidanteffectonthebrainbymaintainingantioxidantenzymeandvitaminlevels.Weinvestigatedtheeffectsofmelatoninonantioxidantabilityinthecerebralcortexandbloodoftraumaticbraininjuryrats.Resultsshowedthatthecerebralcortexβ-carotene,vitaminC,vitaminE,reducedglutathione,anderythrocytereducedglutathionelevels,andplasmavitaminClevelweredecreasedbytraumaticbraininjurywhereastheywereincreasedfollowingmelatonintreatment.Inconclusion,melatoninseemstohaveprotectiveeffectsontraumaticbraininjury-inducedcerebralcortexandbloodtoxicitybyinhibitingfreeradicalformationandsupportingantioxidantvitaminredoxsystem.

简介：Theactiveingredientofginseng,ginsenosidesRg1,hasbeenshowntoscavengefreeradicalsandimproveantioxidantcapacity.ThisstudyhypothesizedthatginsenosidesRg1hasaprotectiveroleinhumanneuroblastomacellsinjuredbyH_2O_2.GinsenosidesRg1atdifferentconcentrations(50and100μM)wasusedtotreatH_2O_2(150μM)-injuredSH-SY5Ycells.ResultsdemonstratedthatginsenosideRg1elevatedthesurvivalrateofSH-SY5YcellsinjuredbyH_2O_2,diminishedtheamountofleakedlactatedehydrogenase,andincreasedsuperoxidedismutaseactivity.GinsenosideRg1effectivelysuppressedcaspase-3immunoreactivity,andcontributedtoheatshockprotein70geneexpression,inadose-dependentmanner.TheseresultsindicatethatginsenosideRg1hasprotectiveeffectsonSH-SY5YcellsinjuredbyH_2O_2andthatitsmechanismofactionisassociatedwithanti-oxidationandtheinhibitionofapoptosis.

简介：BACKGROUND:Thepathwaysinduced/activatedbymercurypoisoningthatleadtomusclepainremainunclear.Thepresentstudyaddressedthestructuralchangesobservedintheperipheralnervefollowingmercurypoisoning.OBJECTIVE:Toestablishthemercurypoisonratmodel,ratswereintragastricallyadministeredmercury.Thecorrelationbetweenpost-mercurypoison-inducedmuscularpainandtibialnervemorphologicalchangeswereobserved.DESIGN:Observationalcontrastanimalstudy.SETTING:ShangdongAcademyofOccupationalHealthandOccupationalMedicine.MATERIALS:ThirtyadultSpragueDawleyratsofequalgender.Mercurychloride(HgCl2,analyticalgrade:99.99%;batchnumber:990402)wasprovidedbyShanghaiChemicalReagentFactory,andsodiumdimercaptopropanesulfonate(DMPS)injectionbyShanghaiHarvestPharmaceuticalCo.,Ltd.(batchnumber:0309011).METHODS:ThisstudywasperformedattheAnimalExperimentalCenterofShangdongAcademyofOccupationalHealthandOccupationalMedicinefromDecember2005toJanuary2006.Ratswererandomlydividedintohigh-dosemercury,low-dosemercury,andcontrolgroups,with10ratsineachgroup.Ratsinthetwomercurygroupswereintragastricallyadministered17mg/kgand8.5mg/kgHgCl2solution,respectively,onceadaytoestablisharatmodelofsubacutemercurypoisoning.Ratsinthecontrolgroupwereintragastricallyadministered2mLsaline,onceaday.Intragastricadministrationinthethreegroupslastedfor(20±2)days.Aftermodelestablishment,ratsinthetwomercurygroupswereinjectedDMPSonceadaytoremovemercury.Theinjectionlastedfor3daysafterevery4-dayinterval.Sevendayswasregardedasonetreatmentcycle,andthereweretwotreatmentcyclesintotal.MAINOUTCOMEMEASURES:Mercury-inducedmuscularpainstatus;ultrastructuralchangesoftherighttibialnervefollowingmodelestablishmentandmercuryremovalundertransmissionelectronmicroscope.RESULTS:Thirtyratswereincludedinthefinalanalysis.Muscularpainsta

简介：Brief-pulsestimulationat50Hzhasbeenshowntoterminateafterdischargesobservedinepilepsypatients.However,theoptimalpulsestimulationparametersforterminatingcorticalelectricalstimulation-inducedafterdischargesremainunclear.Inthepresentstudy,weexaminedtheeffectsofdifferentbrief-pulsestimulationfrequencies(5,50and100Hz)oncorticalelectricalstimulation-inducedafterdischargesin10patientswithrefractoryepilepsy.Resultsdemonstratedthatbrief-pulsestimulationcouldterminatecorticalelectricalstimulation-inducedafterdischargesinrefractoryepilepsypatients.Inconclusion,(1)abrief-pulsestimulationwasmoreeffectivewhentheafterdischargedidnotextendtothesurroundingbrainarea.(2)Ahigherbrief-pulsestimulationfrequency(especially100Hz)wasmorelikelytoterminateanafterdischarge.(3)Alowcurrentintensityofbrief-pulsestimulationwasmorelikelytoterminateanafterdischarge.

简介：BACKGROUND:Themostprominentcharacteristicofbrainagingisdecreasedlearningandmemoryability.Thefunctionsoflearningandmemoryarecloselyrelatedtointracerebralacetylcholinesterase(AChE)andmonoamineneurotransmitteractivity.PreviousstudieshaveshownthatSchisandrachinensispolysaccharidehasananti-agingeffect.OBJECTIVE:ToexploretheeffectsofSchisandrachinensispolysaccharideonAChEactivityandmonoamineneurotransmittercontent,aswellaslearningandmemoryabilityinaD-galactose-inducedagingmousebrainmodelcomparedwiththepositivecontroldrugKangnaoling.DESIGN,TIMEANDSETTING:Completelyrandomized,controlledexperimentbasedonneurobiochemistrywasperformedatthePharmacologicalLaboratory,HenanUniversityofTraditionalChineseMedicinefromSeptembertoDecember2003.MATERIALS:SchisandrachinensiswaspurchasedfromHenanProvincialMedicinalCompany.Schisandrachinensispolysaccharidewasobtainedbywaterextractionandalcoholprecipitation.KangnaolingpelletswereprovidedbyLiaoningTianlongPharmaceutical(batchNo.20030804;statedrugpermitNo.H21023095).Atotalof50six-week-oldKunmingmicewererandomlydividedintofivegroups:blankcontrol,model,Kangnaoling,highandlowdosageSchisandrachinensispolysaccharidegroups,with10micepergroup.METHODS:Miceintheblankcontrolgroupweresubcutaneouslyinjectedwith0.5mL/20gnormalsalineintothenapeoftheneckeachday,whiletheremainingmiceweresubcutaneouslyinjectedwith5%D-galactosesalinesolution(0.5mL/20g)inthenapefor40daystoinduceabrainagingmodel.Onday11,miceinthehighandlowdosageSchisandrachinensispolysaccharidegroupswereintragastricallyinfusedwith20mg/mLand10mg/mLSchisandrachinensispolysaccharidesolution(0.2mL/10g),respectively.MicefromtheKangnaolinggroupwereintragastricallyinfusedwith35mg/mLKangnaolingsuspension(0.2ml/10g),andthemiceinthemodelgroupwereintragastricallyinfusedwiththesamevolumeofnormalsal

简介：Psychologicaldepressionisdrawingaccumulatingattentionnowadays,duetotheskyrocketingincidenceworldwideandtheenormousburdensitincurs.Physicalexercisehasbeenlongrecognizedforitstherapeuticeffectsondepressivedisorders,althoughknowledgeoftheunderlyingmechanismsremainslimited.Suppressedhippocampalneurogenesisinadultbrainshasbeenregarded,atleastpartly,contributivetodepression,whereasphysicalexercisethatrestoresneurogenesisaccordinglyexertstheanti-depressiveaction.Severalrecentpublicationshavesuggestedthepotentialroleofadiponectin,aproteinhormonesecretedbyperipheralmatureadipocytes,inmediatingphysicalexercise-triggeredenhancementofhippocampalneurogenesisandalleviationofdepression.Here,webrieflyreviewthesenovelfindingsanddiscussthepossibilityofcounteractingdepressionbymodulatingadiponectinsignalinginthehippocampuswithinterventionsincludingphysicalexerciseandadministrationofpharmacologicalagents.更多还原

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简介：BACKGROUND:Mailuoning,aChineseherb,hasbeenwidelyusedinChinatotreatacuteischemicstroke,andthemajorcomponentexhibitsanti-oxidativeeffects.However,thepreciseanti-oxidationpathwayremainsuncertain.OBJECTIVE:TovalidatetheprotectiveeffectsofMailuoningonH2O2-inducedprimarycorticalneuroninjuryinembryonicmice.DESIGN,TIMEANDSETTING:ComparativeobservationandinvitroexperimentswereperformedattheJiangsuKeyLaboratoryforMolecularMedicinefromJanuary2008toSeptember2009.MATERIALS:Mailuoning(NanjingJinlingMedicalCompany,China),reactiveoxygenspecies(ROS)kit(BeyotimeBiotechnology,China),superoxidedismutase(SOD),Cu/ZnSODkit,malondialdehyde(MDA)kits(NanjingJiancheng,China),mitochondrialmembranepotential(GMS10013.1,GENMED,USA)andcatalaseactivityassaykit(BeyotimeBiotechnology,China)wereutilizedforthepresentstudy.METHODS:MouseembryoniccorticalneuronswereisolatedandculturedwithculturemediumcontainingH2O2(80μmol/L)and/orMailuoning(1.25μg/mL)for24hours.MAINOUTCOMEMEASURES:Neuronalviabilityanddeathweredetectedbymethylthiazolyltetrazdiumandflowcytometry;ROSproductionwasdeterminedbyflowcytometry;mitochondrialmembranepotentialwasdetectedusingfluorescentstaining;SODactivitywasdetectedusingamodifiednitrobluetetrazoliummethod;Cu/ZnSODandcatalaseactivitywasdetectedbyspectrophotometry;andMDAwasdeterminedusingthelipidperoxidationmethod.RESULTS:H2O2increasedROSproductionandMDAconcentration(P<0.05),anddecreasedmitochondrialmembranepotential,SOD,Cu/ZnSODandcatalaseactivity(P<0.05);thenumberofsurvivingneurons(P<0.05)wasalsoreduced.Mailuoningreversedthesechanges.CONCLUSION:MailuoningprotectsH2O2-inducedinjuryincorticalcellsbyinhibitingROSandMDA,increasingdepolarizationofmitochondrialmembrane,andenhancingSODandcatalaseactivity.

简介：BACKGROUND:Culturesfrommultipleportionsofumbilicalcordbloodmesenchymalstemcellshavebeenshowntoundergomorerapidproliferationandattachmentthansingleportions.OBJECTIVE:Toobservegrowthofbasicfibroblastgrowthfactor(bFGF)-inducedculturesofhumanamnion-derivedmesenchymalstemcells(AMSCs)anddifferentiationintoneuronal-likecells.DESIGN,TIMEANDSETTING:Comparativeobservation.ThestudywasperformedattheLaboratoryofMicrobiologyandImmunology,BasicMedicalSchoolofZhengzhouUniversityfromJanuarytoMay2008.METHODS:Amniafromfull-term,uterine-incisiondeliveryweredonatedby12healthywomen.AMSCswereobtainedbycellseparationandculturetechniques,andwerepassagedandinducedbybFGF.Fromthethirdpassage,atotalof1mLAMSCs,atadensityof1.0×10~4/mL,wasseparatelyharvestedfromsixsamples,whichservedasgroupA.Atotalof1mLAMSCs,atadensityof1.0×10~4/mL,washarvestedseparatelyfromtheremainingsixsamples,whichservedasgroupB.Atotalof0.5mLfromthesixsamplesofgroupAand0.5mLfromthesixsamplesofgroupBwerecombinedtoformgroupC.MAINOUTCOMEMEASURES:Differencesincellquantityamongthethreegroupswerecomparedbycellquantificationand3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide(MTT)analysis.Expressionofaglialcellmarker,neuron-specificenolase,andnestinwasdetectedinthethreegroupsbyimmunocytochemistry.RESULTS:CellquantificationandMTTanalysisoflivecells,aswellasAMSCabsorbance,weresignificantlygreateringroupCcomparedwithgroupsAandBat18daysofculture(P<0.05),andnosignificantdifferencewasobservedbetweengroupsAandB.Glialfibrillaryacidicprotein,neuron-specificenolase,andnestinwereexpressedinallgroupsfollowingbFGFinduction.CONCLUSION:MixedAMSCculturespromotedproliferation,andbFGF-inducedAMSCsdifferentiatedintoneuronal-likecells.

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.

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：ThepresentstudyestablishedachronicexperimentalautoimmuneencephalomyelitismodelinC57BL/6miceinducedbymyelinoligodendrocyteglycoproteinpeptidesandcompleteFreund'sadjuvant.Onsetlatencywas12days,withanincidencerateof100%.Neuropathologicalcharacteristicsincludedperivascularinflammatorycellinfiltration,demyelination,neuronaldegeneration,andaxonaldamagewithincerebralandmyelicwhitematter.Electronmicroscopyrevealedswollenmitochondria,completeorgandisappearance,andfusedorbrokenmyelinsheathstructure,whichwereaccompaniedbymyelinsheathreconstruction.Moreover,axonaldamagewasnotconsistentwithdemyelinationdistribution,andseverityofaxonaldamagedidnotcorrelatewithdemyelination.Resultssuggestedthataxonaldamageinanexperimentalautoimmuneencephalomyelitismodelisnotsecondarytoinflammatorydemyelination.

简介：BACKGROUND:Highincidenceofstrokeatinterchangeperiodofautumnandwinterwasdemonstratedbyepidemiologicalsurvey,andthespecificcausesshouldbefurtherinvestigated.OBJECTIVE:Toinvestigatetheinfluenceofartificialcoldexposureontheincidenceofstrokeinrenovascularhypertensiverats(RHR),andanalyzetheassociationwithbloodpressureandcold-inducibleRNAbindingprotein(CIRP)mRNAexpressioninbraintissue.DESIGN:Acompletelyrandomizedgroupingdesign,arandomizedcontrolanimaltrial.SETTINGS:LabofNeurology,theFirstAffiliatedHospitalofSunYat-senUniversity;DepartmentofChemistry,OpenlaboratoryofChemicalBiology,InstituteofMolecularTechnologyforDrugDiscoveryandSynthesis,UniversityofHongKong.MATERIALS:MaleSDrats(n=460),weighing80-100gwereobtainedfromGuangdongProvinceHealthAnimalUnit.AmodifiedRXZ-300Aintelligentartificialclimatecabinet(NingboJiangnanInstrumentCo.,Ltd.,China).METHODS:TheexperimentwereprocessedintheLabofNeurology,theFirstAffiliatedHospitalofSunYat-senUniversityandtheOpenLaboratoryofChemicalBiology,InstituteofMolecularTechnologyforDrugDiscoveryandSynthesis,UniversityofHongKongfromOctober2004toNovember2005.Rats(n=400)wereoperatedtoestablish2-kidney2-clipRHRmodelasdescribedpreviously.Thesham-operatedrats(n=60)servedasnormotensivecontrols.Eightweekslater,300ofRHRwererandomlyselectedaccordingtotheirsystolicbloodpressure(SBP)anddividedinto3sub-groups(n=100pergroup):mildhypertensivegroup(SBPof160-200mmHg),moderatehypertensivegroup(SBPof200-220mmHg)andseverehypertensivegroup(SBP>220mmHg).Eachgroupwasfurtherdividedintotwogroups(n=50)underACEandnon-ACE.Normalsham-operatedSDrats(n=60),SBP<140mmHg,wererandomlydividedintotwogroups:Sham-operatedcontrolgroup(n=30)underACEandnon-ACE.ToestablishtheACEandnon-ACEtreatment,ratswerehousedindividuallyinartifici