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

简介：BACKGROUND:ThedetectionofdifferentialgeneexpressioninbrainispossiblebycDNAmicroarraytechnology,andthescreeningofdifferentiallyexpressedgenesmightprovideabiologicalbasisforgene-targetedtherapyfortumors.OBJECTIVE:TodetectthedifferentialexpressionofgenesamongastrocytomaSHG-44(WHOgradeIV),CHG-5(WHOgradeII),andATRA-treatedSHG-44celllinesbycDNAmicroarray.DESIGN:Laboratoryexperimentsinvitro.SETTING:DepartmentofNeurobiology,theThirdMilitaryMedicalUniversity.MATERIALS:TheexperimentwasperformedattheDepartmentofNeurobiologyintheThirdMilitaryMedicalUniversityoftheChinesePLAfromJanuarytoOctober2007.TheSHG-44cellline(WHOgradeⅣ)wasestablishedbyProf.ZiweiDu,andtheCHG-5cellline(WHOgradeII)wassetupbyProf.XiuwuBianfromtheThirdMilitaryMedicalUniversityoftheChinesePLA.ThecDNAmicroarraycontaining9182knowngeneswaspreparedandprovidedbyDr.YangZhongattheCityUniversityofHongKong.METHODS:ToscreendifferentiallyexpressedgenesfromthegeneexpressionprofilesdetectedbycDNAmicroarraycomparisonsweremadebetweenCHG-5andSHG-44cellsandbetweenSHG-44cellswithorwithouttreatmentwith10μmol/LATRA.SomedifferentiallyexpressedgeneswereselectedrandomlyforNorthernBlotanalysistoconfirmtheresultsofthemicroarray.Thedeterminationcriteriafordifferentialgeneexpressionwereasfollows.①TheratioofCy5signaltoCy3wasgreaterthan2.0orlessthan0.5.②Theresultsofthetriplicatemicroarrayhybridizationsshowedthesametrendinthreeexperiments.③Ageneappearedatleasttwotimesonthetriplicatemicroarrayhybridizations,andthe3rdvaluedidnotshowacontradictorytrend.AnormalizedratioofCy5intensitytoCy3greaterthan2.0orlessthan0.5wasconsideredtorepresentup-regulatedordown-regulatedgeneexpression,respectively.MAINOUTCOMEMEASURES:Theidentificationofgenesthatweresimilarlyregulated(overlapping)dur

简介：Recentadvancesinstemcelltechnologieshaveopenednewavenuesforthetreatmentofanumberofdiseasesstilllackingeffectivetherapeuticoptions.Celltransplantationhasemergedasamongthemostpromisingclinicalinterventionfordisorderssuchasinjuries,diabetes,liver

简介：Traumaticinjuriestospinalcordelicitdiversesignalingpathwaysleadingtounselectiveandcomplexpathologicaloutcomes:deathofmultipleclassesofneuralcells,formationofcysticcavitiesandglialscars,disruptionofaxonalconnections,anddemyelinationofsparedaxons,allofwhichcancontributemoreorlesstodebilitatingfunctionalimpairmentsfoundinpatientswithspinal

简介：Mitochondriaplayanimportantroleinneuronalapoptosiscausedbycerebralischemia,andtheroleismediatedbytheexpressionofmitochondrialproteins.Thisstudyinvestigatedtheinvolvementofmitochondrialproteinsinhippocampalcellapoptosisaftertransientcerebralischemia-reperfusioninjuryinagedratsusingacomparativeproteomicsstrategy.Ourexperimentalresultsshowthattheagedratbrainissensitivetoischemia-reperfusioninjuryandthattransientischemialedtocellapoptosisinthehippocampusandchangesinmemoryandcognitionofagedrats.Differentialproteomicsanalysissuggestedthatthisphenomenonmaybemediatedbymitochondrialproteinsassociatedwithenergymetabolismandapoptosisinagedrats.Thisstudyprovidespotentialdrugtargetsforthetreatmentoftransientcerebralischemia-reperfusioninjury.

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

简介：Intraperitonealinjectionofrecombinanthumaninterleukin-2(rhIL-2)inhibitsneuronalapoptosisinthechronicocularhypertensionretinalganglioncelllayer.IntravitreousinjectionwasperformedonretinalganglioncellsinaWistarratmodelofchronicallyelevatedintraocularpressuretoobservetheeffectsofLY294002andAG490onretinalganglioncellsurvival,macrophageactivation,andPI3K/AktandJAK/STATactivation.ThenumberofretinalganglioncellsintherhIL-2treatmentgroupwasmuchgreaterthaninthenormalcontrolandphosphate-bufferedsalinegroups.WesternblotanalysisrevealedlowAktandSTAT3proteinexpressionintheretinaafter3-hourintravitreousinjectionsofrhIL-2.However,proteinexpressionwasincreasedat12hours,butdecreasedagainat24hours,withverylowexpressionat96hours.LY294002andAG490,whichareinhibitorsofthePI3K/AktandJAK/STAT3signalpathways,preventedupregulationofAktandSTAT3proteinexpressionintheretina,respectively.IntravitreousinjectionofrhIL-2exhibitedneuroprotectiveeffectsbydecreasingretinalganglioncelllayerdamageinaratmodelofchronicglaucoma.TheseresultssuggestthatintravitrealinjectionofrhIL-2couldinducethePI3K/AktandJAK/STAT3signalingpathwaystoprotectretinalganglioncellsinchronicallyelevatedintraocularpressuremodels.