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简介：AIMTo评估β的可靠性；在试验性的绿内障model.METHODSGlaucoma老鼠的一个网膜的中心房间(RGC)标记当模特儿的-III-Tubulin蛋白质被把聚苯乙烯microbeads注入C57BL/6J老鼠的前面的房间建立，在intraocular压力(IOP)被提高以后，当时，他们的视网膜是获得的14d和28d。网膜的扁平的山和节是由fluorogold(FG)和β的双labeled；-III-Tubulin抗体或由β标记单人赛；-III-Tubulin抗体，然后，RGC被认为并且比较注射眼睛的respectively.RESULTSIOP显著地被提高并且在22.8±到达了山峰；0.7公里Hg在白天14在注射以后，然后落下到11.3±；0.7公里Hg在白天28。RGC数字由标记的FG和β数了；-III-Tubulin抗体标记是64807±；4930和64614±；5054分别地在控制组织，没有重要差别。在白天14，RGC在里面试验性的组与控制组相比显著地减少了，但是标记数的FG和β之间没有重要差别；在试验性的组或在控制组把数的任何一个标记的-III-Tubulin抗体。结果在白天是类似的28，与进一步的RGCloss.CONCLUSIONOur，结果建议β；-III-Tubulin蛋白质没被IOP举起影响并且能在绿内障的试验性的模型为RGC被用作一个可靠标记。

简介：ObjectiveTostudytheeffectofsalicylateontheexpressionandfunctionofNMDAreceptorsinspiralganglionneurons(SGNs).MethodsThemRNAofNR1subunitofNMDAreceptorinmodiolustissuesweredetectedbyRealtimefluorescencequantitativePCR(FQ-PCR).NMDAreceptorwhole-cellcurrentswererecordedusingpatchclampinacuteisolatedSGNs.ResultsComparedwiththecontrolgroup,salicylatesignificantlyincreasedthemRNAlevelofNR1subunitinSGNs.NMDAofconcentrationsrangingfrom0.1mMto10mMevokednocurrentinSGNs.NMDA(0.1mMand0.5mM)appliedwithsalicylate(5mM),however,inducedinwardcurrents(212.6±15.2pA,n=5;607.9±44.3pA,n=5)inadose-dependentmanner,whichcouldbeinhibitedbyAPV.SalicylatealonedidnotproduceanycurrentinSGNs.ConclusionSalicylateincreasestheexpressionofNMDAreceptorsandfacilitatesthecurrentsmediatedbyNMDAreceptorsinSGNs.

简介：ObjectiveTostudygentamicininjurymechanismsusingpostnatalmousecochlearspiralgangcells(SGC).MethodsSGCswereisolatedusingacombinatorialapproachofenzymaticdigestionandmechanicalseparationfromP2～6Kunmingmousecochleae.After4days,culturedSGCswerefixedwith4%paraformaldehydeatroomtemperatureforimmunocytochemicalexaminationusingthemethodsofS-Pandthemonoclonalantibodyagainstmouseneurofilamentprotein(Neurofilament-68/200Kda,NF-L+H).SGCswererandomlydividedintoablankcontrolgroupandthreegentamicintreatmentgroups(mediumgentamicinconcentrationat50mg/L,100mg/Land150mg/Lrespectively),SGCswerecollectedandexaminedunderatransmissionelectronmicroscopeafterbeingculturedfor48h.ResultsSGCprimaryculturewassuccessful.SGCcytoplasmandneuritesweredyedbrownishyellowbythemonoclonalmouseneurofilamentproteinantibody.SGCsshowedclassicalbipolarneuronappearance.Underthetransmissionelectronmicroscope,.gentamicintreatedSGCsshowedmorphologicalfeaturesdifferentcomparedtothoseintheblankcontrolgroup,whichmightindicateapoptosis.ConclusionOurresultsindicatethatgentamicinhasdirecttoxiceffectsoncochlearSGCsinmiceandtheinjurymechanismiscloselyrelatedwithapoptosis.Damagetomitochondriamayplayanimportantroleintheprocess.

简介：Injurytoaxonsclosetotheneuronalbodiesinthemammaliancentralnervoussystemcausesalargeproportionofparentingneuronstodegenerate.Itisknownthatopticnervetransectionclosetotheeyeinrodentsleadstoalossofabouthalfofretinalganglioncellsin1weekandabout90%in2weeks.Usinglowlevellasertreatmentinthepresentstudy,wedemonstratedthattreatmentwithhelium-neon(660nm)laserwith15mWpowercoulddelayretinalganglioncelldeathafteropticnerveaxotomyinadulthamsters.Theeffectwasmostapparentinthefirstweekwithashortperiodoftreatmenttime(5minutes)inwhich65–66%ofretinalganglioncellssurvivedtheopticnerveaxotomywhereas45–47%ofretinalganglioncellsdidsoinopticnerveaxotomycontrols.Wealsofoundthatsingledoseandearlycommencementoflaserirradiationwereimportantinprotectingretinalganglioncellsfollowingopticnerveaxotomy.Thesefindingsthusconvincinglyshowthatappropriatelasertreatmentmaybeneuroprotectivetoretinalganglioncells.更多还原

简介：AIM:ToinvestigatetheroleofBrn-3bindifferentiationprocessofstemcellsderivedfromretinalMiillercellsintotheganglioncell.METHODS:ThepassageculturemethodofMiillercellsfromretinaofnewbornSpragueDawleyratswascarriedoutbyrepeatedincompletepancreaticenzymedigestionmethod.Thecellsweredetectedbyfluorescenceactivatedcellsorter(FACS),immunohistochemistrytechnologyandreversetranscription-polymerasechainreaction(RT-PCR)todeterminethepurity.Thethirdpassageofcellswasinducedintheserum-freededifferentiationmedium.TheexpressionofthespecificmarkersKi-67andnestinofretinalstemcellswasmeasuredbyRT-PCRandWesternblot.Thecellproliferationofretinalstemcellswasdetectedby5-Ethynyl-2’-deoxyuridine(Edu)staining.Thecellswererandomlydividedinto5groupsasfollows:groupA:Brn-3bsiRNAgroup;groupB:Brn-3bcontrolsiRNAgroup;groupC:pGC-Brn-3b-greenfluorescentprotein(GFP)group;groupD:pGC-GFPgroup;groupE:controlgroup(withoutanyhandling).ThepurifiedMullercellswereculturedfor3-7d,then,thepercentageofganglioncellswascountedbyimmunofluorescencestaining.RESULTS:FACSdemonstratedthepurityofretinalMullercellswasmore97.44%.Afewsphericalcellspheresappeared.Immunofluorescencestainingshowedthatstemcellswithinthesphereswerepositiveforretinalstemcell-specificmarkersnestin(redfluorescence,92.94%±6.48%)andKi-67(greenfluorescence,85.96%±6.04%).Meanwhile,RT-PCRanalysisshowedcellspheresintheculturetohaveexpressedabatteryoftranscriptscharacteristicofstemcellssuchasnestinandKi-67,whichwereabsentintheMullercells.WesternblotanalysisfurtherconfirmedtheexpressionofnestinandKi-67inthecellspheresbutnotintheMullercells.Edustainingshowedmostofthenucleiwithinthecellsphereswerestainedred(82.80%±6.65%),suggestingthenewcellsphereshadthecapacityforeffectiveproliferation.ThestatisticsresultshowedthedifferencebetweenBrn-3bsiRNAgroupand

简介：ObjectiveToinvestigatetheclinicaloutcomesoffacialneverdecompressionviaacombinedsubtemporal-supralabyrinthineapproachtogeniculateganglionformanagementoffacialparalysisintemporalbonefracture.MethodsEighteenpatientswithunilateralfacialparesisduetotemporalbonefractureweretreatedbetweenMarch2003andMarch2011.FacialfunctionwasHouse-Brackmann(HB)gradeⅢin6patients,HBgradeⅤin9patientsandHBgradeⅥin3patients.Thepreoperativemeanairconductionthresholdwas52dBHLforthe15caseswithlongitudinaltemporalbonefractureandshowedseveresensorineuralhearinglossinthe3caseswithtransversetemporalbonefracture.Fracturelinesweredetectedin15casesontemporalboneaxialCTscansandossiculardisruptionwasdeterminedin11casesbyvirtualCTendoscopy.Thegeniculateganglionorthetympanicmastoidsegmentofthefacialnerveshowedanirregularmorphologyoncurvedplanarreformationimagesofthefacialnervecanal.Afteranintactcanalwallmastoido-epitympanectomy,theossicularchaindamagewasevaluated.Iftheossicularchainwasintact,thesupralabyrinthinerecesswasopenedbydrillingthroughthecellsbetweenthetegmentympaniandossicularchain.Iftheossicularchainwasdisrupted,theincuswasremovedtoaccessthesupralabyrinthinerecess.Thegeniculateganglionandthedistallabyrinthinesegmentofthefacialnervewereexposed.Aftercompletingfacialnervedecompression,thedislocatedincuswasreplaced,orafracturedincuswasreshapedtobridgethespacebetweenthemalleusandthestapes.ResultsPronouncedgangliongeniculatumswellingwasfoundin15casesoflongitudinaltemporalbonefracture,withgreaterpetrosusnervesdamagein3casesandbleedingin5cases.Disruptedossicularchainswereseenin11cases,includingdislocatedincusresultingincrushingofthehorizontalportionofthefacialnervein3casesandfractureoftheincuslongprocessin1case.In3casesoftransversefractures,

简介：AIM:Toinvestigatetheneuroprotectiveeffectofgastrodinonretinalganglioncells(RGCs)inanacuteocularhypertension(AOH)ratmodelandtoidentifyitspossiblemechanism.METHODS:AOHratmodelwasperformedinarandomlyselectedeyebyanteriorchamberperfusionandeitherreceivedanintraperitonealinjectionwithvariousconcentrationsofgastrodinornormalsaline.After2wk,theratsweresacrificed.FluoroGoldwasusedtolabelsurvivalRGCs.Immunostainingwithanti-Iba1intheretinalflatmountstocalculatethemicrogliadensityintheganglioncelllayer(GCL).Changesinmicroglialcytokines,tumournecrosisfactor-alpha(TNF-α)andinducibleNOsynthase(iNOS)wereexaminedwithWesternblotandreversetranscriptionquantitativepolymerasechainreaction.Expressionlevelsoftotalandphosphorylatedp38mitogenactivatedproteinkinase(MAPK)weredeterminedbyWesternblot.RESULTS:ResultsshowedthatAOHinducedsignificantlossofRGCsandseveremicrogliaactivationintheGCL.Besides,AOHincreasedthephosphorylationofp38MAPKandpromotedthereleaseofmicroglialcytokinesintheretinas.Intraperitonealinjectionwithdose-dependentgastrodinsignificantlyreducedthelossofRGCsandinhibitedretinalmicrogliaactivation,accompaniedwiththedecreasedexpressionlevelsofmicroglialcytokinesandp38MAPKphosphorylation.CONCLUSION:GastrodinexertsaneuroprotectiveeffectonRGCsinanacuteglaucomaanimalmodelviainhibitingmicrogliaactivationandmicroglial-mediatedneuroinflammation.ThefindingdemonstratesthepotentialapplicationofgastrodinintheneuroprotectivetherapyofacuteglaucomaandotherretinalneurodegenerativediseasescharacterizedbymicrogliaactivationandRGCsdeath.

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简介：Excessivenoise,ototoxicdrugs,infections,autoimmunediseases,andagingcancauselossofspiralganglionneurons,leadingtopermanentsensorineuralhearinglossinmammals.Stemcellshavebeenconfirmedtobeabletodifferentiateintospiralganglionneurons.Littlehasbeenreportedonadiposetissue-derivedstemcells(ADSCs)forrepairofinjuredspiralganglionneurons.Inthisstudy,wehypothesizedthattransplantationofneuralinduced-humanADSCs(NI-hADSCs)canrepairtheinjuredspiralganglionneuronsinguineapigswithneomycin-inducedsensorineuralhearingloss.NI-hADSCswereinducedwithculturemediumcontainingbasicfibroblastgrowthfactorandforskolinandtheninjectedtotheinjuredcochleae.GuineapigsthatreceivedinjectionofHanks’balancedsaltsolutionintothecochleaewereusedascontrols.Hematoxylin-eosinstainingshowedthatat8weeksaftercelltransplantation,thenumberofsurvivingspiralganglionneuronsinthecelltransplantationgroupwassignificantlyincreasedthanthatinthecontrolgroup.Alsoat8weeksaftercelltransplantation,immunohistochemicalstainingshowedthatagreaternumberofNI-hADSCsinthespiralganglionsweredetectedinthecelltransplantationgroupthaninthecontrolgroup,andtheseNI-hADSCsexpressedneuronalmarkersneurofilamentproteinandmicrotubule-associatedprotein2.Within8weeksaftercelltransplantation,theguineapigsinthecelltransplantationgrouphadagraduallydecreasedauditorybrainstemresponsethreshold,whilethoseinthecontrolgrouphadalmostnoresponseto80dBofclicksorpuretoneburst.ThesefindingssuggestthatalargeamountofNI-hADSCsmigratedtothespiralganglions,survivedforaperiodoftime,repairedtheinjuredspiralganglioncells,andtherebycontributedtotherecoveryofsensorineuralhearinglossinguineapigs.

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.