简介:AIM:ToinvestigatetheregulationofEaf2proteininmouselenscellsapoptosisinducedbyultraviolet(UV)radiation.METHODS:AneyeofEaf2geneknockoutmiceornormalcontrolmicewasexposedtoUVradiation,andtheotheronewasnon-exposed.AlloflenseswereanalyzedbyTUNELandcaspase3activityassaystodeterminethedifferenceoftheapoptosisinducedbyUVradiation.Inaddition,exposedandnon-exposedlenseswereanalyzedbyquantifiedp53expressionandreal-timereversetranscription-polymerasechainreaction(RT-PCR)ofBax,Bid,Apaf-1,PumaandNoxa,tocompareEaf2geneknockoutmiceandnormalcontrolmice.RESULTS:UVradiationcausedapoptosisoflenscellsinnormalcontrolmiceandEaf2knockoutmice.Activityofcaspase3wassignificantlyhigherinnormalcontrolmicethanEaf2knockoutmice.Expressionofp53proteinwassignificantlyhigherinlensesexposedtoUVradiationthannonexposedlenses,butwassimilarbetweenEaf2geneknockoutmiceandnormalcontrolmiceinthesameUVcondition.AfterexposingtoUVradiation,theanalysisofreal-timeRT-PCRdemonstratedthatmRNAlevelsofPumaandNoxaweresignificantlyhigherinlensesofnormalcontrolmicethanEaf2geneknockoutmice,andthatmRNAlevelsofBax,BidandApaf-1werenotsignificantlydifferentbetweengeneknockoutmiceandnormalcontrolmice.CONCLUSION:Eaf2increaseslenscellsapoptosisinducedbyultravioletradiation.AndEaf2up-regulatesexpressionofthePumaandtheNoxatoactonlenscellsapoptosisafterUVradiation.
简介:AIM:Toinvestigatethediffusioncharacteristicsofwaterofopticnerveandopticradiationinhealthyadultsanditsrelatedfactorsbydiffusiontensorimaging(DTI)at3T.METHODS:Atotalof107healthyvolunteersperformedheadconventionalMRIandbilateralopticnerveandopticradiationDTI.TheprimarydataofDTIwasprocessedbypost-processingsoftwareofDTIstudio2.3,obtainingfractionalanisotropyvalue,meandiffusivityvalue,principalenginevalue,orthogonalenginevaluebymeasuring,andanalyzedbytheSPSS13.0statisticalsoftware.RESULTS:Thebilateralopticnerveandopticradiationfiberspresentedgreencolorindirectionalencodedcolor(DEC)mapsandpresentedhighsignalinfractionalanisotropy(FA)maps.TheFAvalueoftheleftopticnervewas0.598±0.069andtherightwas0.593±0.065;themeandiffusivity(MD)valueoftheleftopticnervewas(1.324±0.349)×10-3mm2/sandtherightwas(1.312±0.350)x10-3mm2/s;theprincipalenginevalue(λ?)oftheleftopticnervewas(2.297±0.522)×10-4mm2/sandtherightwas(2.277±0.526)×10-3mm2/s;theorthogonalenginevalue(λ⊥)oftheleftopticnervewas(0.838±0.285)×10-3mm2/sandtherightwas(0.830±0.280)×10-3mm2/s;theFAvalueoftheleftopticradiationwas0.636±0.057andtherightwas0.628±0.056;themeandiffusivity(MD)valueoftheleftopticradiationwas(0.907±0.103)×10-3mm2/sandtherightwas(0.889±0.125)×10-3mm2/s;theprincipaleigenvalue(λⅡ)oftheleftopticradiationwas(1.655±0.210)×10-3mm2/sandtherightwas(1.614±0.171)×10-3mn2/s;theorthogonalenginvalue(λ⊥)oftheleftopticradiationwas(0.531±0.103)×10-3mm2/sandtherightwas(0.524±0.152)×10-3m
简介:AIM:Toexaminetheexpressionofsurvivinandvascularendothelialgrowthfactor(VEGF)duringthedevelopmentofretinalneovascularization(NV)inamousemodel.·METHODS:Awell-characterizedmurinemodelofretinalNVwasusedtostudytheexpressionofsurvivinandVEGF.NVoftheretinawasinducedinmicebyexposureto75%O2frompostnataldayP7toP12,followedbyreturntoroomairfromP12toP17.ExpressionofsurvivinandVEGFproteinwasanalyzedbyImmunohistochemistry.Inaddition,mousemodelofproliferativeretinopathywasanalyzedbyretinalfluoresceinangiographyandquantificationanalysis.·RESULTS:Thenormalmicehadbothsuperfiekalanddeepvascularlayersthatextendedfromtheopticnervetotheperiphery.Inintraocularpressure(IOP)micewerecharacterizedbyrepresentatypicalpatternofpathologicalretinalNV.Therearelessorlittlenucleiofnewvesselsvascularendothelialcellbreakingthroughtheinnerretinalthaninretinopathyofprematurity(ROP)mice,largeclustersofbloodvesselswereadherenttotheinternallimitingmembrane(ILM)(0.27±0.20vs23.38±1.027,t=9.454,P<0.001).DuringtheangiogenicperiodfromP13toP17,survivinandVEGFproteinexpressionincreasedinexperimentalretinascomparedwithcontrolsamples(2.56±0.46vs3.34±0.40,t=17.43,P<0.01:2.18±0.75vs4.34±0.25,t=19.61,P<0.01).ProteinlevelsofVEGFandsurvivnhassignificantlypositivecorrelation(P<0.05,r=0.411).·CONCLUSION:CorrelationwasmadeattheproteinlevelsofsurvivinexpressioncomparedwiththatofVEGFinamurinemodelofretinalNV,whichsuggestsatemporalroleforsurvivinandVEGFinnewvesselformationinresponsetohypoxicstimulation.