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简介:AIM:Todeterminetheclinicalfeatures,diagnosisandtreatmentoftheprimarySjogrensyndrome(SS)relatedopticneuritis.METHODS:Theclinicaldataof8patients(12eyes)withprimarySSrelatedopticneuritiswereanalyzedretrospectively.RESULTS:Eightof128consecutivepatientswithopticneuritisresultedfromvariedcausesfulfilledthediagnosticcriteriafortheprimarySS.Theypresentedinitiallywiththesignsandsymptomsofnon-specificopticneuritis,and5patientspresentingwithoutdrynessshowedachronicinflammationofsubmandibularglandorparotidgland,andlymphocyteinfiltrationwasdemonstratedbylabialglandbiopsyin2patients.Therewereserumpositivetitersforanti-SjogrensyndromeA(SSA)in7patientsandanti-SjogrensyndromeB(SSB)in8patients.Anti-aquaporin-4(AQP4)antibodywasnegativeinallthe8patients.Bothglucocorticoidsandimmunosuppressiveagentwereadministered,andvisualacuityelevatedin8eyes(66.7%),3patients(37.5%)recurredinthefollow-up.CONCLUSION:PrimarySSrelatedopticneuritisislesscommonandeasilymisdiagnosed.Theconventionaltherapiesforopticneuritiscouldnotcontroltherecurrence.
简介:Leber'scongenitalamaurosis(LCA)andrecentgenetherapyadvancementfortreatinginheritedretinopathieswereextensiveliteraturereviewedusingMEDLINE,PubMedandEMBASE.Adeno-associatedviralvectorswerethemostutilisedvectorsforoculargenetherapy.Conephotoreceptorcellsmightuseanalternatepathwaywhichwasnotreliantoftheretinalpigmentepithelium(RPE)derivedretinoidisomerohydrolase(RPE65)toaccessthe11-cisretinaldehydechromophore.Researcheffortsdedicatedontheprogressionofagene-basedtherapyforthetreatmentofLCA2.Suchgenetherapyapproacheswereextremelysuccessfulincanine,porcineandrodentLCA2models.TherecombinantAAV2.hRPE65v2adenoassociatedvectorcontainedtheRPE65cDNAandwasreplicationdeficient.ItsinvitroinjectionintargetcellsinducedRPE65proteinproduction.Thegenetherapytrialsthatweresofarconductedforinheritedretinopathieshavegeneratedpromisingresults.PhaseIclinicaltrialstocureLCAandchoroideremiademonstratedthatadeno-associatedviralvectorscontainingRPEgenesandphotoreceptorsrespectively,couldbesuccessfullyadministeredtoinheritedretinopathypatients.AphaseIIItrialispresentlyongoingandifsuccessful,itwillleadthewaytoadditionalgenetherapyattemptstocuremonogenic,inheritedretinopathies.
简介:Aim:ToverifywhetherpartialintraoperativeTenon'scapsuleresection(PTCR)withadjunctiveMitomycinCiseffectiveindevelopingthin,avascularblebsineyesundergoingAhmedglaucomavalveinsertionandtoassesstheefficacyandsafetyofthisprocedure.Methods:ThisstudywasconductedinfourLatinAmericacountries(Argentina,Brazil,ColombiaandPeru).AhmedglaucomavalveimplantinsertionwithPTCR(groupA)andwithoutPCTR(groupB)wasperformedinneovascular
简介:目的:探讨线粒体膜电位(△ψm)、Caspase3在As2O3诱导ACC-2细胞凋亡中的作用。方法:进行ACC-2细胞培养,将As2O3建立不同药物浓度梯度(0,1.0,2.0,4.0,8.0μmol/L)分别作用于ACC-2细胞,用Rh123染色,流式细胞仪检测8.0μmol/LAs2O3作用前、后(24h),ACC-2细胞的线粒体膜电位(△ψm)变化;用多功能酶标仪进行Caspase3活性检测。结果:空白对照组ACC-2细胞内Rh123荧光强度最强,8.0μmol/LAs2O3处理组ACC-2细胞内Rh123荧光强度减弱,其差异有显著性(P〈0.05);随着As2O3药物浓度的增高(0,1,2,4,8μmol/L),ACC-2细胞的Caspase3酶活力单位逐渐增加。结论:As2O3作用于ACC-2细胞,可通过降低线粒体膜电位从而引起细胞凋亡。随着As2O3药物浓度的增高,ACC-2细胞的Caspase3酶活力单位逐渐增加,Caspase3被激活,细胞可发生不可逆转的凋亡过程。
简介:AIMTo在Descemet的家根据厚度评估视觉尖酸和endothelial房间密度剥去自动化endothelialkeratoplasty(DSAEK)在外科以后的年。
简介:AIMTo在划分的类型2糖尿病的patients.METHODSWe估计在choroidal厚度(CT)和糖尿病的retinopathy(医生)的早阶段之间的关联83个糖尿病的病人(51-80岁;50女性)进非糖尿病的retinopathy,组(NDR)和温和/中等的nonproliferative糖尿病患者retinopathy(NPDR)组织,并且把他们与26个非糖尿病的控制题目作比较(51-78岁;16女性)。Subfovealchoroidal厚度(SFCT)和parafovealchoroidal厚度(PFCT)用提高的深度成像被测量光谱域的光连贯断层摄影术(EDI10月)。眼睛的健康地位,疾病持续时间,身体团索引,和血红素A1c(HbA1c)是NDR,NPDR,和控制组的recorded.RESULTSThe平均数年龄68.0是戠牥晥?景吗?
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