简介:目的:观察MoriaM2型90与110μm角膜刀制作角膜瓣在准分子激光角膜原位磨镶术(laserinsitukeratomileusis,LASIK)的疗效和并发症,探讨MoriaM2型90刀头在LASIK中应用的有效性、安全性和优点。方法:选取通过术前检查并自愿行LASIK手术的患者105例202眼,按随机数字表分成两组,使用MoriaM2型90刀头LASIK患者51例98眼,110刀头LASIK患者54例104眼做对照,术后即使用光学相干断层扫描仪(OCT)检测两组角膜瓣厚度,观察两组术后1d;1wk;1,3mo裸眼视力、矫正视力和角膜瓣形态、对合情况、并发症。结果:90刀头组术后角膜瓣厚度为118.3±15.2μm,110刀头组术后角膜瓣厚度为130.5±17.1μm,有显著性差异。90刀头组均未发现层间点状金属碎屑,110刀头组有层间点状金属碎屑个例(12例),有显著性差异。两组角膜瓣形态、对合情况、术后反应、术后裸眼视力相当。结论:应用90刀头LASIK的疗效及并发症和110刀头LASIK相当,但90刀头保留角膜基质床相对较厚,可矫治的屈光度更大,术后层间点状金属碎屑并发症更少,具有更好的安全性和更宽的适应范围。
简介:AIM:Toassesstheeffectofmyopiaonthethicknessofretinalnervefiberlayer(RNFL)measuredby3Dopticalcoherencetomography(3D-OCT)inagroupofnonglaucomatousChinesesubjects.METHODS:Twohundredandfifty-eighteyesof258healthyChinesemyopicindividualswererecruitedandfourgroupswereclassifiedaccordingtotheirsphericalequivalent(SE):lowmyopia(n=42,-0.50
简介:目的观察1,25(OH)2D3对高糖诱导牛视网膜血管内皮细胞(BRECs)中血管内皮生长因子(VEGF)的表达水平变化及对细胞凋亡水平的影响。方法将分离培养的BRECs分为三组,分别为正常糖组、高糖组和高糖处理组。正常对照组细胞培养液含5mmol/L葡萄糖,高糖组细胞培养液含30mmol/L葡萄糖,高糖处理组细胞培养液含30mmol/L葡萄糖和50nM,1,25(OH)2D3。培养48h后收集细胞蛋白。蛋白免疫印迹法检测细胞VEGF及细胞凋亡相关蛋白Bax和Bcl-2表达水平;PI/Hoechst双染色法检测细胞凋亡。结果相比于正常糖组,高糖组中VEFG水平和Bax/Bcl-2比值显著增加;而在高糖处理组中表达水平远远低于高糖组,差异均有统计学意义(P〈0.05)。高糖的细胞凋亡水平高于正常糖组,而经过1,25(OH)2D3处理后,其细胞凋亡水平则有所下降,差异均有统计学意义(P〈0.05)。结论1,25(OH)2D3可以抑制高糖诱导BRECs中VEGF表达增加及细胞凋亡。
简介:AIM:Topresenttheoutcomeofmodifiedgridlaserphotocoagulation(GLP)indiffusediabeticmacularedema(DDME)ineyeswithoutextrafovealand/orvitreofovealtraction.METHODS:InclusioncriteriafortheretrospectivestudywereDDMEeyesofpatientswithtypeⅡdiabetesmellitusthathad≥4monthsoffollow-upfollowingGLP.Onlyoneeyeperpatientwasanalyzed.Using3-Dspectral-domainopticalcoherencetomography(3-DSDOCT),eyesthathadeitherextrafovealorvitreofovealtraction,orhadbeenpreviouslytreatedbyanintravitrealmedication(s)wereexcluded.TreatedDDMEeyesweredividedinto4groups:A)'Classic'DDMEthatinvolvedthecentralmacula;B)edemadidnotinvolvethemacularcenter;C)eyesassociatedwithcentralepiretinalmembrane(ERM);D)DDMEthatwasassociatedwithmacularcapillarydropout≥2disc-diameter(DD).RESULTS:GLPoutcomein35DDMEeyesafter4-24(mean,13.1±6.9)monthswasasfollows:GroupA)18eyeswith'classic'DDME.Followingoneor2(mean,1.2)GLPtreatments,best-correctedvisualacuity(BCVA)improvedby1-2Snellenlinesin44.4%(8/18)ofeyes,andworsenedby1linein11.1%(2/18).Centralmacularthickness(CMT)improvedby7%-49%(mean,26.6%)in77.8%(14/18)ofeyes.CausesofCMTworsening(n=4)werecommonlyexplainable,predominantly(n=3)associatedwithemergenceofextrafovealtraction,5-9monthspost-GLP.GroupB)GLP(s)inDDMEthatdidnotinvolvethemacularcenter(n=6)resultedinimprovedBCVAby1-2linesin2eyes.However,thecentralmaculabecameinvolvedintheedemaprocessaftertheGLPin3(50%)eyes,associatedwithanemergenceofextrafovealtractioninoneoftheseeyes4monthsfollowingtheGLP.GroupC)GLPfailedinall5eyesassociatedwithcentralERM.GroupD)GLPwasofpartialbenefitin2of6treatedeyeswithmacularcapillarydropout≥2DD.CONCLUSION:EyeswithDDMEthatinvolvedthemacularcenterwerefoundtoachievefavourableoutcomesafterGLP(s)duringmid-termfollow-up,unlesscomplicatedpre-GLPorpost-GLPbyvltreoretinalinterfaceabnormalities,oftenextrafovealtra