简介：AIM:Tocomparetheregularityandaccuracyoflaserinsitukeratomileusis(LASIK)flapscreatedbytheZiemerFEMTOLDV'Classic'(Ziemer'Classic')andZiemerFEMTOLDVCrystalLinefemtosecondlaser(ZiemerCrystalLine).METHODS:Fourier-domainopticalcoherencetomography(RTVueOCT)wasusedtomeasurethemorphologyof200LASIKflapsof100consecutivepatientscreatedwiththeZiemerClassic(100flaps)ortheZiemerCrystalLine(100flaps)atoneweekpostoperatively.Flapthicknesswasevaluatedat36specifiedmeasurementpointsoneachflap.Forallprocedureswithbothlasers,thenominalflapthicknesswas110μm.RESULTS:ThemeanflapthicknessoftheZiemerCrystalLinegroup(102.49±2.68μm)wasthinnerthanthatoftheZiemerClassicgroup(107.65±5.09μm)(P<0.01).Averagethicknessofallflapswasuniformwithin4μmatallmeasurementpoints.TheflapsintheZiemerCrystalLinegroupweremoreregularthanthoseintheZiemerClassicgroupwhenmeasuredfromthecentertotheperiphery.Themaximumdeviationfromthenominal110μmof36measurementswas8μmintheZiemerClassicgroup,whileintheZiemerCrystalLinegroupitwas9μm.Withinthe3600measurementsonthe100eyes,differencesgreaterthan20μmwereobserved0.14%intheZiemerClassicgroup,and0.04%intheZiemerCrystalLinegroup.CONCLUSION:TheflapscreatedwiththeZiemerFEMTOLDVCrystalLinefemtosecondlaseraremoreuniformandthinnerthanthosecreatedbytheZiemerFEMTOLDVClassicfemtosecondlaser.

简介：目的：观察多西环素对碱烧伤大鼠角膜炎症细胞浸润的抑制作用。方法：健康SD大鼠32只，随机分为对照组、多西环素组，每组16只大鼠。建立角膜碱烧伤模型后，多西环素组予3g／L多西环素眼液点眼，对照组予眼液溶媒点眼。分别于碱烧伤后第3，7，14，21d观察计算炎症指数，角膜取材后进行病理切片及炎症细胞计数，行ICAM-1的ELISA检测。结果：多西环素组各时间点结膜充血、角膜水肿较对照组轻，炎症指数均明显低于对照组，差异有统计学意义（P〈0．05）。多西环素组各时间点炎症细胞计数少于对照组（P〈0．05）。多西环素组各时间点大鼠角膜的ICAM-1表达低于对照组（P〈0．05）。结论：多西环素可以抑制碱烧伤大鼠角膜的炎症细胞浸润，其机制可能是抑制ICAM-1的表达。

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