简介：Simulationcanbedefinedasmalingering,orsometimesfunctionalvisualloss(FVL).Itmanifestsaseithersimulatinganophthalmicdisease(positivesimulation),ordenialofophthalmicdisease(negativesimulation).Consciousbehaviorandcompensationorindemnityclaimsareprominentfeaturesofsimulation.Sincesomeauthorssuggestthatthisisamanifestationofunderlyingpsychopathology,evenconversionisincludedinthiscontext.Intoday’sworld,everyophthalmologistcanfacewithsimulationofophthalmicdiseaseordisorder.Incaseofsimulationsuspect,thephysician’sresponsibilityistoprovethesimulationconsideringthedisease/disorderfirst,andsimulationasanexclusion.Insimulationexaminations,thephysicianshouldbefirmandsmarttoselectappropriatetest(s)toconvincenotonlythesubject,butalsothejudgeincaseofindemnityorcompensationtrials.Almostallophthalmicsensoryandmotorfunctionsincludingvisualacuity,visualfield,colorvisionandnightvisioncanbethesubjectofsimulation.Examinermustbeskillfulinselectingthemostappropriatetest.Apartfromthoseintheliterature,weincludedallkindsofsimulationinophthalmology.Inaddition,simulationexaminationtechniques,suchas,useofOCT(opticalcoherencetomography),frequencydoublingperimetry(FDP),andmodifiedpolarizationtestswerealsoincluded.Inthisreview,wemadeathoroughliteraturesearch,andaddedourexperiencestogivethereadersup-to-dateinformationonmalingeringorsimulationinophthalmology.

简介：90D裂隙灯显微镜前置镜是双凸透镜（图1），检查时是利用裂隙灯较强光源，检查时所获的眼底图像立体感好，可以很清楚地显示视盘小凹，血管变异，黄斑裂孔或囊肿，视网膜裂孔，眼内占位等病变，并且由于检查过程中不接触角膜，

简介：AIM:Toassesstheeffectofmyopiaonthethicknessofretinalnervefiberlayer(RNFL)measuredby3Dopticalcoherencetomography(3D-OCT)inagroupofnonglaucomatousChinesesubjects.METHODS:Twohundredandfifty-eighteyesof258healthyChinesemyopicindividualswererecruitedandfourgroupswereclassifiedaccordingtotheirsphericalequivalent(SE):lowmyopia(n=42,-0.50D),moderatemyopia(n=120,-3.0D≤SE<-6.0D),highmyopia(n=58,-6.0D≤SE<-8.0D)andextremehighmyopia(n=38,SE≥-8.0D).TheRNFLthicknessprofileincludingsuperior,nasal,inferiorandtemporalquadrantandeachofthe12clock-hourthicknessesweremeasuredby3DOCT.TheRNFLthicknessesamongfoursamplegroupswereperformedbyone-wayanalysisofvariance(onewayANOVA)andleastsignificantdifferencetest(LSDtest).CorrelationsbetweenRNFLthicknessandaxiallength/sphericalequivalentwereperformedbylinearregressionanalysis.RESULTS:TheoverallRNFLparametersshownsignificantdifferencesbetweengroupsexcluding7,9,10,11o’clockhourthickness.TheRNFLthicknessofsuperior,nasal,inferior,averageand1,2,3,4,5,6,12o’clocksectorsweredecreasedwiththeincreasingaxiallengthandhigherdegreeofmyopia.Incontrast,asaxiallengthandthedegreeofmyopiaincreased,thetemporaland8,9o’clocksectorsthicknesseswereincreased.Aconsiderableproportionofmyopiceyeswereclassifiedasoutsidethenormallimits.Sixo’clockwasthemostnotableofthetotal,which43.4%wereoutsidethenormallimits.CONCLUSION:OnthemeasurementofRNFL,thecharacteristicsofRNFLwiththechangeofthedegreeofmyopiawereobserved.Asthedegreeofmyopiaincreases,theRNFLthicknessmeasuredby3D-OCTincludingtheaverageandsuperior,nasal,inferiorsectorsdecreases.AndduetothechangeofRNFLthickness,itshouldbeconsideredwhenusingOCTtoaccessforthedamageofglaucomaespeciallypeoplewithmyopia.

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