简介:目的:通过对Q值调整非球面切削与标准化LASIK术后视觉质量的观察来分析Q值引导个性化切削技术的临床效果。方法:对2008-01/05等效球镜低于-12.00D的46例88眼进行非球面切削或标准化LASIK术后进行随访,按术前屈光度数将其分为A组(〈-6.00D)和B组(-6.00~-12.00D)两组,对比各组非球面切削与标准化LASIK术后1mo裸眼视力、Q值、夜间眩光、夜间视物质量及满意率(后3者采取问卷调查)。结果:A、B组内非球面切削与标准化LASIK术后裸眼视力差异无统计学意义(t=1.18,P〉0.05;t=0.62,P〉0.05);A、B组内非球面切削与标准化LASIK术后Q值差异无统计学意义(t=-0.93,P〉0.05;t=-0.372,P〉0.05);A组内非球面切削与标准化LASIK术后眩光、夜间视物质量差异无统计学意义(眩光:χ^2=2.397,P>0.05;夜间视物质量:χ2=1.263,P〉0.05);B组内非球面切削与标准化LASIK术后眩光、夜间视物质量差异有统计学意义(眩光:χ^2=10.85,P〈0.01;夜间视物质量:χ^2=10.85,P〈0.01);术后效果满意率达到98%。结论:非球面切削能明显改善-6.00D以上的术后主观视觉质量。
简介:AIM:Toassesstheeffectofmyopiaonthethicknessofretinalnervefiberlayer(RNFL)measuredby3Dopticalcoherencetomography(3D-OCT)inagroupofnonglaucomatousChinesesubjects.METHODS:Twohundredandfifty-eighteyesof258healthyChinesemyopicindividualswererecruitedandfourgroupswereclassifiedaccordingtotheirsphericalequivalent(SE):lowmyopia(n=42,-0.50
简介:目的评价不增加切口的20G标准三通道玻璃体手术治疗严重眼外伤脉络膜上腔出血的疗效。方法对2011年10月至2014年10月间我科收治的29例(29眼)严重眼外伤合并脉络膜上腔出血的病人采取玻璃体手术治疗,置灌注后,通过板层的20G玻切穿刺口引流脉络膜上腔积血,再通过此切口行玻璃体手术,处理玻血和或网膜损伤,术终眼内填充气体或硅油。结果25例患者术中脉络膜上腔出血充分引流完全复位,4例患者残留少量积血,表现为小块脉络膜隆起,注入硅油后,术后一月复查网膜复位。所有患者术后视力均有改善。结论采用不增加切口的三通道玻切的巩膜切口可以有效引流外伤性脉络膜上腔出血,达到理想疗效。
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