简介：目的：比较原发性开角型青光眼和高眼压患者及拥有健康眼球表面的正常人群的泪膜功能和印象细胞学检查的数值。方法：此前瞻性研究中纳入了原发性开角型青光眼患者11例11眼（平均年龄：62.7±6.1岁）,高眼压患者12例12眼（平均年龄：62.8±6.4岁）及健康人12例12眼（平均年龄：62.9±6.03岁）。这些患者均是最近被诊断出患有原发性开角型青光眼及高眼压,且之前未接受过抗青光眼方面的治疗。均行结膜印迹细胞学检查、泪膜破裂时间和基础泪液分泌试验。每组印迹细胞学检查的样本根据Nelson分级法分为0-3级。应用Kruskal-Wallis检验和Dunn多重比较检验进行统计分析。结果：原发性开角型青光眼患者,高眼压患者及正常人群平均基础泪液分泌值分别为10.4±1.3,10.9±1.2和11.1±1.1mm/5min,其差距没有统计学意义（P=0.33）；三组的泪膜破裂时间分别为11.2±1.1,11.3±1.1和11.8±1.2s,其差距没有统计学意义（P=0.35）。原发性开角型青光眼患者中6眼（54.5%）为0级,5眼（45.5%）为1级。高眼压患者中6眼（50%）为0级,6眼（50%）为1级,健康人中6眼（50%）为0级,6只眼（50%）为1级（P=0.97）。结论：氧化应激可能会导致青光眼,眼表疾病,泪腺功能障碍及机体杯状细胞所分泌的黏液减少。原发性开角型青光眼患者,高眼压症患者及健康人群间的印象细胞学检查数值并无显著差异。

简介：AIM:Toestablishanuntransfectedhumancornealstromal(HCS)celllineandcharacterizeitsbiocompatibilitytoacellularporcinecornealstroma(aPCS).·METHODS:PrimaryculturewasinitiatedwithapurepopulationofHCScellsinDMEM/F12media(pH7.2)containing20%fetalbovineserumandvariousnecessarygrowthfactors.Theestablishedcelllinewascharacterizedbygrowthproperty,chromosomeanalysis,tumorigenicityassay,expressionofmarkerproteinsandfunctionalproteins.Furthermore,thebiocompatibilityofHCScellswithaPCSwasexaminedthroughhistologicalandimmunocytochemistryanalysesandwithlight,electronmicroscopies.·RESULTS:HCScellsproliferatedtoconfluence2weekslaterinprimarycultureandhavebeensubculturedtopassage140sofar.AcontinuousuntransfectedHCScelllinewithapopulationdoublingtimeof41.44hoursatpassage80hasbeendetermined.Resultsofchromosomeanalysis,morphology,combinedwiththeresultsofexpressionofmarkerproteinandfunctionalproteinssuggestedthatthecellsretainedHCScellproperties.Furthermore,HCScellshavenotumorigenicity,andwithexcellentbiocompatibilitytoaPCS.·CONCLUSION:Anuntransfectedandnon-tumorigenicHCScelllinehasbeenestablished,andthecellsmaintainedpositiveexpressionofmarkerproteinsandfunctionalproteins.Thecellline,withexcellentbiocompatibilitytoaPCS,mightbeusedforinvitroreconstructionoftissue-engineeredHCS.

简介：目的研究视网膜色素上皮(retinalpigmentepithelium,RPE)细胞中端粒酶逆转录酶(telomerasereversetranscriptase,TERT)表达及其反义寡核苷酸(antisenseolgonucleotides,ASODN)对其表达和细胞增生的抑制作用,为增生性玻璃体视网膜病变(prliferativevitreoretinopathy,PVR)治疗探索基因治疗新途径.方法体外培养兔眼RPE细胞,在不同时间采用链霉亲合素-生物素化过氧化物酶复合物(strepoavidin-biotin-enzymecomplex,SABC)免疫组织化学法检测TERT的表达;不同浓度的TERTASODN和正义寡核苷酸(senseoligodeoxynucleotides,SODN)分别作用于体外培养的RPE细胞,采用免疫组织化学方法检测TERT的表达;四唑盐比色法(MTT)检测在不同浓度的TERTASODN和SODN作用下RPE细胞生长活性及其生长抑制率.结果体外培养兔眼RPE细胞可表达TERT,在5,10μmo/LASODN作用下,TERT的表达明显受抑制;TERTASODN能明显抑制RPE细胞增生活性,并呈剂量依赖性.结论TERTASODN能序列特异性地抑制RPE细胞TERT表达和增生活性.

简介：AIM:ToidentifythegeneticdefectinaChinesefamilywithbilateralprogressivechildhoodposteriorcataract.METHODS:Atwo-generationfamilywasrecruitedinthisstudy.Familyhistoryandclinicaldatawererecorded.AllreportedcandidategenesassociatedwithcongenitalposteriorcataractwerescreenedbydirectDNAsequencing.·RESULTS:Allaffectedindividualspresentedposterioropacitiesinthelens.Directsequencingofthecandidategenesshowedaheterozygousc.2668C>TvariationinEPHA2gene,whichresultedinthereplacementofargininebycysteineatcodon890(p.R890C).Thismutationwasfoundintwoaffectedindividuals,butwasnotobservedin200normalcontrols.·CONCLUSION:Wereportanovelmutation(p.R890C)intheEPHA2receptortyrosinekinasegene.ThefindingexpandsthemutationspectrumofEPHA2inassociationwithposteriorcataract.

简介：AIM:ToinvestigatetheinterferingeffectofY-27632,aROCK-Iselectiveinhibitor,onthesignaltransductionpathwayoftransforminggrowthfactor-β1(TGF-β1)inocularTenoncapsulefibroblasts(OTFS)invitro.METHODS:AfterOTFSfrompassages4to6invitrowereinducedbyTGF-β1andthentreatedbyY-27632,thechangesoftheOTFScellcycleswereanalyzedviaflowcytometry,andtheproteinsexpressionoftheα-smoothmuscularactin(α-SMA),connectivetissuegrowthfactor(CTGF),collagenIwerecalculatedbyWesternblot.AfterOTFStreatedbythedifferentconcentrationsofY-27632,theexpressionlevelsoftheα-SMA,CTGFandcollagenImRNAwereassayedbyRT-PCR.RESULTS:Y-27632hadnomarkedlyeffectontheOTFScellcycles.AftertreatedbyTGF-β1,OTFSinG1periodsignificantlyincreased.ThecellcyclesdistributionbybothTGF-β1andY-27632hadnoremarkabledifferencefromthatincontrolgroup.Y-27632significantlyinhibitedtheproteinsexpressionsofbothα-SMAandCTGF,whiletosomeextentinhibitedthatofcollagenI.TGF-β1significantlypromotedtheproteinsexpressionsofα-SMA,CTGFandcollagenI.AfterOTFStreatedbybothTGF-β1andY-27632,ofα-SMA,theproteinexpressionwassimilarwiththatincontrolgroup(P=0.066>0.05),buttheproteinexpressionofCTGForcollagenI,respectively,wassignificantlydifferentfromthatincontrolgroup(P=0.000<0.01).Thedifferencesofexpressionsoftheα-SMA,CTGFandcollagenImRNAin30,150,750μmol/LY-27632groupwerestatisticallysignificant,comparedwiththoseincontrolgroup,respectively(α-SMA,P=0.002,0.000,0.000;CTGF,P=0.014,0.002,0.001;collagenI,P=0.003,0.002,0.000).CONCLUSION:BlockingtheRho/ROCKsignalingpathwaybyusingofY-27632couldinhibitthecellularproliferationandtheexpressionofbothCTGFandα-SMAwhateverOTFSinducedbyTGF-β1ornot.Y-27632suppressedtheexpressionofcollagenImRNAwithoutinduction.

简介：AIM:Toinvestigatethelevelsofserumsolubleintercellularadhesionmolecules-1(sICAM-1)andneutrophilicexpressionofCD18inpatientswithvariousstagesofdiabeticretinopathyandtodeterminetheirdifferentexpressionpatterninthedevelopmentofdiabeticretinopathy(DR).·METHODS:LevelsofserumsICAM-1andCD18onthesurfaceofneutrophileweremeasuredin41DRpatients,theywereclassifiedinthreesubgroupsaccordingtothestageofretinopathyasdeterminedbyfund’sophthalmoscopy;10controlsubjectswerealsostudied.sICAM-1weremeasuredbyenzyme-linkedimmunosorbentassayandCD18byflowcytometry.·RESULTS:TheneutrophilicCD18expressionandserumsICAM-1levelwereallsignificantlyelevatedinalldiabeticsubgroupscomparedtocontrolsubjects(P<0.01).ThedifferencesofCD18andsICAM-1amongthediabeticsubgroupsweresignificantinCD18butnotinsICAM-1.TheprogressionofretinopathywasassociatedwithanincreasebothinCD18andinsICAM-1levelsbysimplecorrelationanalysis(β=0.74,P<0.001;β=0.38,P<0.01,respectively).ButstepwisemultipleregressionanalysisrevealedthatonlyCD18wasindependentdeterminantofretinopathy(β=1.04,P<0.01).·CONCLUSION:OurresultsconfirmthecontributionofendothelialandneutrophilicactivationinthedevelopmentofDRasindicatedbyincreasedlevelsofCD18andsICAM-1.However,adirectimplicationofCD18andICAM-1intheprogressionofDRcanbesupportedonlyintheCD18butnotICAM-1.CD18andICAM-1mayplaydifferentroleinthedevelopmentofdiabeticretinopathy.