简介：目的探讨胬肉术中完整，安全，彻底剥离角膜上的变性组织的技巧性，安全性。方法25例胬肉术中以逆向撕皮法，剥离胬肉组织，术后观察有无结膜变性组织残留及角膜上皮修复情况。结果25例眼用此方法均能完整，彻底的剥离附着在角膜上的变性组织，无残留胬肉组织，上皮修复较快。结论胬肉术中以角膜上皮全层为厚度行结膜变性组织的剥离方法简单，可行，安全性高的术式，尤其适用于初学者。

简介：AIM:ToInvestigatethegeneticfindingsandphenotypiccharacteristicsofaChinesefamilywithNorriedisease（ND）.METHODS:MoleculargeneticanalysisandclinicalexaminationswereperformedonaChinesefamilywithND.MutationsintheNorriediseasepseudoglioma（NDP）geneweredetectedbydirectsequencing.Haplotypeswereconstructedandcomparedwiththephenotypesinthefamily.Evolutionarycomparisonsandmutantopenreadingframe（ORF）predictionwerealsoundertaken.RESULTS:TwofamilymemberswithocularmanifestationswerediagnosedwithND.Nosignsofsensorineuralhearinglosswereobservedineitherpatient,whileoneofthemshowedsignsofmildmentalretardation.AnovelheterozygousmutationintheNDPgene,c.-12delAAT,wasdetectedinbothpatients.ThemutationandthemutationbearinghapiotypecosegregatedwiththeNDphenotypeinmalesandwastransmittedfromtheirmothersand/orgrandmothers（Ⅱ:2）.ThemalewithoutNDdidnotharborthemutation.Themutationoccurredatthehighlyconservednucleotides.DRFfinderpredictedthatthemutationwouldleadtotheproductionofatruncatedproteinthatlacksthefirst11N-terminalaminoacids.CONCLUSION:Anovelmutation,c.-12delAATintheNDPgene,wasidentifiedinaChinesefamilywithND.ThismutationcausedNDwithoutobvioussensorineuralhearingloss.Mentaldisorderwasfoundinonebutnottheotherpatients.Theclinicalheterogeneityinthefamilyindicatedthatothergeneticvariantsandepigeneticfactorsmayalsoplayaroleinthediseasepresentation.

简介：AIM:ToidentifythefunctionofST2andexploretheroleofIL-33/ST2signalinginregulatingthepro-allergiccytokineproductioninhumancornealepithelialcells(HCECs).METHODS:HumancornealtissuesandculturedprimaryHCECsweretreatedwithIL-33indifferentconcentrationswithoutorwithdifferentinhibitorstoevaluatetheexpression,locationandsignalingpathwaysofST2inregulatingproductionofpro-allergiccytokineandchemokine.TheexpressionofmRNAwasdeterminedbyreversetranscriptionandrealtimePCR,andproteinproductionwasmeasuredbyenzyme-linkedimmunosorbentassay(ELISA),immunohistochemicalandimmunofluorescentstaining.ST2proteinwasdetectedindonorcornealepithelium,andST2signalwasenhancedbyexposuretoIL-33.·RESULTS:IL-33significantlystimulatedproductionofpro-allergiccytokinesthymicstromallymphopoietin(TSLP)andchemokine(CCL2,CCL20,CCL22)inHCECsatbothmRNAandproteinlevels.Thesestimulatedproductionsofpro-allergicmediatorsbyIL-33wereblockedbyST2antibodyorsolubleST2protein(P<0.05).Interestingly,theIκB-αinhibitorBAY11-7082orNF-κBactivationinhibitorquinazolineblockedNF-κBp65proteinnucleartranslocation,andalsosuppressedtheproductionsofthesepro-allergiccytokinesandchemokineinducedbyIL-33.CONCLUSION:ThesefindingsdemonstratethatIL-33/ST2signalingplaysanimportantroleinregulatingIL-33inducedpro-allergicresponses.IL-33andST2couldbecomenovelmoleculartargetsfortheinterventionofallergicdiseasesinocularsurface.

简介：AIM:ToinvestigatetheexpressionsoftypeIcollagen,α2integrinandβ1integrinintheposteriorscleraofguineapigswithdefocusmyopiaandwhetherbasicfibroblastgrowthfactor(bFGF)injectioninhibitstheformationanddevelopmentofmyopiabyupregulatingtheexpressionoftypeIcollagen,α2integrinandβ1integrin.METHODS:After14daysoftreatment,therefractivestateandaxiallengthweremeasuredandthelevelsoftypeIcollagen,α2integrinandβ1integrinwereassayedintheposteriorscleraeofgroupsofguineapigsthatworeamonocular-7Dpolymethylmethacrylate(PMMA)lensorhad-7DlenswearfollowedbytheperibulbarinjectionofPhosphateBufferSolution(PBS)orbFGF.Theuntreatedfelloweyeservedasacontrol.Guineapigswithnotreatmentservedasnormalgroup.·RESULTS:Theresultsshowedthat14daysofmonoculardefocusincreasedaxialeyelengthandrefraction,whilebFGFdeliveryinhibitedthemmarkedly.Further,itwasalsofoundthatthemonocular-7DlenscoulddecreasethelevelsoftypeIcollagen,α2integrinandβ1integrinexpressions,while,unlikePBS,bFGFincreasedthemsignificantlyincomparisontocontralateralcontroleyesandnormaleyes.CONCLUSION:bFGFcanpreventtheformationanddevelopmentofdefocusmyopiabyupregulatingtheexpressionsoftypeIcollagen,α2integrinandβ1integrin.Takentogether,ourresultsdemonstratethatbFGFpromotesscleraremodelingtopreventmyopiainguineapigs.

简介：AIM:Toevaluatetheaccuracyofsphericalequivalent(SE)estimatesofadouble-passsystemandtocompareitwithretinoscopy,subjectiverefractionandatablemountedautorefractor.METHODS:Non-cycloplegicrefractionwasperformedon125eyesof65healthyadults(age23.5±3.0years)fromOctober2010toJanuary2011usingretinoscopy,subjectiverefraction,autorefraction(AutokeratorefractometerTOPCONKR-8100,Japan)andadoublepasssystem(OpticalQualityAnalysisSystem,OQAS,VisiometricsS.L.,Spain).Nineconsecutivemeasurementswiththedouble-passsystemwereperformedonasubgroupof22eyestoassessrepeatability.ToevaluatethetruenessoftheOQASinstrument,theSElaboratorybiasbetweenthedoublepasssystemandtheothertechniqueswascalculated.RESULTS:TheSEmeancoefficientofrepeatabilityobtainedwas0.22D.SignificantcorrelationscouldbeestablishedbetweentheOQASandtheSEobtainedwithretinoscopy(r=0.956,P<0.001),subjectiverefraction(r=0.955,P<0.001)andautorefraction(r=0.957,P<0.001).ThedifferencesinSEbetweenthedouble-passsystemandtheothertechniquesweresignificant(P<0.001),butlackedclinicalrelevanceexceptforretinoscopy;Retinoscopygavemorehyperopicvaluesthanthedouble-passsystem-0.51±0.50Daswellasthesubjectiverefraction-0.23±0.50D;Moremyopicvalueswereachievedbymeansofautorefraction0.24±0.49D.CONCLUSION:Thedouble-passsystemprovidesaccurateandreliableestimatesoftheSEthatcanbeusedforclinicalstudies.Thistechniquecandeterminethecorrectfocuspositiontoassesstheocularopticalquality.However,ithasarelativelysmallmeasuringrangeincomparisonwithautorefractors(-8.00to+5.00D),andrequirespriorinformationontherefractivestateofthepatient.

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:ToInvestigatetheeffectsoftransforminggrowthfactorβ2(TGF-β2)andconnectivetissuegrowthfactor(CTGF)ontransdifferentiationofhumanlensepithelialcells(HLECs)culturedinvitroandsynthesisofextracellularmatrix(ECM).METHODS:HLECsweretreatedwithTGF-β2(0,0.5,1.0,5,10μg/L)andCTGF(0,15,30,60,100μg/L)fordifferenttimes(0,24,48,72h)invitroandtheexpressionofα-smoothmuscleactin(α-SMA),themaincomponentoftheextracellularmatrixtypeⅠcollagen(Col-1)andfibronectin(Fn)weremeasuredbyusingreal-timepolymerasechainreaction(PCR)andwestern-blot.RESULTS:TGF-β2andCTGFsignificantlyincreasedexpressionofα-SMAmRNAandprotein(P<0.05,P<0.001),FnmRNAandprotein(P<0.001),Col-1mRNAandprotein(P<0.001).TGF-β2couldinduceHLECsexpressionofCTGFmRNAandproteinindosedependentmanner(P<0.05,P<0.001).TGF-β2andCTGFcouldinduceHLECstoexpressα-SMA,FnandCol-1intime-dependentmanner.EachtimeofTGF-β2andCTGFinducedHELCsexpressionofα-SMA,Fn,Col-1mRNAandproteinwassignificantincreasecomparedwithcontrol(P<0.05,P<0.001).CONCLUSION:TGF-β2andCTGFcouldinduceHLECsepithelialmesenchymaltransitionandECMsynthesis.