简介：AIM:Toadaptthelowvision-relatedqualityoflife(LVQOL)instrumentintoTurkishlanguageandtoassessitsvalidityandreliability.METHODS:Thestudywasconductedin387patientsattendingtheCentreofLowVisionRehabilitation,FacultyofMedicine,AnkaraUniversity.Forstatisticalanalyses,theSpearman’scorrelationcoefficient,Cronbach’salphacoefficientandConfirmatoryFactorAnalysis(CFA)wereused.RESULTS:AccordingtoresultsofCFA,theiteminthe'Adjustment'subscalebecauseofhavingthefactorloadingbelow0.40,wasexcludedfromthequestionnaire.ThereliabilityofthequestionnairewasassessedaccordingtoCronbach’salphacoefficients.Thereliabilityofthe'DistanceVision,Mobility,andLighting'subscalewas?琢=0.863;ofthe'Adjustment'subscalewas?琢=0.694;'ReadingandFineWork'was?琢=0.791,and'ActivitiesofDailyLiving'was?琢=0.770.Sotheseresultsindicatethatthequestionnaireisreliabletomeasurethevisionrelatedqualityoflifeoflow-visionpatients.Thecorrelationsbetweenthesubscaleswerealsoanalyzed,andthecorrelationbetween'Adjustment'and'ReadingandFineWork'wasfoundtobethelowest(rs=0.336,P<0.001),whereasthestrongestcorrelationwasfoundbetweenthe'ReadingandFineWork',and'ActivitiesofDailyLiving'.Additionally,the'Adjustment'dimensionshowedthestrongestcorrelationwithonly'DistanceVision,Mobility,andLighting'dimension.CONCLUSION:Afterremovingthelastitemintheseconddimension,theTurkishadaptationofalldimensionsoftheLVQOLhasbeenshowntobereliable,validandsuitableforuseinpatientswithlowvisioninTurkey.

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: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: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.

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