简介：目的分析评价眼科激光对视网膜静脉阻塞的疗效。方法对32例经眼底荧光血管照影明确诊断的视网膜静脉阻塞的患者采用光凝治疗，治疗后预约定期随诊，并复查各项检查。结果治疗后视力增加17例，不变者10例，稍下降者5例，黄斑水肿明显减轻者21例，占65．62％；不变者5例，占15．62％；消失者6例，占18．75％，激光治疗后较激光治疗前的暗点数增加者20例，占60％，暗点数减少5例，占15．62％，不变者7例，占21．87％。并发症：激光治疗前有新生血管者5例，术后2例完全退缩。结论视网膜静脉阻塞早期行激光治疗可促进出血吸收，缩短病程，降低新生血管及玻璃体病变等并发症，是切实可行的治疗方法。

简介：目的分析剥脱综合征（ES）患者和正常人眼轴及中央前房深度与眼压的相关性。方法2010年1月～2012年1月间来本院就诊的Es患者106例（106眼）、正常人69例（69眼），均为维吾尔族。观察Es眼和非ES眼眼轴长度、中央前房深度及眼压有无差异，分析眼轴及中央前房深度与眼压的相关性。结果ES患者眼轴长度为（22．89±0．91）mm，正常人眼轴长度为（23．12±0．97）mm，差异无统计学意义（P=0．12）；ES患者前房深度为（2．84±0．41）mm，正常人前房深度为（2．93±0．39）mm，差异无统计学意义（P=0．14）；ES患者眼压为（26．72±15．70）mmHg（1mmHg=0．133kPa），正常人眼压为（14．39±2．19）mmHg，差异有统计学意义（P=0．00）。Es患者眼轴与眼压具有相关性（r=-0．412，P=0．00）；正常人眼轴与眼压不具有相关性（r=-0．102，P=0．405）。ES患者中央前房深度与眼压具有相关性（r=-0．33，P=0．001）；正常人中央前房深度与眼压不具有相关性（r=-0．102，P=0．406）。结论维吾尔族ES患者的眼压较正常人高，其眼轴及中央前房深度与眼压具有负相关性。（中国眼耳鼻喉科杂志，2013，13：170—172）

简介：目的探讨单纯泪道探通术与泪道探通联合洛美沙星凝胶治疗婴幼儿泪道阻塞的不同效果.方法将100例泪道阻塞患儿按来院顺序随机分成A组与B组各50例,A组行泪道探通联合洛美沙星凝胶治疗,B组行单纯泪道探通术.比较2组疗效.结果2组患儿实施治疗后差异显著（p＜0.05）,泪道探通联合洛美沙星凝胶治疗优于单纯泪道探通术.结论泪道探通联合洛美沙星凝胶填充治疗婴幼儿泪道阻塞能保持泪道正常生理结构,更好的巩固探通后的效果,防止细菌再生,降低二次阻塞的发生,值得推广.

简介：AIM:ToinvestigatetheeffectofY-27632onthesurvivalandneuriteoutgrowthoftheculturedretinalneurocytes.METHODS:Afterthepostnatalday2-3,Sprague-Dawleyretinalneurocyteswereculturedfor48hours,theculturemediawasreplacedwithserum-freemedia(controlgroup)andserum-freemediacontained30μmol/LY-27632(Y-27632group),andthecellswerecontinuallyculturedanother48hours.Theculturedretinalneurocyteswereidentifiedwithanti-neuronspecificenolase(NSE)immunocytochemistry.ThesurvivalstateofthosecellswasestimatedbyMTTassay,andtheneuriteoutgrowthofthosecellswasevaluatedbythecomputerizedimage-analysissystem.RESULTS:Comparedwiththecontrolgroup,theabsorbancevaluesofcellssurvivalinY-27632groupincreased12.90%and33.33%respectivelyafter72and96hoursculture.Y-27632hadnosignificanteffectonthediameterofculturedretinalneurocytes.Comparedwiththecontrolgroup,Y-27632inducedastableimprovementofneuriteoutgrowthofretinalneurocytesafter72and96hoursculture(P=0.001).CONCLUSION:Y-27632couldpromotethesurvivalandneuriteoutgrowthoftheearlypostnatalculturedretinalneurocytes.

简介：AIM:ExcessivedissolveofcornealtissueinducedbyMMPswhichwereactivatedbycytokinsandchemokineswillleadtocornealulcer.ThemolecularmechanismofLipoxinA4(LXA4)oncornealcollagendegradationinthreedimensionswasinvestigated.·METHODS:Rabbitcornealfibroblastswereharvestedandsuspendedinserum-freeMEM.TypeIcollagen,DMEM,collagenreconstitutionbufferandcornealfibroblastsuspensionweremixedonice.Theresultantmixturesolidifiedinanincubator,afterwhichtestreagentsandplasminogenwasoverlaidandthecultureswerereturnedtotheincubator.Thesupernatantsfromcollagengelincubationswerecollectedandtheamountofhydroxyprolineinthehydrolysatewasmeasured.ImmunoblotanalysisofMMP-1,-3andTMMP-1,-2wasperformed.MMP-2,-9wasdetectedbythemethodofGelatinzymography.Cytotoxicityassaywasmeasured.RESULTS:LXA4inhibitedcornealcollagendegradationinadoseandtimemanner.LXA4inhibitedtheIL-1βinducedincreasesinthepro-MMP-1,-2,-3,-9andactiveMMP-1,-2,-3,-9inaconcentrationdependentmanner.LXA4alsoinhibitedtheIL-1βinducedincreasesinTIMP-1,-2.CONCLUSION:Asapotentanti-inflammationreagent,LXA4caninhibitcornealcollagendegradationinducedbyIL-1βincornealfibroblaststhusinhibitingcornealdissolvingpathologyprocess.

简介：Thekeratoprosthesis(KPro;artificialcornea)isaspecialrefractivedevicetoreplacehumancorneabyusingheterogeneousformingmaterialsfortheimplantationintothedamagedeyesinordertoobtainacertainvision.Themainproblemsofartificialcorneaarethebiocompatibilityandstabilityofthetissueparticularlyinpenetratingkeratoplasty.Thecurrentstudiesoftissue-engineeredscaffoldmaterialsthroughcomprisingcompositesofnaturalandsyntheticbiopolymerstogetherhavedevelopedanewwaytoartificialcornea.Althoughawideagreementthatthelong-termstabilityofthesedeviceswouldbegreatlyimprovedbythepresenceofcorneacells,modificationofkeratoprosthesistosupportcorneacellsremainselusive.Mostofthestudiesoncornealsubstratematerialsandsurfacemodificationofcompositeshavetriedtoimprovethegrowthandbiocompatibilityofcorneacellswhichcannotonlyreducethestimulusofheterogeneousmaterials,butalsomoreimportantlycontinuousandstablecorneacellscanpreventthedestructionofcollagenase.Thenecrosisofstromaandspontaneousextrusionofthedevice,allowformaintenanceofaprecornealtearlayer,andplaytheroleofensuringagoodopticalsurfaceandresistingbacterialinfection.Asaresult,improvementincornealcellshasbeenthemainaimofseveralrecentinvestigations;someefforthasfocusedonbiomaterialforitswellbiologicalpropertiessuchaspromotingthegrowthofcorneacells.Thepurposeofthisreviewistosummarythegrowthstatusofthecornealcellsaftertheimplantationofseveralartificialcorneas.

简介：AIM:Todeterminethehistopathologicalchangesofrifampicinappliedintravitreallyonretinalganglioncellsbymeansofstereologicalandhistopathologicalmethods.METHODS:Forthisstudytwenty-fourNewZealandadultrabbitsweredividedintofourgroups(n=6foreachgroup).50μg/0.1mL(group1),100μg/0.1mL(group2),150μg/0.1mL(group3)and200μg/0.1mL(group4),rifampicinwereinjectedintothevitreousoftherighteyesofanimals,theirlefteyeswereusedascontrol(group5).Afterthe28thdayofapplication,animalswereanesthetisedwithxylazine(8mg/kg,IM)andthentheireyeswereenucleatedimmediately.Patternsweretakenawayandeyeswerepreparedforbothstereologicalandelectromicroscopicobservation.RESULTS:Dependingonthehighdoseofrifampicin,somehistopathologicalchangessuchascytoplasmicdilatationanddamagedmembranewereobservedontheelectromicroscopiclevel.Usingquantitativeexamination,whichwasdoneatthelightmicroscopiclevel,itwasshownthatthenumberofneuronsdecreasedlinearlyasrifampicindoseincreasedwhencomparedwiththecontrolgroup.CONCLUSION:Basedonthesefindings,low-doserifampicin(50μg/0.1mL)maybeusefulfortreatmentoftheoculardiseases.

简介：AIM:Toevaluatetheeffectofbrinzolamide-timololfixedcombinationonintraocularpressure(IOP)aftercataractsurgery.METHODS:Thestudyincluded92eyesof87patientswhounderwentcataractsurgeryandintraocularlensimplantation.Patientsscheduledforphacoemulsificationwereassignedto1of2groups.Thetreatmentgroupreceived1dropofbrinzolamide-timololfixedcombinationimmediatelyaftersurgery,andthecontrolgroupreceivednotreatment.TheIOPwasmeasuredpreoperativelyandat2hand24hpostoperatively.RESULTS:ThemeanIOPchangewaslowerinthetreatmentgroupthaninthecontrolgroupat2hpostoperatively.ThedifferencebetweenthemeanIOPvaluesofthetwogroupsat2hpostoperativelywasfoundtobestatisticallysignificant.Twenty-fourhoursafterthesurgery,themeanIOPchangewasstillhigherinthecontrolgroupwhencomparedtothetreatmentgroup.CONCLUSION:ThefixedcombinationbrinzolamidetimololcaneffectivelyreduceIOPaftercataractsurgery.

简介：AIM:ToinvestigatetheeffectofintravitrealinjectionofDL-alpha-aminoadipicacid(DL-α-AAA)onocularrefractivestateandretinaldopamine,transforminggrowthfactor-β2(TGFβ2),vasoactiveintestinalpolypeptide(VIP)inguineapigform-deprivedmyopia.METHODS:Four-week-oldpigmentedguineapigswererandomlyassignedto4groups:normalcontrol,deprivation,deprivationplusDL-α-AAA,deprivationplussaline.Formdeprivationwasinducedwiththeself-madetranslucenteyeshields,andlastedfor14days.8μgDL-α-AAAwasinjectedintothevitreouschamberofdeprivedeyes.Thecornealradiusofcurvature,refractionandaxiallengthweremeasured.Retinaldopaminecontentwasevaluatedbythehigh-performanceliquidchromatographywithelectrochemicaldetection,andTGFβ2andVIPproteinweredetectedbyWesternblotting.RESULTS:Fourteendaysofeyeocclusioncausedtheaxiallengthtoelongateandbecomemyopicintheform-deprivedeyes,withthedecreaseofretinaldopamineandtheincreaseofTGFβ2andvasoactiveintestinalpolypeptide(VIP)protein.IntravitrealinjectionofDL-α-AAAcouldinhibitthemyopicshiftfrom(-3.65±1.06)Dto(-1.48±0.63)D,P<0.01duetogogglesoccludingandcausethedecreaseofretinalTGFβ2proteininthedeprivedeyes.However,intravitrealinjectionofDL-α-AAAhadnosignificanteffectonretinaldopamineandVIPproteinindeprivedeyes.RetinalTGFβ2proteincorrelatedhighlywiththeocularrefraction(y=-3.34+0.31/x,F=74.75,P<0.001)andaxiallength(y=8.39-0.02/x,F=48.32,P<0.001)indifferenttreatmentgroups.·CONCLUSION:IntravitrealinjectionofDL-α-AAAiseffectivelyabletosuppressthedevelopmentofformdeprivationmyopia,whichmaybeassociatedwithretinalTGFβ2proteininguineapigs.

简介：AIM:TodiscusstheimpactofLyciumBarbarumPolysaccharide(LBP)andDanshensupurifiedfromTraditionalChineseMedicine(TCM)onvascularendothelialgrowthfactor(VEGF)ofrabbitswithretinalneovascularization.METHODS:Fortyrabbitsweredividedintonormalcontrolgroup,modelcontrolgroup,LBPgroupandDanshensugroup.Animalsinthenormalcontrolgroupwerefedinthenormaloxygenenvironment.Animalsintheotherthreegroupswereputintotheenvironmentwith70%oxygenfor5daysinordertobuildthemodelofoxygen-inducedvascularproliferationretinopathy.AndthendifferentTCMextractwasinjectedintotheabdominalcavitiesoftheseannimals.After7days,theVEGFcontentofintheserumofrabbitwasmeasuredbydoubleantibodysandwichmethod.RESULTS:DataanalysisindicatedthatVEGFcontentwasasfollows:Danshensugroupwaslowerthanmodelcontrolgroup(12.92±3.84ng/Lvs19.32±4.15ng/L,P<0.05);LBPgroupandnormalcontrolgroupwerelowerthanmodelcontrolgroup(12.92±3.84ng/L,9.26±1.61ng/Lvs19.32±4.15ng/L,P<0.01);totalbloodviscosity,plasmaviscosity,cholesterolcontent,fibrinogencontentandtriacylglycerolcontentafterperitonealinjectionofLBPandDanshensuwereobviouslylowerthanbeforeinjection.CONCLUSION:TCMextract-LBPandDanshensucanprominentlyreducethecontentofVEGFintheprocessofvascularproliferativeretinopathyofrabbit;canpreventtheoccurrenceofretinalmicrovasculardiseasebyimprovingpartialoxygen-deficientenvironmentoraffectingallkindsofnewgrowthfactor.

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