简介：AIM:Topresentretinalmicrostructure,metabolismandfunctionabnormalitiesinthecourseofmultipleevanescentwhitedotsyndrome(MEWDS)byHeidelbergspectralismodalityimagingplatformandobserveitsoutcomebyEDI-SD-OCTandtwowavelengthautofluorescence.METHODS:Acaseofmultipleevanescentwhitedotsyndromeina23-year-oldfemalepresentedinitiallywitha15-dayhistoryoffloatersandacentralscotomaintherighteye.Toestablishthediagnosis,multimodalityimagingwasperformed,namely,bluelight-fundusautofluorescence(BL-FAF,excitation488nm,emission>500nm),near-infraredfundusautofluorescence(NIR-FAF,excitation787nm,emission>800nm)usingaconfocalscanninglaserophthalmoscope,fundusfluoresceinangiography(FFA),indocyaninegreenangiography(ICGA),spectrum-domainenhancedepthimagingopticalcoherencetomography(SD-EDI-OCT),multifocalelectroretinography(mf-ERG)andfundusphotograghwereperformedandfollowedupattheeighthmonthafterinitiallyvisiting.RESULTS:Opticalcoherencetomography(OCT)showedatransientdisruptionofthefovealphotoreceptoroutersegmentsincorrespondencetofovealgranularity.NIR-FAFshowedhypoautofluorescentareas,≤40μminsize,mostlyconcentratedaroundtheposteriorpoleanditstemporalsidelessthanthatinBL-FAF.Mf-ERGshowpinnacledisappearedinfoveaandmaculaandresponsesdecreasedmarkedlycomparedwiththefolloweye.Attheeighthmonthfollowup,hyperfluorescenceinBL-FAFweredisappear,while,NIR-FAFHypofluorescentspotsinearlystageofsuchlesionwerereduced.ButOCTdemonstratedthestructurewasrecoveredinresidualHypofluorescentareainNIR-FAF.Thesubfovealchoroidalthicknesswasdecreasedfrom372μmto307μmslightlyandcostlinewasrecovered.CONCLUSION:MEWDSisabenignself-healingdiseaseandthereisnopathologicalevidencetoinvestigatethenaturalcourseofsuchdisease.SD-OCTallowshighlydetailedimagesapproachinghistopathologytocertifythemicrostructura

简介：AIM:Toinvestigatewhether15-Lipoxygenase-1(15-LOX-1)playsanimportantroleintheregulationofangiogenesis,inhibitinghypoxia-inducedproliferationofretinalmicrovascularendothelialcells(RMVECs)andtheunderlyingmechanism.METHODS:PrimaryRMVECswereisolatedfromtheretinasofC57/BL6JmiceandidentifiedbyanevaluationforFITC-markedCD31.ThehypoxiamodelswereestablishedwiththeBio-bagandevaluatedwithablood-gasanalyzer.ExperimentswereperformedusingRMVECstreatedwithandwithouttransferAd-15-LOX-1orAd-vectorbothunderhypoxiaandnormoxiaconditionat12,24,48,72hours.Theefficacyofthegenetransferwasassessedbyimmunofluorescencestaining.CellsproliferationwasevaluatedbytheCCK-8method.RNAandproteinexpressionsof15-LOX-1,VEGF-A,VEGFR-2,eNOsandPPAR-rwereanalyzedbyreal-timereversetranscriptionpolymerasechainreaction(RT-PCR)andWesternblot.RESULTS:RoutineevaluationforFITC-markedCD31showedthatcellswerepure.Theresultsofblood-gasanalysisshowedthatwhenthecultureswereexposedtohypoxiaformorethan2hours,thePo2was4.5to5.4Kpa.WeverifiedRMVECscouldbeinfectedwithAd-15-LOX-1orAd-vectorviaFluorescencemicroscopy.CCK-8analysisrevealedthattheproliferativecapacitiesofRMVECsinhypoxicgroupweresignificantlyhigherateachtimepointthantheywereinnormoxicgroup(P<0.05).Inahypoxiccondition,theproliferativecapacitiesofRMVECsin15-LOX-1groupweresignificantlyinhibited(P<0.05).Real-timeRT-PCRanalysisrevealedthattheexpressionsofVEGF-A,VEGF-R2andeNOsmRNAincreasedinhypoxiagroupcomparedwithnormoxiagroup(P<0.01).However,theexpressionsof15-LOX-1,PPAR-rmRNAdecreasedinhypoxiagroupcomparedwithnormoxiagroup(P<0.01).Italsoshowedthatinahypoxiccondition,theexpressionsofVEGF-A,VEGF-R2andeNOsmRNAdecreasedsignificantlyin15-LOX-1groupcomparedwithhypoxiagroup(P<0.01).However,15-LOX-1andPPAR-rmRNAincreasedsigni