简介：AIMTo与rhegmatogenous在病人评估错过的网膜的裂缝(MRB)和以后的玻璃的分开(PVD)的原因和协会经历vitreo的病人的网膜的分开(RRD).METHODSCase表为在一个第三级的眼睛照顾中心的RRD的网膜的外科回顾地被评估。从屏蔽的378个记录，253为MRB的分析被包括，191个病人为PVD的分析被包括，取决于包括标准。在检查上注意的RRD和网膜的裂缝的特征与为可能的associations.RESULTSOverall在外科期间检测的MRB和PVD的地位相比，27%病人有MRB。当错过的网膜的眼泪与完全的PVD的存在被联系时，网膜的洞通常与格子退化在病人被错过。为奔流外科操作的病人显著地与错过是的一个网膜的裂缝的机会与MRB(P=0.033)被联系1.91作为与有自然透镜的病人相比。先进proliferativevitreoretinopathy(PVR)和网膜的bullae是为在检查期间错过一个网膜的裂缝的最普通的原因。PVD在52%盒子中是在场的并且错误地在16%被估计。网膜的bullae，pseudophakia/aphakia，近视，和马鞋网膜的眼泪强烈与PVD的存在被联系。创伤的RRD很少与网膜的bullae与PVD.CONCLUSIONPseudophakic病人，和病人被联系或先进PVR应该小心地为MRB被屏蔽。尽管Weiss戒指是PVD的好指示物，它可能仍然完了在一些情况中诊断了。PVD与网膜的bullae和pseudophakia被联系，并且相反地与创伤的RRD。

简介：AbstractClinical ophthalmologists consider each retinal disease as a completely unique entity. However, various retinal diseases, such as uveitis, age-related macular degeneration, diabetic retinopathy, and primary open-angle glaucoma, share a number of common pathogenetic pathways. Whether a retinal disease initiates from direct injury to the blood-retinal barrier (BRB) or a defect/injury to retinal neurons or glia that impairs the BRB secondarily, the BRB is a pivotal point in determining the prognosis as self-limiting and recovering, or developing and progressing to a clinical phenotype. The present review summarizes our current knowledge on the physiology and cellular and molecular pathology of the BRB, which underlies its pivotal role in the initiation and development of common retinal diseases.

简介：Purpose:Toinvestigatewhetherthemixedbeta-blocker,metipranolol,possessescalciumandsodiumchannelblockingactivitiesandbluntstheeffectsofretinalischaemiaasreportedforthebetal-antagonist,betaxolol(Expt.EyeResearch1999,69,331-342).Methods:RatretinasorratbrainsynaptosomeswereexposedtoradioactivecalciumorsodiumandNM-

简介：Paediatricretinaldetachment(PRD)isanuncommonandchallengingdisease;itdiffersfromadultdetachmentsinetiology,anatomicalcharacteristics,managementandprognosis.PRDscanbeparticularlychallenging,evenforthemostexpertpaediatricsurgeonsduetothehigherprevalenceoftotalretinaldetachments,latediagnosisandbilateralinvolvementwithrespecttothosewhichoccurinadulthood.Moreover,theanatomicalsuccess,whenachieved,isfrequentlynotrelatedtoafunctionalrecover.Postsurgicaladverseevents,refractiveerrorsandamblyopiamayadditionallyunderminethefinaloutcome.Uptodatetherearefewreviewsregardingtheapproachofretinaldetachmentinchildren,mainlydealingwithrhegmatogenousretinaldetachment.Inthisreview,rhegmatogenous,retinopathyofprematurityrelatedandCoats'-relatedPRDswereconsidered.Theavailableliteraturefromthelastdecadeswerereviewedandsummarized.Epidemiology,etiologyandclinicalpresentation,togetherwiththerapeuticapproachesandoutcomeshavebeenreviewedanddiscussed.

简介：AIM:ToinvestigatetheroleofBrn-3bindifferentiationprocessofstemcellsderivedfromretinalMiillercellsintotheganglioncell.METHODS:ThepassageculturemethodofMiillercellsfromretinaofnewbornSpragueDawleyratswascarriedoutbyrepeatedincompletepancreaticenzymedigestionmethod.Thecellsweredetectedbyfluorescenceactivatedcellsorter(FACS),immunohistochemistrytechnologyandreversetranscription-polymerasechainreaction(RT-PCR)todeterminethepurity.Thethirdpassageofcellswasinducedintheserum-freededifferentiationmedium.TheexpressionofthespecificmarkersKi-67andnestinofretinalstemcellswasmeasuredbyRT-PCRandWesternblot.Thecellproliferationofretinalstemcellswasdetectedby5-Ethynyl-2’-deoxyuridine(Edu)staining.Thecellswererandomlydividedinto5groupsasfollows:groupA:Brn-3bsiRNAgroup;groupB:Brn-3bcontrolsiRNAgroup;groupC:pGC-Brn-3b-greenfluorescentprotein(GFP)group;groupD:pGC-GFPgroup;groupE:controlgroup(withoutanyhandling).ThepurifiedMullercellswereculturedfor3-7d,then,thepercentageofganglioncellswascountedbyimmunofluorescencestaining.RESULTS:FACSdemonstratedthepurityofretinalMullercellswasmore97.44%.Afewsphericalcellspheresappeared.Immunofluorescencestainingshowedthatstemcellswithinthesphereswerepositiveforretinalstemcell-specificmarkersnestin(redfluorescence,92.94%±6.48%)andKi-67(greenfluorescence,85.96%±6.04%).Meanwhile,RT-PCRanalysisshowedcellspheresintheculturetohaveexpressedabatteryoftranscriptscharacteristicofstemcellssuchasnestinandKi-67,whichwereabsentintheMullercells.WesternblotanalysisfurtherconfirmedtheexpressionofnestinandKi-67inthecellspheresbutnotintheMullercells.Edustainingshowedmostofthenucleiwithinthecellsphereswerestainedred(82.80%±6.65%),suggestingthenewcellsphereshadthecapacityforeffectiveproliferation.ThestatisticsresultshowedthedifferencebetweenBrn-3bsiRNAgroupand

简介：AIMTo探索在网膜的血容器的氧浸透怎么在ischemic和non-ischemic分支被改变网膜的静脉吸藏(BRVO).METHODSFiftyBRVO眼睛被划分成ischemic(n=26)和non-ischemic(n=24)组，基于宫底荧光黄angiography。健康个人(n=52和n=48，分别地)也为二个组作为控制被招募。堵塞容器和中央容器的吝啬的氧浸透被oximetry在BRVO和控制groups.RESULTSIn测量ischemicBRVO组，堵塞小动脉氧浸透(SaO2-一，106.0%±；14.3%)，而不是堵塞小静脉氧浸透(SaO2-V,60.8%±；9.4%)，看了增加什么时候与那些相比在一样的象限容器(SaO2-A,86.1%±；16.5%)在contralateral眼睛(P<；0.05)。中央容器的氧浸透堵塞容器与那些显示出类似的趋势。在non-ischemicBRVO组，堵塞，中央SaO2-V和SaO2-A没显示出重要变化。在ischemic和non-ischemicBRVO，当时，中央SaO2-A显著地被增加与健康individuals.CONCLUSIONObvious变化在相比堵塞，中央SaO2-A在ischemicBRVO组被发现，显示在小动脉的氧新陈代谢的混乱可以参予ischemicBRVO的致病。

简介：网膜的退化疾病可以导致外部视网膜并且接着的退化，盲目。但由于内部视网膜的维护，编码并且处理视觉神经原回答仍然能自然地被执行。因此，一台有效网膜的修复术设备可以被mimicking开发外部视网膜的功能：把视觉光变成人工的刺激并且把刺激送到试图唤起神经回答的视网膜。作为为当前的网膜的修复术的二个主要发展中方向，epiretinal(嗯)并且subretinal(SR)修复术两个都正在经历试验性的舞台并且拥有优点和限制。在电源供应的进一步的调查，biocompatibility，仍然要求的etc.are。另外，尽管他们不是足够成熟的也商业地被使用，suprachoroidaltransretinal刺激(圣)和在网膜的修复术的一些另外的选择也被看作有希望的导致neurotransmitter的刺激研究方向。

简介：Severalfeaturesofretinalvesselscanbeusedtomonitortheprogressionofdiseases.Changesinvascularstructures,forexample,vesselcaliber,branchingangle,andtortuosity,areportentsofmanydiseasessuchasdiabeticretinopathyandarterialhypertension.Thispaperproposesanautomaticretinalvesselsegmentationmethodbasedonmorphologicalclosingandmulti-scalelinedetection.First,anilluminationcorrectionisperformedonthegreenbandretinalimage.Next,themorphologicalclosingandsubtractionprocessingareappliedtoobtainthecruderetinalvesselimage.Then,themulti-scalelinedetectionisusedtofinethevesselimage.Finally,thebinaryvasculatureisextractedbytheOtsualgorithm.Inthispaper,forimprovingthedrawbacksofmulti-scalelinedetection,onlythelinedetectorsat4scalesareused.Theexperimentalresultsshowthattheaccuracyis0.939forDRIVE(digitalretinalimagesforvesselextraction)retinaldatabase,whichismuchbetterthanothermethods.

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简介：DearEditor,Retinalarterialmacroaneurysm(RAM),whichusuallyoccurswithinthefirstthreeordersofarterialbifurcation,isacquiredfusiformorsacculardilatationsofretinalarterioles~([1-2]).Aging,thefemalegender,andsystemicvascularpa-

简介：<正>DearEditor,Wepresentacaseof'Rhegmatogenousretinaldetachmentfollowingelectricalshockinjury'forevaluationforpublicationinyourjournal.Toourknowledge,thisisthefirstcaseofretinaltearsandretinaldetachmentcausedbyanelectricalshockreportedintheliterature.That

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简介：AIM:Toinvestigatewhetherphotoreceptornecroptosisinducedbyz-VAD-FMK(pancaspaseinhibitor)wasinvolvedtheactivationofautophagyandwhetherNecrostatin-1,aspecificnecroptosisinhibitor,couldinhibitthisinductionofautophagyafterexperimentalretinaldetachment.METHODS:ExperimentalretinaldetachmentmodelswerecreatedinSprague-Dawleyratsbysubretinalinjectionofsodiumhyaluronateandsubretinalinjectionsofz-VAD-FMK,vehicleorz-VAD-FMKplusNecrostatin-1.Threedaysafterretinaldetachment,morphologicchangeswereobservedbytransmissionelectronmicroscopy.Inotheranimals,retinasweresubjectedtoimmunoprecipitationandWesternBlotting,thenprobedwithanti-RIP1,phosphoserine,LC-3IIorcaspase8antibody.RESULTS:Itwasprovedbyimmunoprecipitationandwesternblotting,thatphotoreceptornecroptosiswasmediatedbycaspase-8inhibitionandreceptorinteractingproteinkinase(RIP1)phosphorylationactivation.TransmissionelectronmicroscopeandwesternblottingresultsindicatedthatphotoreceptornecroptosiswasinvolvedtheLC-3IIandautophagosomesinduction.WealsodiscoveredNecrostatin-1couldinhibitRIP1phosphorylationandLC-3IIinduction.CONCLUSION:Thesedatafirstlyindicatephotoreceptornecroptosisisassociatedwiththeactivationofautophagy.Necrostatin-1protectsphotoreceptorsfromnecroptosisandautophagybydown-regulationofRIP1phosphorylationandLC-3II.

简介：基因治疗是为网膜的退化疾病的潜在地有效的治疗。定期聚类interspaced短palindromic重复(CRISPR)/CRISPR-associated蛋白质9(Cas9)系统在眼的研究作为一个新编辑染色体的工具被开发了。在研究的最近的进展证明CRISPR/Cas9在在视网膜炎pigmentosa(RP)和leber的vivo产生动物模型以及基因治疗被使用了先天的黑(LCA)。它被与象联系adeno的病毒(AAV)那样的另外的技术结合也为诊所作为一次潜在的尝试显示出并且导致pluripotent干细胞(iPSCs)。在这评论，我们加亮在指向网膜的退化使用CRISPR/Cas9的进一步的前景的主要的点。我们也在治疗网膜的退化疾病强调这种技术的潜在的应用程序。

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简介：Toobservetheprocessofinvasion,retinaofratwasusedasamodeltosubstitutetheinnerlimitingmembraneofretinaforthebasementmembrane.RetinainvadedbyesophagealcarcinomacellsandB16melanomacellsupontheinnerlimitingmembranewasstudiedbyscanningandtransmissionelectronmicroscopy.Theresultsshowedthattheinnerlimitingmembranewasdestroyedbybothkindsoftumorcells.Theprocessofdestructionwasfollowedbyaseriesoftransformationsintheinnerlimitingmembrane,i.e.folding,swelling,thickening,andgranularchange.Theinnerlimitingmembranewasdissolvedfocallyasaresultoftransformation,andthentumorcellsinvadedtheretinathroughthesedissolvedregions.Itseemsthat,asabarrier,theinnerlimitingmembraneplaysasimilarroleasthebasementmembrane.

简介：AIM:Todeterminewhetherretinalcirculatorychangesplayaroleinthepathogenesisofmaculardisordersinpatientswhoareotherwisehealthy.METHODS:Patientswithmaculardisordersthatrequiredangiographicimagingwereincludedinthisprospectivecaseseries.Afteracompleteocularexam,fluoresceinangiographywasperformedusingastandardizedtechniqueontheHRA-II(HeidelbergEngineering,Heidelberg,Germany)withspecialfocusontheposteriorpole.Onlypatientswithgoodqualityimageswereincludedintheanalysis.Circulatoryparametersrecordedincludedthearm-choroidtime,choroid-retinalartery,andfinallytheretinalartery-veintime.Zonalasymmetry(betweentheupperandlowerzonesdividedbyalinepassingthroughthecentreofthefovea)intransittimes,ifanywasalsonoted.Appropriatestatisticalanalysiswasdone.Circulationtimeswerecomparedwithagematchedhistoricalcontrols.Changesinretinaldyetransittimesrelativetohistoricalagematchedcontrols,ifany,werenotedandcomparedbetweenvariousdisorders.RESULTS:Atotalof156eyesof156patients(120males)wereincludedinthestudy.Meanage:49.14±14.93y.Maculardisordersstudiedwereagerelateddegeneration,polypoidalvasculopathy,centralserouschorioretinopathy(CSCR)andparafovealtelangiectasia.DelayedcirculationtimewasnotedinCSCRpatientsonly.CONCLUSION:CSCRpatientsappeartohavedelayedarterialfilling,retinalcirculatorydisturbancesdonotseemtocontributetothepathogenesisofothermaculardisorders.

简介：Leber'scongenitalamaurosis(LCA)andrecentgenetherapyadvancementfortreatinginheritedretinopathieswereextensiveliteraturereviewedusingMEDLINE,PubMedandEMBASE.Adeno-associatedviralvectorswerethemostutilisedvectorsforoculargenetherapy.Conephotoreceptorcellsmightuseanalternatepathwaywhichwasnotreliantoftheretinalpigmentepithelium(RPE)derivedretinoidisomerohydrolase(RPE65)toaccessthe11-cisretinaldehydechromophore.Researcheffortsdedicatedontheprogressionofagene-basedtherapyforthetreatmentofLCA2.Suchgenetherapyapproacheswereextremelysuccessfulincanine,porcineandrodentLCA2models.TherecombinantAAV2.hRPE65v2adenoassociatedvectorcontainedtheRPE65cDNAandwasreplicationdeficient.ItsinvitroinjectionintargetcellsinducedRPE65proteinproduction.Thegenetherapytrialsthatweresofarconductedforinheritedretinopathieshavegeneratedpromisingresults.PhaseIclinicaltrialstocureLCAandchoroideremiademonstratedthatadeno-associatedviralvectorscontainingRPEgenesandphotoreceptorsrespectively,couldbesuccessfullyadministeredtoinheritedretinopathypatients.AphaseIIItrialispresentlyongoingandifsuccessful,itwillleadthewaytoadditionalgenetherapyattemptstocuremonogenic,inheritedretinopathies.