简介:糖尿病视网膜病变(diabeticretinopathy,DR)是糖尿病最严重和最常见的微血管并发症之一,也是一种世界范围内主要的致盲性眼病。其发病机制相当复杂,目前尚未完全明确。经典理论包括多元醇代谢异常、糖基化终产物的形成增加、蛋白激酶C的活化、氧化应激等。近年来,随着分子生物学的发展,分子基础研究已成为目前DR发病机制研究的焦点和热点。目前已知与DR有关的细胞因子有VEGF,IGF-1,bFGF,TNF等。多种细胞因子通过信号转导系统形成复杂的网络系统,引起新生血管生成,破坏血-视网膜屏障等多种改变,从而导致DR的发生发展。本文就细胞因子表达异常与DR的关系进行综述。
简介:目的探讨复方樟柳碱对视网膜挫伤的临床效果。方法将42例视网膜挫伤患者根据入院时间分为两组,06年初到08年底18例作为对照组,09年初至2011年10月24例为试验组。两组均使用ATP40mg+辅酶A100单位+肌苷200mg组成的能量合剂和250ml丹参注射液,试验组加用复方樟柳碱注射液2ml颞浅动脉旁注射,观察两组的疗效。结果试验组24例,16例治愈,6例好转,2例无效,治愈与好转率之和为91.67%。对照组18例,8例治愈,3例好转,7例无效,治愈与好转率之和为61.11%。两组治愈和好转之和比较,差异有显著意义(X^2=4.0332,P〈0.05)。结论复方樟柳碱对于视网膜挫伤效果明显。
简介:目的:观察应用复方樟柳碱注射液、激素冲击及补充能量综合治疗青少年急性视神经炎的疗效。方法:将65例82眼青少年急性视神经炎患者随机分为两组,治疗组33例41眼,对照组32例41眼;治疗组在与对照组同样的全身用药的同时,于患眼颞浅动脉旁注射复方樟柳碱注射液,1次/d,2mL/次,于14,30,60d观察两组患者治疗前后病程时间、视力、视觉诱发电位及眼底荧光血管造影的变化。结果:于14,30,60d观察两组患者治疗后的疗效,治疗组均比对照组的有效率高,两组比较差异有统计学意义(P〈0.05)。结论:加用复方樟柳碱颞浅动脉旁注射较传统激素冲击及补充能量综合治疗青少年急性视神经炎,可以缩短病程,减小激素用量,提高患者视力。
简介:目的:观察早期视网膜激光光凝(PRP)联合复方樟柳碱颞浅动脉旁皮下注射治疗放射性视网膜病变(RR)的临床疗效。方法:在我院确诊为因鼻咽癌外照射后发生RR的患者21例41眼,早期行双眼视网膜激光光凝联合复方樟柳碱颞浅动脉旁穴位注射治疗,观察治疗后3mo最佳矫正视力(BCVA)、毛细血管无灌注区变化、视网膜新生血管及并发症情况。结果:治疗后观察3mo,视力提高6眼(14.6%),视力不变31眼(75.7%),下降4眼(9.7%)。2眼虹膜新生血管消退,1眼行睫状体光凝术;9眼(75%)视网膜新生血管消退;22眼(68.7%)原视网膜无灌注区消失,7眼(21.8%)原视网膜无灌注区(NPA)缩小〉5个DA,总有效率90.5%。1眼发生玻璃体出血,未见视盘及虹膜新生血管和新生血管性青光眼等并发症以及与治疗相关的并发症。结论:早期PRP与复方樟柳碱颞浅动脉旁穴位注射治疗是有效的、合理的中西医结合治疗方法。
简介:AIM:Toinvestigatethelevelsofserumsolubleintercellularadhesionmolecules-1(sICAM-1)andneutrophilicexpressionofCD18inpatientswithvariousstagesofdiabeticretinopathyandtodeterminetheirdifferentexpressionpatterninthedevelopmentofdiabeticretinopathy(DR).·METHODS:LevelsofserumsICAM-1andCD18onthesurfaceofneutrophileweremeasuredin41DRpatients,theywereclassifiedinthreesubgroupsaccordingtothestageofretinopathyasdeterminedbyfund’sophthalmoscopy;10controlsubjectswerealsostudied.sICAM-1weremeasuredbyenzyme-linkedimmunosorbentassayandCD18byflowcytometry.·RESULTS:TheneutrophilicCD18expressionandserumsICAM-1levelwereallsignificantlyelevatedinalldiabeticsubgroupscomparedtocontrolsubjects(P<0.01).ThedifferencesofCD18andsICAM-1amongthediabeticsubgroupsweresignificantinCD18butnotinsICAM-1.TheprogressionofretinopathywasassociatedwithanincreasebothinCD18andinsICAM-1levelsbysimplecorrelationanalysis(β=0.74,P<0.001;β=0.38,P<0.01,respectively).ButstepwisemultipleregressionanalysisrevealedthatonlyCD18wasindependentdeterminantofretinopathy(β=1.04,P<0.01).·CONCLUSION:OurresultsconfirmthecontributionofendothelialandneutrophilicactivationinthedevelopmentofDRasindicatedbyincreasedlevelsofCD18andsICAM-1.However,adirectimplicationofCD18andICAM-1intheprogressionofDRcanbesupportedonlyintheCD18butnotICAM-1.CD18andICAM-1mayplaydifferentroleinthedevelopmentofdiabeticretinopathy.
简介:AIM:ToevaluatetheeffectofCollagencross-linkingonthepreventionofmeltinginrabbitcorneasafteralkaliburn.·METHODS:TwentyNewZealandwhiterabbitswererandomlydividedintomodelcontrolgroupandcollagencross-linkingtreatmentgroup.Thesecondgroupofrabbitsreceivedcollagencrosslinkedtreatment.Bothgroupswereappliedwithantibioticeyedropstopreventinfection.Thecorneaswereevaluatedformelting,opacity,pathologicalandimmunohistochemistry,recordthechangeswhen28daysaftertheanimalswerekilled.·RESULTS:Inthecontrolgroup,6outof8rabbitsshowedcornealmeltingafterinjury(14±4)days,whiletwocornealperforated.Incollagencross-linkingtreatmentgroup,onerabbitshowedcornealmeltingafterinjury23days,withoutcornealperforation;cornealdissolutionratebetweenthetwogroupswassignificantlydifferent(P<0.05).Pathologicalexaminationsuggestedthatinthetreatmentgroup,mildcornealedema,milddamagetocollagenfibers,inflammatorycellinfiltrationwassignificantlylessthanthecontrolgroup.Immunohistochemistryshowedthatcornealcollagenfibersarrangedinneatrowsinthecontrolgroup.·CONCLUSION:Collagencross-linkingtreatmentnotonlycanpreventanddelaythecornealmeltingafteralkaliburn,butalsocanreducethedestructionofcornealcollagenfibersandinfiltrationofinflammatorycellsinthecornealtissue.
简介:AIM:Todeterminetheproliferativepotentialandthemaintenanceofstemcellactivityinstoredhumanlimbaltissues,andcorrelatethiswiththepreservationtime,cellviabilityandtheexpressionofstemcellmarkers.METHODS:Thirtylimbalrimsweresplitinto4partsandstoredincornealpreservationmediumat4℃for0,1,4,or7days.ThelimbalstemcellandmitoticmarkersP63,CK19,proliferatingcellnuclearantigen(PCNA),andKi67weredeterminedbyimmunohistochemicalstaining.Theproliferativepotentialoflimbalepithelialcellswasassessedbycellviability,theabilityofgeneratingstratifiedepithelium,andcolonyformingassay.RESULTS:Thestoredtissuesmaintainedlimbalstratifiedstructureto7daysandexhibitedcomparableexpressionlevelofstemcellandmitoticmarkers.Theproportionofviablecellsdecreasedwiththeprolongedpreservationtime,whilecolonyformingefficiencydecreasedfromthe1stdayanddisappearedatthe4thday.Wheninoculatedonamnioticmembrane,thecellspreservedfor1dayformedastratifiedepithelium,whilethecellsfrom4days’preservationformedadiscontinuouslayer.CONCLUSION:Thecolonyformingefficiencyoflimbalepithelialstem/progenitorcellsdecreasedrapidlywiththeincreasingpreservationtime,whiletheexpressionlevelofmarkersandcapacityofformingepithelialmonolayeronamnioticmembranedecreasedgradually.Thelimbalepithelialstemcellslosttheirfunctionearlierthanthelostexpressionlevelofstemcellmarkers.Thismayhelpustobetterchoosetheappropriatepreservationgraftsforfuturelimbalstemcelltransplantation.
简介:<正>DearSir,IamProf.BeuyJoobfromSanitation1MedicalAcademicCenter,Bangkok,Thailand.Iwritetodiscusstherecentpublicationonproteomicanalysisindiabeticretinopathy(DR).Liuetal[1]concludedthattheirapproachbytwodimensionalfluorescencedifferencegelelectrophoresis(2D-DIGE)combinedwithmatrix-assistedlaser
简介:目的:通过检测高度近视性弱视者弱视眼黄斑区视网膜神经节细胞厚度,探讨该类弱视的程度与视网膜神经节细胞厚度的关系。方法:选取先天性高度近视(10g/L阿托品眼膏散瞳后〉-4.00DS)并伴有弱视患者12例20眼。年龄3.5~15岁。采用傅立叶域光学相干断层扫描仪(fourier-domainopticalcoherencetomography,FD-OCT)测量弱视眼的黄斑区神经节细胞厚度以及黄斑区视网膜厚度,并比较神经节细胞层厚度占视网膜层厚度的比例与患者弱视及近视程度的相关性。结果:我们发现高度近视患者近视程度与最佳矫正视力无明显相关性,近视程度高的患者其神经节细胞层相对厚度有变薄现象。结论:先天性近视性弱视的患者黄斑中心区神经节细胞层厚度占视网膜厚度的比例有下降。
简介:世界各地糖尿病增加是主要由于2型糖尿病患者的人数在上升。2型糖尿病越来越常见是因为:随着人的寿命延长,糖尿病更多发生在中老年人中。随着人们越来越多地迁移到市区,运动减少,吃得更多,不健康的食物,越来越多的人正变得肥胖成为2型糖尿病的主要原因。糖尿病增加一系列的眼部疾病风险,包括白内障,但是与糖尿病有关盲的主要原因是糖尿病视网膜病变(DR)。糖尿病视网膜病变通常在患糖尿病后的十至二十年之间发生并且当糖尿病未确诊及未治疗时发展更快。
简介:目的:探讨中老年人群高脂血症、糖尿病与年龄相关性白内障(age-relatedcataract,ARC)的关系。方法:采用以医院为基础的病例对照研究方法,病例组由年龄45~85岁的360例ARC患者所组成;对照为与病例同期入住相同医院,未患与ARC有关眼病的360例患者,对照组与病例采取1:1匹配方式。采用自行设计的调查表对研究对象进行调查,内容包括人口学特征、生活方式、疾病既往史等,同时收集研究对象的临床生化检测资料,包括空腹血糖、高密度脂蛋白胆固醇(HDL-C)、总胆固醇(TC)及甘油三酯(TG)等。采用多因素Logistic回归分析,估计研究因素与ARC关联的比值比(OR)及其相应的95%可信区间(CI)。结果:调整了年龄和性别因素后,高脂血症、高脂血症病程、TC及TG与发生ARC的危险性无关(P〉0.05),仅HDL-C下降与发生ARC的危险性升高有关(OR=1.519,95%CI:1.093~2.110,P=0.013)。在调整了多种潜在性混杂因素后,经多因素Logistic回归分析的结果显示,空腹血糖受损的研究对象发生ARC的危险性升高了73%(OR=1.734,95%CI:1.102~2.725,P〈0.001),而已确诊的糖尿病患者发生ARC的危险性升高了94%(OR=1.938,95%CI:1.293~2.906,P〈0.001)。糖尿病病程也与ARC呈显著性正相关,糖尿病病程〈10a和10~19a的病例发生ARC的危险性分别是未患糖尿病对照的2倍(OR=2.347,95%CI:1.502~3.752,P=0.010)和3倍(OR=2.683,95%CI:1.267~5.683,P〈0.001)。结论:HDL-C下降及糖尿病可使中老年人群发生ARC的危险性增加。
简介:目的:探讨眼附属器B细胞非霍杰金淋巴瘤(B—cellnon-Hodgkinlymphoma,NHL)中Skp2,p27和PTEN的表达。方法:收集1995年到2011年青岛大学附属医院眼科石蜡包埋标本,用免疫组化法分别检测眼附属器B细胞NHL(n=30)标本中Skp2,p27和PTEN的表达,以眼部反应性淋巴组织增生(n=10)作为对照组。以患者的年龄、性别、发病部位,病理类型作为眼附属器B细胞NHL的的分类标准。结果:Skp2,p27和PTEN的表达与患者的年龄、性别、发病部位无关,而与病例类型有关。眼附属器B细胞NHLSkp2表达率与眼部反应性淋巴组织增生相比显著增高。p27,PTEN表达率与反应性淋巴组织增生相比显著降低。随眼附属器B细胞NHL病理分级的提高,Skp2的表达显著增高,p27和PTEN的表达显著降低。在黏膜相关淋巴组织结(mucosa—associatedlymphoidtissue,MALT)外边缘区B细胞淋巴瘤(diffuselargeB—celllymphoma,DLBCL)中,Skp2分别与p27,VFEN成负相关,p27和PTEN成正相关。结论:Skp2的表达升高,p27,PTEN蛋白的缺失以及可能与眼附属器B细胞NHL的发生有关;其中在MALT外边缘区DLBCL中,三种蛋白存在相关性。联合三种蛋白的检测眼附属器B细胞NHL的不同病理类型有重要意义。
简介:目的:观察增生型糖尿病视网膜病变(proliferativediabeticretinopathy,PDR)的多焦视网膜电图(multifocalelectroreti-nogram,mf-ERG)的图像特征及临床意义。方法:对临床确诊的PDR患者40例44眼(PDR组)和正常对照组40例40眼进行mf-ERG检查,并对所得数据进行统计分析。结果:PDR患者组mf-ERG1~5环的反应密度均低于正常对照组,且有显著性差异,N1波潜伏期在4环、P1波潜伏期在2~5环与正常对照组相比显著延长。结论:Mf-ERG可有效地评价PDR患者视网膜的功能。
简介:AIM:Toestablishanuntransfectedhumancornealstromal(HCS)celllineandcharacterizeitsbiocompatibilitytoacellularporcinecornealstroma(aPCS).·METHODS:PrimaryculturewasinitiatedwithapurepopulationofHCScellsinDMEM/F12media(pH7.2)containing20%fetalbovineserumandvariousnecessarygrowthfactors.Theestablishedcelllinewascharacterizedbygrowthproperty,chromosomeanalysis,tumorigenicityassay,expressionofmarkerproteinsandfunctionalproteins.Furthermore,thebiocompatibilityofHCScellswithaPCSwasexaminedthroughhistologicalandimmunocytochemistryanalysesandwithlight,electronmicroscopies.·RESULTS:HCScellsproliferatedtoconfluence2weekslaterinprimarycultureandhavebeensubculturedtopassage140sofar.AcontinuousuntransfectedHCScelllinewithapopulationdoublingtimeof41.44hoursatpassage80hasbeendetermined.Resultsofchromosomeanalysis,morphology,combinedwiththeresultsofexpressionofmarkerproteinandfunctionalproteinssuggestedthatthecellsretainedHCScellproperties.Furthermore,HCScellshavenotumorigenicity,andwithexcellentbiocompatibilitytoaPCS.·CONCLUSION:Anuntransfectedandnon-tumorigenicHCScelllinehasbeenestablished,andthecellsmaintainedpositiveexpressionofmarkerproteinsandfunctionalproteins.Thecellline,withexcellentbiocompatibilitytoaPCS,mightbeusedforinvitroreconstructionoftissue-engineeredHCS.
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:糖尿病视网膜病变(DR)是作为一种常见的糖尿病并发症,对其发病机制的研究一直是关注的焦点。经典的糖尿病视网膜病变的发病机制假说集中与多元醇通路的异常、蛋白质非酶糖基化产物的堆积、蛋白激酶C及氨基己糖途径有关。聚腺苷二磷酸核糖聚合酶(PARP)作为统一机制中的一个关键分子,与DR发病机制及其防治密不可分,对其进行适当干预,可成为DR治疗的重要方法之一。