Prevalence of retinal pathologies in people over 60 years:the Tehran Geriatrics Eye Study

AIM:To determine the prevalence of some retinal pathologies in people over 60y and their association with demographic and ocular factors.METHODS:A cross-sectional study was conducted in Tehran using multistage cluster sampling.After selecting subjects aged 60 and over,optometric,and ophthalmic examinations were done.For retinal examination,a 90 D lens was used and indirect ophthalmoscopy was performed after instilling tropicamide drops.Biometry was done using the IOL Master for all participants.RESULTS:Of 3791 people that were invited through cluster sampling,3310 participated in the study(response rate=82%).The prevalence of retinal pigmented epithelium(RPE)change,drusen,geographic atrophy(GA),hypertensive retinopathy(HTR),nonproliferative diabetic retinopathy(NPDR),proliferative diabetic retinopathy(PDR),choroidal neovascularization(CNV),central retinal artery occlusion(CRAO),myopic retinopathy(MR),branch retinal vein occlusion(BRVO),and central retinal vein occlusion(CRVO)was 27.42%,11.08%,4.52%,3.03%,4.05%,0.54%,0.82%,0.39%,0.20%,0.49%,and 0.19%,respectively.After removing the effect of age,the odds of NPDR were 1.68 times higher in women compared to men(P=0.014).After removing the effect of sex,the odds of drusen,RPE change,GA,CNV,BRVO,and CRVO increased with age.CONCLUSION:There is a higher prevalence of RPE change,drusen,GA,CNV and a lower prevalence of MR and CRAO in the elderly population of Tehran aged over 60y compared to global average values.Considering the correlation of most of the diseases with age and their effects on vision,attention should be paid to these diseases and the related screening programs to prevent vision impairment.

Overexpression of Twist1 in vascular endothelial cells promotes pathological retinal angiogenesis in mice

Retinal angiogenesis is a critical process for normal retinal function.However,uncontrolled angiogenesis can lead to pathological neovascularization(NV),which is closely related to most irreversible blindness-causing retinal diseases.Understanding the molecular basis behind pathological NV is important for the treatment of related diseases.Twist-related protein 1(TWIST1)is a well-known transcription factor and principal inducer of epithelial-mesenchymal transition(EMT)in many human cancers.Our previous study showed that Twist1 expression is elevated in pathological retinal NV.To date,however,the role of TWIST1 in retinal pathological angiogenesis remains to be elucidated.To study the role of TWIST1 in pathological retinal NV and identify specific molecular targets for antagonizing pathological NV,we generated an inducible vascular endothelial cell(EC)-specific Twist1 transgenic mouse model(Tg-Twist1iEC+).Whole-mount retinas from Tg-Twist1iEC+mice showed retarded vascular progression and increased vascular density in the front end of the growing retinal vasculature,as well as aneurysm-like pathological retinal NV.Furthermore,overexpression of Twist1 in the ECs promoted cell proliferation but disturbed cell polarity,thus leading to uncontrolled retinal angiogenesis.TWIST1 promoted pathological NV by activating the Wnt/β-catenin signaling pathway and inducing the expression of NV formation-related genes,thereby acting as a‘valve’in the regulation of pathological angiogenesis.This study identified the critical role of TWIST1 in retinal pathological NV,thus providing a potential therapeutic target for pathological NV.

Pathological,Ultrastructural and Immunohistochemical Observations of Adenoma of Retinal Pigment Epithelium

Purpose: To Study the clinical, pathological, ultrastructural and immunohistchemicalcharacters of adenoma of the retinal pigment epithelium in order to offer evidence todiagnose this tumor.Methods: Routine paraffin slices HE stain, histochemistry PAS and VG stain,transmission electron microscopy, and immunohistochemistry for S-100 and vimentinwith LSAB method were used.Results: The tumor cells were oval and cuboidal in shape. Part of the tumor had atubular arrangement. Around the sheets of tumors cells there was a large amount ofuniform red stick-like substances. The above matter represented positive in PAS stain.Most of the above matter was yellow, while less of the matter showed red in VG stain.Transmission electron microscopy showed that there were tight junctions between tumorcells. Immunohistochemistry showed positive for S-100, negative for vimentin.Conclusions: The ultrastructural and immunohistochemical characters of the adenoma ofretinal pigment epithelium are consistent with the retinal pigment epithelium.

Upregulation of Nogo receptor expression induces apoptosis of retinal ganglion cells in diabetic rats

The Nogo receptor is an essential factor for neuronal apoptosis, but the changes in Nogo receptor expression in the retina and the effects of the Nogo receptor on retinal ganglion cell apoptosis in diabetes mellitus remain unclear. We found that Nogo receptor expression was mainly visible in retinal ganglion cells of a rat model of diabetes mellitus induced by streptozotocin. At 12 weeks after onset of diabetes mellitus, Nogo receptor and Rho kinase expression signiifcantly increased in the retina, and retinal ganglion cell apoptosis was apparent. When RNA interference was used to suppress Nogo receptor expression in rat retina, Rho kinase expression was obviously inhibit-ed, and retinal ganglion cell apoptosis was evidently reduced in rats with diabetes mellitus. These results indicate that upregulation of Nogo receptor expression is an important mechanism of retinal ganglion cell apoptosis in rats with diabetes mellitus.

Protection of retinal ganglion cells against optic nerve injury by induction of ischemic preconditioning

AIM： To explore if ischemic preconditioning （IPC） can enhance the survival of retinal ganglion cells （RGCs） after optic nerve axotomy. METHODS： Twenty-four hours prior to retinal ischemia 60min or axotomy, IPC was applied for ten minutes in groups of （n=72） animals. The survival of RGCs, the cellular expression of heat shock protein 27 （HSP27） and heat shock protein 70 （HSP70） and the numbers of retinal microglia in the different groups were quantified at 7 and 14d post-injury. The cellular expression of HSP27 and HSP70 and changes in the numbers of retinal microglia were quantified to detect the possible mechanism of the protection of the IPC. RESULTS： Ten minutes of IPC promoted RGC survival in both the optic nerve injury （IPC-ONT） and the retinal ischemia 60min （IPC-IR60） groups, examined at 7d and 14d post-injury. Microglial proliferation showed little correlation with the extent of benefit effects of IPC on the rescue of RGCs. The number of HSP27-positive RGCs was significantly higher in the IPC-ONT group than in the sham IPC-ONT group, although the percentage of HSP27-positive RGCs did not significantly differ between groups. For the IPC-IR60 group, neither the number nor the percentage ofthe HSP27-positive RGCs differed significantly between the IPC and the sham-operated groups. The number of HSP70-positive RGCs was significantly higher for both the IPC-ONT and the IPC-IR60 experimental groups, but the percentages did not differ. CONCLUSION： The induction of IPC enhances the survival of RGCs against both axotomy and retinal ischemia.

Rhegmatogenous Retinal Detachment in Pierre Robin Anomaly—A Suspicion for Stickler Syndrome: Case Report

Stickler syndrome (SS) is an autosomal dominant inherited genetic disorder that presents with hearing loss, a cleft palate, epiphyseal dysplasia, and degeneration, similar to arthritis and well known to be associated with rhegmato-genous retinal detachments. A particular group of physical features called Pierre Robin sequence is also common in people with stickler syndrome. Pierre Robin sequence includes a cleft palate, glossoptosis, and micrognathia. We describe a case report of a family diagnosed with stickler syndrome presenting with Pierre Robin sequence and share some universal management steps for rhegmatogenous retinal detachment in stickler syndrome. Genetic testing is important to support the diagnosis and conduct screenings of family members.

中药单体干预增生性玻璃体视网膜病变的研究进展

增生性玻璃体视网膜病变(PVR)是导致孔源性视网膜脱离手术失败和复发的主要原因。目前临床治疗PVR多以手术为主,但存在一定不足,因此,需要寻找新的药物疗法。中药单体兼有中药与化学药的双重优势,我国传统中药与中药单体在PVR治疗尤其是视网膜保护方面具有独特优势,逐渐成为了研究热点。本文对近年来中药单体治疗PVR的文献进行综述,发现姜黄素、藏红花素、槲皮素等中药单体可通过降低血小板源性生长因子、转化生长因子、表皮生长因子等因子的表达,抑制上皮细胞—间充质转化的生物学过程,防止PVR的发生。这些中药单体的发现对后续新药的研发可提供新的选择,为PVR的治疗提供更多元化的方法。

伴白质脑病和系统性损害的视网膜血管病家系特点分析

目的探讨伴白质脑病和系统性损害的视网膜血管病(retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations,RVCL-S)家系的临床、组织病理及分子遗传学特点。方法回顾性分析RVCL-S家系的临床资料并绘制家系图,总结其临床表现、影像学、组织病理及分子遗传学特点。结果家系1:男性发病3例,年龄分别为10岁、29岁和40岁。家系2:男性发病1例,年龄为32岁。2家系患者均表现为视网膜血管病、白质脑病及多系统损害,后者包括肝、肾、消化道受累等;2家系无症状携带者4例。家系1-Ⅱ2颅脑CT示左侧侧脑室后角旁片状低密度,伴颅内多发高密度钙化,颅脑MRI平扫示侧脑室旁病变;家系1-Ⅱ5颅脑MRI平扫及增强示额颞叶皮层病变伴周围水肿及占位效应,环形强化明显。家系2-Ⅱ1颅脑MRI平扫及增强先后出现右侧及左侧额叶病变,伴周围水肿及强化,占位效应明显。家系1-Ⅱ5病变脑组织手术病理示内皮细胞增生性病变;家系2-Ⅱ1脑病变2次手术病理均符合“脑梗死”样表现;小肠壁内小血管示内皮细胞增生性病变。家系1-Ⅱ2存在TREX1 D272Rfs杂合突变,其2女1子均为无症状突变携带者。家系2-Ⅱ1基因存在TREX1 S246Ifs杂合突变,其父亲、母亲均未发现该突变,其子为无症状突变携带者。结论RVCL-S临床主要表现为视网膜血管病、神经系统受累及多系统损害。影像学见颅内病变可呈占位性,伴周围水肿及强化;病理特点为小血管内皮细胞增生及管腔狭窄。基因结果证实存在TREX1基因突变。

微RNA-140-5p靶向调节血管内皮生长因子表达对高糖诱导的人视网膜血管内皮细胞增殖、迁移和管腔形成的影响

目的 探讨微RNA(miR)-140-5p靶向调节血管内皮生长因子(VEGF)表达对高糖诱导的人视网膜血管内皮细胞(hRECs)增殖、迁移和管腔形成的影响。方法 将对数生长期hRECs细胞分为正常对照组、高糖组、miR-140-5p组、阴性对照(NC)组、高糖+miR-140-5p组。正常对照组和高糖组细胞不做任何转染,miR-140-5p组和高糖+miR-140-5p组细胞转染miR-140-5p模拟物(miR-140-5p mimics),NC组细胞转染阴性对照模拟物(mimics NC)。高糖组和高糖+miR-140-5p组细胞用含30 mmol·L^(-1)葡萄糖的培养基制备高糖模型。应用实时荧光定量聚合酶链式反应法检测各组细胞中miR-140-5p表达水平,噻唑蓝法检测各组细胞增殖能力,Transwell法检测各组细胞迁移能力,管腔形成实验检测各组细胞成管能力,Western blot法检测各组细胞中VEGF蛋白的表达。将40只Sprague Dawley大鼠随机分成正常对照组、糖尿病模型组、糖尿病+NC组、糖尿病+miR-140-5p组,每组10只。除正常对照组外,其余各组大鼠腹腔注射65 mg·kg^(-1)链脲佐菌素制备糖尿病模型,正常对照组和糖尿病模型组大鼠尾静脉注射200μL生理盐水,糖尿病+miR-140-5p组大鼠尾静脉注射200μL miR-140-5p,糖尿病+NC组大鼠尾静脉注射200μL mimics NC,每日1次,持续给药7 d;再继续饲养8周,大鼠麻醉后,取视网膜,苏木精-伊红染色观察miR-140-5p对糖尿病模型大鼠视网膜血管生成的影响。结果 高糖组、高糖+miR-140-5p组细胞中miR-140-5p相对表达量显著低于正常对照组,miR-140-5p组细胞中miR-140-5p相对表达量显著高于正常对照组(P<0.01);NC组与正常对照组细胞中miR-140-5p相对表达量比较差异无统计学意义(P>0.05)。miR-140-5p组、NC组、高糖+miR-140-5p组细胞中miR-140-5p相对表达量显著高于高糖组(P<0.01)。NC组、高糖+miR-140-5p组细胞中miR-140-5p相对表达量显著低于miR-140-5p组(P<0.01)。高糖+miR-140-5p组细胞中miR-140-5p相对表达量显著低于NC组(P<0.05)。培养24、48、72 h时,高糖组细胞增殖率均显著高于正常对照组(P<0.01),miR-140-5p组、NC组与正常对照组细胞增殖率比较差异均无统计学意义(P>0.05)。培养24 h时,高糖+miR-140-5p组与正常对照组细胞增殖率比较差异无统计学意义(P>0.05);培养48、72 h时,高糖+miR-140-5p组细胞增殖率显著高于正常对照组(P<0.01)。培养24、48、72 h时,miR-140-5p组、NC组、高糖+miR-140-5p组细胞增殖率均显著低于高糖组(P<0.05)。培养24、48、72 h时,NC组与miR-140-5p组细胞增殖率比较差异均无统计学意义(P>0.05)。培养24 h时,高糖+miR-140-5p组细胞增殖率与miR-140-5p组、NC组比较差异无统计学意义(P>0.05);培养48、72 h时,高糖+miR-140-5p组细胞增殖率显著高于miR-140-5p组和NC组(P<0.01)。高糖组迁移细胞数显著高于正常对照组,miR-140-5p组、NC组迁移细胞数显著低于正常对照组(P<0.01)。高糖+miR-140-5p组与正常对照组迁移细胞数比较差异无统计学意义(P>0.05)。miR-140-5p组、NC组、高糖+miR-140-5p组迁移细胞数显著低于高糖组(P<0.01)。NC组、高糖+miR-140-5p组迁移细胞数均显著高于miR-140-5p组(P<0.01)。高糖+miR-140-5p组迁移细胞数显著高于NC组(P<0.01)。高糖组管腔形成数量显著高于正常对照组,miR-140-5p组、NC组细胞管腔形成数量显著低于正常对照组(P<0.01);高糖+miR-140-5p组与正常对照组细胞管腔形成数量比较差异无统计学意义(P>0.05)。miR-140-5p组、NC组、高糖+miR-140-5p组细胞管腔形成数量均显著低于高糖组(P<0.01)。NC组、高糖+miR-140-5p组细胞管腔形成数量均显著高于miR-140-5p组(P<0.05)。高糖+miR-140-5p组细胞管腔形成数量显著高于NC组(P<0.05)。高糖组、高糖+miR-140-5p组细胞中VEGF蛋白相对表达量显著高于正常对照组,miR-140-5p组细胞中VEGF蛋白相对表达量显著低于正常对照组(P<0.05);NC组与正常对照组细胞中VEGF蛋白相对表达量比较差异无统计学意义(P>0.05)。miR-140-5p组、NC组、高糖+miR-140-5p组细胞中VEGF蛋白相对表达量显著低于高糖组(P<0.01)。NC组、高糖+miR-140-5p组细胞中VEGF蛋白相对表达量显著高于miR-140-5p组(P<0.01)。高糖+miR-140-5p组细胞中VEGF蛋白相对表达量显著高于NC组(P<0.05)。正常对照组大鼠靠近视乳头处的视网膜血管整体呈“树状结构”,内极部毛细血管分布较致密,外极部毛细血管分布较疏松,血管壁均匀。糖尿病模型组大鼠视网膜血管的“树状结构”被破坏,毛细血管分布不均匀,毛细血管瘤形成。糖尿病+NC组大鼠视网膜血管损伤与糖尿病模型组相当。糖尿病+miR-140-5p组大鼠视网膜血管的损伤情况有所好转,毛细血管瘤减少。结论 miR-140-5p可以抑制hRECs在高糖条件下的增殖、迁移及成管能力,缓解糖尿病大鼠视网膜血管病变,其作用可能是通过miR-140-5p靶向调控VEGF的表达而实现。

中药小分子抑制新生血管形成机制的研究进展

一系列中药复方在临床实践和基础实验中被证明能够抑制病理性新生血管形成。中药小分子是中药复方中实际发挥药效的活性成分,特定中药小分子通过不同途径抑制血管内皮细胞生长因子的表达,从而抑制新生血管形成,为相关血管新生疾病的治疗提供了新思路。新生血管形成在糖尿病性视网膜病变等视网膜新生血管疾病中扮演了重要的角色,也对恶性肿瘤的发生、发展具有重要作用。本文概述了新生血管形成的过程和机制,并以黄酮类、皂苷类、生物碱等中药小分子为主,讨论了中药小分子抑制新生血管形成的机制。

两种常用大鼠视神经钳夹伤模型造模效果的比较

背景视神经钳夹伤（ONC）动物模型是外伤性视神经损伤致病机制及治疗方法相关基础研究的主要工具，目前常用的造模方法有经眼眶上缘开神经鞘膜视神经钳夹法和经球结膜外眦部夹伤视神经法，但关于2种模型优劣评价的研究很少。目的比较2种常用大鼠ONC模型的造模效果，为相关的实验研究中造模方法的选择提供依据。方法采用随机分配方法将8～10周龄健康成年雄性SD大鼠24只分为经眶上缘开神经鞘膜ONC组和经眶上缘开神经鞘膜ONC20s、40s、60s组，分别采用经眶上缘开神经鞘膜视神经夹伤法（20s）及经球结膜外眦部夹伤视神经法在大鼠的-侧眼建立ONC动物模型，各组大鼠的正常对侧眼作为对照。于造模后14d记录各组大鼠闪光视觉诱发电位（F—VEP）P。波；制备大鼠视神经组织切片，采用苏木精-伊红染色法观察大鼠视神经的组织病理学改变；采用免疫荧光法观察并计数大鼠视网膜组织中Brn-3a阳性视网膜神经节细胞（RGCs）。对2种造模方法的造模过程和检测结果进行比较。结果造模后14d，经眶上缘开神经鞘ONC组和经球结膜ONC20s组、40S组、60s组大鼠的F—VEPP。波潜伏期较各自的正常对侧眼均明显延长，差异均有统计学意义（t=-11．64、-8．04、-6．50、-10．84，均P〈0．01）；经眶上缘开神经鞘ONC组大鼠P．波潜伏期与经球结膜ONC20s、40s、60s组大鼠比较均明显延长，差异均有统计学意义（P=0．01、0．02、0．05）；各组大鼠术眼P．波振幅与其正常对侧眼比较差异均无统计学意义（均P〉0．05）。造模后14d，免疫荧光检测显示各组大鼠模型眼视网膜上Brn-3α表达阳性RGCs数均较正常对侧眼明显减少，经眶上缘开神经鞘ONC组大鼠视网膜上Brn-3a表达阳性RGCs数为（13．60±2．14）个／视野，为其正常对侧眼的47．49％，经球结膜ONC20s、40s和60s组中Brn-3a阳性RGCs数分别为（18．74±3．61）、（15．84±2．31）和（14．58±3．23）个／视野，分别为其正常对侧眼的67．70％、56．69％和50．17％，经眶上缘开神经鞘ONC组大鼠视网膜中Brn．3a阳性RGCs数与经球结膜ONC40s和60s组比较，差异均无统计学意义（均P〉0．05）。组织病理学检查显示，各组大鼠造模眼神经胶质细胞核排列紊乱，细胞基质空泡化，可见大量炎性细胞浸润，以眶上缘开神经鞘ONC组更为严重。结论与经球结膜ONC模型鼠比较，经眶上缘开视神经鞘ONC模型大鼠视神经形态结构损害更为严重，视神经的传导功能更为迟缓，RGCs的存活率更低。

1种视网膜眼底图像增强的新方法

目的:提高视网膜眼底图像中血管和病灶部位的可视性,便于临床诊断。方法:首先,对采集到的视网膜眼底图像进行数学形态学处理,以弱化背景,使图像得到初步增强;然后,运用有限对比度自适应直方图均衡化算法改善光照不均的现象;最后,利用二维匹配滤波算法进一步强化血管和病灶部位信息,提高血管与背景的对比度。结果:该方法能很好地弱化背景,增强对比度,凸显感兴趣区域,也对视盘区域血管的分割和病灶部位的识别有极大地帮助。结论:该方法可有效地增强正常和病变的眼底图像,辅助医师诊断。

眼底血管病理学改变特征研究

眼底血管是活体能唯一观察到的人体终末血管,许多疾病在眼底血管有病理改变,通过这些病理改变的研究,可以实现利用眼底血管改变诊断疾病,本文总结了眼底血管的部分常见病理学改变,以及引起这些改变的常见疾病,希望可以将部分疾病与眼底血管改变对应起来,以利于临床疾病的诊断。

外伤性视神经损伤后视神经及视网膜形态的动态观察

目的 :了解外伤性视神经损伤后的病理变化、溃变特点与时相间的关系。方法 :参照Allen脊髓损伤法 ,造成视神经眶尖段间接 6 0 0gcm力冲击、挤压伤。伤后对视神经和视网膜行形态学动态观察。结果 :①伤后 4 8h ,视神经轻度肿胀和空泡反应 ;1周时损伤处视神经出现溃变 ,神经胶质细胞增生 ,视网膜神经节细胞 (retinalganglioncells,RGCs)形态改变不明显 ;2周时神经纤维轴束间空泡样改变 ,局灶性坏死 ,RGCs核固缩和细胞数量减少。术后 3月 ,视神经损伤部位直径缩小 ,形成胶质疤痕 ,RGCs数量明显减少 ,核固缩细胞增多。②RGCs数量于术后 4 8h、1周、2周、1月和 3月分别比正常对照组低 3 35 %、13 2 3%、19 74 %、2 3 2 0 %、2 9 2 8%。③视网膜细胞在 4 8h内出现凋亡。结论 :本实验模型可造成明确的视神经和视网膜损伤 ,神经元的损伤程度从节细胞、中间神经元、感光细胞的次序依次递减。视网膜和视神经损伤的严重程度与时间呈相关性。RGCs数量在 4 8h至 1周时下降速率最快。

视网膜缺血再灌注后RGC凋亡分子机制研究进展

视网膜缺血再灌注(retinal ischemia reperfusion,RIR)损伤是常见的眼科疾病,主要表现为神经节细胞的凋亡,可造成视神经损害等严重的疾病,对患者的视觉功能和生活质量造成严重的影响。细胞凋亡是在基因控制下的自我消亡过程,受多种基因调控。我们结合文献,综述了不同基因在RIR后神经节细胞凋亡中的作用。

实验性网脱复位后未脱离区域视网膜组织形态学观察

目的:研究视网膜脱离(RD)复位后未发生脱离区域的视网膜组织形态改变。方法:将20只健康成年新西兰灰兔随机分为空白对照组2只和实验组18只,实验组在显微镜下行视网膜下注射透明质酸钠建立视网膜脱离自动复位动物模型,分别于术后10d、20d、30d处死实验兔并摘除眼球进行组织学观察。结果:未发生脱离区域的视网膜在复位早期表现为色素上皮层基本正常,感光细胞层、双极细胞层排列紊乱,感光细胞、双极细胞、神经节细胞均有变性。结论:RD复位后视网膜上光感受器的不完全再生,双极细胞和神经节细胞的不可逆变化,均可影响视功能的提高。

特发性黄斑裂孔内界膜的组织病理学特征及细胞成分研究

背景 研究特发性黄斑裂孔（IMH）内界膜的组织病理结构和细胞成分对理解IMH的发病机制,从而预防IMH的发病具有重要意义,但目前的研究报道结果不一致.目的 研究IMH内界膜的组织病理学特征及细胞成分,检测内界膜中胶质纤维酸性蛋白（GFAP）、CD45及CD44的表达分布情况,探讨IMH的发生机制.方法 收集2012年2月至2013年8月在广州医科大学附属第二医院行玻璃体切割联合内界膜剥离的IMH患者7例7眼的内界膜标本,制备石蜡切片,采用苏木精-伊红染色进行组织病理学观察,观察内界膜的组织结构及细胞成分;采用免疫组织化学法检测和定位内界膜中GFAP的表达;采用免疫荧光染色法检测内界膜中CD45及CD44的表达.结果 7例IMH内界膜石蜡切片均可见波浪弯曲状红染膜状结构,其中2例内界膜厚度均匀一致,含较少细胞,其他5例内界膜厚度不均,散在分布有色素上皮细胞、神经胶质细胞、成纤维细胞、巨噬细胞和淋巴细胞.免疫组织化学检测显示,GFAP表达于内界膜外层.免疫荧光染色表明,CD45阳性T淋巴细胞散在分布于内界膜组织中,黏附分子CD44多表达于内界膜的内层细胞.结论 IMH的内界膜上细胞成分较少,但Ⅲ期以上裂孔内界膜中存在神经胶质细胞和CD45阳性T淋巴细胞,表明IMH的发生过程伴有增生和免疫炎症反应.CD44作为黏附分子在内界膜中表达上调,促进IMH的增生和免疫炎症反应过程.

视网膜色素上皮细胞的生理功能及其参与的病变

视网膜色素上皮细胞能够维持光感受器的更新、再生,对维持视网膜外层的内环境稳定有重要意义,而且还是增生性玻璃体视网膜病变中最重要的细胞成分。视网膜色素上皮细胞参与了糖尿病视网膜病变、年龄相关性黄斑变性、视网膜色素变性等疾病的发生发展,是视网膜中被研究最多的细胞,虽来源于神经外胚叶,但其在特定的条件下能够分化和分裂的特性,让研究者看到了利用RPE来治疗相应的视网膜变性类疾病、遗传性疾病的希望。

屈光手术前严重视网膜病变的诊治和激光屈光手术的选择

目的:探讨激光屈光术前视网膜病变的及早诊断和处理方法及屈光手术方式的选择和疗效。方法:对预施准分子激光屈光手术的患者,扩瞳行三面镜检查,对有视网膜严重病变如裂孔伴格子样变性和囊样变性等的患者进行治疗,并随访后决定是否行屈光手术及选择何种术式。屈光术后随访24mo以上。结果:共检查648眼,52眼有视网膜裂孔及伴需处理的格子样变性或囊样变性区,占8.0%,有5眼因为视网膜病变严重,在处理眼底病变并随访后,未行准分子激光屈光手术。其余47眼在行激光处理视网膜病变后3wk以上,或冷凝手术3mo以后,查眼底原有视网膜裂孔牢固闭合、格子样变性囊样变性区激光光凝包绕确切并无新裂孔出现且视网膜无脱离,对其中26眼行LASEK手术、21眼行LASIK手术。结论:屈光手术不可忽视视网膜病变,应该将眼底的三面镜检查作为术前的常规检查项目。一旦发现格子样变性、囊样变性区和裂孔等病变,应及时采取预防性激光光凝等治疗,定期随访,如需行近视矫治手术应考虑手术的方法与时机。

单纯高度近视和病理性近视患者眼后段结构的形态学改变

目的对比单纯高度近视和病理性近视患者视盘区域、眼球壁等形态学改变,探讨用于评价高度近视眼的可测量指标。方法收集18～45岁高度近视患者29例52眼,采用深度扫频光学相干断层扫描仪DRI-OCT Atlantis等影像设备检测相关数据,将患眼分成单纯高度近视组和病理性近视组。对比两组视盘、近视弧、脉络膜萎缩弧形态;不同区域的视网膜、神经纤维层、脉络膜、巩膜的厚度等形态特征。结果本研究中单纯高度近视组27眼,病理性近视组25眼。两组患者年龄比较差异无统计学意义(P=0. 08),病理性近视组比单纯高度近视组的屈光度更大、眼轴更长、最佳矫正视力更差,差异均有统计学意义(均为P <0. 01)。单纯高度近视组、病理性近视组患者的视盘水平长度分别为(1440±419)μm和(1228±331)μm;垂直长度分别为(1906±430)μm和(2085±304)μm;两组比较差异均无统计学意义(均为P> 0. 05)。视盘椭圆指数分别为0. 78±0. 16、0. 63±0. 16,两组比较差异有统计学意义(P <0. 01)。按照视盘椭圆指数0. 8以上为正常分类(8眼因视盘界限难以确定未纳入该项分析),单纯高度近视组中视盘正常形态13眼、异常12眼,病理性近视组视盘正常形态3眼、异常16眼,两组差异有统计学意义(P=0. 01)。两组单侧弧和环形弧分布差异无统计学意义(P=0. 84)。两组单纯近视弧和色素上皮脉络膜萎缩区分布差异有统计学意义(P <0. 01)。视网膜厚度:单纯高度近视组和病理性近视组患者视网膜厚度中心区域差异无统计学意义(P> 0. 05);病理性近视组患者的其余各区域视网膜厚度均比单纯高度近视组薄,差异均有统计学意义(均为P <0. 05)。神经纤维厚度:两组颞侧区域神经纤维厚度差异无统计学意义(P> 0. 05);病理性近视组的其余各区域神经纤维厚度均比单纯高度近视组薄,差异均有统计学意义(均为P <0. 01)。病理性近视组患者各区域脉络膜厚度比单纯高度近视组薄,差异均有统计学意义(均为P <0. 05)。单纯高度近视组均未完整显示全层巩膜厚度;病理性近视组19眼可显示全层巩膜厚度。结论单纯高度近视进展为病理性近视时,主要表现为近视加深、眼轴变长、最佳矫正视力下降,脉络膜萎缩弧增加,视网膜厚度、神经纤维厚度大部分区域更薄;脉络膜厚度普遍变薄。