Objective: Extensive retinal ischemia caused by proliferative diabetic retinopathy (PDR) may develop into neovascular glaucoma (NVG). We searched for the proteins which might participate in neovascularization through the analysis of aqueous humor (AH) proteomics in patients with NVG secondary to PDR to increasing the understanding of the possible mechanism of neovascularization. Methods: We collected 12 samples (group A) of AH from patients with NVG secondary to PDR as the experimental group and 7 samples (group B) of AH from patients with primary acute angle-closure glaucoma (PAACG) & diabetes mellitus without diabetic retinopathy (NDR) as the control group. Differential quantitative proteome analysis of the aqueous humor samples was performed based on the data-independent acquisition (DIA) method. The differentially expressed proteins were functionally annotated by Ingenuity Pathway Analysis (IPA). The important differentially expressed proteins were validated in another group (group A: 5 samples and group B: 5 samples) by parallel reaction monitor (PRM) approach. Results: A total of 636 AH proteins were identified, and 82 proteins were differentially expressed between the two groups. Functional annotation showed that the differentially expressed proteins were mainly associated with angiogenesis and cell migration. Signaling pathways analysis showed that the proteins up-regulated in group A were mainly related to Liver X receptor/Retinoid X receptor (LXR/RXR) activation and acute reaction. Conclusions: This study presented a pilot work related to NVG secondary to PDR, which provided a better understanding of the mechanisms governing the pathophysiology of NVG.

青光眼是全球第2位致盲眼病,是一类以特征性视神经萎缩和视野缺损为共同特征的疾病,最主要的危险因素是病理性眼压升高.目前该病发病机制、发展过程尚不完全清楚,在研究该病病理生理中,高眼压动物模型的建立起到很大作用,作为人类研究疾病的载体,动物模型是探索疾病发病机制的有力工具.本文就国内外学者研究过程中常用的高眼压实验动物模型(包括实验诱导模型和转基因模型)进行系统概括并简要分析各种模型的优缺点.

眼科学属于临床医学中的三级学科,课程学时数相对较少,每一章节有各自的特点,内容琐碎且相对独立,总体上给学生"形散"而"神也散"的印象[1],这就对眼科理论教学提出了更高的要求。传统的眼科教学多采用以幻灯为基础的讲授式教学法,授课教师由若干名教师组成教学团队。这种教学方法存在一些弊端:虽然有集体备课之名,但教师之间很少有沟通,讲课时"各自为战",讲授的知识点缺乏连贯性[2]。另外,传统大课的授课教师主宰课堂,学生始

Objective In recent years,alcoholic poisoning has occurred due to drinking fake wine.The aim of this study was to investigate the variation of cell autophagy level,in the process of sodium formate inducing retinal photoreceptor cells (661 w) damaged.Methods 661W cells were exposed to 15 and 30 mM concentration of sodium formate for 24h respectively,then,the autophagy level was detected by monodansylcadaverine staining.The autophagy formation of 661W cells was observed by transmission electron microscopy.The expression of microtubule associated protein LC3,p-mTOR,Beclin 1,JNK and p-JNK were evaluated by western blotting.Intracellular reactive oxygen species (ROS) were detected using 2',7'.dichlorofluorescein diacetate (DCFH.DA) staining,followed by flow cytometric analysis.Results Compared with the control group,sodium formate at concentrations of 15 or 30 mM markedly increased the level of autophagy level was observed under fluorescence microscope.Autophagosomes were observed under transmission electron microscope.Western blotting showed that the levels of LC3-Ⅱ.Beclin 1,p JNK exhibited increased.while the expression of p-mTOR protein was decreased.And flow cytometry showed that the level of reactive oxygen species increased.Conclusion Sodium formate can induce autophagy of 661W cells.Autophagy may be involved in the process of visual impairment caused by fakes poisoning.

Objective Methanol intoxicated accidents caused by drinking fake wine take place now and then in the world.Some people become blindness due to methanol selective neurotoxicity.This study was to investigate the effects of sodium formate exposure on photoreceptor cells (661W cells).Methods 661W cells were exposed to dfferent con-centrations of sodium formate for 6-24 h.The cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphen-yl-2H-tetrazolium bromide (MTT)assays.Then,661W cells were exposed to 15mM and 30 mM sodium formate for 24 h.Apoptosis was determined by Hoechst 33342/propidium iodide (PI)staining,visualized under a fluorescence micro-scope,and annexin V-FITC staining using flow cytometry.The activation of Bax,Bcl-2,cleaved-caspase-3 and cleaved-caspase-9,was evaluated by western blotting.Results MTT assay showed that,sodium formate treatment induced a decrease in 661W cell viability in a time-and dose-dependent manner;DCFH-DA staining and flow cytometry showed that ,sdium formate induces 661W cells apoptosis.Western blotting showed that,661W cells exposed to sodium formate for 24 h increased levels of Bax,cleaved-caspase-3 and cleaved-caspase-9,but decreased levels of Bcl-2.Conclusion These results suggest that sodium formate treatment reduced the cell viability in a time-and dose-dependent manner and triggers caspase-dependent apoptosis of 661W cells.

Glaucomais a group of diseases characterized by optic nerve damage and visual field defect, and pathological high intraocular pressure is a risk factor for glaucoma. Glaucoma is affected by the interaction of multiple genes and environmental factors, and inflammation may be involved in the pathogenesis of glaucoma. A great deal of studies have confirmed that high expression of connective tissue growth factor(CTGF), tumor necrosis factor-α(TNF-α), interleukins(ILs), nuclear factor-kappa B(NF-κB)and various cytokines in the aqueous humor of patients with glaucoma, which have a close correlation with pathogenesis of glaucoma.This article reviews the progress of inflammatory cytokines and their relationship with glaucoma.

目的:探讨17-β雌二醇(E2)对压力诱导的视网膜神经节细胞(RGC-5细胞)凋亡的保护作用,并阐明其可能作用机制.方法:RGC-5细胞分为正常对照组、单纯加压组和加压联合E2组.取处于对数生长期细胞,应用MTT法检测各组细胞相对存活率;Hoe33342核染色法检测各组细胞凋亡形态;Western blotting法检测各组细胞凋亡相关蛋白bax、bcP2、P53、iASPP和cleaved-caspase-3表达水平.结果:MTT法检测,与对照组比较,单纯加压组及加压联合E2组细胞存活率均降低(P＜0.05);加压联合E2组细胞存活率高于单纯加压组(P＜0.05).细胞染色检测,加压联合E2组细胞核浓缩及凋亡小体出现率低于加压组.与对照组比较,单纯加压组及加压联合E2组bax、P53和cleaved-caspase3表达水平均升高(P＜0.05),bcl-2和iASPP表达水平均降低(P＜0.05);与单纯加压组比较,加压联合E2组bax、P53和cleaved-caspase-3表达水平降低(P＜0.05),bcl-2和iASPP表达水平升高(P＜0.05).结论:E2对加压条件下RGC-5细胞有保护作用,可以减少加压条件下的RGC-5细胞的凋亡.

Incidents associated with methanol intoxication resulting from the consumption of fake wine occur not infrequently worldwide. Certain individuals are made blind due to methanol poisoning. The present study aimed to investigate the effects of sodium formate exposure on photoreceptor cells (661W cells). The 661W cells were exposed to sodium formate for 6‑24 h and cell viability was determined using a 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5‑diphenyl‑2H‑tetrazolium bromide (MTT) assay. Subsequently, the 661W cells were exposed to 15 or 30 mM sodium formate for 24 h. The level of apoptosis was determined using Hoechst 33342/propidium iodide staining, visualizing the cells under a fluorescence microscope, and annexin V‑fluorescein isothiocyanate staining, using flow cytometric analysis. Intracellular reactive oxygen species (ROS) were measured using 2',7'‑dichlorofluorescein diacetate (DCFH‑DA) staining, followed by flow cytometric analysis. Autophagy of the 661W cells was measured by monodansylcadaverine staining. The activation of phosphorylated c‑Jun N‑terminal kinase (p‑JNK), B‑cell lymphoma (Bcl‑2), Bcl‑2‑associated X protein, cleaved caspase‑3, cleaved caspase‑9 and microtubule‑associated protein 1A/1B‑light chain 3 (LC3) was assessed by western blotting. The effects of Z‑VAD‑fmk (a pan‑caspase inhibitor) and SP600125 (a JNK inhibitor) on the viability of the sodium formate‑induced 661W cells were determined using an MTT assay. Sodium formate treatment induced a decrease in the viability of the 661W cells in a time‑ and a dose‑dependent manner. In addition, sodium formate at concentrations of 15 or 30 mM markedly increased the level of apoptosis and the ROS levels, as measured by DCFH‑DA staining of the 661W cells. Additionally, 661W cells exposed to sodium formate for 24 h exhibited increased levels of p‑JNK, Bax, cleaved caspase‑3, cleaved caspase‑9 and LC3II (the phosphatidylethanolamine‑modified form of LC3), although the level of Bcl‑2 was decreased. Furthermore, cell cytotoxicity and autophagy were induced upon treatment with sodium formate. Z‑VAD‑fmk and SP600125 were able to effectively circumvent the effects of sodium formate on cell viability. These results suggested that the cytotoxicity induced by sodium formate induces the activation of the JNK signaling pathway, leading to caspase‑dependent apoptosis. Increased levels of autophagy were also observed during the process of 661W cell damage induced by sodium formate.

先天性葡萄膜外翻(CEU)是由于瞳孔缘虹膜色素上皮层过度增生并向前覆盖于虹膜前基质表面所致,属于一种罕见的先天性异常.几乎100％的先天性葡萄膜外翻都会先后出现进展性青光眼,多数患者伴随其他眼部畸形和全身异常[1-3].我院现有1例双眼先天性葡萄膜外翻伴继发性青光眼病例如下。

Objective This study was to explore the expression of iASPP on pressure-induced apoptosis of cultured retinal ganglion cells (RGC-5 cells).Methods The RGC-5 cells were cultured under the pressure of 60mmHg and 80mmHg for 48 hours.Cell viability were determined by MTT assays.Cells apoptosis was determined by Hoe33342. The expression of iASPP and P53 was determined by using semi-quantitative RT-PCR and Western blot respective. Results MTT assay showed that the RGC-5 cells viability was decreased in a pressure-dependent manner.As the pressure was up,the apoptosis of RGC-5 cells was increased,the expression of P53 was elevated and the expression of iASPP was decreased.Conclusion The reduced expression of iASPP gene may increase the activity of p53 and promote the apoptosis of RGC-5 cells under pressure.Enhancing expression of iASPP may play a role as a neuroprotect.

Objective To study the influence of the specific inhibitor of autophagy 3-methyladenine(3-MA)in apoptosis of retinal ganglion cells(RGCs),and to clarify the protective effect of 3-MA on RGCs under hypoxic micro-environment.Methods The RGCs at logarithmic growth phase were collected and divided into control group(PBS),3-MA group(6mmol·L-13-MA),CoCl2 group(300μmol·L-1 CoCl2)and 3-MA combined with CoCl2 group(6 mmol·L-1 3-MA+300μmol·L-1 CoCl2).MTT method was conducted to evaluate the optimal concentration of CoCl2 and the inhibitory rate of proliferation of RGCs in various groups;Acridine orange/Ethidium bromide(AO/EB)staining was used to detect the morphology of RGCs;Monodansylcadaverine(MDC)staining was used to detect the autophagic vacuoles of RGCs;Western blotting method was used to test the expression levels of apoptotic proteins P53,Bax,caspase-9,caspase-3,iASPP and autophagic protein LC3in RGCs in various groups.Results The 30%inhibitory concentration(IC30)of CoCl2 was 300μmol·L-1.Compared with CoCl2 group,the inhibitory rate of proliferation of RGCs in 3-MA+CoCl2 group was decreased(P0.05).The apoptosisbody and autophagic vacuole in RGCs in various groups were observed under fluorescence microscope.The Western blotting results showed that compared with control group,the expression levels of P53,Bax,caspase-9, caspase-3,and LC3in RGCs in the other groups were increased(P0.05)and the expression level of iASPP was decreased(P0.05);compared with CoCl2 group,the expression levels of P53,Bax,caspase-9,caspase-3,and LC3in RGCs in 3-MA +CoCl2 group were decreased(P0.05)and the expression level of iASPP was increased(P0.05);compared with 3-MA group,the expression levels of P53,Bax,caspase-9,caspase-3,and LC3in RGCs in 3-MA +CoCl2 group were increased(P0.05)and the expression level of iASPP was decreased(P 0.05).Conclusion Under hypoxic micro-environment,the inhibitor of autophagy 3-MA has protective effect on apoptosis of RGCs induced by CoCl2.

Simvastatin is a cholesterol-lowering drug which exhibits numerous pleiotropic effects including anticancer activity. Yet, the anti-cancer effects in choroidal melanoma remain poorly characterized. Therefore, in this study, we investigated the effects of simvastatin on OCM-1 cells growth, apoptosis and cycle. Simvastatin showed an inhibitory effects on OCM-1 cells viability in dose-dependent (2-10 mu M) and time-dependent (24-72 h) manner. Further study suggested that simvastatin-induced inhibition OCM-1 cells proliferation was associated with G1 phase arrest, decreased protein and mRNA expression of proliferation marker cyclin D1, cyclin E, cyclin dependent kinase (CDK)2 and increased expression of CDK inhibitory protein P21. In addition, simvastatin resulted in an increase in levels of reactive oxygen species (ROS) in OCM-1 cells and simvastatin significantly triggered apoptosis in OCM-1 cells, which was characterized by increased chromatin condensation, activation of caspase-9 and cleaved-caspase-3, increased expression mitochondrion-related apoptosis protein of P53, Bax and decreased expression of Bcl2 and iASPP. Collectively, our study demonstrated that simvastatin can efficiently inhibit proliferation and induce apoptosis in OCM-1 cells. (C) 2013 Elsevier Ltd. All rights reserved.

例1,患者,男,21岁,因右眼胀痛、眼红伴视力下降1年余来诊.既往史:19年前曾诊断为"右眼青光眼",行右眼抗青光眼手术(具体不详).入院查体:视力右眼手动/眼前,左眼0.8;眼压右眼59 mmHg(1 mmHg=0.133 kPa),左眼15 mmHg;右侧颜面部及上睑可见片状血管瘤;球结膜混合性充血,结膜及巩膜血管扩张,角膜水肿,直径约13 mm,前房深,瞳孔圆,直径约8 mm,对光反射迟钝,12:00位可见虹膜根部切除孔,眼底视盘色苍白,生理凹陷深,杯盘比(C/D)≈1.0,血管偏鼻侧,呈屈膝状爬行.左眼未见明显异常.B型超声检查:右眼脉络膜血管瘤.房角检查:房角结构紊乱.入院诊断:(1)右眼抗青光眼术后眼压失控.(2)右侧Sturge-Weber综合征.(3)右侧视神经萎缩.

患者女,61岁.因双眼畏光伴异物感1个月,于2010年5月6日入院就诊于我院门诊.患者缘于1个月前无明显诱因出现双眼畏光伴轻微异物感,自行休息后无缓解,遂就诊于当地医院,诊断为“角膜炎(双)”,予“氧氟沙星滴眼液(泰利必妥)”、“小牛血去蛋白提取物眼用凝胶(速高捷)”治疗2周后,上述症状末见明显缓解,视物模糊加重,为求进一步诊治来我院就诊.眼部检查:视力:右眼0.3,左眼0 4,双眼矫正不应.眼压:右眼12 mm Hg,左眼15 mm Hg。

例1患者女,71岁.因右眼视力渐进性下降20年,加重伴胀痛2个月入院.既往:30年前曾有急性发作史.眼部检查:视力:右眼:0.15,左眼:0.8.眼压:右眼:24mm Hg(已用噻吗洛尔滴眼液1周),左眼:22 mm Hg.右侧颜面部及上、下睑皮肤可见明显色素沉着(图1).右眼:球结膜充血,巩膜表面散在斑块状色素沉着,前房浅,虹膜纹理模糊,较左眼色深且基质隐窝少,瞳孔圆,直径3 mm,对光反射(-),晶状体混浊,眼底视盘色苍白,病理性凹陷,C/D=0.9,后极部视网膜可见大量色素沉着;左眼:球结膜充血,前房浅,虹膜纹理模糊,瞳孔圆,直径3 mm,对光反射(-),晶状体混浊,眼底视盘色淡,病理性凹陷,C/D=0.5.

Objective To investigate the epidemiological feature,complication and the therapeutic of patients with penetrating ocular trauma. Methods A retrospective analysis on clinical data was performed on 292 patients with penetrating ocular trauma. Results The ratio of male and female was 5.49∶1;the ratio of right eye injure and left eye injure was 1.05∶1;the high incidence was in 20-50 years groups;the major causes of injury were foreign bodies and fight;the complications were cataract,intraocular foreign bodies and hyphema. Conclusion Ocular injury is one of main caused of blindness.The analysis on personage and cause of ocular injure patients show that most of eye injuries may be prevented.

BACKGROUND:Ahmed glaucoma valve(AGV) is usually implanted at the superotemporal area of eyes.Corneal endothelial cells cannot regenerate,so the repair of the endothelial cells mainly depend on the extension and progradation of the healthy cells in other area.Therefore,changes of density and shape are observed in the corneal endothelial cells after AGV implantation.OBJECTIVE:To observe the changes of density and morphology of corneal endothelial cells after AGV implantation.METHODS:Ahmed glaucoma valves were implanted in 34 eyes of 34 patients with refractory glaucoma.Density and morphology of corneal endothelial cells were evaluated in the superotemporal,superonasal,infratemporal,infranasal,and central corneal areas to calculate mean value of total cornea before and at 3 and 6 months after surgery.Percentage of hexagonal cells was statistically summarized.RESULTS AND CONCLUSION:Mean density of corneal endothelial cells was statistically decreased following AGV implantation(P<0.05),In particular,the decrease was obvious in the superotemporal area.Density of corneal endothelial cells was not changed in central area before and after AGV implantation.Morphological changes demonstrated that hexagonal cells were increased,but polygon cells were increased(P<0.05).Density of corneal endothelial cells was gradually decreased,and morphology was also changed at 6 months after AGV implantation,suggesting that more care should be taken during intra-operation in order to minimize damage to the endothelium and prolong monitoring time of corneal endothelial cells following AGV implantation.

OBJECTIVE:To investigate the expression of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) in the sclera of lamina cribrosa in rat chronic elevated intraocular pressure (IOP) and its the relationship with the pathogenesis of glaucoma.METHODS:It was an experimental study. Chronic ocular hypertension (OHT) model was induced in the left eyes of 43 Wistar rats by cauterizing episcleral venous while the right eyes were used as control. The rats were divided into three groups: 13 for immunohistology, 15 for Western blotting, and 15 for RT-PCR by randomly computerized assignment and sacrificed at week 12 after OHT induction. The expression of MMP-2, MMP-9, TIMP-1, and TIMP-2 in the sclera lamina cribrosa was detected using immunohistology, Western blotting, and RT-PCR technique, respectively. Repeated measures ANOVA of two-factor Studies in SAS statistic software were used to analyze the data.RESULTS:After 12 weeks, compared with control eyes, the IOP of rat OHT eyes was significantly (F = 1519.67, P < 0.01) elevated. The expression of MMP-2 and MMP-9 was increased in cell nucleus and cytoplasm in sclera lamina cribrosa in rat OHT when compared to control eyes with negative expression. No expressions of TIMP-1, TIMP-2 in sclera lamina cribrosa were found in both OHT and control eyes. The mean gray-scale values of MMP-2, MMP-9, TIMP-1, and TIMP-2 in OHT were significantly (F = 405.55, F = 436.11, F = 1167.77, and F = 4629.64, P < 0.01) higher than control eye by Western blotting (193.88 +/- 8.84 vs 117.38 +/- 10.76, 202.65 +/- 8.37 vs 134.13 +/- 5.06, 283.63 +/- 5.65 vs 186.88 +/- 7.14, and 284.75 +/- 5.50 vs 183.0 +/- 5.58), while by RT-PCR (200.50 +/- 3.25 vs 181.88 +/- 9.36, 200.13 +/- 2.95 vs 181.75 +/- 5.85, 201.88 +/- 3.14 vs 179.25 +/- 9.21, and 195.50 +/- 3.55 vs 179.75 +/- 7.12), respectively.CONCLUSION:The increased expression of MMP-2, MMP-9, TIMP-1, and TIMP-2 in lamina cribrosa in rat OHT eye indicates that MMPs and TIMPs may be involved in the pathogenesis of glaucoma.

Objectives To observe the relation of postoperation visual field and postoperation IOP of advanced glaucoma with tubular visual field.Methods 32 patients(44 eyes) were divided into three groups by postoperation IOP.Group A:15 eyes,postoperation IOP18 mmHg,group B:15 eyes,postoperation IOP is between 18 mmHg and 12 mmHg,group C:14 eyes,postoperation IOP is between 12 mmHg and 5 mmHg.The vision,MD and postoperative satisfaction among three groups of subjects were compared. Results Group A:the MD of postoperation descend,and the discrepancy is statistically significant,which means visual field is still decreasing even if postoperation IOP18 mmHg,group B:the MD of postoperation is lightly promoting,and the discrepancy is not statistically significant,which means the depression of postoperation IOP is partly helpful to the aggravation of visual field and development of advanced glaucoma,group C:the MD of postoperation is obviously promoting,and the discrepancy is statistically significant, which means controlling the postoperation IOP within 12～5 mmHg can obviously promote the visual field of advanced glaucoma.Conclusions We should control the postoperation IOP of advanced glaucoma within 12～5 mmHg,and testing visual field regularly is instructive to monitoring the variation of visual field of advanced glaucoma.

Objective:To establish menopausal rat models with ovariectomized rats by injecting different levels of progesterone,detect the changes of nitric oxide level in serum,observe the effect of progesterone on apoptosis of retinal ganglial cells.Methods:The levels of progesterone and nitric oxide in serum were detected by RIA and colorimetry,respectively;the apoptosis of retinal ganglial cells was detected by TUNEL technique.Results:The level of nitric oxide increased with progesterone level,there was a negative correlation between apoptosis of retinal ganglial cells and progesterone level.Conclusion:Proper progesterone can inhibit the apoptosis of retinal ganglial cells by promoting the production of nitric oxide,in order to protect optic nerve.