川芎嗪防治增殖性玻璃体视网膜病变的实验研究

目的探讨川芎嗪对实验性增殖性玻璃体视网膜病变(PVR)的疗效.方法将30只新西兰大白兔的60只眼随机分为3组,分别在玻璃体腔内注入自血0.1ml及生理盐水0.1ml、自血0.1ml加川芎嗪0.2mg、自血0.1ml加川芎嗪0.5mg,观察川芎嗪对眼内纤维增生的抑制作用.结果注入川芎嗪的实验组玻璃体增生较对照组少,高浓度组的川芎嗪较低浓度组抑制作用无明显差异.结论川芎嗪对防治PVR有效,本研究为川芎嗪应用于临床提供了依据.     

四川省整合防盲资源开展大规模白内障防盲手术的探讨

目的:探索四川省整合利用各种防盲资源,提高大规模白内障防盲手术项目的效率与质量的方法,推动防盲工作的发展。方法:分析比较2000年以来由卫生与残联各自单独与合作开展大规模白内障防盲复明手术项目效果。结果:四川省卫生与残联合作2004/2006高质高效完成8548例白内障防盲复明手术,取得了显著成果。手术质量与工作效率较卫生、残联各自单独开展有较大提高。结论:以政府为主导协调整合各方防盲资源开展防盲工作,是防盲工作可持续发展的方向。     

年龄相关性黄斑变性的眼底荧光造影特点(英文)

目的:探讨眼底荧光素血管造影(fundus fluorescein angiog-raphy, FFA)在年龄相关性黄斑变性(age-related macular degeneration, AMD)患者中的特征及临床意义。方法:用日本Nikon NF-505眼底照相机对112例149眼进行FFA检查。结果:在149眼中,萎缩型90眼(60.4%),渗出型59眼(39.6%),依据CNV造影特点和CNV与黄斑中心凹的距离分为中心凹下CNV包括经典型7眼,隐匿型26眼,盘状瘢痕化9眼,旁中心凹CNV包括经典型2眼,隐匿型12眼,中心凹外CNV3眼均为隐匿型。结论:FFA可以发现AMD患者的CNV,并能分辨其性质和部位,有助于指导治疗和评价预后。     

玻璃体腔注射曲安奈德治疗糖尿病黄斑囊样水肿的护理

黄斑区弥漫性水肿是导致糖尿病视网膜病变病人视力严重下降的主要原因，目前常用的治疗方法为激光格栅样光凝及药物保守治疗，但效果都不理想^[1]。曲安奈德是一种长效糖皮质激素，玻璃体腔注射具有很强的抗炎作用，能有效地改善黄斑水肿^[1,2]。我科采用此方法治疗22例（25眼）弥漫性黄斑水肿病人，效果较满意。现将护理报告如下。     

五味子乙素对视网膜母细胞瘤移植癌裸鼠存活和VEGF表达的影响

目的：探究五味子乙素对视网膜母细胞瘤移植癌裸鼠存活和血管内皮生长因子(VEGF)表达的影响。方法：裸鼠随机分为4组：移植瘤模型 (Y79) 组、五味子乙素低中高剂量(10、20、50 mg/kg BW)组。末端脱氧核苷酸转移酶介导的dUTP缺口末端标记法(TUNEL)染色,检测肿瘤组织细胞凋亡。免疫组化染色检测肿瘤组织中VEGF表达。蛋白印迹检测肿瘤组织中VEGFR2、P-P38、P38、P-Hsp27和Hsp27蛋白水平。结果：五味子乙素(10、20、50 mg/kg)组裸鼠肿瘤体积小于移植瘤模型组(P<0.01)。同时,五味子乙素(10、20、50 mg/kg)组裸鼠存活率高于移植瘤模型组(P<0.01)。与移植瘤模型组相比,五味子乙素(10、20、50 mg/kg)组肿瘤组织细胞凋亡升高(P<0.01)。另外,五味子乙素(10、20、50 mg/kg)组肿瘤组织中VEGF表达低于移植瘤模型组(P<0.01)。与移植瘤模型组相比,五味子乙素(10、20、50 mg/kg)组肿瘤组织VEGFR2蛋白水平及P-P38/P38和P-Hsp27/Hsp27比值下降(P<0.01)。结论：五味子乙素可减弱视网膜母细胞瘤移植癌裸鼠肿瘤生长,提高存活率,降低VEGF表达,抑制VEGF信号通路活化。     

IGF-1系统与糖尿病视网膜病变的研究进展

糖尿病视网膜病变(DR)是导致患者失明的重要原因.引起DR的确切机制尚不十分清楚,有关胰岛素样生长因子-1(IGF-1)等多种生长因子参与其病理过程的观点日益受到人们重视[1].IGF-1系统具有复杂的生物学效应,随着重组人胰岛素样生长因子-1(rh IGF-1)的成功合成及对其结构与功能的深入研究,人们发现IGF-1在DR的发展中发挥着相当重要的作用,本文就此相关进展作一综述.     

高度近视眼伴后巩膜葡萄肿黄斑裂孔性视网膜脱离治疗的临床研究

目的:研究高度近视眼伴后巩膜葡萄肿黄斑裂孔性视网膜脱离的临床治疗效果及不同手术方式的有效性。方法:回顾性分析2003-05/2008-05诊断治疗的高度近视眼伴后巩膜葡萄肿黄斑裂孔性视网膜脱离91眼,分析视网膜复位情况及最佳矫正视力。结果:在这些视网膜脱离的治疗中,有6种手术方式:单纯黄斑区巩膜外垫压12眼,5眼(42%)首次术后视网膜回贴;单纯玻璃体腔气体充填15眼,6眼(40%)首次术后视网膜回贴;平坦部玻璃体切除联合球内气体充填20眼,14眼(70%)首次术后视网膜回贴;平坦部玻璃体切除、视网膜前膜剥离联合球内气体充填16眼,11眼(69%)首次术后视网膜回贴;巩膜环扎、玻璃体切除、视网膜前膜剥离联合球内气体充填25眼,18眼(72%)首次术后视网膜回贴;巩膜环扎、玻璃体切除联合硅油填充13眼,10眼(77%)首次术后视网膜回贴。64眼(70%)首次手术治疗后视网膜回贴,85眼(93%)视网膜回贴。结论:玻璃体切除联合球内惰性气体或硅油填充是治疗高度近视眼伴后巩膜葡萄肿黄斑裂孔性视网膜脱离的最有效方法。     

翼状胬肉切除联合自体游离结膜瓣移植术疗效观察

目的:通过对翼状胬肉切除联合自体游离结膜瓣移植术治疗翼状胬肉的观察,分析该手术方式的临床疗效。方法:利用眼科手术显微镜分别对30例38眼进行翼状胬肉切除联合自体游离结膜瓣移植术。结果:通过上述手术方式,患者术后不适反应较轻、角膜创面愈合快,随访1年,复发2眼(5.26%)。结论:翼状胬肉切除联合自体游离结膜瓣移植术能有效地减少术后复发及瘢痕形成。     

Effects of travoprost on actin cytoskeleton and β-catenin in the human trabecular meshwork cells treated with Dexamethasone

Objective To investigate the effect of travoprost on changes of actin cytoskeletal and β-catenin protein in the cultured human trabecular meshwork (HTM) cells treated with dexamethasone (DEX). Methods It was a control experiment study. The HTM cells were cultured in vitro and divided into control group, DEX (1 × 10-6mol/L) group, travoprost (1 × 10-6mol/L) group, and DEX (1 ×10-6mol/L) plus travoprost (1 × 10-6mol/L) group. F-actin in the HTM cells was detected by FITC-phallodin and observed under a fluorescence microscope. The expression of β-catenin was determined by immunofluorescence and western-blot. Statistical analysis was performed using SPSS13.0 software. The difference of β-catenin expression among groups was analyzed through variance analysis and, further by q test. Results The cultured HTM cells were identified by immunohistochemistry. A reorganization of actin cytoskeletal and a formation of cross linked actin networks (CLANs) were seen in the HTM cells treated with DEX, which were partially reversed by the treatment with DEX plus travoprost. An increase of the expression of β-catenin was discovered in the HTM cells treated with DEX, which was also partially reversed by the treatment with DEX plus travoprost. The amount of β-catenin protein in untreated control group, DEX group, DEX plus travoprost group and travoprost group were 0. 84 ± 0. 03,1.65 ± 0. 05, 1.21 ± 0. 05, and 0. 65 ±0. 04, respectively. Expression of β-catenin was significantly ( F = 143.07, P ＜ 0. 05 ) different when compared untreated control group with DEX group ( q = 15. 32 ,P ＜0. 05 ), untreated control group with DEX plus travoprost group (q = 11.40,P＜0. 05), DEX group with DEX plus travoprost group (q =9. 38,P ＜ 0. 05 ), DEX group with travoprost group ( q = 16. 55, P ＜ 0. 05 ), and DEX plus travoprost group with travoprost group (q = 14. 31 ,P ＜ 0. 05 ). No difference was found in untreated control group and travoprost group(q = 2. 84, P ＞ 0. 05 ). Conclusions Our results suggest that reversion of the changes of actin organization and β-catenin by travoparost in the HTM cells treated with DEX may partially elucidate the mechanism of action of increasing outflow by which travoprost reduces intraocular pressure.