兔角膜碱烧伤后角膜和房水中VEGF的表达

目的探讨兔角膜碱烧伤后血管内皮生长因子(vascular endothelial growth fac-tor,VEGF)的表达。方法用1mol·L-1氢氧化钠溶液烧伤兔角膜建立角膜碱烧伤动物模型,未烧伤眼作为对照;免疫组织化学方法检测正常对照组以及角膜碱烧伤后1d、4d、7d、10d、14d VEGF蛋白在角膜中的表达情况,同时用酶联免疫吸附测定法(enzymelinkedi mmunosorbent assay,ELISA)检测房水中VEGF蛋白的表达量。结果正常对照组中,VEGF蛋白在角膜上皮细胞和内皮细胞仅有弱阳性表达,基质层表达不明显;房水中VEGF表达量为(0.168±0.038)μg·L-1。碱烧伤后,角膜各层组织中VEGF蛋白表达较对照组增强(P<0.05),其中基质层可见大量炎性细胞浸润,伴随有VEGF蛋白在该区域的集中表达。房水中VEGF的表达量于烧伤后1d为(0.336±0.072)μg·L-1,随后持续升高,至14d达(1.294±0.216)μg·L-1,各检测点均较对照组有显著差异(P<0.05)。同时房水中VEGF表达量与角膜中检测结果呈正相关(P<0.01)。结论角膜碱烧伤后早期角膜组织和房水中VEGF蛋白的表达均显著增高,提示VEGF可能在损伤后的早期修复过程中发挥着作用。     

小鼠角膜碱烧伤后缺氧诱导因子-1α和水通道蛋白-1在角膜中的表达

目的　检测小鼠角膜碱烧伤后缺氧诱导因子-1α（hypoxia inducible factor-1 alpha,HIF-1α）及水通道蛋白-1（aquaporin-1,AQP1）的表达情况,探讨角膜碱烧伤后HIF-1α及AQP1在其损伤机制中的作用。方法　选用健康成年雌性昆明系小鼠48只,左眼为对照组,右眼用1 mol·L^-1 NaOH建立角膜碱烧伤模型,并随机分为碱烧伤后1 d组、4 d组、7 d组、14 d组,每组12只,免疫荧光染色法和实时荧光定量PCR法检测碱烧伤后角膜HIF-1α、AQP1的表达情况。结果　免疫荧光染色结果显示,对照组中HIF-1α在角膜上皮基底膜弱表达,碱烧伤后1 d HIF-1α在角膜上皮层表达开始增强,4 d在角膜上皮层和基质层均表达,至7 d时HIF-1α表达达到峰值;对照组中AQP1在角膜内皮层弱表达,碱烧伤后1 d,AQP1在角膜内皮层表达开始增强,4 d和7 d时AQP1在角膜内皮层和基质层均表达,且表达更强。实时荧光定量PCR结果显示,与对照组（188.70±33.99）相比,碱烧伤后1 d组（269.70±15.68）、4 d组（350.50±67.26）、7 d组（272.10±6.88）的HIF-1α mRNA相对表达量增加,差异均有统计学意义（均为P<0.05）;与对照组（36.43±3.95）相比,碱烧伤后1 d组（61.90±5.45）、7 d组（48.34±1.33）的AQP1 mRNA相对表达量增加,差异均有统计学意义（均为P<0.05）。结论　碱烧伤引起了角膜病理性变化,HIF-1α和AQP1参与碱烧伤后角膜损伤的病理机制。     

缺氧诱导因子-1α及促红细胞生成素在大鼠角膜新生血管中的表达

目的:探讨缺氧诱导因子-1α(hypoxia-inducible factor-1α,HIF-1α)及促红细胞生成素(erythropoietin,EPO)在碱烧伤大鼠角膜组织中的表达,评估其在角膜新生血管(corneal neovascularization,CNV)发生发展中的作用。方法:健康3月龄SD大鼠,随机分为实验组和对照组,碱烧伤法建立CNV模型,分别于造模成功后1,3,5,7,14d测量CNV的长度并计算面积,同时取角膜组织以免疫组织化学检测HIF-1α及EPO的表达部位,并以RT-PCR法检测其mRNA的表达情况,实验数据采用SPSS 20.0处理。结果:碱烧伤后1,3,5,7,14d,CNV的面积随时间逐渐增加,7d生长最为旺盛,14d后生长减慢。免疫组织化学提示:正常角膜各层未见HIF-1α的表达,可见微量EPO,碱烧伤后1d时HIF-1α及EPO免疫活性增强,主要表达于角膜上皮及内皮层。RT-PCR结果显示HIF-1α及EPO mRNA的表达在正常大鼠角膜组织中表达极少,在角膜碱烧伤后3d表达增强,7d达到高峰,14d后明显下降;不同时间点组间比较存在统计学差异(P<0.05)。结论:HIF-1α和EPO与CNV的形成密切相关。     

HIF-1α在大鼠角膜碱烧伤后的作用研究

目的检测大鼠角膜碱烧伤后缺氧诱导因子-1α(HIF-1α)的表达变化,探讨其在角膜碱烧伤损伤机制中的作用。方法建立大鼠角膜碱烧伤模型,采用免疫组织化学与原位杂交技术,检测角膜碱烧伤后不同时间HIF-1α在角膜各层中的表达变化。结果在正常角膜组织中,角膜各层均未见HIF-1α免疫染色,碱烧伤后1d时HIF-1α免疫活性增强,且3d时表达最强,15d时明显下降,30d时仍有高于正常水平的弱表达。原位杂交检测中正常角膜组织有极弱的HIF-1α mRNA表达,碱烧伤后HIF-1α mRNA表达增强,在伤后3d、7d时表达最明显,15d后表达强度恢复至正常组织水平。结论HIF-1α参与碱烧伤后角膜的损伤病理机制,其表达变化影响新生血管形成过程,为寻找角膜碱烧伤新的治疗途径提供了理论依据。     

多西环素对碱烧伤大鼠角膜组织中NF-κB和bcl-2表达的影响

目的 研究多西环素作用下碱烧伤大鼠角膜组织中核因子κB(nuclear factor kappa B,NF-κB)和抗凋亡因子bcl-2表达情况,探索多西环素诱导炎症细胞凋亡的机制. 方法 制备SD大鼠(64只,64眼)一侧眼角膜碱烧伤动物模型,以3g·L-1多西环素眼液滴眼为实验组(32只,32眼),以溶媒滴眼为阴性对照组(32只,32眼).于角膜碱烧伤后第3天、第7天、第14天、第21天分别取下烧伤侧角膜组织行荧光定量RT-PCR,检测角膜组织中bcl-2基因的表达情况,酶联免疫吸附实验(ELISA)检测角膜组织中NF-κB的表达情况.结果 RT-PCR检测显示:烧伤后第3天、第7天、第14天阴性对照组bcl-2 mRNA的相对表达量分别为0.87±0.15、0.91±0.14、0.99±0.13,第3天、第7天、第14天多西环素组bcl-2 mRNA的相对表达量分别为0.30±0.15、0.22±0.08、0.42±0.06,多西环素组与阴性对照组相比bcl-2 mRNA表达显著下降(均为P＜0.05).ELISA检测显示:角膜碱烧伤后第3天、第7天阴性对照组NF-κB蛋白相对含量分别为(45.87±1.15)ng·L-1、(47.52±2.34)ng·L-1,第3天、第7天多西环素组NF-κB蛋白相对含量分别为(23.30±2.15)ng·L-1、(24.96±7.14)ng·L-1,角膜碱烧伤后第3天、第7天时多西环素组NF-κB与阴性对照组相比表达有显著下降(均为P＜0.05).角膜烧伤后第3天、第7天时NF-κB蛋白表达量与bcl-2 mRNA相对表达量呈明显正相关(r =0.746,P＜0.05;r =0.772,P＜0.05).结论 多西环素作用于碱烧伤大鼠角膜可下调NF-κB、bcl-2基因的表达,这可能是多西环素诱导炎症细胞凋亡、减轻炎症反应的机制之一.     

BMPR-IA在实验性大鼠角膜碱烧伤中的表达及意义

目的 探讨大鼠角膜碱烧伤后,骨形态发生蛋白受体IA(BMPR-IA)在角膜中的表达及意义.方法 采用1moL/L的氢氧化钠溶液烧灼大鼠角膜表面,建立角膜碱烧伤动物模型;分别于烧伤后1 d、3 d、5 d、7 d、14 d处死大鼠,摘除角膜作病理切片,用免疫组织化学染色方法检测正常对照组及角膜碱烧伤后不同时段BMPR-IA在角膜各层次中的表达,并用计算机图像分析系统进行结果分析.结果 正常大鼠角膜组织表达BMPR-IA;角膜碱烧伤后,BMPR-IA在角膜上皮层的着染程度明显增强,且浸润的新生血管内皮细胞和炎细胞均染色阳性.在各实验组中,烧伤后1 d组表达最强(P＜0.05).烧伤后3 d、5 d时表达逐渐下降,至14 d时表达恢复正常水平.结论 碱烧伤后,角膜组织中BMPR-IA的表达显著增高,提示BMPR-IA在角膜损伤修复过程的早期发挥重要作用.     

HIF在兔角膜碱烧伤后CNV生成中的作用研究

目的研究缺氧诱导因子(hypoxia inducible factor,HIF)以及诱导性一氧化氮合成酶(inducible nitric oxide synthase,iNOS)和血管内皮生长因子(vascular endothelial growth factor,VEGF)在角膜碱烧伤后角膜新生血管(corneal neovascularization,CNV)形成中的作用及机制。方法 建立兔CNV动物模型,将其随机分为对照组和3个实验组,对照组结膜下注射生理盐水,实验组注射不同剂量的三氧化二砷。观察兔CNV的生长情况,并记录CNV的生长面积。用免疫组织化学方法检测兔角膜HIF、iNOS以及VEGF的表达。结果 对照组6 d、12 d、15 d、21 d、28 d CNV的面积分别为:(53.86±20.60)mm2、(87.21±25.80)mm2、(128.31±40.10)mm2、(114.42±29.40)mm2、(78.15±35.13)mm2。各实验组CNV面积均小于对照组,差异均有统计学意义(均为P<0.05)。免疫组织化学方法检测角膜HIF-1α、iNOS及VEGF蛋白的表达:VEGF表达集中在角膜上皮下基质,存在于血管内皮细胞、炎性细胞胞浆内,呈深黄色。在7 d有较高表达,14 d达到高峰,28 d时明显降低,且对照组明显高于实验组,各实验组的表达随三氧化二砷剂量的增加而减少。蛋白的表达与CNV面积呈正相关。结论 角膜碱烧伤后CNV的形成可能与HIF-1α有关。三氧化二砷通过抑制HIF-1α和iNOS、VEGF表达而抑制兔CNV的形成。     

缺氧诱导因子1α在碱烧伤后兔角膜新生血管形成中的作用

目的 观察碱烧伤后兔角膜新生血管形成的不同时期缺氧诱导因子1α（HIF-1α）在角膜内的表达,探讨HIF-1α对角膜新生血管形成的影响.方法 实验研究.取30只健康家兔,采用随机数字表法分成5组,每组各6只兔,右眼采用1 mol/L氢氧化钠溶液建立角膜碱烧伤模型,左眼作为自身对照.分别于碱烧伤前和碱烧伤后1、3、5、7、14 d,在裂隙灯显微镜下观察家兔角膜新生血管增生情况,HE染色观察角膜组织病理学特征,并采用免疫组织化学法检验角膜组织中HIF-1α的表达,计算炎性细胞（多形核白细胞和淋巴细胞）和HIF-1α阳性细胞核数,对其结果行单因素方差分析及相关分析.结果 角膜碱烧伤后,HIF-1α主要表达在角膜基质中的炎性细胞、血管内皮细胞的细胞核中.随着时间的增加,炎性细胞表达增强,HIF-1α表达量也相应增加,并于碱烧伤后5 d达到高峰,以后逐渐减少.碱烧伤后1、3、5、7、14 d,角膜组织中炎性细胞和HIF-1α表达水平的差异均有统计学意义（F=422.086,437.555;P均＜0.05）,且HIF-1α的表达与新生血管的形成在时空上一致.经相关分析,角膜中炎性细胞和HIF-1α阳性细胞表达呈正相关（r=0.860,P＜0.05）.结论 碱烧伤后炎症反应能诱导HIF-1α的表达,而HIF-1α能促进角膜新生血管的形成.     

瘦素和血管内皮生长因子在碱烧伤诱导的大鼠角膜新生血管模型中的表达

目的 观察碱烧伤后不同时期角膜的组织病理学变化,以及瘦素和血管内皮生长因子(vascular endothelial growth factor,VFGF)的表达,探讨它们与角膜新生血管(corneal neovascularization,CNV)的关系.方法 使用碱烧伤诱导大鼠角膜新生血管模型,采用浸润1 mol·L-1 NaOH溶液、直径为3 mm的单片滤纸,准确置于大鼠右眼角膜中央30 s,制作CNV模型.25只SD大鼠右眼为实验眼,随机分成5组,每组5眼,左眼为正常对照眼.每天用裂隙灯显微镜观察角膜新生血管,分别计算新生血管长度和面积.并行HE染色和免疫组织化学检测.结果 碱烧伤后4 d、7 d、14 d、21 d,实验组CNV面积分别为:(2.55±0.15)m2、(4.15±0.36)mm2、(10.21±0.45)mm2、(8.56±0.06)mm2.免疫组织化学检测显示角膜碱烧伤后1 d,实验组瘦素、VEGF的表达开始增高,碱烧伤后14 d达高峰,14 d后瘦素、VEGF的表达下降,21 d后显著下降;其表达部位主要分布在形成的新生血管区域和上皮层;正常对照组瘦素可微弱表达于角膜上皮层和基质层,VEGF没有表达或仅在上皮基底膜有微弱表达.实验组角膜瘦素、VEGF阳性表达率较对照组明显增加(χ2=29.07,P=0.001;χ2=35.51,P=0.001),瘦素与VEGF的表达具有正相关性(r=0.95,P=0.001).结论 瘦素和VEGF表达水平与角膜新生血管的生成具有相关性,瘦素可能成为治疗CNV的靶点.     

大鼠角膜碱烧伤后血小板源生长因子的表达

目的 :检测血小板源生长因子 (PDGF)在大鼠角膜碱烧伤后表达的变化情况。方法 :建立大鼠角膜碱烧伤模型 ,用免疫组化法检测角膜碱烧伤后不同时段PDGF BB在角膜各层次中的表达 ,用RT PCR法检测PDGF B的mRNA在角膜碱烧伤后不同时段表达的变化。结果 :免疫组化检测显示 ,在正常角膜中 ,PDGF BB在上皮层中为弱表达 ,角膜碱烧伤后 ,PDGF BB在角膜各层组织中均有表达且表达逐步增强。各实验组中 ,7d组表达最强 ,而后逐渐下降 ,至 30d组基质层已基本无表达。RT PCR检测显示 ,正常角膜和损伤角膜中均有PDGF B的mRNA表达 ,角膜碱烧伤后 7d组和15d组 ,PDGF B的mRNA表达量最多。结论 :PDGF B在角膜碱烧伤后表达增强 ,且其表达的量随病程的发展而变化 ,PDGF B在角膜的损伤和修复过程中起一定作用。     

Follow-up studies in pattern VECP in demyelinating diseases in children

Spectral sensitivity functions and the transient decrease of sensitivity to short wavelengths after the offset of yellow light (transient tritanopia) were measured by increment threshold techniques in patients suffering from hereditary macular degenerations. Color vision defects were determined by arrangement tests and the anomaloscope. Central areolar choroidal dystrophy was found to produce a mild protan defect and to reduce foveal spectral sensitivity throughout the visible spectrum by a factor of 100; it also abolishes transient tritanopia. Electroretinogram (ERG) was normal, electrooculogram (EOG) subnormal. Stargardt's disease, despite numerous fluorescent macular spots, does not abolish transient tritanopia nor does it reduce spectral sensitivity, although scotopic matches were performed on the Nagel anomaloscope. Only in severe, advanced cases was transient tritanopia reduced and spectral sensitivity found to follow the absorption spectrum of rods. Routine ERGs and EOGs were normal. Vitelliform macular degeneration, despite the ophthalmoscopically pronounced dystrophic macula, produced only very small changes in spectral sensitivity and transient tritanopia, although a widened matching range on the Nagel anomaloscope and electrophysiological abnormalities were found. Apparently damage of the retinal circuit which connects long and short wavelength-sensitive cones, caused by hereditary conditions, is different from that caused by retinotoxic drugs.     

p53 expression in pterygium in two climatic regions in Turkey

Purpose:

To assess accumulation of p53 protein in samples of primary pterygium from people living in two different climatic regions in Turkey.

Materials and Methods:

Group 1 included 101 pterygium specimens from people in Adana located in southern Turkey. Group 2 included 39 pterygium specimens from people in Ankara, located in the middle of Turkey. Climatic conditions throughout the year are sunnier and warmer in Adana than they are in Ankara. The control group (Group 3) included 30 specimens of conjunctiva that had been excised during cataract surgery from 30 patients without pterygium. The pterygial specimens and control conjunctiva were studied by immunohistochemistry using antibodies against p53 protein. Pearson''s chi-square test was used to compare the p53 immunoreactivity.

Results:

The p53 immunoreactivity in Groups 1 and 2 was greater than it was in the control group (P<0.001). There were no differences in p53 immunoreactivity between Groups 1 and 2 (P= 0.060).

Conclusion:

The p53 immunoreactivity was not correlated with ultraviolet irradiation exposure. The p53 immunoreactivity in our pterygium specimens suggests that pterygium could be a result of uncontrolled cell proliferation.     

Trends in Patterns of Anterior Uveitis in a Tertiary Institution in Singapore

Purpose: To report the trends in etiology of patients with anterior uveitis (AU) in Singapore over 6 years.

Methods: A retrospective review of the clinical records of all new patients who presented with anterior uveitis to the uveitis subspecialty clinic from 2005 to 2010 at Tan Tock Seng Hospital, Singapore.

Results: There were 552 new cases of AU. This comprised 59.5% of a total of 928 new patients diagnosed with uveitis from 2005 to 2010. The mean age was 48.0?±?17.2 years. There was a male predominance (62.5%), with a male:female ratio of 1.7:1. The majority were of Chinese ethnicity (69%), followed by Malays (13.2%). Most cases were unilateral (79.5%) and idiopathic (50.4%). Common etiological causes included Fuchs heterochromic iridocyclitis (FHI) (5.6%), ankylosing spondylitis (AS)-related AU (5.1%), herpes simplex virus (HSV) (4.7%), and herpes zoster virus (HZV) (4.5%). There were increasing trends in AS-related AU from 3.2% in 2008 to 6.5% in 2010, and psoriasis-associated AU from 1.7% in 2005 to 4.0% in 2008. There were decreasing trends in the incidence of FHI from 10.6% in 2006 to 4.7% in 2009. No change in incidence of viral etiologies was noted, but cytomegalovirus-related immune-recovery uveitis (IRU) comprised 7.4%. IRU showed an increasing trend from 1.7% in 2005 to 11.9% in 2007, then decreased to 3.3% in 2010. Using the Pearson chi-square test, there was no statistically significant association between ethnicities (Chinese, Malay, Indian) comparing infectious and noninfectious cases (p?=?0.788), idiopathic and nonidiopathic cases (p?=?0.170), or between the various etiologies of uveitis (p?=?0.168).

Conclusions: AU was the predominant form of uveitis seen at our centers. Infectious etiologies (18.5%) are the most common among nonidiopathic cases, with herpes viruses (9.2%) being most prevalent. Despite increased use of polymerase chain reaction (PCR) in the detection of microbial and viral DNA, there was no overall increase in detection of infectious causes for uveitis. The changes in CMV-related immune recovery uveitis from 2005 to 2010 could reflect a change in HIV management in Singapore.     

Changes in Bruch's membrane in experimental hypercholesteremia in rats

PURPOSE: We investigated the effect of high cholesterol diet for the aging changes in Bruch's membrane of rats. METHODS: After feeding a 4% cholesterol diet for 15 weeks to three young rats 3 months old and four aged rats 23 months old, we observed the morphological changes of Bruch's membrane by electron microscopy, and made a comparison with rats fed an ordinary diet. RESULTS: In one young rat fed a high-cholesterol diet, the endothelial basement membrane of the choriocapillaris formed multiple folds separated from the plasma membrane of the endothelium and showed lamellar thickening and crack in some areas. The elastic fiber layer in Bruch's membrane disappeared partly and some new microfibrils appeared. In one aged rat fed a high-cholesterol diet, the endothelial basement membrane of the choriocapillaris showed more lamellar thickening with lumps in some parts. Compared with rats fed an ordinary diet, rats fed a high-cholesterol diet showed thickening of the basement membrane and the changes were more severe. CONCLUSIONS: Our data indicated that high-cholesterol diet might promote age-related changes of Bruch's membrane.     

Orthokeratology practice in children in a university clinic in Hong Kong*

Purposes: The aim of this study was to analyse clinical data of children undergoing orthokeratology (ortho‐k) and to investigate patients’/parents’ perspective on ortho‐k via telephone interviews. Methods: Clinical records of children undergoing ortho‐k from a university optometry clinic were reviewed and the effects of ortho‐k on refraction, vision and cornea were investigated. A telephone interview was conducted to solicit patients’/parents’ perspective of the treatment. Results: One hundred and eight files were reviewed. Median age of the children was nine years (range six to 15); mean (±SD) pre‐treatment refractive sphere was ‐3.56 ± 1.49 D and the median refractive cylinder was ‐0.50 D (range zero to ‐4.25 D). Significant refractive spherical reduction (58 per cent), improvement in unaided vision and corneal topographical changes were noted after only one night of wear. No significant change in astigmatism was found. Corneal staining was the most commonly observed complication with ortho‐k and more than 80 per cent of patients were advised to apply ocular lubricants to loosen the lens before lens removal. Ortho‐k was mainly undertaken for myopic control and about 90 per cent of the respondents reported good/very good unaided vision after ortho‐k and ranked the treatment as satisfactory or very good. Lens binding and ocular discharge were the most frequently reported problems during the treatment. Conclusion: Under close monitoring, overnight ortho‐k is effective and safe for reducing low to moderate myopia and the treatment is well accepted by the children.     

内毒素诱导的大鼠葡萄膜炎的巨噬细胞中Toll样受体4的表达

目的 探讨在内毒素诱导的Wistar大鼠葡萄膜炎中Toll样受体4(TLR4)阳性细胞与虹膜组织中巨噬细胞的动态变化和分布.方法 实验研究.Wistar大鼠50只,用随机数字法随机分为5组,每组10只,分别为正常对照(0 h)组、6 h组、12 h组、24 h组及48 h组.除0 h组外其余各组均足垫部注射霍乱弧菌内毒素200μg,注射后于裂隙灯显微镜下观察双眼前节炎症反应变化.按实验分组于0、6、12、24、48 h处死大鼠.取虹膜一睫状体及脉络膜组织.通过葡萄膜铺片免疫组织化学方法检测TLR4和巨噬细胞的标记CD163的表达.人工计数虹膜中TLR4~+与CD163~+的细胞并计算细胞密度,计算圆形和多形性的CD163~+细胞占所有CD163~+细胞的百分比.进一步采用免疫荧光双标记检测TLR4和CD163共表达的情况.通过单因素方差分析分别对大鼠虹膜内阳性细胞密度以及圆形、多形性CD163~+细胞的百分比进行统计学检验.结果 正常大鼠虹膜睫状体组织不表达TLR4.6 h组有2只大鼠虹膜内可见少量TLR4~+细胞,12～48 h组所有大鼠虹膜内TLR4~+细胞明显增多(F=167.2,P＜0.001),虹膜内TLR4~+细胞密度分别为(506.1±39.5)个/mm~2(12 h组)、(492.3±54.5)个/mm~2(24 h组)及(663.8±150.2)个/mm~2 (48 h组).在注射LPS后12～48 h期间TLR4~+细胞形态无明显变化.0～48 h组大鼠虹膜内均有CD163~+细胞,0 h组圆形和多形性CD163~+细胞百分比为13%,12～48 h组其百分比约为80%,且圆形细胞主要位于虹膜基质层.免疫荧光双标记可见TLR4和CD163的共表达,TLR4位于细胞膜,CD163位于细胞质.5组大鼠脉络膜内均未见TLR4表达.结论 内毒素诱导的大鼠葡萄膜炎中虹膜内TLR4表达增高,部分虹膜固有巨噬细胞表达TLR4.TLR4可能在葡萄膜炎的发生发展中起一定作用.     

弱视眼底光学相干断层扫描的研究进展

弱视是由于视觉发育关键期内各种异常的视觉经验导致单眼或双眼最佳矫正远视力低于正常同龄儿童,而眼部无明显器质性病变。目前普遍观点认为,弱视的发病机理主要源于视皮层。近年来,光学相干断层扫描（OCT）作为一种先进的活体成像技术,促进了对视网膜形态结构的大量研究,同时也被应用到弱视的研究领域。陆续有不同的研究人员利用OCT发现弱视患者眼底视网膜、脉络膜等眼部结构存在改变。笔者将对弱视眼底OCT的研究进展做一综述。     

实验性糖尿病视网膜微血管病变的病理研究

目的：观察糖尿病视网膜病变（diabetic retinopathy,DR）的组织学改变。方法：应用光镜、免疫组织化学、电镜及组织化学电镜等技术,研究在不同时间点Spregue-Dawley(SD)大鼠视网膜毛细血管基底膜中的Ⅳ型胶原蛋白及层黏蛋白和视网膜毛细胞血管基底膜的厚度,以及其负电荷位点数目的变化。结果：随着糖尿病病程的发展,视网膜毛细血管基底膜下不断增厚伴有Ⅳ型胶原蛋白及层黏蛋白的增加,同时负电荷位点数目减少。结论：视网膜毛细血管基底膜增厚,Ⅳ型胶原蛋白及层黏蛋白的增加,负电荷位点数目减少可能是导致DR渗出性病变的病理基础。