(-)-Epigallocatechin-3-gallate,reduces corneal damage secondary from experimental grade II alkali burns in mice

Background

Since recent reports have shown that (-)-Epigallocatechin-3-gallate (EGCG) could be used for treating proliferative and inflammatory disorders, we explored its use for the management of corneal chemical burns.

Modulation of cytokine production from an EpiOcular corneal cell culture model in response to Staphylococcus aureus superantigen

The present study investigated the hypothesis that Staphylococcus aureus enterotoxin B (SEE) produces epithelial cell death and releases inflammatory cytokines that produce stromal infiltration during contact lens induced peripheral ulceration. Epithelial cells were incubated with different doses of SEB for various time periods. Culture supernatants were assayed for cytokines IL- lo, IL-6 and chemotactic agents IL-8 and LTB,. SEE induced the production of IL- I p and IL-8. Epithelial cells exposed for longer periods (48 h) with low concentrations of SEB produced significantly higher levels (N0.02) of IL-Ip and IL-8 (P<0.05) compared t o a 24 h exposure. SEB did not induce the production o f IL-6 and     

角膜地形图与角膜曲率计在白内障手术前后评价

本文应用计算机辅助的角膜地形图系统TMS-1和角膜曲率计TOPCONOM-4同时测定了200例(278眼)的角膜地形图和中央角膜屈光状态。比较了角膜地形图的模拟角膜曲率SIMK值和角膜曲率计的垂直和水平屈光度。结果显示,白内障术前组116例150眼的SIMK平均值分别为44.22D(垂直轴)和44.26D(水平轴),角膜曲率计的中央屈光度垂直轴平均为44.16D,水平轴为44.23D。统计学处理表明,2种组方法的结果之间差异无显著性(P>0.05),第2种术后组67例90眼的SIMK平均值分别为46.37D(垂直轴)和43.06D(水平轴),角膜曲率计的中央屈光度垂直轴平均为46.09D,水平轴平均为42.88D,统计学处理二种方法的结果之间差异无显著性(P>0.05)。研究提示,角膜地形图系统的模拟角膜曲率SIMK值和角膜曲率计的屈光度无论在白内障手术前还是在手术后其结果是一致的,临床应用具有同等的价值。但是,当角膜中央屈光度异常范围小于3毫米,角膜混浊,角膜严重不规则散光时,角膜曲率计不能满足临床需要。而计算机辅助的角膜地形图系统则具有极大的诊断及检测价值。眼科学报 1994;10:85—89。     

Suppurative corneal ulceration in Bangladesh

Suppurative keratitis is an important preventable cause of blindness, particularly in the developing world. This study analyses 142 cases of suppurative keratitis referred to Chittagong Eye Infirmary, Bangladesh. Some 53.5% of cases were bacterial and 35.9% were fungal. The five most common pathogens were: Pseudomonas sp. 24%, Streptococcus pneumoniae 17%, Aspergillus sp. 13%, Fusarium sp. 7% and Curvularia sp. 6%. Gram stain and culture results were consistent in 62.6% of cases. Previous antibiotic treatment was a significant factor for failure of culture isolation and less so for Gram stain failure. On Gram stain, 55.9% of pseudomonal cases were missed, but only 2% of fungal cases were missed. Over all, Gram stain had a sensitivity of 62% and positive predictive value of 84% for bacterial cases, and 98% and 94% for fungal cases, respectively. Fungal ulcers were typically filamentous, but an antecedent history of trauma was not common. The most frequent injury was due to rice grains, but the inoculum appeared to be introduced during eye washing with contaminated water. Pseudomonal ulcers occurred most frequently in the monsoon season, and Fusarium cases were seen only in the hot, dry season.     

角膜缝线的细菌学试验研究

对常用的4种角膜缝线进行细菌的吸附试验和虹吸试验。结装发现3-0黑丝线吸附细菌最多,10-0尼龙线吸附细菌最少。3-0和5-0黑丝线对细菌虹吸试验阳性,9-0和10-0尼龙线虹吸试验阴性。试验证明,10-0尼龙线是角膜手术较理想的缝线。     

环缩酚肽抑制视网膜表达VEGF及PECAM基因和血管增生

[目的]观察两种环缩酚肽衍生物(Hep-A和Hep-B)对氧诱导的小鼠视网膜表达血管内皮生长因子(VEGF)和细胞黏附分子(PECAM;ICAM-1;VCAM-1)基因的影响及血管增生的变化.[方法]建立氧诱导的血管增殖性视网膜病变模型,12 d开始给小鼠皮下注安慰剂(第1组,n=7)、Hep-A 10 mg/kg(第2组,n=6)或者Hep-B 10 mg/kg(第3组,n=6),每天两次.5 d后取出左侧眼,分离视网膜并抽提RNA,用荧光定量PCR测出上述基因含量,并分别求出每个靶基因与标准基因S16含量的比率;右眼经心脏荧光素灌注后取眼球做视网膜平铺片,用图像分析软件定量计算视网膜新生血管的面积.[结果]视网膜中VEGF/S16的mRNA比率为:第1组(0.554±0.050),第2组(0.355±0.037),第3组(0.287±0.051);PECAM/S16为:第1组(2.050±0.249),第2组(1.228±0.153),第3组(1.027±0.210).经ANOVA分析,第2组和第3组分别与第1组比较,视网膜中VEGF基因表达分别减少36%和48.2%(P=0.001);PECAM基因表达分别减少40.1%(P＜0.05)和49.9%(P＜0.01);而VCAM-1和ICAM-1表达无明显差异.视网膜平片检测视网膜新生血管面积:第1组为(1.06±0.03)mm2/眼,第2组为(0.17±0.01)mm2/眼,第3组为(0.11±0.01)mm2/眼;经ANOVA分析,第2组和第3组分别与第1组比较,视网膜新生血管的面积明显减少(P＜0.001).[结论]两种环缩酚肽衍生物均抑制氧诱导的小鼠视网膜表达VEGF和PECAM基因,并抑制其形成视网膜新生血管.     

Long-term effects of glaucoma therapy with 4% pilocarpine gel on corneal clarity and endothelial cell density

Corneal thickness measurements and endothelial cell counts were carried out in 34 patients undergoing treatment for glaucoma with 4% pilocarpine gel between 18 to 78 months after initiation of therapy. The corneal thickness and endothelial cell population were found to be within normal limits in all cases except two, one patient with increased corneal thickness who had recently undergone cataract and glaucoma filtering surgery and another patient with decreased cell count who had an old endothelial scar sustained prior to pilocarpine gel therapy. There was a very close correlation for both of these parameters noticed in patients treated with pilocarpine gel and in age-matched control group of patients with glaucoma. The present study has shown that there are no adverse corneal effects with pilocarpine gel therapy.     

Inhibition of angiogenesis by antibody blocking the action of proangiogenic high-molecular-weight kininogen

Summary.  Previously we demonstrated that domain 5 (D5) of high-molecular-weight kininogen (HK) inhibits neovascularization in the chicken chorioallantoic membrane (CAM) assay and further found that kallikrein cleaved HK (HKa) inhibited FGF2-and VEGF-induced neovascularization, and thus was antiangiogenic. In this study, we sought to demonstrate whether uncleaved HK stimulates neovascularization and thus is proangiogenic. The chick chorioallantoic membrane was used as an in ovo assay of angiogenesis. Low-molecular-weight kininogen stimulates angiogenesis, indicating that D5 is not involved. Bradykinin stimulates neovascularization equally to HK and LK and is likely to be responsible for the effect of HK. A murine monoclonal antibody to HK (C11C1) also recognizes a similar component in chicken plasma as detected by surface plasmon resonance. Angiogenesis induced by FGF2 and VEGF is inhibited by this monoclonal antibody and is a more potent inhibitor of neovascularization induced by VEGF than an integrin α_vβ₃ antibody (LM 609). Our postulate that C11C1 inhibits the stimulation of angiogenesis by HK was confirmed when either C11C1 or D5 completely inhibited angiogenesis in the CAM induced by HK. Growth of human fibrosarcoma (HT-1080) on the CAM was inhibited by GST-D5 and C11C1. These results indicate HK is proangiogenic probably by releasing bradykinin and that a monoclonal antibody directed to HK could serve as an antiangiogenic agent with a potential for inhibiting tumor angiogenesis and other angiogenesis-mediated disorders.     

角膜损伤后神经再生的实验研究

应用神经组织化学技术观察了兔角膜NA能神经及AchE阳性神经在角膜损伤后的再生,证实术后1月,两种神经均有再生轴突进入植片;术后3月可见交界区和植床内神经密度明显增加;同时,对术后两种神经再生的功能意义进行了讨论。     

IL-2-PE40体外抑制γ-干扰素诱导的角膜内皮细胞MHC抗原表达的研究

目的了解正常大鼠角膜内皮细胞在体外经γ-干扰素诱导后，主要组织相容性复合体（major histoeompatibility complex，MHC）-Ⅰ、Ⅱ类抗原异常表达的情况。并观察比较白细胞介素-2-绿脓杆菌外毒素（interleukin-2-pseudomonas exotoxin40。IL-2-PE40）、环胞霉素A（cyclosporine A，CsA）对角膜内皮细胞MHC-Ⅰ、Ⅱ类抗原异常表达的免疫抑制作用。方法采用ACAS-570黏附式细胞分析仪和免疫荧光技术，对体外原代培养经γ-干扰素诱导后的正常大鼠角膜内皮细胞分成A、B2组进行MHC-Ⅰ、Ⅱ类抗原表达的相对量测定，并在培养液中加入新型免疫抑制剂IL-2-PE40和CsA，进一步测定角膜内皮细胞MHC-Ⅰ、Ⅱ类抗原的表达量。结果未加入γ-干扰素前，MHC-Ⅰ类抗原的表达量为97．8±8．1，MHC-Ⅱ类抗原无表达；经γ-干扰素诱导后，MHC—Ⅰ类抗原的表达量为1006．3±13．2，MHC-Ⅱ类抗原表达量为406．5±10．5，γ-干扰素加入前后MHC-Ⅰ、Ⅱ类抗原比较均有统计学意义（P〈0．05）。IL-2．PE40组MHC-Ⅰ类抗原的表达量为618．2±13．5，MHC-Ⅱ类抗原表达量为204．5±7．8，CsA组MHC-Ⅰ类抗原的表达量为609．5±12．9，MHC-Ⅱ类抗原表达量为198．5±6．9，IL-2．PE40组、CsA组分别与注射用水比较，MHC—Ⅰ、Ⅱ类抗原间均有统计学意义（P〈0．05）。IL-2．PE40组与CsA组比较．MHC—Ⅰ、Ⅱ类抗原间差异无统计学意义（P〉0．05）。结论在体外，γ-干扰素可诱导角膜内皮细胞MHC-Ⅰ、Ⅱ类抗原异常表达；IL-2-PE40及CsA均能不同程度的抑制这种表达。[眼科新进展20ff7；27（3）：170．172]