Central corneal thickness, tonometry, and glaucoma risk--a guide for the perplexed

The results of the Ocular Hypertension Treatment Study (OHTS) brought to the forefront the role of central corneal thickness (CCT) as a confounder of applanation tonometry, and established CCT as an independent predictive factor for the development of glaucoma. Ophthalmologists often wonder how to use CCT in daily practice. This article reviews the current CCT literature and provides some basic guidance to clinicians wishing to integrate CCT into their care of glaucoma patients.     

角膜缘干细胞研究现状及展望

角膜缘干细胞的发现是眼科领域的重要进展，角膜缘干细胞移植治疗严重眼表疾病已取得初步效果。但有关角膜缘干细胞的鉴定、分离、体外培养和转归等仍是制约这一领域深入发展的瓶颈，加强对角膜缘干细胞的基础研究对角膜盲的防治有重要意义。     

眼轴长度和屈光度数对视网膜神经纤维层厚度的影响

目的探讨眼轴长度、屈光度数对平均视网膜神经纤维层厚度（mean retinal nerve fiber layer thickness,mRN-FLT）的影响。方法选取不同屈光度数患者90例90眼,用A/B超声仪及HRT-Ⅱ分别测定其眼轴长度及mRNFLT,并进行线性回归分析。结果高中度近视组患者眼轴长度与mRNFLT具有负相关性（P〈0.01）,低度近视组患者眼轴长度与mRNFLT无相关性（P〉0.05）;3组患者屈光度数与mRNFLT均不具相关性（P〉0.05）。结论眼轴长度对中高度近视患者mRNFLT有直接影响,利用HRT-Ⅱ诊断早期青光眼时,应除外这一情况造成的假象。     

眼附属器黏膜相关淋巴组织淋巴瘤的研究进展

黏膜相关淋巴组织（MALT）淋巴瘤是非霍奇金淋巴瘤中结外边缘带淋巴瘤（MZL）的一种特殊类型。眼附属器MALT淋巴瘤是眼眶恶性肿瘤中较常见的一种，可发生在结膜、泪腺、眼睑和眼眶。近年来，国外许多学者在MALT淋巴瘤的临床特点、病理形态学、免疫表型、分子遗传学及分子生物学方面对它的发生机制在基因水平有了新的认识。就国外对眼附属器MALT淋巴瘤的分子遗传学异常在肿瘤细胞内部信号转导通路中作用的研究做一综述。     

儿童眼外伤165例分析

目的研究儿童眼外伤的有关特点。方法对165例儿童眼外伤的相关因素进行统计分析。结果儿童眼外伤有其特点:男性儿童多发,眼部伤情重,并发症多,农村多发,致盲率高等。结论儿童眼外伤是主要的致盲原因之一,重在预防。     

2型糖尿病角膜知觉减退及其与眼表异常的相关性研究

目的 探讨2型糖尿病患者角膜知觉减退及其与眼表异常的相关性.方法 采用前瞻性病例对照研究.采用Cochet-Bonnet角膜知觉测量仪分别测定并比较38例（68眼）2型糖尿病患者（糖尿病组）和33例（57眼）无糖尿病患者（对照组）中央角膜知觉,同时对糖尿病患者行泪膜破裂时间测定（break up time,BUT）、基础泪液分泌试验（Schiemer Ⅰ）及角膜荧光素染色.对角膜知觉与后三者进行相关性研究.结果 糖尿病组角膜知觉为（36.07±14.26）mm,对照组为（52.98±3.89）mm,两者差异有显著性（P＜0.01）.糖尿病患者Schirmer Ⅰ试验平均值为（12.41±3.22）mm,BUT值平均为（8.82±2.70）s,角膜荧光素染色累积分平均值为（3.94±1.66）分.糖尿病患者角膜知觉与泪膜破裂时间（r=0.330,P=0.006）、角膜荧光素染色（r=-O.342,P=0.004）有相关关系,与泪液分泌量无相关关系（P=0.538）.结论 糖尿病患者角膜知觉明显减退,而角膜知觉减退是影响角膜上皮病变、干眼症等眼表疾病的因素之一.     

内皮抑素与眼部新生血管

眼部新生血管导致眼结构和功能的破坏,造成严重的视功能损害,是当前最难解决的眼科难题之一。内皮抑制素(endostatin,ES)是目前公认的最强的血管生成抑制因子之一,已经用于抑制眼部新生血管的实验研究,表明内皮抑制素具有强大的抗眼部新生血管作用。本文就内皮抑素的结构、功能及与眼部新生血管的相关研究进行综述。     

睫状肌收缩与可折叠人工晶状体植入眼伪调节力的关系

目的分析和探讨可折叠人工晶状体（IOL）植入眼睫状肌收缩功能与伪调节力的关系。方法超声乳化白内障吸除及囊袋内可折叠IOL植入术后3个月,采用红外验光仪中调节性微波动分析软件检测瞳孔直径2．0—3．5mm、对光反应良好的50例患者（50只眼）的睫状肌调节性微波动高频成分（HFC）,并与患者术眼的伪调节力、IOL移动度等因素进行相关分析。结果HFC与IOL移动度呈正相关（r=0．702,P〈0．01）,IOL移动度与伪调节力呈正相关（r=0．861,P〈0．01）,HFC与伪调节力呈正相关（r=0．915,P〈0．01）。即IOL植入术后睫状肌的收缩能力越强,则IOL移动度越大,术后伪调节力越强。结论可折叠IOL植入术后术眼的睫状肌收缩可能导致IOL移动,这可能是IOL眼伪调节力增大的重要原因之一。     

角膜屈光手术后的人工晶状体度数计算

角膜屈光手术后用现行的角膜曲率检测方法测量角膜屈光力不精确,导致该类患者白内障手术时人工晶状体度数计算偏低,术后呈较严重的远视状态。随着接受准分子激光角膜屈光手术人数的增加,此问题在未来将日益突出。围绕这一问题,不少学者提出多种修正方案,以期提高角膜屈光手术后人工晶状体度数计算的准确性,本文就此进行综述。     

Clinicopathological analysis of 719 pediatric and adolescents’ ocular tumors and tumor-like lesions: a retrospective study from 2000 to 2018 in China

AIM: To analyze the retinal proteomes with and without conbercept treatments in mice with oxygen-induced retinopathy (OIR) and identify proteins involved in the molecular mechanisms mediated by conbercept. METHODS: OIR was induced in fifty-six C57BL/6J mouse pups and randomly divided into four groups. Group 1: Normal17 (n=7), mice without OIR and treated with normal air. Group 2: OIR12/EXP1 (n=14), mice received 75% oxygen from postnatal day (P) 7 to 12. Group 3: OIR17/Control (n=14), mice received 75% oxygen from P7 to P12 and then normal air to P17. Group 4: Lang17/EXP2 (n=21), mice received 75% oxygen from P7 to P12 with intravitreal injection of 1 μL conbercept at the concentration of 10 mg/mL at P12, and then normal air from P12 to P17. Liquid Chromatography-Mass Spectrometry (LC-MS)/MS data were reviewed to find proteins that were up-regulated after the conbercept treatment. Gene ontology (GO) analysis was performed of conbercept-mediated changes in proteins involved in single-organism processes, biological regulation, cellular processes, immune responses, metabolic processes, locomotion and multiple-organism processes. RESULTS: Conbercept induced a reversal of hypoxia-inducible factor 1 signaling pathway as revealed by the Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis and also induced down-regulation of proteins involved in blood coagulation and fibrin clot formation as demonstrated by the Database for Annotation, Visualization and Integrated Discovery (DAVID) and the stimulation of interferon genes studies. These appear to be risk factors of retinal fibrosis. Additional conbercept-specific fibrosis risk factors were also identified and may serve as therapeutic targets for fibrosis. CONCLUSION: Our studies reveal that many novel proteins are differentially regulated by conbercept. The new insights may warrant a valuable resource for conbercept treatment.