光性视网膜损伤研究进展

本文简要介绍电磁波谱和电磁波对生物的组织效应,并综述光对视网膜的损伤、损伤的影响因素和危险因素以及阈值问题和光性视网膜损伤机理的新看法。某些药物可促发或加重光对视网膜的损伤,糖尿病可能是光性视网膜损伤的危险因素之一。视网膜光损伤阈值受多种因素的影响,但低于角膜和晶体的损伤阈值。光子能量不同的光源,损伤的时间阈值不同,波长不同的光波,导致视网膜损伤所需能量不同。光化学损伤可能是因自由基作用的结果。     

血-视网膜屏障损伤的机制及治疗对策

血-视网膜屏障在维持视网膜微环境稳态中具有重要作用,很多疾病如糖尿病视网膜病变、急性青光眼、早产儿视网膜病变等均会导致血-视网膜屏障损伤。目前对于引起血-视网膜屏障损伤的分子机制尚未完全阐释清楚,本文旨在综述血-视网膜屏障的结构与功能,各种眼部疾病导致的血-视网膜屏障损伤机制及采用药物治疗、激光治疗、手术治疗的治疗对策。     

缺血性视网膜损作机制的研究[下]：损伤的机制和治疗

缺血性视网膜损伤是眼科常见的一种临床表现,本文参阅了大量有关的文献,重点对缺血性视网膜损伤的机制和药物治疗等进行了较为全面的综述。     

缺血性视网膜损伤机制的研究〔下〕——损伤的机制和治疗

缺血性视网膜损伤是眼科常见的一种临床表现。本文参阅了大量有关的文献,重点对缺血性视网膜损伤的机制和药物治疗等进行了较为全面的综述     

视网膜修复与再生的研究进展

视网膜退行性疾病,如年龄相关性黄斑变性、视网膜色素变性等,均是由视网膜细胞变性凋亡而引起.视网膜细胞损伤后难以自我修复.近年来研究者们通过视网膜移植、组织工程学、基因修复、药物保护及视觉假体等方法对视网膜进行修复或促进其再生.     

青光眼视神经保护的研究进展

青光眼是眼科临床中最常见的致盲眼病之一,目前的治疗方法主要是药物和手术控制眼压,单纯的降低眼压并不能有效地防止视网膜神经节细胞程序性死亡所引起的视神经进行性损害.自视网膜神经保护概念提出以来,对视网膜神经节细胞的损伤和保护研究取得了长足进展.文中就视网膜神经节细胞的损伤、死亡机制及对视网膜神经保护措施的研究进展加以综述.     

视网膜缺血--再灌注损伤的保护

视网膜缺血-再灌注损伤是目前研究较多的一个课题,其损伤机制复杂,目前通过各种实验研究探索其损伤机制以及减轻或防止缺血-再灌注损伤的药物和方法很多.现就视网膜缺血-再灌注损伤的保护机制进行总结归纳.     

糖尿病视网膜神经节细胞损伤的研究进展

糖尿病性视网膜病变( diabetic retinopathy,DR)是糖尿病严重并发症之一,可对患者造成严重视功能损害。在视网膜出现微血管病变之前,已经出现视网膜神经节细胞(retinal ganglion cell, RGC)的病变。神经细胞的病理改变是糖尿病早期视功能障碍的重要因素。 RGC的损伤机制可能与高血糖代谢紊乱、氧化应激损伤、神经营养因子缺乏以及谷氨酸兴奋毒性有关。许多实验研究发现神经元保护药物能减少RGC凋亡,一些关于有效性和安全性的临床研究为临床治疗糖尿病视网膜神经细胞病变奠定重要基础。     

抗VEGF药物玻璃体内注射治疗对早产儿视网膜病变神经系统发育的影响

早产儿视网膜病变(ROP)是以视网膜血管异常增生为主要病理特征的儿童致盲眼病。血管内皮生长因子(VEGF)是一种特异性刺激血管内皮细胞增生及新生血管形成的生长因子。早产儿视网膜局部缺血、缺氧环境促使眼内VEGF表达代偿性升高, 进而诱导视网膜血管病理性生长。玻璃体内注射抗VEGF药物可抑制眼内VEGF的生物活性, 从而延缓视网膜新生血管形成, 可有效治疗ROP。然而, ROP患者常伴有血-视网膜屏障损伤, 导致视网膜微环境稳态失衡, 抗VEGF药物易透过血-视网膜屏障及血-脑屏障进入全身血液循环, 可能导致ROP患儿神经系统发育异常。目前抗VEGF药物玻璃体内注射是否影响患儿神经系统发育仍是眼科研究的热点。本文就VEGF在ROP发病机制和神经发育中的作用以及抗VEGF药物玻璃体内注射对ROP患儿神经系统发育的影响进行综述, 以期为临床合理、安全应用抗VEGF药物提供依据。     

玻璃体腔注射促红细胞生成素对大鼠视网膜结构和功能的影响

促红细胞生成素（erythropoietin,EPO）对视网膜光损伤、视网膜缺血-再灌注损伤、高眼压视网膜神经节细胞损伤、视神经损伤诱导的神经节细胞损伤及视神经轴突再生、早期糖尿病视网膜病变视网膜神经元、血-视网膜屏障和变应性视神经脱髓鞘病变均具有保护作用。本研究将重组大鼠EPO注入大鼠玻璃体腔,旨在观察EPO对视网膜的结构和功能的影响以及是否会诱发视网膜新生血管形成。     

Strabisme Alternant - Etude clinique - traitement

The author defines motor and sensory alternation: the term alternation should not be used in isolation, it should always be accompanied by the name of the parameter concerned. Sensory alternation is always found together with motor alternation but the reverse is not true.The examining criteria for a diagnosis of sensory alternation are given, sensory alternation must not be confused with alternating inhibition. Working from clinical observations of cases of motor alternating strabismus, the author selects 2 types of binocular sensory relations which allow one to differentiate between:- cases of primary alternating strabismus- cases of secondary alternating strabismusThese forms will develop in different ways; in both cases a cure is possible providing that the right treatment is prescribed and once prescribed carefully followed, etc. It is always a case of serious forms of strabismus whose developmental period is spread over several years.According to the authors, the frequency of cases of true primary strabismus is from 1–3%, the frequency of cases of secondary alternating strabismus varies according to the type of therapy practised on cases of monocular strabismus with amblyopia. These latter will become cases of alternating strabismus under the influence of certain types of therapy carried out over several years (penalization, rocking, alternated occlusion, etc...).Experimental data on kittens confirm clinical data; kittens placed in abnormal environments during the sensitive period will show modification in the distribution of cortical cells and the absence of binocular cells (either because the excitation of the two eyes was not simultaneous, or not identical: artificial strabismus, occlusion, opaque glasses). This disturbances become irreversible after a certain period of exposure (a function of age, length of exposure, etc...).It is thus necessary to bear in mind: 1) the iatrogenic risks of certain orthoptic treatments, 2) the necessity for a binocular form of treatment as soon as possible, as once a certain stage is passed, cortical plasticity diminishes and the elaboration of normal binocular relations becomes impossible.

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Effects of Adenosine Agonists on Intraocular Pressure and Aqueous Humor Dynamics in Cynomolgus Monkeys

The effects of single or multiple topical doses of the relatively selective A₁adenosine receptor agonists (R)-phenylisopropyladenosine (R-PIA) and N⁶-cyclohexyladenosine (CHA) on intraocular pressure (IOP), aqueous humor flow (AHF) and outflow facility were investigated in ocular normotensive cynomolgus monkeys. IOP and AHF were determined, under ketamine anesthesia, by Goldmann applanation tonometry and fluorophotometry, respectively. Total outflow facility was determined by anterior chamber perfusion under pentobarbital anesthesia. A single unilateral topical application of R-PIA (20–250 μg) or CHA (20–500 μg) produced ocular hypertension (maximum rise=4.9 or 3.5 mmHg) within 30 min, followed by ocular hypotension (maximum fall=2.1 or 3.6 mmHg) from 2–6 hr. The relatively selective adenosine A₂antagonist 3,7-dimethyl-1-propargylxanthine (DMPX, 320 μg) inhibited the early hypertension, without influencing the hypotension. Neither 100 μg R-PIA nor 500 μg CHA clearly altered AHF. Total outflow facility was increased by 71% 3 hr after 100 μg R-PIA. In conclusion, the early ocular hypertension produced by topical adenosine agonists in cynomolgus monkeys is associated with the activation of adenosine A₂receptors, while the subsequent hypotension appears to be mediated by adenosine A₁receptors and results primarily from increased outflow facility.