青光眼动物模型中自噬与视网膜神经节细胞的关系

青光眼的主要病理特征是视网膜神经节细胞(RGCs)渐进性丢失,而其损伤机制尚未明确.自噬是溶酶体降解物质的过程,该过程消除了受损的细胞成分,包括细胞器和长寿蛋白,这对维持细胞内环境的稳定有着重要作用.最近的研究表明,自噬参与了青光眼发病的病理生理过程.本文总结了视神经损害模型、视网膜缺血-再灌注模型、高眼压模型等不同青光眼动物模型中自噬与RGCs的关系,发现在不同青光眼动物模型中,自噬既可促进RGCs存活,又可促进其死亡,而在相同动物模型中,自噬对RGCs的调节也发挥着双刃剑的作用.同时阐述了自噬与具有神经元保护作用的Sirt1之间的相互作用.     

自噬与青光眼关系的研究进展

自噬是溶酶体降解或再循环利用细胞器、蛋白质等胞内物质成分的过程,在细胞内环境稳态中发挥重要作用.近年来的研究表明,自噬与众多眼病包括青光眼的发生和发展有着密切联系.自噬可能是导致小梁网细胞功能异常的重要因素之一,其对视网膜神经节细胞发挥保护作用还是促进其死亡,仍存在争议.目前与青光眼有关的自噬基因的研究主要是OPTN基因,其编码的蛋白质optineurin与正常眼压性青光眼的发生发展相关.通过调控自噬而保护视网膜神经节细胞免于损伤可能是青光眼视神经保护的一种新方法.     

自噬与糖尿病视网膜病变氧化应激的关系

糖尿病视网膜病变(diabetic retinopathy,DR)是糖尿病的微血管和神经并发症,氧化应激是其重要致病机制。自噬是细胞在生理和病理条件下的一种重要调节活动,能够通过降解细胞内多余或损伤的蛋白质和细胞器维持细胞内环境稳态。研究表明,自噬和氧化应激之间具有重要联系,本文从DR早期微血管病变、DR神经病变和DR其它病变等方面综述自噬与氧化应激的具体关系,以期为阐明DR发病机制提供新的思路。     

补体激活与自噬在年龄相关性黄斑变性中的研究进展

年龄相关性黄斑变性(age-related macular degeneration,ARMD)是一种随年龄增长而发病率逐渐上升的黄斑部疾病,目前认为其发病因素与患者的年龄、遗传、吸烟、氧化应激、免疫炎症反应、RPE细胞老化和代谢异常等有关。补体系统在机体防御感染、免疫调节和炎症应答中扮演重要角色,补体系统异常激活引起免疫炎症近年来被认为是ARMD发病的重要原因。而自噬过程也参与了ARMD的发病。正常的自噬是细胞自我保护以及维持稳态的一个重要途径,当自噬被阻断时,可加剧氧化应激损伤,导致ARMD的发展。补体激活与自噬过程的均衡调节是控制ARMD发展的重要手段。     

自噬作用对糖尿病视网膜病变的影响

糖尿病视网膜病变(diabetic retinopathy,DR)发病机制多样,目前尚未完全阐明.自噬可能通过改变细胞内环境、氧化应激、内质网应激、细胞凋亡以及过度自噬等途径对DR的发生发展产生影响.此外,对于DR的治疗,适当提高自噬作用或抑制过度自噬可能具有重要的潜在价值.     

自噬调控眼部疾病进程的研究进展

细胞自噬是一种在生理和病理条件下发生的高度保守的自我降解过程.近年来研究表明,细胞自噬在眼部疾病的发生、发展中起着至关重要的作用.本文就细胞自噬在眼病发病机制中的作用进行了综述,为今后眼病的临床治疗提供新的思路.     

青光眼视神经损伤机制的研究进展

青光眼是目前全球范围内致盲性最高的疾病之一,是以进行性视网膜神经节细胞丧失、不可逆的视野损害等病理性改变为特征,最终导致视神经萎缩及视功能丧失的疾病。目前青光眼的发病机制并不完全清楚,其中视神经损伤的机制有多种学说,包括眼压因素及非眼压因素,非眼压因素包括血管因素、免疫作用、远端轴突病变、氧化应激作用、细胞因子的变化及自噬等机制。本文综述了有关青光眼视神经损伤机制的研究进展,为进一步研究青光眼视神经病变提供依据。     

自噬的分子机制及其在糖尿病视网膜病变中的作用

糖尿病视网膜病变（diabetic retinopathy,DR）是糖尿病微血管并发症之一,具有特征性的眼底表现,是临床上导致糖尿病患者失明的重要原因。近年来DR的发病率显著增长,严重威胁到糖尿病患者的身心健康,已成为关乎民众健康乃至国计民生的社会问题。DR发病机制复杂,多种因素如氧化应激、缺氧、炎症反应、内质网应激、多元醇途径等,均被证实与DR的发病密切相关。近年研究发现,自噬作为机体一种重要的防御机制,参与了DR的发生与发展,其病理过程涉及多种信号转导通路,与氧化应激、缺氧及新生血管形成尤为相关。因此,自噬与DR的关系成为临床研究的热点。     

非动脉炎性前部缺血性视神经病变患者血液流变学指标观察

非动脉炎性前部缺血性视神经病变(NAION)是一种常见的视神经疾病,可严重影响视功能,其发病因素诸多,机制复杂.多项研究表明异常的血液流变学尤其是高血粘度与NAION的发病密切相关[1-4].为了进一步了解血液流变学改变与NAION发病机制的关系,我们对一组NAION患者的血液流变学进行了检测.现将结果报告如下.     

自噬在年龄相关性黄斑变性和视网膜脱离中的研究进展

自噬是维持细胞正常功能和内环境稳定的一种关键的自我保护机制,其在生长发育、适应、肿瘤抑制、老化、先天性和获得性免疫中扮演着重要角色.近年来的研究表明,自噬与众多眼病,如角膜营养不良、白内障、青光眼和视网膜疾病等的发生和发展有着密切联系.在年龄相关性黄斑变性(AMD)中,自噬异常损害视网膜色素上皮(RPE)细胞的功能,促进脂褐质形成并且参与玻璃膜疣的积累.在视网膜脱离(RD)中,自噬既能保护光感受器细胞,也能促进光感受器细胞的死亡.本文就自噬的分子机制、其在AMD和RD中的作用以及自噬作用的转变和水平的变化与损伤的时间、强弱及性质的相关性进行综述.     

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.