凋亡是糖尿病视网膜微血管病变和神经元病变的细胞病理学基础

糖尿病视网膜病变(diabetic retinopathy,DR)不仅是视网膜微血管病变也是神经元病变.在早期糖尿病电生理和心理物理学的改变提示神经元病变出现在微血管病变之前.因此这些手段是目前发现最早期DR的方法.DR的细胞病理学基础是凋亡.但是把调控细胞凋亡作为治疗DR的方法却长期以来被忽视.最新的研究,应用细胞保护剂可以预防和逆转视网膜神经元凋亡,使这种治疗途径初现端倪.     

自噬与HMGB1在糖尿病视网膜微血管病变和神经退行性变中的研究进展

糖尿病视网膜病变（diabetic retinopathy,DR）是由糖尿病所导致的最典型的微血管并发症之一。以往DR发病机制和治疗的研究主要集中在微血管;近年来,许多学者认为DR不仅仅是一种微血管病变,而且还伴有视网膜神经退行性变。近期研究表明,自噬与高迁移率族蛋白B1（high mobility group box protein 1,HMGB1）通过多条通路参与到糖尿病视网膜微血管病变和神经退行性变中,通过调控自噬或 HMGB1可能为DR治疗提供一种新的思路。本文就自噬与 HMGB1 在糖尿病视网膜微血管病变和神经退行性变发病中的研究进展进行综述。     

糖尿病视网膜神经变性机制的研究进展

糖尿病视网膜病变(diabetic retinopathy,DR)一直被认为是微血管病变。然而,大量的研究已经证实,DR不仅会引起视网膜的血管病变,也会引起视网膜神经退行性改变。越来越多的证据也表明,在DR早期未发生视网膜血管病变之前就已经出现了视网膜神经变性,且视网膜神经变性可能参与了微血管异常的发生发展。目前,糖尿病视网膜神经变性的机制尚不十分明确,现就近年来糖尿病视网膜神经变性机制的研究进展做一综述。     

σ-1受体在糖尿病视网膜病变中神经保护作用的研究进展

视网膜微血管病变被认为是糖尿病视网膜病变(diabetic retinopathy,DR)的重要特征之一,近年来越来越多的研究表明,DR同时有视网膜神经元的损害.σ-1受体是一种能与多种抗精神病药物结合的非阿片类蛋白受体,近年来许多研究发现,σ-1受体的激活有视网膜神经保护作用.本文综述了σ-1受体在DR中神经细胞保护作用机制的研究进展,为DR神经损害的研究及防治提供新的思路.     

糖尿病视网膜病变中周细胞功能异常的分子调控机制研究进展

糖尿病视网膜病变(diabetic retinopathy,DR)是导致视功能障碍和视力丧失的主要原因之一,其发病机制复杂,涉及多种细胞、分子,至今尚未完全阐明.DR的主要病理特点是微血管功能紊乱,其中周细胞凋亡是DR的重要标志.周细胞凋亡的主要原因包括高血糖引起的活性氧和糖基化终产物的产生增加,血小板衍生生长因子表达下降,血管生成素2和转化生长因子β的上调以及色素上皮衍生因子水平降低等.近年来,关于糖尿病视网膜微血管病变中周细胞分子调控机制的研究取得很大突破.因此,本文对DR中周细胞功能异常和其分子调控机制做一综述,为防治糖尿病视网膜微血管病变的发生提供新的理论基础.     

糖尿病视网膜病变微血管神经病变发病机制的研究进展

糖尿病视网膜病变(diabetic retinopathy,DR)是糖尿病(diabetic melitus,DM)常见且严重的微血管并发症之一。在国外,DR是工作人群(20～64岁)首位的致盲因素; 在国内,DR的发病率和致盲率也在逐年增加,严重影响患者的生存质量。以往对DR发病机制和治疗的研究主要集中在微血管方面,近年来,随着研究的深入,越来越多的学者认为DR不再单纯是一种微血管病变,同时伴随着视网膜神经退行性改变,但国内外文献对DR的微血管病变与神经退行性改变发病机制的研究多是单一的。本文就DR微血管病变与神经退行性改变之间的关系做一综述。     

内脏脂肪素在糖尿病视网膜病变中的研究进展

糖尿病视网膜病变(DR)是继发于糖尿病的慢性视网膜微血管病变,可致糖尿病患者视力永久丧失。DR的发生与视网膜微血管功能障碍、视网膜组织水肿、出血和继发性新血管增殖有关。有研究显示,在糖尿病患者的脂肪组织、肝脏和肾脏中均发现内脏脂肪素高表达,并且该因子可能存在于视网膜组织中,对DR的发生发展具有一定调控性作用。本综述以内脏脂肪素与DR的相关研究为依据,对内脏脂肪素与DR的关系作论述。     

糖尿病早期视网膜神经元退行性病变最新研究进展

糖尿病视网膜病变(diabetic retinopathy,DR)在早期被认为是一种微血管性疾病,多年来关于DR发病机制的研究主要集中在血管特征的改变上,包括血管渗透性的增加、新生血管的形成和黄斑水肿等.近年大量的视网膜电生理检查发现在糖尿病早期视网膜微血管发生损害前,视网膜神经元即发生一系列病理改变,提示DR是一种神经血管性疾病,这也可以解释DR患者很快发生的视功能减退.现将国内外关于糖尿病早期视网膜神经元退行性病变的最新研究进展作一综述,以期发现有效的视网膜神经元保护策略,从而减缓DR的进程.     

糖尿病视网膜病变神经血管损伤发病机制的研究进展

糖尿病视网膜病变(diabetic retinopathy,DR)曾被认为是糖尿病微血管病变的并发症,如今已被广泛认为是神经血管单元（neurovascular unit,NVU）损伤引起的一类神经血管性疾病。研究表明,在出现临床可检测的微血管病变之前,视网膜神经损伤已经出现,并参与了微血管病变的进展。因此,微血管病变这一观点并没有揭示视网膜神经元、神经胶质细胞和血管间相互联系及影响的重要性。以NVU作为整体研究神经血管损伤及保护机制,寻找临床新的预防和干预DR的措施必定成为未来研究的热点。     

VEGF家族及其受体与糖尿病视网膜病变发病的关系

视网膜新生血管形成和黄斑水肿是糖尿病视网膜病变(diabetic retinopathy,DR)的主要临床表现,也是DR主要的致盲原因。目前研究表明血管内皮生长因子(vascular endothelial growth factor,VEGF)在糖尿病视网膜微血管并发症的发生中发挥重要作用,因此VEGF成为当今DR治疗干预的一个研究热点。本文就VEGF家族及其受体在DR中的表达与DR病变发病的关系研究进展进行综述。     

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.

---

     

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.