微小RNA在视网膜中的表达及其与视网膜疾病的关系

微小RNA(microRNA.miRNAs)是一类调控基因表达的非编码小RNA.miRNA的表达具有组织特异性,并参与细胞生长、发育、分化、增生以及凋亡等过程.近年来,人们也发现miRNA在视网膜不同细胞中呈特异表达,尽管尚无直接证据,但这些差异表达的miRNA可能与视网膜疾病如视网膜色素变性以及糖尿病视网膜病变的发生发展有着密切的联系.本文对miRNA在视网膜中的特异表达以及miRNA在视网膜疾病中的作用等研究现状进行总结,同时对miRNA在视网膜相关疾病的治疗方面的前景进行探讨.     

微小RNA与视网膜发育相关性研究进展

微小RNA(miRNA)是相对分子质量较小、性质稳定的RNA,通过与目的mRNA的部分互补序列碱基互补配对而在转录后水平调节动物、植物的基因表达及抑制蛋白质合成.目前发现在视网膜中表达的miRNA有200多种,miRNA对基因的表达调控影响了视网膜的正常发育,与神经视网膜的发生、视网膜光感受器的分型及正常数量维持、神经节细胞的存活及轴突生长、视网膜色素上皮层的发育均有密切联系.此外,miRNA的调控还与视网膜损伤后的再生有关.miRNA对视网膜发育的调控主要通过直接靶向调节与此有关的某些目的基因的表达,或通过调节某些信号通路组分来实现,在视网膜发育过程中,miRNA功能的正常发挥为视网膜正常形态结构的形成提供了保障,从而为其发挥正常的生理功能提供了物质基础.现就脊椎动物视网膜中miRNA的生物学功能与视网膜发育的相关性研究进展进行综述.     

环状RNA在眼底疾病中的研究进展

环状RNA（circRNA）是一类通过反向剪接生成的新的内源性非编码RNA,具有miRNA"海绵"、调节转录和剪接、调节蛋白之间的相互作用等功能。最近的研究表明,circRNA在视网膜微血管功能障碍、糖尿病视网膜病变、老年性黄斑变性、增生性玻璃体视网膜病变、高同型半胱氨酸血症所致眼病和眼部恶性肿瘤等眼底疾病的发生和发展...     

微小核糖核酸与眼底疾病的相关性研究进展

微小核糖核酸(miRNA)是近年来发现的真核细胞内一类稳定、非编码可调控的核糖核酸(RNA)分子,主要通过与靶基因信使RNA(mRNA)3’端非编码区碱基配对的方式,引起靶标mRNA降解或翻译抑制,从而参与真核生物的生长发育、细胞增生凋亡及肿瘤发生等多种生理和病理过程.miRNA表达变化与眼底新生血管性疾病、糖尿病视网膜病变、视网膜色素变性、视网膜母细胞瘤、脉络膜黑色素瘤等眼底疾病的发生发展存在一定的相关性.进一步探索miRNA与眼底疾病发生发展的相互关系,可能有助于从基因水平上认识、预防和治疗这些眼底疾病.     

哺乳动物视网膜microRNA的表达及功能

microRNAs(miRNAs)是一类长约22个核苷酸的内源性非编码单链RNA,在维系几乎所有组织或器官系统的正常发育和生理功能等方面都起着非常重要的作用,主要通过降解靶基因mRNAs或抑制靶基因mRNAs的翻译,从而沉默特定靶基因发挥作用.据预测人类超过1/3的蛋白编码基因受miRNAs的调控.越来越多的研究表明很多miRNAs在眼部组织中有特异性的表达,其中至少有78个miRNAs在视网膜组织中表达.本文主要就miRNAs在哺乳动物视网膜中的表达及其相关功能的最新研究进展作一综述.     

miRNA在视网膜母细胞瘤中的作用研究进展

视网膜母细胞瘤（RB）是儿童最常见的原发性眼内恶性肿瘤，其发病与基因突变相关。microRNA（miRNA）是一种非编码RNA，能调控基因的表达，目前已成为肿瘤研究的热点之一。本文将对miRNA在RB中相关研究进展作一综述，从而为RB的诊断、治疗提供新思路和新方法。     

环状RNA在糖尿病视网膜病变中的作用研究进展

视网膜微血管功能失调、炎症反应过度激活以及神经元的退行性病变是糖尿病视网膜病变(DR)的主要发病机制。环状RNA(circRNA)是一类主要由前体RNA经剪切加工后具有特殊环状结构的内源性非编码RNA,其广泛存在于视网膜中并参与各种眼底疾病的发生发展。已有研究表明,circRNA在DR视网膜组织中存在异常表达,并且其可作为miRNA的"海绵",通过参与视网膜微血管功能失调、炎症反应及神经元退行性病变过程影响DR的发生发展。未来,对circRNA在DR中的探索将深入阐明DR的病理生理过程,使其有望成为DR诊断的生物标志物及治疗的分子靶点,从而实现DR早期诊断及精准治疗的目标。     

微小RNA在糖尿病视网膜病变发病机制中的作用

微小RNA（micoRNA）是一类高度保守、非编码的小分子RNA,通过与mRNA互补配对在转录后水平降解mRNA或抑制mRNA翻译来负调控靶基因的表达,并可能调控着几乎每一个细胞生理进程.研究发现微小RNA的异常表达谱对于糖尿病视网膜病变（diabetic retinopathy,DR）的发病机制有着至关重要的作用.微小RNA在不同的刺激因素下通过靶向调控核因子-κB、缺氧诱导因子-1/血管内皮生长因子、p53等与DR发生发展密切相关的靶基因,产生不同的细胞生物学效应,从而广泛调节视网膜各类细胞在炎症发生、新生血管形成、增生和凋亡等方面的病理过程.异常表达的微小RNA及其功能靶标的发现不仅丰富了对DR发病机制的阐述,也为DR的早期预防和探索基因靶向治疗提供新的突破点.     

长链非编码RNA在糖尿病视网膜病变中的作用

长链非编码RNA(long non-coding RNA,LncRNA)是一类不编码蛋白质的转录子,长度大于200个核苷酸,主要在表观遗传、转录或转录后水平调节基因的表达.LncRNA的表达异常可能引发各种病理过程.糖尿病视网膜病变(diabetic retinopathy,DR)为多因素疾病,新近的研究表明,许多LncRNA特异表达与DR的发生密切相关.在本文中,我们对LncRNA的相关功能、参与DR发生发展的调控机制以及相关治疗的新近研究进行综述.     

微小RNA在糖尿病视网膜病变新生血管生成中的研究进展

微小RNA(miRNA)是一类内生的、长度约20 ～ 24个核苷酸的具有组织特异性和高度保守的RNA,通过与mRNA互补配对在转录后水平降解mRNA或抑制mRNA翻译来负调控靶基因的表达.多项研究已表明miRNA的亚型基因miR-126、miR-31、miR-200b和miR-29等在一定程度上与糖尿病视网膜病变(DR)的新生血管生成有关,通过一系列调控血管内皮生长因子(VEGF)的表达,进而抑制或促进血管新生,而VEGF是一种新生血管的主要促进因子,能够特异性的刺激血管内皮细胞的增生及新生血管生成,破坏血-视网膜屏障,加快DR的进展.因此,揭示miRNA在DR新生血管形成中的作用及其机制是未来DR机制研究的重要方向,并可为DR的防治提供新的策略.现就miRNA在DR新生血管形成的研究进展作一综述.     

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.