血管内皮生长因子在早产儿视网膜病变中的作用研究进展

视网膜新生血管形成是眼部多种疾病共有的病理特点,其引发的疾病已成为目前致盲的重要原因.VEGF家族在新生血管形成中扮演着重要的角色,其通过影响细胞增生、细胞迁移、诱导毛细血管腔形成,从而促进新生血管的生成和生长.本文以早产儿视网膜病变为例,介绍VEGF家族及其受体,在早产儿视网膜病变的病理过程中的作用和针对其作用机制可采取的相应防治方法.     

血管内皮生长因子抑制剂在糖尿病性视网膜病变中的应用

眼部新生血管是糖尿病性视网膜病变致盲的主要病理改变,而血管内皮生长因子（vascular endothelial growth factor,VEGF）在新生血管形成过程中起关键性刺激作用。VEGF抑制剂主要通过与VEGF结合并阻断其生物活性而起作用,从而达到抑制眼部新生血管生成的目的,在糖尿病性视网膜病变血管渗漏及新生血管形成的治疗中取得了显著的成绩。Bevacizumab（Avastin）是VEGF抑制剂之一,属于重组人源化单克隆抗体,因其疗效良好、价格低廉已被广泛应用于临床。现将VEGF抑制剂（尤其是Avastin）治疗糖尿病性视网膜病变的相关应用进展作一综述。     

β肾上腺素能受体拮抗剂治疗眼部新生血管疾病的研究进展

眼部新生血管形成是糖尿病视网膜病变、早产儿视网膜病变、视网膜中央静脉阻塞和老年性黄斑变性等多种眼部疾病的病理学改变, 严重影响患者视力。β受体在结膜、角膜上皮细胞、角膜内皮细胞、眼外肌、小梁网、睫状肌、晶状体和视网膜中均有表达。β肾上腺素能受体拮抗剂与β受体结合, 通过抑制血管内皮生长因子(VEGF)、缺氧诱导因子-1、白细胞介素-6等促血管生成细胞因子, 降低巨噬细胞相关炎症反应, 增加抗血管生成因子表达来发挥抗血管生成作用。其在治疗角膜新生血管、脉络膜新生血管、早产儿视网膜病变时, 可显著减少新生血管面积, 延缓疾病进展, 联合应用抗VEGF药物可减少抗VEGF药物的给药频率。在有效的治疗浓度下, β肾上腺素能受体拮抗剂表现出良好的耐受性;且其较抗VEGF药物有更广泛的靶点, 为角膜、脉络膜和视网膜新生血管等眼部新生血管性疾病提供了新的治疗策略。     

血管内皮生长因子抑制剂治疗视网膜新生血管性疾病

视网膜新生血管性疾病是致盲的主要病因,早期预防、控制视网膜新生血管的发生发展显得尤为重要。目前,关于视网膜新生血管性疾病的确切发病机制尚不清楚,但对血管内皮生长因子(vascular endothelial growth factor,VEGF)在其形成过程中起关键作用已达成共识,现在已有多种VEGF抑制剂被用于治疗眼部新生血管性疾病。现将治疗视网膜新生血管性疾病的最新几种VEGF抑制剂作一综述。     

VEGF与眼内血管新生

眼内新生血管是很多眼病致盲的重要原因,例如糖尿病视网膜病变、年龄相关性黄斑变性、早产儿视网膜病变、视网膜中央或分支静脉阻塞、角膜炎和眼外伤等.生长因子中的血管内皮生长因子(vascular endothelial growth factor,VEGF)家族是眼内血管新生的关键因素.在一些眼病中,它通过调控病理性血管发生和增加血管通透性而起作用.本文我们主要阐述眼内新生血管的形成机制和治疗方面的新进展,对VEGF 家族的结构、理化特性、VEGF及受体在眼内血管新生中的作用以及针对血管新生的防治措施进行综述.     

色素上皮衍生因子(PEDF)的研究进展

糖尿病性视网膜病变、年龄相关性黄斑变性、中心性渗出性脉络膜视网膜病变等许多眼部疾病的共同特征是视网膜或视网膜下新生血管。色素上皮衍生因子（PEDF）是近年来发现的能有效抑制新生血管形成的因子，与血管内皮生长因子（VEGF）等一起控制了新生血管的发生过程。PEDF有抑制新生血管、营养神经、诱导肿瘤细胞凋亡等作用。本文主要综述其上调下调规律、其作用的研究现况及应用前景。     

肝细胞生长因子与视网膜新生血管形成

视网膜新生血管形成可造成眼部多种组织成分的广泛损害,已成为世界范围的致盲性疾病。其发生及发展过程复杂,需要多种因素参与,包括多种生长因子的相互作用等。肝细胞生长因子(HGF)作为多效性生长因子,对新生血管形成的作用逐渐被认识。本文主要探讨HGF在视网膜新生血管发病机制中的作用以及与血管内皮生长因子(VEGF)的关系。     

眼部新生血管与抗血管内皮生长因子治疗

眼部新生血管性病变是致盲的主要原因之一,可见于多种眼底疾病,其确切的发病机制尚不完全清楚.大量的研究证据表明血管内皮生长因子(VEGF)是新生血管形成的关键调控因子.本文对VEGF的特性、VEGF在眼部新生血管形成中的作用和抗VEGF治疗进行综述.     

密蒙花提取物对高糖下人视网膜血管内皮细胞增生及VEGF表达的影响

糖尿病视网膜病变（diabetic retinopathy,DR）是糖尿病严重的微血管并发症之一,其病理特征为视网膜新生血管形成,血管内皮生长因子（vascular endothelial growth factor,VEGF）能特异性地作用于视网膜血管内皮细胞,是最直接的眼内新生血管形成因子之一。密蒙花是用于治疗眼部疾病的一种中药,具有维生素P样作用,能降低皮肤和小肠血管的通透性及脆性。     

肝细胞生长因子与视网膜新生血管形成

视网膜新生血管形成可造成眼部多种组织成分的广泛损害,已成为世界范围的致盲性疾病.其发生及发展过程复杂,需要多种因素参与,包括多种生长因子的相互作用等.肝细胞生长因子（HGF）作为多效性生长因子,对新生血管形成的作用逐渐被认识.本文主要探讨HGF在视网膜新生血管发病机制中的作用以及与血管内皮生长因子（VEGF）的关系.     

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.