Photoreceptor Function in Retinopathy of Prematurity

早产儿活动性视网膜病变(ROP)是对视网膜缺氧的一种反应，发生在 杆状外节快速发育的年龄。研究人员推测，迅速增加的氧气 发育中的杆状细胞的需求促成了引发ROP的缺氧，并作为一种结果 新陈代谢需求得不到满足，视杆功能受损。同时承认“光感受器假说 ROP“不会被直接测试，光感受器的发展和ROP的知识创造了 该项目的框架。在月经后年龄的ROP受试者中完成的研究记录了 受损的棒子。在新项目的目标1中，将在早产儿测量杆状细胞敏感度Srod 在此期间，ROP通常是活动的。这一点很重要，因为在活动中演示了杆的参与 ROP将为ROP管理提供新的视角，其原则将是：满足氧气 光感受器的需求。将对早产儿视网膜血管进行数值分析。Srod和 血管参数将被分析以预测ROP的结局，高危前期的概率 阈值ROP，以及视网膜和视觉功能的后期发展。在健康ROP受试者中，轻度 视力障碍可能是轻微黄斑病变的常见症状，因为这是神经血管改变的残留物 中心凹和中心凹无血流区的发育。在目标2中，将评估中央视网膜功能 (包括ROP婴儿的多焦ERG)，并跟踪整个儿童早期。迄今的结果显示 视杆功能障碍与早期屈光不正的关系，但关于视网膜的更多信息仍有待发现 ROP儿童发展为早期屈光不正的比例很大。因此， Aim 3的实验将更新屈光测量并分析儿童ROP的视网膜机制 以前在婴儿期进行研究的受试者。对于每一组实验，对十字的分析 切片数据将评估视网膜和视觉参数与ROP结果的显著差异。这个 将评估纵向数据随时间的变化以及随ROP结果的变化。该项目将 获得有关基础疾病过程的新知识，有助于理解屈光不正 ROP的发展，并对常见视力缺陷的基础提供了新的见解。此信息 未来可能会改变婴儿期和有ROP病史的儿童ROP的管理。

Active retinopathy of prematurity (ROP), which is known to be a response to retinal hypoxia, occurs at the age of rapid rod outer segment development. The investigators postulate that rapidly increasing oxygen demands of the developing rods contribute to the hypoxia that instigates ROP, and, as a consequence of unmet metabolic needs, rod function is impaired. While acknowledging that the "photoreceptor hypothesis of ROP" will not be put to direct test, knowledge of the development of the photoreceptors and of ROP creates a framework for the project. Completed studies in ROP subjects at post-term ages document evidence of damaged rods. In Aim 1 of the new project, rod cell sensitivity, Srod, will be measured at pre-term ages during which ROP is typically active. This is important because demonstration of rod involvement in active ROP will warrant a new perspective on ROP management, the principle of which will be: Satisfy oxygen needs of photoreceptors. A numeric analysis of preterm retinal blood vessels will be conducted. Srod and blood vessel parameters will be analyzed for prediction of ROP outcome, the probability of high risk pre- threshold ROP, and post-term development of retinal and visual function. In healthy ROP subjects, mild acuity deficits may be the common sign of a subtle maculopathy as residua of altered neural-vascular development of fovea and foveal avascular zone. In Aim 2, central retinal function will be evaluated (including multifocal ERG in ROP infants) and tracked through early childhood. Results to date demonstrate an association of rod dysfunction and early ametropia, but more remains to be discovered about retinal mechanisms in that substantial proportion of ROP children who develop early ametropia. Accordingly, the experiments of Aim 3 will update refractive measurements and analyze retinal mechanisms in child ROP subjects who were previously studied in infancy. For each set of experiments, the analyses of the cross sectional data will evaluate the retinal and visual parameters for significant variation with ROP outcome. The longitudinal data will be evaluated for change over time and for variation with ROP outcome. The project will obtain new knowledge about the fundamental disease process, contribute to the understanding of refractive development in ROP, and provide new insights into the basis of common acuity deficits. This information may, in the future, change management of ROP in infancy and in children with a history of ROP.