Ocular Biology

The structural basis of lens opacification (cataract), lens structure/function relationships as a consequence of aging, cataract formation and ocular/systemic diseases, and fiber cell elongation/migration in normal lens and models of cataract are being investigated. (Al-Ghoul)

Retinal Ischemic Injury

Responses of the retina to transient circulatory arrest (ischemia) are being examined in rat eyes. This model has been exploited in various ways: 1) to quantitate cell loss following timed no-flow ischemic episodes; 2) to examine factors that contribute to reperfusion injury and the death of retinal neurons once the circulation is restarted; 3) and to show neuroprotective effects of therapeutic agents. Attention is presently focused on responses of the retinal microcirculation during the postischemic period. These phenomena involve postischemic hypoperfusion, biochemical and inflammatory factors contributing to no-reflow effects, damage to and proliferation of capillary cells (endothelium and pericytes), and remodeling of the microcirculation following ischemic injury. Insights from the rat model may provide information specifically relevant to diseases of the eye that are complicated by angiogenic/vasoproliferativ     (Point to image to see capillary degeneration following ischemic injury) events, e.g. in diabetes, age-related macular degeneration, vein occlusions, hypertensive disease, and retinopathy of prematurity. The experimental studies relate more broadly to problems of blood flow and microcirculation in central nervous system disease and stroke.
(Hughes)