Molecular Solutions to Low Injuries Resulting from Battlefield Injuries. Addendum; Annual rept. 15 May 2007-14 Apr 2008

摘要

We hypothesize that targeted molecular intervention can preserve vision threatened by battlefield trauma-induced corneal and retinal inflammation, corneal and retina/optic nerve apoptosis, ocular surface dry eye after refractive surgery, and retinal degeneration. We are studying the consequences of trauma-induced (1) corneal inflammation using a gene therapy approach of providing soluble Fas ligand to the cornea to determine if this ligand can suppress corneal inflammation in mice; (2) retinal inflammation by examining if transforming growth factor-beta, thrombospondin, and somatostatin, in subretinal space, can suppress inflammation within retina secondary to autoimmune uveoretinitis and light-induced damage in mice; (3) corneal cell death by apoptosis and promote regeneration by identifying the anti-apoptotic gene with the greatest capacity to suppress corneal cell apoptosis using mice; (4) retinal cell death and regeneration by using mice to determine if systemic treatment with lithium chloride can prevent collateral damage to retinal neurons and promote optic nerve regeneration; (5) dry eye by determining how to minimize dry eye after LASIK refractive surgery by developing new tests to predict pre-disposition to refractive surgery induced dry eye; and (6) retinal injury by generating stem cell polymer composites.