Costs of Military Eye Injury, Vision Impairment, and Related Blindness and Vision Dysfunction Associated with Traumatic Brain Injury (TBI) without Eye Injury Prepared by

2 TAKE AWAY MESSAGE Based on published data from 2000-2010, the total incident cost of eye injury in the military each year in this timeframe has been $2.282 billion, which represents superficial eye injury, nonsuperficial eye injury that does and does not result in permanent visual impairment or blindness, and vision impairment related to Traumatic Brain Injury (TBI). If we multiply the one-year costs by 11 to account for the period from 2000-2010, the total cost to the economy of all ocular injury and vision impairment related to TBI is$25.107 billion. Of that total, the costs incurred in the first year (all for superficial injury, initial medical care for non-superficial injuries, and rehabilitation for bilateral vision impairment) are $634 million. This is money that has already been spent. The present value of the projected Department of Veterans Affairs (VA) benefits for the remainder of the lives of all service members with ocular injuries in the 11 years under study is$188 million. The present value of the projected costs to the remainder of the economy over the remaining lifetimes of the service members with eye injuries or vision impairment due to TBI is $24.286 billion. This last cost is not to the federal government but to the economy and society as a whole

The Peripheral Serotonergic System and Platelet Aggregation in Cyclosporin A-Induced Hypertensive Rats

Cyclosporin A plays an important role in preventing rejection in allograft transplant recipients. However, the therapeutic use of cyclosporin A is associated with increased incidence of thromboembolic complications and drug-related hypertension. In order to study the mechanisms by which cyclosporin A induces these abnormal pathophysiological situations, we have assessed the platelet serotonin contents and whole blood platelet aggregation in control rats as well as in rats treated (orally) with 30 and 5 mg/kg/day of cyclosporin A, after 2 and 7 weeks of treatment. These doses correspond respectively to CsA "peak" and "trough" concentrations achieved in human blood in clinical practice (immediately following an intake of a daily dose of CsA and when the blood concentration stabilizes, respectively). Both trough and peak doses caused an increase in blood pressure after 2 and 7 weeks. Platelet serotonin content decreased in the cyclosporin-treated groups, in contrast with the control. Collagen-induced whole blood platelet aggregation increased drastically for the peak concentration-treated group, while adenosine 5'-diphosphate-induced platelet aggregation did not reach statistical significance. Finally, in vitro platelet thromboxane A2 generation increased in cyclosporin A concentrations when platelets were stimulated with either collagen or adenosine 5'-diphosphate. In conclusion, both tested cyclosporin A concentrations induced important changes in platelet serotonin and thromboxane content and aggregation, factors which may play a decisive role in the development and/or maintenance of hypertension and thrombotic complications.http://www.sciencedirect.com/science/article/B6T1C-3Y4C5D7-4/1/157b7272bc9cfd3ff94f5888dc32dc2