This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.Nitric oxide availability is reduced in people with sickle cell disease. Possibly, as a consequence, hemostasis is deregulated and circulating inflammatory mediators are present. Excess fibrin deposition in tissues ensues and accounts for much of the morbidity and mortality. We postulate administration of NO may improve hemostatic and inflammatory balance thereby potentially reducing the consequences of sickle cell disease.
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