The goal of the UAB Comprehensive Sickle Cell Center is to develop new strategies to treat and, ultimately, to cure sickle cell disease (SCD). To accomplish this goal, the Center will be organized into two divisions: The Division of Basic and Clinical Research, and the Division of Social, Health Service and Community Based Research (SHSCBR). The major goals of projects included in the Division of Clinical and Basic Research are (1) to develop genetic therapies for SCD using 2 separate approaches (2) to study nitric oxide-dependent vascular functions and the effects of oxygen radicals in sickle cells disease (3) to develop better strategies for preventing pneumococcal infections by vaccination and (4) to elucidate the natural history and risk factors for development of chronic renal insufficiency. The clinical benefits of these studies include: new reduced morbidity from acute vaso-occlusive events, an improved pneumococcal vaccine and a better understanding of stroke in adult patients with SCD. The Division of SHSCBR will (1) establish a sickle cell network which will provide a registry and health service assessment for all patients in Alabama (2) incorporate detailed psychosocial assessment and intervention with behavioral and non-pharmacological pain management strategies and (3) evaluate house staff education, and its impact on SCD patient care. The SHSCBR Division will also provide a liaison with six of the seven State of Alabama sickle cell community organizations, their directors and the ex officio members of the Community Advisory Board of the Center. Clinical Core will be organized in two adult sickle cell clinics at the UAB Kirklin Clinic and Cooper Green Hospital and pediatric clinic located in the UAB- affiliated Children's Hospital of Alabama. The Center will provide quality care for both pediatric and adult sickle cell patients while new therapies are being developed. The Diagnostic Laboratory will provide state of the art diagnosis for the patients and will provide analyses for the basic and clinical research components, including hemoglobin analysis of transgenic animals. The lab presently serves as a reference laboratory for the Neonatal Hemoglobinopathy Screening Program, and for the Department of Public Health Bureau of Clinical Labs in Montgomery. The Center will interact formally with the Neonatal Hemoglobinopathy Screening Program, a component of the State of Alabama Department of Public Health Bureau of Family Health. An administrative core will serve the Center as a whole.

National Institute of Health (NIH)
National Heart, Lung, and Blood Institute (NHLBI)
Comprehensive Center (P60)
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Special Emphasis Panel (ZHL1-CSR-Q (S1))
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University of Alabama Birmingham
Internal Medicine/Medicine
Schools of Medicine
United States
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Coats, Mamie T; Benjamin, W H; Hollingshead, S K et al. (2005) Antibodies to the pneumococcal surface protein A, PspA, can be produced in splenectomized and can protect splenectomized mice from infection with Streptococcus pneumoniae. Vaccine 23:4257-62
Telfair, Joseph; Alexander, Leah R; Loosier, Penny S et al. (2004) Providers' perspectives and beliefs regarding transition to adult care for adolescents with sickle cell disease. J Health Care Poor Underserved 15:443-61
Briles, David E; Hollingshead, Susan K; Paton, James C et al. (2003) Immunizations with pneumococcal surface protein A and pneumolysin are protective against pneumonia in a murine model of pulmonary infection with Streptococcus pneumoniae. J Infect Dis 188:339-48
Liu, Enli; Jelinek, Jaroslav; Pastore, Yves D et al. (2003) Discrimination of polycythemias and thrombocytoses by novel, simple, accurate clonality assays and comparison with PRV-1 expression and BFU-E response to erythropoietin. Blood 101:3294-301
Aslan, Mutay; Ryan, Thomas M; Townes, Tim M et al. (2003) Nitric oxide-dependent generation of reactive species in sickle cell disease. Actin tyrosine induces defective cytoskeletal polymerization. J Biol Chem 278:4194-204
Lim, Dong Gun; Sweeney, Scott; Bloodsworth, Allison et al. (2002) Nitrolinoleate, a nitric oxide-derived mediator of cell function: synthesis, characterization, and vasomotor activity. Proc Natl Acad Sci U S A 99:15941-6
Coles, Barbara; Bloodsworth, Allison; Eiserich, Jason P et al. (2002) Nitrolinoleate inhibits platelet activation by attenuating calcium mobilization and inducing phosphorylation of vasodilator-stimulated phosphoprotein through elevation of cAMP. J Biol Chem 277:5832-40
Coles, Barbara; Bloodsworth, Allison; Clark, Stephen R et al. (2002) Nitrolinoleate inhibits superoxide generation, degranulation, and integrin expression by human neutrophils: novel antiinflammatory properties of nitric oxide-derived reactive species in vascular cells. Circ Res 91:375-81
Robinson, D Ashley; Briles, David E; Crain, Marilyn J et al. (2002) Evolution and virulence of serogroup 6 pneumococci on a global scale. J Bacteriol 184:6367-75
O'Donnell, V B; Freeman, B A (2001) Interactions between nitric oxide and lipid oxidation pathways: implications for vascular disease. Circ Res 88:12-21

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