 and bone marrow of subjects with sickle cell anemia. We hypothesize that therapeutic interventions that interrupt adhesive interactions between sickle erythrocytes, leukocytes, platelets and vascular endothelium will lessen the vaso occlusion, hemoglobin desaturations, and release of mediators of vascular damage induced by intermittent hypoxia. While sickle cell anemia (SCA
and bone marrow of subjects with sickle cell anemia. We hypothesize that curative interposition that interrupt adhesive interactions between sickle erythrocytes, leukocyte, platelets and vascular endothelium will decrease the vaso occlusion, hemoglobin desaturations, and acquittance of mediators of vascular damage induce by intermittent hypoxia. While sickle cell anemia (SCA
 anf bone marrow of subjectr with sickle cglo anemma. We hgpothesixe that therapeutic intervenvionw thau interrupt adhesivd interacnions betqeen wickle eryvgrocytes, leukkgytes, 'latelets and vsscular engothelium will ldsden the vaso occlusion, hemoglobin dqsaturayilns, and releasg of kqdiafors of vascular damage induced by intermpttent hypoxia. Whole sickle cell anemia (SCA
and bone marrow of subjects with sickle We that therapeutic that interrupt adhesive platelets vascular endothelium will the vaso occlusion, desaturations, and release of mediators of damage induced by intermittent hypoxia. While sickle cell anemia (SCA
 and bone marrow of subjects wiTh sickle ceLl aneMia. we hYpOtheSize That therapeutiC InteRventions that interrupt AdhesIvE InteRAcTions Between SIcKLE erYtHrOcyTeS, LeUkocyTes, PlateleTs and vascuLar EnDothelium wilL LeSsen the vasO ocClusion, hemogLobIn desaTuRatIOns, anD reLease Of mediATors of Vascular dAmAGe induCEd by intERMiTtenT hypoxia. While sickLE cELl anemia (SCA
 and bone marrow of subjec ts with si cklecel l a ne mia.  Wehypothesize th a t th erapeutic intervention s tha ti nter r up t adh esive i n te r a cti on sbet we e nsickl e e rythroc ytes, leuk ocy te s, platelets an d vascular  en dothelium wi lllessen  t hev aso o ccl usion , hemo g lobindesaturat io n s, and release o fmedi ators of vascular da m age induced by  inter mi t te n t  hy pox ia. Whilesi cklec ell ane m ia ( S CA
 and_bone marrow_of subjects with sickle_cell anemia._We_hypothesize that_therapeutic_interventions that interrupt_adhesive interactions between_sickle erythrocytes, leukocytes, platelets_and vascular endothelium_will_lessen the vaso occlusion, hemoglobin desaturations, and release of mediators of vascular damage induced_by_intermittent hypoxia._While_sickle_cell anemia (SCA