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2 recommended for adults with 3 or more severe vasoocclusive crises during any 12-month period, with SC
3 ther increased during acute sickling events (vasoocclusive crises in humans or hypoxia/reoxygenation
4 ctors that are hypothesized to contribute to vasoocclusive crises in sickle cell anemia are increased
5 ease, and was further reduced during painful vasoocclusive crises to 34% +/- 9% and 25% +/- 3% of con
11 re was no difference in isoprostanes between vasoocclusive crisis and patients with sickle cell disea
12 one patient 4 d prior to hospitalization for vasoocclusive crisis contained the highest ET-1 level an
13 findings contribute to the understanding of vasoocclusive crisis in patients with SCD and may have t
15 (SpO2) in adult patients with SCD and acute vasoocclusive crisis with simultaneously drawn arterial
16 r treatment of severe pain associated with a vasoocclusive crisis, and use of incentive spirometry in
17 yndrome (pre- and postexchange transfusion), vasoocclusive crisis, and/or at baseline; 12 normal volu
19 function, hemostasis, response to injury and vasoocclusive disease, and to test the prevailing hypoth
23 initiation, progression, and resolution of a vasoocclusive episode may present features of ischemia-r
24 n (BCAM/Lu) receptor, which is implicated in vasoocclusive episodes in sickle cell disease and activa
27 ive in sickle patients presenting with acute vasoocclusive episodes, and only 10+/-13% positive in no
28 e cell disease (SCD), treatment of recurrent vasoocclusive episodes, leading to pain crises and organ
30 gical, and hematological factors involved in vasoocclusive events associated with SCD and to develop
31 electin inhibition has been shown to prevent vasoocclusive events in patients with SCD; however, the
33 olymerization of Hb S promotes hemolysis and vasoocclusive events in the microvasculature of patients
34 kocyte-endothelium interaction contribute to vasoocclusive events in the sickle mice and perhaps in h
35 o evoke, control, and inhibit the collective vasoocclusive or jamming event in sickle cell disease.
36 nary hemodynamics during sickle cell disease vasoocclusive pain and ACS.Clinical trial registered wit
39 abnormal RBC vasoactivity contributes to the vasoocclusive pathophysiology of sickle cell anemia, and