ライフサイエンスコーパス: vasoocclusive

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1 hich inflammation and immune responses cause vasoocclusive complications in sickle-cell disease.

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

6 e useful in treating acute painful episodes (vasoocclusive crises) of sickle cell disease (SCD).

7 kle cell anemia is characterized by periodic vasoocclusive crises.

8 erapeutic intervention for acute sickle cell vasoocclusive crises.

9 r sickle cell disease patients vulnerable to vasoocclusive crises.

10 re was no difference in isoprostanes between vasoocclusive crisis and patients with sickle cell disea

11 one patient 4 d prior to hospitalization for vasoocclusive crisis contained the highest ET-1 level an

12 findings contribute to the understanding of vasoocclusive crisis in patients with SCD and may have t

13 The vasoocclusive crisis is the major clinical feature of si

14 (SpO2) in adult patients with SCD and acute vasoocclusive crisis with simultaneously drawn arterial

15 r treatment of severe pain associated with a vasoocclusive crisis, and use of incentive spirometry in

16 yndrome (pre- and postexchange transfusion), vasoocclusive crisis, and/or at baseline; 12 normal volu

17 ve spirometry in patients hospitalized for a vasoocclusive crisis.

18 function, hemostasis, response to injury and vasoocclusive disease, and to test the prevailing hypoth

19 eviously linked to vascular inflammation and vasoocclusive disease.

20 Degos' disease is a vasoocclusive disorder involving the cutaneous and gastr

21 initiation, progression, and resolution of a vasoocclusive episode may present features of ischemia-r

22 n (BCAM/Lu) receptor, which is implicated in vasoocclusive episodes in sickle cell disease and activa

23 s may lead to novel antiadhesive targets for vasoocclusive episodes in sickle cell disease.

24 nude and humanized SCD mouse models of acute vasoocclusive episodes using intravital microscopy.

25 ive in sickle patients presenting with acute vasoocclusive episodes, and only 10+/-13% positive in no

26 e cell disease (SCD), treatment of recurrent vasoocclusive episodes, leading to pain crises and organ

27 s greater when sickle patients develop acute vasoocclusive episodes.

28 gical, and hematological factors involved in vasoocclusive events associated with SCD and to develop

29 to the pathology of thrombotic disorders and vasoocclusive events in sickle cell disease.

30 kocyte-endothelium interaction contribute to vasoocclusive events in the sickle mice and perhaps in h

31 o evoke, control, and inhibit the collective vasoocclusive or jamming event in sickle cell disease.

32 In patients with moderate to severe vasoocclusive pain, RheothRx was safe and may offer a th

33 abnormal RBC vasoactivity contributes to the vasoocclusive pathophysiology of sickle cell anemia, and

34 The vasoocclusive process in patients with sickle cell disea

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