ライフサイエンスコーパス: intravascular hemolysis

1 herapeutic that prevents complement-mediated intravascular hemolysis.

2 as therapeutics for patients with excessive intravascular hemolysis.

3 ributes to these processes without affecting intravascular hemolysis.

4 eased mortality and morbidity resulting from intravascular hemolysis.

5 the disease result from complement-mediated intravascular hemolysis.

6 PI)-linked membrane proteins, which leads to intravascular hemolysis.

7 n in SCD, and potentially other disorders of intravascular hemolysis.

8 hemoglobin released into blood plasma during intravascular hemolysis.

9 iated with extravascular hemolysis than with intravascular hemolysis.

10 of red cells in PNH patients, manifested by intravascular hemolysis.

11 iciency state and vasculopathy consequent to intravascular hemolysis, (2) chronic pulmonary thromboem

12 cells results in chronic complement-mediated intravascular hemolysis, a process central to the morbid

13 ransfusion with old but not new blood led to intravascular hemolysis, acute hypertension, vascular in

14 Acute intravascular hemolysis after infusions of intravenous R

15 Low levels of intravascular hemolysis after transfusion of aged stored

16 Infusion of a low dose of hemin caused acute intravascular hemolysis and autoamplification of extrace

17 blood cells (RBCs) to complement, leading to intravascular hemolysis and hemoglobinuria.

18 and thus consistent with the hypothesis that intravascular hemolysis and increased endogenous erythro

19 ages to remove senescent erythrocytes led to intravascular hemolysis and increased expression of the

20 ickle cell disease (SCD) is characterized by intravascular hemolysis and inflammation coupled to a 40

21 However, the degree of intravascular hemolysis and microparticle formation in h

22 LDH may represent a convenient biomarker of intravascular hemolysis and NO bioavailability, characte

23 re simultaneous damage to endothelial cells, intravascular hemolysis, and activation of platelets lea

24 or 2 hours after transfusion by 50%, reduced intravascular hemolysis, and lowered the levels of compl

25 ssociated with Hb levels </=6 g/dL at onset, intravascular hemolysis, and previous splenectomy.

26 loantibodies, which fixed complement, led to intravascular hemolysis, and resulted in decreased level

27 ations are consistent with NO depletion from intravascular hemolysis, and they indicate that the path

28 imed at controlling extravascular as well as intravascular hemolysis are also examined.

29 PNH) is characterized by complement-mediated intravascular hemolysis because of the lack from erythro

30 This explains intravascular hemolysis but does not explain the mechani

31 Intravascular hemolysis can be inhibited in patients by

32 Intravascular hemolysis can impair NO bioavailability an

33 es, the development of PH is associated with intravascular hemolysis, cutaneous leg ulceration, renal

34 Intravascular hemolysis describes the relocalization of

35 PNH) is characterized by complement-mediated intravascular hemolysis due to the lack of CD55 and CD59

36 ing erythrocytic sickling, vascular ectasia, intravascular hemolysis, exuberant hematopoiesis, cardio

37 However, when it is released during intravascular hemolysis from the cell into blood plasma,

38 low titer of DL antibody can mediate severe intravascular hemolysis given its propensity to sensitiz

39 ainst terminal complement protein C5 reduces intravascular hemolysis, hemoglobinuria, and the need fo

40 acquired stem cell disorder characterized by intravascular hemolysis, hypercoagulability, and relativ

41 We experimentally produced acute intravascular hemolysis in a canine model in order to te

42 During intravascular hemolysis in human disease, vasomotor tone

43 cells and the lack of clinically significant intravascular hemolysis in patients with IGD.

44 against the complement protein 5, stops the intravascular hemolysis in PNH.

45 We conclude that intravascular hemolysis in SCD releases heme that activa

46 had gastroenteritis followed by progressive intravascular hemolysis, initially attributed to acute p

47 othesized that plasma hemoglobin released by intravascular hemolysis initiates endothelial injury thr

48 n expanding body of research indicating that intravascular hemolysis is a pathological mechanism in s

49 Hp-depleted sera from patients with intravascular hemolysis is severalfold more trypanolytic

50 ion of ILY in ThCD59(RBC) mice induced acute intravascular hemolysis, leading to reduced nitric oxide

51 Intravascular hemolysis leads to impaired bioavailabilit

52 Chronic intravascular hemolysis leads to nitric oxide (NO) deple

53 We recently generated a unique intravascular hemolysis mouse model in which the membran

54 Intravascular hemolysis occurred in 5 patients, of which

55 Intravascular hemolysis occurs in patients on extracorpo

56 ervations confirm that the acute toxicity of intravascular hemolysis occurs secondarily to the accele

57 of inhibiting both the extravascular and the intravascular hemolysis of PNH.

58 e have investigated the impact of persistent intravascular hemolysis on liver dysfunction using the m

59 The degree of intravascular hemolysis post-transfusion and effects on

60 ell disease, ischemia-reperfusion injury and intravascular hemolysis produce endothelial dysfunction

61 sign, we demonstrate that free water-induced intravascular hemolysis produces dose-dependent systemic

62 GPI-AP expression gradually decreased, while intravascular hemolysis progressively increased.

63 Thus, intravascular hemolysis represents an intrinsic mechanis

64 lytic diseases are characterized by enhanced intravascular hemolysis resulting in heme-catalyzed reac

65 ries have discovered that even low levels of intravascular hemolysis severely disrupt nitric oxide bi

66 Intravascular hemolysis showed a positive correlation wi

67 0.58, P < .001) and to laboratory markers of intravascular hemolysis, such as reticulocyte count (r =

68 al nocturnal hemoglobinuria (PNH) is chronic intravascular hemolysis that is a consequence of unregul

69 Our previous studies suggested that during intravascular hemolysis the expression of HO-1 protein i

70 thrombotic microangiopathy characterized by intravascular hemolysis, thrombocytopenia, and acute kid

71 However, direct contribution of acute intravascular hemolysis to fatal PAH has not been invest

72 icate that the pathophysiologic cascade from intravascular hemolysis to NO depletion and its cardiopu

73 rticles test fundamental hypotheses relating intravascular hemolysis to sickle cell disease (SCD) pat

74 Intravascular hemolysis was simulated by infusion of pre

75 A total of 7 instances of intravascular hemolysis were identified in 60 TIPS patie

76 laria (2.5 vs 1 g/dL; P = .0001), markers of intravascular hemolysis were not higher in severe diseas

77 nal hemoglobinuria (PNH) is characterized by intravascular hemolysis, which is effectively controlled

78 Predictive tests for intravascular hemolysis with crossmatch-incompatible ser