ライフサイエンスコーパス: vaso-occlusive

1 ight attenuate the severity of outcomes from vaso-occlusive and hemolytic crises.

2 Unheralded vaso-occlusive cardiovascular events (myocardial infarct

3 ous cellular and soluble participants in the vaso-occlusive cascade.

4 emoglobin (HbF) and decreases morbidity from vaso-occlusive complications in patients with sickle cel

5 Current treatments to reduce vaso-occlusive complications include chronic hydroxyurea

6 mbosis, but also impact on many of the other vaso-occlusive complications of SCD.

7 To determine whether early vaso-occlusive complications predicted subsequent advers

8 nt and pentoxifyllin therapy in another, the vaso-occlusive complications were eliminated.

9 atients at steady state and 6 during painful vaso-occlusive crises (pVOC).

10 Treatment of vaso-occlusive crises (VOC) or events in sickle cell dis

11 A unique feature of SCD is vaso-occlusive crises (VOCs) characterized by episodic,

12 ia/reperfusion (H/R) stress, mimicking acute vaso-occlusive crises (VOCs), increased bone turnover, o

13 vels in subjects with severe SCD (at least 3 vaso-occlusive crises [VOCs] per year) were 18.5 +/- 1.2

14 ase, including the frequency and severity of vaso-occlusive crises and acute chest syndrome episodes.

15 Vaso-occlusive crises are the main acute complication in

16 ocirculation and is characterized by painful vaso-occlusive crises in deep tissues.

17 ism for the increased occurrence of clinical vaso-occlusive crises in individuals with sickle cell di

18 e blood vessel wall, thereby contributing to vaso-occlusive crises in sickle cell disease.

19 hydroxyurea use to decrease the frequency of vaso-occlusive crises is completely defined only in 2 te

20 42, linking hemolysis- and infection-induced vaso-occlusive crises to TLR4 signaling.

21 od disorder that is characterized by painful vaso-occlusive crises, for which there are few treatment

22 ckle cell anemia is characterized by painful vaso-occlusive crises.

23 cute presentations of osteomyelitis (OM) and vaso-occlusive crisis (VOC) bone infarction in children

24 Severe ACS often develops in the course of a vaso-occlusive crisis (VOC), but currently there are no

25 HTRs induced acute vaso-occlusive crisis (VOC), resulting in shortened surv

26 SCD were evaluated at baseline (n = 36), in vaso-occlusive crisis (VOC; n = 12), and during ACS (n =

27 ry and secondary endpoints-rates of clinical vaso-occlusive crisis and hemolytic events, blood transf

28 ther, in men, and likely all patients during vaso-occlusive crisis and the acute chest syndrome, nitr

29 gated the protective effect of IVIG on acute vaso-occlusive crisis caused by neutrophil recruitment a

30 The rate of vaso-occlusive crisis events per person-year was 2.30 in

31 or dysregulation to the development of acute vaso-occlusive crisis in sickle cell disease have been i

32 The pathophysiology of vaso-occlusive crisis in sickle cell disease involves in

33 r the treatment or prevention of pain due to vaso-occlusive crisis in sickle cell disease nor reassur

34 lium and inflammation play a central role in vaso-occlusive crisis in sickle cell disease.

35 Pain due to vaso-occlusive crisis is the major cause of hospital use

36 LA2 (steady state mean = 10.0 +/- 8.4 ng/mL; vaso-occlusive crisis mean = 23.7 +/- 40.5 ng/mL; ACS me

37 n patients with ACS but not in patients with vaso-occlusive crisis or non-SCD patients with pneumonia

38 Features of vaso-occlusive crisis pathophysiology such as red cell a

39 escents with sickle cell anemia, the rate of vaso-occlusive crisis was not significantly lower among

40 The primary end point was the rate of vaso-occlusive crisis, a composite of painful crisis or

41 ing 20 admissions for ACS, 10 admissions for vaso-occlusive crisis, and during 12 clinic visits when

42 ickle cell disease (SCD) is characterized by vaso-occlusive crisis.

43 well as a link with acute chest syndrome and vaso-occlusive crisis.

44 suggest that INO may be beneficial for acute vaso-occlusive crisis.

45 and may be a measurable laboratory marker of vaso-occlusive crisis.

46 symptomatic sickle cell disease nor in acute vaso-occlusive crisis.

47 of hospitalization in children with SCD and vaso-occlusive crisis.

48 whether heterozygosity of Nf1 would lead to vaso-occlusive disease in genetically engineered mice in

49 spholipid syndrome is a rare cause of ocular vaso-occlusive disease, but is associated with significa

50 lopathy, which mirrors features of human NF1 vaso-occlusive disease, identifies a potential therapeut

51 ically less than 3 days to attenuate rebound vaso-occlusive disease.

52 tress in the sickle mouse precipitates acute vaso-occlusive disease.

53 hereby participating in the pathogenesis of vaso-occlusive diseases.

54 ivated VSMCs is a potential strategy against vaso-occlusive disorders such as in-stent restenosis, ve

55 CD98hc is a potential therapeutic target in vaso-occlusive disorders.

56 arbon emulsion (PFE) was tested for its anti-vaso-occlusive effects in the ex vivo mesocecum vasculat

57 proaches to both prevention and treatment of vaso-occlusive episodes in SCD.

58 d to be the initiating event in the periodic vaso-occlusive episodes that characterize sickle cell di

59 th a broad range of complications, including vaso-occlusive episodes, acute chest syndrome (ACS), pai

60 Hydroxyurea (HU) therapy results in fewer vaso-occlusive episodes, and we postulated that HU-relat

61 al of hydroxyurea to reduce the frequency of vaso-occlusive episodes, sickle cell disease (SCD) has c

62 This is a key factor in the initiation of vaso-occlusive episodes, the hallmark of SCD.

63 d hypoxia could lead to an increased risk of vaso-occlusive episodes.

64 Clinical manifestations resemble a vaso-occlusive event and include edema, intraretinal hem

65 tations of tumor cells migrating away from a vaso-occlusive event.

66 c/anoxic focus, often triggered by a central vaso-occlusive event.

67 reatment reduced the median rate of clinical vaso-occlusive events (0 compared with 1.0 per year, P <

68 We hypothesized that sickling-induced vaso-occlusive events and attendant oxidative stress wil

69 nd Akti XII has immediate benefits for acute vaso-occlusive events and survival in SCD mice exceeding

70 of sustained haemolytic anaemia and episodic vaso-occlusive events drive the development of end-organ

71 c cell-cell adhesion and aggregation mediate vaso-occlusive events in patients with sickle cell disea

72 r whether it has immediate benefits in acute vaso-occlusive events in SCD patients.

73 roved clinical efficacy for preventing acute vaso-occlusive events in severely affected adults.

74 duce endothelial injury and facilitate acute vaso-occlusive events in transgenic SAD mice.

75 termine the contribution of LW activation to vaso-occlusive events in vivo, we investigated whether i

76 This interaction may contribute to vaso-occlusive events that are an important cause of mor

77 concentration, reduce hemolysis, and prevent vaso-occlusive events that cause additional increases in

78 on and thus contribute to the association of vaso-occlusive events with physiologic stress.

79 l disease (SCD) is characterized by repeated vaso-occlusive events, which result in substantial morbi

80 e possible role played by such aggregates in vaso-occlusive events.

81 in inflammation, blood flow impairment, and vaso-occlusive events.

82 served in SCD and increases the incidence of vaso-occlusive events.

83 l was related to HbF levels and frequency of vaso-occlusive events.

84 ocytes to endothelium and may play a role in vaso-occlusive events.

85 for children and adolescents with recurrent vaso-occlusive events; recent evidence documents sustain

86 ences blood rheology and plays a key role in vaso-occlusive manifestations of sickle cell disease.

87 mon serious adverse event in both groups was vaso-occlusive pain (11 events in five [8%] patients wit

88 mia (SCA) admitted to the hospital for acute vaso-occlusive pain (VOC).

89 ial Doppler velocity >200 cm/s (n = 2), >/=3 vaso-occlusive pain crises per year (n = 12), or >/=2 ac

90 zed by chronic hemolytic anemia and episodic vaso-occlusive pain crises.

91 patients with sickle cell disease (SCD) with vaso-occlusive pain crisis.

92 3; 95% confidence interval [CI], 0.06-0.91), vaso-occlusive pain episodes (11 studies, 1219 participa

93 onicities are often used during treatment of vaso-occlusive pain episodes (VOE), the major cause of m

94 The MSH analysis suggests that rates of vaso-occlusive pain episodes in these patients were unre

95 ted to initiate or contribute to sickle cell vaso-occlusive pain episodes.

96 nd is associated with increased incidence of vaso-occlusive pain events, acute chest syndrome episode

97 Acute, vaso-occlusive pain is the most characteristic complicat

98 A composite SCA-related clinical outcome (vaso-occlusive painful crisis, dactylitis, acute chest s

99 ransduction in SS RBCs may contribute to the vaso-occlusive pathology observed in sickle cell disease

100 combination of antiangiogenic treatment and vaso-occlusive PDT.

101 erize, thereby reducing the frequency of the vaso-occlusive phenomena associated with the disease.

102 ypothesis that the ability of HU to ease the vaso-occlusive phenomena may, in part, be attributed to

103 integral part of the pathophysiology of the vaso-occlusive phenomenon in sickle cell anemia.

104 The results suggest that PMNs contribute to vaso-occlusive processes and endothelial cell injury in

105 rea (HU) acute administration in diminishing vaso-occlusive processes in sickle cell disease (SCD) mi

106 potentially visually devastating necrotizing vaso-occlusive retinitis affecting both healthy and immu

107 S) are important in governing whether or not vaso-occlusive sickle cell crises will occur.

108 function of the formation and persistence of vaso-occlusive thrombi that limit tumor blood supply.