ライフサイエンスコーパス: atherothrombosis

1 hil extracellular traps in atherogenesis and atherothrombosis.

2 future understanding of the pathogenesis of atherothrombosis.

3 lving HDL regulatory genes and their role in atherothrombosis.

4 ition of fibrinolysis, it could also promote atherothrombosis.

5 ications for both the metabolic syndrome and atherothrombosis.

6 r of generalized endothelial dysfunction and atherothrombosis.

7 s in the treatment of patients with coronary atherothrombosis.

8 pendent risk factor for vascular disease and atherothrombosis.

9 y likely contributing to the pathogenesis of atherothrombosis.

10 etween sVCAM-1 and sICAM-1 in the genesis of atherothrombosis.

11 niae has been hypothesized to play a role in atherothrombosis.

12 atheroma versus later stenotic or occlusive atherothrombosis.

13 ased risk or apparent protective effects for atherothrombosis.

14 identify persons who are prone to premature atherothrombosis.

15 ammation is important in the pathogenesis of atherothrombosis.

16 tion may be important in the pathogenesis of atherothrombosis.

17 r noninvasive imaging of atherosclerosis and atherothrombosis.

18 telet activity effective in the treatment of atherothrombosis.

19 f vorapaxar in 26,449 patients with previous atherothrombosis.

20 that could lead to vascular dysfunction and atherothrombosis.

21 de may differentially affect dysglycemia and atherothrombosis.

22 l of discontinuity in the natural history of atherothrombosis.

23 isruption using a rabbit model of controlled atherothrombosis.

24 nogen facilitate fibrinolysis and may reduce atherothrombosis.

25 lerotic lesions of primary APS patients with atherothrombosis.

26 ve and prothrombotic phenotype that promotes atherothrombosis.

27 venues in the treatment of atherogenesis and atherothrombosis.

28 nt plaque instability that eventually favors atherothrombosis.

29 is a proximate event in the pathogenesis of atherothrombosis.

30 e pathophysiological implications in AMI and atherothrombosis.

31 the broad range of risk for outpatients with atherothrombosis.

32 thrombotic disease or >/= 3 risk factors for atherothrombosis.

33 in the treatment and prevention of vascular atherothrombosis.

34 n human clinical trials for the treatment of atherothrombosis.

35 impair insulin signaling and contributes to atherothrombosis.

36 ncreased platelet aggregation, a hallmark of atherothrombosis.

37 nction, weight homeostasis, and/or premature atherothrombosis.

38 endothelial barrier function in experimental atherothrombosis.

39 and monocytes, to the vessel wall modulating atherothrombosis.

40 which causes plaque necrosis, a precursor to atherothrombosis.

41 fluid shear is an important step regulating atherothrombosis.

42 e or treatment intensity of individuals with atherothrombosis.

43 , thereby contributing to the development of atherothrombosis.

44 Among those with symptomatic atherothrombosis, 15.9% had symptomatic polyvascular dis

45 Of the 68 236 patients with atherothrombosis, 3412 patients (5%) had a history of ca

46 test formally the inflammatory hypothesis of atherothrombosis, an agent is needed that reduces inflam

47 ogrel treatment in patients with symptomatic atherothrombosis and a suggestion of harm in patients wi

48 t links air pollution to the pathogenesis of atherothrombosis and acute myocardial infarction.

49 otentially implicated in the acceleration of atherothrombosis and CV risk in SLE and RA, as well as i

50 ltiple bioactive oxidized lipids that affect atherothrombosis and endothelial function.

51 ) has been implicated in the pathogenesis of atherothrombosis and is expressed by the major cell type

52 s has been implicated in the pathogenesis of atherothrombosis and other vascular disorders accompanie

53 vated after revascularization and related to atherothrombosis and restenosis.

54 at increased risk of developing large vessel atherothrombosis and small vessel dysfunction.

55 ents with prior MI, 7804 patients with known atherothrombosis, and 2101 patients with risk factors al

56 Inflammation plays a major role in atherothrombosis, and measurement of inflammatory marker

57 n predisposes to increased lesion formation, atherothrombosis, and medial degradation.

58 nflammation, type II diabetes, hypertension, atherothrombosis, and myocardial injury.

59 involved in the transition from atheroma to atherothrombosis, and that control of this pattern may b

60 hanisms by which homocysteine contributes to atherothrombosis are complex and their in vivo relevance

61 Racial differences in the pathophysiology of atherothrombosis are poorly understood.

62 Cardiovascular diseases, including atherothrombosis, are the leading cause of morbidity and

63 OX-1 inhibitors) effectiveness in preventing atherothrombosis, as well as its shared (with other anti

64 sis for Continued Health (REACH) registry of atherothrombosis, baseline characteristics and 4-year fo

65 .4%-12.9%); and patients without established atherothrombosis but with risk factors only (n = 8073) h

66 the essential platelet collagen receptor in atherothrombosis, but its inhibition causes only a mild

67 Atherothrombosis can be evaluated according to histologi

68 e of research focused on the final events of atherothrombosis cannot be overestimated.

69 Despite improved understanding of atherothrombosis, cardiovascular prediction algorithms f

70 Six microRNAs, involved in atherothrombosis development, were quantified in purifie

71 latelet function and eventually decelerating atherothrombosis development.

72 iate regression models evaluating markers of atherothrombosis (fibrin, antithrombin and tissue plasmi

73 sis were enrolled in the global Reduction of Atherothrombosis for Continued Health (REACH) Registry a

74 SETTING, AND PARTICIPANTS: The Reduction of Atherothrombosis for Continued Health (REACH) Registry c

75 The Reduction of Atherothrombosis for Continued Health (REACH) Registry i

76 From the international REduction of Atherothrombosis for Continued Health (REACH) registry o

77 The Reduction of Atherothrombosis for Continued Health (REACH) Registry r

78 tional study of patients in the Reduction of Atherothrombosis for Continued Health (REACH) registry w

79 s from the international REACH (Reduction of Atherothrombosis for Continued Health) registry, which e

80 APS patients with atherothrombosis harbor in vivo-activated CD4(+) T cells

81 This second part of the review on atherothrombosis highlights the diffuse nature of the di

82 ia and increased platelet production promote atherothrombosis; however, a potential link between alte

83 ts G protein-coupled receptor contributes to atherothrombosis in human patients.

84 ed with a severalfold increased incidence of atherothrombosis in multiple longitudinal studies.

85 l dysfunction, aberrant vascular repair, and atherothrombosis in murine models of lupus and atheroscl

86 nt an important mechanism for development of atherothrombosis in SLE.

87 s fibrinolysis, endothelial dysfunction, and atherothrombosis in the coronary circulation and may exp

88 A possible cause of accelerated atherothrombosis in the syndrome of insulin resistance a

89 ifferent clinical manifestations of coronary atherothrombosis, in light of comorbidities and/or inter

90 rythematosus (SLE) are at risk for premature atherothrombosis independent of Framingham risk factors.

91 Two cardiovascular outcome trials - Atherothrombosis Intervention in Metabolic Syndrome with

92 in this secondary analysis of the AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome With

93 cardiovascular (CV) events in the AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome with

94 uce the Incidence of Vascular Events and The Atherothrombosis Intervention in Metabolic Syndrome with

95 g data from the recently published AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome with

96 The AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome With

97 Vascular injury and atherothrombosis involve vessel infiltration by inflamma

98 Atherothrombosis is a complex disease in which cholester

99 Atherothrombosis is a process mediated by dysregulated p

100 idence for its role as a causative factor in atherothrombosis is lacking.

101 Atherothrombosis is the leading cause of cardiovascular

102 n activator inhibitor-1 (PAI-1), a marker of atherothrombosis, is also elevated in the metabolic synd

103 endent and may be integrated under the term "atherothrombosis." It is now clear that plaque compositi

104 slipoproteinemia is associated with arterial atherothrombosis, little is known about plasma lipoprote

105 oxidized phospholipids (OxPLs), part of its atherothrombosis might be mediated through this pathway.

106 ase, n = 8273) or 3 or more risk factors for atherothrombosis (n = 12,389) between 2003 and 2004.

107 rtery disease (CAD) may result from coronary atherothrombosis not evident using standard angiography

108 provide a possible explanation for increased atherothrombosis observed in CBS-deficient patients.

109 Atherothrombosis of the coronary and cerebral vessels is

110 C-reactive protein as a causative factor in atherothrombosis or to enable the recommendation of C-re

111 s may significantly enhance understanding of atherothrombosis pathophysiology.

112 , no study has analyzed their involvement in atherothrombosis related to APS and SLE patients.

113 re-miR-124a and/or -125a caused reduction in atherothrombosis-related target molecules.

114 Their role in the primary prevention of atherothrombosis remains controversial because of the un

115 platelet production contributes to enhanced atherothrombosis remains unknown.

116 laques, which have the propensity to develop atherothrombosis, remains an elusive goal in clinical me

117 volved in the development and progression of atherothrombosis responsible for coronary, cerebral, and

118 Venous thromboembolism and atherothrombosis share common risk factors and the commo

119 ovel antiplatelet therapies more relevant to atherothrombosis than to normal hemostasis.

120 In the subgroup with clinically evident atherothrombosis, the rate was 6.9 percent with clopidog

121 plaque inflammation is also associated with atherothrombosis, the relationship between inflammation

122 arette smoke (CS) increases the incidence of atherothrombosis, the release of prostaglandin (PG) E2,

123 Among patients with atherothrombosis, those with a prior history of ischemic

124 thelial dysfunction may increase the risk of atherothrombosis through a reduction in the acute fibrin

125 viously developed in a large population with atherothrombosis to predict CV death, myocardial infarct

126 randomly assigned patients with a history of atherothrombosis to receive vorapaxar (2.5 mg daily) or

127 induced ruptures of coronary plaques trigger atherothrombosis, vessel occlusions, myocardial infarcti

128 al disease or with multiple risk factors for atherothrombosis were enrolled in the global Reduction o

129 c1 gene display prominent medial erosion and atherothrombosis, whereas their macrophages accumulate f

130 platelet therapy would improve biomarkers of atherothrombosis without causing unacceptable bleeding i

131 l antiplatelet therapy reduces biomarkers of atherothrombosis without causing unacceptable bleeding.