ライフサイエンスコーパス: thrombogenicity

1 rome (ACS) to promote premature EC aging and thrombogenicity.

2 all are critical factors in modulating stent thrombogenicity.

3 tissue factor is a key contributor to plaque thrombogenicity.

4 to modulate both platelet numbers and their thrombogenicity.

5 ween inflammation, plaque rupture, and blood thrombogenicity.

6 mong inflammation, plaque rupture, and blood thrombogenicity.

7 mmatory cell viability in determining plaque thrombogenicity.

8 rder to improve prosthetic graft patency and thrombogenicity.

9 significant predictor of a decrease in blood thrombogenicity.

10 5%), showing a significant decrease in blood thrombogenicity.

11 role in both lesion stability and subsequent thrombogenicity.

12 ycemic improvement showed no change in blood thrombogenicity.

13 cules responsible for plaque instability and thrombogenicity.

14 is considered a major regulator of arterial thrombogenicity.

15 Tissue factor (TF) appears to mediate plaque thrombogenicity.

16 Polyester filling was added to enhance thrombogenicity.

17 and platelet deposition, evidencing myosin's thrombogenicity.

18 This is likely due to increased thrombogenicity and a foreign-body reaction.

19 ted/saturated FAs ratios, and the indices of thrombogenicity and atherogenicity depended on specific

20 s it efficiently attenuated inflammation and thrombogenicity and delayed hemodynamic changes.

21 able polymer and a metallic stent surface on thrombogenicity and endothelial cell coverage using diff

22 Our objectives were to quantify the thrombogenicity and extent of vascular injury created by

23 ting hemodynamic milieu and with the stent's thrombogenicity and pro-restenotic potential, thereby in

24 d comparative outcomes with respect to acute thrombogenicity and re-endothelialization among thin-str

25 Acute thrombogenicity and re-endothelialization represent clin

26 ese outcomes indicate differential trends in thrombogenicity and vascular healing among contemporary

27 Thrombogenicity and vascular healing differ among metall

28 ncluding barrier regulation of permeability, thrombogenicity, and leukocyte adherence, as well as pro

29 sed procoagulant mediators increase systemic thrombogenicity, and leukocytes are actively recruited t

30 ition of neointimal thickening, reduction in thrombogenicity, and restoration of endothelium-dependen

31 ts receptors, but the roles of the latter in thrombogenicity are less well-defined.

32 s suggest increased plaque TF expression and thrombogenicity as a novel mechanism for the increased r

33 determinant of both plaque vulnerability and thrombogenicity as they relate to plaque disruption.

34 This dynamic organ regulates blood thrombogenicity as well as contractile, secretory, and m

35 gy for controlling vascular inflammation and thrombogenicity associated with endothelial dysfunction.

36 A comparison in acute thrombogenicity between the Magmaris sirolimus-eluting b

37 pothesized that the observed increased blood thrombogenicity (BT) observed in patients with type 2 di

38 mponents of atherosclerosis including plaque thrombogenicity, cellular migration, endothelial functio

39 EES demonstrated significantly less acute thrombogenicity compared with bioabsorbable EES and biol

40 IX-Padua exhibits similar immunogenicity and thrombogenicity compared with FIX wild type.

41 ittle is known of the effect of EI on vessel thrombogenicity due to delayed arterial healing.

42 have significant limitations with regards to thrombogenicity, durability, and inability to grow or re

43 ow capacity, low transvalvular gradient, low thrombogenicity, durability, easy availability, resistan

44 it of an ideal valve substitute, namely, low thrombogenicity, freedom from anticoagulation, durabilit

45 stem cells, which resemble CDCs in size and thrombogenicity, have been associated with infarction af

46 n TF and TFPI and the regulation of vascular thrombogenicity in a model of vascular remodeling.

47 t thrombosis in animal models suggests stent thrombogenicity in human patients.

48 oth muscle cells, suggesting a cell-mediated thrombogenicity in patients with acute coronary syndrome

49 issue factor may be responsible for coronary thrombogenicity in patients with plaque rupture.

50 in malapposed or overlapping configurations, thrombogenicity increased compared with apposed, length-

51 , atherogenicity index (IA) (0.26-0.60), and thrombogenicity index (IT) (0.20-0.44).

52 direct prediction of the Atherogenicity and Thrombogenicity indexes, which are useful for the interp

53 nt, displaying the lowest atherogenicity and thrombogenicity indices (0.02 and 0.14; 0.12 and 0.34; 0

54 fic inhibition of TF activity reduced plaque thrombogenicity, inhibiting both platelet and fibrin(oge

55 Whether increased blood thrombogenicity is associated with glycemic control has

56 tudy was designed to determine whether blood thrombogenicity is related to chronic glycemic control i

57 The thrombogenicity of a disrupted atherosclerotic lesion is

58 the intrinsic pathway significantly enhances thrombogenicity of atherosclerotic lesions after removal

59 Although thrombogenicity of atherosclerotic plaques has been ascr

60 issue factor (TF) has been implicated in the thrombogenicity of atherosclerotic plaques.

61 ations for control of thrombus formation and thrombogenicity of biomaterials.

62 inflammatory mediators that can increase the thrombogenicity of blood.

63 dy examines the role of tissue factor in the thrombogenicity of different types of atherosclerotic pl

64 This study analyzes the role of TF on thrombogenicity of disrupted human atherosclerotic plaqu

65 t that it is an important determinant of the thrombogenicity of human atherosclerotic lesions after s

66 This study assessed acute thrombogenicity of Magmaris compared with Absorb and the

67 are needed to determine whether the reduced thrombogenicity of Magmaris will result in reductions in

68 to the TF expression and hence to increased thrombogenicity of plaques during the inflammatory respo

69 The thrombogenicity of polymer-coated stents with thin strut

70 The thrombogenicity of the arterial specimens was assessed b

71 anticoagulant function, thereby reducing the thrombogenicity of the thrombus or injured vessel surfac

72 We previously reported on the different thrombogenicity of the various types of human atheroscle

73 not associated with serious adverse events, thrombogenicity, or virus transmission.

74 between improved glycemic control and blood thrombogenicity reduction.

75 atings uniformly reduce rather than increase thrombogenicity relative to matched bare metal counterpa

76 ss relations between dietary fatty acids and thrombogenicity reveals problems that need to be recogni

77 eutic agent in other conditions of increased thrombogenicity, such as acute coronary syndromes, and f

78 durable, with low incidence of infection and thrombogenicity, their widespread application has been l

79 cence under atheroprone low shear stress and thrombogenicity through angiotensin II-induced redox-sen

80 Prosenescent MPs promoted EC thrombogenicity through tissue factor upregulation, shed

81 endent pathway, linking the regulation of TF thrombogenicity to oxidative stress in the vasculature.

82 Thrombogenicity was assessed by exposing all surfaces to

83 Blood thrombogenicity was measured at baseline and after three

84 determine whether smoking influences plaque thrombogenicity, we examined the effect of cigarette smo

85 The indices of atherogenicity and thrombogenicity were also within the values considered t