ライフサイエンスコーパス: atheromatous

1 RNA was expressed in the thickened intima of atheromatous aorta of apolipoprotein E knockout mice.

2 Patients with severe atheromatous aortic disease (AAD) who undergo coronary a

3 Moreover, the expression of this receptor in atheromatous arteries raises the possibility that SR-BI

4 In a collaborative investigation, 71% of atheromatous arteries taken at autopsy from white South

5 VAs, and the basilar artery; 4) intracranial atheromatous branch disease of macroscopically visible b

6 In particular, the expression of Cox-2 in atheromatous, but not in unaffected, arteries has therap

7 te the frequent detection of the organism in atheromatous cardiovascular specimens by these methods,

8 ate in the mechanisms of vascular insult and atheromatous change, and many of these inflammatory prot

9 Platelet deposition on the lipid-rich atheromatous core was significantly higher than on all o

10 ated in the macrophage-rich areas within the atheromatous core, whereas the macrophages close to the

11 nts and is largely caused by embolization of atheromatous debris during manipulation of the diseased

12 e catheter is essential to prevent injecting atheromatous debris into the vascular bed.

13 ned to trap and exclude thrombus and friable atheromatous debris to prevent distal embolization.

14 ndothelial dysfunction and increased risk of atheromatous disease.

15 rred to as cholesterol crystal embolization, atheromatous embolization or atheroembolism) occurs when

16 tissue factor content and macrophages in the atheromatous gruel (r = .98, P < .0001).

17 ng a cascade of events from formation of the atheromatous lesion in response to vascular injury throu

18 Physical disruption of an atheromatous lesion often underlies acute coronary syndr

19 tivity, hepatic steatosis, as well as aortic atheromatous lesion were characterized in Mstn(-/-)/Ldlr

20 d novel vascular risk factors to promote the atheromatous lesion.

21 cells of the immune system, are enriched in atheromatous lesions and in circulation of patients with

22 ible for increased inflammatory responses in atheromatous lesions due to periodontal infections.

23 o test the hypothesis that collagenolysis in atheromatous lesions exceeds that in fibrous human ather

24 ages of atherogenesis and the development of atheromatous lesions for these arterial regions remain t

25 is is implicated in the progression of early atheromatous lesions in animal models, but its role in n

26 nalyses demonstrated 41% reduction in aortic atheromatous lesions in Ldlr(-/-) mice with Mstn deletio

27 or metronidazole showed significantly fewer atheromatous lesions in the proximal aorta and the aorti

28 1 was more frequently present in lipid-rich, atheromatous lesions than in lipid-poor, proliferative o

29 s, we examined autopsy specimens of coronary atheromatous lesions using in vitro imaging techniques w

30 lagen loss and the subsequent instability of atheromatous lesions, a common trigger of acute coronary

31 Ox-LDL has been demonstrated in atheromatous lesions, anti-ox-LDL antibodies have been d

32 Extracts of atheromatous lesions, however, contained both Cox-1 and

33 e of the presence of viable C. pneumoniae in atheromatous lesions.

34 C. pneumoniae to influence the generation of atheromatous lesions.

35 perhomocysteinemia have so far not displayed atheromatous lesions.

36 demonstrated the presence of the organism in atheromatous lesions.

37 tion of PAI-1 compared with u-PA observed in atheromatous material extracted from vessels of diabetic

38 taneous interventions, the amount of visible atheromatous material from large-lumen-guiding catheters

39 In contrast, atheromatous (n = 7) lesions contained both Cox-1 and Co

40 ical characteristics into fibrous (n=10) and atheromatous (n=10) lesions.

41 oactive stents promotes the formation of an "atheromatous" neointima after 6 months in this experimen

42 ic stenosis involves an active inflammatory, atheromatous, osteogenic process.

43 ce fed methionine-rich diets had significant atheromatous pathology in the aortic arch even with norm

44 abetes, aortic dimension, the presence of an atheromatous plaque and smoke in the left atrium.

45 We found that both the coronary atheromatous plaque burden and smoking habit are associa

46 The core of an atheromatous plaque contains lipids, macrophages, and ce

47 hought to play an important role in coronary atheromatous plaque destabilization.

48 Atheromatous plaque disruption often presents as complex

49 s have been developed that ablate or section atheromatous plaque during percutaneous coronary interve

50 Metformin attenuated Ang-II-induced atheromatous plaque formation and aortic aneurysm in Apo

51 regressing angiotensin II (Ang-II)-mediated atheromatous plaque formation in ApoE(-/-) mice.

52 sease, but the paucity of neutrophils in the atheromatous plaque has led to neglect of its potential

53 ynamic therapy (PDT) agent that localizes in atheromatous plaque in which it can be activated by far-

54 al for atraumatic and effective debulking of atheromatous plaque through a biological mechanism, the

55 play a significant role in atherogenesis and atheromatous plaque vulnerability and may determine rapi

56 ent reductions in the inflammatory status of atheromatous plaque, and suggest that this effect may ha

57 h, composition, and rupture of intracoronary atheromatous plaque-factors that define the natural hist

58 ole for secretory SMCs in the development of atheromatous plaque.

59 m (Lu-Tex) is a photosensitizer that targets atheromatous plaque.

60 ET-1 and its precursor, big ET-1, within the atheromatous plaque.

61 que in the coronary arteries is a marker for atheromatous-plaque burden and is predictive of future r

62 In our study, atheromatous plaques (ATH) and macroscopically intact ti

63 therosclerotic lesions (P < 0.004) and fewer atheromatous plaques (P < 0.008) when compared with ApoE

64 overexpression of collagenolytic enzymes in atheromatous plaques and implicated MMPs in the destabil

65 e-related increase in the incidence of aorta atheromatous plaques and periaortic vascular channels in

66 ynthesis may influence both the stability of atheromatous plaques and the development of restenotic l

67 ity lipoprotein (OxHDL) within the intima of atheromatous plaques as well as in plasma; however, its

68 Fibrous and atheromatous plaques but not normal arteries contained N

69 nical events but may evolve into complicated atheromatous plaques characterized by an accumulation of

70 Finally, atheromatous plaques contained higher levels of proinfla

71 have demonstrated a high incidence of CMV in atheromatous plaques from the coronary circulation.

72 Improved understanding of the biology of atheromatous plaques has led to the concept of plaque vu

73 associated with irregularity and rupture of atheromatous plaques in both the carotid and coronary ar

74 al microbiota to the bloodstream and then to atheromatous plaques in carotid or other peripheral arte

75 t C pneumoniae can frequently be detected in atheromatous plaques in coronary arteries.

76 tic and asymptomatic patients would identify atheromatous plaques independently of stenosis.

77 showed that the enhanced glycolytic flux in atheromatous plaques of ApoE(-/-) mice was associated wi

78 lut1 connects the enhanced glucose uptake in atheromatous plaques of ApoE(-/-) mice with their myelop

79 Histological analysis of the atheromatous plaques showed no difference between lesion

80 abounded in the macrophage-rich shoulders of atheromatous plaques with histological features of vulne

81 o cause clinical manifestations (vulnerable, atheromatous plaques) or those less frequently associate

82 ies have been detected in circulation and in atheromatous plaques, and immune complexes (ICs) formed

83 PA and vWF may correlate with instability of atheromatous plaques, and that their decrease after coro

84 Pathological changes consisting of atheromatous plaques, atherosclerotic microaneurysms ext

85 mutans has been found with high frequency in atheromatous plaques.

86 racterized by the presence of lesions called atheromatous plaques.

87 as reference segments and 1318 segments with atheromatous plaques.

88 , a pathogen also linked to endocarditis and atheromatous plaques.

89 s plaques < or = abdominal aortic aneurysm < atheromatous plaques; and correlate with macrophage cont

90 ere shown to interact in vitro with a rabbit atheromatous protein extract by time-resolved fluorescen

91 This report demonstrates that atheromatous rather than fibrous plaques might be prone

92 I in the vicinity of macrophages and SMCs in atheromatous regions with massive deposits of oxLDL, sup

93 fied valves and were especially prominent in atheromatous regions.

94 The demonstration by IVUS of atheromatous remodeling permits the safe use of balloons

95 in 102 patients, IVUS was performed, and if atheromatous remodeling was present, PTCA was repeated w

96 pothesized that angiographically unsuspected atheromatous remodeling with vessel expansion (the Glago

97 y (CABG) is widely used for the treatment of atheromatous stenosis of coronary arteries.

98 significantly higher levels of expression in atheromatous than in fibrous plaques.

99 hesis that routine ablation or sectioning of atheromatous tissue is beneficial during percutaneous co

100 In addition, atheromatous tissue obtained from 20 patients undergoing

101 ades endothelium, has been detected in human atheromatous tissue, and accelerates atheroma formation

102 ion of whether this detection is specific to atheromatous tissue.

103 ts, and endothelial cells) of human coronary atheromatous tissue.

104 sm was detected frequently by ICC and PCR in atheromatous tissues (approximately 50% of subjects) but

105 Extracts of atheromatous tissues had approximately twofold greater e

106 lagen type I and increased collagenolysis in atheromatous versus fibrous lesions.

107 ated increased levels of MMP-1 and MMP-13 in atheromatous versus fibrous plaques.

108 everal years follow-up, although these large atheromatous vulnerable plaques may angiographically see