ライフサイエンスコーパス: fatty streak

1 sed deals primarily with very early lesions (fatty streaks).

2 t showed only early atherosclerotic lesions (fatty streaks).

3 e the cellular events seen in the developing fatty streak.

4 aired glucose intolerance had more extensive fatty streaks.

5 fed animals were limited to raised foam cell fatty streaks.

6 ded progressive increase in stage from early fatty streak (10 weeks) to large complex plaques without

7 A lipid-enriched fatty streak along the vessel wall can ensue.

8 l role in the development of atherosclerotic fatty streak and plaque formation.

9 bendothelial space during the development of fatty streaks and atherosclerotic lesions.

10 that a greater amount of MMP-2 is present in fatty streaks and atherosclerotic plaques as compared wi

11 xamining lesions that are more advanced than fatty streaks and careful histologic and immunologic exa

12 Fatty streaks and clinically significant raised lesions

13 The extent of fatty streaks and fibrous plaques in the aorta and coron

14 The association between fatty streaks and fibrous plaques was much stronger in t

15 The extent of both fatty streaks and raised lesions (fibrous plaques and ot

16 BMI in young men was associated with both fatty streaks and raised lesions in the RCA and with AHA

17 mass index >/=30 kg/m(2)) had more extensive fatty streaks and raised lesions than nonobese men, and

18 abdominal aorta, smokers had more extensive fatty streaks and raised lesions than nonsmokers, and hy

19 nt, foam cell formation, the generation of a fatty streak, and an increase in smooth muscle cell cont

20 bits fed normal chow for 11 months developed fatty streaks, and some had more advanced atheroscleroti

21 Ath diet showed extensive oil red O-staining fatty streak aortic sinus lesions (20,537+/-2,957 micron

22 ccumulates within the fibrin clot with time, fatty streaks are formed that develop into occlusive ath

23 est recognizable atherosclerotic lesions are fatty streaks composed of lipid-laden macrophages (foam

24 In contrast, macrophages in human fatty streaks contain little or no myeloperoxidase.

25 In the earliest fatty streaks, DCs are found next to the vascular endoth

26 gen-4 (VLA-4) integrin/ligand interaction in fatty streak development using murine models.

27 lusion that M-CSF participates critically in fatty streak formation and progression to a complex fibr

28 then tested if other mechanisms involved in fatty streak formation depended upon IL-6.

29 of human atherosclerotic lesions and reduced fatty streak formation in EC-specific STAT3 knock-out mi

30 egnancy is associated with markedly enhanced fatty streak formation in human fetal aortas and acceler

31 rolemia is associated with greatly increased fatty streak formation in human fetal arteries and accel

32 during pregnancy is associated with enhanced fatty streak formation in human fetuses and faster progr

33 associated with a marked increase in aortic fatty streak formation in human fetuses and faster progr

34 or platelets and was shown to be involved in fatty streak formation in LDL receptor-deficient mice on

35 percholesterolemia per se may cause enhanced fatty streak formation in offspring and whether interven

36 stosterone replacement significantly reduced fatty streak formation in Tfm mice compared with placebo

37 lemia, remarkable lipoprotein oxidation, and fatty streak formation in the arteries.

38 iological testosterone replacement inhibited fatty streak formation in the Tfm mouse, an effect that

39 prone areas is one of the earliest events in fatty streak formation leading to atherogenesis.

40 o determine the role of eNOS in diet-induced fatty streak formation through the use of eNOS-deficient

41 However, fatty streak formation was reduced by 62% in animals fed

42 role of bioactive oxidized phospholipids in fatty streak formation was tested using C57BL/6J LDL R-/

43 To evaluate T helper-cell phenotype in fatty streak formation, wild-type C57Bl/6 mice (IA(b)+IE

44 r receptor activity contributes to excessive fatty streak formation.

45 may regulate early monocyte recruitment and fatty streak formation.

46 n important link between hyperlipidaemia and fatty streak formation.

47 tions from the aortic root were examined for fatty streak formation.

48 the long-term susceptibility of children to fatty-streak formation and subsequent atherosclerosis.

49 nical manifestations of atherosclerosis, but fatty-streak formation begins in fetuses and is greatly

50 oxidation may contribute to the reduction of fatty-streak formation in eNOS-deficient mice.

51 Losartan inhibited fatty-streak formation through mechanisms that may inclu

52 rosclerosis, the effect of AT(1) blockade on fatty-streak formation, plasma lipids, and surrogate mar

53 After 8 weeks on the atherogenic diet, the fatty streaks formed in the aortic sinus of LDLR-/-vWf-/

54 AHA grade 2 or 3 lesions (fatty streaks), grade 4 or 5 lesions, and stenosis > or

55 -2 was expressed in atherosclerotic plaque > fatty streak > normal aortic wall in a ratio of approxim

56 ted controls, losartan reduced the extent of fatty streak in the aorta, the coronary arteries, and th

57 percent of the intimal surface covered with fatty streaks in the aorta (P for trend=0.01).

58 atrophy of pancreatic islets of Langerhans, fatty streaks in the aorta, and hypertension (P<0.01).

59 Findings The largest fatty streaks in the aortic arch of children younger tha

60 enic diet, the LDLR-/- P/E-/- mice developed fatty streaks in the aortic sinus that were five times s

61 These were limited to fatty streaks in the apoE(-/-) P(-/-) mice, whereas 70%

62 vs. 0.12 percent in nonsmokers, P=0.02) and fatty streaks in the coronary vessels (8.27 percent vs.

63 iet for 8-20 wk formed significantly smaller fatty streaks in the cusp region of the aortae than did

64 f cholesterol and its esters, referred to as fatty streaks, in the intima of large muscular arteries.

65 tration of male mice increased the extent of fatty streak lesion formation in the aortic origin compa

66 Early fatty streak lesion formation in these mice was not affe

67 eases HDL cholesterol and greatly diminishes fatty streak lesion formation.

68 BALB/cJ have revealed an association between fatty streak lesion size and a decrease in high density

69 normal diet-fed B6Tg2576 mice also developed fatty streak lesions (early atherosclerosis) in the aort

70 decrease in the development of diet-induced fatty streak lesions compared with the apo B transgenics

71 ining showed that endothelial cells on human fatty streak lesions expressed increased levels of P-sel

72 s in vivo was suggested by their presence in fatty streak lesions from cholesterol-fed rabbits and by

73 ce fed with atherogenic diet developed early fatty streak lesions in the aortic root, elevated plasma

74 at weaning displayed increases (P < 0.01) in fatty streak lesions in the proximal aorta and aortic si

75 These mice developed spontaneous aortic fatty streak lesions on a chow diet.

76 dietary conditions designed to induce either fatty streak lesions or complex atherosclerotic lesions.

77 play an integral role in the development of fatty streak lesions, an initial step in atherogenesis.

78 wever, immediately upon development of early fatty streak lesions, the arterial LDL residence time in

79 To induce fatty streak lesions, these mice were fed a Western diet

80 al to macrophage accumulation in established fatty streak lesions.

81 d resistant (C3H/HeJ) to diet-induced aortic fatty streak lesions.

82 overexpression decreases formation of early fatty-streak lesions in mice independent of lipoprotein

83 of MIF-deficient mice developed only early, fatty streak-like lesions, whereas >80% of LDLr-/- mice

84 etuses (p<0.0001), which suggests that fetal fatty streaks may regress after birth.

85 = 7) express stromelysin-3 in situ, whereas fatty streaks (n = 5) and normal arterial specimens (n =

86 roducts of fatty acid oxidation found in the fatty streaks of atherosclerotic arteries due to a lack

87 ncy with previous military studies: minimal (fatty streaking only), moderate (10%-49% luminal narrowi

88 percent, and 11.0 percent, respectively, for fatty streaks (P for trend=0.01) and 0.6 percent, 0.7 pe

89 rosclerosis, including the initiation of the fatty streak, promotion of plaque instability, and remod

90 Fatty streaks resembled those of human type II lesions i

91 usceptible mice, C57BL/6J (BL/6), but not in fatty streak resistant mice, C3H/HeJ (C3H).

92 Analysis of fatty streaks revealed a similar pattern of oxidation pr

93 Fatty streaks seldom cause clinical events but may evolv

94 y 52%, and apoJ levels increased 2.8-fold in fatty streak susceptible mice, C57BL/6J (BL/6), but not

95 oam cells" are the primary components of the fatty streak, the earliest atherosclerotic lesion.

96 es of atherosclerotic plaques from the early fatty streak to mature calcified lesion.

97 N activities and the IL-6 -/- mice developed fatty streaks to a greater degree than wild-type mice.

98 rtic tree, ranging in appearance from simple fatty streaks to complex fibrous plaques.

99 cipate in all stages of atherosclerosis from fatty streaks to mature lesions.

100 vessel walls by 78% and the average lesion (fatty streak type) development by 81%.

101 colocalized with focal apo(a) deposition and fatty-streak type atherosclerotic lesions.

102 The density of macrophages in the fatty streaks was comparable between LDLR-/- P/E+/+ and

103 Fatty streaks were more extensive in black subjects than