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 aortas (media layer) or with early atheroma (fatty streak and fibrolipidic, media and intima layers)

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

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

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

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

13 Fatty streaks and clinically significant raised lesions

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

46 r receptor activity contributes to excessive fatty streak formation.

47 may regulate early monocyte recruitment and fatty streak formation.

48 n important link between hyperlipidaemia and fatty streak formation.

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

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

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

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

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

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

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

56 -2 was expressed in atherosclerotic plaque > fatty streak > normal aortic wall in a ratio of approxim

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

82 al to macrophage accumulation in established fatty streak lesions.

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

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

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

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

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

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

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

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

91 Fatty streaks resembled those of human type II lesions i

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

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

94 Fatty streaks seldom cause clinical events but may evolv

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

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

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

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

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

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

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

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

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

104 Fatty streaks were more extensive in black subjects than