ライフサイエンスコーパス: disturbed flow

1 s in a flume in response to laminar flow and disturbed flow.

2 ion of atherosclerotic plaques at regions of disturbed flow.

3 thelia subjected to surgically induced acute disturbed flow.

4 and used to compute shear stress metrics of disturbed flow.

5 vascular remodeling after acute induction of disturbed flow.

6 d diminished in atheroprone areas subject to disturbed flow.

7 plaques preferentially develop at sites with disturbed flow.

8 HDAC-2/3/5 levels in ECs in areas exposed to disturbed flow.

9 to cell cycle progression in ECs induced by disturbed flow.

10 nd such cells were more frequent at sites of disturbed flow.

11 cal inflammation of artery walls at sites of disturbed flow.

12 n compared with atheroprone areas exposed to disturbed flow.

13 Atherosclerotic plaque develops at sites of disturbed flow.

14 ylation in vascular endothelium subjected to disturbed flow.

15 downstream inflammatory genes in regions of disturbed flow.

16 rms in regions of the vasculature exposed to disturbed flow.

17 in areas of vasculature that are subject to disturbed flow.

18 glycemic conditions under both "normal" and "disturbed" flow.

19 to laminar shear stress (12 dynes/cm(2)) or disturbed flow (+/- 5 dynes/cm(2) at 1Hz) in a parallel

20 cation (dye transfer) throughout the zone of disturbed flow (84.2 and 68.4% inhibition at 5 and 30 h,

21 In contrast, downregulation of miR-126-5p by disturbed flow abrogated EC proliferation at predilectio

22 similarly blunted inflammation in models of disturbed flow and diet-induced atherogenesis but did no

23 This study tested in vivo the involvement of disturbed flow and of neutrophils, hyaluronan, and Toll-

24 Recent in vitro studies have shown that disturbed flow and oxidative conditions induce the expre

25 fic protease 2 on endothelial function under disturbed flow and suggest that SUMOylation of p53 and E

26 tion of inflammatory signaling at regions of disturbed flow, and flow-dependent vascular remodeling.

27 rtic arch (AA) endothelia exposed to chronic disturbed flow, and in mouse carotid artery endothelia s

28 Since regions of disturbed flow are the focal points of atherosclerotic c

29 exposed to reduced shear stress (low and/or disturbed flow) are predisposed to atherogenesis.

30 ance imaging, is a measure of energy loss in disturbed flow as it occurs, for instance, in aortic ste

31 In mice, disturbed flow as the result of partial carotid artery l

32 The maladaptation of endothelial cells to disturbed flow at arterial bifurcations increases permea

33 SUMOylation of p53 and ERK5 was induced by disturbed flow but not by steady laminar flow.

34 Only ECs in the lesser curvature exposed to disturbed flow, but not those in the greater curvature a

35 Recently, we showed that disturbed flow caused by a partial ligation of mouse car

36 ar stress; TXNIP expression was increased in disturbed flow compared with steady flow areas.

37 y bind to endothelial cells (ECs) exposed to disturbed flow condition in pro-atherogenic regions.

38 he combinatorial effects of high glucose and disturbed flow conditions elicit significantly different

39 referentially in arterial regions exposed to disturbed flow conditions including oscillatory shear st

40 e known to maintain endothelial homeostasis, disturbed flow conditions including those the endotheliu

41 referentially in arterial regions exposed to disturbed flow conditions, including oscillatory shear s

42 g that elevated glucose in conjunction with "disturbed" flow conditions results in significantly high

43 ascular niches associated with "normal" and "disturbed" flow conditions typically seen in vivo along

44 vature region of the arch that is exposed to disturbed flow, consistent with our in vitro data.

45 suggest that SUMOylation of p53 and ERK5 by disturbed flow contributes to the atherosclerotic plaque

46 ) as a mechanosensitive miRNA upregulated by disturbed flow (d-flow) in endothelial cells, in vitro a

47 Hemodynamic disturbed flow (DF) is associated with susceptibility to

48 Disturbed flow (DF) occurs in arterial bifurcations and

49 In the arterial circulation, regions of disturbed flow (DF), which are characterized by flow sep

50 Regions with disturbed flow displayed a focal enrichment and luminal

51 In contrast to laminar shear stress, disturbed flow failed to induce endothelial cell CD59 pr

52 In contrast, disturbed flow had opposite effects.

53 re fluid flow behavior can be classified as "disturbed flow" (i.e., low shear stress recirculation an

54 Atherosclerosis develops at sites of disturbed flow in large arteries, but the mechanisms gui

55 Here, we identified an important role for disturbed flow in lymphatic vessels, in which it coopera

56 ritical role of the activation of YAP/TAZ by disturbed flow in promoting atheroprone phenotypes and a

57 e hypothesized that septal branches generate disturbed flow in the LAD and PDA in a similar fashion t

58 ation-sensitive gene perturbation induced by disturbed flow in vitro and in vivo.

59 was observed in endothelial cells exposed to disturbed flow in vitro.

60 and inflammatory gene expression at sites of disturbed flow in vivo, whereas inhibiting PKA by PKA in

61 nd oscillatory flow in vitro and at sites of disturbed flow in vivo.

62 aque localization correlates with regions of disturbed flow in which endothelial cells (ECs) align po

63 Although disturbed flows in the branches and curved regions are p

64 (Cx43) was studied in a model of controlled disturbed flows in vitro.

65 Exposure to disturbed flow, including oscillatory shear stress, stim

66 inhibition in arterial wall ameliorates the disturbed flow-induced atherosclerosis through, at least

67 To examine the role of the disturbed flow-induced p53 and ERK5 SUMOylation, we used

68 inhibited YAP/TAZ activities to diminish the disturbed flow-induced proliferation and inflammation.

69 aorta, also suggesting a crucial role of the disturbed flow-induced SUMOylation of proteins, includin

70 Disturbed flow induces peroxynitrite production, which a

71 P/TAZ knockdown significantly attenuated the disturbed flow induction of EC proliferative and proinfl

72 dysfunction caused by the combined action of disturbed flow, inflammatory mediators and oxidants deri

73 Together, our results demonstrate that disturbed flow influences endothelial function and induc

74 In blood vessels, disturbed flow is associated with vascular diseases, suc

75 Although disturbed flow is thought to play a central role in the

76 cytokines or exposure to hemodynamic-induced disturbed flow leads to a proadhesive and prothrombotic

77 was observed in these cells, suggesting that disturbed flow leads to posttranscriptional modification

78 selectively bound to arterial ECs exposed to disturbed flow not only in the partially ligated carotid

79 Here, we explored whether disturbed flow patterns activate an innate immune respon

80 associated with chronic inflammation due to disturbed flow patterns.

81 -ICAM-1 specifically bound to endothelium in disturbed flow regions, reducing endothelial ICAM-1 expr

82 st that shear stress gradients in regions of disturbed flow regulate intercellular communication thro

83 Gene ontology analyses show that disturbed flow regulates genes involved in cell prolifer

84 d endothelial cells (ECs) to the atheroprone disturbed flow resulted in YAP/TAZ activation and transl

85 marily affects the regions of the aorta with disturbed flow that are prone to atherosclerosis.

86 lood, Ni et al use an in vivo mouse model of disturbed flow that results in accelerated atheroscleros

87 s cultured under conditions of "normal" and "disturbed flow" under hyperglycemic conditions suggestin

88 ith increased PKCzeta activity in regions of disturbed flow versus unidirectional flow.

89 therosclerotic lesions develop in regions of disturbed flow, whereas laminar flow protects from ather

90 for atherosclerosis than regions exposed to disturbed flow with low shear stress.

91 e arterial tree is atheroprotective, whereas disturbed flow with oscillation in branch points and the

92 atory, and proliferative responses of ECs to disturbed flow with OSS.

93 osclerotic lesion localization to regions of disturbed flow within certain arterial geometries, in hu

94 We evaluated whether inducing disturbed flow would cause the development of advanced c

95 oscillation frequency of 1 Hz, as occurs in disturbed flow zones prone to atherosclerosis, failed to