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1  in areas of vasculature that are subject to disturbed flow.
2 res where vascular endothelium is exposed to disturbed flow.
3 educes EndMT and atherosclerosis in areas of disturbed flow.
4 pathway limits Klf2 expression in regions of disturbed flow.
5 at Jag1 promotes atherosclerosis at sites of disturbed flow.
6 xity and vorticity were high in regions with disturbed flow.
7 s in a flume in response to laminar flow and disturbed flow.
8 ylation in vascular endothelium subjected to disturbed flow.
9 ion of atherosclerotic plaques at regions of disturbed flow.
10 thelia subjected to surgically induced acute disturbed flow.
11  and used to compute shear stress metrics of disturbed flow.
12 vascular remodeling after acute induction of disturbed flow.
13 d diminished in atheroprone areas subject to disturbed flow.
14 plaques preferentially develop at sites with disturbed flow.
15 HDAC-2/3/5 levels in ECs in areas exposed to disturbed flow.
16  to cell cycle progression in ECs induced by disturbed flow.
17 nd such cells were more frequent at sites of disturbed flow.
18 cal inflammation of artery walls at sites of disturbed flow.
19 n compared with atheroprone areas exposed to disturbed flow.
20  Atherosclerotic plaque develops at sites of disturbed flow.
21  downstream inflammatory genes in regions of disturbed flow.
22 rms in regions of the vasculature exposed to disturbed flow.
23 glycemic conditions under both "normal" and "disturbed" flow.
24  to laminar shear stress (12 dynes/cm(2)) or disturbed flow (+/- 5 dynes/cm(2) at 1Hz) in a parallel
25 cation (dye transfer) throughout the zone of disturbed flow (84.2 and 68.4% inhibition at 5 and 30 h,
26 In contrast, downregulation of miR-126-5p by disturbed flow abrogated EC proliferation at predilectio
27 s and cultured human coronary artery EC that disturbed flow activates the JAG1-NOTCH4 signaling pathw
28 duced by oxLDL in vitro and by dyslipidemia, disturbed flow and ageing in vivo.
29  similarly blunted inflammation in models of disturbed flow and diet-induced atherogenesis but did no
30 xplanation for the close association between disturbed flow and intracranial aneurysms.
31 This study tested in vivo the involvement of disturbed flow and of neutrophils, hyaluronan, and Toll-
32      Recent in vitro studies have shown that disturbed flow and oxidative conditions induce the expre
33 fic protease 2 on endothelial function under disturbed flow and suggest that SUMOylation of p53 and E
34 tion of inflammatory signaling at regions of disturbed flow, and flow-dependent vascular remodeling.
35 rtic arch (AA) endothelia exposed to chronic disturbed flow, and in mouse carotid artery endothelia s
36 tein CCN1 is induced in endothelial cells by disturbed flow, and is expressed in advanced atheroscler
37 dentify potential compounds that can inhibit disturbed flow- and BMP-induced Smad1/5 activation and a
38 of half doses of each [1/2(K + A)] inhibited disturbed flow- and BMP4-induced Smad1/5 activation in h
39  activation and inflammation in both models, disturbed flow- and high fat diet-induced atherosclerosi
40                             Since regions of disturbed flow are the focal points of atherosclerotic c
41  exposed to reduced shear stress (low and/or disturbed flow) are predisposed to atherogenesis.
42 ance imaging, is a measure of energy loss in disturbed flow as it occurs, for instance, in aortic ste
43                                     In mice, disturbed flow as the result of partial carotid artery l
44    The maladaptation of endothelial cells to disturbed flow at arterial bifurcations increases permea
45                                              Disturbed flow at atheroprone regions primes plaque infl
46  superficial erosion, including experiencing disturbed flow, basement membrane breakdown, endothelial
47   SUMOylation of p53 and ERK5 was induced by disturbed flow but not by steady laminar flow.
48  Only ECs in the lesser curvature exposed to disturbed flow, but not those in the greater curvature a
49 EPAS1 attenuates atherosclerosis at sites of disturbed flow by maintaining EC proliferation via fatty
50                     Recently, we showed that disturbed flow caused by a partial ligation of mouse car
51 ar stress; TXNIP expression was increased in disturbed flow compared with steady flow areas.
52 y bind to endothelial cells (ECs) exposed to disturbed flow condition in pro-atherogenic regions.
53 he combinatorial effects of high glucose and disturbed flow conditions elicit significantly different
54 referentially in arterial regions exposed to disturbed flow conditions including oscillatory shear st
55 e known to maintain endothelial homeostasis, disturbed flow conditions including those the endotheliu
56 referentially in arterial regions exposed to disturbed flow conditions, including oscillatory shear s
57 g that elevated glucose in conjunction with "disturbed" flow conditions results in significantly high
58 ascular niches associated with "normal" and "disturbed" flow conditions typically seen in vivo along
59 vature region of the arch that is exposed to disturbed flow, consistent with our in vitro data.
60  suggest that SUMOylation of p53 and ERK5 by disturbed flow contributes to the atherosclerotic plaque
61 laminar flow (S-flow) in healthy arteries to disturbed flow (D-flow) in aneurysmal arteries, platelet
62 ) as a mechanosensitive miRNA upregulated by disturbed flow (d-flow) in endothelial cells, in vitro a
63 expression was markedly repressed by chronic disturbed flow, demonstrating that eNOS expression is re
64 s (increasing from 0.22 to 0.48), indicating disturbed flow development.
65 t arterial curvatures and bifurcations where disturbed flow (DF) activates endothelium, therapies tar
66             This work presents evidence that disturbed flow (DF) induces GCX degradation, leading to
67                                  Hemodynamic disturbed flow (DF) is associated with susceptibility to
68                                              Disturbed flow (DF) occurs in arterial bifurcations and
69 ally develops at arterial regions exposed to disturbed flow (DF), but much less at regions of unidire
70      In the arterial circulation, regions of disturbed flow (DF), which are characterized by flow sep
71 as well as endothelial stiffening induced by disturbed flow (DF), which was also oxLDL dependent.
72                                   Linear and disturbed flow differentially regulate gene expression,
73                                 Regions with disturbed flow displayed a focal enrichment and luminal
74      We conclude that JAG1-NOTCH4 sensing of disturbed flow enhances atherosclerosis susceptibility b
75         In contrast to laminar shear stress, disturbed flow failed to induce endothelial cell CD59 pr
76 , which features a diffuser shape, minimizes disturbed flow formation and prevents thrombosis because
77                                 In contrast, disturbed flow had opposite effects.
78 stasis, but its potential role in sensing of disturbed flow has not been previously studied.
79 re fluid flow behavior can be classified as "disturbed flow" (i.e., low shear stress recirculation an
80 cific phosphorylation alterations induced by disturbed flow in ECs to contribute to atherosclerosis.
81 cific phosphorylation alterations induced by disturbed flow in endothelial cells (ECs).
82         Atherosclerosis develops at sites of disturbed flow in large arteries, but the mechanisms gui
83    Here, we identified an important role for disturbed flow in lymphatic vessels, in which it coopera
84 ow induced NF-kB activation and induction of disturbed flow in mouse carotid arteries.
85 ritical role of the activation of YAP/TAZ by disturbed flow in promoting atheroprone phenotypes and a
86 e hypothesized that septal branches generate disturbed flow in the LAD and PDA in a similar fashion t
87 ation-sensitive gene perturbation induced by disturbed flow in vitro and in vivo.
88 was observed in endothelial cells exposed to disturbed flow in vitro.
89 and inflammatory gene expression at sites of disturbed flow in vivo, whereas inhibiting PKA by PKA in
90 mmunostaining of murine aortic EC exposed to disturbed flow in vivo.
91  enhance NF-kappaB at disease-prone sites of disturbed flow in vivo.
92 nd oscillatory flow in vitro and at sites of disturbed flow in vivo.
93 aque localization correlates with regions of disturbed flow in which endothelial cells (ECs) align po
94                                     Although disturbed flows in the branches and curved regions are p
95  (Cx43) was studied in a model of controlled disturbed flows in vitro.
96 ary to the widely accepted notions of highly disturbed flow, in this study, we demonstrate that the a
97                                  Exposure to disturbed flow, including oscillatory shear stress, stim
98  inhibition in arterial wall ameliorates the disturbed flow-induced atherosclerosis through, at least
99                                         This disturbed flow-induced EC phospho-YY1(S118) is mediated
100 uman atherosclerosis, and demonstrating that disturbed flow-induced endothelial activation required I
101 trate a role for the Nck adaptor proteins in disturbed flow-induced endothelial activation.
102                                              Disturbed flow-induced microRNA-92a (miR-92a) has been l
103                   To examine the role of the disturbed flow-induced p53 and ERK5 SUMOylation, we used
104 s-related phosphoprotein vinculin (VCL) with disturbed flow-induced phosphorylation at serine 721 (VC
105 inhibited YAP/TAZ activities to diminish the disturbed flow-induced proliferation and inflammation.
106 aorta, also suggesting a crucial role of the disturbed flow-induced SUMOylation of proteins, includin
107 tioxidant genes NQO1, CYB5B, and WWP2, and a disturbed flow-induced super-enhancer in endothelium whi
108  Review, we discuss this emerging concept of disturbed-flow-induced reprogramming of endothelial cell
109 de new insights into the mechanisms by which disturbed flow induces endothelial phospho-YY1(S118) to
110                                              Disturbed flow induces peroxynitrite production, which a
111 P/TAZ knockdown significantly attenuated the disturbed flow induction of EC proliferative and proinfl
112 dysfunction caused by the combined action of disturbed flow, inflammatory mediators and oxidants deri
113       Together, our results demonstrate that disturbed flow influences endothelial function and induc
114                            In blood vessels, disturbed flow is associated with vascular diseases, suc
115                                     Although disturbed flow is thought to play a central role in the
116 cytokines or exposure to hemodynamic-induced disturbed flow leads to a proadhesive and prothrombotic
117 was observed in these cells, suggesting that disturbed flow leads to posttranscriptional modification
118 nd proatherogenic fibronectin deposition and disturbed flow-mediated endothelial cell inflammation.
119 ter expression in the atheroprone regions of disturbed flow (n=5).
120 selectively bound to arterial ECs exposed to disturbed flow not only in the partially ligated carotid
121                In this study, the effects of disturbed flow on the regulation of vascular endothelial
122 jected to well-defined atherosclerosis-prone disturbed flow or atherosclerosis-protective unidirectio
123                    Here, we explored whether disturbed flow patterns activate an innate immune respon
124 Both type III and type V TAAAs showed highly disturbed flow patterns with varying helicity values pre
125 disease-prone regions of arteries exposed to disturbed flow patterns, and promote vascular inflammati
126  associated with chronic inflammation due to disturbed flow patterns.
127                           We postulated that disturbed flow plays important role in modulating phosph
128 ifferentially regulate gene expression, with disturbed flow priming endothelial cells (ECs) for a pro
129 s was further confirmed to be present in the disturbed flow regions in experimental animals and human
130 -ICAM-1 specifically bound to endothelium in disturbed flow regions, reducing endothelial ICAM-1 expr
131 st that shear stress gradients in regions of disturbed flow regulate intercellular communication thro
132             Gene ontology analyses show that disturbed flow regulates genes involved in cell prolifer
133 ow-induced atherosclerosis demonstrated that disturbed flow reprogrammes arterial endothelial cells i
134 ner, demonstrating that IRAK-1 activation by disturbed flow required Nck1 in vitro and in vivo, showi
135 % inhibitions of EC proliferation induced by disturbed flow, respectively, whereas EC inflammation wa
136 d endothelial cells (ECs) to the atheroprone disturbed flow resulted in YAP/TAZ activation and transl
137 netic proteins (BMPs)] and mechanical (e.g., disturbed flow) stimulations and hence may serve as a pr
138 marily affects the regions of the aorta with disturbed flow that are prone to atherosclerosis.
139 lood, Ni et al use an in vivo mouse model of disturbed flow that results in accelerated atheroscleros
140 s cultured under conditions of "normal" and "disturbed flow" under hyperglycemic conditions suggestin
141 ith increased PKCzeta activity in regions of disturbed flow versus unidirectional flow.
142  Using cultured endothelial cells exposed to disturbed flow, we demonstrate that neutrophil microvesi
143 therosclerotic lesions develop in regions of disturbed flow, whereas laminar flow protects from ather
144 phosphoproteomics analysis of ECs exposed to disturbed flow with low and oscillatory shear stress (0.
145  for atherosclerosis than regions exposed to disturbed flow with low shear stress.
146                                              Disturbed flow with lower average shear stress decreases
147 e arterial tree is atheroprotective, whereas disturbed flow with oscillation in branch points and the
148 atory, and proliferative responses of ECs to disturbed flow with OSS.
149 osclerotic lesion localization to regions of disturbed flow within certain arterial geometries, in hu
150                We evaluated whether inducing disturbed flow would cause the development of advanced c
151  oscillation frequency of 1 Hz, as occurs in disturbed flow zones prone to atherosclerosis, failed to

 
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