ライフサイエンスコーパス: shear stress

1 nsport from momentum transport (i.e. fluidic shear stress).

2 growth on a collagen surface under arterial shear stress.

3 hrombotic phenotype on collagen matrix under shear stress.

4 factors known to be activated by oscillatory shear stress.

5 they may overestimate volumetric outflow and shear stress.

6 h, sea surface temperature, salinity and bed shear stress.

7 system, while decoupling mass transport from shear stress.

8 vival and viability during exposure to fluid shear stress.

9 strength to overcome prevailing hemodynamic shear stress.

10 ed VWF multimers, preferentially under fluid shear stress.

11 othelial cells respond to blood flow-induced shear stress.

12 llagen and impaired thrombus formation under shear stress.

13 canal (SC), theoretically increasing luminal shear stress.

14 ral changes in electroactive biofilms due to shear stress.

15 n 30 min after exposure to arterial rates of shear stress.

16 signaling molecule during cell migration and shear stress.

17 inutes of experimentally-induced oscillatory shear stress.

18 lignment of endothelial cells in response to shear stress.

19 gic (5%) O2 and stimulated with histamine or shear stress.

20 scosity above a critical, material-dependent shear stress.

21 N-cadherin, alpha-SMA) in EC exposed to low shear stress.

22 plications of physiological and pathological shear stress.

23 nced by hyperglycemia, oxidative stress, and shear stress.

24 r 5 minutes in the presence of 1.0 dyn/cm(2) shear stress.

25 bsequently shown by others to be due to lung shear stress.

26 signaling scales with the magnitude of fluid shear stress.

27 an anisotropic hydrogel string under modest shear stress.

28 ces EC production of NO in response to fluid shear stress.

29 ds that support slow leukocyte rolling under shear stress.

30 iPSCs), to study their vulnerability to flow shear stress.

31 proliferation, phenotypes induced by laminar shear stress.

32 for cross-fiber, and 0.039 +/- 0.011 kPa for shear stress.

33 n fluorescent protein (GFP) and subjected to shear stress.

34 ral and material properties as a function of shear stress.

35 nction of the strength and duration of fluid shear stress.

36 ause they were grown in the absence of fluid shear stress.

37 of flow and produce nitric oxide under high shear stress.

38 ertical sides of the healing-gap due to high shear stress.

39 leased from endothelial cells in response to shear stress.

40 city upon the filaments bundling promoted by shear stresses.

41 f cellular deformation at moderate-to-higher shear stresses.

42 are subjected to in vivo like fluid flow and shear stresses.

43 odstream of animals is associated with large shear stresses.

44 (MC) with high specificity under a range of shear stresses.

45 ess experiments under unidirectional laminar shear stress (12 dyn/cm(2)) versus oscillatory shear str

46 ed arterioles exposed to 1 h of intraluminal shear stress (20 dynes cm(-2) ) subsequently exhibited g

47 Under predominantly shear stresses (25 degrees ), aging significantly decrea

48 ear stress (12 dyn/cm(2)) versus oscillatory shear stress (+/-5 dyn/cm(2)) conditions.

49 w patterns that exert low or low oscillatory shear stress, a mechanical environment that promotes vas

50 erstanding of the mechanism by which laminar shear stress activates lymphatic proliferation.

51 moted melanoma cell invasion, survival under shear stress, adhesion to endothelial cells under contin

52 igh shear stress (before TAVI) and under low shear stress (after TAVI).

53 on, was assessed in response to flow-induced shear stress and ACh.

54 must incorporate design elements that reduce shear stress and avoid stasis to reduce the frequent adv

55 nthase (eNOS) promoter, we tested effects of shear stress and elevated flow rate on reporter expressi

56 VWF interaction, which is regulated by fluid shear stress and exhibits "catch bond" characteristics.

57 re at the outlet of the system produces high shear stress and high levels of NO, which inhibits contr

58 osity in platelet releasates produced higher shear stress and higher LTGF-beta1 activation.

59 lls did not migrate against the direction of shear stress and increased proliferation rates specifica

60 and decreased by 20% and 22% with increasing shear stress and inhibition of non-muscle myosin II moto

61 hanically stimulated rat cortical neurons by shear stress and local indentation.

62 sociated with the direction of the mean wall shear stress and of the gradient of harmonic phase-avera

63 ches are required for precise computation of shear stress and pressure gradient whereas models that h

64 ity and actin disruption induced by Yoda1 or shear stress and prevented Piezo1-induced monocyte adhes

65 es, where it integrates responses to laminar shear stress and regulates junctional integrity through

66 IH reduced vascular shear stress and steepened the relationship between dias

67 We observed that IGPR-1 is activated by shear stress and tensile force and that flow shear stres

68 s release RNA in response to increased fluid shear stress and that administration of RNase inhibitor

69 The magnitude of the reduction in the shear stress and the local friction coefficients have be

70 expression analysis after fluid flow-induced shear stress and the relocalization of components of the

71 suggest that pulsed wave stimulation induces shear stress and thus increases algal lipid production.

72 Reductions in vessel wall shear stress and, consequently, nitric oxide production

73 rasensitive resolution in film thickness and shear stress, and control over the crystallographic alig

74 stem behavior, such as advection regimes and shear stress, and derive estimates for relevant quantiti

75 ssure-induced wall stress, flow-induced wall shear stress, and exogenous sources of angiotensin II, w

76 how that endothelial NOTCH1 is responsive to shear stress, and is necessary for the maintenance of ju

77 arious mechanical stimuli including stretch, shear stress, and osmotic pressure.

78 The monitored evolution of slip-velocity, shear stress, and slip-distance revealed three slip styl

79 ntal arcade configurations that concentrated shear stresses, and (3) repetitive, localized biting.

80 Thus, deleterious effects of shear stress are initiated by Piezo1 but require TRPV4.

81 r, little is known about how cues from fluid shear stress are translated into responses that pattern

82 nd factor (VWF) of mixed ABOs under arterial shear stress, as compared with those from non-O subjects

83 We demonstrate that high shear stress, as present in patients with aortic valve s

84 ditions and conditions designed to mimic the shear stress associated with tidal breathing.

85 eas they exhibit progressive increase in the shear stress at higher V, which is reminiscent of a tran

86 ood flow streamlines, as well as lower blood shear stress at the wall, blood vorticity, inner wall ci

87 Here we demonstrate that fluid shear stress, at arterial flow magnitudes, maximally act

88 he activation status of monocytes under high shear stress (before TAVI) and under low shear stress (a

89 reased cytosolic free calcium to a threshold shear stress between 8 and 21 Pa; the propagation of thi

90 anches on coronary hemodynamics by comparing shear stress between coronary models with and without th

91 Endothelial cells are critical sensors of shear stress but the mechanisms by which they decode com

92 While complex shear stresses can activate LTGF-beta1, the mechanisms u

93 Under physiological shear stress, caps of polymerized pFn at bacterial poles

94 We discovered that high and prolonged shear stress caused sustained [Ca(2+)](i) elevation that

95 humans) support the hypothesis that elevated shear stress causes the vascular endothelium to become m

96 essary for SDF-1alpha-induced adhesion using shear stress, cell morphology alterations, and crawling

97 We quantify all normal and shear stress components and demonstrate vector magnetic

98 ew model, correlating the optically measured shear stress concentration factor and flexural strength

99 il is an essential driver of EndMT under low shear stress conditions and may promote early atherogene

100 We hypothesised that shear stress counteracts the inflammatory effects of oxi

101 ood-brain barrier (BBB) recapitulate in vivo shear stress, cylindrical geometry, and cell-ECM interac

102 Furthermore, fluid-shear stress decreases cilioplasmic, but not cytoplasmic

103 rate that the expression of this receptor is shear stress dependent and downregulated in patients rec

104 r highly controlled conditions, showing that shear stress-dependent calcium influx and monocyte adhes

105 ood samples from NSML patients also showed a shear stress-dependent elevation of platelet responses o

106 the temporal correlation of the interaction shear stress determines an effective viscosity of the ti

107 We hypothesized that different types of shear stress differentially activate LTGF-beta1.

108 , here we sense the evolution of the maximum shear stress distribution on the beams under loading.

109 stress induced by diverse mechanisms such as shear stress, DNA damage, and heat shock.

110 This process continues until the effective shear stress drops and dislocation activities stop.

111 ses of seabed sediments, the period when bed shear stress due to combined current-wave action under n

112 multimeric blood protein, senses changes in shear stress during bleeding and responds by binding pla

113 genetic studies, we could recapitulate high shear stress effects on isolated human monocytes under h

114 Oscillatory shear stress elevated circulating markers of endothelial

115 al concentrations of high levels of Reynolds shear stress, enstrophy, and temperature fluctuations.

116 the mechanisms by which they decode complex shear stress environments to regulate physiological and

117 model and the experimental measurements, the shear stress exerted by the cilia is deduced.

118 d viable after filtration due to the minimal shear stress exerted over cells during the procedure, wh

119 nce supporting the hypothesis that increased shear stress exerts insulin-sensitizing effects in the v

120 s have the capacity to quantify and localize shear stress experienced by endothelial cells.

121 /dm) mice, were investigated in the in vitro shear stress experiments under unidirectional laminar sh

122 Here we show that shear stress favours mitochondrial biogenesis and metabo

123 dramatically stiffen in response to applied shear stress featuring power law rheology with exponents

124 om MLO-A5 cells exposed to fluid flow-driven shear stress (FFCM) increased the tensile forces and inc

125 nse mechanical cues by changes in fluid flow shear stress (FFSS) across their dendritic projections.

126 llatory, normal laminar and elevated laminar shear stress for a period of 72 hours.

127 weather conditions exceeds the critical bed shear stress for erosion (tau cr ) accounts for 63% of t

128 expression change in response to oscillatory shear stress frequency.

129 cultured endothelial cells, 1 h of increased shear stress from 3 to 20 dynes cm(-2) caused a signific

130 ize confinements to the flat distribution of shear stress from the anisotropic microchannel walls and

131 wth is distinctly enhanced by elevated fluid shear stress (FSS), the underlying regulatory mechanism

132 pacity in response to acute changes in fluid shear stress (FSS); however, it is not known whether GFR

133 sturbed blood flow with increased retrograde shear stress further deteriorates the already impaired e

134 study were: (1) to test whether oscillatory shear stress further exacerbates endothelial dysfunction

135 Although shear stress generated by fluid flow is known to trigger

136 and laser-derived deformability at any given shear stress >=1 Pa.

137 how a significant drop in cell viability for shear stresses >11.8 kN/m(2).

138 r stimulated platelets, even if the imparted shear stress has low magnitude and brief exposure time.

139 dic measurements also highlight the key role shear-stress has in enabling this interaction.

140 stimulate an increase in limb blood flow and shear stress have the potential to have profound metabol

141 In a culture model of blood flow-induced shear stress, human coronary artery endothelial cells fa

142 In response to high shear stress, HUVECs and SC cells expressed more SEAP an

143 ng: (i) changes in blood flow patterns (i.e. shear stress), (ii) increased inflammation and productio

144 xide from all other cells while enduring the shear stress imposed by navigating small vessels and sin

145 response of primary rat astrocytes to fluid shear stress in a model of traumatic brain injury (TBI),

146 d of healthy volunteers were exposed to high shear stress in a viscometer or microfluidics channel to

147 n and A1A2A3 tridomain fragment of VWF under shear stress in an ex vivo shear flow microfluidic chamb

148 WIST1 and HOX family genes, are regulated by shear stress in arteries in adults.

149 ced expression of the chemokine Cxcl12 Under shear stress in culture, Dach1 overexpression stimulated

150 changes in gene expression induced by fluid shear stress in cultured osteocytes and stimulation of P

151 telets is unclear, despite the importance of shear stress in platelet function and life-threatening t

152 urface machining on the ceramic, the maximum shear stress in the reaction layer is decreased, which c

153 Fluid shear stress in the vasculature is the driving force for

154 SFKs [7], which is maximally induced by low shear stress in vitro and in vivo [8].

155 red for the response of endothelial cells to shear stress in vitro and in vivo and regulates the site

156 Induction of disturbed shear stress in vivo and in vitro resulted in complex FN

157 that there would be an optimal range of wall shear stress in which bacterial upstream twitching is mo

158 ction is then applied to generate rotational shear stresses in any desired direction.

159 rein we tested the hypothesis that increased shear stress, in the absence of muscle contraction, can

160 Shear stress increases Jagged1 levels and Notch activati

161 Organs and cells must adapt to shear stress induced by biological fluids, but how fluid

162 Here, we show that (disturbed) shear stress induced by vortices is a sufficient conditi

163 traumatic brain injury (TBI), we found that shear stress induced Ca(2+) entry.

164 The underlying concept, a shear-stress induced permeabilisation of biocatalytic re

165 Inhibition of this phosphorylation prevented shear stress-induced actin fiber assembly and endothelia

166 studies included endothelial cell adhesion, shear stress-induced cell alignment, blood pressure meas

167 ion with rapid relaxation to circular shape, shear stress-induced deformation, and rapid fluorescence

168 ole of the transcription factor Snail in low shear stress-induced EndMT.

169 nction and is protective against oscillatory shear stress-induced endothelial dysfunction in patients

170 gen administration abrogated the oscillatory shear stress-induced increase in CD31+/CD41b- microparti

171 ow) types of ICWs at varying degrees of flow shear stress-induced membrane deformation, as determined

172 Shear stress-induced molecular and cellular responses we

173 siological experiments demonstrate that high shear stress-induced multimeric cochlin produces a quali

174 rosine kinase 2 restores insulin-induced and shear stress-induced NO production.

175 mplicated in high venous pressure- and fluid shear stress-induced vascular hyperpermeability in endot

176 Low shear stress induces dedifferentiation of EC through a p

177 Shear stress induces phosphorylation of vimentin at seri

178 demonstrate that Piezo1 activation by fluid shear stress initiates a calcium signal that causes TRPV

179 lood components with artificial surfaces and shear stress inside extracorporeal membrane oxygenation

180 The oscillatory shear stress intervention induced significant decreases

181 is that acute exposure of venous ECs to high shear stress is associated with inflammatory responses t

182 f von Willebrand factor (VWF) as a result of shear stress is dependent on VEGFR2.

183 ural tube-paraxial mesoderm interfaces where shear stress is highest.

184 The application of shear stress is known to enhance tight junction formatio

185 their crosstalk with the redox system under shear stress is lacking.

186 Conversely, physiologically high shear stress is protective.

187 nt at the cell-cell contacts; however, under shear stress, it redistributes along the cell borders in

188 and thus are consistent with the notion that shear stress may be a principal mechanism by which physi

189 the mouse vessels, suggesting that disturbed shear stress may lead to sustained NF-kB activation ther

190 How integrin binding under shear stress mechanosignals a functional shift in iMo to

191 (2+)](i) elevation was responsible for fluid shear stress-mediated and Piezo1-mediated disruption of

192 shear stress and tensile force and that flow shear stress-mediated IGPR-1 activation modulates remode

193 vanced this field by integrating specialized shear-stress models with systems biology approaches, inc

194 c core size was also reduced in the model of shear stress-modulated vulnerable plaque formation.

195 esion development was assessed in a model of shear stress-modulated vulnerable plaque formation.

196 tic endothelial cells exposed to oscillatory shear stress (n=3 in triplicate).

197 es of turbidity currents, in the form of bed shear stress obtained by numerical simulations, match ob

198 so known as erosion, depends on the critical shear stress of a particle and is influenced by the part

199 tion was developed to determine the critical shear stress of different MP particles on natural sedime

200 In this study, the critical shear stresses of 14 MP particles with different shapes,

201 Critical shear stresses of the MP particles were between 0.002 an

202 erfaces at the proportional limit under pure shear stresses of torsion.

203 Shear stress on arteries produced by blood flow is impor

204 cell (PBMEC) culture to assess the impact of shear stress on barrier formation using the Kirkstall Qu

205 ered to enhance hemocompatibility and reduce shear stress on blood components.

206 The effect of shear stress on Ca(2+) entry in human platelets and Meg-

207 tulated that increased blood flow-associated shear stress on endothelial cells is an underlying mecha

208 tulated that increased blood flow-associated shear stress on endothelial cells is an underlying mecha

209 f atheroprone and atheroprotective pulsatile shear stress on endothelial cytoskeleton remodeling and

210 vealed the significant effect of hemodynamic shear stress on RBC-induced microvascular injury.

211 his condensation significantly increases the shear stresses on the packaged DNA while also reducing t

212 is suggest that elevated tidal range and bed shear stress optimized mangrove development along tide-i

213 l cells, Piezo1 channel activation by either shear stress or a chemical agonist Yoda1 activated a dis

214 ible to rupture by extrinsic forces, such as shear stress or compression.

215 the cell through hemichannels and following shear stress or membrane damage.

216 We first confirmed that either fluid shear stress or the Piezo1 agonist, Yoda1, led to an ele

217 TP in response to changes in blood flow (via shear stress) or hypoxia, to act on P2 receptors on endo

218 s-associated protein (YAP) under oscillatory shear stress (OSS) in the atheroprone phenotype of endot

219 hnique, the cells are perfused under defined shear stresses over a monolayer of endothelial cells (ex

220 Here, we assessed the impact of shear stress patterns and flow directionality on the beh

221 Blood flow and vascular shear stress patterns play a significant role in inducin

222 ange their migratory behavior in response to shear stress patterns, according to flow directionality.

223 alcium channel, was identified to induce the shear stress phenotypes and cell proliferation in LECs r

224 ain- or loss-of-function phenotype and under shear stress, platelet translocation pause times on coll

225 Haemodynamic shear stress plays a critical role in maintaining endoth

226 We also examined the velocity and shear stress profiles for flow over the permeable layer

227 molecular mechanosensors to directly detect shear stress profiles that will ultimately lead to ather

228 We find that increased shear stress reduces biofilm development time while incr

229 pment but also drives atherosclerosis in low shear stress regions of adult arteries.

230 A shear stress-regulated temporal rise in p38 phosphorylat

231 we describe these studies, which reveal that shear stress regulates diverse processes and demonstrate

232 The mechanisms underlying shear stress-regulation of EndMT are uncertain.

233 es fit the established simple bedload flux - shear stress relations for dryland channels very well, b

234 and platelets with endothelia under vascular shear stress requires mechanically specialized interacti

235 Furthermore, caveolar-mediated shear stress response activates YAP/TAZ.

236 Endothelial cells show impaired shear stress response and reduced levels of endothelial

237 experimental study and mechanistic model of shear stress response.

238 Steady laminar flow induced the classic shear stress responses commonly in blood vascular endoth

239 te laminar flow commonly induces the classic shear stress responses in blood endothelial cells and ly

240 ption rates, nitric oxide production levels, shear stress responses, and TNFalpha-induced leukocyte a

241 The application of shear stress resulted in a reorientation and enhancement

242 capsule with DMSO, ultrasound, or mechanical shear stress resulted in capsule alterations that affect

243 release nitric oxide in response to elevated shear stress secondary to metabolic dilatation of arteri

244 Pressure drop, wall shear stress, secondary flow degree, helicity, maximal v

245 We hypothesized that downregulation of a shear stress-sensitive transcription factor, Kruppel-lik

246 entify the key mechanoreceptor mediating the shear stress sensitivity of monocytes.

247 ltered the two parameters that contribute to shear stress: shear rate and solution viscosity.

248 the ratio of the excess shear modulus to the shear stress should be inversely proportional to the cri

249 spatial and temporal complexity of the wall shear stress should be taken into account when studying

250 at Snail was expressed preferentially at low shear stress sites that are predisposed to atheroscleros

251 We reported that hydrodynamic shear stress (SS) mechanoregulates inflammation in human

252 TM expression is regulated by shear stress (SS) via Kruppel-like factor 2 (KLF2).

253 Mechanistically, shear stress stimulated activation of AKT Ser/Thr kinase

254 in 5% O2 (>5 d) decreased histamine- but not shear stress-stimulated endothelial (e)NOS activity.

255 f superoxide, whereas insulin-stimulated and shear stress-stimulated eNOS activations were blunted.

256 Shear stress stimulates lipophagy, contributing to the p

257 odilator activity, given its contribution to shear stress stimuli and diverse biochemical reactions w

258 tric oxide signalling through alterations in shear stress stimuli and haemoglobin scavenging of nitri

259 Statistical covariation for the shear stress stimulus did not alter FMD, indicating that

260 atation occurred in the face of an unaltered shear stress stimulus for vasodilatation and reduced res

261 s, and improved FMD after accounting for the shear stress stimulus.

262 Comparison of energy barriers and ideal shear stresses suggests that the favorable modes are pri

263 ng blood generates a frictional force called shear stress that has major effects on vascular function

264 ed, from which characteristics such as ideal shear stress, the dislocation Burgers vector, and possib

265 trate-induced allosteric activation; without shear stress, the distal T8-CUB domains markedly inhibit

266 lectin and pilin domains are separated under shear stress, the FimH-ligand interaction switches in a

267 gical functions of S1P are tightly linked to shear stress, the key biophysical stimulus from blood fl

268 In response to oscillatory shear stress, the transcription factors Tal1, Gata2, and

269 obes regulate cell adhesion strength at high shear stress through intricate molecular mechanisms incl

270 The resolution of high shear stress through TAVI reduces Mac-1 activation, cell

271 composites not only promotes the interfacial shear stress to a high level and thus results in signifi

272 pathway that translates laminar flow-induced shear stress to activation of lymphatic sprouting.

273 nd (3) cultured endothelial cells exposed to shear stress to decrease CSE expression and treated with

274 under static conditions or exposed to fluid shear stress to decrease CSE expression; and (3) culture

275 to seed, culture, and apply calibrated fluid shear stress to hEMVs (takes 1-7 d); and how to assess v

276 s and G was computed as the ratio of imposed shear stress to measured shear strain.

277 ing motifs are sufficient to bear normal and shear stress to promote significant and tunable adhesive

278 er permeability can be modulated by applying shear stress to the droplet interfaces, inducing flow pa

279 eutrophil rolling over E-selectin at precise shear stress transmits tension and catch-bond formation

280 Shear stress triggers DLL4-dependent proteolytic activat

281 Indeed, shear stress triggers rapid increases in force across PE

282 interact with endothelia under physiological shear stress, using recently developed live cell imaging

283 (TM) cells might detect aqueous humor fluid shear stress via interaction of the extracellular matrix

284 an aortic endothelium or rVCAM-1 under fluid shear stress was assessed using a microfluidic-based art

285 n Combined analysis of lumen volume and wall shear stress was associated with enlargement of abdomina

286 nded joints are subject to mixed tensile and shear stresses when the restoration is in occlusal servi

287 terns in the vasculature to generate complex shear stress, which activates higher levels of TGF-beta1

288 nfluences atherosclerosis by generating wall shear stress, which alters endothelial cell (EC) physiol

289 Finally, this shear stress, which can easily be measured in the clinic

290 de by the endothelium in response to luminal shear stress, which increases secondary to arteriolar di

291 d of the gradient of harmonic phase-averaged shear stresses, which surprisingly do not match the over

292 Perfusion of TEBVs at a physiological shear stress with enzyme-modified low-density-lipoprotei

293 pal TM transducer of physiological levels of shear stress, with both shear and the Piezo1 agonist Yod

294 adient across the stenosis (DeltaP) and wall shear stress (WSS) - by performing the largest simulatio

295 The combined role of wall shear stress (WSS) and circumferential wall stresses (CW

296 The ABM also considers wall shear stress (WSS) dependent leukocyte TEM and compensat

297 dothelial cells (ECs) to acute arterial wall shear stress (WSS) in the arterial circulation, and the

298 Our simulations reveal elevated wall shear stress (WSS) in wild type and AG1478 compared to g

299 migration; whereas intensities of fluid wall shear stress (WSS) typical of venous or arterial flow in

300 ice that generates spatial gradients in wall shear stress (WSS), such as are found at sites of valve

301 men volumes, maximal wall pressure, and wall shear stress [WSS]) to identify relevant parameters for