ライフサイエンスコーパス: shear stress

1 h which blood was sampled (e.g., by avoiding shear stress).

2 an anisotropic hydrogel string under modest shear stress.

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

4 ds that support slow leukocyte rolling under shear stress.

5 proliferation, phenotypes induced by laminar shear stress.

6 +) T cells under conditions of physiological shear stress.

7 ress functional Kir2.1 channels sensitive to shear stress.

8 lar factors, including proteases, Na(+), and shear stress.

9 s was evidenced only under conditions of low shear stress.

10 ing eNOS activity not present in response to shear stress.

11 signaling molecule during cell migration and shear stress.

12 me, but increased with the magnitude of wall shear stress.

13 ides elevated resistance of the EPS layer to shear stress.

14 elevated distribution of peak systolic wall shear stress.

15 e scaling theory for the energy and residual shear stress.

16 re significantly enhanced by increasing wall shear stress.

17 T were altered in the BOECs with exposure to shear stress.

18 anges of cancer cells upon exposure to fluid shear stress.

19 lugdunensis requires mechanisms to overcome shear stress.

20 VWF self-association is accelerated by shear stress.

21 an atheroprotective transcription factor by shear stress.

22 misorientation from the direction of maximum shear stress.

23 igration of CCR4+ huTreg under physiological shear stress.

24 full-length VWF proteolysis as a function of shear stress.

25 inutes of experimentally-induced oscillatory shear stress.

26 e of cell types, inflammatory mediators, and shear stress.

27 es including oxidative stress, wounding, and shear stress.

28 0 that are required for a robust response to shear stress.

29 ancer cells to elevated levels of flow-based shear stress.

30 ge dislocation velocity at very high applied shear stress.

31 low (P<0.002) and multidirectional (P<0.002) shear stress.

32 lignment of endothelial cells in response to shear stress.

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

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

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

36 plications of physiological and pathological shear stress.

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

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

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

40 signaling scales with the magnitude of fluid shear stress.

41 rotecting the biomass from environmental and shear stresses.

42 odstream of animals is associated with large shear stresses.

43 MMP-1 expression is detected in fluid shear stress (20 dyn/cm(2))-activated and osteoarthritic

44 High wall shear stress (60.5 dyne/cm(2)), however, led to decrease

45 Blood viscosity decreases with shear stress, a property essential for an efficient perf

46 Neutrophils rolling at high shear stress (above 6 dyn/cm(2)) form tethers in the rea

47 resence of the ADAM10 inhibitor corroborated shear stress-activated Notch signaling to modulate trabe

48 ss-mediated inflammatory activation and that shear stress activates ERK5 signalling while attenuating

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

50 a obtained in the present study suggest that shear stress activates TRPM4 current by triggering Ca(2+

51 up that exposes cells to linearly increasing shear stress along the length of the flow channel floor.

52 in an asymmetry in average velocity and wall shear stress along the length of the stenosis.

53 othesize that substrate topography and fluid shear stress alter the cellular contractile forces, infl

54 bloodstream by conferring resistance to the shear stress and attack from natural killer cells.

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

56 Arterial hemodynamic shear stress and blood vessel stiffening both significan

57 lls in response to a variety of magnitude of shear stress and circulating time.

58 atriumm58 (wea) mutants resulted in reduced shear stress and downregulation of Notch signaling and t

59 ltaneous calculation of blood flow velocity, shear stress and drug distribution.

60 bryogenesis, but its role in EC responses to shear stress and focal atherosclerosis is unknown.

61 s of binding of cancer cells on the level of shear stress and in the presence of small molecule inhib

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

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

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

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

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

67 endothelial senescence under atheroprone low shear stress and thrombogenicity through angiotensin II-

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

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

70 e, solution exchange rate in a microchamber, shear stress, and time to fill up a single microwell wit

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

72 through stenotic regions producing high wall shear stresses, and plaque-derived tissue factor driving

73 Shear stress antagonises endothelial dysfunction by incr

74 marrow, where external forces such as fluid shear stress, apart from the physical characteristics of

75 Endothelial responses to fluid shear stress are essential for vascular development and

76 Mechanisms by which blood cells sense shear stress are poorly characterized.

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

78 nce, cardiac myocytes are subjected to fluid shear stress as a result of blood flow and the relative

79 ut a state diagram with particle density and shear stress as variables.

80 tance Sd </= 30 mum, driven by the transient shear stress associated with TB-induced jetting flow.

81 r presence is felt globally in terms of wall shear stresses at the channel walls.

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

83 Vanishing velocity and vanishing shear stress boundary conditions are applied to the flui

84 strain, shear strain, system size, pressure, shear stress, bulk modulus, and shear modulus are all re

85 llebrand factor (VWF) self-association under shear stress can be modulated by the high-density lipopr

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

87 It is proposed that the shear stresses cause the amorphization and that pressure

88 dothelial migration (TEM) are potentiated by shear stress caused by blood flow.

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

90 wall stress (CPWS), strain (CPWSn) and flow shear stress (CFSS) were recorded, and cap index, lipid

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

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

93 Blood flow-induced shear stress controls endothelial cell (EC) physiology d

94 In conclusion, shear stress counteracts endothelial dysfunction by supp

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

96 its bulk room temperature critical resolved shear stress (CRSS) is ~33-43 MPa, ~10 times higher than

97 constants for the affinity of reactions, the shear-stress dependent adsorption time of molecules on s

98 R inhibitor dalotuzumab (MK-0646) and showed shear stress-dependent resistance to the IGF-1R blockade

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

100 eld with an uncertainty of 0.06% and 2D wall shear stress distribution at the resolution of ~65 muPa.

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

102 r of 2D dynamic simulations using stochastic shear stress distributions and a geometry based on the c

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

104 Fluid shear stress due to blood flow on the vascular endotheli

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

106 Atrial myocytes are subjected to shear stress during the cardiac cycle under physiologica

107 Oscillatory shear stress elevated circulating markers of endothelial

108 In response to fluid shear stress, endothelial cells released ATP, which acti

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

110 hly deformed polylobed shapes for increasing shear stresses, even for semidilute volume fractions of

111 Shear stress evoked a rapid increase in whole cell curre

112 hology adjusts during incision such that bed shear stresses exceed the threshold for erosion by a sma

113 the endothelium under the influence of fluid shear stress exerted by flowing blood.

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

115 ed from the endothelium in response to fluid shear stress exerted by the flowing blood.

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

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

118 expression change in response to oscillatory shear stress frequency.

119 al cell subjected to a step increase of wall shear stress from zero to a finite physiologically relev

120 owing blood exerts a frictional force, fluid shear stress (FSS), on the endothelial cells that line t

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

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

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

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

125 ich is physically challenging because of the shear stress generated by blood flow.

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

127 High shear stresses generated at the biofilm-burst interface

128 It is proposed that the shear stresses generated by the uniaxial strain state of

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

130 Mature artery-type shear stress (high, uniform laminar) specifically down-r

131 ary hemodynamics and fluid flow-induced high shear stress (HSS) are characteristic hallmarks in the p

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

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

134 imers defects under instantaneous changes in shear stress in an aortic stenosis rabbit model and in p

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

136 es a new insight to the roles of circulatory shear stress in cellular responses of circulating tumor

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

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

139 disease and is triggered by increasing fluid shear stress in preexisting collateral arteries.

140 rom the vessel center and peak systolic wall shear stress in the ascending aorta were quantified.

141 al blood flow pattern and peak systolic wall shear stress in the ascending aorta.

142 umor cells constantly experience hemodynamic shear stress in the circulation.

143 yers in flow-based assays that mimic in vivo shear stress in the sinusoids.

144 The role of fluid shear stress in vasculature development and remodeling i

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

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

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

148 ing of these effects, which are dominated by shear stresses in highly fluctuating turbulent flow, has

149 Cellular responses to shear stress including cell viability and proliferation

150 The data obtained suggest that shear stress indirectly activates the monovalent cation

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

152 tch with calcium ion transport and ii) fluid shear stress induced nitric oxide production (NO).

153 ultured EC exposed to flow revealed that low shear stress induced Snail expression.

154 We present a biochemical model of the wall shear stress-induced activation of endothelial nitric ox

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

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

157 lucidate which integrin heterodimers mediate shear stress-induced endothelial cell activation and ear

158 , the role these integrins play in mediating shear stress-induced endothelial cell activation remains

159 ccur early during atherogenesis and regulate shear stress-induced endothelial cell activation.

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

161 rosine kinase 2 improved insulin-induced and shear stress-induced eNOS activation in hIRECO EC.

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

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

164 Shear stress-induced molecular and cellular responses we

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

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

167 2 receptors have been shown to mediate fluid shear stress-induced stimulation of NO formation.

168 otide exchange factor GEF-H1 as critical for shear stress-induced transendothelial neutrophil migrati

169 Low shear stress induces dedifferentiation of EC through a p

170 We discovered that fluid shear stress induces the synthesis of insulin growth fac

171 , von Willebrand factor, under physiological shear stress induces unfolding of this mechanosensory do

172 However, the mechanism by which fluid shear stress initiates these processes is unclear.

173 The oscillatory shear stress intervention induced significant decreases

174 the frictional force from blood flow (fluid shear stress) into biochemical signals that regulate gen

175 The application of high shear stress is a key methodological determinant acceler

176 s our landscape and occurs when a sufficient shear stress is exerted by a fluid on a sedimented layer

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

178 Raised endothelial shear stress is protective against atherosclerosis but s

179 Triggered by shear-stress, it adheres to platelets at sites of vascul

180 tic gene network to monitor endothelial cell shear stress levels and directly modulate expression of

181 uch as vasoprotective unidirectional laminar shear stress (LSS) and atherogenic oscillatory shear str

182 cytes and examined their response to laminar shear stress (LSS).

183 work varied logarithmically as a function of shear stress magnitude.

184 nteractions between these two proteins under shear stress may be an important mechanism by which atri

185 (tp1:gfp) Notch reporter line, revealed that shear stress-mediated Notch activation localizes to the

186 n, sedimentation, and using a novel in vitro shear stress model, we show that histones induce erythro

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

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

189 Here, we assessed whether shear stress modulates trabeculation to influence contra

190 kinase phosphorylation in response to fluid shear stress occurred more rapidly in ECs cultured on mo

191 a level, total bilirubin level, and RCD at a shear stress of 1.7 Pa were each independently correlate

192 A shear stress of approximately 16 dyn cm(-2) was applied

193 low MRI underestimates the maximum principal shear stress of laminar viscous stress (PLVS), and overe

194 VS), and overestimates the maximum principal shear stress of Reynolds stress (PRSS) with increasing v

195 designed to capture platelets under the high shear stress of rheological blood flow.

196 RCD at shear stresses of 1.7 Pa and 30 Pa was reduced significa

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

198 -DIB) device is presented as a tool to apply shear stress on biological lipid membranes.

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

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

201 activator Yoda1 mimicked the effect of fluid shear stress on endothelial cells and induced vasorelaxa

202 the concept that VWF splicing is affected by shear stress on endothelial cells.

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

204 Fluid-structure simulations showed that shear stress on the surface did not depend on sample sti

205 ts of interstitial flow and associated fluid shear stress on the tumor cell function have been largel

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

207 rculating blood generates frictional forces (shear stress) on the walls of blood vessels.

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

209 in vessels of diameter </=300 mum, with high shear stress or strong flow acceleration, and with sharp

210 ected, cultured proximal tubule cells, fluid shear stress or the addition of cyclic nucleotides enhan

211 Taylor cone tip, presumably due to the high shear stress or/and viscous drag forces operating there.

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

213 e of ENaC to extracellular Na(+), mechanical shear stress, or alpha-chymotrypsin-mediated proteolysis

214 We found that oscillatory shear stress (OSS), which promotes lymphatic vessel matu

215 ear stress (LSS) and atherogenic oscillatory shear stress (OSS).

216 ment (P=0.11), and higher peak systolic wall shear stress (P=0.0926).

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

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

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

220 We observe large-amplitude and localized shear stress peaks that precede rupture fronts and propa

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

222 Our results imply that, at high endothelial shear stress, PI16 contributes to inhibition of protease

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

224 Haemodynamic shear stress plays a critical role in maintaining endoth

225 downstream part of carotid plaques where low shear stress prevails.

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

227 We also show that shear stress, rather than shear rate, is the key control

228 , TWIST1 was expressed preferentially at low shear stress regions as evidenced by quantitative polyme

229 nt, TWIST is expressed preferentially at low shear stress regions of adult arteries where it promotes

230 tor 16 (PI16) mRNA are among the most highly shear stress regulated transcripts in human coronary art

231 Further studies showed that shear stress regulates NMHC IIA expression and localizat

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

233 ment supply drives the magnitude of bankfull shear stress relative to the critical stress required to

234 The ionic currents regulated by shear stress remain poorly understood.

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

236 inase (MAPK) signaling is linked to both the shear stress response and AP-1 up-regulation.

237 esults identify GEF-H1 as a component of the shear stress response machinery in neutrophils required

238 experimental study and mechanistic model of shear stress response.

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

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

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

242 a1a morpholino oligonucleotides (MO) reduced shear stress, resulting in downregulation of Notch signa

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

244 lar identity and activation mechanism of the shear stress-sensitive current (Ishear ) in rat atrial m

245 The present study aimed to characterize the shear stress-sensitive membrane current in atrial myocyt

246 Kruppel-like Factor 2 (KLF2) is a shear stress-sensitive transcription factor that regulat

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

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

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

250 role in mechanosensing of atherosusceptible shear stress (SS) by signaling enhanced inflammation.

251 Though alterations in shear stress stimulate arteriogenesis, the migration of

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

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

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

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

256 ls respond optimally within a range of fluid shear stress that approximate physiological shear.

257 aling relation between pressure and residual shear stress that yields insight into why the shear and

258 ynamics, such as cardiac output and vascular shear stress, that are similar to exercise, and thus may

259 Under shear stress the C1q-VWF interaction was enhanced, resem

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

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

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

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

264 ld, and through the mediation of anisotropic shear stresses, the active nematic reversibly self-assem

265 hesion to activated platelets under arterial shear stress, these advantages seem not readily translat

266 The shear-stress threshold exhibits an inverse square-root r

267 ere exists a microbubble oscillation-induced shear-stress threshold, on the order of kilopascals, bey

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

269 The ex vivo perfusion of arterial laminar shear stress to isolated veins further confirmed the cor

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

271 The mechanism that couples shear stress to migration has not been fully elucidated.

272 at fill the channel banks create just enough shear stress to move the median-sized gravel particles o

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

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

275 ties of neutrophils under static conditions, shear stress triggered GEF-H1-dependent spreading and cr

276 Shear stress triggers DLL4-dependent proteolytic activat

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

278 ast, the square sum of the turbulent viscous shear stress (TVSS), which is used for blood damage inde

279 provides the rheological basis to elucidate shear stress underlying developmental cardiac mechanics

280 telet aggregation using an aggregometer, and shear stress using a cone-and-plate viscometer.

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

282 d EC revealed that TWIST1 was induced by low shear stress via a GATA4-dependent transcriptional mecha

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

284 When fluid shear stress was applied, human MSCs with higher contrac

285 The resolved shear stress was estimated to be 13.8 GPa for the partia

286 though incremental activation by insulin and shear stress was impaired.

287 frequency component elements of hemodynamic shear stress waveforms encountered in cardiovascular blo

288 aintained when physiologically relevant wall shear stresses were applied.

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

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

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

292 preclinical IVM, and thereby have lower wall shear stress, which influences delivery of drugs and cel

293 uch as Na(+), Cl(-), protons, proteases, and shear stress, which modulate gating behavior.

294 ing the redox state in response to different shear stresses, which may promote the development of nov

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

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

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

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

299 We found that increased wall shear stress (WSS) was mainly caused by the increasing s

300 od flow (Q), wall shear rate (WSR), and wall shear stress (WSS) were measured in arterioles and venul