ライフサイエンスコーパス: vWF

1 vWF acts as a simple prognostic biomarker in AF and, whi

2 vWF and VEGF-C expression decreased in BDL Kit(W-sh) mic

3 vWF is an independent predictor of long-term outcome in

4 vWF multimers and degradation fragments were quantified

5 vWF protein forms long multimers from homodimers that fi

6 vWF significantly predicted mortality with a hazard rati

7 vWF was associated with CVD among participants with diab

8 vWF-Ag correlated with HVPG (r = 0.69; P < 0.0001) and p

9 vWF-Ag equals Model for End-Stage Liver Disease (MELD) i

10 vWF-Ag is a new, simple and noninvasive predictor of CSP

11 vWF-Ag may become a valuable marker for the prediction o

12 We used R687E type 2B and G561S type 2M vWF-A1 mutations to study binding between flowing platel

13 A vWF-Ag cut-off value at 315% can clearly stratify patien

14 Importantly, a vWF-Ag cutoff at 413% identified patients at risk for de

15 Using a vWF-Ag cut-off value of >/= 241%, the AUC for detection

16 In compensated patients with a vWF-Ag >315% median time to decompensation or death was

17 with microspheres bearing a tridomain A1A2A3 vWF fragment with the R1450E mutation in a shear-depende

18 The relationship to abnormal vWF metabolism is unknown.

19 The mean stop time for all vWF-A1 molecules reveals catch-slip transitions at diffe

20 viable and exhibit normal survival, although vWF-mediated platelet-endothelial interactions are signi

21 eight vWF multimers (+40+/-5%, P<0.0001) and vWF degradation fragments (+53+/-6%, P<0.0001).

22 of clinical outcome at day 21 (P=0.008), and vWF levels at day 21 was a weak independent inflammatory

23 p = 0.003), TG: HDL-C ratio (p = 0.010), and vWF levels (p = 0.004).

24 PAI-1 (10 vs 7 ng/mL, overall P = .02), and vWF (142% vs 87%, overall P < .01) levels in asthmatic p

25 ETP, PAI-1, and vWF levels increased with increasing asthma severity.

26 : FVII activity/antigen, FVIII activity, and vWF antigen.

27 lial nitric oxide synthase, VE-cadherin, and vWF indicated functional promoter activity in cell types

28 demonstrated surface expression of CD31+ and vWF+, alpha-SMA+ cells and were found in the "interstiti

29 dothelial markers was observed with CD34 and vWF and least for CD31.

30 gher densities of CD15+ and Ki-67+ cells and vWF-positive vessels as histologic markers that differen

31 platelet activation, thrombin, collagen, and vWF are known to induce in vitro calcium mobilization in

32 tion, we found a correlation between ETP and vWF with neutrophil but not eosinophil counts.

33 on with high expression of tissue factor and vWF, and low expression of the ectonucleotidase CD39.

34 ants across the fibrinogen, FVII, FVIII, and vWF traits that were independent of previously identifie

35 H-E, Von Kossa, and vWF staining showed complete cell death, with a sharply

36 verning WPB docking with plasma membrane and vWF secretion remains undefined.

37 (IQR) increase in PAI-1 (IQR 16.8 ng/ml) and vWF (IQR 66.8% of control) conditioned on baseline chara

38 MELD-Na and vWF-Ag were comparable and independent in their predicti

39 Osteoprotegerin and vWF levels increased in participants following inoculati

40 s that the plasma levels of CXCL16, PTX3 and vWF at the start of treatment are independently associat

41 ecules (IL-6, HMGB1, HSP70, HSP90, S100B and vWF) were effectively neutralised by the TiO(2)-NPs in e

42 In contrast, plasma levels of sRAGE and vWF were not predictive of ALI.

43 e functional relationship between STXBP5 and vWF is unknown.

44 von Willebrand factor antigen (vWF-Ag) is elevated in patients with liver cirrhosis, bu

45 The von Willebrand factor (vWF) antigen (vWF-Ag) correlates with portal pressure and seems capabl

46 rom mice expressing a vWD-type 2B-associated vWF (vWF/p.V1316M), platelets from a patient with the sa

47 al vascular architecture and LVAD-associated vWF degradation were consistent findings in multiple spe

48 port that the endothelial surface-associated vWF formed at exocytosis recruits soluble plasma vWF and

49 he waiting list (area under the curve [AUC], vWF-Ag = 0.739; MELD-Na = 0.764).

50 Deviations from average vWF ligand size or healthy GPIbalpha-vWF-A1 binding kine

51 isolated buffer-perfused mouse lungs, basal vWF levels were significantly reduced in Galpha12(-/-),

52 Significant associations were found between vWF and cardiovascular events, stroke, mortality and ble

53 ation was critically dependent on bloodborne vWF and autocrine platelet stimulation.

54 ibitors abolished platelet spreading on both vWF and fibrinogen, indicating a role for PI3K in integr

55 on of the small GTPase Rap1 were impaired by vWF/p.V1316M following exposure to platelet agonists (th

56 Endothelial progenitor cells were CD31+, vWF+, and alpha-SMA- before seeding confirmed by immunoh

57 perfusion (500 s(-1), 10 min) over collagen, vWF, and collagen/vWF microspots, the amount of platelet

58 1), 10 min) over collagen, vWF, and collagen/vWF microspots, the amount of platelet deposition on the

59 t of fibrin(ogen) deposition on the collagen/vWF spots was approximately 2 times greater in compariso

60 mount of platelet deposition on the collagen/vWF spots was approximately 2 times greater in compariso

61 Combining vWF-Ag levels with MELD-Na improves risk stratification

62 In contrast, vWF was retained in Weibel-Palade storage granules of ar

63 hort course of cyclosporine did not decrease vWF release and platelet aggregation in PVG.1U (C6+) rec

64 hermore, Akt1- or Akt2-deficiency diminished vWF-induced cGMP elevation, and their inhibitory effects

65 site-as the main driving force defining DNA-vWF recognition.

66 n-size modulation, upon establishment of DNA-vWF interactions, to indirect steric hindrance and parti

67 nknown molecular mechanism governing the DNA-vWF interaction by integrating atomistic, coarse-grained

68 alpha12 and Galphaq/11 in basal vs evoked EC vWF secretion may provide promising new therapeutic stra

69 g that Galpha12 plays a prominent role in EC vWF secretion required for hemostasis and thrombosis.

70 l cells, flow provoked increased endothelial vWF secretion in the stenotic outlet region, contributin

71 Both PR3 and elastase induced endothelial vWF release, with elastase inducing the highest response

72 Accordingly, this study aimed to evaluate vWF-Ag as an adjunct surrogate marker for risk stratific

73 in minigene peptide blocked basal and evoked vWF secretion.

74 ause lung endothelial cells strongly express vWF.

75 Von Willebrand factor (vWF) adsorbs and immobilizes platelets at sites of injur

76 idenced by release of von Willebrand factor (vWF) and accompanied by platelet aggregation.

77 ologic degradation of von Willebrand factor (vWF) and bleeding from gastrointestinal angiodysplasia a

78 , granules containing von Willebrand factor (vWF) and P-selectin, which induce leukocyte rolling and

79 rombosis that include von Willebrand factor (vWF) and platelets.

80 luate vascular cells, von Willebrand factor (vWF) and vascular endothelial growth factor (VEGF)-C exp

81 The von Willebrand factor (vWF) antigen (vWF-Ag) correlates with portal pressure an

82 (PAI-1) antigen, and von Willebrand factor (vWF) antigen predicted incident diabetes independent of

83 ation and activity of von Willebrand factor (vWF) at poststenotic sites.

84 ce of variant type 2B von Willebrand factor (vWF) binding to blood platelets.

85 igens on secretion of von Willebrand factor (vWF) from endothelial cells (ECs).

86 he primary hemostatic von Willebrand factor (vWF) functions to sequester platelets from rheological b

87 c sequence within the von Willebrand factor (vWF) gene facilitates expression by endothelial cells re

88 ons of the biopolymer von Willebrand Factor (vWF) immersed in flow.

89 Collagen and/or von Willebrand Factor (vWF) in 5% glycerol was contact printed onto glass slide

90 I), VIII (FVIII), and von Willebrand factor (vWF) influence risk of hemorrhage and thrombosis.

91 Von Willebrand factor (vWF) is a biomarker of endothelial dysfunction.

92 von Willebrand factor (vWF) is a multimeric plasma glycoprotein with three tand

93 Von Willebrand factor (vWF) is inconsistently associated with cardiovascular di

94 t intron of the human von Willebrand factor (vWF) is required for gene expression in the endothelium

95 , angiopoietin-2, and von Willebrand Factor (vWF) levels were measured as biomarkers of endothelial a

96 von Willebrand factor (vWF) mediates platelet adhesion and thrombus formation v

97 VIII) and its carrier von Willebrand factor (vWF) play key roles in hemostasis.

98 nogen in concert with von Willebrand factor (vWF) potentiates S. aureus-platelet binding via shear-de

99 The platelet von Willebrand factor (vWF) receptor, glycoprotein Ib-IX (GPIb-IX), mediates pl

100 von Willebrand factor (vWF) secretion by endothelial cells (ECs) is essential f

101 ssect a mechanism for von Willebrand factor (vWF) secretion from endothelial cells mediated via Gaq/1

102 function mutations in von Willebrand factor (vWF) that enhance its binding to the glycoprotein Ib-IX-

103 CD31 and von Willebrand Factor (vWF) transcripts were predominantly expressed in the RNA

104 as baseline levels of von Willebrand factor (vWF) was an independent predictor of clinical outcome at

105 disease pigs, plasma von Willebrand factor (vWF) was significantly increased after lung transplantat

106 dothelial cells store von Willebrand Factor (vWF), a glycoprotein essential to haemostasis in Weibel-

107 ing the production of von Willebrand factor (vWF), a key initiator of the clotting cascade.

108 efore aimed to assess von Willebrand factor (vWF), a marker of endothelial damage, as potential bioma

109 coagulation factors, von Willebrand factor (vWF), and tissue factor (TF), were demonstrated in const

110 hesive blood protein, von Willebrand Factor (vWF), interacts with the extracellular DNA of NETs to po

111 The unfolding of von Willebrand Factor (vWF), one of the largest multimeric proteins in our body

112 t of the A1 domain of von Willebrand Factor (vWF), the ligand for receptor glycoprotein 1b on platele

113 uctures ("quanta") of von Willebrand factor (vWF), the main WPB cargo.

114 coprotein Ibalpha and von Willebrand factor (vWF), type 2M has decreased binding affinity between the

115 for the detection of von Willebrand factor (vWF), vascular endothelial growth factor (VEGF), insulin

116 ibrin, platelets, and von Willebrand factor (vWF), were identified predominantly in glomerular capill

117 rkers VE-cadherin and von Willebrand factor (vWF).

118 nd LDL-C), and plasma von Willebrand factor (vWF).

119 rkers CD31, CD34, and von Willebrand factor (vWF); and cytokeratins and CD68, markers for retinal pig

120 , -CD146, -CD45, and -von Willebrand factor (vWF)] designed to match the surface antigens on ovine pe

121 Endothelial von Willebrand Factor (vWF)release and calcium signaling were used as PAR activ

122 with the A1 domain of von Willebrand factor (vWF-A1).

123 and immunostains for von Willebrand factor (vWF; blood vessels), Ki-67 (dividing cells), CD15 (neutr

124 aspects of GPIbalpha-von-Willebrand-factor (vWF)-mediated interplatelet binding at high shear rates,

125 (H-E), Von Kossa, and von Willibrand factor (vWF) staining and terminal deoxynucleotidyl transferase

126 [PAI-1], D-dimer, and von Willebrand factor [vWF]) were measured in plasma.

127 ns of most (eg, CD31, von Willebrand factor [vWF], VE-cadherin, and intercellular adhesion molecule-2

128 oxide synthase(eNOS), von Willebrand factor(vWF), and CD31 after cardiac hypertrophy.

129 For vWF, 400 SNPs exceeded the threshold and marked 8 loci o

130 8 per IQR for PAI-1 (1.01-1.37) and 1.39 for vWF (1.09-1.77).

131 QR for PAI-1 (95% CI 1.41-1.70) and 1.49 for vWF (1.21-1.85).

132 ction (area under the curve [AUC] = 0.71 for vWF-Ag versus AUC = 0.65 for MELD; P = 0.2).

133 or WPB fusion at the plasma membrane and for vWF secretion.

134 n, while intron processing is irrelevant for vWF expression by megakaryocytes.(1)

135 c effects were measured by an ELISA for free vWF A1 binding sites and by a platelet function analyzer

136 istence of TTP-modifying genes distinct from vWF.

137 t different shear stresses (gain-of-function vWF-A1 < wt vWF-A1< loss-of-function vWF-A1).

138 Platelet interactions with loss-of-function vWF-A1 retain the catch-slip bond transition seen in wt-

139 unction vWF-A1 < wt vWF-A1< loss-of-function vWF-A1).

140 PAR1 peptide induced GEC vWF release to the same extent as PR3.

141 cytes admixed within tumors did not generate vWF-positive blood vessels during a similarly defined pe

142 average vWF ligand size or healthy GPIbalpha-vWF-A1 binding kinetics are observed in simulations to h

143 All three peptides inhibited GPIbalpha-vWF-mediated platelet aggregation induced under high she

144 lular trap formation, but involves GPIbalpha-vWF and CD40-CD40L-dependent platelet interactions.

145 The GPIbalpha-vWF-A1 bond formation rate is predicted to have piecewis

146 peptide specifically disrupted the GPIbalpha-vWF-A1 interaction.

147 dentify peptide antagonists of the GPIbalpha-vWF-A1 interaction.

148 n of two unactivated platelets via GPIbalpha-vWF-GPIbalpha bridging is developed and integrated with

149 e we show that increasing force on GPIbalpha/vWF bonds first prolonged ("catch") and then shortened (

150 lar Dynamics (MD) simulations of non-grafted vWF multimers subject to a shearing flow were used as in

151 poietic specific-surface (CD45) and granular vWF antibodies, as well as uncoated bare glass and subst

152 Higher vWF-Ag levels were associated with varices (odds ratio [

153 Immunohistochemical (anti-human vWF, CD45, GFAP, and Iba-1) and motor neuron histologica

154 with intron-containing and intronless human vWF promoter-luciferase constructs.

155 hat could be normalized by infusion of human vWF.

156 In humans, vWF levels predict the risk of myocardial infarction and

157 of platelet tethering to surface-immobilized vWF-A1 under hydrodynamic shear flow.

158 P5) as a candidate gene linked to changes in vWF plasma levels, though the functional relationship be

159 sting involvement of hypertonic signaling in vWF up-regulation.

160 of severe hypernatremia reversibly increases vWF mRNA in endothelial cells in culture and the rate of

161 WR increases vWF mRNA in liver and lung and raises vWF protein in blo

162 etylpenicillamine decreases ceramide-induced vWF release in a dose-dependent manner, whereas the NO s

163 nine methyl ester increases ceramide-induced vWF release.

164 d in Galpha12(-/-), whereas thrombin-induced vWF secretion was defective in both EC-Galphaq(-/-);Galp

165 d human umbilical vein ECs, thrombin-induced vWF secretion was reduced by 40%, whereas basal secretio

166 3, inhibited both basal and thrombin-induced vWF secretion, whereas overexpression of activated Galph

167 Exogenous ceramide induces vWF release from endothelial cells in a dose-dependent m

168 ombosis; however, the factors that influence vWF levels are not completely understood.

169 NAC also inhibited vWF-dependent platelet aggregation and collagen binding.

170 between flowing platelets and insolubilized vWF mutants.

171 Intraluminal vWF deposition was accompanied with thrombus formation,

172 by influencing the adhesive activity of its vWF cargo, may represent a novel mode of regulation of p

173 atelets may allow ADAMTS-13 to deplete large vWF multimers, causing bleeding.

174 used by adhesion of platelets to ultra-large vWF (ULVWF) multimers.

175 independent of its reported cognate ligands vWF, P-selectin or Mac-1, offering a potential target ag

176 ers such as TUBB3, an early neuronal marker; vWF, VEGFA, VEGFC and IL-8, endothelial markers; and PPA

177 To mimic the subendothelial matrix, vWF was microarrayed over sonicated type I collagen micr

178 Maximal vWF:Ag/Hb ratio expressed as percentage of baseline leve

179 Notably, maximal vWF:Ag/Hb ratio was lower in the FE 202158 than the argi

180 nked immunosorbent assay was used to measure vWF.

181 2 activation caused PR3 or elastase-mediated vWF release.

182 that RNA splicing plays a role in mediating vWF expression in the vasculature.

183 Furthermore, the mesangial vWF deposition was detectable in young eNOSKO mice in wh

184 A 26-year-old man with mild vWF deficiency (FvW:antigen 39 IU/dL; FvW:ristocetin cof

185 association between the A domains, modulates vWF-GPIbalpha binding and platelet activation under shea

186 The Ashwell receptor normally modulates vWF homeostasis and is responsible for thrombocytopenia

187 ch LacZ was targeted to the endogenous mouse vWF locus in the absence or presence of the native first

188 3-month waiting-list mortality (AUC, MELD-Na-vWF = 0.804).

189 significantly reduced vWF levels but normal vWF multimers and impaired laser-induced thrombus format

190 By contrast, fibrinogen, but not vWF, supports the adhesion of early growth phase S. aure

191 Most notably, vWF showed additional prognostic value beyond that achie

192 In the absence of vWF, platelet activation was normal, but platelet adhere

193 w paradigm in the function and activation of vWF.

194 that the post-exocytic adhesive activity of vWF towards platelets and plasma vWF at the endothelial

195 Based on IDI and NRI, addition of vWF to CHA2DS2-VASc statistically improved its predictiv

196 For major bleeding, the addition of vWF to HAS-BLED improved the c-index but not IDI or NRI.

197 ls with thrombin, and measured the amount of vWF released into the media.

198 dition of W6/32 did not change the amount of vWF released.

199 evaluation of a novel aptamer antagonist of vWF.

200 In particular, combined assessment of vWF and NT-proBNP improved risk prediction in this vulne

201 This might be explained by associations of vWF with type 2 diabetes mellitus and insulin resistance

202 exocytosis by measuring the concentration of vWF released into the media.

203 Concentrations of vWF were assessed in 457 patients with HFpEF enrolled as

204 s formation, whereas mesangial deposition of vWF was associated with mesangial matrix expansion.

205 The effect of vWF on prognosis was calculated using a Cox regression m

206 reduction of STXBP5 increased exocytosis of vWF and P-selectin.

207 in mediating lineage-specific expression of vWF in the endothelium.

208 Ultimately, inclusion of vWF-Ag into the MELD-Na equation significantly improved

209 g macromolecular conformation information of vWF multimers were used for training the RFA.

210 to endothelial injuries and the infusion of vWF concentrate.

211 Inhibition of vWF A1 binding activity was achieved with an EC(90) valu

212 e- and concentration-dependent inhibition of vWF activity and platelet function with duration of effe

213 nockin mice, the loss of the first intron of vWF resulted in a significant reduction of reporter gene

214 s have been associated with plasma levels of vWF and increased venous thrombosis risk.

215 Mice lacking Stxbp5 had higher levels of vWF in the plasma, increased P-selectin translocation, a

216 Higher levels of vWF were associated with risk of CVD in people with type

217 he waiting list displayed elevated levels of vWF-Ag (P < 0.001).

218 that in type 2B vWD, prolonged lifetimes of vWF bonds with GPIbalpha on circulating platelets may al

219 bleeding tendency that is linked to loss of vWF multimers and/or thrombocytopenia.

220 A single measurement of vWF-Ag at listing for OLT predicts early mortality.

221 is, are the primary activation mechanisms of vWF, and unfold the multimeric protein at flow rates tha

222 n allows copackaging of a variable number of vWF quanta within the continuous lumen of the trans-Golg

223 ng of liver revealed increased production of vWF protein by endothelium and increased number of micro

224 factor NFAT5 and its binding to promoter of vWF gene, suggesting involvement of hypertonic signaling

225 endothelial cells in culture and the rate of vWF secretion from them.

226 the activation and mechanical regulation of vWF activity during blood clotting.

227 There was enhanced release of vWF during activated neutrophil-endothelial cell cocultu

228 C6, but C6 deficiency limits the release of vWF from arterial endothelial cells.

229 centrations of complement, on the release of vWF from Weibel-Palade bodies (WPBs) in human umbilical

230 The release of vWF occurs during coculture and is sensitive to serine p

231 c oxide likely contributed to the release of vWF, leading to thrombus formation in this model.

232 ease (vWD), on the structure and rheology of vWF A1 domain adhesiveness to the platelet GPIbalpha rec

233 Indeed, although the storage of vWF in Weibel-Palade bodies (WPBs) of endothelial cells

234 gulate GPIbalpha binding and the strength of vWF-platelet interactions, which affects the vWD functio

235 kt1 or Akt2 diminished platelet spreading on vWF but not on immobilized fibrinogen.

236 do not elicit significant WPB exocytosis or vWF secretion from ECs in the absence of exogenous compl

237 ed platelets expressing either P-selectin or vWF, the cold ischemia time was significantly longer (88

238 FVIII, 5 loci were identified and overlapped vWF findings.

239 Pathologic vWF metabolism may be a mechanistic link between LVAD su

240 In the tissue factor-mediated pathway, vWF plays a role in platelet accumulation during thrombu

241 Plasma vWF level increased during the postoperative days, presu

242 activity of vWF towards platelets and plasma vWF at the endothelial surface reflects the size of thei

243 , no correlation was observed between plasma vWF level and severity of TTP, implying the existence of

244 CASA/Rk (a mouse strain with elevated plasma vWF) resulted in the appearance of spontaneous thrombocy

245 L; factor VIII 99%; normal multimeric plasma vWF pattern) was referred to our institution and underwe

246 ficantly contributes to prediction of plasma vWF and risk of stroke.

247 o increased the digestion of purified plasma vWF.

248 of the mesenteric venules and reduced plasma vWF multimers.

249 formed at exocytosis recruits soluble plasma vWF and that this process is reduced by treatments that

250 9, and P < 0.001, respectively) while plasma vWF was increased (P = 0.014) in IGT subjects compared t

251 published cutoff at a MELD-Na of 20 points (vWF-Ag, OR = 10.873, 95% confidence interval [CI], 3.160

252 Therefore, catch bonds may prevent vWF multimers from agglutinating platelets.

253 and the A1A2A3 domain complex in preventing vWF to bind spontaneously to GPIbalpha in solution under

254 verexpression of activated Galpha12 promoted vWF secretion.

255 ifies a role for the shear-sensitive protein vWF in transducing hemodynamic forces that are present a

256 by low levels of the prothrombotic proteins vWF, P-selectin, and ICAM1 and high levels of the antith

257 reases vWF mRNA in liver and lung and raises vWF protein in blood.

258 sodium within the physiological range raises vWF sufficiently to increase coagulability and risk of t

259 ontrol platelets pretreated with recombinant vWF/p.V1316M.

260 Here, we examined whether NAC could reduce vWF multimers, which polymerize in a manner similar to m

261 12(-/-) mice exhibited significantly reduced vWF levels but normal vWF multimers and impaired laser-i

262 Moreover, H(1)RKO-vWF(H1R) Tg mice exhibited decreased BBB permeability an

263 the von Willebrand factor promoter (H(1)RKO-vWF(H1R) Tg) were Bphs-resistant.

264 W6/32, L2, or L243 did not evoke significant vWF release above control IgG.

265 t has been recently demonstrated that single vWF molecules only adsorb significantly to collagen abov

266 We hypothesized that vWF-Ag levels may correlate with portal pressure, measur

267 en receptor signaling, further implying that vWF/p.V1316M acts directly on or downstream of Ca2+ rele

268 eta3 activation, was normal, indicating that vWF/p.V1316M acts downstream of Ca2+ release and upstrea

269 s or insulin resistance, which suggests that vWF may be a risk factor unique to these populations.

270 tively inhibited the interaction between the vWF-A1 domain and GPIbalpha-Fc in a concentration-depend

271 nts had 25% mortality after 53 months if the vWF-Ag was <315% compared to 15 months in patients with

272 shear-induced adsorption only occurs if the vWF-surface bonds are slip-resistant such that force-ind

273 Mutations in the vWF A1 domain that cause type 2B von Willebrand disease

274 tranded DNA binds to a specific helix of the vWF A1 domain, via three arginines.

275 medications) with the lowest quartile of the vWF distribution as the referent, the hazard ratio (HR)

276 eatening illness caused by deficiency of the vWF-cleaving protease ADAMTS13.

277 th statins produce shorter WPBs and that the vWF they release at exocytosis displays a reduced capabi

278 imately 4 times greater in comparison to the vWF spots.

279 mately 18 times greater in comparison to the vWF spots.

280 ectin in eNOSKO mice was consistent with the vWF behavior and suggested exocytosis of the Weibel-Pala

281 tality of 25% after 37 and 7 months if their vWF-Ag was <315% and >315%, respectively (P = 0.002).

282 glycoprotein Ibalpha (GPIbalpha) binding to vWF, which initiates platelet adhesion to injured vessel

283 In vitro, NAC reduced soluble plasma-type vWF multimers in a concentration-dependent manner and ra

284 er an initial description of type 2B variant vWF, the consequence of this spontaneous variant vWF bin

285 the consequence of this spontaneous variant vWF binding to platelets is viewed as a dysregulation of

286 emistry was employed to measure vascularity (vWF), neurogenesis (BrdU TUJ1, DCX and NeuN), synaptogen

287 The patient received factor VIII/vWF concentrate both during and after surgery without an

288 ice expressing a vWD-type 2B-associated vWF (vWF/p.V1316M), platelets from a patient with the same mu

289 01) and accumulation of low-molecular-weight vWF multimers (+40+/-5%, P<0.0001) and vWF degradation f

290 ificant degradation of high-molecular-weight vWF multimers (-9+/-1%, P<0.0001) and accumulation of lo

291 et aggregation/thrombi (e.g., stroke), where vWF levels directly correlate with severity of disease p

292 s were assessed by HVPG measurement, whereas vWF-Ag levels were measured by enzyme-linked immunosorbe

293 We tested whether vWF predicted incident CVD in 3799 Framingham Offspring

294 utathione [tGSH]) and plasma von Willebrand (vWF) factor levels were also measured.

295 ue expressed CARD8 and CARD8 correlated with vWF, CD163 and the expression of inflammatory genes, suc

296 The interaction of GPIbalpha with vWF-A1 under conditions of high shear stress is the firs

297 <315% compared to 15 months in patients with vWF-Ag >315% (P < 0.001).

298 ths compared with 59 months in patients with vWF-Ag <315%.

299 shear stresses (gain-of-function vWF-A1 < wt vWF-A1< loss-of-function vWF-A1).

300 oated microspheres to roll more slowly on WT vWF and WT A1 domains as flow increased from suboptimal