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

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

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

17 The relationship to abnormal vWF metabolism is unknown.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

39 e functional relationship between STXBP5 and vWF is unknown.

40 dU labeling of neuroproliferative zones, and vWF-immunoreactive vascular profiles, without and with i

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

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

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

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

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

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

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

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

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

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

51 affect integrin activation, as indicated by vWF-induced fibrinogen binding, but affected cell spread

52 Human platelet aggregation induced by vWF or low-dose thrombin was inhibited by PKG inhibitors

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

54 When expressed in AtT-20 cells, vWF leads to the de novo formation of cigar-shaped organ

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

56 1), 10 min) over collagen, vWF, and collagen/vWF microspots, the amount of platelet deposition on the

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

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

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

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

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

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

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

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

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

66 in minigene peptide blocked basal and evoked vWF secretion.

67 ause lung endothelial cells strongly express vWF.

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

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

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

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

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

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

74 g with TUNEL and anti-von Willebrand factor (vWF) antibody showed that apoptotic cells in immature gl

75 Circulating plasma von Willebrand factor (vWF) antigen is a marker of generalized endothelial dysf

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

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

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

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

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

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

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

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

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

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

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

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

88 ) Ib-IX-V complex and von Willebrand factor (vWF) is the first step of the hemostatic response to ves

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

90 the platelet receptor von Willebrand factor (vWF) on cold preserved SEC.

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

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

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

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

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

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

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

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

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

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

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

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

103 creased expression of von Willebrand factor (vWF), CD41, and P-selectin in 48%, 30%, and 13% of allog

104 platelet receptor for von Willebrand factor (vWF), glycoprotein Ib-IX, integrin alphaIIb, and mutants

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

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

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

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

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

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

111 d cell model enhanced von Willebrand factor (vWF)-induced activation of the platelet integrin alpha(I

112 receptors, and plasma von Willebrand factor (vWF)-like soluble proteins.

113 main of surface-bound von Willebrand factor (vWF).

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

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

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

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

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

119 with anti-TM and anti-von Willebrand factor (vWF; an endothelial cell marker) antibodies.

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

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

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

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

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

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

126 8 per IQR for PAI-1 (1.01-1.37) and 1.39 for vWF (1.09-1.77).

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

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

129 se hemostasis by increasing the affinity for vWF.

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

131 valine alters the affinity of GPIbalpha for vWF, with mutations K237V and Q232V, respectively, showi

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

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

134 istence of TTP-modifying genes distinct from vWF.

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

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

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

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

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

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

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

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

143 n and dissociation kinetics of the GPIbalpha-vWF-A1 bond.

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

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

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

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

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

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

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

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

152 hat could be normalized by infusion of human vWF.

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

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

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

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

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

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

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

160 nine methyl ester increases ceramide-induced vWF release.

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

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

163 3, inhibited both basal and thrombin-induced vWF secretion, whereas overexpression of activated Galph

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

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

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

167 between flowing platelets and insolubilized vWF mutants.

168 Intraluminal vWF deposition was accompanied with thrombus formation,

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

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

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

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

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

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

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

176 nked immunosorbent assay was used to measure vWF.

177 2 activation caused PR3 or elastase-mediated vWF release.

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

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

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

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

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

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

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

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

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

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

188 w paradigm in the function and activation of vWF.

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

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

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

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

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

194 evaluation of a novel aptamer antagonist of vWF.

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

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

197 Thus, binding of vWF to its major physiological ligands may promote the f

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

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

200 n surfaces coated with limiting densities of vWF-A1, revealed that the Q232V and K237V dissociated 1.

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

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

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

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

205 to endothelial injuries and the infusion of vWF concentrate.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

228 237V, rolled very slowly and continuously on vWF-A1 surface while the loss-of-function mutant, Q232V,

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

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

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

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

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

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

235 Plasma vWF level increased during the postoperative days, presu

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

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

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

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

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

241 is due to the spontaneous binding of plasma vWF to circulating platelets.

242 o increased the digestion of purified plasma vWF.

243 of the mesenteric venules and reduced plasma vWF multimers.

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

245 9, and P < 0.001, respectively) while plasma vWF was increased (P = 0.014) in IGT subjects compared t

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

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

248 verexpression of activated Galpha12 promoted vWF secretion.

249 a cGMP-enhancing agent, sildenafil, promoted vWF- or thrombin-induced platelet aggregation.

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

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

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

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

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

255 12(-/-) mice exhibited significantly reduced vWF levels but normal vWF multimers and impaired laser-i

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

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

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

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

260 ha subunit beta-propeller and a beta subunit vWF type A domain.

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

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

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

264 The results suggest that vWF domain A1 inhibits the cleavage of domain A2, and th

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

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

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

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

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

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

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

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

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

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

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

276 netics of the GPIbalpha interaction with the vWF-A1 domain under dynamic flow conditions.

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

278 Platelet adhesion to vWF was impaired in P2Y12-/- platelets.

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

280 t mice showed impaired platelet responses to vWF or low doses of thrombin and prolonged bleeding time

281 ve analysis showed significantly fewer TUNEL/vWF-labeled cells in glomeruli after anti-TGF-beta1 anti

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

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

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

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

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

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

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

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

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

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

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

293 -Palade bodies of endothelial cells in which vWF is normally stored before regulated secretion.

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

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

296 ld-type or mutant GPIbalpha interacting with vWF-A1-coated surfaces at different shear stresses.

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