ライフサイエンスコーパス: prothrombotic

1 racellular traps (NETs), is procoagulant and prothrombotic.

2 he blood in high numbers, microparticles are prothrombotic.

3 oposed that the PDE5 inhibitor sildenafil is prothrombotic.

4 h as solid tumors, have been suggested to be prothrombotic.

5 maximally activate platelets and render them prothrombotic.

6 syndrome (HUS) is characterized by profound prothrombotic abnormalities.

7 ead and neck trauma, sickle cell anemia, and prothrombotic abnormalities.

8 s suggest that plasmin may drive potentially prothrombotic aCL in genetically susceptible individuals

9 ombotic axis in CRPtg mice may elucidate the prothrombotic actions of CRP in unstable arterial diseas

10 Prothrombotic activation occurs to a greater extent in t

11 tissue injury in several disease states, has prothrombotic activity and is known to interact with Tol

12 rn support oxidation of HMGB1 unleashing its prothrombotic activity and promoting platelet aggregatio

13 novel findings suggest that contrary to the prothrombotic activity of oxidized low-density lipoprote

14 e anticoagulant activity of heparins and the prothrombotic activity of polyP.

15 Inflammatory cytokines that induced prothrombotic activity on endothelial cells caused the p

16 cleaves von Willebrand factor, reducing its prothrombotic activity.

17 Heparin-induced thrombocytopenia is a prothrombotic adverse drug effect induced by platelet-ac

18 induces heparin-induced thrombocytopenia, a prothrombotic adverse drug reaction caused by immunoglob

19 complexes activate platelets, leading to the prothrombotic adverse drug reaction heparin-induced thro

20 hrombocytopenia (HIT) is a relatively common prothrombotic adverse drug reaction of unusual pathogene

21 osed mechanisms linking inflammation and the prothrombotic AF state include endothelial activation/da

22 opose elevated plasma FVIII is an etiologic, prothrombotic agent after moderate but not extensive vas

23 gerated fluid-phased thrombosis dependent on prothrombotic agents such as tissue factor to a platelet

24 ing long-haul air travel, is associated with prothrombotic alterations in the hemostatic system in he

25 We examined the expression of several prothrombotic and antithrombotic genes in 25 biopsies wi

26 ETs) may result in chromatin release that is prothrombotic and cytotoxic.

27 A significant increase in relevant prothrombotic and inflammatory parameters in 43 APS pati

28 Moreover, some of the reactive Abs are prothrombotic and interfere with inactivation of thrombi

29 d myelopoiesis, platelet activation promotes prothrombotic and proatherogenic platelet/leukocyte aggr

30 e are concerns that tranexamic acid may have prothrombotic and proconvulsant effects.

31 hen released into the circulation, it exerts prothrombotic and proinflammatory activities by modulati

32 eosinophils may provoke the development of a prothrombotic and proinflammatory endothelial/endocardia

33 Solid-phase immunoglobulins initiated prothrombotic and proinflammatory functions in human mac

34 les fuse with the plasma membrane, releasing prothrombotic and proinflammatory messenger molecules.

35 ole for sphingolipids in contributing to the prothrombotic and proinflammatory phenotype of the obese

36 ecrease in platelet CD40L suggests that this prothrombotic and proinflammatory protein was derived pr

37 of a soluble form of CD40 ligand (sCD40L), a prothrombotic and proinflammatory protein with GP IIb/II

38 le of VWF and coresidents of the WPBs in the prothrombotic and proinflammatory response of endothelia

39 In endothelium, parmodulins inhibit prothrombotic and proinflammatory signaling without bloc

40 Considering that P-selectin induces prothrombotic and proinflammatory signaling, we studied

41 Its activation by thrombin stimulates prothrombotic and proinflammatory signaling, whereas its

42 nce diabetic subjects are characterized by a prothrombotic and proinflammatory status, we hypothesize

43 cular ATP and ADP, thereby eliminating these prothrombotic and proinflammatory stimuli.

44 have generally detrimental effects that are prothrombotic and proinflammatory.

45 /GOX causes lung injury combining oxidative, prothrombotic, and inflammatory components characteristi

46 biology and exhibits striking prohemostatic, prothrombotic, and proinflammatory effects in vivo.

47 ocket of thrombin promotes the procoagulant, prothrombotic, and signaling functions of the enzyme.

48 ge of substrates mediating its procoagulant, prothrombotic, and signaling functions.

49 t biological functions as a proinflammatory, prothrombotic, and vessel permeability-regulating factor

50 These prothrombotic autoantibodies, commonly found to be eleva

51 priming, triggering and yielding activated "prothrombotic behavior" for stimulated platelets, even i

52 ing time, but significantly reduced platelet prothrombotic capacity after carotid injury.

53 nflammation, to be a master regulator of the prothrombotic cascade involving platelets and myeloid le

54 dysfunction in cerebral SVD, and endothelial prothrombotic changes may be important in mediating the

55 arrier, impaired cerebral autoregulation and prothrombotic changes, is believed to be important in me

56 Heparin-induced thrombocytopenia (HIT) is a prothrombotic complication of heparin therapy caused by

57 the de novo synthesis of proinflammatory and prothrombotic compounds and might thus have a role as an

58 included the presence of a mechanical valve, prothrombotic condition, and an acute infection at the t

59 r to standard care in the prevention of most prothrombotic conditions.

60 evated plasma levels of the proinflammatory, prothrombotic cytokine CD40 ligand (sCD40L).

61 n bronchoalveolar fluid concentration of the prothrombotic cytokine IL-6.

62 risks of these outcomes are exacerbated by a prothrombotic diathesis and hypokalaemia.

63 se that anti-A2 antibodies contribute to the prothrombotic diathesis in antiphospholipid syndrome.

64 o induce anti-PF4/polyanion antibodies and a prothrombotic diathesis.

65 , reduce microalbuminuria and ameliorate the prothrombotic diathesis.

66 ascular TF has been reported in a variety of prothrombotic diseases, but there is debate as to whethe

67 scular injury and circulate in patients with prothrombotic diseases, we hypothesized that PS exposed

68 Heparin-induced thrombocytopenia is a prothrombotic disorder caused by antibodies to platelet

69 Heparin-induced thrombocytopenia (HIT) is a prothrombotic disorder initiated by antibodies against c

70 HIT is a prothrombotic disorder that typically presents with a 50

71 heparin-induced thrombocytopenia (HIT)-like prothrombotic disorder.

72 ations between arterial perinatal stroke and prothrombotic disorders, but population-based, controlle

73 in sickle cell disease and more recently in prothrombotic disorders, moyamoya, and nitric oxide regu

74 rombotic events in the absence of associated prothrombotic disorders.

75 in hematopoietic cells was the source of the prothrombotic effect in deep vein thrombosis.

76 nclude that platelet TLR4 contributes to the prothrombotic effect of cellular Fn-EDA+, suggesting ano

77 ism and cell types involved in mediating the prothrombotic effect of Fn-EDA+ still remain unknown.

78 thrombosis and has been shown to enhance the prothrombotic effect of FVL in vitro.

79 ally blocks, and 15H8 completely blocks, the prothrombotic effect of fXII in this model.

80 These observations demonstrate the prothrombotic effect of modest variations in the level o

81 ies released by activated neutrophils have a prothrombotic effect, mediated in part by inhibition of

82 following vascular injury in vivo and these prothrombotic effects appear to be mediated through the

83 Besides its well-known prothrombotic effects Fg seems to have other destructive

84 rmine whether carbamylated LDL (cLDL) exerts prothrombotic effects in vascular cells and platelets an

85 We found that cLDL induces prothrombotic effects in vascular cells and platelets by

86 ested notions, we were unable to demonstrate prothrombotic effects of AF-related remodeling.

87 In this study, we examined the prothrombotic effects of anti-CD40L ICs in vivo.

88 isolated from patients with CKD mimicked the prothrombotic effects of cLDL on vascular cells, platele

89 hin subunit B (His95Arg), might modulate the prothrombotic effects of estrogen and help to explain th

90 agonists may obviate the proinflammatory and prothrombotic effects of sCD40L.

91 that CRP may have direct proinflammatory and prothrombotic effects on monocytes and endothelial cells

92 findings have clearly demonstrated that the prothrombotic effects seen in a mouse model of this synd

93 The implications of prothrombotic effects, which extend downstream beyond th

94 e related to oestrogen's proinflammatory and prothrombotic effects.

95 yclin/thromboxane in favor of thromboxane, a prothrombotic eicosanoid.

96 ed increases in circulating inflammatory and prothrombotic elements, notably lower viremia levels, le

97 Solid tumors generate a prothrombotic environment capable of platelet activation

98 procedural events might also be related to a prothrombotic environment or state generated by the impl

99 m-targeted thromboprophylaxis triggered by a prothrombotic enzyme illustrates a novel approach to tim

100 nclusion, the H2S pathway is involved in the prothrombotic events occurring in hyperhomocysteinemic p

101 subset of such antibodies is associated with prothrombotic events such as stroke and with adverse pre

102 ted adverse reactions, such as a bleeding or prothrombotic events.

103 ue factor has been recognized as a potential prothrombotic factor initiating thrombosis after vascula

104 nd Shea report that the morning surge of the prothrombotic factor plasminogen activator inhibitor-1 (

105 inhibits fibrinolysis, is a key circulating prothrombotic factor that rises in the morning in humans

106 We sought to confirm that carriers of this prothrombotic factor V Leiden mutation do not have an in

107 de reduced expression of proinflammatory and prothrombotic factors in adipose tissue and increased ex

108 h an adverse cardiovascular risk profile and prothrombotic factors that, along with migraine-specific

109 cells, including induction of cytokines and prothrombotic factors.

110 robably mediated through increased levels of prothrombotic factors.

111 Such a prothrombotic fibrin clot phenotype has been suggested a

112 has relevance to the primary haemostatic and prothrombotic function of platelets.

113 BM chimeras revealed that P2X7 receptor prothrombotic function was present in both hematopoietic

114 t antibody (14E11) that selectively inhibits prothrombotic FXI activation by activated FXII (FXIIa) m

115 re polymicrobial abdominal infection induces prothrombotic FXI activation, to the detriment of the ho

116 of the pedigree supported the presence of a prothrombotic gene on chromosome 11q23 (nominal P < .000

117 The factor V Leiden mutation (R506Q), a prothrombotic gene polymorphism, disrupts the activity o

118 emiological findings associating variants in prothrombotic genes with atherogenesis and atherothrombo

119 erandrogenic conditions, and the presence of prothrombotic genetic disorders is needed to address thi

120 row therapeutic window, and is paradoxically prothrombotic in certain settings (ie, can precipitate "

121 ) may inhibit tPA activity and, thus, may be prothrombotic in the host.

122 nt function of APC and are thus likely to be prothrombotic in the host.

123 and migration, and in platelets SR-BI may be prothrombotic in the setting of dyslipidemia.

124 CD40L is a proinflammatory and prothrombotic ligand in the tumor necrosis factor family

125 extensive vascular damage with multifaceted prothrombotic local imbalance are characteristics of pur

126 urse of inflammation, myocardial injury, and prothrombotic markers after radiofrequency ablation for

127 Prothrombotic markers are elevated at 1 week after ablat

128 Inflammatory and prothrombotic markers are elevated in individuals with m

129 Inflammatory and prothrombotic markers are predictors for a change in kid

130 er with increasing number of inflammatory or prothrombotic markers that were above the median (below

131 A5 anticoagulant shield may be an important prothrombotic mechanism in the aPL syndrome.

132 eover, they define a previously unrecognized prothrombotic mechanism that is not detected by conventi

133 hydroxychloroquine (HCQ), might affect this prothrombotic mechanism.

134 n incomplete understanding of the underlying prothrombotic mechanisms and by uncertainties about risk

135 d a molecule, A1-A1, which interferes with 2 prothrombotic mechanisms in APS: the binding of beta2GPI

136 To better understand the potential prothrombotic mechanisms underlying the formation of the

137 terial and venous thrombosis through similar prothrombotic mechanisms.

138 nticoagulant therapy include thrombin, a key prothrombotic mediator.

139 m by which CO interrupts proinflammatory and prothrombotic mediators of ischemic injury.

140 othelial exocytosis of granules that contain prothrombotic mediators such as von Willebrand Factor (V

141 ndoxyl sulfate (IS) is a potent CKD-specific prothrombotic metabolite that induces tissue factor (TF)

142 LA dilation and dysfunction form a prothrombotic milieu characterized by blood stasis and e

143 Tissue factor (TF), a potent prothrombotic molecule, is expressed by macrophages and

144 increased generation of proinflammatory and prothrombotic molecules and reactive oxygen species trig

145 mbosis, involving elevated expression of the prothrombotic molecules plasminogen activator inhibitor-

146 ts as risk modifiers of pregnancy failure in prothrombotic mothers.

147 The generation of prothrombotic MPs required P2X7 receptor-dependent produ

148 Our findings demonstrate that fetal prothrombotic mutations can cause localized activation o

149 by reports suggesting that co-inheritance of prothrombotic mutations may ameliorate the clinical phen

150 not with disease progression before PVT, or prothrombotic mutations.

151 have significantly elevated plasma levels of prothrombotic N-Hcy-fibrinogen.

152 in aPC generation and may contribute to the prothrombotic nature of HIT.

153 We suggest that the prothrombotic nature of smoking could be a cause of elev

154 Due to its prothrombotic nature, early recognition of HIT and promp

155 Associated conditions were hematologic, prothrombotic, neoplastic, immune, and exposure to toxin

156 er, disulfide HMGB1 facilitates formation of prothrombotic neutrophil extracellular traps (NETs) medi

157 ency ablation (RFA) to create a quantifiable prothrombotic nidus.

158 ng polymers are able to scavenge effectively prothrombotic nucleic acids and other polyphosphates in

159 Alterations in circulating prothrombotic or antifibrinolytic mediators in the "flui

160 discuss the evidence for the existence of a prothrombotic or hypercoagulable state associated with t

161 triad for thrombogenesis, and accord with a prothrombotic or hypercoagulable state in this arrhythmi

162 Atrial fibrillation is associated with a prothrombotic or hypercoagulable state, which may contri

163 ities, thus fulfilling the requirement for a prothrombotic or hypercoagulable state.

164 oxidative stress in the pathogenesis and the prothrombotic or proinflammatory status of antiphospholi

165 -to-adiponectin ratio) (73%), and much lower prothrombotic PAI-1 levels (19%).

166 ependent JNK2 activation is involved in this prothrombotic pathway.

167 ion as key modulators of proinflammatory and prothrombotic pathways in obesity, are also reviewed.

168 ollowed by activation of proinflammatory and prothrombotic pathways.

169 es of TSP-4 (P387) and may contribute to the prothrombotic phenotype associated with this variant.

170 This is the first report of a prothrombotic phenotype directly attributable to the pre

171 latelet SR-BI deficiency protected mice from prothrombotic phenotype in 2 types of dyslipidemia assoc

172 These studies reveal a potent vascular prothrombotic phenotype in Gla-deficient mice and sugges

173 de and biliverdin administration rescued the prothrombotic phenotype in Hmox1-/- mice.

174 e platelet surface and are consistent with a prothrombotic phenotype in Ser-700 individuals.

175 enhanced procoagulant activity, assembling a prothrombotic phenotype in vivo.

176 broaden our mechanistic understanding of the prothrombotic phenotype observed during cellular damage

177 static and flow conditions, and, in vivo, a prothrombotic phenotype occurred in mice with a platelet

178 als, thus highlighting a proinflammatory and prothrombotic phenotype of DGKepsilon-deficient ECs.

179 on the endothelium, thereby perpetuating the prothrombotic phenotype of the endothelium.

180 ed disturbed flow leads to a proadhesive and prothrombotic phenotype that promotes atherothrombosis.

181 In addition, shorter bleeding times and a prothrombotic phenotype were observed in mice lacking TU

182 tial therapies designed to reverse patients' prothrombotic phenotype, such as selective plasma factor

183 electin glycoprotein ligand-1 did not have a prothrombotic phenotype.

184 disease activity, endothelial function, and prothrombotic phenotype.

185 a central role in the hyperglycemia-related prothrombotic phenotype.

186 pocynin, Tempol) abrogates the hypertensive, prothrombotic phenotype.

187 eased platelet sensitivity to agonists and a prothrombotic phenotype.

188 on compared with wild-type mice indicating a prothrombotic phenotype.

189 ced platelet reactivity and the accompanying prothrombotic phenotype.

190 s between dyslipidemia, oxidant stress and a prothrombotic phenotype.

191 ing activity of TSP-1 underlies the observed prothrombotic phenotype.

192 ) particles, a process that induces an overt prothrombotic phenotype.

193 lyzed to elucidate the acute hypoxia-induced prothrombotic phenotype.

194 Dyslipidemia is associated with a prothrombotic phenotype; however, the mechanisms respons

195 ized low-density lipoprotein (oxLDL)-induced prothrombotic platelet signaling and the inhibition of e

196 The effect of prothrombotic polymorphism, factor V Leiden (Arg506Gln;

197 nts that contribute to vascular bed-specific prothrombotic potential.

198 ecreasing VWF multimers size and hence their prothrombotic potential.

199 elin displayed a shorter bleeding time and a prothrombotic profile.

200 Tipping the balance toward a prothrombotic, proinflammatory phenotype results from mu

201 l. report possible mechanisms underlying the prothrombotic, proinflammatory state accompanying hyperc

202 idant systems in VSMCs may contribute to its prothrombotic, proinflammatory, and atherogenic effects.

203 A1-A1 inhibits prothrombotic properties of beta2GPI/antibody complexes

204 ceptor/counterreceptor systems regulates the prothrombotic properties of PMN-derived MPs.

205 The results suggest that these prothrombotic properties should be considered when devel

206 Histones may combine microbicidal with prothrombotic properties to fight invading microbes and

207 ins (N-Hcy-protein) with autoimmunogenic and prothrombotic properties.

208 rates N-Hcy-protein with autoimmunogenic and prothrombotic properties.

209 by microscopy, with no influence on platelet prothrombotic properties.

210 ion, selective fibrinopeptide A release, and prothrombotic properties.

211 ts, we investigated alterations in levels of prothrombotic proteins (plasminogen activator inhibitor

212 ccine-induced alterations in levels of these prothrombotic proteins do not appear to play a role in i

213 uman AF, but whether acute onset AF alone is prothrombotic remains unclear.

214 cripts for genes regulating the inflammatory/prothrombotic response were diminished in Egr-1-/-/apoE-

215 sion of Egr-1 leading to proinflammatory and prothrombotic responses in diabetic atherosclerosis.

216 eedback loop that limits proinflammatory and prothrombotic responses in human monocytes stimulated wi

217 iting events are often involved; one or more prothrombotic risk factors are common; recurrence is com

218 xcessive permeability to PFC-NP may indicate prothrombotic risk in damaged atherosclerotic vasculatur

219 The prothrombotic role for calpain was further confirmed by

220 To investigate the prothrombotic role of oxidative stress during aging, we

221 s usually abnormal, but echocardiography and prothrombotic screening are commonly negative.

222 s abrogated by coxibs, which may explain the prothrombotic side-effects for this class of drugs.

223 Insulin resistance, inflammation and a prothrombotic state acutely emerge.

224 from alveolar macrophages is required for a prothrombotic state and acceleration of thrombosis follo

225 (s) may act as critical modulators linking a prothrombotic state and hyperlipidemia.

226 A prothrombotic state and increased platelet reactivity ar

227 A prothrombotic state and increased platelet reactivity ar

228 mbotic and hemostatic markers that promote a prothrombotic state and inflammation, cross-reactive sys

229 f inflammation are related to indexes of the prothrombotic state and may be related to the clinical v

230 monstrate that GPx-3 deficiency results in a prothrombotic state and vascular dysfunction that promot

231 lots to lysis, and thereby contribute to the prothrombotic state associated with homocysteinemia.

232 Our results suggest that the prothrombotic state associated with hypercholesterolemia

233 ch fetal loss is triggered when the maternal prothrombotic state coincides with fetal gene defects th

234 vascular endothelium and its transition to a prothrombotic state during an inflammatory response.

235 a relationship between inflammation and the prothrombotic state in atrial fibrillation (AF).

236 The prothrombotic state in cancer can be reproduced by treat

237 The many signs and symptoms of the prothrombotic state in cancer range from asymptomatic ba

238 ded to examine the mechanisms leading to the prothrombotic state in cancer, the potential prognostic

239 t activation of monocytes contributes to the prothrombotic state in HIT and showed that HIT antibodie

240 key role in platelet hyperreactivity and the prothrombotic state in the setting of hyperlipidemia by

241 ctivated by HIT antibodies contribute to the prothrombotic state in vivo, but the mechanism by which

242 that a potential mechanism for an increased prothrombotic state is the post-translational modificati

243 can cause a platelet rebound phenomenon and prothrombotic state leading to major adverse cardiovascu

244 nderstanding of the events that initiate the prothrombotic state may improve approaches to antithromb

245 us, in obese patients, clinical markers of a prothrombotic state may indicate a risk for the developm

246 f inflammation in the pathophysiology of the prothrombotic state of AF has not been studied in detail

247 gesting that these drugs may contribute to a prothrombotic state provides support for this concern.

248 eased circulating protein C is a marker of a prothrombotic state that has been associated with poor c

249 Asthmatic patients have a prothrombotic state that increases with asthma severity.

250 Obesity also leads to a proinflammatory and prothrombotic state that potentiates atherosclerosis.

251 a2AR signaling promoted the development of a prothrombotic state that was sufficient to accelerate ar

252 It is unknown whether these patients have a prothrombotic state under stable conditions.

253 iated conditions (e.g., a proinflammatory or prothrombotic state) in the absence of offspring obesity

254 d blood pressure, elevated plasma glucose, a prothrombotic state, and a proinflammatory state.

255 d blood pressure, elevated plasma glucose, a prothrombotic state, and a proinflammatory state.

256 tein [CRP] and interleukin-6 [IL-6]) and the prothrombotic state, including markers of platelet activ

257 re, we examined whether NAFLD is linked to a prothrombotic state, independently of metabolic risk fac

258 deficiency abrogates the ADAMTS13-deficient prothrombotic state, suggesting VWF as the only relevant

259 dothelial microparticles (MPs), leading to a prothrombotic state, which may contribute to acute occlu

260 chanisms contributing to the obesity-induced prothrombotic state.

261 platelet hyperreactivity and thus identify a prothrombotic state.

262 nfer that loss of DGKE function results in a prothrombotic state.

263 lease of large quantities of chromatin and a prothrombotic state.

264 ies can lead to a limb- and life-threatening prothrombotic state.

265 kle cell disease (SCD) is characterized by a prothrombotic state.

266 (EC) abnormalities might contribute to this prothrombotic state.

267 nt recipients manifest features of a chronic prothrombotic state.

268 other risk factors, predisposes to an early prothrombotic state.

269 lipidemia may contribute to development of a prothrombotic state.

270 diate the elevation of PAI-1 that promotes a prothrombotic state.

271 r dysfunction and a chronic inflammatory and prothrombotic state.

272 ms by which adherent leukocytes can induce a prothrombotic state.

273 in (PGI2) contribute to a proatherogenic and prothrombotic state.

274 lows that the presence of a tumour confers a prothrombotic state.

275 s well as sustained insulin resistance and a prothrombotic state.

276 lement cascade but hypothetically leads to a prothrombotic state.

277 hages attenuated PM-induced IL-6 release and prothrombotic state.

278 h can augment platelet function leading to a prothrombotic state.

279 of the cyclooxygenase-2 enzyme to promote a prothrombotic state; observational data suggesting an in

280 d establish premonitory, proinflammatory and prothrombotic states in anticipation of either injury or

281 ctions, malposition of the catheter tip, and prothrombotic states.

282 1 may represent a possible target to prevent prothrombotic states.

283 ficient to decrease abnormal TF activity and prothrombotic status in COX-2 knockout mice.

284 xia upregulates fundamental inflammatory and prothrombotic stress genes.

285 crofluidics combined with micropatterning of prothrombotic substrates provides devices for measuring

286 to interact in an additive manner to yield a prothrombotic system.

287 risk of hypercoagulopathy with an increased prothrombotic tendency also warrants consideration.

288 on during inflammation and contribute to the prothrombotic tendency associated with inflammation.

289 This prothrombotic tendency was associated with increased gen

290 eatment duration is unclear, but because the prothrombotic tendency will persist in patients with adv

291 er-induced IL-6 production and the resultant prothrombotic tendency.

292 mplement-dependent membrane perturbations to prothrombotic TF activation on myeloid cells.

293 owever, the molecular pathways that generate prothrombotic TF in vivo are poorly defined.

294 r-dependent signaling pathway that generates prothrombotic TF, defining a link between inflammation a

295 (or autoimmune HIT), defined as a transient prothrombotic thrombocytopenic disorder without proximat

296 s well as the NFkappaB-related expression of prothrombotic tissue factor.

297 Endothelial cells secrete prothrombotic ultralarge von Willebrand factor (VWF) mul

298 b and trigger the AP, and the release of the prothrombotic von Willebrand factor.

299 nship between the magnitude of the effective prothrombotic zone and the interval distance between TF

300 We define an effective prothrombotic zone that extends well beyond the dimensio