ライフサイエンスコーパス: prothrombotic

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

2 maximally activate platelets and render them prothrombotic.

3 stones, which are highly proinflammatory and prothrombotic.

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

5 he blood in high numbers, microparticles are prothrombotic.

6 oposed that the PDE5 inhibitor sildenafil is prothrombotic.

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

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

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

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 They involve prohemorrhagic and prothrombotic alterations at each of these steps.

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

26 y, characterized by compensatory increase in prothrombotic aminophospholipids (aPL) in circulating ce

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

28 Externalised PS is prothrombotic and attractive to phagocytes and activated

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

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

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

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

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

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

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

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

37 ents of blood coagulation and platelets have prothrombotic and proinflammatory functions independent

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

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

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

41 Resolution of detrimental I/RI-generated prothrombotic and proinflammatory responses is essential

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

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

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

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

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

47 have generally detrimental effects that are prothrombotic and proinflammatory.

48 The increased inflammatory, prothrombotic, and procoagulant responses following seve

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

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

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

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

53 inus rhythm present an opportunity to detect prothrombotic atrial remodeling through measurement of P

54 These prothrombotic autoantibodies, commonly found to be eleva

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

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

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

58 g immunothrombosis may, in part, explain the prothrombotic clinical presentations in COVID-19, and NE

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

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

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

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

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

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

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

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

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

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

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

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

71 Heparin-induced thrombocytopenia (HIT) is a prothrombotic disorder mediated by complexes between pla

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

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

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

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

76 rombotic events in the absence of associated prothrombotic disorders.

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

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

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

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

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

82 lasminogen activator (tPA), exacerbating the prothrombotic effect.

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 e a better adaptive response to protect from prothrombotic effects of hyperhomocysteinemia than CBS(-

90 role for COX1-derived prostacyclin from the prothrombotic effects of platelet COX1.

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

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

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

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

95 ABC treatment led to an inflammatory, prothrombotic endothelial phenotype that promoted platel

96 Solid tumors generate a prothrombotic environment capable of platelet activation

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

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

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

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

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

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

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

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

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

106 robably mediated through increased levels of prothrombotic factors.

107 cells, including induction of cytokines and prothrombotic factors.

108 provide evidence that organ involvement and prothrombotic features in COVID-19 are linked by immunot

109 Such a prothrombotic fibrin clot phenotype has been suggested a

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

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

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

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

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

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

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

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

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

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

120 ing mediators (SPMs) and proinflammatory and prothrombotic lipid mediators during DVT progression in

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

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

123 Prothrombotic markers are elevated at 1 week after ablat

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

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

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

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

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

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

130 terial and venous thrombosis through similar prothrombotic mechanisms.

131 nticoagulant therapy include thrombin, a key prothrombotic mediator.

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

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

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

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

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

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

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

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

140 modifies the thrombotic risk of this common prothrombotic mutation.

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

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

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

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

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

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

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

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

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

150 hanosensitive-dependent production of highly prothrombotic neutrophil extracellular traps.

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

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

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

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

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

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

157 ependent JNK2 activation is involved in this prothrombotic pathway.

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

159 ollowed by activation of proinflammatory and prothrombotic pathways.

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

161 CD69 deficiency promotes a prothrombotic phenotype characterized by increased VWF a

162 In addition, a systemic prothrombotic phenotype has been reported in patients wi

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

164 o revealed a quantifiable net shift toward a prothrombotic phenotype in HFD-fed mice.

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

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

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

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

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

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

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

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

173 Deletion of COX2 from ECs also resulted in a prothrombotic phenotype that was independent of local va

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

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

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

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

178 disease activity, endothelial function, and prothrombotic phenotype.

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

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

181 eased platelet sensitivity to agonists and a prothrombotic phenotype.

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

183 ced platelet reactivity and the accompanying prothrombotic phenotype.

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

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

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

187 and ensuing fibrin formation, resulting in a prothrombotic phenotype.

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

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

190 ecreasing VWF multimers size and hence their prothrombotic potential.

191 Patients showed typical lymphopenia, higher prothrombotic profile, and higher markers of inflammatio

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

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

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

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

196 E model and probed a set of metabolites with prothrombotic propensity in the inferior vena cava (IVC)

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

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

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

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

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

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

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

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

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

206 phenotype characterized by low levels of the prothrombotic proteins vWF, P-selectin, and ICAM1 and hi

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

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

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

210 d with imminent DVT, suggesting that it is a prothrombotic risk factor and promotional mechanism.

211 egrating TG and PG measurements may define a prothrombotic risk factor in diet-induced obesity.

212 Obesity is a prevalent prothrombotic risk factor marked by enhanced fibrin form

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

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

215 While the prothrombotic risk of severe hyperlipidemia has been est

216 The prothrombotic role for calpain was further confirmed by

217 ents aPL signaling, indicating a paradoxical prothrombotic role for TFPI.

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

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

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

221 of the development of a hypercoagulable and prothrombotic state among individuals afflicted by advan

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

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

224 A prothrombotic state and increased platelet reactivity ar

225 A prothrombotic state and increased platelet reactivity ar

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

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

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

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

230 Our results suggest that the prothrombotic state associated with hypercholesterolemia

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

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

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

234 The prothrombotic state in cancer can be reproduced by treat

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

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

237 Several mechanisms of the prothrombotic state in these patients have been proposed

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

239 On the other hand, a prothrombotic state increases the risk of thromboembolic

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

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

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

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

244 areness and mechanistic understanding of the prothrombotic state of COVID-19 patients are driving eff

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

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

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

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

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

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

251 disease 2019 (COVID-19) is associated with a prothrombotic state with a high incidence of thrombotic

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

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

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

255 ublished evidence for the concept of LC as a prothrombotic state, discuss discordant data, and highli

256 pathophysiological mechanisms involved: the prothrombotic state, hemodynamic and hormonal changes, r

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 lement cascade but hypothetically leads to a prothrombotic state.

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

262 chanisms contributing to the obesity-induced prothrombotic state.

263 platelet hyperreactivity and thus identify a prothrombotic state.

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

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

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

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

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

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

270 lipidemia may contribute to development of a prothrombotic state.

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

272 as well as by propelling platelets to a more prothrombotic state.

273 r dysfunction and a chronic inflammatory and prothrombotic state.

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

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

276 nt recipients manifest features of a chronic prothrombotic state.

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

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

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

280 1 may represent a possible target to prevent prothrombotic states.

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

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

283 xia upregulates fundamental inflammatory and prothrombotic stress genes.

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

285 ink between mortality, d-dimer values, and a prothrombotic syndrome has been reported in patients wit

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