ライフサイエンスコーパス: thrombosis

1 tion (AMR), complement activation, and graft thrombosis.

2 or in combination increase cancer-associated thrombosis.

3 r primary and secondary prevention of venous thrombosis.

4 the relatively higher incidence of scaffold thrombosis.

5 diac death, reinfarction, and definite stent thrombosis.

6 sis, inflammation, vascular dysfunction, and thrombosis.

7 nuous-flow pump that was engineered to avert thrombosis.

8 ber of granule-containing MCs decreased with thrombosis.

9 implicated to play a role in hemostasis and thrombosis.

10 elial cell death and desquamation, and mural thrombosis.

11 thmias, arteriosclerosis, stroke, and venous thrombosis.

12 or vena cava (IVC) ligation to induce venous thrombosis.

13 play a major role in hemostasis and arterial thrombosis.

14 voked VTE, pulmonary embolism, and deep-vein thrombosis.

15 3- kinase (PI3K) and contributes to arterial thrombosis.

16 ically been considered passive bystanders in thrombosis.

17 recruitment and NET formation at the site of thrombosis.

18 in did not exhibit increased inflammation or thrombosis.

19 selective antagonist of PAR1 used to prevent thrombosis.

20 rocoagulant-anticoagulant equilibrium toward thrombosis.

21 ependent manner, even after establishment of thrombosis.

22 h BVS than EES, particularly TVMI and device thrombosis.

23 come measure was definite or probable device thrombosis.

24 e increased risk of late and very late stent thrombosis.

25 lation of platelet function, haemostasis and thrombosis.

26 event can be exacerbated by inflammation and thrombosis.

27 identifies a novel mechanism for controlling thrombosis.

28 sfer of in vitro differentiated MCs restored thrombosis.

29 lecule targeting of Mac-1:GPIbalpha inhibits thrombosis.

30 ontribution to biliary complications from HA thrombosis.

31 nes, with widespread pulmonary microvascular thrombosis.

32 gical evidence of hemorrhage organization or thrombosis.

33 nslating into lower risk of subsequent stent thrombosis.

34 ed with the FeCl3 model of mesenteric artery thrombosis.

35 ted tuberculosis complicated by splenic vein thrombosis.

36 The confluence was narrowed but without thrombosis.

37 eling contributes to in-stent restenosis and thrombosis.

38 latory support is associated with subsequent thrombosis.

39 and plays a critical role in hemostasis and thrombosis.

40 rotection conferred by miR-223 deficiency on thrombosis.

41 the morbidity and mortality associated with thrombosis.

42 uring plasmatic coagulation, hemostasis, and thrombosis.

43 on, but it is not clear if it contributes to thrombosis.

44 , but not in the normal circulation to avoid thrombosis.

45 ell-rich areas are susceptible to subsequent thrombosis.

46 whether in the presence or absence of venous thrombosis.

47 gation and contraction during hemostasis and thrombosis.

48 pendent predictor of 3-year TLF and scaffold thrombosis.

49 data sets on the effect of OC use and venous thrombosis.

50 or grade 1 and 2 arterial and grade 1 venous thrombosis.

51 ortal vein, and 3 (3.1%) had post-transplant thrombosis.

52 helial cell damage, platelet activation, and thrombosis.

53 rdiac death, myocardial infarction, or stent thrombosis.

54 children but is complicated by bleeding and thrombosis.

55 rdiac death, myocardial infarction, or stent thrombosis.

56 ogical hemostasis or pathological process of thrombosis.

57 iods (74% and 76%) were not related to stent thrombosis.

58 upper limb ischemia caused by radial artery thrombosis.

59 is associated with increased risk of venous thrombosis.

60 dies evaluating leaflet immobility and valve thrombosis.

61 evention or treatment of subclinical leaflet thrombosis.

62 herapeutic target for prevention of arterial thrombosis.

63 tality, 43.7% disability, and 9.8% deep vein thrombosis.

64 ependent feedback loops enhances the risk of thrombosis.

65 spital are at increased risk of bleeding and thrombosis.

66 ormed ferric chloride-induced carotid artery thrombosis.

67 telet-specific CLEC-2 knockout mice restored thrombosis.

68 se inactivation, increase the risk of venous thrombosis.

69 seminated complement-dependent macrovascular thrombosis.

70 tening complications of thrombocytopenia and thrombosis.

71 6 points, P<0.001) or medically managed pump thrombosis (0 versus 5 points, P=0.02), and fewer nondis

72 .64 [95% CI 1.03-2.61], p=0.0376) and device thrombosis (0.5% [11 of 2085] vs none [0 of 1183], p<0.0

73 juries (14 with neonatal cerebral sinovenous thrombosis, 11 with hypoxic ischemic encephalopathy, and

74 ervention (62%), arrhythmia treatment (32%), thrombosis (12%), and protein-losing enteropathy (8%).

75 BVS (8.6% vs. 5.9%; p = 0.03), as was device thrombosis (2.3% vs. 0.7%; p = 0.01).

76 to harm: 41; p = 0.003; I(2) = 0%) and stent thrombosis (2.4% vs. 0.7%; absolute risk difference: +1.

77 chemic stroke, and 1 (0.1%) with deep venous thrombosis; 28 patients (2.4%) died for cardiovascular c

78 ridine had greater reductions in MI or stent thrombosis (3.0% vs. 6.1%; p < 0.001) compared with subj

79 three (23.5%) patients had MPV (single site) thrombosis, 55 (56.1%) had multiple site-thrombosis (MPV

80 r patients with symptomatic superficial-vein thrombosis a less burdensome and less expensive oral tre

81 The rate of stent thrombosis, a safety indicator, did not differ between g

82 n lung injury and repair such as coagulation/thrombosis, acute phase response signaling and complemen

83 of LLH was associated with a greater risk of thrombosis (adjusted hazard ratio, 15; 95% confidence in

84 ce interval, 1.37-2.42; P<0.0001), and stent thrombosis (adjusted hazard ratio, 2.26; 95% confidence

85 y outcomes in patients with superficial-vein thrombosis and additional risk factors given either riva

86 aspirin for secondary prevention in arterial thrombosis and aspirin with anticoagulants for primary a

87 complications, including arterial or venous thrombosis and bleeding.

88 ial because of its potential risks on venous thrombosis and breast cancer.

89 roup died during the study (pulmonary artery thrombosis and cardiorespiratory failure); neither death

90 opathy associated with cerebral venous sinus thrombosis and disseminated primary JCPyV infection orig

91 gA-aB2GP1 was the main risk factor for graft thrombosis and early graft loss.

92 ful imaging tool for the detection of venous thrombosis and for the estimation of a complete burden o

93 lipid syndrome is characterized by recurrent thrombosis and gestational morbidity in patients with an

94 plasma VWF levels, International Society of Thrombosis and Haemostasis Bleeding Assessment Tool (IST

95 rombocythemia (ET) are at high risk for both thrombosis and hemorrhage.

96 sessed by using the International Society of Thrombosis and Hemostasis Scientific and Standardization

97 tion and implicated in thrombus stability in thrombosis and hemostasis.

98 Sildenafil is associated with reduced device thrombosis and ischemic stroke during ongoing LLH on Hea

99 Device thrombosis and ischemic stroke were associated with an i

100 s characterized by recurrent arterial/venous thrombosis and miscarriages in the persistent presence o

101 combined myocardial infarction (MI) or stent thrombosis and moderate/severe bleeding were assessed in

102 ound no difference in terms of target lesion thrombosis and mortality among groups, and no patient un

103 er rates of restenosis, although early stent thrombosis and neointimal hyperplasia causing vessel ren

104 od platelets are critical for hemostasis and thrombosis and play diverse roles during immune response

105 us thromboembolism (which includes deep vein thrombosis and pulmonary embolism), but the evidence is

106 ficial-vein thrombosis can lead to deep-vein thrombosis and pulmonary embolism.

107 le for normal hemostasis, but contributes to thrombosis and serves as a bridge between inflammation a

108 cenarios that one may encounter in pediatric thrombosis and suggests a logical approach to such situa

109 is based on an individual patient's risk of thrombosis and the severity of the bleeding.

110 th the clinical relevance of subclinical BPV thrombosis and the value of empirical oral anticoagulati

111 o promote platelet activation with resultant thrombosis and thrombocytopenia.

112 ely tested to assess the risk of bleeding or thrombosis and to monitor response to anticoagulant ther

113 ding and cell-surface thiol-redox control of thrombosis and vascular remodeling.

114 with myocardial infarction, 0.1% with stent thrombosis, and 0.1% with ischemic stroke).

115 6 with myocardial infarction, 113 with stent thrombosis, and 83 with ischemic stroke), and 232 indivi

116 rogression or recurrence of superficial vein-thrombosis, and all-cause mortality at 45 days in the pe

117 rogression or recurrence of superficial vein-thrombosis, and all-cause mortality, and was not associa

118 rom nutrient digestion to blood coagulation, thrombosis, and beyond.

119 ies to reduce the daily risk of bleeding and thrombosis, and different thresholds for transfusion, ma

120 ction not related to stent thrombosis, stent thrombosis, and ischemic stroke) and bleeding events (GU

121 cterized by venous thromboembolism, arterial thrombosis, and obstetric morbidities in the setting of

122 ificant roles in vasoregulation, hemostasis, thrombosis, and vascular remodeling.

123 adverse events of bleeding, stroke, and pump thrombosis; and they must become more cost-effective.

124 The reported relative risks for thrombosis, any bleeding, and major bleeding with antipl

125 The reported incidence rates of thrombosis, any bleeding, and major bleeding without ant

126 However, effects of RBCs on thrombosis are difficult to assess because humans and mi

127 recognition signaling mechanisms that impact thrombosis are poorly defined.

128 ogy of the pancreas varied widely with graft thrombosis as the most common finding.

129 We defined subclinical leaflet thrombosis as the presence of reduced leaflet motion, al

130 y on the same side as the isolated calf vein thrombosis as well as on the opposite side.

131 of the patients with HM II were free of pump thrombosis at 3 years compared with 90% of the patients

132 ischemia-driven revascularization, or stent thrombosis at 48 h after randomization.

133 ischemia-driven revascularization, or stent thrombosis at 48 hours.

134 thrombin may be as important as platelets to thrombosis at sites of arterial injury and that platelet

135 tients were eligible if they had symptomatic thrombosis (at least 5 cm in a supragenual superficial-v

136 f large pathogens and are also implicated in thrombosis, autoimmunity, and cancer.

137 vent-free at 12 months, rates of MI or stent thrombosis between 12 and 30 months were similar between

138 (eltrombopag: acute kidney injury, arterial thrombosis, bone pain, diarrhoea, myocardial infarction,

139 f mechanisms that contribute to pathological thrombosis but have a lesser impact on hemostasis.

140 sm (eg, factor V Leiden) are associated with thrombosis but result in less severe bleeding when co-in

141 These data suggest RBCs promote arterial thrombosis by enhancing platelet accumulation at the sit

142 hat eosinophils contributed to intravascular thrombosis by exhibiting a strong endogenous thrombin-ge

143 ue factor can directly affect hemostasis and thrombosis by modulating the size and density of intra-

144 Superficial-vein thrombosis can lead to deep-vein thrombosis and pulmonar

145 re, atrial fibrillation, stroke, deep venous thrombosis, cardiovascular death, and total mortality.

146 Thrombosis caused 1.3% of the graft losses in open kidne

147 Coronary artery thrombosis caused by plaque erosion may be on the rise i

148 We propose segmenting coronary artery thrombosis caused by plaque rupture into cases with or w

149 Skin inflammation; thrombosis clotting times; and percentage of splenic mon

150 ed recanalization and reduced progression of thrombosis, compared with patients who do not receive an

151 Central venous access device (CVAD)-related thrombosis (CRT) is a common complication among patients

152 te device-oriented adverse events and device thrombosis cumulatively at 2 years and between 1 and 2 y

153 nishing ADAMTS13, and blocking microvascular thrombosis despite persistent ADAMTS13 deficiency.

154 develops in patients with proximal deep-vein thrombosis despite treatment with anticoagulant therapy.

155 Results There was no evidence of IVC thrombosis, device migration, caval penetration, or pulm

156 The risk of thrombosis during anticoagulant therapy with these treat

157 int was occurrence of objectively documented thrombosis during DOAC therapy for acute HIT.

158 transfusion or intracranial hemorrhage) and thrombosis during ECMO support; (2) to identify factors

159 RATIONALE: Deep vein thrombosis (DVT) and its complication pulmonary embolism

160 Deep vein thrombosis (DVT) and pulmonary embolism are collectively

161 Deep venous thrombosis (DVT) remains a common and serious cardiovasc

162 Deep vein thrombosis (DVT) with its major complication, pulmonary

163 t properties can predict recurrent deep vein thrombosis (DVT), we studied 320 consecutive patients ag

164 Importantly, in vivo thrombosis experiments after bone marrow transplantation

165 a were proteins involved in inflammation and thrombosis, followed by changes in regulatory ECM protei

166 platelet miR-223 is a regulator of arterial thrombosis following endothelial injury through effects

167 egative regulator of platelet activation and thrombosis for many years, but more recent findings sugg

168 regated into pathways that are essential for thrombosis formation and pathways that are important for

169 portion of patients with subclinical leaflet thrombosis had aortic valve gradients of more than 20 mm

170 Transcatheter heart valve (THV) thrombosis has been increasingly reported.

171 Better understanding of the pathogenesis of thrombosis has fostered 2 new approaches to achieving th

172 jury and that platelets contribute to venous thrombosis has prompted trials comparing anticoagulants

173 use mortality, restenosis, or definite stent thrombosis (hazard ratio, 0.65; 95% confidence interval,

174 es in recurrent myocardial infarction, stent thrombosis, heart failure, or target vessel revasculariz

175 At 2 years, rates of thrombosis, hemorrhage, and transformation were not sign

176 play a key role in pathological states like thrombosis, hemostasis and inflammation.

177 Important adverse events (eg, thrombosis, hepatobiliary, and bone marrow fibrosis) wer

178 4 [95% CI, 1.00-1.09]; P=0.03) but not stent thrombosis (HR, 1.07 [95% CI, 0.99-1.16]; P=0.10) or spo

179 Patients were classified as having THV thrombosis if there was any evidence of hypoattenuated l

180 IgA aB2GP1 only are at risk of experiencing thrombosis if they are B2A-CIC positive.

181 entified as a biomarker of cancer-associated thrombosis in a general cancer population and may reflec

182 bogenic properties and induces microvascular thrombosis in a perfusion system.

183 NETs have been reported to directly promote thrombosis in animal models.

184 l provide useful insight into the genesis of thrombosis in blood-wetted devices, and provide a tool f

185 The incidence of graft thrombosis in group 1 (31.2%) was significantly higher t

186 bosuppressor genes based on perinatal lethal thrombosis in mice homozygous for F5(L) (F5(L/L) ) and h

187 we identified predictors of out-of-hospital Thrombosis in Myocardial Infarction (TIMI) major or mino

188 that provides an explanation for the lack of thrombosis in patients with gain-of-function VWD.

189 entary technique for the detection of venous thrombosis in such of cases.

190 ndaparinux for treatment of superficial-vein thrombosis in terms of symptomatic deep-vein thrombosis

191 rget lesions had higher rates of MI or stent thrombosis in the first 12 months after PCI (3.9% vs. 2.

192 One patient died of thrombosis in the superior mesenteric artery.

193 ischemia-driven revascularization, or stent thrombosis) in patients >/=75 years old (odds ratio [OR]

194 lmonary bypass because of extended vena cava thrombosis; in 2 patients, a simultaneous sternotomy was

195 rial (GIFT) of Warfarin to Prevent Deep Vein Thrombosis included patients aged 65 years or older init

196 12%) of 890 patients had subclinical leaflet thrombosis, including five (4%) of 138 with thrombosis o

197 In contrast, in a model of vein thrombosis induced by flow restriction in the inferior v

198 esolving and can lead to arterial damage and thrombosis-induced organ infarction.

199 Risk markers related to atherosclerosis, thrombosis, inflammation, cardiac injury, and fibrosis a

200 Platelet cross-linking during arterial thrombosis involves von Willebrand Factor (VWF) multimer

201 ts included target lesion revascularization, thrombosis, ipsilateral amputation, binary restenosis, a

202 Venous thrombosis is a multicausal disease involving intravenou

203 Vessel thrombosis is a severe complication after renal transpla

204 Thrombosis is caused by the activation of platelets at t

205 , the mechanism by which intact NETs promote thrombosis is largely unknown.

206 However, the role of Mac-1 in thrombosis is undefined.

207 ch as myocardial infarction, including stent thrombosis, ischemic stroke, or death from cardiovascula

208 ted VWF release, prolonged bleeding time and thrombosis, largely due to defective endothelial secreti

209 ion poised to enhance vascular inflammation, thrombosis, leakage, and wall instability; these changes

210 platelets, coagulation, and flow in arterial thrombosis, little attention has been paid to factors af

211 de pulmonary embolism, recurrent deep venous thrombosis, loss of central venous access, and postthrom

212 of PE (obesity, pregnancy, cancer, deep vein thrombosis, major procedure, spinal cord paralysis, veno

213 ts play a critical role in atherogenesis and thrombosis-mediated myocardial ischemia, processes that

214 e to formation of thrombi in a FeCl3-induced thrombosis model was significantly shortened in the TRAF

215 In a FeCl3-induced thrombosis model, we found that compared with wild-type

216 nt than hirulog-1 in a murine carotid artery thrombosis model.

217 nM), with excellent preclinical efficacy in thrombosis models and aqueous solubility suitable for in

218 te) thrombosis, 55 (56.1%) had multiple site-thrombosis (MPV and other), 17 (17.3%) had cavernous tra

219 Two eltrombopag recipients (arterial thrombosis n=1; myocardial infarction n=1) and no placeb

220 events (n = 7), cataracts (n = 4), deep vein thrombosis (n = 3), cerebral infarction (n = 2), headach

221 harmacological triggering protocol to induce thrombosis (n=22).

222 tes to responses to oxPCCD36 and accelerated thrombosis observed in hyperlipidemia.

223 Inflammation and thrombosis occur together in many diseases.

224 myocardial infarction and sinus venous tract thrombosis occurred as a complication of trichinellosis

225 INTERPRETATION: Subclinical leaflet thrombosis occurred frequently in bioprosthetic aortic v

226 Definite or probable device thrombosis occurred in 31 patients in the scaffold group

227 Deep vein thrombosis occurred in 5 patients.

228 overy without new, progressive, or recurrent thrombosis occurred in all 10 Hamilton patients with acu

229 Suspected or confirmed pump thrombosis occurred in no patients in the centrifugal-fl

230 ic event (myocardial infarction and/or stent thrombosis) occurred in 8.2% of DCS and 10.6% of BMS pat

231 omplications, except in some studies showing thrombosis of 1 of the 2 grafts.

232 Patients with thrombosis of any other vein were excluded.

233 Subclinical leaflet thrombosis of bioprosthetic aortic valves after transcat

234 thromboembolism, cancer, autoimmune disease, thrombosis of non-varicose veins).

235 thrombosis, including five (4%) of 138 with thrombosis of surgical valves versus 101 (13%) of 752 wi

236 surgical valves versus 101 (13%) of 752 with thrombosis of transcatheter valves (p=0.001).

237 Seventeen patients had either device thrombosis or ischemic stroke.

238 dent of the presence or absence of deep vein thrombosis or pulmonary embolism at the time of IVC filt

239 thrombosis in terms of symptomatic deep-vein thrombosis or pulmonary embolism, progression or recurre

240 ome was a composite of symptomatic deep-vein thrombosis or pulmonary embolism, progression or recurre

241 urgical bleeding, thromboembolic event, pump thrombosis, or neurological event) in the short-term coh

242 n use with venous thromboembolism, deep vein thrombosis, or pulmonary embolism in adults were include

243 ed data on venous thromboembolism, deep vein thrombosis, or pulmonary embolism outcomes.

244 The Canakinumab Anti-Inflammatory Thrombosis Outcomes Study (CANTOS) used computer-generat

245 nalysis in the Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS), a randomised trial o

246 .007), disability (P = 0.012), and deep vein thrombosis (P = 0.048).

247 , reducing endothelial cell injury and local thrombosis (P<0.05).

248 Pancreatic allograft thrombosis (PAT) remains the leading cause of nonimmunol

249 oses patients to the potential risk of stent thrombosis, perioperative myocardial infarction, or both

250 therapy-associated bleeding and pathological thrombosis pose serious risks to hospitalized patients.

251 t, neurology consultation, Holter, deep vein thrombosis prophylaxis, oral hypoglycemic intensificatio

252 plications (myocardial infarction, deep vein thrombosis, pulmonary embolism, and pneumonia).

253 ver cirrhosis complicated with portal venous thrombosis (PVT) has been mainly treated with transjugul

254 atocellular carcinoma (HCC) with portal vein thrombosis (PVT) treated with (90)Y radioembolization.

255 subsequently develop into portal vein tumour thrombosis (PVTT).

256 the long-term annual MACE rate and the stent thrombosis rate appeared constant for both stent types,

257 ture review plus these new data identified a thrombosis rate of 1 of 46 patients (2.2%; 95% CI, 0.4%-

258 Stent thrombosis rates were low: definite (7 of 697 [1.0%] vs

259 Vascular inflammation and thrombosis require the concerted actions of several diff

260 score, the HM3 group demonstrated less pump thrombosis requiring reoperation (0 versus 36 points, P<

261 esion failure and definite or probable stent thrombosis, respectively.

262 vents, hospitalizations, and vascular access thrombosis, respectively.

263 Analysis of IVC thrombosis revealed greater thrombus weight, length, mye

264 addition, a supraannular neosinus may reduce thrombosis risk because of reduced flow stasis.

265 sociated with reduced bleeding and increased thrombosis risk in humans.

266 d in rates of postoperative ileus, deep vein thrombosis, small bowel obstruction, urinary stricture,

267 Platelet hyperreactivity and accelerated thrombosis, specifically in dyslipidemia, have been mech

268 and MACE (composite of cardiac death, stent thrombosis, spontaneous myocardial infarction, or target

269 Stent thrombosis (ST) is a serious complication following coro

270 end points were definite and probable stent thrombosis (ST), clinically relevant bleeding, all-cause

271 (myocardial infarction not related to stent thrombosis, stent thrombosis, and ischemic stroke) and b

272 er studies and cross referenced with in vivo thrombosis studies.

273 mas [89%]) included in the Vienna Cancer and Thrombosis Study, a prospective observational cohort stu

274 associated with a higher incidence of device thrombosis than the metallic stent through 2 years of fo

275 Among patients with acute proximal deep-vein thrombosis, the addition of pharmacomechanical catheter-

276 crease in MI risk, mainly unrelated to stent thrombosis; the magnitude of risk is highest in the earl

277 mote pathogen clearance but also can lead to thrombosis; the pathways that negatively regulate NETosi

278 evaluate risk factors that contribute to THV thrombosis through the combination of retrospective clin

279 hey can differ notably from those supporting thrombosis, thus presenting therapeutic opportunities.

280 ecreased platelet accumulation and increased thrombosis times compared with mice transplanted with ER

281 f miR-223 was responsible for differences in thrombosis times.

282 tial target to treat or prevent pathological thrombosis, to inhibit contact activation in extracorpor

283 vestigated the role of APP in hemostasis and thrombosis, using APP knockout (KO) mice.

284 1, 46.4% of patients experienced any type of thrombosis versus 10.4% in group 2 (P<0.001) and 8.6% in

285 hermore, the contribution of very late stent thrombosis (VLST) to these events remains poorly underst

286 We estimated that the odds of graft thrombosis was 1.67 times higher in DCD organs (95% CI,

287 Subclinical leaflet thrombosis was associated with increased rates of TIAs a

288 leaflet motion (p=0.10), subclinical leaflet thrombosis was associated with increased rates of transi

289 Prosthetic leaflet thrombosis was detected in 1 patient at follow-up and re

290 48 hours following IVC ligation, IVC thrombosis was evident in 60% of WT mice and 25% of pcsk

291 Subclinical leaflet thrombosis was less frequent among patients receiving an

292 on to the aPL thrombophilic effect, arterial thrombosis was related to accelerated atherosclerosis in

293 ophil and NK cell infiltration and capillary thrombosis were also significantly reduced by GS-492429

294 SAPIEN 3 valves with leaflet thrombosis were on average 10% further expanded (by diam

295 ng target lesion revascularization and stent thrombosis, were followed for 1 year.

296 sa lesions, the management of basilar artery thrombosis, which may have a longer time window for reca

297 or morbidity of recipients with grade 1 or 2 thrombosis who were or were not anticoagulated.

298 Reduction of MI or stent thrombosis with continued thienopyridine beyond 12 month

299 g therapeutic role, as they inhibit arterial thrombosis with limited risk of bleeding.

300 These findings link hemostasis-thrombosis with the AP of complement and open new therap