ライフサイエンスコーパス: thrombosis

1 d had no history to suggest past deep venous thrombosis).

2 nd related mechanisms of thrombus formation (thrombosis).

3 ivo (tail-bleeding assay and FeCl(3)-induced thrombosis).

4 er cell necrosis, together with central vein thrombosis.

5 nts (84.6%) had cannula-associated deep vein thrombosis.

6 rdial infarction, or definite-probable stent thrombosis.

7 onography of both legs showed no deep venous thrombosis.

8 aggregates is a critical process in arterial thrombosis.

9 hrombosis, and two had an oxygenator or pump thrombosis.

10 fection and presenting with left portal vein thrombosis.

11 and anti-beta2GPI antibodies) and recurrent thrombosis.

12 echanisms that differentiate hemostasis from thrombosis.

13 ange of complications related to portal vein thrombosis.

14 nus thrombosis, along with left jugular vein thrombosis.

15 impacts on platelet reactivity and arterial thrombosis.

16 veal a mechanism by which Slc44a2 influences thrombosis.

17 ay an important role in stent restenosis and thrombosis.

18 associated liver disease or porto-mesenteric thrombosis.

19 and the use of antiplatelet agents to limit thrombosis.

20 n had ischemia, possibly due to small-vessel thrombosis.

21 e SLC44A2 rs2288904-A polymorphism in venous thrombosis.

22 ardiomyopathy and severe pulmonary edema and thrombosis.

23 , which in turn increased the risk of device thrombosis.

24 referred to here as an unexplained arterial thrombosis.

25 tional relationship between inflammation and thrombosis.

26 factor (VWF) plays a major role in arterial thrombosis.

27 del, when assayed as ferric chloride-induced thrombosis.

28 ecognized contributor to venous and arterial thrombosis.

29 them developed cannula-associated deep vein thrombosis.

30 mainstay for the prevention and treatment of thrombosis.

31 ment with eltrombopag might increase risk of thrombosis.

32 ntribution of NETs to atherosclerosis and to thrombosis.

33 or the management of acute cancer-associated thrombosis.

34 ral and jugular cannula-associated deep vein thrombosis.

35 lating cells involved in both hemostasis and thrombosis.

36 BS)-deficient patients are prone to vascular thrombosis.

37 ted with a slightly increased risk of venous thrombosis.

38 te endpoints; and definite or probable stent thrombosis.

39 ffector cells of hemostasis and pathological thrombosis.

40 to play an important role in restenosis and thrombosis.

41 sive inward remodeling, medial fibrosis, and thrombosis.

42 ients (42.2%) were found to have deep venous thrombosis.

43 pro-inflammatory conditions such as arterial thrombosis.

44 ially increase the risk of both bleeding and thrombosis.

45 ad central venous catheter-related deep vein thrombosis.

46 on likely caused by pulmonary angiopathy and thrombosis.

47 ic loci including SLC44A2 which may regulate thrombosis.

48 2.7 years), the incidence of definite stent thrombosis (1% versus 5%; hazard ratio, 9.20 [95% CI, 1.

49 ]; aHR, 0.92; 95% CI, 0.72-1.18) or arterial thrombosis (1.2% [n = 12 of 1014] vs 1.5% [n = 15 of 100

50 emic infarct (23.3%), one with a deep venous thrombosis (1.4%), eight with multiple microhemorrhages

51 .3% versus 1.0%; P=0.46), and definite stent thrombosis (1.8% versus 1.0%; P=0.15) did not differ sig

52 Of 13 PNF cases, 2 were due to early venous thrombosis, 2 to arterial thrombosis, and 2 to failure o

53 the composite of definite or probable stent thrombosis (5% versus 11%; hazard ratio, 2.52 [95% CI, 1

54 er >2500 ng/mL, adjusted odds ratio [OR] for thrombosis, 6.79 [95% CI, 2.39-19.30]; adjusted OR for b

55 n) and the incidence of postoperative venous thrombosis, 78 patients with brain tumors that were oper

56 talization; however, data examining rates of thrombosis after discharge are limited.

57 s disease 2019 were screened for deep venous thrombosis after ICU admission with 102 duplex ultrasoun

58 Cannula-associated deep vein thrombosis after venovenous extracorporeal membrane oxyg

59 and left transverse and sigmoid venous sinus thrombosis, along with left jugular vein thrombosis.

60 ions revealed a mild ascites and portal vein thrombosis although the patient received proper anticoag

61 as no difference in incidence of deep venous thrombosis among different pharmacologic prophylaxis reg

62 which can present as acute vasospasm, acute thrombosis and accelerated atherosclerosis, of cancer th

63 Accurate assessment of blood thrombosis and antithrombotic therapy is essential for t

64 es insights into the molecular mechanisms of thrombosis and bleeding disorders related to fibrinogen

65 ole of hypercoagulable disorders in arterial thrombosis and discuss our approach to thrombophilia wor

66 between persistent leukocytosis and risk of thrombosis and disease evolution in polycythemia vera (P

67 y membership and hazard of 2 major outcomes: thrombosis and disease evolution to myelofibrosis, myelo

68 Data from the International Society of Thrombosis and Haemostasis (ISTH) registry were obtained

69 g as defined by the International Society on Thrombosis and Haemostasis (ISTH) was a secondary safety

70 modification of the International Society on Thrombosis and Haemostasis criteria for major bleeding.

71 ajor bleeding, with International Society on Thrombosis and Haemostasis major bleeding a secondary sa

72 th a trend for more International Society on Thrombosis and Haemostasis major bleeding with clopidogr

73 ssociated with more International Society on Thrombosis and Haemostasis major bleeding within 365 day

74 We conclude that the rates of thrombosis and hemorrhage appear to be similar following

75 of coagulation disorders (thrombocytopenia, thrombosis and hemorrhage) are risk factors for SARS-CoV

76 prior infarctions or resolved intravascular thrombosis and included calcifications in pulmonary vess

77 Thrombosis and infections are two grave, interrelated pr

78 sttransplant cure, extensive mesenteric vein thrombosis and intestinal infarction, total intestinal a

79 Therefore, clinicians should always consider thrombosis and other hypercoagulable diseases in patient

80 titis and is associated with splanchnic vein thrombosis and pancreatic head necrosis.

81 r stricture development were splanchnic vein thrombosis and pancreatic head parenchymal necrosis.

82 ffectiveness in reducing catheter associated thrombosis and pathogen colonization, as an alternative

83 Thrombosis and platelet activation play a central role i

84 sses, such as left ventricular assist device thrombosis and profiling of leukocyte activation, contin

85 eneral's Call to Action to Prevent Deep Vein Thrombosis and Pulmonary Embolism in 2008 has been lower

86 Deep vein thrombosis and pulmonary embolism, collectively defined

87 olism (VTE), which includes both deep venous thrombosis and pulmonary embolism, is a common and poten

88 the drug of choice for preventing deep vein thrombosis and pulmonary embolism.

89 (7.7%) had both cannula-associated deep vein thrombosis and pulmonary embolism.

90 inogen concentrates may increase the risk of thrombosis and should be restricted to rare patients wit

91 Bin2fl/fl,Pf4-Cre mice in models of arterial thrombosis and stroke.

92 red to understand the mechanism of increased thrombosis and the benefit of aggressive antithrombotic

93 central regulator of platelet activation in thrombosis and thrombo-inflammatory disease settings.

94 Secondary outcomes were thrombosis and thrombosis-related major complications an

95 Evidence of thrombosis and vasculitis was detected in mice with seve

96 spholipid syndrome (APS) is characterized by thrombosis and/or pregnancy morbidity in the presence of

97 68.5% of samples collected within 1 year of thrombosis), and only 6.8% of systemic lupus erythematos

98 e subgroups of pediatric VTE (eg, renal vein thrombosis), and will be important to ultimately guide t

99 ue to early venous thrombosis, 2 to arterial thrombosis, and 2 to failure of desensitization and deve

100 isease models, including pulmonary fibrosis, thrombosis, and acute respiratory distress syndrome.

101 verse cardiovascular events, splanchnic vein thrombosis, and bleeding in a cohort with cirrhosis and

102 e infection, pulmonary embolism, deep venous thrombosis, and death.

103 schemic and hemorrhagic stroke, venous sinus thrombosis, and endothelialitis.

104 ndophenotype modules governing inflammation, thrombosis, and fibrosis in the human interactome (P < 0

105 bute to inflammation-associated lung damage, thrombosis, and fibrosis.

106 ischaemic heart disease and coronary artery thrombosis, and one patient assigned fluoxetine had a su

107 s ventilator-associated pneumonia, deep vein thrombosis, and pressure sores; and shortened the durati

108 macrophage, complement, platelet activation, thrombosis, and proinflammatory markers, including C-rea

109 ed for provoked/unprovoked events, deep vein thrombosis, and pulmonary embolism.

110 ing myocardial infarction, stroke, deep vein thrombosis, and pulmonary embolism.

111 d infection, gastrointestinal bleeding, pump thrombosis, and readmission and reduced hazards for card

112 nts had femoral cannula-associated deep vein thrombosis, and two had an oxygenator or pump thrombosis

113 ection, hemorrhage, renal failure, deep vein thrombosis, and uncontrollable intracranial hypertension

114 lity rate in COVID-19, strategies to prevent thrombosis are of critical importance.

115 Left sided abscess and portal vein thrombosis are rare and hence reported.

116 Whereas chronic platelet activation and thrombosis are well-recognized features of human SLE, th

117 y hematopoiesis, pulmonary hypertension, and thrombosis, are related to the chronic hemolytic anemia

118 he relationship between oxidative stress and thrombosis as most nutrients are believed to possess ant

119 who had deep vein thrombosis or central-line thrombosis as their most recent VTE.

120 latelet activation and pathological arterial thrombosis, as tested in vivo by carotid occlusion assay

121 or screening for lower extremity deep venous thrombosis at or above a concentration of 3,000 ng/mL (m

122 nt period or asymptomatic proximal deep-vein thrombosis at the end of treatment.

123 al of the commonest manifestations of venous thrombosis at the lower extremities.

124 To date, anticoagulant therapy for thrombosis at unusual sites is generally accepted, but t

125 PTE in COVID-19 might be a pulmonary artery thrombosis because of severe lung inflammation and hyper

126 s who did not receive L-ASP or who developed thrombosis before L-ASP, AT supplementation did not have

127 markedly higher in patients with deep venous thrombosis, both for maximum value and value on day of u

128 vention and treatment of bioprosthetic valve thrombosis (BPVT), anticoagulation is effective, but the

129 ms plus imaging-confirmed proximal deep vein thrombosis but no chest imaging.

130 Anucleate platelets form blood-clots during thrombosis, but also play a crucial role in inflammation

131 hogenesis in humans include inflammation and thrombosis, but the mechanistic details underlying these

132 vailing dogma is that inhibition of vascular thrombosis by antagonizing platelet integrin alphaIIbbet

133 Aspirin prevents thrombosis by inhibiting platelet cyclooxygenase (COX)-1

134 hat Slc44a2 controls platelet activation and thrombosis by regulating mitochondrial energetics.

135 ects including in-stent restenosis and stent thrombosis can be avoided and long-term medication of an

136 sts (VKA) for treatment of cancer associated thrombosis (CAT).

137 lymphoblastic leukemia (ALL) are at risk for thrombosis, caused in part by the use of l-asparaginase

138 Subclinical leaflet thrombosis, characterized by hypoattenuated leaflet thic

139 )) have increased bleeding times and delayed thrombosis compared to wild-type (Slc44a2(WT)) controls.

140 t prevails in COVID-19, hypercoagulation and thrombosis contribute to the lethality of subjects infec

141 us resulting in 38.7% with PE or deep venous thrombosis, despite 40% receiving prophylactic anticoagu

142 view provides an overview of haemostasis and thrombosis, details the current landscape of antithrombo

143 most common therapy used to prevent circuit thrombosis during extracorporeal membrane oxygenation, b

144 arkers at initial presentation predictive of thrombosis during hospitalization included platelet coun

145 t-lesion revascularization or access-circuit thrombosis during the 6 months after the index procedure

146 omboembolism (VTE), which includes deep vein thrombosis (DVT) and pulmonary embolism (PE), is the thi

147 Deep vein thrombosis (DVT) is a common but unpredictable complicat

148 diagnosis of recurrent ipsilateral deep vein thrombosis (DVT) is challenging, because persistent intr

149 ncidence rates for lower extremity deep vein thrombosis (DVT) range from 88 to 112 per 100 000 person

150 hem have proximal limb-threatening deep vein thrombosis (DVT).

151 athogenesis, including vascular dysfunction, thrombosis, dysregulated inflammation, and respiratory c

152 infarction, stroke, aortic dissection, valve thrombosis, endocarditis, and urgent cardiac interventio

153 qualitative differences such that deep vein thrombosis exclusively afflicted the immunosuppressed pa

154 Patients with device thrombosis exhibited a greater coagulation activation 7

155 heparin or other polyanions, but the risk of thrombosis extends beyond exposure to heparin implicatin

156 Levels of D-dimers, a marker of thrombosis, failed to correlate with any measured indica

157 atelet-COX-1-ko mice would be protected from thrombosis, forming less pro-thrombotic TxA(2) and PGE(2

158 Patients found to have deep venous thrombosis had no difference in time to intubation (p =

159 tanding of the mechanisms of haemostasis and thrombosis has revealed new targets for attenuating thro

160 igher rates of multivessel thrombosis, stent thrombosis, higher modified thrombus grade post first de

161 cases (16.7%) of lower extremity deep venous thrombosis identified.

162 antiplatelet agent, adjunctive treatment for thrombosis, immunomodulatory therapy, complement inhibit

163 Prolonged air leak in 141, deep venous thrombosis in 64, Atrial fibrillation in 42, chylothorax

164 Autopsy revealed deep venous thrombosis in 7 of 12 patients (58%) in whom venous thro

165 eported the frequent occurrence of pulmonary thrombosis in a series of autopsies of patients with COV

166 or diminish the incidence of bleeding and/or thrombosis in adult patients on venovenous extracorporea

167 bodies activate complement and contribute to thrombosis in APS, whereas patients with CAPS have under

168 type in CBS(-/-) patients and the absence of thrombosis in Cbs(-/-) mice.

169 the rate of recanalization according to the Thrombosis in Cerebral Infarction (TICI) scale and funct

170 ontribution of platelets to inflammation and thrombosis in COVID-19 patients.

171 onstrate endothelial disruption and vascular thrombosis in histopathologic sections of lungs from bot

172 ROS1 and SERPINC1 result in perinatal lethal thrombosis in homozygotes and markedly increased VTE ris

173 partial agonist drugs in inhibiting vascular thrombosis in humanized mice, but neither causes serious

174 mmaRIIA expression in lupus mice also led to thrombosis in lungs and kidneys.

175 reduces ferric-chloride-induced experimental thrombosis in mice and suppresses blood coagulation in a

176 ted that the underlying cause of portal vein thrombosis in our case was coronaviruses.

177 of and risk factors for venous and arterial thrombosis in patients hospitalized with COVID-19 in 4 N

178 sible for complement activation and vascular thrombosis in patients with antiphospholipid syndrome (A

179 lue in assessing the threat of postoperative thrombosis in patients with benign and malignant brain t

180 of fibrinolytic dysfunction in bleeding and thrombosis in patients with cirrhosis.

181 the development of systemic inflammation and thrombosis in SARS-CoV-2-infected patients with cancer,

182 ding to accelerated elastic fiber damage and thrombosis in severe COVID-19 due to impaired activation

183 clerotic disease and in reducing the risk of thrombosis in the setting of plaque disruptions.

184 two patients, superior mesenteric vein (SMV) thrombosis in two patients, and intraluminal haemorrhage

185 The cumulative incidence of thrombosis (including arterial and venous events) at day

186 ial therapies to prevent COVID-19-associated thrombosis, including heparin, FXII inhibitors, fibrinol

187 ) at non-platelet sites leading to predicted thrombosis increase.

188 omodulin (a natural endothelial inhibitor of thrombosis, inflammation, and vascular leakage) and alle

189 ing the International Network Against Venous Thrombosis (INVENT) consortium multi-ancestry genome-wid

190 ata from the International Network on Venous Thrombosis (INVENT) consortium to examine whether single

191 a therapeutic range to minimize bleeding and thrombosis is important for personalized treatment of NO

192 Lower extremity deep venous thrombosis is prevalent in coronavirus disease 2019 dise

193 Deep venous thrombosis is very common in critically ill patients wit

194 mposed of pulmonary embolism and deep venous thrombosis, is a significant cause of maternal mortality

195 te RV dysfunction, with or without deep vein thrombosis, is more common, but acute LV systolic dysfun

196 g cause of maternal mortality, and deep vein thrombosis leads to maternal morbidity, with postthrombo

197 erogenous population, with variation in age, thrombosis location, and underlying medical comorbiditie

198 rate of graft failure due to hepatic artery thrombosis <=14 days from initial LT was observed in HEH

199 The lack of associations with SVS suggests thrombosis may be less important for this stroke subtype

200 isplayed antithrombotic efficacy in a rabbit thrombosis model.

201 which show excellent efficacy in preclinical thrombosis models with minimal effects on hemostasis.

202 induced femoral cannula-associated deep vein thrombosis more frequently than femorojugular cannulatio

203 berrant NET formation to pulmonary diseases, thrombosis, mucous secretions in the airways, and cytoki

204 contribute to the pathogenesis of deep vein thrombosis, myocardial infarction and stroke.

205 (1 of them due to needing heparin for venous thrombosis, none required interventions).

206 Death may be caused by the thrombosis observed in segmental and subsegmental pulmon

207 n, endothelial activation, and microvascular thrombosis occur in the context of coronavirus disease 2

208 One symptomatic thrombosis occurred and resolved under aspirin and antic

209 Device-related thrombosis occurred in 5 patients (6.4%), and all of the

210 presence of large abscess cavity along with thrombosis of left portal vein.

211 coronary syndromes most commonly arise from thrombosis of lipid-rich coronary atheromas that have la

212 Thrombosis of small and mid-sized pulmonary arteries was

213 oratory values, clinical outcome, and venous thrombosis of the patients were recorded.

214 of such nutrients in experimental models of thrombosis or analyzed biomarkers of clotting, platelet,

215 r 2 of 162 children (1.2%) who had deep vein thrombosis or central-line thrombosis as their most rece

216 significantly associated with the hazard of thrombosis or disease evolution.

217 matic or incidental acute proximal deep-vein thrombosis or pulmonary embolism to receive oral apixaba

218 amputation for ischemia) and VTE (deep vein thrombosis or pulmonary embolism) were assessed.

219 reduces the risk of VTE events (deep venous thrombosis or pulmonary embolism).

220 r surgery or confirmed symptomatic deep vein thrombosis or pulmonary embolism).

221 ant therapy for suspected pulmonary arterial thrombosis or thromboembolism.

222 I showing ischemic infarcts, cerebral venous thrombosis, or chronic lesions unrelated to the current

223 nt ischemic attack, systemic embolism, valve thrombosis, or hospitalization for heart failure), or ma

224 nts of the primary end point, definite stent thrombosis, or stroke.

225 rdial infarction, definite or probable stent thrombosis, or unplanned revascularization or rehospital

226 Although the Canakinumab Anti-Inflammatory Thrombosis Outcomes Study (CANTOS) established the role

227 In the Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS), inhibition of the IL

228 The incidence of definite/probable stent thrombosis over 10 years was low and comparable in both

229 link between inflammation, innate immunity, thrombosis, oxidative stress, and cardiovascular disease

230 flow with higher incidence of hepatic artery thrombosis (P = 0.043) and biliary complication (P = 0.0

231 n was not related to presence of deep venous thrombosis (p = 0.35).

232 -3,735 ng/mL] for no evidence of deep venous thrombosis; p < 0.0001).

233 itical interactions between inflammatory and thrombosis pathways lead to SARS-CoV-2-induced vascular

234 In haemostasis and thrombosis, platelet, coagulation and anticoagulation pa

235 ar in the incidence of reoperation, vascular thrombosis, posttransplant lymphoproliferative disease,

236 e platelet activation-related phenotypes and thrombosis potential in whole blood, isolated platelets,

237 PAGly) fostering platelet responsiveness and thrombosis potential.

238 The frequency of thrombosis preceding MPN was similar for cases and contr

239 d International Myeloma Working Group (IMWG) thrombosis prevention recommendations and compared with

240 helial anticoagulant protein S, required for thrombosis prevention.

241 COVID-19, together with the roles for strict thrombosis prophylaxis, laboratory and imaging studies,

242 )thrombotic complications, such as deep vein thrombosis, pulmonary embolism, and stroke.

243 ous thromboembolism was defined as deep vein thrombosis, pulmonary embolism, or both, diagnosed great

244 of symptomatic distal or proximal deep-vein thrombosis, pulmonary embolism, or venous thromboembolis

245 ng from repeated thrombophlebitis, deep vein thrombosis, pulmonary embolism, transitory ischemic atta

246 Portal vein thrombosis (PVT) occurs frequently in hepatocellular car

247 llular carcinoma (HCC) and portal vein tumor thrombosis (PVTT) is 2-6 months; conventionally liver tr

248 Venous thrombosis rarely occurs at unusual sites such as cerebr

249 good hemostasis (81.8%) coupled with a 3.8% thrombosis rate.

250 Stent thrombosis rates were 2.0% DCS and 2.2% bare metal stent

251 the major difference being increased risk of thrombosis rather than bleeding.

252 ion (RD, 0.003 [CI, -0.010 to 0.017]), stent thrombosis (RD, 0.003 [CI, -0.005 to 0.010]), and stroke

253 Secondary outcomes were thrombosis and thrombosis-related major complications and postoperative

254 utcomes, in-stent restenosis (ISR) and stent thrombosis remain clinically significant issues for vasc

255 However, thrombosis remained frequent in spite of IMWG-guided thr

256 for confounders, the occurrence of arterial thrombosis remained independently associated with the ri

257 the centrifugal pump, and one had oxygenator thrombosis requiring circuit replacement.

258 of SLC44A2 that is protective against venous thrombosis results in severely impaired binding to both

259 (NCT01895777) and had an unresolved clinical thrombosis risk factor requiring further anticoagulation

260 Stent thrombosis risk was significantly reduced by both ticagr

261 iari Syndrome) and in those with portal vein thrombosis (second section); and we briefly comment on t

262 ignificantly reduced proteinuria, glomerular thrombosis, serum creatinine, and glomerular macrophage

263 plication was cannula-associated deep venous thrombosis (six patients, 23.1%).

264 lity, and the secondary endpoints were stent thrombosis (ST) or restenosis and peri-procedural compli

265 cularization); 2) definite or probable stent thrombosis (ST); or 3) spontaneous (non-ST or non-proced

266 ce in ischemic cholangiopathy (IC), vascular thrombosis/stenosis or graft, and patient survival was s

267 re significantly higher rates of multivessel thrombosis, stent thrombosis, higher modified thrombus g

268 ocardial infarction, definite/probable stent thrombosis, stroke, or urgent vessel revascularization.

269 atory virus that can lead to venous/arterial thrombosis, stroke, renal failure, myocardial infarction

270 In vitro and in vivo thrombosis studies proved these predictions.

271 at CT pulmonary angiography had deep venous thrombosis, thus resulting in 38.7% with PE or deep veno

272 clinical presentation ranging from isolated thrombosis to acute respiratory distress syndrome (ARDS)

273 %) had isolated cannula-associated deep vein thrombosis, two patients (15.4%) had isolated pulmonary

274 nciding cerebral infarction and venous sinus thrombosis unveiling the diagnosis of celiac disease.

275 ombus stability in a mouse model of arterial thrombosis using intravital microscopy.

276 markers, and therapeutic targets relevant to thrombosis, vascular inflammation, and other platelet-as

277 0,770 ng/mL] for lower extremity deep venous thrombosis vs 2,087 ng/mL [interquartile range, 638-3,73

278 o determine whether lower-extremity arterial thrombosis was associated with COVID-19 and whether it w

279 Femoral deep vein thrombosis was diagnosed in 5 of 12 patients with RV fai

280 Femoral artery thrombosis was documented in 6 (9%) infants without any

281 Cannula-associated deep vein thrombosis was found in 75 patients (71.4%) despite it h

282 oral associated cannula-associated deep vein thrombosis was identified in 10 patients (76.9%), and si

283 ular associated cannula-associated deep vein thrombosis was identified in seven patients (53.8%), a f

284 Venous thrombosis was induced by inferior vena cava ligation in

285 The rate of definite or probable stent thrombosis was infrequent and similar between the 2 arms

286 The incidence of stent thrombosis was low and comparable in both groups.

287 stent group; however, the incidence of stent thrombosis was lower in the stent-only group, as was tar

288 Subclinical leaflet thrombosis was more frequent in transcatheter compared w

289 Thrombosis was not associated with inferior progression-

290 ow involvement, and microvascular injury and thrombosis were also detected.

291 egarding the secondary causes of portal vein thrombosis were normal.

292 Bleeding, blood product transfusions, and thrombosis were not different in the two groups.

293 ures, primary nonfunction and hepatic artery thrombosis were observed in the total cohort and in 32 v

294 drome can be broadly defined as breakthrough thrombosis while on standard oral anticoagulation treatm

295 in patients with Covid-19 showed widespread thrombosis with microangiopathy.

296 sis has revealed new targets for attenuating thrombosis with the potential for less bleeding, includi

297 hibition is protective in models of arterial thrombosis, with only minor effects on hemostasis.

298 s knock-out or inhibition in animals reduced thrombosis without causing abnormal bleeding.

299 lagen-induced platelet activation and reduce thrombosis without deleterious effects on hemostasis.

300 Inhibiting thrombosis without generating bleeding risks is a major