ライフサイエンスコーパス: thrombus

1 erent modelling scenarios (e.g. with/without thrombus).

2 n (P = .008) independently helped predict LV thrombus.

3 for simulating the formation and growth of a thrombus.

4 lity to distinguish between an old and fresh thrombus.

5 rove accurate assessment of the exact age of thrombus.

6 as up-regulated in HCC and portal vein tumor thrombus.

7 nd stiffness and post-triggering to identify thrombus.

8 lets and fibrin) components within a growing thrombus.

9 t in mice with a thrombus vs those without a thrombus.

10 platelets, and fibrin accumulating within a thrombus.

11 ficity (95.5%) in discriminating pannus from thrombus.

12 tion of interactions between platelets and a thrombus.

13 For predicting the occurrence of LV thrombus, a multiple regression model was applied.

14 Furthermore, thrombus accumulation was found to increase with decreas

15 ormation for the diagnosis and therapy of LV thrombus after STEMI.

16 ERIAL/The object of this study was to assess thrombus age in patients with saphenous vein insufficien

17 Thrombus and edema were detected in 35 (81.4%) and 32 (7

18 acomechanical thrombolysis") rapidly removes thrombus and is hypothesized to reduce the risk of the p

19 CD4(+) and CD8(+) T cells infiltrate the thrombus and vein wall rapidly on deep vein thrombosis i

20 nchymal forward diastole flow), splenic vein thrombus, and edema.

21 secutive heart cycles in endoleak, organized thrombus, and fresh thrombus areas were 0.78% +/- 0.22,

22 Areas of endoleak, solid organized thrombus, and fresh thrombus were identified and segment

23 s implanted, less multivessel stenting, less thrombus, and less no-reflow.

24 enic thrombus, whereas mixed echogenicity of thrombus appeared on 11 patients.

25 oons is part of the haemostatic response and thrombus architecture.

26 t-positive area varied up to 13.45% of total thrombus area.

27 rent between endoleak and organized or fresh thrombus areas (P < .000) and between organized and fres

28 s (P < .000) and between organized and fresh thrombus areas (P < .0002).

29 s in endoleak, organized thrombus, and fresh thrombus areas were 0.78% +/- 0.22, 0.23% +/- 0.02, 0.10

30 Spectroscopic thrombus aspirate analysis showed persistence of intraco

31 in 221 of 9155 patients (2.4%) randomized to thrombus aspiration and 262 of 9151 (2.9%) randomized to

32 c attack occurred in 66 (0.8%) randomized to thrombus aspiration and 46 (0.5%) randomized to PCI alon

33 As a result, thrombus aspiration can no longer be recommended as a ro

34 Routine thrombus aspiration during PCI for ST-segment-elevation

35 Routine thrombus aspiration during PCI for STEMI did not reduce

36 rials to determine the benefits and risks of thrombus aspiration during PCI in patients with ST-segme

37 Thrombus aspiration during percutaneous coronary interve

38 The 3 eligible randomized trials (TAPAS [Thrombus Aspiration During Percutaneous Coronary Interve

39 ported contradictory results at 1 year after thrombus aspiration in ST elevation myocardial infarctio

40 tion in Acute Myocardial Infarction], TASTE [Thrombus Aspiration in ST-Elevation Myocardial Infarctio

41 recombinant tissue plasminogen activator and thrombus aspiration or maceration, with or without stent

42 de a rationale for future trials of improved thrombus aspiration technologies in this high-risk subgr

43 Myocardial Infarction] thrombus grade >/=3), thrombus aspiration was associated with fewer cardiovasc

44 follow-up of the largest randomised trial of thrombus aspiration, we aimed to clarify the longer-term

45 Myocardial Infarction 3 flow restoration by thrombus aspiration.

46 found, which was immediately recanalized by thrombus aspiration.

47 Patients with LV thrombus at 6 months were restudied at 1 year.

48 In the subgroup with high thrombus burden (TIMI [Thrombolysis in Myocardial Infarc

49 In the high thrombus burden group, the trends toward reduced cardiov

50 A more detailed thrombus burden quantification is required to investigat

51 to further develop strategies for minimizing thrombus burden, these results may help identify patient

52 mes, and predictors of left ventricular (LV) thrombus by using sequential cardiac magnetic resonance

53 d within filters in 99% of patients included thrombus, calcification, valve tissue, artery wall, and

54 he immediate and long-term safety as well as thrombus-capturing efficacy for 5 weeks after implantati

55 the circulation loop showed microparticles (thrombus/coagulum and tissue).

56 ween aggregates, suggesting a level of intra-thrombus communication.

57 yeloma growth and simultaneously eradicating thrombus complication.

58 To better understand thrombus composition, we analyzed thrombi retrieved from

59 ential platelet processes such as spreading, thrombus consolidation, and clot retraction.

60 side branch >/=2.5 mm, vein bypass graft, or thrombus-containing lesion.

61 ow for exact determination of the age of the thrombus depending on changes of its elasticity.

62 For both problems, the simulated thrombus deposition agreed very well with experimental o

63 owth in an injured blood vessel and in vitro thrombus deposition in micro-channels (1.5 mm x 1.6 mm x

64 n microscopy demonstrated significantly less thrombus deposition to Magmaris as a percentage of the t

65 tion and prognostic implications of coronary thrombus, detected by coronary angiography, in a populat

66 Biodistribution and thrombus detection was investigated in cynomolgus monkey

67 this mechanism, and how it may contribute to thrombus development.

68 ow-up of 181 weeks +/- 168, patients with LV thrombus displayed a very low rate of stroke (0%), perip

69 ha2-antiplasmin inactivation on experimental thrombus dissolution and bleeding.

70 olytic efficacy, essentially by accelerating thrombus dissolution and preventing rethrombosis.

71 er, t-PA does not always result in efficient thrombus dissolution and subsequent blood vessel recanal

72 m assembles at the site of pulmonary emboli, thrombus dissolution is halted by alpha2-antiplasmin.

73 Thrombus dissolution was markedly accelerated in mice wi

74 Despite greater thrombus dissolution, alpha2-antiplasmin inactivation al

75 rix metalloproteinases (MMPs) participate in thrombus dissolution.

76 When tPA is introduced at the clot or thrombus edge, lysis proceeds as a front.

77 Elastography as a method of thrombus evaluation, provides information about relative

78 umulates on the endothelium and the platelet thrombus following injury.

79 Data on left ventricular (LV) thrombus formation after primary percutaneous coronary i

80 adhesion and bleeding defects due to delayed thrombus formation after vessel injury.

81 ance to elucidate the mechanisms of platelet thrombus formation after vessel wall injury.

82 phosphate has been associated with increased thrombus formation and activation of coagulation factor

83 fully restored injury-induced microvascular thrombus formation and brain damage.

84 istic studies suggests that RBCs can promote thrombus formation and enhance thrombus stability.

85 hesion of platelets is crucial in predicting thrombus formation and growth following a thrombotic eve

86 ypothesis that targeting factor XII prevents thrombus formation and has a beneficial effect on outcom

87 n mice minimize trauma-induced microvascular thrombus formation and improve outcome, as reflected by

88 PK drives thrombus formation and inflammation via activation of th

89 adhesion and aggregation, and downregulates thrombus formation and inflammation.

90 scent albumin marker to simultaneously track thrombus formation and protein transport following injur

91 Accordingly, thrombus formation and stabilization under high arterial

92 LAAI, an unexpectedly high incidence of LAA thrombus formation and stroke was observed despite OAC t

93 (AF) and underlies the potential for atrial thrombus formation and subsequent stroke.

94 -Infestin-4) on trauma-induced microvascular thrombus formation and the subsequent outcome in 2 mouse

95 This study evaluated the incidence of LAA thrombus formation and thromboembolic events after LAAI.

96 vascular thiol isomerases that contribute to thrombus formation are yet to be defined at the molecula

97 A comprehensive understanding of thrombus formation as a physicochemical process that has

98 Because extracellular PDI is critical for thrombus formation but its extracellular substrates are

99 bosis, systemic delivery of miR-181b reduced thrombus formation by 73% in carotid arteries and prolon

100 n of platelet function and the prevention of thrombus formation by GLP-1R agonists represent potentia

101 tration of cLDL in mice accelerated arterial thrombus formation compared to treatment with native LDL

102 led pulmonary fibrin deposition, and trebled thrombus formation compared with wildtype littermates in

103 ng anti-CLEC-2 antibody, INU1, resulted in a thrombus formation defect in vivo and ex vivo, revealing

104 egulator of platelet activation and arterial thrombus formation dynamics.

105 Anti-miR-148a also reduced thrombus formation following intravascular platelet acti

106 oietic cell DREAMs are required for platelet thrombus formation following laser-induced arteriolar in

107 Here, we visualized thrombus formation in an in vivo murine model and an end

108 ner, reduces fibrin accumulation and impedes thrombus formation in blood under flow.

109 on of miR-30c increases PAI-1 expression and thrombus formation in DM2.

110 intravenous injection of exenatide inhibited thrombus formation in normoglycemic and hyperglycemic mi

111 Thrombus formation in the cerebral microcirculation has

112 nd in vivo, the absence of APP did not alter thrombus formation in the femoral artery.

113 ation, adhesion, spreading, aggregation, and thrombus formation in vitro and in vivo.

114 greater inhibition of platelet function and thrombus formation in vitro than chrysin under physiolog

115 Results showed effective inhibition of thrombus formation in vivo and enhancement of vascular t

116 negative role in platelet activation and in thrombus formation in vivo.

117 platelets and whether cLDL enhances arterial thrombus formation in vivo.

118 ts of cLDL on vascular cells, platelets, and thrombus formation in vivo.

119 tg) mice, indicating a higher propensity for thrombus formation in vivo.

120 ctivation of the LOX-1 receptor and enhances thrombus formation in vivo.

121 binding and inhibit platelet aggregation and thrombus formation in vivo.

122 receptor 2-mediated platelet activation and thrombus formation in vivo.

123 ed stent was the most important correlate of thrombus formation in VLST.

124 Thus, after a short time, thrombus formation is governed by alphaIIbbeta3 binding

125 he use of fibrinolytic agents to prevent new thrombus formation is limited by an increased risk of bl

126 c conditions in the absence of secreted PDI, thrombus formation is suppressed and maintains a quiesce

127 The time to occlusive thrombus formation lengthened in these mice and correlat

128 associated complications either by enhancing thrombus formation or by initiating various signaling ev

129 which platelet polyphosphate contributes to thrombus formation remains unclear.

130 dent FVIII activation sets the threshold for thrombus formation through contact phase-generated FIXa.

131 ocytes are actively recruited to the site of thrombus formation through interactions with platelets a

132 o1, which may contribute to Ca(2+) entry and thrombus formation under arterial shear.

133 Incubation with exenatide also inhibited thrombus formation under flow conditions in ex vivo perf

134 ntrol, exposure to fire simulation increased thrombus formation under low-shear (73+/-14%) and high-s

135 Arterial thrombus formation was analyzed in a murine carotid arte

136 Unexpected evidence of pulmonary artery thrombus formation was found in 19% of SSc-PAH patients.

137 High inhibition efficiency of L-PGMA NPs in thrombus formation was further confirmed in vivo with a

138 Thrombus formation was greater in mice transplanted with

139 l PVs were successfully isolated; no char or thrombus formation was observed.

140 x-4) or by chelation of extracellular Ca(2+) Thrombus formation was studied on collagen-coated surfac

141 l cell injury in the kidney that may lead to thrombus formation when severe or manifest by multilayer

142 rect inhibition of FXIa can block pathologic thrombus formation while preserving normal hemostasis.

143 herogenic lipoproteins and platelet-mediated thrombus formation with a specific focus on stroke.

144 sists well beyond red cell escape and mature thrombus formation, (3) the most critical events for lim

145 provide evidence for a novel role of ERp5 in thrombus formation, a function that may be mediated thro

146 nological synapse formation, shear-dependent thrombus formation, and agonist-driven blood clotting.

147 quires integrin activation for adherence and thrombus formation, and thus regulation of talin present

148 on a phenomenological mathematical model of thrombus formation, coagulation and platelet function ca

149 After each exposure, ex vivo thrombus formation, fibrinolysis, platelet activation, a

150 ha2beta1-collagen interaction and subsequent thrombus formation, however its practical application su

151 e suppression activates platelets, increases thrombus formation, impairs vascular function, and promo

152 These mediators can influence all aspects of thrombus formation, including platelet activation and ad

153 shown to potentiate platelet activation and thrombus formation, involving both CD40-dependent and -i

154 ity, immunogenicity risks and the hazards of thrombus formation, still need to be addressed.

155 ular traps (NETs) have been shown to promote thrombus formation.

156 planin expression in the venous wall trigger thrombus formation.

157 activity and plays an important role during thrombus formation.

158 hese observations suggest RBCs contribute to thrombus formation.

159 al cells on vascular injury, is required for thrombus formation.

160 oteins, among them vitronectin, critical for thrombus formation.

161 bleeding times and faster occlusive arterial thrombus formation.

162 I and FIX supports efficient FVIII-dependent thrombus formation.

163 ng a mechanistic explanation for the lack of thrombus formation.

164 that precedes development of carotid artery thrombus formation.

165 eta3 to support stable platelet adhesion and thrombus formation.

166 d PAI-1 in the treatment of lenti-miR-30c to thrombus formation.

167 d following vessel injury and participate in thrombus formation.

168 functions thus plays a role in pathological thrombus formation.

169 apex with the typical 3-layer appearance and thrombus formation.

170 ibute significantly to platelet function and thrombus formation.

171 nfluences blood coagulation and pathological thrombus formation.

172 ase in platelets) in platelet activation and thrombus formation.

173 erase (PDI), all of which serve to stabilize thrombus formation.

174 yphosphate make significant contributions to thrombus formation.

175 diminished both in vitro and in vivo during thrombus formation.

176 in subsequent platelet activation and stable thrombus formation.

177 ss in platelet function and life-threatening thrombus formation.

178 D) equations to represent three processes in thrombus formation: initiation, propagation and stabiliz

179 siological mechanisms that may lead to valve thrombus formation; and 3) provide perspective on the im

180 sisted thrombolysis, percutaneous mechanical thrombus fragmentation, or percutaneous or surgical embo

181 ortened plasma-clotting times, and increased thrombus frequency in the inferior vena cava.

182 ys and autoradiography using a fresh cardiac thrombus from an explanted human heart.

183 M1 occlusion with thrombus generated 50% mortality.

184 In vivo studies of thrombus generation in mice demonstrate that vitronectin

185 TIMI [Thrombolysis in Myocardial Infarction] thrombus grade >/=3), thrombus aspiration was associated

186 me and a significant decrease in the rate of thrombus growth (P < .05 vs wild-type), but not in the i

187 eceptor-2 (Tlr2)-deficient mice have reduced thrombus growth after carotid artery injury relative to

188 n alphaIIbbeta3 function, thereby supporting thrombus growth and consolidation.

189 gations, the spatial and temporal details of thrombus growth as a multicomponent process are not full

190 IN1, induced abnormal secretion and affected thrombus growth at arterial shear rate, indicating a rol

191 robiota restored a significant difference in thrombus growth between the genotypes.

192 del the processes of platelet deposition and thrombus growth in a continuous flow blood pump and ther

193 two illustrative benchmark problems: in vivo thrombus growth in an injured blood vessel and in vitro

194 ver, administration of VWF rescues defective thrombus growth in Tlr2(-/-) mice in vivo.

195 s regulated by gut microbiota and determines thrombus growth in Tlr2(-/-) mice.

196 Tsp1(-/-)/Vwf(+/-) mice exhibited delayed thrombus growth kinetics and prolonged occlusion time (P

197 ury-induced carotid artery thrombosis model, thrombus growth rate and the time to occlusion were prol

198 elium and favors platelet integrin-dependent thrombus growth.

199 ncreased the rate of platelet deposition and thrombus growth.

200 tic segmentation of the AAA and intraluminal thrombus (ILT) from medical images, the entire analysis

201 ed with either with 68Ga, 111In, or 99mTc as thrombus imaging agents for PET and SPECT.

202 recently reported the high target uptake and thrombus imaging efficacy of the novel fibrin-specific P

203 wed malapposed scaffold struts surrounded by thrombus in 7.1%, 9.0%, and 8.9% of struts in cases 1, 2

204 31 patients presented uniform, hypoechogenic thrombus in B-mode image.

205 (67%) patients, who were more likely to have Thrombus in Myocardial Infarction flow 0 or 1 in the cul

206 In this setting, thrombus in the left atrial appendage has been found to

207 culosis and a clinically unsuspected partial thrombus in the splenic vein on imaging.

208 eficiency causes prolonged bleeding, reduced thrombus incidence, thrombus size, fibrin and platelet d

209 pplication of alpha2AP-PFCs>60 minutes after thrombus induction no longer resulted in detectable 19F

210 w tailoring of pharmacotherapy to potentiate thrombus instability, through fragmentation of platelet

211 also assessed thrombin generation, platelet-thrombus interactions, and platelet accumulation in thro

212 les accumulated preferentially at the plaque-thrombus interface.

213 2) mobile mass detected on THV suspicious of thrombus, irrespective of dysfunction and in absence of

214 The spontaneous lysis of a coronary thrombus is a natural protective mechanism against lasti

215 Moreover, the homogeneity of the thrombus is also changed.

216 roups: systemic TEC, defined as intracardiac thrombus, ischemic stroke, or systemic arterial embolus;

217 minutes, HIT antigen was detected within the thrombus itself at the interface between the platelet co

218 , CHADS2 score and CHA2DS2-Vasc, left atrial thrombus (LAT), the five-grades of LASEC and video inten

219 ary efficacy end point was the percentage of thrombus load reduction from baseline to 15 hours accord

220 Yet, thrombus-mediated bloodflow occlusion was driven primari

221 utrophils did not affect onset, severity, or thrombus morphology.

222 utrophil and monocyte recruitment and delays thrombus neovascularization and resolution.

223 bstructions were identified: 1) pre-pump via thrombus obstructing the inflow cannula (26 events; 0.03

224 ores and increased mortality compared to the thrombus occlusion group.

225 re-prone based on the absence or presence of thrombus on the corresponding post-trigger magnetic reso

226 th transplant failure than does splenic vein thrombus or edema.

227 TEC, defined as Fontan conduit/right atrial thrombus or pulmonary embolus.

228 without apparent epicardial coronary artery thrombus or stenosis.

229 ay be able to help characterize endoleak and thrombus organization, regardless of the size, pressure,

230 Finally, improved imaging of ventricular thrombus plus the availability of non-vitamin K antagoni

231 s multicenter cohort of patients with STEMI, thrombus prevalence assessed by cardiac magnetic resonan

232 Inhibition of factor XIIa (FXIIa) provides thrombus protection without bleeding complications.

233 ce of significant residual intrastent plaque/thrombus protrusion (hazard ratio [HR], 2.35; P<0.01), i

234 P=0.002) and the residual intrastent plaque/thrombus protrusion (HR, 2.83; P=0.008) were confirmed a

235 ulprit lesion and residual intrastent plaque/thrombus protrusion was associated with adverse outcome.

236 cifically that of residual intrastent plaque/thrombus protrusion) on outcome.

237 In these studies, thrombus quantification has been based on a 2-dimensiona

238 VWF, and this was inversely correlated with thrombus red blood cell content.

239 An arterial thrombus required urgent revision 8 h after the operatio

240 Furthermore, our simulations showed that thrombus resistance imparted by fibrin was approximately

241 a supplemented fibrinogen level of 48%, the thrombus resistance increased by approximately 2.7-fold.

242 al blood resulted in a nonlinear increase in thrombus resistance, and for a supplemented fibrinogen l

243 harmacologic inhibition by pifithrin impairs thrombus resolution and is associated with increased fib

244 ies define mechanisms by which p53 regulates thrombus resolution by increasing inflammatory vascular

245 onist of p53, quinacrine, accelerates venous thrombus resolution in a p53-dependent manner, even afte

246 , and organ damage could not be reversed, as thrombus resolution was not achieved.

247 leukocytes are involved in fibrinolysis and thrombus resolution, and can regulate clearance of plate

248 Despite the clinical importance of venous thrombus resolution, the cellular and molecular mediator

249 mor suppressor gene p53 in regulating venous thrombus resolution.

250 tion and remain in the tissue throughout the thrombus resolution.

251 n thrombosis and its consequences for venous thrombus resolution.

252 tory response in venous thrombosis affecting thrombus resolution.

253 LV thrombus resolved in 22 of 25 patients (88%) restudied w

254 to 15 hours according to the length-adjusted thrombus score, obtained from standardized venograms and

255 lpha gain-of-function mutation to expand the thrombus shell.

256 Thrombus site expression of key fibrinolytic molecules w

257 Thrombus size correlated with elevated gal3 and interleu

258 Thrombus size was reduced 50% by GsMTx-4, independently

259 longed bleeding, reduced thrombus incidence, thrombus size, fibrin and platelet deposition in the lig

260 n in contracting clots and determines venous thrombus size, suggesting FXIII(a) is a potential target

261 ans by which fibrinolytic enzymes can reduce thrombus size.

262 e production of NO which, in turn, modulates thrombus size.

263 ture comprised of a linear fluid phase and a thrombus (solid) phase.

264 The thrombus solidifies significantly during the process of

265 smin inactivation showed a unique pattern of thrombus specificity, because unlike r-tPA, it did not d

266 xactly the same manner as the myocardium and thrombus specimen.

267 experimental evidence for the importance of thrombus stability and highlight the need for physiologi

268 in blood-lymph separation and implicated in thrombus stability in thrombosis and hemostasis.

269 flow conditions, review techniques to assess thrombus stability in vitro, and describe novel imaging

270 Thrombus stability is thus a direct determinant of clini

271 attention has been paid to factors affecting thrombus stability, despite evidence linking impaired sp

272 s can promote thrombus formation and enhance thrombus stability.

273 a, pharmacologic inhibition of GSK3 restores thrombus stability.

274 system and that this system is critical for thrombus stabilization and growth have identified factor

275 telet agents and anticoagulants that perturb thrombus structure affect the re-establishment of a tigh

276 promote their selective delivery and improve thrombus targeting.

277 clusion (defined as an isolated intracranial thrombus that impedes ascending blood flow) in the conte

278 und definitively helps to diagnose the tumor thrombus, the extent, and helps in redefining the TNM st

279 In CoreValve/Evolut Rs with thrombosis, the thrombus volume increased linearly with implant depth (R

280 THV deployment geometries were analyzed, and thrombus volumes were computed through manual 3-dimensio

281 a substantially higher extent in mice with a thrombus vs those without a thrombus.

282 Autologous thrombus was administered from below the filter in seven

283 The incidence of LV thrombus was as follows: (a) nonanterior infarction, LVE

284 In the control group, no LAA thrombus was detected and no stroke occurred (P<0.001).

285 Results LV thrombus was detected in 27 of 392 patients (7%): 18 (5%

286 here was no evidence of dissolution, and the thrombus was either near the injection site (M1) or flus

287 Splenic vein thrombus was identified in 10 of 20 failed transplants (

288 In the remaining 47 patients, LAA thrombus was identified on transesophageal echocardiogra

289 At PVR-TIPS completion, persistence of MPV thrombus was noted in 33 of 43 (77%) cases.

290 Each iatrogenic-administered thrombus was successfully captured by the filter until r

291 Analysis of IVC thrombosis revealed greater thrombus weight, length, myeloid cell recruitment, and m

292 er confirmed in vivo with a 50% reduction of thrombus weight.

293 of both uncovered and malapposed struts with thrombus were consistent among early- and newer-generati

294 ndoleak, solid organized thrombus, and fresh thrombus were identified and segmented by comparing the

295 No perforations, steam pops, or thrombus were noted.

296 gically detected as a clot was classified as thrombus, whereas a mass which was surgically detected a

297 dy 21 patients still presented hypoechogenic thrombus, whereas mixed echogenicity of thrombus appeare

298 tractile forces onto the fibrin network of a thrombus, which over time increases clot density and dec

299 genicity within it raised the suspicion of a thrombus, which was confirmed on a contrast-enhanced CT

300 eria were: symptoms for longer than 3 weeks, thrombus within 3 cm of the sapheno-femoral junction, in