ライフサイエンスコーパス: thrombus

1 bus detection (p = 0.13 vs. patients without thrombus).

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

3 astography probably corresponds with chronic thrombus.

4 d complement iC3b and C5b-9 in a human brain thrombus.

5 tion fraction to up to 3 patients without LV thrombus.

6 ld be administered to dissolve the occluding thrombus.

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

8 rove accurate assessment of the exact age of thrombus.

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

10 mic stroke and patients with an intracardiac thrombus.

11 tion of interactions between platelets and a thrombus.

12 for simulating the formation and growth of a thrombus.

13 model which simulates the initiation of the thrombus.

14 ng in platelets and is required for a stable thrombus.

15 fied atherosclerotic plaque and intraluminal thrombus.

16 modality imaging ruled out the presence of a thrombus.

17 ch sufficiently reduced TPA flux through the thrombus.

18 19 pneumonia even in the absence of arterial thrombus.

19 on, noninducibility or left atrial appendage thrombus.

20 d by a reduction of leukocyte content in the thrombus.

21 tact to collagen fibers at the bottom of the thrombus.

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

23 , microsurgery, targeted drug/cell delivery, thrombus ablation, and wound healing are reviewed from t

24 In aortic aneurysmal disease, a thrombus adherent to the aortic wall within the expandin

25 ictating the deformation and remodeling of a thrombus after its formation in hemostasis.

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

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

28 lasminogen, and alpha2AP, which changed with thrombus age.

29 ist released by platelets was limited to the thrombus and a boundary layer downstream, thus restricti

30 from both knockout mice, collagen-dependent thrombus and fibrin formation under flow were enhanced.

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

32 ufficient to balance drag forces on an early thrombus and keep it intact.

33 were analyzed (maximal diameter and surface, thrombus and lumen volumes, maximal wall pressure, and w

34 ith annualized rates of 3.7% and 0.8% for LV thrombus and matched non-LV thrombus patients, respectiv

35 activation leads to the formation of a firm thrombus and thus the sealing of a damaged blood vessel.

36 lial matrix, by fibrin and fibrinogen in the thrombus, and by a remarkable number of other ligands.

37 eplacement (TTVR), including valve function, thrombus, and endocarditis.

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

39 e interval [CI]: 79%, 100%) had at least one thrombus, and only 69% of control patients (95% CI: 50%,

40 d device position, absence of device-related thrombus, and peridevice leak of <=5 mm.

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

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

43 , conduction abnormalities, and intracardiac thrombus are common in patients with cardiac amyloidosis

44 e while deformations throughout the wall and thrombus are inferred from optical coherence tomography.

45 ctions between flowing and coagulated blood (thrombus) are crucial in dictating the deformation and r

46 3 to 5.26; p = 0.002) and a smaller baseline thrombus area (HR: 0.66; 95% CI: 0.45 to 0.96; p = 0.031

47 probe (p = 0.047) and a smaller nonenhancing thrombus area compared to intact AAAs (p = 0.001).

48 justed mean difference in post-randomization thrombus area was similar between groups: -218.2 mum(2)

49 of the aneurysm wall to size of nonenhancing-thrombus-area predicted AAA rupture with high sensitivit

50 ng of bonds between platelets and treats the thrombus as an evolving porous, viscoelastic material, w

51 ation and more proresolving monocytes in the thrombus, as well as an increased number of cells in an

52 herefore, to describe the temporal trends in thrombus aspiration (TA) use in Sweden before, during, a

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

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

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

56 Thrombus aspiration during percutaneous coronary interve

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

58 and after dissemination of the TASTE trial (Thrombus Aspiration in ST-Elevation Myocardial Infarctio

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

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

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

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

63 use of glycoprotein IIb/IIIa inhibitors and thrombus aspiration.

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

65 us because of its unique ability to identify thrombus based on tissue characteristics related to avas

66 rdiography for the detection of intracardiac thrombus because of its unique ability to identify throm

67 ch and observe in real-time formation of the thrombus, blockage of cerebral perfusion and eventually

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

69 tion, there is a strong signal toward higher thrombus burden and poorer outcomes.

70 utic measures to efficiently reduce existent thrombus burden are scarce.

71 Thrombus burden as measured by the Modified Miller Index

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

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

74 f thrombus resolution, significantly reduced thrombus burden, with significantly less neutrophil infi

75 cular to left ventricular diameter ratio and thrombus burden.

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

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

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

79 Venous thrombus weights were measured and thrombus composition was determined by Martius scarlet b

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

81 : (1) a priming role of platelet adhesion in thrombus contraction and subsequent fibrin formation; (2

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

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

84 LV thrombus detected by LGE CMR but not by echocardiography

85 te contemporary antithrombotic treatment, LV thrombus detected by LGE CMR is associated with a 4-fold

86 nostic significance of left ventricular (LV) thrombus detected by LGE CMR is unknown.

87 lso compared outcomes among patients with LV thrombus detected by LGE CMR stratified by whether the L

88 study of consecutive adult patients with LV thrombus detected by LGE CMR who were matched on the dat

89 tients received anticoagulant therapy before thrombus detection (p = 0.13 vs. patients without thromb

90 Biodistribution and thrombus detection was investigated in cynomolgus monkey

91 as no effect on models of arterial or venous thrombus development, but remarkably prevents experiment

92 lpha2AP appears essential for stasis-induced thrombus development, which suggests that targeting alph

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

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

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

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

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

98 Thrombus dissolution was markedly accelerated in mice wi

99 Despite greater thrombus dissolution, alpha2-antiplasmin inactivation al

100 3-kinase dose dependently modulate platelet thrombus dynamics.

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

102 ectomy in the anterior cerebral circulation, thrombus embolization resulting in Willisian collateral

103 o vessel occlusion and significantly reduced thrombus embolization.

104 We recently reported that peri-thrombus endothelium is targeted by HIT antibodies, but

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

106 inly due to a high incidence of intracardiac thrombus even among patients who received adequate antic

107 on generates drag forces which the fluid and thrombus exert on one another.

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

109 gen all attenuated along with a reduction in thrombus formation (both in vitro and in vivo).

110 on on biomaterials and related mechanisms of thrombus formation (thrombosis).

111 Pathogenic thrombus formation accounts for the etiology of many ser

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

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

114 esterol increased platelet responsiveness in thrombus formation and ensuing fibrin formation, resulti

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

116 een published on the role of lamellipodia in thrombus formation and stability.

117 Accordingly, thrombus formation and stabilization under high arterial

118 The identification of a ruptured plaque with thrombus formation and subsequent occlusion or downstrea

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

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

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

122 tive phenotyping approach of platelet-fibrin thrombus formation has revealed interaction mechanisms o

123 event or block VWF oligomerization attenuate thrombus formation in a murine model of HIT.

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

125 we studied platelet activation and arterial thrombus formation in Apoe(-/-) and Ldlr(-/-) mice fed a

126 tion in the lungs, but the cancer-associated thrombus formation in CLEC-2-depleted mice was significa

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

128 y inoculated in the back skin showed massive thrombus formation in the lungs, but the cancer-associat

129 croscopy demonstrated reduced post-traumatic thrombus formation in the pericontusional cortical micro

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

131 c ligand, SR12813, was observed to attenuate thrombus formation in vivo in humanised PXR transgenic m

132 om vascular cells, is essential for complete thrombus formation in vivo, but other extracellular ERp5

133 Consequently, targeting of EETs diminished thrombus formation in vivo, which identifies this approa

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

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

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

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

138 mounts of serotonin that they release during thrombus formation or acute inflammation.

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

140 which platelet polyphosphate contributes to thrombus formation remains unclear.

141 Given that coagulation is involved in the thrombus formation stage on atherosclerotic plaque ruptu

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

143 Platelet aggregation responses, as well as thrombus formation under arterial flow conditions on col

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

145 tive Ca2+ signaling translated into impaired thrombus formation under flow and a protection of Bin2fl

146 differ between a static spreading assay and thrombus formation under flow.

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

148 gation at low doses of collagen and impaired thrombus formation under shear stress.

149 addition to its effects on acute thrombosis, thrombus formation was also markedly suppressed in alpha

150 Markedly, thrombus formation was enhanced in blood from chimeric m

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

152 Thrombus formation was quantified by intravital microsco

153 No significant thrombus formation was seen in alpha2AP(-/-) mice (P < .

154 Similarly, arterial thrombus formation was significantly reduced in response

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

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

157 elet aggregation, oxygen radical output, and thrombus formation, and carotid occlusion, while tail he

158 exhibited prolonged bleeding times, impaired thrombus formation, and reduced survival following major

159 ipodium formation is not required for stable thrombus formation, and that morphological changes of pl

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

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

162 isorders indicated characteristic defects in thrombus formation, in cases of factor V, XI or XII defi

163 While thrombin is the key protease in thrombus formation, other coagulation proteases, such as

164 oles of factor XIIIa-specific cross-links in thrombus formation, regression, or probability for embol

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

166 en-dependent platelet aggregation, adhesion, thrombus formation, superoxide anion generation, and sur

167 eptor 1), leading to platelet activation and thrombus formation, which can be inhibited by rivaroxaba

168 onstrated poor vascularization and increased thrombus formation.

169 e electrical isolation (LAAEI) could lead to thrombus formation.

170 therosclerotic plaque rupture and subsequent thrombus formation.

171 itrullinates plasma proteins, thus affecting thrombus formation.

172 ects of PXR ligands on platelet function and thrombus formation.

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

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

175 that precedes development of carotid artery thrombus formation.

176 in subsequent platelet activation and stable thrombus formation.

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

178 planin expression in the venous wall trigger thrombus formation.

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

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 In vivo studies of thrombus generation in mice demonstrate that vitronectin

184 attributes including patient survival, tumor thrombus, genetic profile, and the liver-specific proteo

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

186 hrombosis, stent thrombosis, higher modified thrombus grade post first device with consequently highe

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

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

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

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

193 boundary layer downstream, thus restricting thrombus growth into the vessel lumen.

194 f GPVI and CLEC-2 agonists and a decrease in thrombus growth on a collagen surface under arterial she

195 ncreased the rate of platelet deposition and thrombus growth.

196 To confirm or rule out a suspected thrombus, he underwent gadolinium-enhanced cardiac magne

197 control patients, mainly due to intracardiac thrombus identified on transesophageal echocardiogram (1

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

199 Our prior work implicated intraluminal thrombus (ILT) in AAAs to be a potential source of syste

200 he association of preprocedural intraluminal thrombus (ILT) volume with aneurysm sac growth following

201 Magnetic resonance direct thrombus imaging (MRDTI), a technique without intravenou

202 n 1 patient and intraluminal local transient thrombus in a second patient.

203 31 patients presented uniform, hypoechogenic thrombus in B-mode image.

204 (67%) patients, who were more likely to have Thrombus in Myocardial Infarction flow 0 or 1 in the cul

205 shape, distance to the first bifurcation and thrombus in the left atrial appendage.

206 septal aneurysms (8), septal bags (6) and 1 thrombus in the left atrial appendage.

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

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

211 les accumulated preferentially at the plaque-thrombus interface.

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

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

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

215 level of inter-observer agreement was venous thrombus (kappa = 0.600).

216 prognosis and management of left ventricular thrombus (LVT).

217 ive, thereby allowing us to study effects of thrombus microstructure and properties on its deformatio

218 Moreover, we combine this proposed thrombus model with a particle-based model which simulat

219 n input variable in the proposed phase-field thrombus model.

220 neutrophils did not affect onset, severity, thrombus morphology, or liver fibrin deposition.

221 tor XII did not alter VT onset, severity, or thrombus morphology.

222 by echocardiography versus patients with LV thrombus not detected by echocardiography (P=0.25).

223 The volume fraction of a thrombus obtained from the particle simulation is mapped

224 3 of the CA patients (31%) with intracardiac thrombus on transesophageal echocardiogram received adeq

225 without apparent epicardial coronary artery thrombus or stenosis.

226 troke, major bleeding, filter migration, CCA thrombus, or stenosis.

227 Although coronary thrombus overlying a disrupted atherosclerotic plaque ha

228 us patients compared with the matched non-LV thrombus patients (P<0.001), with annualized rates of 3.

229 e of embolism was significantly higher in LV thrombus patients compared with the matched non-LV throm

230 Of 157 LV thrombus patients, 155 were matched to 400 non-LV thromb

231 and 0.8% for LV thrombus and matched non-LV thrombus patients, respectively.

232 nce of embolism compared with matched non-LV thrombus patients.

233 bus patients, 155 were matched to 400 non-LV thrombus patients.

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

235 t is able to rapidly interrupt arterial-type thrombus propagation at exceedingly low doses (<2 ug/kg,

236 monia underwent DECTPA to diagnose pulmonary thrombus (PT); 11 underwent surveillance DECTPA 14 +/-11

237 the ATTRACT trial (Acute Venous Thrombosis: Thrombus Removal With Adjunctive Catheter-Directed Throm

238 The ATTRACT trial (Acute Venous Thrombosis: Thrombus Removal with Adjunctive Catheter-Directed Throm

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

240 murine endothelial cells and improved venous thrombus resolution and pulmonary vaso-occlusions in End

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

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

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

244 was the proportion of children with complete thrombus resolution, and freedom from recurrent venous t

245 ension (CTEPH) is characterized by defective thrombus resolution, pulmonary artery obstruction, and v

246 PM that was enriched at the natural onset of thrombus resolution, significantly reduced thrombus burd

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

248 nction but was associated with faster venous thrombus resolution, whereas endothelial TGFbetaRII dele

249 bo-inflammatory disease in vivo and improves thrombus resolution.

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

251 Although this might reduce mural-thrombus risk, the relatively more complex vortex phenom

252 The mean thrombus score using any of the three scoring systems yi

253 that platelets rather form filopodia in the thrombus shell, and are flattened with filopodium-like s

254 of tissue plasminogen activator (tPA) at the thrombus site.

255 The primary endpoint was thrombus size at the post-randomization visit with plate

256 on, at which time ex vivo assays to quantify thrombus size under dynamic flow conditions and platelet

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

258 ans by which fibrinolytic enzymes can reduce thrombus size.

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

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

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

262 We found that rivaroxaban reduced arterial thrombus stability in a mouse model of arterial thrombos

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

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

265 Thrombus stability is thus a direct determinant of clini

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

267 s can promote thrombus formation and enhance thrombus stability.

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

269 ssed platelet adhesion, platelet activation, thrombus structure and fibrin clot formation in real tim

270 Kinetics of platelet activation, thrombus structure and fibrin formation were assessed by

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

272 ian, three-dimensional, phase-field model of thrombus that is calibrated with existing in vitro exper

273 rta, often with a false lumen and intramural thrombus that thickens the wall.

274 bolism was not different in patients with LV thrombus that was also detected by echocardiography vers

275 ional study to integrate the initiation of a thrombus through platelet aggregation with its subsequen

276 and effective release of tPA at the site of thrombus, thus achieving efficient clot dissolution whil

277 nd increases the exposure of an intracranial thrombus to alteplase (recombinant tissue plasminogen ac

278 e thrombolysis by increasing the exposure of thrombus to endogenous and exogenous thrombolytics.

279 igation of platelet morphology in an induced thrombus under flow revealed that platelets rather form

280 In addition, RP101075 treatment reduced thrombus volume, which was accompanied by a reduction of

281 were positively correlated with AAA size and thrombus volume.

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

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

284 Autologous thrombus was administered from below the filter in seven

285 cted by LGE CMR stratified by whether the LV thrombus was also detected by echocardiography or not.

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

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

288 An entrapped thrombus was found in the filter in 6 patients.

289 Device thrombus was observed in 34 patients (4.1%) and was not

290 Device-related thrombus was seen in 2.7%.

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

292 LV thrombus was the only independent predictor of the compo

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

294 Venous thrombus weights were measured and thrombus composition

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

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

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

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

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

300 Transesophageal-echocardiogram revealed thrombus within the left atrium and ventricle.