ライフサイエンスコーパス: thrombi

1 )F-labeled small molecule for PET imaging of thrombi.

2 ases inflammatory injury and enlarges venous thrombi.

3 selectively targets nascent over preexisting thrombi.

4 rrently prevented the development of nascent thrombi.

5 , arrhythmias, and embolic events from mural thrombi.

6 ted to the scaffolds of particulate coronary thrombi.

7 eceptors, enabled the efficient detection of thrombi.

8 telets were the major source of HMGB1 within thrombi.

9 s for the growth, embolization, and lysis of thrombi.

10 ammatory cells and rare intravascular fibrin thrombi.

11 R4-P2Y12 dependent stabilization of platelet thrombi.

12 e robotic surgery for level II and level III thrombi.

13 ogated the ability of platelets to stabilize thrombi.

14 l I (67%), level II (30%) and level III (3%) thrombi.

15 s mediate platelet cross-linking in arterial thrombi.

16 date, including level I (n=4) and high level thrombi.

17 e structure of the body and head of the same thrombi.

18 patients (5.9%) developed distal superficial thrombi.

19 th the primary tumours and renal vein tumour thrombi.

20 lebrand factor, and inability to form stable thrombi.

21 igration," specifically mediated by platelet thrombi.

22 ys act together to produce fibrin-containing thrombi.

23 et VWF during the formation of platelet-rich thrombi.

24 detecting left atrial/LA appendage (LA/LAA) thrombi.

25 which requires Galpha13 and greatly expands thrombi.

26 the stable formation of occlusive arteriolar thrombi.

27 more fibrotic and higher vascularized venous thrombi.

28 but WT mice had more AGEs incorporated into thrombi.

29 imaging of evolving and dissolving arterial thrombi.

30 the viscoelastic scaffold of blood clots and thrombi.

31 -blood or plasma-fibrin clots and in in vivo thrombi.

32 orming either hemostatic plugs or pathologic thrombi.

33 acteristics were correlated with presence of thrombi.

34 1.2%, and 1.1% were positive for left atrial thrombi.

35 gnificant difference in the presence of lead thrombi.

36 with total cross-linked alpha(2)AP in plasma thrombi.

37 antial part of extracellular traps in murine thrombi.

38 e, although both may exacerbate pre-existing thrombi.

39 platelets are hyperreactive and form larger thrombi.

40 n average, 79% of glomeruli contained fibrin thrombi.

41 were more strongly incorporated into venous thrombi.

42 more neutrophils and H3Cit compared to fresh thrombi.

43 ensity of intra- and extravascular clots and thrombi.

44 nd more specifically NETs in ischemic stroke thrombi.

45 able to pharmacological r-tPA for dissolving thrombi.

46 ed to uncover the effects of NAC on arterial thrombi.

47 NETs form important constituents of cerebral thrombi.

48 to disseminated microvascular platelet rich-thrombi.

49 ed platelets in the inner core of developing thrombi.

50 he VWF that cross-link platelets in arterial thrombi.

51 ils were detected extensively throughout all thrombi.

52 wing 100% of the glomeruli containing fibrin thrombi.

53 antibody resulted in development of smaller thrombi.

54 hallmark of NETs, was observed in almost all thrombi.

55 Fresh (range: 5-27 days) and old thrombi (4-26 months) could be discriminated without ove

56 eal echocardiography follow-up, there were 3 thrombi (4.8%) and 13 (20%) with residual leak.

57 incidence of premature deaths, the number of thrombi (7 in 249 plaques), and also the degree of infla

58 14) and inflammation (CD68) were detected in thrombi (8 of 8) by immunohistochemistry.

59 physiological fibrinolysis fails to dissolve thrombi acutely and r-tPA (recombinant tissue-type plasm

60 scar and protection against intraventricular thrombi after acute infarction.

61 ected the location of lung emboli and venous thrombi after DVT-PE, revealing significant differences

62 GSAO(+) platelets form in occluding murine thrombi after ferric chloride injury and are attenuated

63 ation between old and fresh left ventricular thrombi after myocardial infarction would be of clinical

64 Factor XIII (FXIII) stabilizes thrombi against fibrinolysis by cross-linking alpha2-ant

65 ere functional in stabilizing FXIII-depleted thrombi against lysis.

66 ranulomatous meningitis and vasculitis, with thrombi and abundant angioinvasive fungi, with extensive

67 showed peritubular capillary and vasa recta thrombi and capillary basement membrane alterations prim

68 ulation (RPA) and occlusion of platelet-rich thrombi and clot shrinkage have been studied after flow

69 lar traps (EETs), which are present in human thrombi and constitute a substantial part of extracellul

70 sibility of (64)Cu-FBP8 PET to detect source thrombi and culprit emboli after deep vein thrombosis an

71 platelet aggregation, the formation of large thrombi and delayed clot retraction compared with wild-t

72 All thrombi and emboli contained few biconcave red blood cel

73 little description of how the composition of thrombi and emboli depends on their vascular origin and

74 ucible differences among arterial and venous thrombi and emboli related to their origin, destination

75 The structures within all of the thrombi and emboli were very tightly packed, in contrast

76 and/or death due to features of PAH: in situ thrombi and endothelial injury, angioproliferative remod

77 Thrombi and extensive vascular damage with multifaceted

78 e results highlight the susceptibility of LV thrombi and liver sinusoidal vessels to plasmin-mediated

79 tween the primary tumours, renal vein tumour thrombi and metastases.

80 s with at least 6-month-old chronic residual thrombi and normal D-dimer levels.

81 FXIII into depleted plasma stabilized plasma thrombi and normalized gamma-dimers and alpha-polymers f

82 cture and composition of arterial and venous thrombi and pulmonary emboli using high-resolution scann

83 s comprised the major constituents of venous thrombi and pulmonary emboli.

84 nique for the diagnosis of acute deep venous thrombi and pulmonary thromboemboli.

85 major component of both arterial and venous thrombi and represents an ideal candidate for imaging of

86 is a major component of arterial and venous thrombi and represents an ideal candidate for molecular

87 ears promising to disaggregate platelet-rich thrombi and restore vessel patency in acute thrombotic d

88 Noninvasive detection of deep venous thrombi and subsequent pulmonary thromboembolism is a se

89 ing could identify inflamed, recently formed thrombi and thereby improve the diagnosis of recurrent D

90 c are thought to become passively trapped in thrombi and therefore have not been considered a modifia

91 We used ICE to examine leads for thrombi and to measure the pulmonary artery systolic pre

92 antibody-mediated rejection with glomerular thrombi and transplant glomerulopathy.

93 on, immunohistological examinations of brain thrombi and vulnerable plaque material from patients wit

94 ms that give rise to the T1 signal in venous thrombi and whether changes in T1 relaxation time are in

95 T and PET probes with preformed 125I-labeled thrombi and with a nonbinding control probe using SPECT/

96 stability, through fragmentation of platelet thrombi and/or enhanced endogenous fibrinolysis, to redu

97 Willebrand factor (VWF) within platelet-rich thrombi, and cleavage depends on allosteric activation o

98 idans streptococci, was measured in 78.2% of thrombi, and periodontal pathogens were measured in 34.7

99 laques suddenly precipitate life-threatening thrombi; and the concepts of plaque burden, activity, an

100 In fresh thrombi, anticoagulation with phenprocoumon results in t

101 study is warranted to determine whether lead thrombi are a clinically relevant source of pulmonary em

102 and that platelets immobilized in occlusive thrombi are activated over time to produce IL-1beta.

103 chanical and chemical stability of clots and thrombi are affected by both the structure of the fibrin

104 However, because nonpathologic thrombi are also lysed, these drugs, although potentiall

105 ice have shown that stabilized non-occluding thrombi are covered by a fibrin network ('fibrin cap').

106 Evidence has emerged to suggest that thrombi are dynamic structures with distinct areas of di

107 Widespread thrombi are found among donor lungs rejected for transpl

108 These results imply that in vivo clots or thrombi are more dynamic structures than previously beli

109 drive the formation of infection-associated thrombi are poorly understood.

110 hat, in COVID-19, inflammatory microvascular thrombi are present in the lung, kidney, and heart, cont

111 It has long been assumed that clots and thrombi are stable structures until proteolytic digestio

112 hance thrombus formation and embolization of thrombi around the device into the circulation; on the o

113 N) fibril assembly through direct effects of thrombi as well as by virtue of mechanical strain.

114 elets after aggregation and were depleted in thrombi aspirated from MI patients, indicating the relea

115 patients and (2) prognostic relevance of LV thrombi at 1-year follow-up.

116 with elevated hematocrit (RBC(HIGH)) formed thrombi at a faster rate and had a shortened vessel occl

117 okinase prevented degradation of fibrin-rich thrombi at the LV valves and largely resolved the blood-

118 Thrombi because of superficial intimal erosion character

119 hat they are not only present in plaques and thrombi but also they may play a causative role in trigg

120 s should allow delayed enrichment on growing thrombi but not on the initial sealing layer of platelet

121 is a very sensitive method for detection of thrombi, but has some limitations, e.g. inability to dis

122 healing and to restore flow past obstructive thrombi, but little is known about the structure of cont

123 linical trials assessing detection of LA/LAA thrombi by cardiac computed tomography when compared wit

124 oduct that results from ordered breakdown of thrombi by the fibrinolytic system.

125 Fresh and old intracavitary thrombi can be reliably differentiated by deformation im

126 While thrombi can form under a variety of circumstances, lack

127 entify potential aetiologies such as cardiac thrombi, cardiac tumours, aortic arch disease and other

128 ternative to TEE for the detection of LA/LAA thrombi/clot, avoiding the discomfort and risks associat

129 henotypic reversion characterized by smaller thrombi comparable to those formed in WT mice, and resto

130 h COVID-19 (95% CI: 70%, 99.8%) had proximal thrombi compared with 47% of control patients (95% CI: 2

131 rate that Bambi-deficient mice form unstable thrombi compared with Bambi(+/+) mice.

132 a delayed time to the formation of occlusive thrombi compared with wild-type (WT) in a FeCl(3)-induce

133 ogical analysis of tissue sections show that thrombi contain very low numbers of bacteria.

134 Arterial thrombi contained a surprisingly large amount of fibrin,

135 Thrombi contained on average 20.3% +/- 10.1% VWF, and th

136 Older thrombi contained significantly more neutrophils and H3C

137 To study how they are incorporated into thrombi despite a lack of free activated integrin, we in

138 pped") platelets to become incorporated into thrombi despite their lack of active integrins.

139 Hemostatic thrombi develop a characteristic architecture in which a

140 In all patients, the thrombi dissolved with subcutaneous heparin.

141 ditions associated with platelet aggregation/thrombi (e.g., stroke), where vWF levels directly correl

142 s interactions, and platelet accumulation in thrombi ex vivo, in vitro, and in silico.

143 bonuclease accelerated the lysis of coronary thrombi ex vivo.

144 le.Properties of Ablation Lesions and Atrial Thrombi Experimental GroupControl (n=16)ATR (n=16)CHF (n

145 IVC thrombi extracted from Def(++) mice were composed of a f

146 Venous thrombi, fibrin- and rbc-rich clots triggered by inflamm

147 , and a failure to generate stable occlusive thrombi following FeCl3 injury of carotid arteries.

148 urden provides a test of the hypothesis that thrombi form in healthy vessels to trap or remove bacter

149 d spontaneous echocardiographic contrast and thrombi formation (16/51).

150 Hemostatic thrombi formed after a penetrating injury have a distinc

151 Hemostatic thrombi formed after a penetrating injury have a heterog

152 nd that cl-nanozyme can be cross-linked into thrombi formed after I/R injury in the brain, and this e

153 indings, compound exocytosis was observed in thrombi formed after severe laser injury of the vessel w

154 ion of platelet FXIII-A using Chandler model thrombi formed from FXIII-depleted plasma.

155 Neutrophils were abundantly present in thrombi formed in both groups, whereas extracellular cit

156 aster muscle arterioles, we herein show that thrombi formed in Cc2(-/-) mice were larger and more sta

157 this relation on measurements from occlusive thrombi formed in our flow chamber experiments, along wi

158 Previous studies have shown that hemostatic thrombi formed in response to penetrating injuries have

159 in fibrin deposition were observed in venous thrombi formed in sickle mice.

160 plex organization of the "caps." In platelet thrombi formed in whole blood on collagen under arterial

161 Occlusive thrombi formed under high flow shear rates develop very

162 Using a novel model of whole blood thrombi, formed under flow, we examine dose-dependent fi

163 Also common are thrombi forming on lesions without rupture (plaque erosi

164 Venous thrombi from alpha2AP(+/+) mice contained plasminogen ac

165 boli mirrored the most distal part of venous thrombi from which they originated, which differed from

166 lar citrullinated histones were seen only in thrombi from wild-type mice.

167 donor kidneys with diffuse glomerular fibrin thrombi (GFT) are safe to use.

168 f diseases; however, the mechanisms by which thrombi guide leukocytes to sites of vascular injury rem

169 months in the fresh thrombus group, 16 of 17 thrombi had disappeared (94%), and in 1 patient the thro

170 tory cells in contraction of blood clots and thrombi has not been investigated.

171 he imaging-triggered approach, we discovered thrombi in 32 (10.8%) of all 296 atherosclerotic coronar

172 We identified focal kidney fibrin thrombi in 6 of 42 (14%) autopsies.

173 Time to formation of thrombi in a FeCl3-induced thrombosis model was signific

174 Platelets stabilized FXIII-depleted thrombi in a transglutaminase-dependent manner.

175 ited thrombin and the formation of occlusive thrombi in AD; preserved cognition, cerebral perfusion,

176 ic enteritis with patchy necrosis and fibrin thrombi in arterioles (n = 2).

177 cardiac computed tomography assessing LA/LAA thrombi in comparison with TEE.

178 Thrombi in control and RBC(HIGH) mice did not differ in

179 cruitment of additional platelets to growing thrombi in flowing blood in vitro and translated into re

180 cted in atherosclerotic lesions and arterial thrombi in humans and mice.

181 nd showed strong binding to platelets within thrombi in infected mouse lungs.

182 correct bleeding in vivo and form occlusive thrombi in mesenteric vessels after FeCl(3) treatment.

183 of deep vein thrombosis and analyzed venous thrombi in peptidylarginine deiminase 4 (PAD4)-deficient

184 unable to form occlusive venous and arterial thrombi in response to endothelial injury, a defect that

185 d the presence of disseminated platelet-rich thrombi in terminal arterioles and capillaries of major

186 gen consumption and the deposition of fibrin thrombi in the glomerular capillaries.

187 with Bambi(+/+) bone marrow formed unstable thrombi in the laser-induced thrombosis model that reced

188 E) is the gold standard for the exclusion of thrombi in the left atrial appendage (LAA) before ablati

189 urrent DVT from 6-month-old chronic residual thrombi in the leg veins.

190 rs concomitant with the appearance of venous thrombi in the lung.

191 life-threatening disorders characterized by thrombi in the microvasculature resulting in thrombocyto

192 o test this, we generated occlusive VWF-rich thrombi in the middle cerebral artery (MCA) of mice.

193 Presence of tumor thrombi in the portal veins (venous metastases) is a cli

194 xert a thrombolytic effect in VWF-containing thrombi in the setting of stroke.

195 associated intramural hematoma (n = 9), and thrombi in the true or false lumens (n = 11).

196 acterized by increased fibrin deposition and thrombi in the vasculature, indicative of a further incr

197 ite the presence of occasional microvascular thrombi in various organ tissues.

198 g inflammatory vascular remodeling of venous thrombi in vivo, and the potential therapeutic applicati

199 ced sonothrombolysis for aged CVC associated thrombi in vivo.

200 facilitates reduction of aged CVC associated thrombi in vivo.

201 ctivity and promoted generation of occlusive thrombi in wild-type mice, whereas SIRT1 activation was

202 han their healthy counterparts; these larger thrombi induced by cancer were not seen in Gas6(-/-) mic

203 Thrombi induced in carotid arteries of C57Bl6 mice in vi

204 vasculature, leading to bacterial and blood thrombi, infectious vasculitis and vascular leakage.

205 Both toxins induced glomerular platelet-rich thrombi, interstitial hemorrhage, and tubular injury.

206 results suggest that stability of occlusive thrombi involves additional and as-yet-unidentified mech

207 The formation of platelet thrombi is determined by the integrin alphaIIbbeta3-medi

208 ic surgery for selected level I and II caval thrombi is feasible.

209 trated that the inner structure of occlusive thrombi is heterogeneous and primarily determined by the

210 en the extent of glomeruli containing fibrin thrombi is less than 50% and donor renal function is pre

211 e formation of gap junctions within platelet thrombi is required for the control of clot retraction.

212 Welsh and colleagues determine how platelet thrombi limit the loss of plasma-borne proteins from the

213 cluding platelet aggregometry, platelet-rich thrombi lysis assays, thromboelastography (ROTEM), and h

214 ctedly, mice lacking platelet PITPalpha form thrombi normally at sites of intravascular injuries.

215 Two days after siRNA injection, thrombi (occlusive) were observed in vessels (large and

216 ecruitment and migration induced by platelet thrombi occurred most prominently in veins but could als

217 rimary structural protein of blood clots and thrombi, occurs through binding of knobs 'A' and 'B' in

218 H3Cit was more abundant in thrombi of cardioembolic origin compared to other etiolo

219 experimentally observed distinctions between thrombi of different physical etiology.

220 cluded pulmonary blood vessels with vascular thrombi often exhibited endothelial necrosis surrounded

221 eter values, the model produced stable dense thrombi on a similar timescale to the experiments.

222 ss, Cyfip1-deficient platelets formed stable thrombi on collagen fibers ex vivo and in 2 models of oc

223 the kidneys, which led to highly conspicuous thrombi on PET and SPECT images.

224 ult in targeting of S. aureus to fibrin-rich thrombi or elastin-rich tissues.

225 FbetaRII-KO endothelial cells, murine venous thrombi, or endarterectomy specimens and plasma of CTEPH

226 % of control patients (95% CI: 50%, 84%) had thrombi (P = .02).

227 17.8211.6+/-17.6231.5+/-29.0176.8+/-22.2N of thrombi per dog5.4+/-0.44.7+/-0.35.6+/-0.46.5+/-0.4Prese

228 ates from platelet aggregates at the base of thrombi, primarily in association with fibrin.

229 have demonstrated that the fibrin network of thrombi progressively compacts over a 2-hour period.

230 agents by focusing on the destabilization of thrombi rather than the prevention of platelet aggregati

231 In contrast, 14 of the 15 old thrombi remained unchanged in size and deformation (1 th

232 ed thrombus scoring) relative to those whose thrombi resolved (median, 25th/75th percentile): 92.5 (8

233 Central venous catheter (CVC) thrombi result in significant morbidity in children, and

234 e-dependently dissolved these t-PA-resistant thrombi resulting in fast restoration of MCA patency and

235 understand thrombus composition, we analyzed thrombi retrieved from ischemic stroke patients and foun

236 Sixty-eight thrombi retrieved from ischemic stroke patients undergoi

237 PET quantification of the venous thrombi revealed that probe uptake was greater in younge

238 ing antibody to alpha2AP into FXIII-depleted thrombi revealed that the stabilizing effect of platelet

239 gnificantly reduced the occurrence of atrial thrombi, reversed action potential alterations, and fina

240 asound and intravenous microbubbles dissolve thrombi (sonothrombolysis) and increase angiographic rec

241 ocytes, were also observed in human arterial thrombi taken from patients.

242 of APP in blood cells, developed much larger thrombi than control animals, and were more sensitive to

243 WT mice with cancer developed larger thrombi than their healthy counterparts; these larger th

244 le (PFO) may permit arterial embolization of thrombi that accumulate on the leads of cardiac implanta

245 AC administration promotes lysis of arterial thrombi that are resistant to conventional approaches su

246 Hypercoagulability increases risk of thrombi that cause cardiovascular events.

247 ttle is known about the exact composition of thrombi that cause ischemic stroke.

248 Thrombi that complicate superficial erosion seem more pl

249 Platelet thrombi that form in coronary and carotid arteries also

250 dicated that platelet aggregation stabilizes thrombi that form in the lymphatic vascular environment

251 ombosis model that receded more rapidly than thrombi that formed in Bambi(+/+) mice receiving Bambi(-

252 The formation of a fibrin cap prevents small thrombi that frequently develop in the absence of major

253 lpha2AP-PFCs can visualize freshly developed thrombi that might still be susceptible to pharmacologic

254 hrough luminal narrowing or by precipitating thrombi that obstruct blood flow to the heart (coronary

255 During infection, mice developed thrombi that persisted for weeks within the liver.

256 however, these valves lacked the fibrin-rich thrombi that prevent blood from entering the lymphatic s

257 Fibrin is a biopolymer that gives thrombi the mechanical strength to withstand the forces

258 ht cleave the VWF multimers inside occlusive thrombi, thereby leading to their dissolution and arteri

259 roy pathological, life-threatening clots and thrombi (thrombolysis).

260 Small arterial, venous thrombi, thrombotic depositions on damaged endothelial s

261 that form tightly adherent, shear-resistant thrombi to prevent blood loss after vessel injury.

262 These thrombi typically were found in arteries presenting with

263 disintegration/fibrinolysis of platelet-rich thrombi under arterial flow conditions, review technique

264 ation impairs the platelet's ability to form thrombi under flow and spread normally as a consequence

265 omographic imaging for detecting subclinical thrombi upon both surgically implanted and THVs, has gen

266 ve and specific identification of developing thrombi using background-free 19F magnetic resonance ima

267 study were to assess the (1) incidence of LV thrombi using cardiac magnetic resonance in a multicente

268 lue for the total amount of bacterial DNA in thrombi was 16 times higher than that found in their blo

269 The incidence of LA/LAA thrombi was 8.9% (SD, +/-7).

270 The presence of thrombi was associated with larger infarcts (P<0.001), l

271 and oral viridans streptococci DNA-positive thrombi was found (odds ratio, 13.2; 95% confidence inte

272 The presence of thrombi was independently associated with the incidence

273 The ability of scFvSCE5-scuPA to lyse thrombi was lost in plasminogen-deficient mice, but coul

274 Interestingly, ex vivo lysis of patient thrombi was more successful when adding DNase 1 to stand

275 al thrombosis model, the formation of stable thrombi was significantly impaired, preventing vessel oc

276 in our clinical analysis of coronary artery thrombi, we identified female patients with stent thromb

277 t sites of endothelial injury; however, only thrombi were capable of inducing directed intravascular

278 Thrombi were characterized by immunostaining, flow cytom

279 LV thrombi were detected in 26 patients (3.5%) in the overa

280 After 6-month mean follow-up, asymptomatic thrombi were detected in 4 patients (1 bilateral, 4 unil

281 ying this threshold value in substudy-II, 17 thrombi were echocardiographically classified as fresh (

282 usive thrombi within 5 hours after ligation; thrombi were even larger in plasminogen-deficient mice (

283 Venous thrombi were induced in both wild-type (WT) and Gas6-def

284 nt flow venous thrombosis model Pecam-1(-/-) thrombi were larger, persisted for longer periods of tim

285 Fibrin-containing platelet thrombi were observed at the LVV and in the terminal TD

286 No lead-associated thrombi were observed.

287 atory-masked analyses for the presence of LV thrombi were performed.

288 RFA, and then hearts were removed and atrial thrombi were quantified by histomorphometry.

289 ient for an open-heart surgery, in which two thrombi were removed.

290 mouse model of ischemic stroke, although the thrombi were resistant to fibrinolysis or traditional an

291 Finally, excised thrombi were used for histology.

292 saggregating the external layer of occlusive thrombi, which is constituted of platelet aggregates for

293 hat delayed enrichment of CD39 on developing thrombi will allow for a low and safe systemic concentra

294 Developing thrombi with a diameter<0.8 mm could be visualized unequ

295 (18)F-GP1 bound to thrombi with a mean clot-to-blood ratio of 95.

296 as a genuine retraction process, as treating thrombi with blebbistatin to inhibit myosin IIa-mediated

297 ted by performing ex vivo lysis of retrieved thrombi with DNase 1 and t-PA.

298 rrying Fibgamma390-396A and produced smaller thrombi with fewer rbc than WT mice.

299 lpha2AP(+/+) mice developed large, occlusive thrombi within 5 hours after ligation; thrombi were even

300 omoting platelet adhesion and enlargement of thrombi within the microfluidic channels.