ライフサイエンスコーパス: thrombi

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

2 nd more specifically NETs in ischemic stroke thrombi.

3 able to pharmacological r-tPA for dissolving thrombi.

4 R4-P2Y12 dependent stabilization of platelet thrombi.

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

6 ogated the ability of platelets to stabilize thrombi.

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

8 s mediate platelet cross-linking in arterial thrombi.

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

10 patients (5.9%) developed distal superficial thrombi.

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

12 th the primary tumours and renal vein tumour thrombi.

13 lebrand factor, and inability to form stable thrombi.

14 igration," specifically mediated by platelet thrombi.

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

16 NETs form important constituents of cerebral thrombi.

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

18 which requires Galpha13 and greatly expands thrombi.

19 were more strongly incorporated into venous thrombi.

20 to disseminated microvascular platelet rich-thrombi.

21 the stable formation of occlusive arteriolar thrombi.

22 but WT mice had more AGEs incorporated into thrombi.

23 imaging of evolving and dissolving arterial thrombi.

24 the viscoelastic scaffold of blood clots and thrombi.

25 ed platelets in the inner core of developing thrombi.

26 orming either hemostatic plugs or pathologic thrombi.

27 acteristics were correlated with presence of thrombi.

28 1.2%, and 1.1% were positive for left atrial thrombi.

29 gnificant difference in the presence of lead thrombi.

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

31 further enhance lysis of alpha(2)AP depleted thrombi.

32 d treat the formation of venous and arterial thrombi.

33 ects, reducing the size and the stability of thrombi.

34 ombi structurally similar to human deep vein thrombi.

35 associated with left atrial appendage (LAA) thrombi.

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

37 ils were detected extensively throughout all thrombi.

38 wing 100% of the glomeruli containing fibrin thrombi.

39 antibody resulted in development of smaller thrombi.

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

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

42 ases inflammatory injury and enlarges venous thrombi.

43 selectively targets nascent over preexisting thrombi.

44 rrently prevented the development of nascent thrombi.

45 , arrhythmias, and embolic events from mural thrombi.

46 ted to the scaffolds of particulate coronary thrombi.

47 more neutrophils and H3Cit compared to fresh thrombi.

48 eceptors, enabled the efficient detection of thrombi.

49 telets were the major source of HMGB1 within thrombi.

50 ensity of intra- and extravascular clots and thrombi.

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

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

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

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

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

56 scar and protection against intraventricular thrombi after acute infarction.

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

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

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

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

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

62 microscopy revealed extensive platelet-rich thrombi along the entire length of the graft in HO-1(-/-

63 enable them to form shear-resistant arterial thrombi, an essential element in the pathogenesis of hum

64 ild-type mice showed increased platelet-rich thrombi and a higher percentage of occluded vessels.

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

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

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

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

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

70 Thrombi and extensive vascular damage with multifaceted

71 s independent of platelets' capacity to form thrombi and instead relies on the secretion of their gra

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

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

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

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

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

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

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

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

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

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

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

83 Devices for aspiration of thrombi and thrombus-derived vasoconstrictor, thrombogen

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

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

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

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

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

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

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

91 In fresh thrombi, anticoagulation with phenprocoumon results in t

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

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

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

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

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

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

98 Widespread thrombi are found among donor lungs rejected for transpl

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

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

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

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

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

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

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

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

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

108 Thrombi because of superficial intimal erosion character

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

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

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

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

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

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

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

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

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

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

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

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

121 Blood clots and thrombi consist primarily of a mesh of branched fibers m

122 lysis of IC-injected mice revealed pulmonary thrombi consisting of platelet aggregates and fibrin.

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

124 Older thrombi contained significantly more neutrophils and H3C

125 On DW images, 15 of 19 neoplastic thrombi demonstrated same SI and four showed lower SI th

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

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

128 Hemostatic thrombi develop a characteristic architecture in which a

129 to anti-CD40L ICs and had pulmonary platelet-thrombi devoid of fibrin.

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

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

132 bonuclease accelerated the lysis of coronary thrombi ex vivo.

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

134 with control mice, elevated FVIII stabilized thrombi (fewer emboli) after short injury, but it had no

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

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

137 ndent increase in PDI was observed in murine thrombi following injury.

138 Hemostatic thrombi formed after a penetrating injury have a distinc

139 Hemostatic thrombi formed after a penetrating injury have a heterog

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

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

142 Plasma model thrombi formed from FXIII or alpha(2)AP depleted plasma

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

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

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

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

147 /-) mice, while small, hemostatically active thrombi formed in venules.

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

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

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

151 c status based on the lysis of platelet-rich thrombi from native blood using the point-of-care GTT ca

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

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

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

155 Each of the six bland thrombi had lower SI than the primary HCC (P < .001).

156 Laparoscopic management of IVC tumor thrombi has been demonstrated in animal models and more

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

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

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

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

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

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

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

164 ke place within seconds to successfully form thrombi in flowing blood.

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

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

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

168 imulates the formation of occlusive platelet thrombi in mice but not in the size- and flow-matched ca

169 her may prevent the development of occlusive thrombi in mice fed a high-fat diet.

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

171 s, unlike ADAP+/+ platelets, formed unstable thrombi in response to carotid artery injury.

172 rrhage and placental disruption, with fibrin thrombi in some maternal blood sinusoids.

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

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

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

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

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

178 In comparison, thrombi in the micro- and macrovasculature of clopidogre

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

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

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

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

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

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

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

186 ced sonothrombolysis for aged CVC associated thrombi in vivo.

187 facilitates reduction of aged CVC associated thrombi in vivo.

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

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

190 Thrombi induced in carotid arteries of C57Bl6 mice in vi

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

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

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

194 Spontaneous lysis of platelet-rich thrombi is an important defense mechanism against lastin

195 The formation of occlusive thrombi is complex, involving the integration of many mo

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

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

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

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

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

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

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

203 al components of hemostatic and pathological thrombi, may represent biologically relevant substrates

204 rombotic angiopathy with platelet and fibrin thrombi, neuronal necrosis in various states of resoluti

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

206 Mobile thrombi, not routinely recognized on transthoracic echoc

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

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

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

210 g with thrombi versus 33 +/- 7 mm Hg without thrombi (odds ratio, 1.11; 95% confidence interval, 1.03

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

212 experimentally observed distinctions between thrombi of different physical etiology.

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

214 Mobile thrombi on cardiovascular implantable electronic device

215 Thrombi on ICE were mobile, averaged 18 +/- 5.9 mm long

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

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

218 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

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

220 eficient mice led to the rapid resolution of thrombi produced by ionophore treatment of the mesenteri

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

222 Ibeta-null platelets failed to form arterial thrombi properly in vivo.

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

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

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

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

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

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

229 Sixty-eight thrombi retrieved from ischemic stroke patients undergoi

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

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

232 the ADC of HCC was lower than 2 and when the thrombi showed similar SI as the primary HCC when qualit

233 ena cava (IVC) results in the development of thrombi structurally similar to human deep vein thrombi.

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

235 elets postdrug administration formed smaller thrombi than cells before therapy and were less responsi

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

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

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

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

240 Hypercoagulability increases risk of thrombi that cause cardiovascular events.

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

242 Platelet thrombi that form in coronary and carotid arteries also

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

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

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

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

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

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

249 n essential role in wound healing by forming thrombi that plug holes in the walls of damaged blood ve

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

251 Catheter-related arterial thrombi that threaten life, organ or limb are the most c

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

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

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

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

256 These thrombi typically were found in arteries presenting with

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

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

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

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

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

262 rtery systolic pressure: 39 +/- 9 mm Hg with thrombi versus 33 +/- 7 mm Hg without thrombi (odds rati

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

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

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

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

267 The presence of thrombi was independently associated with the incidence

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

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

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

271 te accumulation within developing arteriolar thrombi was visualized by situ microscopy.

272 Thrombi were associated with higher pulmonary artery sys

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

274 Thrombi were characterized by immunostaining, flow cytom

275 thrombus on unenhanced PET/CT, and in all 7, thrombi were confirmed on contrast-enhanced CT.

276 es to glycoprotein IX (CD42a), and pulmonary thrombi were detected by near-infrared imaging technolog

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

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

279 Fifth-eight intracardiac thrombi were identified in 42 patients (27%).

280 Right and/or left ventricular thrombi were identified in 5 patients (predominantly by

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

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

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

284 No lead-associated thrombi were observed.

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

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

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

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

289 Thrombi were seen with ICE in 26 of 86 patients (30%) bu

290 Finally, excised thrombi were used for histology.

291 ion between bland and neoplastic portal vein thrombi when the ratio of the ADC of the thrombus to the

292 RBC-PAs incorporate into nascent thrombi, which are focally lysed from within, an attract

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

294 Thrombi, which were composed of fibrin, platelets, and v

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

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

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

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

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

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