ライフサイエンスコーパス: clot

1 model represents a three-dimensional fibrin clot.

2 nformation about relative shrinkage of blood clot.

3 ows that S. epidermidis can rupture a fibrin clot.

4 ases also involved in the formation of blood clots.

5 s and forms the structural scaffold of blood clots.

6 re and after induction of PE with autologous clots.

7 racterize the viscoelasticity of contracting clots.

8 ately 50% at 1 nM macrophage uptake of blood clots.

9 rginate to near a vessel wall and form blood clots.

10 stemic fibrinolysis or disrupting hemostatic clots.

11 PMs promote macrophage phagocytosis of blood clots.

12 ith changes in the elastic modulus of fibrin clots.

13 anuclear cells that are essential for blood clotting.

14 ociated with a reduced likelihood of circuit clotting.

15 into fibrin split products without inducing clotting.

16 signing new antithrombotics disrupting blood clotting.

17 thrombus formation, and agonist-driven blood clotting.

18 that are key regulators of inflammation and clotting.

19 on during clot formation, or abrogate plasma clotting.

20 raction which is central to preventing blood clotting.

21 to aid blood flow, prevent pooling and thus clotting.

22 the site of vascular injury is essential in clotting.

23 vascular injury, where flowing blood forms a clot, a dynamic and heterogeneous fibrin-based biomateri

24 ntensity (r(2)=0.07, P<0.01), and fibrinogen clotting ability (r(2)=0.073, P<0.01) CONCLUSIONS: In BD

25 d failure (ALF), yet a wide heterogeneity in clotting abnormalities exists.

26 will enable the assessment of the effects of clotting-activators and anticoagulants (including non-ph

27 form and stable coatings with increased anti-clot activity and low cytotoxicity.

28 e methodology, in order to maximize its milk-clotting activity (MCA).

29 mutations S478A/L480A/Q481A was deficient in clotting activity and unable to efficiently activate the

30 ng assay, this peptidase showed maximal milk clotting activity at 60-65 degrees C and maintenance of

31 and colleagues demonstrated that the venom's clotting activity does not require factor VII, but does

32 ple fluorometric in vitro assay to determine clotting activity in platelet poor plasma after exposure

33 fic approach through characterization of the clotting activity of venom from Daboia russelii, disting

34 ets and are preferentially incorporated into clots after laser injury.

35 melanocyte stimulating hormone), and a blood-clotting agent can be anchored to erythrocytes, protecte

36 otential to be employed as an efficient milk-clotting agent in the production of dairy products.

37 otential to be employed as an efficient milk-clotting agent.

38 c events (1.1%/year), whereas 13 with apical clots and anticoagulation did not incur embolic events.

39 role in wound healing by stabilizing fibrin clots and cross-linking extracellular matrix proteins.

40 f TAFIa stimulates the degradation of fibrin clots and may help to prevent thrombosis.

41 In vitro fibrin clots and rats with aortic EE were treated with an antip

42 f inflammatory cells in contraction of blood clots and thrombi has not been investigated.

43 size and density of intra- and extravascular clots and thrombi.

44 thrombin and rIIa(S478A) were able to induce clotting and activate factor V and factor VIII with rate

45 factor (VWF) is a blood protein involved in clotting and is proposed to be activated by flow, but th

46 marks a haplotype associated with increased clotting and platelet aggregation attributable to a prom

47 exhibit unique properties analogous to blood clotting and thereby be useful in self-healing applicati

48 on of blood pressure, vascular permeability, clotting and transendothelial migration of leukocytes an

49 a), forming plasmin-resistant abnormal blood clots, and increased fibrin deposition is found in the b

50 confirm that UHRA does not incorporate into clots, and that clots are stable with normal fibrin morp

51 , hypoxia led to increases in cell adhesion, clotting, and fibrin deposition; these increases were el

52 device infection-that of an infected fibrin clot-and show that the common blood-borne pathogen Staph

53 ytic potential resulting from alterations in clot architecture and elevated levels of plasma FXIII an

54 oduced by high thrombin resulted in weakened clot architecture as analyzed by magnetic tweezers in pu

55 ay distinct roles in fibrin crosslinking and clot architecture.

56 y relevant, as overly softened and stiffened clots are associated with bleeding and thrombotic disord

57 in, and complement C3) confirmed that denser clots are independently related to mortality risk.

58 RA does not incorporate into clots, and that clots are stable with normal fibrin morphology.

59 potent anticoagulant activity in an in vitro clotting assay (aPTT EC1.5x = 0.27 muM) and excellent se

60 In a milk-clotting assay, this peptidase showed maximal milk clott

61 -associated hypercoagulation, using in vitro clotting assays and in vivo cancer models.

62 ex vivo that are more reliable than standard clotting assays.

63 e slowly than the others because the caseins clotted at the gastric pH.

64 hen localized as nanoparticles, accelerating clotting at 10-200 fold lower concentrations, particular

65 PolyP has increased propensity to clot blood with increased polymer length and when locali

66 In a second cohort, infusion of 1 ml of clotted blood into a sulcus caused spreading depolarizat

67 heparin (4 U/mL) inhibits 72% of the active clot-bound thrombin after approximately 10 min at 92 s(-

68 gatran (20 and 200 nM) inhibits (50 and 93%) clot-bound thrombin reversibly (87 and 66% recovery).

69 This model illustrates that clot-bound thrombin stability is the result of a constan

70 tidylserine (PS) on adherent leukocytes, and clot burden after 48 hours were significantly reduced in

71 le to provide data on the entire spectrum of clotting but are not validated in acute bleeding.

72 not only stabilizing the skin and the fibrin clot, but is also important for the correct intracellula

73 is a carboxypeptidase that stabilizes fibrin clots by removing C-terminal arginines and lysines from

74 erall, thrombin is robustly generated within clots by the extrinsic pathway followed by late-stage FX

75 ivity was indicated by the regularisation of clotting by lipopolysaccharide-binding protein (LBP).

76 bacterium Bacillus subtilis, induces plasma clotting by proteolytically converting ProT into active

77 The resultant embolization of the infected clot can contribute to the systemic dissemination of the

78 hat fibrin(ogen) polymerisation during blood clotting can be affected strongly by LPS.

79 The contact pathway of the plasma clotting cascade is dispensable for normal hemostasis, b

80 scades are: the complement system, the blood clotting cascade, the fibrinolytic system, and the kalli

81 Data for clotted circuits are presented as median (interquartile

82 Survival probability for clotted circuits was compared using log-rank test.

83 ue plasminogen activator every 8 hours until clot clearance of third and fourth ventricles) or a comb

84 combined treatment approach of IVF and-upon clot clearance of third and fourth ventricles-subsequent

85 t at 250 mL/min was not more likely to cause clotting compared with 150 mL/min (hazards ratio, 1.00 [

86 out anticoagulation was more likely to cause clotting compared with use of heparin strategies (hazard

87 -triggered platelet aggregation in vitro and clot consolidation in vivo.

88 Platelet-driven blood clot contraction (retraction) is thought to promote woun

89 il and quantify the structural mechanisms of clot contraction at the level of single platelets.

90 ted monocytes reduced the extent and rate of clot contraction back to control levels with non-activat

91 revealed platelet-driven mechanisms of blood clot contraction demonstrate an important new biological

92 Clot contraction is composed of 3 sequential phases, eac

93 ), and platelet-fibrin interactions modulate clot contraction may generate novel approaches to reveal

94 telet-driven reduction in blood clot volume (clot contraction or retraction) has been implicated to p

95 Blood clot contraction plays an important role in prevention o

96 et count all promote 1 or more phases of the clot contraction process.

97 Notwithstanding its importance, clot contraction remains a poorly understood process, pa

98 ack into whole blood, the extent and rate of clot contraction were increased compared to addition of

99 contrary, addition of tissue factor enhanced clot contraction, mimicking the effects of tissue factor

100 tudy the influence of activated monocytes on clot contraction.

101 Circuit clotting data were analyzed for repeated events using ha

102 er rate of increase in D-dimer levels during clot degradation (D-Drate; all P < .05).

103 traction rate (CRR), fibrinolysis rate (FR), clot density (CD) (by confocal microscopy), plasma level

104 ork of a thrombus, which over time increases clot density and decreases clot size.

105 , but little is known about the influence of clot density on outcome in patients on hemodialysis.

106 Reliable clot diagnostic systems are needed for directing treatme

107 is a viable therapeutic alternative for many clotting disorders and for other hepatic diseases where

108 y similar to the one generally used for milk clotting during cheese making, and exhibited a satisfact

109 IX and Alprolix exhibit a linear response in clotting efficacy up to 150 IU/kg, where they appear to

110 Two different milk clotting enzymes, belonging to the aspartic protease fam

111 y models, PLT/uPA-T did not lyse preexisting clots, even when administration was delayed by as little

112 A major clotting event that led to premature termination of the

113 ion study (GWAS) of 6135 self-reported blood clots events and 252 827 controls of European ancestry b

114 nts in haemophilia care, the availability of clotting factor concentrates for all affected individual

115 from 133 plant species eliminated 105 (human clotting factor VIII heavy chain [FVIII HC]) and 59 (pol

116 oxaban, a direct oral inhibitor of activated clotting factor Xa, might be more suitable than conventi

117 bleeding with adequately sustained levels of clotting factor, after a single therapeutic intervention

118 n their outer membrane leaflet and activated clotting factors assemble into enzymatically active comp

119 emostasis and the development of recombinant clotting factors for the treatment of the common inherit

120 redicted that restoring the normal levels of clotting factors II, IX, and X while simultaneously rest

121 When binding of purified clotting factors to immobilized myosin was monitored usi

122 treatment relies on replacement therapy with clotting factors, either at the time of bleeding (ie, on

123 t involves frequent intravenous infusions of clotting factors, which is associated with variable hemo

124 n thrombocytopenia and low concentrations of clotting factors, which may cause profuse hemorrhagic co

125 d clot formation time, and increased maximum clot firmness.

126 omboelastography was used to measure time to clot formation (r-time) in both rhesus and human blood,

127 oduced cell-derived microparticles on fibrin clot formation and its properties.

128 rform this cleavage function to impede blood clot formation around the worms in vivo.

129 Ib compared with that of uPA-T, and prevents clot formation in a microfluidic system.

130 show that the ARFOE-OCE is sensitive to the clot formation kinetics and can differentiate the elasti

131 oagulation metrics, including reaction time, clot formation kinetics and maximum shear modulus.

132 measured effects of hematocrit in 2 in vivo clot formation models.

133 Bacteria present during clot formation produce a visibly disorganized microstruc

134 mboelastography (TEG) demonstrated increased clot formation rate, associated with portal vein platele

135 gnificantly increased coagulation, decreased clot formation time, and increased maximum clot firmness

136 ly 78% of its normal level and hence improve clot formation under dilution.

137 uencies using 4 set-points and the effect of clot formation using a chemical trigger.

138 aggregation, thrombin activation, and fibrin clot formation within (and downstream of) NETs in vivo.

139 rinogen, affect fibrin polymerization during clot formation, or abrogate plasma clotting.

140 metabolic processing, and increase in fibrin clot formation, with significant upregulation of fibrino

141 a multicausal disease involving intravenous clot formation.

142 nd neonatal porcine islets prolonged time to clot formation.

143 A dark clot formed at the site of injury in most species tested

144 hodology to follow volume changes in a blood clot formed in vitro.

145 Clots formed in blood from TM-AC cases had the same visc

146 neration kinetics and transport within blood clots formed under hemodynamic flow.

147 may home to endothelium, can be activated by clot-forming elements, and are susceptible to platelet-m

148 d significantly thinner fibers compared with clots from fibrinogen of control individuals (mean+/-SD

149 Of note, sigmaPre2 could generate fibrin clots from fibrinogen, either in solution or in blood pl

150 Lysis of plasma clots from TM-AC cases was significantly delayed compare

151 f for FXIII-A2B2 Compared with gammaA/gammaA clots, FXIII-A2B2 activation peptide release was 2.7-fol

152 It has been demonstrated that fibrin clots generated from plasma samples obtained from patien

153 metrics for rate and molecular mechanisms of clot growth, thrombotic risk, pharmacological response,

154 tree with occlusion of the lumen from blood clots has been reported.

155 n and thromboembolism; the increase in model clot heterogeneity shows that S. epidermidis can rupture

156 , intracranial herniation of orbital fat and clot in the confluence of sinuses.

157 log colony-forming units (CFUs)/g of fibrin clots in 6 hours.

158 These results suggest that subarachnoid clots in sulci/fissures are sufficient to induce spreadi

159 tional triggers) and reproducibly results in clots in the large veins of the head and fibrin depositi

160 in vitro changes in the size of contracting clots in whole blood and in variously reconstituted samp

161 hey are effective inhibitors of human plasma clotting in vitro.

162 Blood clotting in vivo is catalyzed by thrombin, which simulta

163 ied various methods of creating intraluminal clots, including the application of such new technologie

164 tion, changes in the elastic property of the clots increase the shear modulus of the sample, altering

165 xygenase-2 in ipsilateral cortex remote from clots/infarcts.

166 farcts were significantly larger after blood clot infusion compared to mass effect controls using fib

167 Systems as varied as blood clotting, intracellular calcium signaling, and tissue in

168 ng surgical aspiration followed by alteplase clot irrigation.

169 The major structural component of a blood clot is a mesh of fibrin fibers.

170 protein, fibrinogen, into a polymeric fibrin clot, is conserved in all vertebrates.

171 for purified blood proteases or human plasma clotting isotropically.

172 Unwanted clots lead to heart attack and stroke that result in a l

173 ch release high levels of platelets found as clot-like accumulations in the heart.

174 ctionalized beads, polymerization affords a "clot-like" scaffold of beads and polymer.

175 which could explain how protamine instigates clot lysis and increases bleeding after surgery.

176 Fibrin clot structure and clot lysis are crucially involved in development of card

177 lectron microscopy, confocal microscopy, and clot lysis assays, we confirm that UHRA does not incorpo

178 red fibrinolytic degradation (+25% prolonged clot lysis time [CLT]) and a 5% slower rate of increase

179 The molecule inhibited clot lysis, alluding to its promise as an allosteric reg

180 lpha2AP to fibrin and consequently prolonged clot lysis.

181 Clots made of purified fibrinogen from patients on hemod

182 is influences this in vitro model of a blood clot mechanically and structurally on both microscopic a

183 mental cues to mediate contraction and alter clot mechanics is unknown.

184 imen analysed here is evidence of an ancient clotting mechanism not dissimilar to those of today, rap

185 gle-platelet contraction forces in different clot microenvironments.

186 t received: BC (untreated, filled with blood clot), NAT (natrosol gel alone), and DOX (10% doxycyclin

187 amyl-epsilon-lysyl crosslinks into the blood clot network.

188 off-hour admission, and absence of proximal clot occlusion.

189 were required in 31.1%, and patient-related clots occurred in 12.8%.

190 ompared to mass effect controls using fibrin clots of equal volume.

191 trations of short-chain polyP can accelerate clotting of flowing blood plasma under flow at low to su

192 hetic polyP was more effective at triggering clotting of flowing blood plasma when localized on a sur

193 lization of short-chain polyP can accelerate clotting of flowing blood.

194 alpha2AP inhibits plasmin on the fibrin clot or in the circulation by forming plasmin-antiplasmi

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

196 tient data were collected until each circuit clotted or was ceased electively for nonclotting reasons

197 se was 2.7-fold slower in Fibgamma(390-396A) clots (P < .02).

198 ers were associated with formation of sulcal clots (P < 0.01), a high likelihood of adjacent cortical

199 nd inhibit activators of the intrinsic blood clotting pathway, such as polyphosphate (polyP) and extr

200 hase) of denser fibrin networks (-12% fibrin clot permeability [Ks]) and 4% higher maximum absorbance

201 Such a prothrombotic fibrin clot phenotype has been suggested as a new risk factor f

202 lored problem, despite applications in blood clotting, plasmonics, industrial packaging and transport

203 rinogen, the main protein component of blood clots, plays an important role in this circulatory dysfu

204 The restricted proteolysis and milk-clotting potential are attractive properties for the use

205 areas inside the visual surface advert to a clotting principle, rather similar to those of today, an

206 ignaling, protein and lipid homeostasis, and clotting processes.

207 To assess whether abnormal clot properties can predict recurrent deep vein thrombos

208 We demonstrate that unfavorably altered clot properties may predict recurrent DVT after anticoag

209 Plasma clot properties were evaluated after 3 months of anticoa

210 e extract prepared at pH 3 had the best milk-clotting properties (MCA/PA ratio).

211 efficient way to produce rennet with better clotting properties, leading to higher yield, moisture,

212 eliminary step to produce rennet with better clotting properties.

213 employed to produce mainly proteins or milk-clotting proteases.

214 ious studies have investigated only a single clotting protein and lipid composition and have yielded

215 , Petersen et al. (2017) show that the blood clotting protein fibrinogen inhibits nerve repair by pre

216 worms are capable of cleaving the host blood clotting protein fibronectin and that this activity can

217 al methods presents challenges for comparing clotting protein-lipid interactions.

218 ant serpin that irreversibly inactivates the clotting proteinases factor Xa and thrombin by forming c

219 -carboxyglutamic acid-rich domain-containing clotting proteins with lipids.

220 many protein-lipid interactions among blood-clotting proteins.

221 ective removal or dissolution of large blood clots remains a challenge in clinical treatment of acute

222 PM profiles in patients with CAD and promote clot remodeling.

223 onary artery disease and their potential for clot remodeling.

224 eter evacuation followed by thrombolysis for clot removal is safe and can achieve a good functional o

225 ents a safe and effective strategy to hasten clot resolution that may reduce shunt rates.

226 gate with a polymerized fibrin matrix, blood clots result from hundreds of unique reactions within an

227 nces spreading on fibrinogen and accelerates clot retraction (see figure).

228 on on collagen I under flow, and accelerated clot retraction and spreading on fibrinogen.

229 Insights into the mechanisms regulating clot retraction at sites of vascular injury have been ha

230 d spreading on Fg and fibronectin and faster clot retraction compared with wild-type.

231 In vitro clot retraction experiments indicated that subthreshold

232 of clot retraction, and show that promoting clot retraction is a novel and complementary means by wh

233 We evaluated the clot retraction rate (CRR), fibrinolysis rate (FR), clot

234 Clot retraction rate negatively correlated with FENO and

235 Clot retraction refers to the process whereby activated

236 d that subthreshold doses of tPA facilitated clot retraction through a plasmin-dependent mechanism.

237 a-granule secretion, platelet spreading, and clot retraction were not markedly affected.

238 inolytic system as an important regulator of clot retraction, and show that promoting clot retraction

239 ysis of fibrin polymers markedly facilitated clot retraction.

240 g on fibrinogen and thrombin-mediated fibrin clot retraction.

241 ch as spreading, thrombus consolidation, and clot retraction.

242 ernational normalized ratio had no effect on clotting risk.

243 Paramount in the clot's capability to stem haemorrhage are its changing m

244 onal revascularization protocol with a blood clot scaffold.

245 er time increases clot density and decreases clot size.

246 ed thrombin binding to fibrin contributes to clot stability and is resistant to inhibition by antithr

247 rocess is considered important for promoting clot stability and maintaining blood vessel patency.

248 y disorganized microstructure that increases clot stiffness and triggers mechanical instability over

249 DP%): P = 0.018; ADP-induced platelet-fibrin clot strength (MAADP): P = 0.030].

250 Fibrin clot structure and clot lysis are crucially involved in

251 eover, we investigated the interplay between clot structure and its mechanical properties, such as hy

252 rombin and fibrinogen gamma' modulate fibrin clot structure and strength.

253 that patients on hemodialysis with a denser clot structure had increased all-cause and cardiovascula

254 Thus, in patients on hemodialysis, a denser clot structure may be a potent independent risk factor f

255 We determined fibrin clot structure parameters and effect on mortality in a p

256 effects of thrombin and fibrinogen gamma' on clot structure.

257 he number of tPA molecules in the system and clot structure.

258 ilar in gammaA/gammaA and Fibgamma(390-396A) clots, suggesting fibrinogen residues gamma390-396 accel

259 ectly activating factor X, and a form of the clotting test is used in the diagnosis of lupus anticoag

260 Thus, by combining the venom clotting test with the quick clotting time (prothrombin

261 (aPTT) and ''Prothrombinase complex-induced Clotting Test'' (PiCT) have been compared with the stand

262 This implies that it is easier to dissolve clots that consist of fewer thick fibers than those that

263 ) and 4% higher maximum absorbance of plasma clots that displayed impaired fibrinolytic degradation (

264 risk of bleeding due to lysis of hemostatic clots that prevent hemorrhage in damaged blood vessels.

265 pecific binding and adverse effects on blood clotting that limit their use.

266 In animals injected with the clot, there was no evidence of dissolution, and the thro

267 ining the venom clotting test with the quick clotting time (prothrombin time), it was possible to dia

268 compatibility of PAEC, as shown by increased clotting time (WT: 84.3 +/- 11.3 min, p < 0.001; GTKO.hC

269 By applying a clotting time analysis based on a phenomenological mathe

270 hrombin-thrombomodulin complex, prolongs the clotting time by generating pharmacological quantities o

271 e serine residue (FXII-S544A), shortened the clotting time of FXII-deficient plasma and enhanced thro

272 ically modified PAEC significantly prolonged clotting time of human blood (115.0 +/- 16.1 min, p < 0.

273 ther the diluted thrombin time or the ecarin clotting time.

274 s evidenced by the reduction of viscoelastic clotting time.

275 basis of the diluted thrombin time or ecarin clotting time.

276 X-deficient plasma, as well as FXa-initiated clotting times in FX-deficient plasma.

277 the ability of TFPI to prolong TF-initiated clotting times in FXI- or FIX-deficient plasma, as well

278 heparin was administered with goal-activated clotting times of 300 to 400 seconds for all LV procedur

279 human fIIa(MZ), significant prolongation of clotting times was observed for fII(MZ) plasma.

280 tor-bearing microparticles, shortened plasma-clotting times, and increased thrombus frequency in the

281 , different hemolysis levels, differences in clotting times, the number of freeze-thaw cycles, and di

282 , X), which corresponded to increased plasma clotting times.

283 Skin inflammation; thrombosis clotting times; and percentage of splenic monocytes, neu

284 The clot-to-blood ratio for (18)F-GP1 was investigated by an

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

286 ycle length may have a significant impact on clot trajectory and thus embolic stroke propensity throu

287 icted the effect of localization of polyP on clotting under flow, and this was tested in vitro using

288 es evidence that self-reported data on blood clots used in a GWAS yield results that are comparable w

289 mg every 8 h for up to nine doses) to remove clots using surgical aspiration followed by alteplase cl

290 /mum(2)), we measured thrombin released from clots using thrombin-antithrombin immunoassay.

291 Platelet-driven reduction in blood clot volume (clot contraction or retraction) has been im

292 completely lysed or surgically detected as a clot was classified as thrombus, whereas a mass which wa

293 In the second model, an autologous clot was injected via a micro-catheter into the M1 segme

294 The dark coloration of the clots was due to melanin deposition.

295 Median circuit life for first circuit (clotted) was similar for both groups (150 mL/min: 9.1 hr

296 Conversely, protamine binds to the fibrin clot, which could explain how protamine instigates clot

297 s within this region help generate a stiffer clot, which is more resistant to fibrinolysis.

298 unt range: 4-20 in 6 h) and persistent thick clots with patchy or extensive infarction of circumscrib

299 olar vessels, permitting evaluation of blood clotting within small sample volumes under pathophysiolo

300 , major catheter dysfunction occurred before clotting within the circuit.

301 g, dermal fibroblasts are recruited into the clotted wound by a concentration gradient of platelet-de