ライフサイエンスコーパス: fibrin clot

1 s between monomer units that assemble into a fibrin clot.

2 residues within the noncovalently associated fibrin clot.

3 roscale model represents a three-dimensional fibrin clot.

4 r XIII activation to be localized around the fibrin clot.

5 ly affects the structure of the cross-linked fibrin clot.

6 eity shows that S. epidermidis can rupture a fibrin clot.

7 ommodate variability in the structure of the fibrin clot.

8 ation by thrombin self-assembles to form the fibrin clot.

9 eceptors of stromal cells migrating into the fibrin clot.

10 es the local concentration of Lp(a) within a fibrin clot.

11 ompeted for 125I-TSP1 incorporation into the fibrin clot.

12 , the stable incorporation of Lp(a) into the fibrin clot.

13 ion are exposed, resulting in formation of a fibrin clot.

14 localization to the platelet surface and the fibrin clot.

15 e on the role of Cl- in the formation of the fibrin clot.

16 ich, in turn, leads to the generation of the fibrin clot.

17 wounds, platelet releasate was added to the fibrin clot.

18 his large glycoprotein is transformed into a fibrin clot.

19 ds were sealed with a freshly made exogenous fibrin clot.

20 ture to probe oxidative rearrangement of the fibrin clot.

21 r XIII (FXIII) is the main stabilizer of the fibrin clot.

22 eutrophil activation but was distinct from a fibrin clot.

23 form aggregates, and mediate retraction of a fibrin clot.

24 covalent cross-linking of alpha(2)-AP to the fibrin clot.

25 XIIIa that incorporates cross-links into the fibrin clot.

26 min in the bloodstream at sites distant from fibrin clots.

27 injury by preventing the formation of airway fibrin clots.

28 e could reduce the plasmin-mediated lysis of fibrin clots.

29 was completely abolished in the presence of fibrin clots.

30 interfere with the plasmin-mediated lysis of fibrin clots.

31 botic state via acceleration in formation of fibrin clots.

32 t catalyzes covalent cross-link formation in fibrin clots.

33 thickness by scanning electron microscopy of fibrin clots.

34 XIIIa-induced cross-linking were studied in fibrin clots.

35 fibrin cross-linking were incorporated into fibrin clots.

36 lated with changes in the elastic modulus of fibrin clots.

37 it did not block contraction of recombinant fibrin clots.

38 and lysine residues and rapidly cross-links fibrin clots.

39 ibrin clots when compared with gammaA/gammaA fibrin clots.

40 sslink the adjacent gamma-chain C-termini of fibrin clots.

41 tures of individual fibrinogen molecules and fibrin clots.

42 nd spreading when compared with the WT recFN-fibrin clots.

43 ormed polymers similar to those derived from fibrin clots.

44 the stability and function of intravascular fibrin clots.

45 tive form (plasmin), which then degrades the fibrin clots.

46 of fibrinogen oxidation on the formation of fibrin clots.

47 325R) platelets were defective in retracting fibrin clots.

48 lasmin and increased the dissolution time of fibrin clots.

49 sminogen resulted in a longer lysis time for fibrin clots (16.25 vs. 11.96 min, p = 0.007).

50 mpromising specific activation of proUK on a fibrin clot, a Lys300-->His mutation (M5) was developed.

51 of wound repair, new capillaries invade the fibrin clot, a process that undoubtedly requires an inte

52 The important role of Cl- in structuring the fibrin clot also clarifies the role played by the releas

53 s fibrinogen and promotes the formation of a fibrin clot and functions as an anticoagulant when it ac

54 nds were characterized by persistence of the fibrin clot and prolonged inflammation.

55 fibrin alpha and gamma chains stabilize the fibrin clot and protect it from mechanical and proteolyt

56 ntial for fibroblast invasive migration into fibrin clot and that PDGF, the stimulus for migration, i

57 portant role in wound healing by stabilizing fibrin clots and cross-linking extracellular matrix prot

58 n with host prothrombin and fibrinogen, form fibrin clots and enable the establishment of staphylococ

59 lytically active plasmin dissolves preformed fibrin clots and extracellular matrix components.

60 le matrix component of whole-blood or plasma-fibrin clots and in in vivo thrombi.

61 om Malawian children with CM showed cerebral fibrin clots and loss of EPCR, colocalized with sequeste

62 ition of TAFIa stimulates the degradation of fibrin clots and may help to prevent thrombosis.

63 Adsorption of fibrinogen on fibrin clots and other surfaces strongly reduces integri

64 cilitate the early deposition of bacteria in fibrin clots and promote endocarditis.

65 In vitro fibrin clots and rats with aortic EE were treated with a

66 n is essential for fibroblast migration into fibrin clots and that platelet-derived growth factor, th

67 perty to the plasma membrane, which promotes fibrin clotting and provides a signal for cell removal b

68 IGFBP-3 also binds specifically to native fibrin clots, and addition of exogenous IGFBP-3 increase

69 sity and branching, incorporate into nascent fibrin clots, and impede fibrinolysis in vitro.

70 ulated but not resting neutrophils dissolved fibrin clots, and this activity was not only uPA- and Pl

71 medical device infection-that of an infected fibrin clot-and show that the common blood-borne pathoge

72 l velocity of fibrin clot formation, altered fibrin clot architecture, increased fibrin clot stiffnes

73 When fibrin clots are formed in vitro in the presence of cert

74 ectin with fibrin and its incorporation into fibrin clots are thought to be important for the formati

75 conversion of the coiled-coils occurs in the fibrin clot as a part of forced protein unfolding.

76 s an important role in formation of platelet-fibrin clot at the area of damaged vessel wall.

77 rix and surrounded by fibronectin-containing fibrin clots at 24 hours.

78 efficients of FX((a)) in fibrin and platelet-fibrin clots at 37 degrees C was 2.3 x 10(-7) and 5.3 x

79 atherogenic lipoprotein, accumulates within fibrin clots attached to blood vessel walls.

80 overage of the implant surface with detached fibrin clot-blended graft material (31.4%).

81 e protein fibrinogen pack together to form a fibrin clot, but a crystal structure for fibrinogen is n

82 ion is not only stabilizing the skin and the fibrin clot, but is also important for the correct intra

83 rocoagulant, cleaving fibrinogen to make the fibrin clot, but the thrombin-thrombomodulin (TM) comple

84 FXIIIA promoted GBS entrapment within fibrin clots by crosslinking fibronectin with ScpB, a fi

85 alpha polymer formation and stabilization of fibrin clots by factor XIIIa.

86 TAFIa) is a carboxypeptidase that stabilizes fibrin clots by removing C-terminal arginines and lysine

87 However, leukocyte adhesion to the fibrin clot can be detrimental at the early stages of wo

88 gration of PDL cells from collagen gels into fibrin clots compared to controls when neither was prese

89 muscle cell lines can contract and adhere to fibrin clots composed of either fibronectin-depleted pla

90 covalent incorporation of these recFNs into fibrin clots confirms that glutamines 3 and 4 are major

91 Fibrin clots contained an abnormal 35-kDa constituent re

92 roduced by intraperitoneal implantation of a fibrin clot containing Escherichia coli in conscious, an

93 r (tPA), but not streptokinase, is slowed in fibrin clots containing Abeta(42), and clot lysis by pla

94 e infected by intraperitoneal inoculation of fibrin clots containing Escherichia coli at 10(8), 10(9)

95 Fibrin clots containing Escherichia coli were surgically

96 ed a prolongation of the reptilase time, and fibrin clots containing the abnormal fibrinogen were mor

97 ither plasma clot contraction or recombinant fibrin clot contraction by human newborn smooth muscle c

98 gy between the core structures of plasmin, a fibrin clot-degrading enzyme, and factor D, a complement

99 mplex prothrombinase plays a pivotal role in fibrin clot development through the production of thromb

100 tips of capillary sprouts as they invade the fibrin clot during angiogenesis of cutaneous wound repai

101 s catalytic activity is stabilization of the fibrin clot during coagulation.

102 were indeed incorporated into the insoluble fibrin clot during the coagulation of plasma.

103 rder to mediate transmission of force to the fibrin clot during the process of clot retraction.

104 gth and stability of platelet aggregates and fibrin clots during blood coagulation.

105 ystem as an exquisite biological sensor, the fibrin clot end-product was replaced with a synthetic ma

106 s confirm the findings of others that venous fibrin clots entrap red cells.

107 ion with immobilized fibrinogen, retracted a fibrin clot faster, and showed markedly enhanced thrombu

108 The differences between coarse and fine fibrin clots first reported by Ferry have been interpret

109 ate that for maximal cell attachment to a FN-fibrin clot, FN must be cross-linked to fibrin by factor

110 ram of events is initiated by formation of a fibrin clot, followed by migration of keratinocytes, con

111 The rate of fibrin clot formation and clot architecture was restored

112 RU-505 restored Abeta-induced altered fibrin clot formation and degradation in vitro and inhib

113 ally produced cell-derived microparticles on fibrin clot formation and its properties.

114 coagulation cascade plays a critical role in fibrin clot formation at extravascular sites, the expres

115 transfusion improved hemostasis by enhancing fibrin clot formation at the site of vascular injury in

116 with its target antigen beta2GP1, leading to fibrin clot formation due to exposure of anionic phospho

117 Intravascular fibrin clot formation follows a well-ordered series of r

118 his disease, we examined its relationship to fibrin clot formation in AD.

119 platelet activation, thrombus structure and fibrin clot formation in real time using flowing whole b

120 DNA 60-18[29] inhibits thrombin-catalyzed fibrin clot formation in vitro.

121 In addition, local fibrin clot formation may be implicated in host defense

122 Thrombin generation (TG) and fibrin clot formation represent the central process of b

123 atelet aggregation, thrombin activation, and fibrin clot formation within (and downstream of) NETs in

124 consequences: increased initial velocity of fibrin clot formation, altered fibrin clot architecture,

125 static functions for thrombin in addition to fibrin clot formation, and identify a previously unrecog

126 gulation factors to perform its key roles in fibrin clot formation, platelet aggregation, and wound h

127 e deficient in CD40L showed markedly delayed fibrin clot formation, suggesting a role for the ligand

128 gulation was assessed using assays including fibrin clot formation, thrombin generation, fibrinolysis

129 educed metabolic processing, and increase in fibrin clot formation, with significant upregulation of

130 s, such as increased platelet activation and fibrin clot formation, Wnt signalling, and hypoxia pathw

131 ocin signaling pathway and common pathway of fibrin clot formation.

132 ration of fibrinogen was shown to accelerate fibrin clot formation.

133 ed with the inhibition of thrombin-catalyzed fibrin clot formation.

134 in complex, plays a procoagulant role during fibrin clot formation.

135 s structure, which may then lead to abnormal fibrin clot formation.

136 tructures present during the early stages of fibrin-clot formation from the beginning of polymerizati

137 Ex vivo fibrin clots formed from patients with COVID-19 appeared

138 In vitro and in vivo experiments showed that fibrin clots formed in the presence of Abeta are structu

139 ivators were included in clotting reactions, fibrin clots formed in the presence of polyphosphate exh

140 Fibrin clots formed in the presence of polyphosphate had

141 de, thereby helping protect the newly formed fibrin clot from premature plasmin degradation.

142 Of note, sigmaPre2 could generate fibrin clots from fibrinogen, either in solution or in b

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

144 flow-through assays corroborated these data; fibrin clots had a higher maximum turbidity in patients

145 ncorporation into a fibrin gel, or after the fibrin clot has been degraded by plasmin.

146 he sheer size and the insoluble character of fibrin clots, have restricted our ability to develop nov

147 d translation of ADDSs that spare hemostatic fibrin clots hold promise for extending the utility of A

148 ibution of Abeta to AD is via its effects on fibrin clots, implicating fibrin(ogen) as a potential cr

149 ul in maintaining the experimentally imposed fibrin clot in this model may have lesser clinical signi

150 Transduced cells retracted a fibrin clot in vitro similar to megakaryocytes derived f

151 illed 7 log colony-forming units (CFUs)/g of fibrin clots in 6 hours.

152 on and form a 'macrophage barrier' to shield fibrin clots in place of the lost mesothelium in mice.

153 uretted, resulting in the formation of fresh fibrin clots in the newly formed wound spaces.

154 nt GBS exhibited decreased entrapment within fibrin clots in vitro and increased dissemination during

155 In study 2, porcine fibrin clots in vitro were pretargeted with biotinylated

156 magnetic resonance imaging when targeted to fibrin clots in vitro.

157 Scanning electron microscopy images of fibrin clotted in the presence of increasing concentrati

158 ffective inhibitor of thrombin bound to aged fibrin clots, in purified systems and in plasma clots, a

159 tivities beyond the classical dissolution of fibrin clots, including cell migration, tissue repair, a

160 The physical properties of fibrin clots, including size, age, and cellular composit

161 itor alpha(2)-antiplasmin (alpha(2)-AP) into fibrin clots increases their resistance to fibrinolysis.

162 n and factor XIII resulted in a cross-linked fibrin clot, indicating that a major portion of the secr

163 They affect the structure and stability of fibrin clots indirectly through acceleration of thrombin

164 ogen following modification by tryptase, and fibrin clotting initiated with Ancrod was stopped and pa

165 ), and likely FIX((a)), to diffuse 1 mm in a fibrin clot is 4 hours, and in the presence of platelets

166 Formation of a stable fibrin clot is dependent on interactions between factor

167 The fibrin clot is gelatinous matter formed upon injury to s

168 Platelet retraction of a fibrin clot is mediated by the platelet fibrinogen recep

169 Incorporation of fibronectin into fibrin clots is important for the formation of a provisi

170 Emerging evidence indicates that fibrin clotting is regulated by different external facto

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

172 the major enzyme responsible for dissolving fibrin clots, is regulated by plasminogen activators, pl

173 s, released by the addition of excess C3, on fibrin clot lysis and structure was assessed in turbidim

174 C3 and abolished C3-induced prolongation of fibrin clot lysis by interfering with C3-fibrinogen inte

175 ted, PEGylated liposomes to induce efficient fibrin clot lysis in a fibrin-agar plate model and the e

176 dy sulfur-containing amino acid metabolites, fibrin clot lysis time (CLT) and maximum absorbance (Abs

177 absence of C3, adhiron A6 failed to modulate fibrin clot lysis time (mean 644 s [SE 13] and 620 [14]

178 This study explored relationships between fibrin clot lysis time at randomization and clinical out

179 Longer fibrin clot lysis time has been shown to predict adverse

180 Shorter pre-treatment fibrin clot lysis time independently predicted higher bl

181 brinolysis, whereas MLR captures the rate of fibrin clot lysis.

182 Fibrin clots made at 10% to 100% of plasma levels of pro

183 Fibrin clots made from prothrombin concentrations less t

184 The gammaA/gamma' fibrin clots made in the presence of factor XIII showed

185 anges in the secondary structure of hydrated fibrin clots made of human blood plasma in vitro.

186 acterized by an accelerated breakdown of the fibrin clot - makes such assessments challenging by obfu

187 mation resumed promptly and independently of fibrin clot matrix maturation.

188 ing fibrinogen alters adhesive properties of fibrin clots may have important implications for control

189 Causative fibrin clots may originate from the venous system and pa

190 The viscoelastic properties of Dusart fibrin clots measured with a torsion pendulum indicated

191 Fiber thickness and pore size of fibrin clots, measured by permeation experiments and vis

192 Here, we describe a non-classical fibrin clotting mechanism mediated by SARS-CoV-2 infecte

193 n BM CD34+ cells were cultured in serum-free fibrin clot medium with rhIL-11, IL-3, or rhIL-11 plus I

194 e defective retraction of fibrin in platelet-fibrin clots mimicking treatment of human platelets with

195 FXIII-dependent cross-linking, making formed fibrin clot more susceptible to embolization.

196 E1 but not P1/GE1 became incorporated into a fibrin clot more than GE1 alone.

197 ed Abeta can bind to fibrin(ogen) and render fibrin clots more resistant to degradation.

198 ls are elevated in acute COVID BALF samples, fibrin clotting occurs only with the presence of viral i

199 mensional spatiodynamics within a dissolving fibrin clot of defined composition.

200 usion compared to mass effect controls using fibrin clots of equal volume.

201 Exposed fibrin clots on the damaged peritoneum, in which the mes

202 alpha2AP inhibits plasmin on the fibrin clot or in the circulation by forming plasmin-ant

203 mpete for the holes and dissolve a preformed fibrin clot, or increase the fraction of soluble oligome

204 , potently stimulating their invasion of the fibrin clot over a period of several days.

205 een quantified in fibrin clot permeation and fibrin clot perfusion systems as a function of clot age

206 % lag phase) of denser fibrin networks (-12% fibrin clot permeability [Ks]) and 4% higher maximum abs

207 ced by decreased plasminogen and a decreased fibrin clot permeability.

208 ctivity of argatroban has been quantified in fibrin clot permeation and fibrin clot perfusion systems

209 rfusion in DCD livers, potentially promoting fibrin clot persistence in vasculature.

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

211 Analysis of fibrin clots prepared using plasma from FXIII 34Leu subj

212 that binding of fibrinogen to the surface of fibrin clot prevents cell adhesion by creating an antiad

213 teine (Hcy) and Hcy-thiolactone (HTL) affect fibrin clot properties and are linked to cardiovascular

214 Factors that influence fibrin clot properties and stroke are not fully understo

215 -containing amino acid metabolites influence fibrin clot properties and the risk of stroke.

216 sulfur-containing amino acid metabolites and fibrin clot properties were significantly different in s

217 in cleavage covalently cross-links preformed fibrin clots protecting them from premature fibrinolysis

218 talin to activate integrins is required for fibrin clot retraction by platelets.

219 These effects were selective because fibrin clot retraction, a response also dependent on alp

220 r is it required for alpha v beta 3-mediated fibrin clot retraction, suggesting that fibrinogen may h

221 ncluding adhesion, platelet aggregation, and fibrin clot retraction.

222 e phosphorylation of pp125(FAK), and greater fibrin clot retraction.

223 nylalanines markedly reduced beta3-dependent fibrin clot retraction.

224 preading on fibrinogen and thrombin-mediated fibrin clot retraction.

225 d in platelet adhesion and platelet-mediated fibrin clot retraction.

226 a complex with endogenous a(v) and retracted fibrin clots similarly to wild-type beta(3).

227 t due to simple trapping of platelets by the fibrin clot, since ligand binding, signal transduction,

228 Accurate assessment of fibrin clot stability can predict bleeding risk in coagu

229 which raises the possibility that it affects fibrin clot stability.

230 altered fibrin clot architecture, increased fibrin clot stiffness, and reduced rate of clot lysis.

231 The presence of high platelet-fibrin clot strength (MA >=68 mm) and low fibrinolytic a

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

233 Platelet-fibrin clot strength (PFCS) is linked to major adverse c

234 c aggregometry and thrombin-induced platelet-fibrin clot strength (TIP-FCS) measured by thrombelastog

235 idogrel responsiveness (ADP-induced platelet-fibrin clot strength [MA(ADP)]) was determined by thromb

236 I patients, AMI patients had higher platelet-fibrin clot strength [maximal amplitude (MA): 66.5 +/- 7

237 Fibrin clot structure and clot lysis are crucially invol

238 ds to beta-amyloid (Abeta), thereby altering fibrin clot structure and delaying clot degradation.

239 Our objective is to determine whether the fibrin clot structure and function differ between critic

240 We found aberrant fibrin clot structure and function in critically ill pat

241 sms may play an important role in modulating fibrin clot structure and increasing its resistance to f

242 hich thrombin and fibrinogen gamma' modulate fibrin clot structure and strength.

243 gamma', total fibrinogen concentration, and fibrin clot structure in 2010 apparently healthy black S

244 We now report that polyphosphate enhances fibrin clot structure in a calcium-dependent manner.

245 Fibrinogen gamma' is known to influence fibrin clot structure in purified experimental models, b

246 We hypothesize that this alteration in fibrin clot structure is an important determinant of the

247 We determined fibrin clot structure parameters and effect on mortality

248 tigate the effect(s) of this polymorphism on fibrin clot structure using recombinant techniques.

249 Importantly, fibrin clot structure was also affected by the prothromb

250 of tissue factor pathway inhibitor, enhances fibrin clot structure, and greatly accelerates factor XI

251 vides a rationale for this risk, as abnormal fibrin clot structure, strength and stability correlates

252 ese findings defined mechanisms that control fibrin clot structure, strength and stability.

253 locked polyphosphate-mediated enhancement of fibrin clot structure, suggesting that pyrophosphate is

254 lpha, and the splice variant gamma' modulate fibrin clot structure.

255 bin concentration on thrombin generation and fibrin clot structure.

256 Platelet poor plasma was used to analyze fibrin clot structure; the functional implications were

257 Fibrin clot structures were essentially indistinguishabl

258 cluded genes that promote the degradation of fibrin clots such as tissue plasminogen activator (t-PA)

259 Further, we show that FN-fibrin clots support increased cell spreading when compa

260 quired dysfibrinogenemia is characterized by fibrin clots that are composed of abnormally thin, tight

261 hrombin alone cleaves fibrinogen to make the fibrin clot, the thrombin-TM complex cleaves protein C t

262 takes from the onset of coagulation for the fibrin clot to mostly dissolve in the blood sample durin

263 0.1 x 10(10) colony-forming units/kg)-laden fibrin clots to produce peritonitis and bacteremia.

264 Fibrin clot turbidimetry was performed, and lysis time d

265 Optimal enhancement of fibrin clot turbidity by polyphosphate required >/= 250m

266 The ability of polyphosphate to enhance fibrin clot turbidity was independent of factor XIIIa ac

267 Incorporation of polyP into fibrin clots was reduced in Ip6k1(-/-) mice, thereby alt

268 Scanning electron microscopy revealed that fibrin clots were denser in psoriatic individuals, compa

269 Fibrin clots were examined in which cross-linking was co

270 In this study, various in vitro, platelet-fibrin clots were prepared on TF:VIIa-coated surfaces an

271 When the Q3 recFN-fibrin clots were used as substrates for cell adhesion,

272 dded, slower lysis was seen in gammaA/gamma' fibrin clots when compared with gammaA/gammaA fibrin clo

273 ly on capillary sprouts invading the central fibrin clot whereas the closely related integrin alphaVb

274 ta chain of fibrin increase the turbidity of fibrin clots, whether they are generated by the direct i

275 Conversely, protamine binds to the fibrin clot, which could explain how protamine instigate

276 nts and control subjects was used to prepare fibrin clots, which were subsequently digested with plas

277 As Lp(a) accumulates within the fibrin clot with time, fatty streaks are formed that dev

278 lastic moduli of individual fibrin fibers in fibrin clots with or without ligation, using optical twe

279 ield microscopy to detect the formation of a fibrin clot within plugs and using fluorescent microscop

280 containing blood and transport of the solid fibrin clots within plugs, (ii) using a hydrophilic glas