ライフサイエンスコーパス: fibrin clot

1 roscale model represents a three-dimensional fibrin clot.

2 residues within the noncovalently associated fibrin clot.

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

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

5 ommodate variability in the structure of the fibrin clot.

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

7 eceptors of stromal cells migrating into the fibrin clot.

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

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

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

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

12 localization to the platelet surface and the fibrin clot.

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

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

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

16 his large glycoprotein is transformed into a fibrin clot.

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

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

19 eutrophil activation but was distinct from a fibrin clot.

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

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

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

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

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

25 was completely abolished in the presence of fibrin clots.

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

27 botic state via acceleration in formation of fibrin clots.

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

29 thickness by scanning electron microscopy of fibrin clots.

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

31 fibrin cross-linking were incorporated into fibrin clots.

32 it did not block contraction of recombinant fibrin clots.

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

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

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

36 tures of individual fibrinogen molecules and fibrin clots.

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

38 ormed polymers similar to those derived from fibrin clots.

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

40 of fibrinogen oxidation on the formation of fibrin clots.

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

42 325R) platelets were defective in retracting fibrin clots.

43 lasmin and increased the dissolution time of fibrin clots.

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

45 injury by preventing the formation of airway fibrin clots.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

85 Fibrin clots contained an abnormal 35-kDa constituent re

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

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

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

89 Fibrin clots containing Escherichia coli were surgically

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

123 Fibrin clots formed in the presence of polyphosphate had

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

155 Fibrin clots made from prothrombin concentrations less t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

174 % lag phase) of denser fibrin networks (-12% fibrin clot permeability [Ks]) and 4% higher maximum abs

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

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

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

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

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

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

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

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

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

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

185 nylalanines markedly reduced beta3-dependent fibrin clot retraction.

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

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

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

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

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

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

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

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

194 Fibrin clot structure and clot lysis are crucially invol

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

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

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

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

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

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

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

202 We determined fibrin clot structure parameters and effect on mortality

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

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

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

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

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

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

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

210 bin concentration on thrombin generation and fibrin clot structure.

211 Fibrin clot structures were essentially indistinguishabl

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

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

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

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

216 0.1 x 10(10) colony-forming units/kg)-laden fibrin clots to produce peritonitis and bacteremia.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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