ライフサイエンスコーパス: fibrin

1 ances alphaMbeta2-dependent cell adhesion to fibrin.

2 rginines and lysines from partially degraded fibrin.

3 s involve both the gamma and alpha chains of fibrin.

4 e of CPN1 in the conversion of fibrinogen to fibrin.

5 ipid, ultimately leading to the formation of fibrin.

6 thrombin is formed, leading to generation of fibrin.

7 nteractions of platelets with fibrinogen and fibrin.

8 to alphaIIbbeta3 and converts fibrinogen to fibrin.

9 al distributions of thrombin, platelets, and fibrin accumulating within a thrombus.

10 ty in a factor XII-dependent manner, reduces fibrin accumulation and impedes thrombus formation in bl

11 n domain was approximately twice that of the fibrin accumulation domain.

12 s unaffected by introducing hirudin to block fibrin accumulation or a Gi2alpha gain-of-function mutat

13 The C-terminal portion of the fibrin alpha chain extends into the alphaC region (210-6

14 platelet polyP and the downstream substrate fibrin, alphaFXIIa is a highly efficient and favorable p

15 Both fibrinogen- and fibrin-alphaIIbbeta3 interactions were partially inhibit

16 Given that fibrin amplifies pathological inflammation in several di

17 fibrin clearance and shows that interstitial fibrin and collagen are cleared by different subsets of

18 e-derived matrix metalloproteinases regulate fibrin and collagen turnover.

19 single alphaIIbbeta3 molecules to polymeric fibrin and compare it to alphaIIbbeta3 binding to monome

20 eading to faster crosslinking of alpha2AP to fibrin and consequently prolonged clot lysis.

21 to alphaIIbbeta3 inhibitors, suggesting that fibrin and fibrinogen have distinct binding requirements

22 mpared the interaction of alphaIIbbeta3 with fibrin and fibrinogen to explore their differential effe

23 are it to alphaIIbbeta3 binding to monomeric fibrin and fibrinogen.

24 resent in the lung, whereas the GPVI ligands fibrin and histone were induced during pneumonia.

25 the t-PA concentration, is regularly lysing fibrin and induced Thrombolysis In Myocardial Infarction

26 transglutaminase that covalently cross-links fibrin and other proteins to fibrin to stabilize blood c

27 e HIT-like monoclonal antibody KKO increased fibrin and platelet deposition at sites of injury, follo

28 thrombin generation in vitro and to restore fibrin and platelet deposition in an intravital laser in

29 , reduced thrombus incidence, thrombus size, fibrin and platelet deposition in the ligated inferior v

30 lood over myosin-coated surfaces also caused fibrin and platelet deposition, evidencing myosin's thro

31 Fibrin and polyP70 acted synergistically to enhance alph

32 t study, we investigated the contribution of fibrin and staphylokinase (Sak) to biofilm formation.

33 through forced unbinding via degradation of fibrin and tPA release.

34 ally tuned the microstructural parameters of fibrin and used a combination of optical tweezers and fl

35 densely packed core, not the accumulation of fibrin, and (4) drugs that affect platelet accumulation

36 from myosin, chemotaxis receptor, vimentin, fibrin, and phenylalanine zippers that vary in size and

37 including experimentally-imaged collagen and fibrin architectures, we find that measurements applied

38 ECM protein biopolymers such as collagen or fibrin are commonly used for 3D cell culture models of t

39 ests that the alphaIIbbeta3-binding sites in fibrin are not confined to its known gamma-chain and RGD

40 agglutinins, proteins that bind polymerized fibrin, are key virulence strategies for the pathogenesi

41 rated thrombin was captured by intrathrombus fibrin as thrombin-antithrombin was largely undetectable

42 ting injuries have a core of densely packed, fibrin-associated platelets overlaid by a shell of less-

43 od forms a clot, a dynamic and heterogeneous fibrin-based biomaterial.

44 -CMs + adult CFs, or mESC-CMs + fetal CFs in fibrin-based hydrogel.

45 Cultivation of LEPC on fibrin-based hydrogels incorporating LN-511-E8 resulted

46 nt was able to prevent sprout formation in a fibrin bead assay, suggesting that p120*VE-Cad interacti

47 or follicles transplanted within VEGF-loaded fibrin beads.

48 d, ligand-free state and a Mn(2+)-activated, fibrin-bound state.

49 of this study is to assess the stability of fibrin-bound thrombin under venous flow conditions and t

50 ound that alphaIIbbeta3 binding to polymeric fibrin can be segregated into two binding regimes, one w

51 Each molecule of fibrin can bind approximately 1.6 thrombin molecules at

52 n endocytic pathway engaged in extravascular fibrin clearance and shows that interstitial fibrin and

53 However, given that a failure of efficient fibrin clearance can impede normal wound repair, the pre

54 this alphaC region blocked plasmin-mediated fibrin cleavage at this site, resulting in the generatio

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

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

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

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

59 % lag phase) of denser fibrin networks (-12% fibrin clot permeability [Ks]) and 4% higher maximum abs

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

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

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

63 Fibrin clot structure and clot lysis are crucially invol

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

65 We determined fibrin clot structure parameters and effect on mortality

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

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

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

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

70 roscale model represents a three-dimensional fibrin clot.

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

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

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

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

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

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

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

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

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

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

81 hrombin) and structural (i.e., platelets and fibrin) components within a growing thrombus.

82 tion between C19MC amplification and reduced fibrin content and TF expression, indicative of reduced

83 and RBC(HIGH) mice did not differ in size or fibrin content, and there was no difference in levels of

84 mation, exosite-mediated thrombin binding to fibrin contributes to clot stability and is resistant to

85 ng that targeting platelet interactions with fibrin could increase the therapeutic indices of antithr

86 MARCKS peptides colocalize with, and inhibit fibrin cross-linking, of adherent platelets.

87 that these glutamines play distinct roles in fibrin crosslinking and clot architecture.

88 n of increased levels of a plasmin-resistant fibrin degradation fragment.

89 D-dimer is a soluble fibrin degradation product that results from ordered bre

90 Reduced levels of D-dimer (fibrin degradation product) were evident in ticks fed on

91 on to a 3-BRS comprising C-reactive protein, fibrin degradation product, and heat shock protein-70 im

92 stment for risk factors, C-reactive protein, fibrin degradation product, and heat shock protein-70.

93 METHODS AND C-reactive protein, fibrin degradation product, heat shock protein-70, and s

94 ing levels of biomarkers C-reactive protein, fibrin degradation products, and heat shock protein-70 r

95 ovel intracellular pathway for extravascular fibrin degradation.

96 (uPAR), which facilitates activation of the fibrin-degrading protease plasmin, were upregulated in C

97 lize on the activated platelet membrane in a fibrin-dependent manner and decorated fibrin strands ext

98 Extravascular fibrin deposition accompanies many human diseases and ca

99 Initial fibrin deposition at the vessel wall over 6 hours in thi

100 diac function and decreased infarct size and fibrin deposition in a time-dependent manner.

101 in clots in the large veins of the head and fibrin deposition in the liver.

102 This was corroborated by strongly reduced fibrin deposition in the liver.

103 esistant abnormal blood clots, and increased fibrin deposition is found in the brains of AD patients

104 staining of infected bone revealed increased fibrin deposition surrounding bacterial abscesses in obe

105 in bone were also increased, further linking fibrin deposition to S. aureus expression of clfA and in

106 ogical activity (smooth muscle cell loss and fibrin deposition) in the FP-PES compared with PES and b

107 d) cell-specific HIF1alpha doubled pulmonary fibrin deposition, and trebled thrombus formation compar

108 RVXB markedly reduced fibrin deposition, suggesting reduced intrahepatic micro

109 nct contributions to platelet activation and fibrin deposition.

110 eutrophils did not affect quantitative liver fibrin deposition.

111 gy of thrombin generation and the subsequent fibrin deposition.

112 to increases in cell adhesion, clotting, and fibrin deposition; these increases were eliminated in HI

113 Coagulation cascade activation and fibrin deposits have been implicated or observed in dive

114 stochemical studies identified extravascular fibrin deposits within white adipose tissue and liver as

115 irms the new concept of an important role of fibrin derivatives in global ischemia/reperfusion injury

116 The fibrin-derived peptide Bbeta15-42 (FX06) has been proven

117 usion injury, which can be attenuated by the fibrin-derived peptide Bbeta15-42.

118 Monomeric fibrin displayed a higher probability of interacting wit

119 itor-1 (PAI-1), S. aureusclfA expression and fibrin-encapsulated abscess communities in bone were als

120 All mice transplanted with fibrin-encapsulated follicles resumed cycling, and live

121 The study identifies a novel fibrin endocytic pathway engaged in extravascular fibrin

122 Surprisingly, however, fibrin endocytosis was unimpeded by the absence of the f

123 Analysis of fibrin expression in human tumor biopsies showed signifi

124 o determine whether fibrinogen glycation and fibrin fiber diameter have an effect on the mechanical p

125 Our finding, therefore, implies that fibrin fibers do not have a homogeneous cross section of

126 oscopy to measure the interactions of single fibrin fibers for the first time, to our knowledge.

127 mine the mechanical properties of individual fibrin fibers formed from blood plasma.

128 Fibrin fibers were studied using turbidimetry, atomic fo

129 tural component of a blood clot is a mesh of fibrin fibers.

130 ffect on the mechanical properties of single fibrin fibers.

131 retraction of platelet filopodia attached to fibrin fibers.

132 number of molecules present with respect to fibrin fibers.

133 tion is governed by alphaIIbbeta3 binding to fibrin fibers.

134 ich activates host prothrombin and generates fibrin fibrils that protect the pathogen against phagocy

135 Thrombin-catalyzed fibrin formation and fibrin susceptibility to plasmin-in

136 bolism through a negative regulation of both fibrin formation and neutrophil function.

137 , prolonged coagulation time, and attenuated fibrin formation by 50%.

138 generation of FXa and promoted TF-dependent fibrin formation in recalcified plasma.

139 fewer lung metastases due to a reduction of fibrin formation surrounding the tumor cells, rendering

140 difference in reaction time (time to initial fibrin formation) greater than 1 minute between heparina

141 In closed system models of fibrin formation, exosite-mediated thrombin binding to f

142 e factor (TF) pathway of coagulation through fibrin formation, incorporates the accumulation of blood

143 However, fibrin formation, the exposure of negatively charged pho

144 d on activated platelets and thereby inhibit fibrin formation.

145 regation, radial migration and cross-linking fibrin formations.

146 Mn-FBP binds the soluble fibrin fragment DD(E) with Kd = 110 nM.

147 However, failure to clear fibrin from the fracture site in plasminogen-deficient m

148 ular graft grown from donor fibroblasts in a fibrin gel to address this critical unmet need.

149 Three gel conditions, which were fibrin gel, fibrin-Matrigel mixed gel and fibrin-hyaluro

150 scale dependent mobility of nanoparticles in fibrin gels and in sputum from patients with cystic fibr

151 f diverse biopolymers such as collagen gels, fibrin gels and Matrigel.

152 Compared with gels containing MSCs alone, fibrin gels engineered with increased compressive stiffn

153 This multiscale adaptation mechanism endows fibrin gels with the remarkable ability to sustain recur

154 In fibrin gels, both methods showed an immobile fraction of

155 ane matrix, agarose gels, alginate gels, and fibrin gels, but not in polyacrylamide gels.

156 ected by being cultured and grown in 3D soft fibrin gels.

157 Perfusate analysis demonstrated reduced fibrin generation in TLN-treated kidneys correlating wit

158 s normal level) in diluted blood can restore fibrin generation to approximately 78% of its normal lev

159 ivity and promotes platelet accumulation and fibrin generation.

160 euticals Ltd, Ramat-Gan, Israel), or Tisseel fibrin glue (Baxter Corp., Deerfield, IL).

161 t using Vicryl sutures (Ethicon, NJ), Evicel fibrin glue (Omrix Biopharmaceuticals Ltd, Ramat-Gan, Is

162 cation and pterygium recurrence with Tisseel fibrin glue compared with Evicel fibrin glue.

163 Tisseel fibrin glue for the repositioning of conjunctival autogr

164 operative day was significantly lower in the fibrin glue groups compared with the suture group (P = 0

165 (flap time) was significantly shorter in the fibrin glue groups compared with the Vicryl group: 5.46

166 in the sutures group (P = 0.019 sutures vs. fibrin glue groups).

167 in the Tisseel group (P = 0.027 sutures vs. fibrin glue groups).

168 groups receiving 10-0 Vicryl sutures, Evicel fibrin glue, or Tisseel fibrin glue.

169 cryl sutures, Evicel fibrin glue, or Tisseel fibrin glue.

170 ith Tisseel fibrin glue compared with Evicel fibrin glue.

171 ted using an amniotic membrane scaffold with fibrin glue.

172 re fibrin gel, fibrin-Matrigel mixed gel and fibrin-hyaluronan mixed gel, were investigated to optimi

173 ough the L1 peptides YIGSR and A99 linked to fibrin hydrogels (FHs) promote intact salivary epithelia

174 Gly-Pro-Arg-Pro amide, confirming a role for fibrin in amplifying plasminogen binding to PS-exposing

175 study, we hypothesized that the presence of fibrin in tumor extracellular matrix contributes to hind

176 e proteins with host matrix proteins such as fibrin initiates agglomeration; our present results show

177 hich blood cells, fibrin(ogen), and platelet-fibrin interactions modulate clot contraction may genera

178 alphaIIbbeta3-fibrin interactions were also less sensitive to inhibiti

179 extracellular matrix, inducing compaction of fibrin into bundled agglomerates tightly associated with

180 Fibrin is also less sensitive to alphaIIbbeta3 inhibitor

181 Lysis of intact fibrin is initiated by t-PA, and uPA activates the remai

182 These results demonstrate that fibrin is more reactive with alphaIIbbeta3 than fibrinog

183 sed intravital microscopy to investigate how fibrin is removed from extravascular space.

184 In addition to a central role in hemostasis, fibrin is thought to enhance bone repair by supporting i

185 (125)I-fibrin or fluorescein isothiocyanate-fibrin labeled emboli in anesthetized mice.

186 However, the high degradation rate of fibrin leads to the dissociation of cytokines even befor

187 elial gaps, thickened basement membrane, and fibrin-like intraluminal deposits, which are classic sig

188 lowed by late-stage FXIa contributions, with fibrin localizing thrombin via its antithrombin-I activi

189 Fibrin made from a fibrinogen gamma'/gamma' variant lack

190 and colocalization of LPS with TCPs in such fibrin material, which indicates the presence of TCP-LPS

191 Diffusivity of nanocarriers in fibrin matrices was limited and could be improved signif

192 Three gel conditions, which were fibrin gel, fibrin-Matrigel mixed gel and fibrin-hyaluronan mixed ge

193 lary-like structures were also formed in the fibrin-Matrigel mixed gel by coculturing brain microvasc

194 First, fibrin-Matrigel mixed gel was found to promote neural st

195 eural networks were constructed in 2-8 mg/ml fibrin-Matrigel mixed gel.

196 ability of thrombin (0-1400 nM) adhered to a fibrin matrix (0.1-0.4 mg/mL fibrinogen, 10 nM thrombin)

197 atelets, and growth factors within the dense fibrin matrix and can be used as healing biomaterial.

198 ed improved migration in a three-dimensional fibrin matrix and during resolution of peritoneal inflam

199 active thrombin remains stably adhered to a fibrin matrix over a range of venous shear rates (46-184

200 d multicellular aggregate with a polymerized fibrin matrix, blood clots result from hundreds of uniqu

201 primary dermal fibroblasts embedded in a 3D fibrin matrix.

202 ic response of the underlying model collagen/fibrin matrix.

203 The mechanism of fibrin-mediated fibrosis was linked to interferon (IFN)g

204 contractile stress generated by the platelet-fibrin meshwork.

205 es had the following order: fibrin polymer > fibrin monomer > fibrinogen.

206 clots, and that clots are stable with normal fibrin morphology.

207 ed to multiple fibers, platelets densify the fibrin network by pulling on fibers transversely to thei

208 tion in clots was positively correlated with fibrin network density; however, FXIIIa inhibition reduc

209 telets transduce contractile forces onto the fibrin network of a thrombus, which over time increases

210 ation of mice, we have demonstrated that the fibrin network of thrombi progressively compacts over a

211 ithin fibers correlates with strength of the fibrin network.

212 let contractility prevented shrinkage of the fibrin network.

213 h faster formation (-9% lag phase) of denser fibrin networks (-12% fibrin clot permeability [Ks]) and

214 We demonstrate that fibrin networks adapt to moderate strains by remodeling

215 eta3 activation and fibrinogen conversion to fibrin occur simultaneously, although the relative contr

216 t the mechanistic links between the thrombin/fibrin(ogen) axis and obesity-associated pathologies are

217 Progressive MS cases with severe fibrin(ogen) deposition have significantly reduced neuro

218 Fibrin(ogen) deposition is neurotoxic in animal models o

219 Motor cortical fibrin(ogen) deposition was significantly over-represent

220 MS cases with high levels of extracellular fibrin(ogen) had significantly upregulated PAI-1 express

221 o investigate the extent and distribution of fibrin(ogen) in progressive MS cortex and elucidate its

222 t time, we provide unequivocal evidence that fibrin(ogen) is extensively deposited in progressive MS

223 proof of concept that targeting thrombin or fibrin(ogen) may limit pathologies in obese patients.

224 e raised in T2D, and we recently showed that fibrin(ogen) polymerisation during blood clotting can be

225 ocytosis was unimpeded by the absence of the fibrin(ogen) receptors, alphaMbeta2 and ICAM-1, the myel

226 The extent and distribution of fibrin(ogen) was assessed and related to measures of dem

227 the provenance and putative neurotoxicity of fibrin(ogen), and its potential impact on clinical disab

228 ding of the mechanisms by which blood cells, fibrin(ogen), and platelet-fibrin interactions modulate

229 nonmuscle myosin II, red blood cells (RBCs), fibrin(ogen), factor XIIIa (FXIIIa), and thrombin on the

230 tested the hypothesis that disruption of the fibrin(ogen)-alphaMbeta2 interaction in Fibgamma(390-396

231 Fibrin(ogen)-alphaMbeta2 interaction inhibited iNOS indu

232 s characterize a novel mechanism whereby the fibrin(ogen)-integrin-alphaMbeta2 interaction reduces bi

233 bp, and sdrC), all with binding affinity for fibrin(ogen).

234 e, was assessed and related to the extent of fibrin(ogen).

235 differentiation of the role of fibrinogen vs fibrin oligomer or polymer in antimicrobial host defense

236 We determined the effect of fibrin on the diffusion, intratumoral distribution, and

237 s induced by jugular vein infusion of (125)I-fibrin or fluorescein isothiocyanate-fibrin labeled embo

238 1, the myeloid cell integrin-binding site on fibrin or the endocytic collagen receptor, the mannose r

239 Fibrin placed into the dermis of mice underwent cellular

240 a3-ligand complexes had the following order: fibrin polymer > fibrin monomer > fibrinogen.

241 the Aalpha chain of fibrinogen such that no fibrin polymer is formed in vivo, allowing for the first

242 e findings establish for the first time that fibrin polymer is the molecular form critical for antimi

243 RA does not interact with fibrinogen, affect fibrin polymerization during clot formation, or abrogate

244 ss Gly-Pro-Arg-Pro (GPRP) was added to block fibrin polymerization.

245 s with tranexamic acid reduced retraction of fibrin polymers in vivo.

246 tion revealed that incomplete proteolysis of fibrin polymers markedly facilitated clot retraction.

247 erstanding of alphaIIbbeta3 interaction with fibrin polymers.

248 udy evaluates contributions of platelet-rich fibrin (PRF) combined with conventional flap surgery on

249 ch in growth factors (PRGF) or platelet-rich fibrin (PRF) compared with a control xenograft defect fi

250 bony defects (IBDs); recently, platelet-rich fibrin (PRF) has been suggested as a grafting material.

251 Platelet-rich fibrin (PRF) has recently been applied in osseous regene

252 Platelet-rich fibrin (PRF) is a leukocyte and platelet preparation tha

253 Platelet-rich fibrin (PRF) is a platelet concentrate having sustained

254 Platelet-rich fibrin (PRF) is a pool of growth-promoting factors and c

255 Platelet-rich fibrin (PRF) is a reservoir of concentrated platelets th

256 Platelet-rich fibrin (PRF) is an autologous non-transfusional hemo-com

257 is to evaluate the effects of platelet-rich fibrin (PRF) membranes on the outcomes of clinical treat

258 Platelet-rich fibrin (PRF) promotes tissue regeneration by releasing v

259 Platelet-rich fibrin (PRF), a second-generation platelet concentrate,

260 Platelet analogs such as platelet-rich fibrin (PRF), being rich sources of growth factors, have

261 pic bead coated with fibrinogen or monomeric fibrin produced by treating the immobilized fibrinogen w

262 thrombin-mediated activation of the platelet fibrin receptor (GPIIbIIIa).

263 ammation through the podoplanin and collagen/fibrin receptors, C-type-lectin-like-2 (CLEC-2) and glyc

264 AR ligand urokinase prevented degradation of fibrin-rich thrombi at the LV valves and largely resolve

265 irculation; however, these valves lacked the fibrin-rich thrombi that prevent blood from entering the

266 t of biofilm matrix, and dissolution of this fibrin scaffold greatly increased susceptibility of biof

267 tile forces exerted by platelets against the fibrin scaffold.

268 The fibrin shield can be marked with R-specific antibodies,

269 phylococcal surface, generating a protective fibrin shield that inhibits phagocytosis.

270 o evasive strategies, assembly of protective fibrin shields via coagulases and protein A-mediated B c

271 present in acute wound fluids as well as in fibrin sloughs from patients with infected wounds.

272 e and thrombus imaging efficacy of the novel fibrin-specific PET probe (64)Cu-FBP8.

273 talloproteinases that cleave fibrinogen into fibrin split products without inducing clotting.

274 n in human tumor biopsies showed significant fibrin staining in nearly all tumor types evaluated.

275 e in a fibrin-dependent manner and decorated fibrin strands extending from platelet aggregates.

276 thrombin and fibrinogen gamma' in modulating fibrin structure under fully hydrated conditions.

277 Thrombin-catalyzed fibrin formation and fibrin susceptibility to plasmin-induced lysis were sign

278 patients fibrinogen function and structure, fibrin susceptibility to plasmin-lysis, plasma redox sta

279 ted mechanism for clearance of extravascular fibrin that is accomplished by a specific proinflammator

280 s in a matrix of natural proteins, including fibrin, that provide physical support and cues to the ce

281 Host-derived fibrin, the main substrate cleaved by Sak-activated plas

282 neys when the extent of glomeruli containing fibrin thrombi is less than 50% and donor renal function

283 ies showing 100% of the glomeruli containing fibrin thrombi.

284 uman embryonic stem cells in 3D multilayered fibrin tissue constructs.

285 unoglobulin M, immunoglobulin G, complement, fibrin, tissue factor, fibrinogen-like protein 2, tissue

286 al wound repair, the precise contribution of fibrin to bone fracture repair, whether supportive or de

287 tly cross-links fibrin and other proteins to fibrin to stabilize blood clots and reduce blood loss.

288 Consequently, cellular fibrin uptake was diminished by elimination of CCR2-expr

289 Cellular fibrin uptake was strictly dependent on plasminogen and

290 ge subpopulation constituted the majority of fibrin-uptaking cells.

291 r biopsies were examined for the presence of fibrin, using light microscopy after Maurits, Scarlet an

292 We show how fibrous networks composed of fibrin utilize irreversible changes in their hierarchica

293 This assumption was supported using the fibrin variants alphaD97E or alphaD574E with mutated RGD

294 showed that thrombus resistance imparted by fibrin was approximately 30-fold higher than that impart

295 In contrast to our hypothesis, fibrin was entirely dispensable for long-bone fracture r

296 IIbbeta3 binding to fibrinogen and monomeric fibrin, we found that alphaIIbbeta3 binding to polymeric

297 Retinal folds and subretinal fibrin were identified in a greater proportion of eyes i

298 a mathematical model of thrombin adhesion to fibrin, which demonstrates that thrombin initially binds

299 on a prototypical hierarchical biomaterial, fibrin, which is one of the most resilient naturally occ

300 GPVI as a platelet receptor for polymerized fibrin with 2 major functions: (1) amplification of thro