ライフサイエンスコーパス: fibrin

1 cellular traps associated with platelets and fibrin.

2 binding sites and mediating the formation of fibrin.

3 prothrombinase to 15 muM thrombin to 90 muM fibrin.

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

5 ipid, ultimately leading to the formation of fibrin.

6 bin, self-polymerize to form water-insoluble fibrin.

7 mutant wounds that contain less collagen and fibrin.

8 ion (10%), chemosis (4%), hypopyon (4%), and fibrin (3%).

9 ch fibrin (L-PRF) and advanced platelet-rich fibrin (A-PRF) has further confused many readers, since

10 of this fundamental mechanical mechanism in fibrin, a key element in wound healing and angiogenesis

11 d PAI-1-dependent tumor growth and increased fibrin abundance, whereas miR-30c mimics inhibited tumor

12 a greater extent of platelet activation and fibrin accumulation on the outside than the inside.

13 s to induce efficient fibrin clot lysis in a fibrin-agar plate model and the encapsulated tPA retaine

14 presence of eosinophil peroxidase, MBP, and fibrin alpha-, beta-, and gamma-chains.

15 ng fibrinolysis by irreversibly crosslinking fibrin and antifibrinolytic proteins.

16 by collagen in the subendothelial matrix, by fibrin and fibrinogen in the thrombus, and by a remarkab

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

18 models had differential abilities to degrade fibrin and launch new vessel sprouts, a finding that was

19 Elastic moduli and failure strains of fibrin and PEG (600) DA hydrogels were calculated from t

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

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

22 CC involved platelets, neutrophils, fibrin, and extracellular DNA.

23 IXa), FIXa (via TF/FVIIa or FXIa), thrombin, fibrin, and FXIa.

24 nt, neutrophil extracellular trap formation, fibrin, and local activation of tissue factor in the thr

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

26 A molecular understanding of fibrin architecture at the level of these cross-links co

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

28 substantial production of FXa, thrombin, and fibrin as compared with controls.

29 splacements of tracer particles suspended in fibrin at different ageing times are obtained.

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

31 e flow stagnation and remote embolisation of fibrin-based clots.

32 g MDA-MB-231 cells + HUVECs in an HLF-laden, fibrin-based ECM within our microfluidic device optimall

33 Fibrin-based engineered heart tissue was generated from

34 nvestigate the effects of using gelatin- and fibrin-based hemostatic hydrogels as a scaffold on pulp

35 utologous blood clot (PC), gelatin-based and fibrin-based hemostatic matrices (GM and FM), or without

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

37 ted significantly higher cell viability than fibrin-based scaffolds after 15 days (P < 0.05).

38 red three-dimensionally in gelatin-based and fibrin-based scaffolds was evaluated by MTT and live/dea

39 An alternative approach to ETFA is the "Fibrin Bead Assay" (FBA), based on the use of Cytodex 3

40 Thrombin-fibrin binding is often described as two independent, si

41 s rendered nonessential either by their high fibrin-binding parameters and short lifetimes or their i

42 Upon activation, fibrinogen forms large fibrin biopolymers that coalesce into clots which assist

43 e study explored the effect of platelet-rich fibrin/biphasic calcium phosphate (PRF/BCP) on different

44 and noninfectious stimuli and, together with fibrin, block the invasion of pathogens.

45 Fibrin both promotes thrombotic events and drives obesit

46 n experimentally-observed residency times of fibrin-bound thrombin.

47 min elution, with most thrombin (>99%) being fibrin-bound.

48 Fibrin can modify multiple aspects of inflammatory cell

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

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

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

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

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

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

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

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

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

58 roscale model represents a three-dimensional fibrin clot.

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

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

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

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

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

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

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

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

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

68 on, this reduced model predicts thrombin and fibrin co-regulation during thrombosis under flow.

69 ad lower portal pressure and livers had less fibrin compared with control mice after pIVCL and bile-d

70 coagulation pathways act together to produce fibrin-containing thrombi.

71 ochemical analyses were performed to analyze fibrin content, amyloid burden, neuroinflammatory activi

72 te measurement of coagulation, platelets and fibrin content.

73 human Lys679Met FXIII-A demonstrated reduced fibrin crosslinking activity in vitro.

74 bitor (PAI-1), and fibrin formation, but not fibrin crosslinking.

75 roenvironment through its ability to promote fibrin degradation and inhibit blood vessel formation.

76 mation and upregulation of components of the fibrin degradation pathway, including plasminogen recept

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

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

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

80 and platelet pathways with the production of fibrin degradation products (D-dimer) and consumption of

81 ogen activator Pla, a protease that promotes fibrin degradation, thwarts T cell-mediated defense agai

82 ewise produce virulence factors that promote fibrin degradation.

83 Affimer F5 reduced fibrin-dependent plasmin generation and was predicted to

84 e data indicate that Pla functions to thwart fibrin-dependent T cell-mediated defense against plague.

85 Infusion of an alpha-FcRn mAb prevented fibrin deposition after microvascular injury in a murine

86 arent, as is an asymmetrical distribution of fibrin deposition and thrombin activity.

87 ated that atorvastatin significantly reduced fibrin deposition at day 7 and macrophage accumulation a

88 y decline, cerebral hypoperfusion, and toxic fibrin deposition in the AD mouse brain.

89 res of VT, the coagulopathy in the head, and fibrin deposition in the liver.

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

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

92 ckling of RBCs and a significant increase in fibrin deposition were observed in venous thrombi formed

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

94 increased bleeding, bodyweight loss, anemia, fibrin deposition, and loss of colon epithelial and gobl

95 ences in the fractions of endothelial cells, fibrin deposition, macrophages and neutrophils when comp

96 RVXB markedly reduced fibrin deposition, suggesting reduced intrahepatic micro

97 abrogated coagulopathy in the head and liver fibrin deposition.

98 set, severity, thrombus morphology, or liver fibrin deposition.

99 gy of thrombin generation and the subsequent fibrin deposition.

100 ctor and C5a), and multifocal intra-alveolar fibrin deposition.

101 Vascularization, fibrin depositions, macrophage and neutrophil infiltrati

102 fibrin(ogen)/Abeta codeposition, as well as fibrin deposits in HCAA patients, compared to early-onse

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

104 In predicting intrathrombus thrombin and fibrin during 15-min microfluidic experiments, the model

105 anistic studies revealed essential roles for fibrin during T cell-mediated defense against Pla-mutant

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

107 Analysis of fibrin expression in human tumor biopsies showed signifi

108 on clot structure and G2 profoundly altered fibrin fiber arrangement, whereas F5 maintained physiolo

109 thrombin becoming physically trapped within fibrin fibers as they formed.

110 urrounding matrix by pulling on collagen and fibrin fibers.

111 ents with prominent elevation of D-dimer and fibrin/fibrinogen-degradation products, whereas abnormal

112 active barrier involving a neutrophil-rich, fibrin-fibronectin net.

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

114 Among the many factors influencing fibrin formation and structure (concentration, temperatu

115 prothrombotic risk factor marked by enhanced fibrin formation and suppressed fibrinolysis.

116 agonist oral anticoagulants, which attenuate fibrin formation by selective inhibition of factor Xa or

117 from aggregating platelets, which increased fibrin formation in a DNase-dependent manner.

118 rofluidic channels, platelet aggregation and fibrin formation induced by 5B9 with heparin was strongl

119 al TG and PG in HFD-fed mice produced normal fibrin formation kinetics but delayed fibrinolysis.

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

121 patial regulation of platelet activation and fibrin formation that could not be inferred from studies

122 ockout mice, collagen-dependent thrombus and fibrin formation under flow were enhanced.

123 platelet activation, thrombus structure and fibrin formation were assessed by fluorescence microscop

124 plasminogen activator inhibitor (PAI-1), and fibrin formation, but not fibrin crosslinking.

125 onsiveness in thrombus formation and ensuing fibrin formation, resulting in a prothrombotic phenotype

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

127 also promote vessel occlusion independent of fibrin formation.

128 cantly to coagulation, platelet function and fibrin formation.

129 esion in thrombus contraction and subsequent fibrin formation; (2) a surface-independent role of tiss

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

131 In tumors, extravascular fibrin forms provisional scaffolds for endothelial cell

132 findings indicate that the immunotherapeutic fibrin gel 'awakens' the host innate and adaptive immune

133 e anti-CD47 antibody are encapsulated in the fibrin gel and scavenge H(+) in the surgical wound, allo

134 ignificantly inhibited 3D spheroid growth in fibrin gel assays.

135 modulus by a factor of two compared with the fibrin gel formed by directly mixing fibrinogen and thro

136 ip comprises a fluidic channel filled with a fibrin gel in which CD34(+) cells and BM-derived stromal

137 further confirmed in HHSEC and the HUVEC 3D fibrin gel model, respectively.

138 n Umbilical Vein Endothelial Cell (HUVEC) 3D fibrin gel model.

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

140 Fibrin gels have been extensively used for three-dimensi

141 ffers experimental insights on the ageing of fibrin gels while presenting a white noise functional st

142 ellular matrix (ECM: collagen, Matrigel, and fibrin gels with or without free HLFs) that we used.

143 m tumor cells in soft three-dimensional (3D) fibrin gels with unidentified mechanisms.

144 We embedded fibroblast cells in 3D fibrin gels, and monitored band formation by real-time c

145 ing multicellular processes in reconstituted fibrin gels.

146 strengthening, but they require thrombin and fibrin generation and are unable to measure platelet for

147 in high-shear microvessels does not require fibrin generation or extracellular trap formation, but i

148 ivity and promotes platelet accumulation and fibrin generation.

149 ; 48.5%), stromal patching (10 cases; 9.9%), fibrin glue (8 cases; 7.9%), and suturing of the defect

150 Tisseel fibrin glue for the repositioning of conjunctival autogr

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

152 vious amniotic membrane graft placement with fibrin glue.

153 Implantation of acellular or endothelialized fibrin grafts with an external ultrathin poly(epsilon-ca

154 in the jejunum and proximal ileum covered by fibrin; histological report showed macrophages with posi

155 inding to cells, but formation of fibrinogen/fibrin-histone aggregates prevented cell death.

156 During thrombosis, thrombin generates fibrin, however fibrin reversibly binds thrombin with lo

157 land regeneration in vivo when compared with fibrin hydrogel (FH) alone; however, L(1p)M-FH produce o

158 aminin-111 peptides chemically conjugated to fibrin hydrogel (L(1p)M-FH) promote cell cluster formati

159 human dermal fibroblasts, encapsulated in a fibrin hydrogel and allowed to compact under passive ten

160 Significantly, the resulting robust cellular fibrin hydrogel constructs can be differentiated down os

161 rombin construct, giving rise to spontaneous fibrin hydrogel nucleation and growth at near human plas

162 on laser radiation at lambda = 532 nm within fibrin hydrogels at pulse energies of E(p) = 12, 18 uJ a

163 h limbal epithelial stem/progenitor cells on fibrin hydrogels pre-incubated with LN-511-E8 resulted i

164 echanisms of Lp(a), including (i) binding to fibrin, (ii) stimulation of smooth-muscle cell prolifera

165 The reduction in fibrin in the mutant is further explained by reduced myo

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

167 mbi contained a surprisingly large amount of fibrin, in addition to platelets.

168 physiologically relevant ECMs-collagen I and fibrin-in a matter of minutes.

169 l video microscopy showed how fibrinogen and fibrin influence NETosis and neutrophil responses to ext

170 ment F1.2 in the presence and absence of the fibrin inhibitor Gly-Pro-Arg-Pro.

171 They show that fibrin interacts with phosphatidylserine exposed on the

172 , in wound healing or angiogenesis, in which fibrin is contracted by fibroblast cells.

173 a combination of leukocyte and platelet-rich fibrin (L-PRF) + autogenous bone graft (ABG) may be a cl

174 de names such as leukocyte and platelet-rich fibrin (L-PRF) and advanced platelet-rich fibrin (A-PRF)

175 e disinfectant, leukocyte- and platelet-rich fibrin (L-PRF), on a mature oral multispecies biofilm on

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

177 ncorporated within VWF A1 HBD-functionalized fibrin matrices accelerated wound healing, with increase

178 Incorporation of the VWF A1 HBD into fibrin matrices enables sequestration and slow release o

179 In vivo, VWF A1 HBD-functionalized fibrin matrices increased angiogenesis and GF retention

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

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

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

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

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

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

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

187 migration of cultured macrophages through a fibrin matrix did not occur in the absence of plasminoge

188 r 3 days in vitro and then injected within a fibrin matrix into subcutaneous pockets on the dorsal fl

189 NTM) of different shapes using stem cells, a fibrin matrix, and 3D printed molds.

190 Thrombin also binds to the formed fibrin matrix, but this interaction is not well understo

191 Utilizing a three-dimensional fibrin-matrix based model we show that TIE2-L914F mutant

192 Fibrin mediated cellular remodeling, stable tunica intim

193 We report that fibrin-mediated angiogenesis was inhibited and tumor gro

194 tracted from Def(++) mice were composed of a fibrin meshwork that was denser and contained a higher p

195 Here, we developed cell-laden fibrin microbeads that can be pre-cultured to form primi

196 In this study, we utilized novel electrospun fibrin microfiber sheets of different stiffnesses (50.0

197 Using surface topography in a hollow fibrin microfiber tube, we enable immediate, controlled

198 Nonocclusive fibrin microthrombi (without ischemic injury) were ident

199 COVID-19 cases frequently have cardiac fibrin microthrombi, without universal acute ischemic in

200 entrapped sickle red cells make the attached fibrin more resistant to fibrinolysis by tissue plasmino

201 ances fibrin polymerization kinetics, alters fibrin morphology, and inhibits fibrinolysis.

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

203 variations necessary to alter significantly fibrin multiscale structure as observed in the literatur

204 gation of the influence of this parameter on fibrin multiscale structure.

205 aggregates is a major determining factor for fibrin multiscale structure.

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

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

208 provide a novel methodology for stabilizing fibrin networks with potential future clinical implicati

209 ding proteins, termed Affimers, to stabilize fibrin networks with the potential to control excessive

210 CD69-deficiency increased fibrin(ogen) accumulation in the ischemic tissue, and pl

211 Moreover, platelet recruitment and fibrin(ogen) accumulation were significantly higher in F

212 However, fibrin(ogen) and proteases controlling its deposition an

213 esence of SAA increased amyloid formation of fibrin(ogen) as determined both with auto-fluorescence a

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

215 stream or downstream (71%), as was extensive fibrin(ogen) buildup (87%).

216 yte proliferation after PHx, indicating that fibrin(ogen) contributes to liver regeneration after PHx

217 We tested the hypothesis that fibrin(ogen) contributes to liver regeneration by promot

218 Platelets use lamellipodia to scan for fibrin(ogen) deposited on the inflamed vasculature and t

219 m whereby coagulation-dependent intrahepatic fibrin(ogen) deposition drives platelet accumulation and

220 he role of coagulation system activation and fibrin(ogen) deposition in models of inflammatory diseas

221 Intrahepatic fibrin(ogen) deposition was abolished in mice with liver

222 Moreover, increased intrahepatic fibrin(ogen) deposition was evident in livers of patient

223 Fibrin(ogen) deposition was noted in the peritoneal cavi

224 Thrombin-dependent intrahepatic fibrin(ogen) deposition was recently reported after part

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

226 69 expression, as well as platelet function, fibrin(ogen) deposition, and VWF (von Willebrand factor)

227 patic coagulation, evidenced by intrahepatic fibrin(ogen) deposition.

228 generation primarily by driving intrahepatic fibrin(ogen) deposition.

229 Indeed, fibrin(ogen) deposits are a near-universal feature of ti

230 l hepatectomy (PHx) in mice, but the role of fibrin(ogen) deposits in liver regeneration has not been

231 Consistent with the protective function of fibrin(ogen) in mice, low postoperative plasma fibrinoge

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

233 ioglycollate, with a significant increase in fibrin(ogen) in the plasminogen-deficient mice.

234 ase in coagulation, but a decreased platelet/fibrin(ogen) interaction.

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

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

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

238 mposed by the interaction of leukocytes with fibrin(ogen) through the integrin alpha(M)beta(2) recept

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

240 coagulation by inducing amyloid formation in fibrin(ogen), as well as by propelling platelets to a mo

241 the thrombin-generating potential underlying fibrin(ogen)-dependent bacterial clearance.

242 ought to characterize possible mechanisms of fibrin(ogen)-mediated antimicrobial responses.

243 Fibrin(ogen)-mediated bacterial clearance was dependent

244 that SAA causes atypical coagulation with a fibrin(ogen)-mediated increase in coagulation, but a dec

245 )beta(2)-binding motif on the gamma chain of fibrin(ogen).

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

247 f the occipital cortex showed an increase of fibrin(ogen)/Abeta codeposition, as well as fibrin depos

248 2.6; 95% CI, 1.02-6.5), and anterior chamber fibrin on examination (OR, 2.7; 95% CI, 1.1-6.3).

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

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

251 flammation, but without injection, hypopyon, fibrin, or severe pain.

252 e in presenting VA (P = 0.0004), presence of fibrin (P = 0.02), and trended toward receiving only obs

253 (m) = 1.5 x 10(5) m(-1)s(-1)), as well as to fibrin, platelet proteins, and blood clots under flow in

254 lure via the formation of crystal clots with fibrin, platelets, and extracellular DNA as critical com

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

256 nt function, supporting a suspected role for fibrin polymerization in this mechanism.

257 ial peptide alpha-defensin-1, which enhances fibrin polymerization kinetics, alters fibrin morphology

258 alpha-Defs accelerate fibrin polymerization, increase fiber density and branch

259 Fibrinogen levels, fibrin polymerization, platelet activation, and micropar

260 rd hydrogels (8 mg/ml, S8) supplemented with fibrin possessed a gelation rate and a storage modulus c

261 regenerative material such as platelet rich fibrin (PRF) and bisphosphonates as alendronate (ALN).

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

263 G) with and without autologous platelet-rich fibrin (PRF) in the treatment of intrabony defects in ch

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

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

266 eneration material with either platelet rich fibrin (PRF) membrane or collagen membrane (CM) treated

267 Platelet-rich fibrin (PRF) membranes can preserve alveolar ridge dimen

268 Platelet-rich fibrin (PRF) serves as a reservoir of bioactive molecule

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

270 The multiscale structure of the fibrins produced from those two fibrinogen preparations

271 srupts the ideal ordering of monomers inside fibrin protofibrils and fibers.

272 To predict intraclot fibrin reaching 30 mg/mL by 15 min, the model required f

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

274 rombosis, thrombin generates fibrin, however fibrin reversibly binds thrombin with low affinity E-dom

275 Although fibrin sealants are considered to minimize blood loss, t

276 ites (KD = 2.8 muM) and high affinity gamma'-fibrin sites (KD = 0.1 muM).

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

278 extent of lysis propagation and the shape of fibrin spatial distribution during lysis.

279 The following fibrin-specific ROTEM (FIBTEM S) variables were also rec

280 und high concentrations of plasma D-dimer, a fibrin split product, suggestive of a concurrent consump

281 were thoroughly determined by measuring the fibrin-stabilizing factor; fibronectin; alpha, beta, and

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

283 ophage response to statin therapy, using the fibrin-targeted, near-infrared fluorescence molecular im

284 platelet-specific receptor for collagen and fibrin that triggers platelet activation through immunor

285 drugs used for inhibiting the dissolution of fibrin, the main structural component of blood clots, ar

286 Here we focus on fibrin, the primary component of a blood clot.

287 hether donor kidneys with diffuse glomerular fibrin thrombi (GFT) are safe to use.

288 We identified focal kidney fibrin thrombi in 6 of 42 (14%) autopsies.

289 ischemic enteritis with patchy necrosis and fibrin thrombi in arterioles (n = 2).

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

291 On average, 79% of glomeruli contained fibrin thrombi.

292 of inflammatory cells and rare intravascular fibrin thrombi.

293 integrative phenotyping approach of platelet-fibrin thrombus formation has revealed interaction mecha

294 -diameter vascular grafts by electrospinning fibrin tubes and poly(epsilon-caprolactone) fibrous shea

295 bservations of colloidal tracer particles in fibrin undergoing gelation, we introduce an analytical f

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

297 cus on lymphocytic vasculitis, intravascular fibrin, vessel caliber, extent of injury, C4d positivity

298 vivo, crosslinking of alpha2-antiplasmin and fibrin was impaired and fibrinolysis was enhanced.

299 feedback loops, and cleaves fibrinogen into fibrin, which polymerizes into fibers to form a stabiliz

300 studied the interdomain dynamics of MMP1 on fibrin without crosslinks using single-molecule Forster