ライフサイエンスコーパス: blood clot

1 ate extensive invadopodia when embedded in a blood clot.

2 ter, are the major structural component of a blood clot.

3 ides information about relative shrinkage of blood clot.

4 fibronectin has to be incorporated into the blood clot.

5 l fibrin generation and stabilization of the blood clot.

6 rupture as they attempt to migrate under the blood clot.

7 d in patients who did not receive autologous blood clot.

8 ecules and gives mechanical stability to the blood clot.

9 lapse or provide sufficient stability of the blood clot.

10 myosins from motor proteins, and fibrin from blood clot.

11 proteases also involved in the formation of blood clots.

12 of the viscoelastic properties of incipient blood clots.

13 embolized using a suspension of small-sized blood clots.

14 bers, which are key structural components of blood clots.

15 olymers and forms the structural scaffold of blood clots.

16 Xa plays a critical role in the formation of blood clots.

17 e conversion of fibrinogen to fibrin to form blood clots.

18 save lives by generating plasmin to dissolve blood clots.

19 n molecules to plasmin, which then dissolves blood clots.

20 proximately 50% at 1 nM macrophage uptake of blood clots.

21 to marginate to near a vessel wall and form blood clots.

22 hese SPMs promote macrophage phagocytosis of blood clots.

23 ibrin fibers form the structural scaffold of blood clots.

24 uclear cell fragments that are essential for blood clotting.

25 by partial loss of pigmentation and impaired blood clotting.

26 platelet stimulation and platelet-activated blood clotting.

27 siologic activator of the contact pathway of blood clotting.

28 identified as a regulatory driving force in blood clotting.

29 shown to be a crucial step in the process of blood clotting.

30 wth by obstructing tumor circulation through blood clotting.

31 depleted protein production and inefficient blood clotting.

32 way inhibitor (TFPI) is a major regulator of blood clotting.

33 uid flow in the regulation of propagation of blood clotting.

34 ts are anuclear cells that are essential for blood clotting.

35 ments lacking nuclei that play a key role in blood clotting.

36 sed by blood-sucking insects to inhibit host blood clotting.

37 for designing new antithrombotics disrupting blood clotting.

38 sed inflammation, microvascular density, and blood clotting.

39 ndent thrombus formation, and agonist-driven blood clotting.

40 h those involved in mammalian complement and blood clotting.

41 nd pharmacological role in the modulation of blood clotting.

42 posure of anionic phospholipids that support blood clotting.

43 , interaction which is central to preventing blood clotting.

44 genic effects on bone, lipid metabolism, and blood clotting.

45 and the mice have no overt abnormalities in blood clotting.

46 enzyme gene (ACE) may be related to abnormal blood clotting.

47 ivity of tissue factor that is distinct from blood clotting.

48 erto undiscovered, shape that contributes to blood clotting.

49 mechanical regulation of vWF activity during blood clotting.

50 a activation of FV is pivotal for plasma and blood clotting.

51 ctor IX and prolonged human plasma and whole blood clotting.

52 The study shows that rapid injection of blood clots (3 ml/30s) produced a model where there is a

53 lots (34.98 microm2/s), and slowest in whole-blood clots (3.55 microm2/s).

54 ammatory response occurred in and around the blood clot after ICH, characterized by the infiltration

55 mone (melanocyte stimulating hormone), and a blood-clotting agent can be anchored to erythrocytes, pr

56 During human blood clotting, alpha2-antiplasmin (alpha2AP) becomes co

57 he 20 patients (15%) who received autologous blood clot and 10 of the 14 (71%) who did not (P <.001).

58 who had deep lesions and received autologous blood clot and in 15 of the 32 patients (47%) who had de

59 le fibrin fibers determine the behavior of a blood clot and, thus, have a critical influence on heart

60 ctivators generate plasmin to degrade fibrin blood clots and other proteins that modulate the pathoge

61 ibrin fibers form the structural scaffold of blood clots and perform the mechanical task of stemming

62 hysiologic process in animals that dissolves blood clots and promotes wound healing, blood vessel gro

63 in and other proteins to fibrin to stabilize blood clots and reduce blood loss.

64 Blood clots and thrombi consist primarily of a mesh of b

65 role of inflammatory cells in contraction of blood clots and thrombi has not been investigated.

66 of fibrin, the primary structural protein of blood clots and thrombi, occurs through binding of knobs

67 ymer that forms the viscoelastic scaffold of blood clots and thrombi.

68 rk that is the major structural component of blood clots and thrombi.

69 , serving to activate the contact pathway of blood clotting and accelerate factor V activation.

70 e activation of various proteins involved in blood clotting and bone metabolism.

71 the roles that polyP plays in modulating the blood clotting and complement systems in health and dise

72 It is a potent modulator of the blood clotting and complement systems in hemostasis, thr

73 gulatory actions is its ability to influence blood clotting and fibrinolysis.

74 ns is critical for platelet aggregation upon blood clotting and for leukocyte extravasation to inflam

75 being involved in signalling, vasodilation, blood clotting and immunity and as an intermediate in mi

76 rtant roles in vivo, ranging from regulating blood clotting and inflammation to directly counteractin

77 ear polymers of orthophosphate that modulate blood clotting and inflammation.

78 the rate of mixing, and surface chemistry in blood clotting and its chemical model.

79 ny important biological responses, including blood clotting and pain perception.

80 s may exhibit unique properties analogous to blood clotting and thereby be useful in self-healing app

81 inogen activator inhibitor (PAI-1), controls blood clotting and tissue remodeling events that involve

82 lation reverses the prometastatic effects of blood clotting and tumor cell integrin alphavbeta3.

83 (Abeta), forming plasmin-resistant abnormal blood clots, and increased fibrin deposition is found in

84 vides biophysical and biochemical support to blood clots, and subsequent degradation of fibrin by pla

85 eosinophils, mast cells, mononuclear cells), blood clotting, and microvascular density within the tum

86 f the VKOR gene extends our understanding of blood clotting, and should facilitate development of new

87 ogical processes, including viral infection, blood clotting, and signal transduction, and as such, th

88 extracellular processes such as virus entry, blood clotting, antibody-mediated immune response, infla

89 The mechanical properties of the blood clot are important for its functioning but complic

90 Substances released by platelets during blood clotting are essential participants in events that

91 generated in a tissue factor-initiated whole blood clotting assay unless exogenous FV was added, cons

92 telets interact with fibrin polymers to form blood clots at sites of vascular injury.

93 e levels of PCB activity thereby stabilizing blood clots at sites where there is a breach in the inte

94 rne TF activity that incorporates within the blood clot, balancing the need for adequate hemostasis w

95 ons to hemostasis appear to be to accelerate blood clotting but are not required for blood clotting t

96 Retraction of the blood clot by nucleated cells contributes both to hemost

97 essing platelets modulate the lysis of whole blood clots by providing direct and indirect binding sit

98 a potent hemostatic regulator, accelerating blood clotting by activating the contact pathway and pro

99 owed that fibrin(ogen) polymerisation during blood clotting can be affected strongly by LPS.

100 ted allosteric enzyme involved in vertebrate blood clotting, can be converted into a K+-specific enzy

101 integral membrane protein that triggers the blood clotting cascade and for which membrane anchoring

102 Seven proteins in the human blood clotting cascade bind, via their GLA (gamma-carbox

103 , the cell-surface protein that triggers the blood clotting cascade in hemostasis and thrombotic dise

104 The blood clotting cascade is selectively involved in lung m

105 ctor VIII (FVIII), an important co-factor in blood clotting cascade, elicits unwanted anti-FVIII anti

106 our cascades are: the complement system, the blood clotting cascade, the fibrinolytic system, and the

107 mbin is a dual action serine protease in the blood clotting cascade.

108 hat is exposed upon injury and initiates the blood clotting cascade.

109 iginally well characterized in the mammalian blood clotting cascade.

110 ptidomimetic drugs such as inhibitors of the blood clotting cascade.

111 malian serpin antithrombin in localizing the blood-clotting cascade, suggesting that serpin inhibitio

112 n is a dual-action protein that mediates the blood-clotting cascade.

113 aterials, and one cylinder was filled with a blood clot (CL).

114 stroke, treatment could be given to break up blood clots compared with blacks (92% versus 84%, P<0.05

115 ty of 4% to 20% of normal and improved whole blood clotting compared with factor VIII-deficient mice.

116 ecretory pathway (receptors, growth factors, blood-clotting components, and even many viral envelope

117 Platelet-driven blood clot contraction (retraction) is thought to promot

118 The revealed platelet-driven mechanisms of blood clot contraction demonstrate an important new biol

119 Blood clot contraction plays an important role in preven

120 In total, only five blood-clotted CSF samples (0.5%) were inhibited.

121 s of inverse lag times and maximal slopes of blood clotting curves in buffers containing Na+ and Cl-

122 alysis of the mechanical properties of whole-blood clots defines a unique property of the incipient c

123 polyphosphate exerts differential effects on blood clotting, depending on polymer length.

124 We found that contracted blood clots develop a remarkable structure, with a meshw

125 ase is widely recognized to be a form of the blood clotting disorder hemophilia, its molecular basis

126 Two genes implicated in blood-clotting disorders, von Willebrand factor (vWA) an

127 A microscale mathematical model of blood clot dissolution based on coarse-grained molecular

128 The results of simulations indicate that the blood clot dissolution process progresses by a blood-flo

129 icroscopy experimental studies on a model of blood clot dissolution, as well as with clinical observa

130 , is the key step in fibrinolysis leading to blood clot dissolution.

131 that regulate the process of fibrinolysis or blood clot dissolution.

132 be exploited to facilitate the design of new blood clot-dissolving drugs.

133 te streptokinase, which activates the host's blood clot-dissolving protein, plasminogen.

134 sociation study (GWAS) of 6135 self-reported blood clots events and 252 827 controls of European ance

135 ed by peptides of +3 to +5 net charge and by blood clotting factor V.

136 idues (gamma-carboxyglutamic acid domain) of blood clotting factor VII was carried out to identify si

137 Active site-inhibited blood clotting factor VIIa (fVIIai) binds to tissue fact

138 Blood clotting factor VIIa is involved in the first step

139 VWF also is a carrier protein for blood clotting factor VIII, and this interaction is requ

140 upon expression of a misfolding-prone human blood clotting factor VIII, or after partial hepatectomy

141 s covalently linked to fibrin when activated blood clotting factor XIII (FXIIIa) catalyzes the format

142 he basis of orthologs of genes for mammalian blood clotting factors being present in its genome.

143 ified factor VIIa and to active site-blocked blood clotting factors Xa or IXa was studied.

144 e lectins and to membrane-binding domains of blood-clotting factors V and VIII.

145 As the structural backbone of blood clots, fibrin networks carry out the mechanical ta

146 may provide an effective strategy to enhance blood clot formation and act as a rapid pan-hemostatic a

147 al role for fibrin crosslinking during whole blood clot formation and consolidation and establish FXI

148 to the von Willebrand factor, a key step in blood clot formation and wound healing.

149 lp2 perform this cleavage function to impede blood clot formation around the worms in vivo.

150 itable for advanced numerical simulations of blood clot formation during flow in blood vessels.

151 Blood clot formation is crucial to maintain normal physi

152 Thrombosis, or blood clot formation, and its sequelae remain a leading

153 and IIa (also known as thrombin) to prevent blood clot formation.

154 Blood-clot formation that results in the complete occlus

155 ng methodology to follow volume changes in a blood clot formed in vitro.

156 Previous work has shown that blood clots formed in the presence of the beta-amyloid p

157 bin generation kinetics and transport within blood clots formed under hemodynamic flow.

158 At higher settings, a blood clotting formed, leading to complete and permanent

159 producing the protease plasmin that removes blood clots from the vasculature, a process called fibri

160 here complement the current understanding of blood clotting from the molecular to the physiological l

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

162 Conversely, the presence of blood clots in stool (LR, 0.05; 95% CI, 0.01-0.38) decre

163 nism through which cancer cells can colonize blood clots in the lung vasculature.

164 Blood clots in the stool make a UGIB much less likely.

165 lecular relaxivity enable EP-2104R to detect blood clots in vivo.

166 e to release tryptase, and thrombin mediates blood clotting in early wounds.

167 K epoxide reductase, a protein required for blood clotting in humans, as part of a disulfide bond fo

168 ompted by previous observations of defective blood clotting in rabbits deficient in the sixth compone

169 the spatiotemporal dynamics of initiation of blood clotting in the complex network of hemostasis.

170 The extensive blood clotting in the eotaxin-transfected tumors was ass

171 long been considered dispensable for normal blood clotting in vivo because hereditary deficiencies i

172 Blood clotting in vivo is catalyzed by thrombin, which s

173 wound healing is a complex process involving blood clotting, inflammation, migration of keratinocytes

174 Infarcts were significantly larger after blood clot infusion compared to mass effect controls usi

175 nduced by introducing a preformed autologous blood clot into the right atrium using a 7-French introd

176 nistered IV following the injection of small blood clots into the brain vasculature.

177 rabbits by introducing tantalum-impregnated blood clots into the right atrium, and the rabbits were

178 Systems as varied as blood clotting, intracellular calcium signaling, and tis

179 Hemostasis and thrombosis (blood clotting) involve fibrinogen binding to integrin a

180 The formation of a blood clot involves the interplay of thrombin, fibrinoge

181 Mammalian blood clotting involves numerous components, most of whi

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

183 A blood clot is a meshwork of fibrin fibers built up by th

184 In the model, a blood clot is assumed to be an assembly of blood cells i

185 The main structural component of the blood clot is fibrin, a fibrous network that forms withi

186 The blood clot is much coarser in D2O, as indicated in clott

187 e forms of tissue factor (TF) into a growing blood clot is necessary for normal fibrin generation and

188 Dissolution of the fibrin blood clot is regulated in large part by plasminogen act

189 Interstitial fluid flow within blood clots is a biophysical mechanism that regulates cl

190 Contraction of blood clots is necessary for hemostasis and wound healin

191 Pathologic blood clotting is a leading cause of morbidity and morta

192 phosphate (S1P) released by platelets during blood clotting is a potent, specific, and selective endo

193 Blood clotting is a process by which a haemostatic plug

194 Thrombus (blood clot) is implicated in a number of life threatenin

195 Thrombosis, or malignant blood clotting, is associated with numerous cardiovascul

196 Tissue factor, the physiologic trigger of blood clotting, is the membrane-anchored protein cofacto

197 DVT by intrajugular injection of a preformed blood clot labeled with (125)I-fibrinogen.

198 We have developed a reconstituted blood clot lysis assay which eliminates the need for on-

199 dermidis influences this in vitro model of a blood clot mechanically and structurally on both microsc

200 expression of the principal initiator of the blood clotting mechanism, tissue factor (TF), and blocki

201 such as dyslipidemia, oxidative stress, and blood clotting mechanisms, we hereby report the synthesi

202 ntal analysis, we determined the quantity of blood clot (mg) in brain that produce neurologic dysfunc

203 the biopsy track was sealed with autologous blood clot (n = 50) and those who did not receive autolo

204 50) and those who did not receive autologous blood clot (n = 50).

205 eatment received: BC (untreated, filled with blood clot), NAT (natrosol gel alone), and DOX (10% doxy

206 A blood clot needs to have the right degree of stiffness a

207 a-glutamyl-epsilon-lysyl crosslinks into the blood clot network.

208 -epsilon-lysyl cross-links within the fibrin blood clot network.

209 mRNA quantitation from blood clots of the same patients showed relatively eleva

210 suggest that the previously noted effects of blood clotting on lung metastasis might be mediated in p

211 received laser irradiation, were filled with blood clot or PRP, respectively, and then irradiated aga

212 ontrol) and 2) PRP, defects were filled with blood clot or PRP, respectively; 3) LLLT and 4) PRP/LLLT

213 d PRP-BMA, in which defects were filled with blood clot or PRP-bma, respectively.

214 assisted injection method to introduce large blood clots or macroscopic emboli into the middle cerebr

215 Embolization with blood clots or microspheres increased mean pulmonary art

216 ed with intravenous injections of autologous blood clots or repeated injections of 300 mum microspher

217 We therefore extracted DNA from blood clots or sera from 92 kuru patients, and analyzed

218 perimental lung embolization with autologous blood clots or with the infusion of microspheres increas

219 deep lesions and did not receive autologous blood clot (P <.001).

220 vity and inhibit activators of the intrinsic blood clotting pathway, such as polyphosphate (polyP) an

221 Blood clots perform an essential mechanical task, yet th

222 unexplored problem, despite applications in blood clotting, plasmonics, industrial packaging and tra

223 at fibrinogen, the main protein component of blood clots, plays an important role in this circulatory

224 from inverse lag times and maximal slopes of blood clotting plots, which are also anion and cation de

225 serpin, antithrombin, to inhibit its target blood-clotting proteases by generating new protease inte

226 nally and a C-terminal region related to the blood clot protein fibrinogen.

227 Here, Petersen et al. (2017) show that the blood clotting protein fibrinogen inhibits nerve repair

228 t the worms are capable of cleaving the host blood clotting protein fibronectin and that this activit

229 Proteolysis of the blood-clotting protein von Willebrand factor (VWF) obser

230 n; 5) assess the role of insulin resistance, blood clotting, protein kinase C isoforms, and signal tr

231 in addition to its known role in regulating blood clotting, protein S may also be an important autoc

232 in activates the primary serpin inhibitor of blood clotting proteinases, antithrombin, both by an all

233 49 of antithrombin, the primary inhibitor of blood clotting proteinases, has previously been implicat

234 antithrombin, the principal inhibitor of the blood-clotting proteinases factor Xa and thrombin, is ac

235 ing of many protein-lipid interactions among blood-clotting proteins.

236 onal assays, such as endotoxin-induced whole blood clotting, prothrombin time, as well as factor X an

237 platelets is very efficient at accelerating blood clotting reactions but is less efficient at initia

238 mechanisms by which polyphosphate modulates blood clotting reactions remain to be elucidated.

239 Effective removal or dissolution of large blood clots remains a challenge in clinical treatment of

240 aggregate with a polymerized fibrin matrix, blood clots result from hundreds of unique reactions wit

241 In addition, D3 also inhibited whole blood clot retraction, in contrast to AP3 and C3, sugges

242 e platelet aggregation, vasoconstriction and blood clotting; saliva of these organisms also has anti-

243 raditional revascularization protocol with a blood clot scaffold.

244 d with the increasing volume of the subdural blood clot (sham: 9+/-3 mm3; 200 microl: 81+/-19 mm3; P<

245 activation, and phosphatidylserine exposure, blood clotting simulations require prediction of platele

246 Thrombin (0.01, 0.1, and 1 unit/mL) and blood clot solution (0.5% and 5%) induced delayed after

247 Thrombin (0.01, 0.1, and 1 unit/mL) and blood clot solution (0.5% and 5.0%) increased LA diastol

248 Blood clot solution (0.5% and 5.0%), respectively, reduc

249 were not changed by thrombin (1 unit/mL) and blood clot solution (5%).

250 and after the administration of thrombin or blood clot solution in control and dabigatran-treated ra

251 ol/L) attenuated the effects of thrombin and blood clot solution in PVs and LA.

252 We investigated the effects of thrombin, blood clot solution, and dabigatran on PVs and LA.

253 Fibrin, the structural scaffold of blood clots, spontaneously polymerizes through the forma

254 itions for the primary intention healing and blood clot stability were ensured by a proper flap desig

255 esentery tissue, lung parenchyma, cornea and blood clots--stiffen as they are strained, thereby preve

256 ndividuals who participated in the Genes and Blood Clotting Study (GABC) or the Trinity Student Study

257 onse to infection includes activation of the blood clotting system, leading to extravascular fibrin d

258 tion of thrombin, which enhances the overall blood-clotting system, both by accelerating fibrin gener

259 ry agent and a potent modulator of the human blood-clotting system.

260 SNPs initiate the contact pathway of the blood-clotting system; short-chain polyP accelerates the

261 ss-links between fibrin molecules in nascent blood clots that greatly increase the mechanical stabili

262 her organisms by using a fibrin gel to mimic blood clots that normally form after injury and that are

263 tamin K2 is a critical nutrient required for blood clotting that also plays an important role in bone

264 h nonspecific binding and adverse effects on blood clotting that limit their use.

265 role, including the ectoenzyme that triggers blood clotting, the plasma serine protease, factor VIIa,

266 rin, a fibrous network that forms within the blood clot, thereby increasing its mechanical rigidity.

267 Cross-linking is thought to fortify blood clots; though, the role of alpha-alpha cross-links

268 rin alpha(IIb)beta3 initiates the process of blood clotting through binding fibrinogen.

269 to 2.5 months and normalization of the whole blood clotting time (WBCT) for about a month.

270 njury in HemA mice, and fully corrects whole blood clotting time (WBCT) in HemA dogs immediately afte

271 Coagulation tests (whole blood clotting time [WBCT], activated clotting time [ACT

272 Whole blood clotting time analysis confirmed that hemostasis w

273 st, siRNA-mediated knockdown of KLF2 reduced blood clotting time and flow rates.

274 rombin time, partial correction of the whole blood clotting time and thromboelastography parameters,

275 Despite normalization of blood clotting time and thrombus stability after r-FVIII

276 se-dependent partial correction of the whole blood clotting time and, at higher doses, of the activat

277 nfected cells, KLF2 overexpression increased blood clotting time as well as flow rates under basal an

278 Whole blood clotting time in FIX-deficient mice was corrected

279 unction were normal; however, when the whole blood clotting time was measured at 25 degrees C in plas

280 sed onto a factor VIIInull background, whole blood clotting time was partially corrected, equivalent

281 Whole-blood clotting times and FeCl3 carotid artery injury cor

282 Activated clotting times and whole blood clotting times were normalized, activated partial

283 creased levels of liver function enzymes and blood clotting times, decreased levels of platelets, mul

284 rate blood clotting but are not required for blood clotting to happen.

285 Willebrand factor receptor, functions during blood clotting to promote platelet adhesion and activati

286 that the threshold response of initiation of blood clotting to the size of a patch of stimulus is a r

287 isolated mouse islets were transplanted in a blood clot under the renal capsule of cynolmogus monkeys

288 function, was added to human plasma or whole blood clots, urokinase (UK)-induced clot lysis was enhan

289 provides evidence that self-reported data on blood clots used in a GWAS yield results that are compar

290 ial phosphatidylserine (PS) in apoptosis and blood clotting using annexin V.

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

292 ther design, thrombin, an enzyme involved in blood clotting, was captured by thrombin-AR-modified cel

293 Here, inspired by blood clotting, we show that polymer-colloid composite a

294 rget diseased sites, such as solid tumors or blood clots, where up-regulated proteases cleave the pep

295 d LPA are both liberated by platelets in the blood clot, which is known to be critical in stabilizing

296 ibrin is the main protein constituent of the blood clot, which is stabilized by factor XIIIa through

297 The autologous blood clot, which ranged from 0.5 to 4.5 mL, was injecte

298 n addition, we show that manual injection of blood clots, which produces a lower baseline hemorrhage

299 of COX-2 in neurons was observed around the blood clot with a peak at 6 h.

300 arteriolar vessels, permitting evaluation of blood clotting within small sample volumes under pathoph