ライフサイエンスコーパス: blood clot

1 lapse or provide sufficient stability of the blood clot.

2 uced similar or inferior results compared to blood clot.

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

4 ate extensive invadopodia when embedded in a blood clot.

5 focus on fibrin, the primary component of a blood clot.

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

7 fibronectin has to be incorporated into the blood clot.

8 hosphate (BCP), bovine bone mineral (BBM) or blood clot.

9 l fibrin generation and stabilization of the blood clot.

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

11 ides information about relative shrinkage of blood clot.

12 ibrin fibers form the structural scaffold of blood clots.

13 of the viscoelastic properties of incipient blood clots.

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

15 ereby effectively promoting the formation of blood clots.

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

17 proteases also involved in the formation of blood clots.

18 olymers and forms the structural scaffold of blood clots.

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

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

21 hese SPMs promote macrophage phagocytosis of blood clots.

22 erto undiscovered, shape that contributes to blood clotting.

23 mechanical regulation of vWF activity during blood clotting.

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

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

26 uclear cell fragments that are essential for blood clotting.

27 by partial loss of pigmentation and impaired blood clotting.

28 platelet stimulation and platelet-activated blood clotting.

29 siologic activator of the contact pathway of blood clotting.

30 identified as a regulatory driving force in blood clotting.

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

32 wth by obstructing tumor circulation through blood clotting.

33 depleted protein production and inefficient blood clotting.

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

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

36 iates tissue factor induction and subsequent blood clotting.

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

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

39 sed inflammation, microvascular density, and blood clotting.

40 h those involved in mammalian complement and blood clotting.

41 ccessful at representing the biochemistry of blood clotting.

42 roles in the maintenance of haemostasis via blood clotting.

43 ing to reduced protein function and abnormal blood clotting.

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

45 for designing new antithrombotics disrupting blood clotting.

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

47 , interaction which is central to preventing blood clotting.

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

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

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

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

52 roteins in blood and vasculature, such as in blood clots and on the extracellular matrix.

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

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

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

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

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

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

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

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

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

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

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

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

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

66 r events such as ferroptosis, apoptosis, and blood clotting and diseases such as arthritis, diabetes,

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

68 We suggest that the exuberant blood clotting and immune hyper-reaction seen in patient

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

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

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

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

73 by lipopolysaccharide (LPS) induced systemic blood clotting and massive thrombosis in tissues.

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

75 bition of TF abolishes inflammasome-mediated blood clotting and protects against death.

76 Furthermore, anomalous blood clotting and structural changes in blood component

77 pread endothelial damage, complement-induced blood clotting and systemic microangiopathy - in disease

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

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

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

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

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

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

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

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

86 omposition changes, with clinical metrics of blood clotting, and with the sharp transition between mi

87 o physiological processes such as digestion, blood clotting, and wound healing.

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 of fibrin, the main structural component of blood clots, are associated with adverse events due to l

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

92 n by in vitro fluorogenic activity and whole blood clotting assays.

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

94 Blood clotting at the vascular injury site is a complex

95 Blood clotting at wound sites is critical for preventing

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

97 and has roles in platelet activation during blood clotting, bone formation and T cell activation.

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

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

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

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

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

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

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

105 The blood clotting cascade is selectively involved in lung m

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

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

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

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

110 hat is exposed upon injury and initiates 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 ecretory pathway (receptors, growth factors, blood-clotting components, and even many viral envelope

116 To reveal an association between the blood clot contraction (retraction) and the incidence of

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 d a long-lasting effect on normalizing whole blood clot contraction.

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

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

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

124 Sickle trait whole blood clots demonstrated an intermediate phenotype in re

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

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

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

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

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

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

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

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 Thus, TMEM173 is a key regulator of blood clotting during lethal bacterial infections.

135 Anucleate platelets form blood-clots during thrombosis, but also play a crucial r

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

137 dividual biological components contribute to blood clotting events in the presence of influenza infec

138 ELISA and failure in the detection of human blood clotting factor IX by voltammetry.

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

140 Hemophilia A is a monogenic disease with a blood clotting factor VIII (FVIII) deficiency caused by

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

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 amin K cycle, activating vitamin K-dependent blood clotting factors.

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

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

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

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

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

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

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

152 With blood clot formation inside an artery resulting from inf

153 Blood clot formation is crucial to maintain normal physi

154 role lipid metabolites play in regulation of blood clot formation under pathologic conditions.

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

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

157 Blood-clot formation that results in the complete occlus

158 ting blood clot was also more rigid than the blood clot formed by thrombin solution.

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

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

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

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

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

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

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

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

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

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

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

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

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

172 Control of blood clotting in root canal systems is one of the most

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

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

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

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

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

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

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

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

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

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

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

184 Mammalian blood clotting involves numerous components, most of whi

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

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

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

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

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

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

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

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

193 Blood clotting is a process by which a haemostatic plug

194 Our data reveal that blood clotting is the major cause of host death followin

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

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

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

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

199 Furthermore, almost complete blood clot lysis was achieved in 75 min, showing conside

200 o a cohesive modelling framework to show how blood clotting may be connected to influenza virus infec

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

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

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

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

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

206 , 30 seconds (TCN30), or 60 seconds (TCN60); blood clot (NC), and non-demineralized autogenous bone (

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

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

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

210 For blood clotting on collagen/tissue factor (1 TF-molecule/

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

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

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

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

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

216 Embolization with blood clots or microspheres increased mean pulmonary art

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

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

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

220 on 24 immature premolars with an autologous blood clot (PC), gelatin-based and fibrin-based hemostat

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 nzyme that plays many important roles in the blood clotting process; it activates platelets, cleaves

226 ed plasma levels of FVIII and restoration of blood clotting properties in a dose-dependent manor for

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

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

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

230 The blood-clotting protein fibrinogen has been implicated in

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

232 49 of antithrombin, the primary inhibitor of blood clotting proteinases, has previously been implicat

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

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

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

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

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

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

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

240 raditional revascularization protocol with a blood clot scaffold.

241 ny of these biomolecules inhibit the central blood-clotting serine proteinase thrombin that is also t

242 of this integrated model, we demonstrate how blood clot severity may depend on circulating prothrombi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

262 sphate, and when activated, platelets induce blood clotting (the first step in wound healing) in part

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

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

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

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

267 ied inflammasome activation as a trigger for blood clotting through pyroptosis.

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

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

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

271 Whole blood clotting time analysis confirmed that hemostasis w

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

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

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

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

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

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

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

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

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

281 The adhesion of blood clots to wounds is necessary to seal injured vascu

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

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

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

285 as well as to fibrin, platelet proteins, and blood clots under flow in vitro Abeta40 also increased t

286 nd tortuous arteriolar vessels would analyze blood clotting under flow, while requiring a small blood

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

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

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

290 The resulting blood clot was also more rigid than the blood clot forme

291 he number of RBCs extruded from sickle whole blood clots was significantly reduced compared with the

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 Human whole blood clots were mounted in a flow system and visualized

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

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

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

298 clots within 30 min and anticoagulated human blood clots within 20-100 s.

299 isparate operating conditions, where chicken blood clots within 30 min and anticoagulated human blood

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