ライフサイエンスコーパス: clotting

1 acylcarnitines inhibited factor Xa-initiated clotting.

2 system is regulated to prevent uncontrolled clotting.

3 the site of vascular injury is essential in clotting.

4 ajor functional receptor in platelets during clotting.

5 ndiscovered, shape that contributes to blood clotting.

6 lls delayed their ability to activate plasma clotting.

7 he forces of centrifugation of blood without clotting.

8 ociated with a reduced likelihood of circuit clotting.

9 ical regulation of vWF activity during blood clotting.

10 vation of FV is pivotal for plasma and blood clotting.

11 X and prolonged human plasma and whole blood clotting.

12 cell fragments that are essential for blood clotting.

13 ssion of neointimal hyperplasia and in-stent clotting.

14 tial loss of pigmentation and impaired blood clotting.

15 ts of medicinal leeches prevented blood from clotting.

16 let stimulation and platelet-activated blood clotting.

17 ic activator of the contact pathway of blood clotting.

18 that are key regulators of inflammation and clotting.

19 on during clot formation, or abrogate plasma clotting.

20 anuclear cells that are essential for blood clotting.

21 into fibrin split products without inducing clotting.

22 signing new antithrombotics disrupting blood clotting.

23 thrombus formation, and agonist-driven blood clotting.

24 raction which is central to preventing blood clotting.

25 to aid blood flow, prevent pooling and thus clotting.

26 Markedly accelerated clotting (53.3% decrease in clotting time) was observed

27 ntensity (r(2)=0.07, P<0.01), and fibrinogen clotting ability (r(2)=0.073, P<0.01) CONCLUSIONS: In BD

28 d failure (ALF), yet a wide heterogeneity in clotting abnormalities exists.

29 patients with MPNs, the events causing these clotting abnormalities remain unclear.

30 ts younger than 60 years most commonly had a clotting abnormality (n = 23/46, 50%), whereas older pat

31 will enable the assessment of the effects of clotting-activators and anticoagulants (including non-ph

32 nd characterization of caseinolytic and milk-clotting activities from Moringa oleifera flowers.

33 e methodology, in order to maximize its milk-clotting activity (MCA).

34 nity through the neutralization of S. aureus clotting activity and protection from staphylococcal dis

35 mutations S478A/L480A/Q481A was deficient in clotting activity and unable to efficiently activate the

36 ng assay, this peptidase showed maximal milk clotting activity at 60-65 degrees C and maintenance of

37 in its clotting activity, fV(DeltaB9/Q3) had clotting activity comparable with fVa(WT).

38 and colleagues demonstrated that the venom's clotting activity does not require factor VII, but does

39 riifolin S of molecular mass 94kDa with milk clotting activity has been purified from the latex of Eu

40 ple fluorometric in vitro assay to determine clotting activity in platelet poor plasma after exposure

41 The milk-clotting activity indicates the application of M. oleife

42 The effect of temperature on the milk-clotting activity of kiwi fruit, melon and ginger extrac

43 fic approach through characterization of the clotting activity of venom from Daboia russelii, disting

44 Melon extracts showed high milk-clotting activity over a broad temperature range (45-75

45 Milk-clotting activity was analysed using skim milk.

46 llular metalloprotease (AcPs) with high milk-clotting activity was purified from edible mushroom Term

47 Five proteolytic fractions with milk-clotting activity were isolated in a two-step purificati

48 Milk-clotting activity, detected only in the presence of CaCl

49 ed that although fV(Q3) was deficient in its clotting activity, fV(DeltaB9/Q3) had clotting activity

50 pear to be the main enzymes involved in milk-clotting activity.

51 of milk at 70 degrees C resulted in highest clotting activity.

52 melanocyte stimulating hormone), and a blood-clotting agent can be anchored to erythrocytes, protecte

53 otential to be employed as an efficient milk-clotting agent in the production of dairy products.

54 otential to be employed as an efficient milk-clotting agent.

55 thrombin and rIIa(S478A) were able to induce clotting and activate factor V and factor VIII with rate

56 rbidity without altering systemic markers of clotting and anticoagulation.

57 vation of various proteins involved in blood clotting and bone metabolism.

58 les that polyP plays in modulating the blood clotting and complement systems in health and disease.

59 It is a potent modulator of the blood clotting and complement systems in hemostasis, thrombosi

60 roles in vivo, ranging from regulating blood clotting and inflammation to directly counteracting tumo

61 lymers of orthophosphate that modulate blood clotting and inflammation.

62 hemostatic factors has been shown to promote clotting and is associated with increased thrombosis, bu

63 factor (VWF) is a blood protein involved in clotting and is proposed to be activated by flow, but th

64 We performed in vitro assays in which clotting and lysis of human plasma clots or fibrin seala

65 marks a haplotype associated with increased clotting and platelet aggregation attributable to a prom

66 y and inhibit RNA- and polyphosphate-induced clotting and the activation of the intrinsic pathway of

67 exhibit unique properties analogous to blood clotting and thereby be useful in self-healing applicati

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

69 on of blood pressure, vascular permeability, clotting and transendothelial migration of leukocytes an

70 , hypoxia led to increases in cell adhesion, clotting, and fibrin deposition; these increases were el

71 the activity of thrombin, a key regulator of clotting, and produce urinary reporters of disease state

72 processes, including viral infection, blood clotting, and signal transduction, and as such, they are

73 ellular processes such as virus entry, blood clotting, antibody-mediated immune response, inflammatio

74 associated with increased propensity toward clotting, as has been suggested on the basis of isolated

75 potent anticoagulant activity in an in vitro clotting assay (aPTT EC1.5x = 0.27 muM) and excellent se

76 ted in a tissue factor-initiated whole blood clotting assay unless exogenous FV was added, consistent

77 In a milk-clotting assay, this peptidase showed maximal milk clott

78 -associated hypercoagulation, using in vitro clotting assays and in vivo cancer models.

79 Two-stage clotting assays revealed that although fV(Q3) was defici

80 Clotting assays were used to evaluate a causal relations

81 n assays, full genome sequencing, and global clotting assays will significantly improve diagnosis of

82 w assays, full genome sequencing, and global clotting assays will significantly improve diagnosis of

83 ex vivo that are more reliable than standard clotting assays.

84 Preprocedural clotting assessment was inadequate in some cases and wou

85 hen localized as nanoparticles, accelerating clotting at 10-200 fold lower concentrations, particular

86 yst for milk coagulation (initiation of milk clotting at about 20 min and full coagulation at about 2

87 The milk-clotting behavior of the three plant extracts was relate

88 presence of both thrombin-spiked and freshly clotting blood in three minutes with detection limits of

89 hemostasis appear to be to accelerate blood clotting but are not required for blood clotting to happ

90 le to provide data on the entire spectrum of clotting but are not validated in acute bleeding.

91 ivity was indicated by the regularisation of clotting by lipopolysaccharide-binding protein (LBP).

92 bacterium Bacillus subtilis, induces plasma clotting by proteolytically converting ProT into active

93 hat fibrin(ogen) polymerisation during blood clotting can be affected strongly by LPS.

94 , including roles for the complement system, clotting cascade and fibrinolysis.

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

96 more than 30 yrs ago that inhibition of the clotting cascade by natural anticoagulants could decreas

97 tiator of the contact pathway, a limb of the clotting cascade important for thrombosis but dispensabl

98 ssor P14ARF can contribute to activating the clotting cascade in glioblastoma.

99 The contact pathway of the plasma clotting cascade is dispensable for normal hemostasis, b

100 The blood clotting cascade is selectively involved in lung metasta

101 and that challenges such stereotypes as the "clotting cascade" and "primary and secondary hemostasis.

102 III (FVIII), an important co-factor in blood clotting cascade, elicits unwanted anti-FVIII antibodies

103 scades are: the complement system, the blood clotting cascade, the fibrinolytic system, and the kalli

104 imetic drugs such as inhibitors of the blood clotting cascade.

105 lebrand factor (vWF), a key initiator of the clotting cascade.

106 dual-action protein that mediates the blood-clotting cascade.

107 t at 250 mL/min was not more likely to cause clotting compared with 150 mL/min (hazards ratio, 1.00 [

108 out anticoagulation was more likely to cause clotting compared with use of heparin strategies (hazard

109 Circuit clotting data were analyzed for repeated events using ha

110 Brain microhemorrhages in CM suggest a clotting disorder, but whether this phenomenon is import

111 is a viable therapeutic alternative for many clotting disorders and for other hepatic diseases where

112 ogical mechanisms that underlie bleeding and clotting disorders.

113 y similar to the one generally used for milk clotting during cheese making, and exhibited a satisfact

114 IX and Alprolix exhibit a linear response in clotting efficacy up to 150 IU/kg, where they appear to

115 Milk-clotting enzymes are valued as chymosin-like protease su

116 Two different milk clotting enzymes, belonging to the aspartic protease fam

117 A major clotting event that led to premature termination of the

118 In contrast, although clotting factor activation was seen in the blood of CM p

119 ble and persistent expression of circulating clotting factor activity, associated with decreased clin

120 nts in haemophilia care, the availability of clotting factor concentrates for all affected individual

121 Prophylactic application of clotting factor concentrates is the basis of modern trea

122 emophilia can experience from treatment with clotting factor concentrates.

123 r control windows, controlling for levels of clotting factor in the blood.

124 For every 1% increase in clotting factor level, bleeding incidence was lower by 2

125 uctase, cellular responses including altered clotting factor processing and coagulopathy, organ level

126 ibodies that inhibit the function of infused clotting factor remains a major challenge and is conside

127 sodes can no longer be treated with standard clotting factor replacement therapy.

128 ticularly strategies to prolong half-life of clotting factor replacements, the management of inhibito

129 II (FVIII) is a major obstacle in using this clotting factor to treat individuals with hemophilia A.

130 ent 1+2, and soluble P-selectin and also for clotting factor VIII and the thrombin generation potenti

131 from 133 plant species eliminated 105 (human clotting factor VIII heavy chain [FVIII HC]) and 59 (pol

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

133 ers of Kupffer cells and LSECs, the level of clotting factor X, and hepatocyte infectibility did not

134 oxaban, a direct oral inhibitor of activated clotting factor Xa, might be more suitable than conventi

135 bleeding with adequately sustained levels of clotting factor, after a single therapeutic intervention

136 patients provide an early natural history of clotting factor-level changes after injury.

137 ween 2000 and 2010 and collected data on all clotting-factor administration for up to 75 exposure day

138 patients who develop inhibitors to deficient clotting factors and in whom bypassing agents are requir

139 n their outer membrane leaflet and activated clotting factors assemble into enzymatically active comp

140 emostasis and the development of recombinant clotting factors for the treatment of the common inherit

141 redicted that restoring the normal levels of clotting factors II, IX, and X while simultaneously rest

142 velopment, and conservation of virtually all clotting factors in the zebrafish genomic sequence.

143 When binding of purified clotting factors to immobilized myosin was monitored usi

144 is known to cause combined deficiency of VKD clotting factors type 2 (VKCFD2), a disease phenotype re

145 tithrombotic on the basis of inactivation of clotting factors Va and VIIIa; (2) a cytoprotective on t

146 on studies as well as pro- and anticoagulant clotting factors were measured.

147 s (LSECs), hepatocytes, scavenger receptors, clotting factors, and immunoglobulins were analyzed.

148 C virus treatment response, plasma levels of clotting factors, and late-onset Alzheimer disease, has

149 Blood tests included cytokines, clotting factors, apolipoprotein E genotype, and sex hor

150 treatment relies on replacement therapy with clotting factors, either at the time of bleeding (ie, on

151 onsists of the administration of recombinant clotting factors, such as factor VIII (FVIII).

152 t involves frequent intravenous infusions of clotting factors, which is associated with variable hemo

153 n thrombocytopenia and low concentrations of clotting factors, which may cause profuse hemorrhagic co

154 r kallikrein-related peptidases, and several clotting factors.

155 f decreased levels of gamma-carboxylated VKD clotting factors.

156 lational modification of vitamin K-dependent clotting factors.

157 iological vitamin K supplementation restores clotting for VKCFD2 patients and results in high serum l

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

159 PolyP-SNP even retains its clotting function at ambient temperature.

160 Prediction of clotting function under hemodynamic conditions for a pat

161 ressing mutant forms of fibrinogen-retaining clotting function, but lacking either the bacterial ClfA

162 tion (FIX Padua), previously associated with clotting hyperactivity and thrombophilia.

163 elease tryptase, and thrombin mediates blood clotting in early wounds.

164 he impact of TFPI deficiency on bleeding and clotting in hemophilia.

165 However, the precise mechanisms that trigger clotting in large veins have not been fully elucidated.

166 lt hemoglobin (free HbA) are associated with clotting in this mechanical device that can result in th

167 platelet-like particles (PLPs) that augment clotting in vitro under physiological flow conditions an

168 hey are effective inhibitors of human plasma clotting in vitro.

169 Blood clotting in vivo is catalyzed by thrombin, which simulta

170 healing is a complex process involving blood clotting, inflammation, migration of keratinocytes, angi

171 ECs synthesize both the clotting initiator von Willebrand factor (VWF) and the c

172 Systems as varied as blood clotting, intracellular calcium signaling, and tissue in

173 overlap between charge-based aggregation and clotting is a function of mass transfer.

174 Pathologic blood clotting is a leading cause of morbidity and mortality i

175 Blood clotting is a process by which a haemostatic plug is ass

176 Thrombosis, or malignant blood clotting, is associated with numerous cardiovascular dis

177 for purified blood proteases or human plasma clotting isotropically.

178 imen analysed here is evidence of an ancient clotting mechanism not dissimilar to those of today, rap

179 ides information important for understanding clotting mechanisms and the associated clinical implicat

180 as dyslipidemia, oxidative stress, and blood clotting mechanisms, we hereby report the synthesis and

181 trations of short-chain polyP can accelerate clotting of flowing blood plasma under flow at low to su

182 hetic polyP was more effective at triggering clotting of flowing blood plasma when localized on a sur

183 lization of short-chain polyP can accelerate clotting of flowing blood.

184 Tissue factor-induced clotting of plasma led to proteolysis of C5 at a thrombi

185 ug/mL]) was tested by microfluidic assay for clotting on collagen/TF at TF surface concentration ([TF

186 d effect of systemic inflammation and excess clotting on tissue function leads to end-organ disease.

187 ble (</=20 pM) in the context of influencing clotting or fibrinolysis.

188 nd inhibit activators of the intrinsic blood clotting pathway, such as polyphosphate (polyP) and extr

189 the alternative complement and the intrinsic clotting pathway.

190 Because of the propensity for clotting, patients with malignancy are often anticoagula

191 and a complete absence of thrombelastometric clotting patterns, which was reversed by antifibrinolyti

192 nd heparinase partially reverse the abnormal clotting patterns.

193 a Src inhibitor was sufficient to rescue the clotting phenotype in knockin mice to wild-type levels.

194 lored problem, despite applications in blood clotting, plasmonics, industrial packaging and transport

195 The restricted proteolysis and milk-clotting potential are attractive properties for the use

196 areas inside the visual surface advert to a clotting principle, rather similar to those of today, an

197 osphate (polyP) that accelerates the natural clotting process of the body.

198 ignaling, protein and lipid homeostasis, and clotting processes.

199 e extract prepared at pH 3 had the best milk-clotting properties (MCA/PA ratio).

200 Analysis of the clotting properties of bare SNPs, bare polyP, and polyP-

201 efficient way to produce rennet with better clotting properties, leading to higher yield, moisture,

202 limited research has been done on their milk-clotting properties.

203 eliminary step to produce rennet with better clotting properties.

204 In contrast, a fibrinogen-clotting protease ancistron increased the amount of fibr

205 Using the clotting protease thrombin and its zymogen precursor pre

206 binding site of thrombin, a Na(+)-activated clotting protease, generates a construct that is most ac

207 employed to produce mainly proteins or milk-clotting proteases.

208 ious studies have investigated only a single clotting protein and lipid composition and have yielded

209 lia, von Willebrand disease (VWD), and other clotting protein deficiencies lead to significant morbid

210 , which induces polymerization of FN and the clotting protein fibrinogen in addition to enhancing FN

211 , Petersen et al. (2017) show that the blood clotting protein fibrinogen inhibits nerve repair by pre

212 s were induced by proteinase cleavage of the clotting protein fibrinogen, yielding fibrinogen cleavag

213 worms are capable of cleaving the host blood clotting protein fibronectin and that this activity can

214 Several new observations about the nature of clotting protein physiology have been made recently, cre

215 al methods presents challenges for comparing clotting protein-lipid interactions.

216 ant serpin that irreversibly inactivates the clotting proteinases factor Xa and thrombin by forming c

217 -carboxyglutamic acid-rich domain-containing clotting proteins with lipids.

218 ostate-specific antigen) in cleaving seminal clotting proteins, resulting in sperm liquefaction.

219 many protein-lipid interactions among blood-clotting proteins.

220 holipid binding specificities of these seven clotting proteins.

221 nisms by which polyphosphate modulates blood clotting reactions remain to be elucidated.

222 ernational normalized ratio had no effect on clotting risk.

223 elet aggregation, vasoconstriction and blood clotting; saliva of these organisms also has anti-inflam

224 tion, and phosphatidylserine exposure, blood clotting simulations require prediction of platelet [Ca(

225 ast calcium calculator, ideal for multiscale clotting simulations that include spatiotemporal concent

226 Clotting stimulation by immobilized tissue factor induce

227 uals who participated in the Genes and Blood Clotting Study (GABC) or the Trinity Student Study (TSS)

228 Cancer patients often have an activated clotting system and are at increased risk for venous thr

229 f thrombin, which enhances the overall blood-clotting system, both by accelerating fibrin generation

230 nt and a potent modulator of the human blood-clotting system.

231 Ps initiate the contact pathway of the blood-clotting system; short-chain polyP accelerates the commo

232 ectly activating factor X, and a form of the clotting test is used in the diagnosis of lupus anticoag

233 Thus, by combining the venom clotting test with the quick clotting time (prothrombin

234 (aPTT) and ''Prothrombinase complex-induced Clotting Test'' (PiCT) have been compared with the stand

235 amine were more likely to experience circuit clotting than those receiving citrate and calcium (hazar

236 pecific binding and adverse effects on blood clotting that limit their use.

237 entional anticoagulation protocol (activated clotting time >250 s) in 10 procedures (group 1), with a

238 ith an aggressive anticoagulation (activated clotting time >320 s) in 13 procedures (group 3).

239 ibrillation ablation with baseline activated clotting time (ACT) and INR values was performed.

240 Activated clotting time (ACT) is widely used to guide unfractionat

241 We correlated r-TEG values [activated clotting time (ACT), r, k, alpha, maximal amplitude (MA)

242 ial thromboplastin time (aPTT) and activated clotting time (ACT); (2) other factors influencing UFH e

243 ersal of diluted thrombin time (dTT), ecarin clotting time (ECT), activated partial thromboplastin ti

244 ining the venom clotting test with the quick clotting time (prothrombin time), it was possible to dia

245 in HemA mice, and fully corrects whole blood clotting time (WBCT) in HemA dogs immediately after dosi

246 compatibility of PAEC, as shown by increased clotting time (WT: 84.3 +/- 11.3 min, p < 0.001; GTKO.hC

247 By applying a clotting time analysis based on a phenomenological mathe

248 Whole blood clotting time analysis confirmed that hemostasis was imp

249 ally enhanced synergistic effect that lowers clotting time and increases thrombin production at low c

250 given intravenously to maintain an activated clotting time at 270 to 300 s.

251 thrombin time and 81 with an elevated ecarin clotting time at baseline, the median maximum percentage

252 hrombin-thrombomodulin complex, prolongs the clotting time by generating pharmacological quantities o

253 irements to maintain a therapeutic activated clotting time during RFA was reduced by 50% in patients

254 displayed a dose-dependent reduction of the clotting time in buffer, with a 20 microM aptamer achiev

255 cus vesiculosus, decreases bleeding time and clotting time in hemophilia, possibly through inhibition

256 enous administration of PN2KPI prolonged the clotting time of both human and murine plasma, and PN2KP

257 e serine residue (FXII-S544A), shortened the clotting time of FXII-deficient plasma and enhanced thro

258 ically modified PAEC significantly prolonged clotting time of human blood (115.0 +/- 16.1 min, p < 0.

259 binds tightly to factor IXa and prolongs the clotting time of human plasma.

260 intraprocedural heparin, the mean activated clotting time was significantly lower in patients who he

261 antagonist and heparin to maintain activated clotting time>350 seconds; (2) submerged loading of the

262 edly accelerated clotting (53.3% decrease in clotting time) was observed in carotid artery preparatio

263 sma resulted in a dose-dependent increase in clotting time, and a dose-dependent decrease in clot lys

264 However, rennet clotting time, ethanol stability and foaming ability wer

265 ratory of the dilute thrombin time or ecarin clotting time.

266 basis of the diluted thrombin time or ecarin clotting time.

267 r platelet aggregation and lengthened plasma clotting time.

268 BA-T7b is more potent than TBA in prolonging clotting time.

269 ther the diluted thrombin time or the ecarin clotting time.

270 s evidenced by the reduction of viscoelastic clotting time.

271 Shortening of the clotting times and lack of bleeding episodes support the

272 This resulted in improvement of clotting times and thrombin generation in hemophilic pla

273 cordingly, the dilute-thrombin or the ecarin clotting times are best suited for dabigatran and the pr

274 rs and corrected the prolongation of ex vivo clotting times by such inhibitors.

275 eved was sufficient to correct the prolonged clotting times in a mouse model of haemophilia B, and re

276 X-deficient plasma, as well as FXa-initiated clotting times in FX-deficient plasma.

277 the ability of TFPI to prolong TF-initiated clotting times in FXI- or FIX-deficient plasma, as well

278 heparin was administered with goal-activated clotting times of 300 to 400 seconds for all LV procedur

279 ial thromboplastin time and prothrombin time clotting times to baseline at 60 mins.

280 nd doxycycline treatment returned thrombosis clotting times to that of control mice (P=0.69).

281 human fIIa(MZ), significant prolongation of clotting times was observed for fII(MZ) plasma.

282 tor-bearing microparticles, shortened plasma-clotting times, and increased thrombus frequency in the

283 we found significantly reduced bleeding and clotting times, as well as increased in vivo thrombosis,

284 eding during a routine operation, had normal clotting times, but markedly reduced prothrombin consump

285 d levels of liver function enzymes and blood clotting times, decreased levels of platelets, multifoca

286 Expression of the variants shortened clotting times, reduced blood loss after tail-clip assay

287 , different hemolysis levels, differences in clotting times, the number of freeze-thaw cycles, and di

288 , X), which corresponded to increased plasma clotting times.

289 Skin inflammation; thrombosis clotting times; and percentage of splenic monocytes, neu

290 lood clotting but are not required for blood clotting to happen.

291 icted the effect of localization of polyP on clotting under flow, and this was tested in vitro using

292 osphatidylserine (PS) in apoptosis and blood clotting using annexin V.

293 ey component of the contact system, triggers clotting via the intrinsic pathway, and is implicated in

294 sma from HRG-deficient mice, and accelerated clotting was restored to normal with HRG reconstitution.

295 esign, thrombin, an enzyme involved in blood clotting, was captured by thrombin-AR-modified cells and

296 Here, inspired by blood clotting, we show that polymer-colloid composite assembl

297 of cells imposes the potential risk of cell clotting, which may be prevented by the addition of anti

298 me results were obtained after initiation of clotting with various activators and also with clots fro

299 olar vessels, permitting evaluation of blood clotting within small sample volumes under pathophysiolo

300 , major catheter dysfunction occurred before clotting within the circuit.