ライフサイエンスコーパス: clotting

1 aused by disturbed blood flow following fast clotting.

2 in the maintenance of haemostasis via blood clotting.

3 reduced protein function and abnormal blood clotting.

4 ociated with a reduced likelihood of circuit clotting.

5 that are key regulators of inflammation and clotting.

6 on during clot formation, or abrogate plasma clotting.

7 the site of vascular injury is essential in clotting.

8 rease thrombin generation and promote plasma clotting.

9 anuclear cells that are essential for blood clotting.

10 into fibrin split products without inducing clotting.

11 signing new antithrombotics disrupting blood clotting.

12 thrombus formation, and agonist-driven blood clotting.

13 raction which is central to preventing blood clotting.

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

15 acylcarnitines inhibited factor Xa-initiated clotting.

16 system is regulated to prevent uncontrolled clotting.

17 ajor functional receptor in platelets during clotting.

18 ndiscovered, shape that contributes to blood clotting.

19 lls delayed their ability to activate plasma clotting.

20 tissue factor induction and subsequent blood clotting.

21 ul at representing the biochemistry of blood clotting.

22 ions substantially compromises microvascular clotting.

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

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

25 ivity, indicating they had an excellent milk-clotting ability.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 ine patch size threshold in quiescent plasma-clotting always occurs given enough time-whereas the she

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

43 rbidity without altering systemic markers of clotting and anticoagulation.

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

45 ts such as ferroptosis, apoptosis, and blood clotting and diseases such as arthritis, diabetes, and c

46 We suggest that the exuberant blood clotting and immune hyper-reaction seen in patients with

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

48 exin type 9 (PCSK9), adhesion molecules, and clotting and inflammatory factors.

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

50 opolysaccharide (LPS) induced systemic blood clotting and massive thrombosis in tissues.

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

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

53 Furthermore, anomalous blood clotting and structural changes in blood components are

54 endothelial damage, complement-induced blood clotting and systemic microangiopathy - in disease exace

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

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

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

58 ng, electrophysiology, extracellular matrix, clotting, and inflammation.

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

60 tion changes, with clinical metrics of blood clotting, and with the sharp transition between mild and

61 iological processes such as digestion, blood clotting, and wound healing.

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

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

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

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

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

67 of Ir-CPI by using in vitro catheter-induced clotting assays and rabbit experimental models of cathet

68 Clotting assays were used to evaluate a causal relations

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

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

71 n vitro fluorogenic activity and whole blood clotting assays.

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

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

74 Blood clotting at the vascular injury site is a complex proces

75 Blood clotting at wound sites is critical for preventing blood

76 nfection, to identify individuals at risk of clotting based on their circulating prothrombin levels,

77 as roles in platelet activation during blood clotting, bone formation and T cell activation.

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

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

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

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

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

83 cells) and 49 haemostasis traits (including clotting cascade factors and markers of platelet functio

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

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

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

87 of the intrinsic and common pathways of the clotting cascade, as well as several other haematologica

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

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

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

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

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

93 Circuit clotting data were analyzed for repeated events using ha

94 our ability to develop novel treatments for clotting diseases.

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

96 a more quantitative and rapid assessment of clotting disorders and their treatment.

97 fewer platelets with larger sizes leading to clotting disorders termed myosin-9-related disorders (MY

98 ogical mechanisms that underlie bleeding and clotting disorders.

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

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

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

102 Complete deficiency of the central clotting enzyme prothrombin has never been observed in h

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

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

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

106 al biological components contribute to blood clotting events in the presence of influenza infection,

107 venously administered procoagulant PL caused clotting factor activation and depletion, induced a blee

108 port that sustained endogenous production of clotting factor as a result of gene therapy eliminates t

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

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

111 due to eoxPL deficiency, instead activating clotting factor consumption and depletion in the circula

112 VKOR variants can cause vitamin K-dependent clotting factor deficiency or alter warfarin response.

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

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

115 atic control without exposure to immunogenic clotting factor proteins.

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

117 for hemophilia treatment that do not rely on clotting factor replacement, but imply the neutralizatio

118 and destruction that results in a defect in clotting factor synthesis.

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

120 We recently showed that clotting factor VIIa (FVIIa) binding to endothelial cell

121 philia A is a monogenic disease with a blood clotting factor VIII (FVIII) deficiency caused by mutati

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

123 compared comprehensively the bone health of clotting factor VIII, factor IX, and Von Willebrand Fact

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

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

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

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

128 ave general relevance to vitamin K-dependent clotting factors containing epidermal growth factor doma

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

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

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

132 glucose, endothelin, adhesion molecules, or clotting factors in this weight-stable cohort.

133 To determine mechanisms by which clotting factors influence PDAC tumor progression, we ge

134 Therapeutic expression of human clotting factors IX and X following adeno-associated vir

135 ypes of human ECs in primary culture produce clotting factors necessary for FX activation via the int

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

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

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

139 the binding interactions of seven different clotting factors with GLA domains that have never been s

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

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

142 perienced major bleeding received platelets, clotting factors, or other hemostatic agents.

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

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

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

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

147 lational modification of vitamin K-dependent clotting factors.

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

149 evelopment through complex interactions with clotting factors.

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

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

152 haemoglobin, mean cell volume, platelet and clotting function.

153 Finally, the presence of VC1 delayed plasma clotting in a dose-dependent manner.

154 Ir-CPI prevented clotting in catheter and arteriovenous shunt rabbit mode

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

156 eventually have a role in the evaluation of clotting in patients with cirrhosis, but currently lack

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

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

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

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

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

162 clotting index in the hypercoagulable range (clotting index > 3) (median 3.05).

163 Fifty percent of patients had a clotting index in the hypercoagulable range (clotting in

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

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

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

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

168 ng in hemophilia A, the question of how much clotting is enough is at the forefront once again.

169 How much clotting is enough to prevent bleeding is the ultimate q

170 Our data reveal that blood clotting is the major cause of host death following infl

171 for purified blood proteases or human plasma clotting isotropically.

172 hesive modelling framework to show how blood clotting may be connected to influenza virus infection.

173 tion of existing innovations, including anti-clotting measures; cloud-computing for optimized treatme

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

175 ected way that sickle red cells modulate the clotting mechanism.

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

177 bolism was induced by large emboli made from clotting of autologous blood.

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

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

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

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

182 For blood clotting on collagen/tissue factor (1 TF-molecule/mum2)

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

184 They showed a high ratio of milk-clotting over caseinolytic activity, indicating they had

185 Several factors on the intrinsic clotting pathway were significantly associated (P < 3.85

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

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

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

189 nd heparinase partially reverse the abnormal clotting patterns.

190 This discovery sets a time scale for insect clotting phenomena, establishing a materials metric for

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

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

193 dels of thrombosis or analyzed biomarkers of clotting, platelet, and fibrinolysis activation in human

194 utrients affect simultaneously or separately clotting, platelet, and fibrinolysis pathways giving spe

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 brate blood, including human blood, based on clotting principles of insect blood.

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

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

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

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

202 sma levels of FVIII and restoration of blood clotting properties in a dose-dependent manor for at lea

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

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

205 eliminary step to produce rennet with better clotting properties.

206 Using the clotting protease thrombin and its zymogen precursor pre

207 Using the clotting protease thrombin as a model system, we investi

208 Using the trypsin-like, clotting protease thrombin as a relevant model system, w

209 Using the clotting protease thrombin as a relevant model, we unrav

210 In vitro studies indicate that key clotting proteases, such as factor Xa (FXa), can promote

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

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

213 The blood-clotting protein fibrinogen has been implicated in host

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

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

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

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

218 Soluble clotting proteins bind to membrane components in a phosp

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

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

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

222 the capacitive nature of blood obscures the clotting response at frequencies below 10 kHz, leading t

223 ernational normalized ratio had no effect on clotting risk.

224 these biomolecules inhibit the central blood-clotting serine proteinase thrombin that is also the tar

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

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

227 e extent to which current assays can predict clotting status in patients.

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

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

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

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

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

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

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

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

236 , and when activated, platelets induce blood clotting (the first step in wound healing) in part by th

237 flammasome activation as a trigger for blood clotting through pyroptosis.

238 S) variables, with normal ranges indicated: clotting time (38-79 s), clot formation time (34-159 s),

239 n time (34-159 s), amplitude at 10 min after clotting time (43-65 mm), maximum clot firmness (50-72 m

240 had a linear correlation with the activated clotting time (ACT) (Pearson's r = 0.86, P < 0.0001).

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

242 Activated clotting time (ACT) was measured before sheath removal.

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

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

245 ere also recorded: amplitude at 10 min after clotting time (normal range 7-23 mm) and maximum clot fi

246 uiring RBC transfusion (p = 0.01), activated clotting time (p = 0.001), and antithrombin levels (p =

247 ness (p=0.024) and amplitude at 10 min after clotting time (p=0.090) were lowest on days 4-6 of illne

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

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

250 -75; p=0.01); mean amplitude at 10 min after clotting time 45.1 mm (SD 7.0) versus 33.9 mm (SD 8.6; p

251 d cases and moderate to severe cases: median clotting time 56 s (range 42-81; IQR 48-64) versus 69 s

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

253 Whole blood clotting time analysis confirmed that hemostasis was imp

254 is connected to an inline pressure sensor a clotting time analysis is applied, allowing for the accu

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

256 131 patients (72.5%) with an elevated ecarin clotting time and was similar for upper and lower GI ble

257 Over 4 years, we replaced the activated clotting time assay with the anti-Xa heparin activity as

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

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

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

261 Furthermore, this device detects a prolonged clotting time in clinical blood samples drawn from pedia

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

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

264 bleeding decreased from 69% using activated clotting time to 51% (p = 0.03).

265 ne oxygenation changed from hourly activated clotting time to anti-Xa heparin activity assay every 6

266 tudy describes the transition from activated clotting time to anti-Xa heparin activity assay monitori

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

268 tration and diluted thrombin time and ecarin clotting time, and a non-linear relationship with activa

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

270 ensor exhibited no variation in the measured clotting time, even when flexed to a 35 mm bend radius.

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

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

273 s evidenced by the reduction of viscoelastic clotting time.

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

275 ific assays diluted thrombin time and ecarin clotting time.

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

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

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

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

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

281 rporeal membrane oxygenation using activated clotting times to anti-Xa heparin activity assays.

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

283 of heparin to achieve therapeutic activated clotting times were also noted.

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

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

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

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

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

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

290 ples to LPS significantly (P < 0.05) reduced clotting times.

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

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

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

294 tuous arteriolar vessels would analyze blood clotting under flow, while requiring a small blood volum

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

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

297 sses such as immunity, oxygen transport, and clotting, which when perturbed cause a significant globa

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.