ライフサイエンスコーパス: clot

1 te (BCP), bovine bone mineral (BBM) or blood clot.

2 model represents a three-dimensional fibrin clot.

3 ows that S. epidermidis can rupture a fibrin clot.

4 imilar or inferior results compared to blood clot.

5 (FXIII) is the main stabilizer of the fibrin clot.

6 on fibrin, the primary component of a blood clot.

7 effectively promoting the formation of blood clots.

8 stabilizing gel matrix in and around growing clots.

9 rable to that of patients with more proximal clots.

10 ased the number of RBCs released from sickle clots.

11 3 weeks of vaginal bleeding with passage of clots.

12 suggest robust prothrombin penetration into clots.

13 tion and remote embolisation of fibrin-based clots.

14 nous FXIII improves the adhesive strength of clots.

15 ncy reinstitution of bypass; the circuit had clotted.

16 tissue factor induction and subsequent blood clotting.

17 ul at representing the biochemistry of blood clotting.

18 ions substantially compromises microvascular clotting.

19 aused by disturbed blood flow following fast clotting.

20 in the maintenance of haemostasis via blood clotting.

21 reduced protein function and abnormal blood clotting.

22 rease thrombin generation and promote plasma clotting.

23 ociated with a reduced likelihood of circuit clotting.

24 that are key regulators of inflammation and clotting.

25 The model required free thrombin in the clot (~100 nM) to have an elution half-life of ~2 sec, c

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

27 sence of developed vessel networks prevented clot accumulation in the grafts.

28 ets and are preferentially incorporated into clots after laser injury.

29 developed larger, occlusive, neutrophil-rich clots after partial inferior vena cava (IVC) ligation th

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

31 FIBTEM clot amplitude at 5 minutes (CA5) had the largest AUC an

32 e: 1) dimensions of the rotor (radius at the clot and end of the tube); 2) rotor angulation for the t

33 ix component of whole-blood or plasma-fibrin clots and in in vivo thrombi.

34 s in blood and vasculature, such as in blood clots and on the extracellular matrix.

35 ative for COVID-19 regarding the presence of clots and presenting symptoms.

36 onally define the interaction network of the clots and provide molecular details for the interaction

37 In vitro fibrin clots and rats with aortic EE were treated with an antip

38 ed to destroy pathological, life-threatening clots and thrombi (thrombolysis).

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

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

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

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

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

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

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

46 d branching, incorporate into nascent fibrin clots, and impede fibrinolysis in vitro.

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

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

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

50 device infection-that of an infected fibrin clot-and show that the common blood-borne pathogen Staph

51 y relevant, as overly softened and stiffened clots are associated with bleeding and thrombotic disord

52 brin, the main structural component of blood clots, are associated with adverse events due to lack of

53 ognition of hardly removable old hemorrhagic clot as self-blockage site of posterior scleral penetrat

54 obstructions persisted, identifying crystal clots as a primary target to prevent organ failure.

55 that limits NETosis in the formation of the clot, as well as regulating the rate of clot resolution,

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

57 n vitro fluorogenic activity and whole blood clotting assays.

58 CRM(-) hemophilia B mice, the times to first clot at a saphenous vein injury site after the infusions

59 e slowly than the others because the caseins clotted at the gastric pH.

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

61 Blood clotting at wound sites is critical for preventing blood

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

63 monstrate the ability of the system to assay clot biomechanics associated with common antiplatelet tr

64 These catalytic microgelators also served to clot blood, unlike PLGA particles loaded with thrombin.

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

66 terial thrombosis characterized by a greater clot burden and a more dire prognosis.

67 Clot burden was quantified using the CTOI, which reflect

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

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

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

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

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

73 The clot contraction assay has a predictive value in assessi

74 A clot contraction assay, along with other hemostatic and

75 These results indicate that impaired clot contraction in the postoperative period is associat

76 ing that these structures are a signature of clot contraction in vivo.

77 On the 1st postoperative day, clot contraction was significantly suppressed in patient

78 During ex vivo clot contraction, the number of RBCs extruded from sickl

79 ng-lasting effect on normalizing whole blood clot contraction.

80 g from both adhesive and cohesive failure of clots decreases survival from hemorrhage in vivo.

81 or to rebleeding and what mechanisms prevent clot delamination.

82 Sickle trait whole blood clots demonstrated an intermediate phenotype in response

83 haemorrhagic fever is related to defects in clot development and stabilisation that are more marked

84 our ability to develop novel treatments for clotting diseases.

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

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

87 e site of thrombus, thus achieving efficient clot dissolution whilst minimising undesirable side effe

88 minocaproic acid and tranexamic acid inhibit clot dissolution.

89 covalent attachment of serpins that regulate clot dissolution.

90 stability of platelet aggregates and fibrin clots during blood coagulation.

91 Anucleate platelets form blood-clots during thrombosis, but also play a crucial role in

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

93 yme half-lives~1 min] predicted the measured clot elution rate of thrombin-antithrombin (TAT) and fra

94 rm the findings of others that venous fibrin clots entrap red cells.

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

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

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

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

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

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

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

102 atic control without exposure to immunogenic clotting factor proteins.

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

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

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

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

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

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

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

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

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

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

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

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

115 evelopment through complex interactions with clotting factors.

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

117 In the rat bleeding model, the frequency of clot failures correlated positively with blood loss (R =

118 min after clotting time (43-65 mm), maximum clot firmness (50-72 mm), and maximum lysis (>15% at 1 h

119 ting time (normal range 7-23 mm) and maximum clot firmness (9-25 mm).

120 riable fibrinogen thromboelastometry maximum clot firmness (FibTEM-MCF; fibrinogen contribution to cl

121 Maximum clot firmness (MCF) was significantly divergent between

122 e compared at different time points; maximum clot firmness (p=0.024) and amplitude at 10 min after cl

123 e 98-418; IQR 156-296; p=0.006); and maximum clot firmness 54.4 mm (SD 7.2) versus 45.1 mm (SD 12.5;

124 ness (FibTEM-MCF; fibrinogen contribution to clot firmness).

125 6-25; IQR 10-15; p=0.68]; and median maximum clot firmness, 15 mm [range 9-60; IQR 13-21] vs 17 mm [r

126 omboelastography was used to measure time to clot formation (r-time) in both rhesus and human blood,

127 nous inhibitor of fibrinolysis, and enhances clot formation after injury.

128 tion that periodontitis promotes accelerated clot formation and an increased risk of thrombosis.

129 on or genetic depletion of PAI-1 attenuating clot formation and lesion expansion after brain trauma.

130 nding assay to test the relationship between clot formation and lymphangiogenesis in mice, we find th

131 imental system that can simultaneously model clot formation and measure clot mechanics under shear fl

132 While spatio-temporal dynamics of clot formation are well characterized, the cell-biologic

133 s target antigen beta2GP1, leading to fibrin clot formation due to exposure of anionic phospholipids

134 leeding or high-risk procedures may optimize clot formation in advanced liver disease: hematocrit >=2

135 cipated role of leukocytes for microvascular clot formation in inflamed tissue.

136 Following clot formation in PPP, the presence of SAA increased amy

137 et activation, thrombus structure and fibrin clot formation in real time using flowing whole blood.

138 athway, promoting a procoagulatory state and clot formation in the cerebral microvasculature.

139 eleased from activated human neutrophils, on clot formation in vitro and in vivo.

140 With blood clot formation inside an artery resulting from influenza

141 e of margination and shear rate on occlusive clot formation is not fully understood yet.

142 l ranges indicated: clotting time (38-79 s), clot formation time (34-159 s), amplitude at 10 min afte

143 0) versus 33.9 mm (SD 8.6; p<0.0001); median clot formation time 147 s (range 72-255; IQR 101-171) ve

144 ipid metabolites play in regulation of blood clot formation under pathologic conditions.

145 elastometry was used to quantify the rate of clot formation via the intrinsic coagulation pathway.

146 Ir-CPI was as efficient as UFH in preventing clot formation within the extracorporeal circuit and mai

147 odel that is not associated with significant clot formation, also revealed an essential role for VEGF

148 onfirmed alterations of proteins involved in clot formation, immune reaction and free heme binding.

149 BEST PRACTICE ADVICE 1: Global tests of clot formation, such as rotational thromboelastometry, t

150 gnaling pathway and common pathway of fibrin clot formation.

151 tructure, properties, and dynamics of sickle clot formation.

152 nd neonatal porcine islets prolonged time to clot formation.

153 nge in 70.3% of patients indicative of rapid clot formation.

154 del by mapping mutations leading to impaired clot formation.

155 semble multi-protein complexes that regulate clot formation; however, PS is of limited abundance phys

156 lood clot was also more rigid than the blood clot formed by thrombin solution.

157 oli were very tightly packed, in contrast to clots formed in vitro.

158 Interestingly, whole blood, but not plasma clots from SCD patients, was more resistant to fibrinoly

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

160 r size and the insoluble character of fibrin clots, have restricted our ability to develop novel trea

161 n and thromboembolism; the increase in model clot heterogeneity shows that S. epidermidis can rupture

162 contribute to the adhesive strength of bulk clots in a lap-shear test in vitro.

163 eleased from sickle cell trait and nonsickle clots in both mice and humans.

164 ors play in both formation and resolution of clots in deep vein thrombosis (DVT).

165 These results suggest that subarachnoid clots in sulci/fissures are sufficient to induce spreadi

166 reased the stiffness of platelet-rich plasma clots in the presence of FXIIIa.

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

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

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

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

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

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

173 L molecular species formed within minutes of clot initiation.

174 ture wound bleeding consistent with impaired clot integrity.

175 This phenomenon is especially prominent in clots involving sickle erythrocytes (see figure), consis

176 The fibrin clot is gelatinous matter formed upon injury to stop blo

177 nce of flow on the growth and shrinkage of a clot is investigated.

178 The mechanistic reaction of the clot is the first step in providing scaffolding for the

179 n specifically tested if adhesive failure of clots is a major contributor to rebleeding and what mech

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

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

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

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

184 ntal pulmonary embolism, particularly distal clots, is unclear.

185 ility intraventricular haemorrhage size, and clot location).

186 Gylated liposomes to induce efficient fibrin clot lysis in a fibrin-agar plate model and the encapsul

187 In human plasma, F5 and G2 prolonged clot lysis time from 9.8 +/- 1.1 minutes in the absence

188 howed enhanced clot stability and lengthened clot lysis time in blood from F8-/-/PN-1-/- and from pat

189 Compared with 40 healthy volunteers, median clot lysis times (CLTs) were shorter in patients with AD

190 Furthermore, almost complete blood clot lysis was achieved in 75 min, showing considerably

191 al Stroke Trials Archive-ICH trials dataset, Clot Lysis: Evaluating Accelerated Resolution of Intrave

192 05) and 149.3 +/- 9.7 (P < .0001) minutes in clots made from purified fibrinogen.

193 These properties of sickle clots may explain the increased risk of venous thromboem

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

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

196 is influences this in vitro model of a blood clot mechanically and structurally on both microscopic a

197 The changes of clot mechanics under biochemical treatments and shear fl

198 otMAT) that recapitulates dynamic changes in clot mechanics under physiological shear.

199 ultaneously model clot formation and measure clot mechanics under shear flow.

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

201 econds (TCN30), or 60 seconds (TCN60); blood clot (NC), and non-demineralized autogenous bone (PC).

202 Clot nucleation and transformation of viscous blood into

203 larvae of Manduca sexta, we discovered that clot nucleation is a two-step process whereby cell aggre

204 CC caused crystal clots occluding intrarenal arteries and a dose-dependent

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

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

207 tient data were collected until each circuit clotted or was ceased electively for nonclotting reasons

208 ue calculated at either the RCF-minimum, RCF-clot, or RCF-maximum; 5) composition and size of tubes u

209 etween 1.3 and 2.0 times higher in one-stage clot (OS) assays than in chromogenic-substrate (CS) assa

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

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

212 immature premolars with an autologous blood clot (PC), gelatin-based and fibrin-based hemostatic mat

213 d US, or (7) rt-PA, Definity, and US (n = 16 clots per group).

214 decreased plasminogen and a decreased fibrin clot permeability.

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

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

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

218 n seem more platelet-rich than the fibrinous clots precipitated by plaque rupture.

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

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

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

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

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

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

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

226 vage covalently cross-links preformed fibrin clots protecting them from premature fibrinolysis.

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

228 Soluble clotting proteins bind to membrane components in a phosp

229 ective removal or dissolution of large blood clots remains a challenge in clinical treatment of acute

230 teplase and endovascular therapy (mechanical clot removal), both of which are highly time-dependent.

231 t of supratentorial spontaneous ICH aimed at clot removal.

232 the clot, as well as regulating the rate of clot resolution, identifies a new target for therapeutic

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

234 ibit human platelet aggregation but preserve clot retraction.

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

236 s integrated model, we demonstrate how blood clot severity may depend on circulating prothrombin leve

237 ) and occlusion of platelet-rich thrombi and clot shrinkage have been studied after flow arrest.

238 Blood from SP patients clotted significantly (P < 0.05) more rapidly and exhibi

239 bolysis (MISTIE), with the aim of decreasing clot size to 15 mL or less, would improve functional out

240 ated positively with the increase in the IVC clot size.

241 Thromboelastometry studies showed enhanced clot stability and lengthened clot lysis time in blood f

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

243 ly strong effects of these two stimulants on clot stiffening.

244 process that involves platelet adhesion and clot stiffening/contraction in the milieu of fluid flow.

245 reased (maximum amplitude, > 72 mm) in vitro clot strength on thromboelastography (91%; area under th

246 coagulation profiles, an increased in vitro clot strength on thromboelastography was associated with

247 latelet count and function, and a measure of clot strength was above reference range in 60.1% of pati

248 study assessed the ability of using in vitro clot strength, as measured by thromboelastography, to pr

249 with those with a normal or reduced in vitro clot strength.

250 and amount of thrombin generated and overall clot strength.

251 aches can be used to assess platelet-induced clot strengthening, but they require thrombin and fibrin

252 ant Abetas led to a dramatic perturbation of clot structure and delayed fibrinolysis.

253 F5 and G2 had a differential effect on clot structure and G2 profoundly altered fibrin fiber ar

254 that patients on hemodialysis with a denser clot structure had increased all-cause and cardiovascula

255 ngement, whereas F5 maintained physiological clot structure.

256 ified and characterized for their effects on clot structure/fibrinolysis, using turbidimetric and per

257 ssion of FV by the macrophages to form local clots that effectively brought macrophages and bacteria

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

259 The clot, therefore, requires special materials properties.

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

261 Clot time is correctly predicted in individual cases, an

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

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

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

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

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

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

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

269 -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

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

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

272 131 patients (72.5%) with an elevated ecarin clotting time and was similar for upper and lower GI ble

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

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

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

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

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

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

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

280 ific assays diluted thrombin time and ecarin clotting time.

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

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

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

284 del required fibrinogen penetration into the clot to be strongly diffusion-limited (actual rate/ideal

285 ly reversed resistance of whole blood sickle clots to fibrinolysis, in part by decreasing platelet-de

286 The adhesion of blood clots to wounds is necessary to seal injured vasculature

287 l as to fibrin, platelet proteins, and blood clots under flow in vitro Abeta40 also increased the sti

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

289 vessel caused a decrease in TPA flux in the clotted vessel, which increased the PAI-1/TPA ratio, thu

290 The resulting blood clot was also more rigid than the blood clot formed by t

291 bosis; if the results were positive (i.e., a clot was present), CT pulmonary angiography was not perf

292 ber of RBCs extruded from sickle whole blood clots was significantly reduced compared with the number

293 in endothelial cells of the IVC and reduced clot weights in both kynurenine-injected and xenograft-b

294 oma cells exhibited significantly higher IVC clot weights, a biological readout of venous thrombogeni

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

296 large fibrin biopolymers that coalesce into clots which assist in wound healing.

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

298 d organ failure via the formation of crystal clots with fibrin, platelets, and extracellular DNA as c

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

300 te operating conditions, where chicken blood clots within 30 min and anticoagulated human blood clots