ライフサイエンスコーパス: coagulation

1 st common organ failures were 'hepatic' and 'coagulation'.

2 cell cycle differentiation, inflammation, or coagulation.

3 sm, organ function, cytokine production, and coagulation.

4 ibutions to our basic understanding of blood coagulation.

5 agulant markers and markers of activation of coagulation.

6 nvolved in olfaction, nociception, and blood coagulation.

7 hich cleaves FIX in the intrinsic pathway of coagulation.

8 d are thought to be responsible for impaired coagulation.

9 ts in activation of fibrinolysis, but not of coagulation.

10 the TF pathway inhibitor that is involved in coagulation.

11 8; p < 0.05) with disseminated intravascular coagulation.

12 liary dysfunction/disseminated intravascular coagulation.

13 ism unrelated to exaggerated inflammation or coagulation.

14 cyte activation, adhesion, inflammation, and coagulation.

15 tic shock-induced disseminated intravascular coagulation.

16 of sepsis-induced disseminated intravascular coagulation.

17 host-mediated tissue damage, and disordered coagulation.

18 serves as a bridge between inflammation and coagulation.

19 r regulating reproductive hormones and blood coagulation.

20 e Fe/NOM ratio and the presence of Ca(2+) in coagulation.

21 s have also been implicated as activators of coagulation.

22 lled criteria for disseminated intravascular coagulation.

23 ted to sepsis and disseminated intravascular coagulation.

24 d structural dysregulation, iron status, and coagulation.

25 y nascent FXa, can support intrinsic pathway coagulation.

26 ecies available for hydrolysis and effective coagulation.

27 d the proteins associated with apoptosis and coagulation.

28 roliter sample volumes of human blood plasma coagulation (0.009 cP for viscosity range 0.5-3 cP and 0

29 However, the degree to which these coagulation abnormalities affect TBI outcomes and whethe

30 ally 'abnormal' IgE, and decreasing in vitro coagulation abnormalities associated with disease activi

31 in humans and non-human primates, including coagulation abnormalities, hemorrhagic manifestations, p

32 s linked to GGCX mutations, however, show no coagulation abnormalities.

33 These may include low hematocrit and coagulation abnormalities.

34 five patients had disseminated intravascular coagulation according to Japanese Association for Acute

35 ed platelet adhesion, complement activation, coagulation activation and inhibition of fibrinolysis.

36 nd C5b-9 deposition, cellular activation and coagulation activation in WT and GTKO.hCD46.hTBM PAEC.

37 on of prothrombin fragment F1 + 2 (marker of coagulation activation), D-dimer, plasmin-antiplasmin co

38 ascular integrity, and evidence for enhanced coagulation activation.

39 complex may be prohemostatic before further coagulation amplification by thrombin-dependent feedback

40 ct the absence of disseminated intravascular coagulation and allow a better stratification in future

41 mostatic system and innate immunity, and the coagulation and complement cascades.

42 Sepsis concurrently activates both coagulation and complement systems.

43 th reduced markers of systemic intravascular coagulation and end-organ damage in septic mice.

44 site inhibitors of S1A proteases involved in coagulation and fibrinolysis is summarized.

45 nknown whether this results in activation of coagulation and fibrinolysis, as may occur upon graft re

46 serine protease with putative roles in blood coagulation and fibrinolysis.

47 serves as a valuable marker of activation of coagulation and fibrinolysis.

48 apid mixing processes remains unaddressed in coagulation and flocculation of insoluble precipitates (

49 ion and atherosclerosis (PECAM1, rs1867624), coagulation and inflammation (PROCR, rs867186 (p.Ser219G

50 s with influenza had dysregulated indices of coagulation and inflammation compared with controls.

51 Endothelial thrombomodulin (TM) regulates coagulation and inflammation via several mechanisms, inc

52 rin form, providing a molecular link between coagulation and inflammation.

53 et-thrombin axis that promotes intravascular coagulation and microvascular dysfunction in sepsis.

54 This leads to NETosis, induction of coagulation and N2 polarization, which prompts tumorigen

55 Measurements in disseminated intravascular coagulation and no disseminated intravascular coagulatio

56 PE is associated with coagulation and platelet activation and increased extrac

57 w dose ozone into the UF membrane tank after coagulation and the use of a hollow-fibre membrane coate

58 ry and cytokine responses, and activation of coagulation and the vascular endothelium.

59 muscle myosins can directly influence blood coagulation and thrombosis, ex vivo studies of the effec

60 f Fe precipitates, leading to more effective coagulation and widening the pH range of water treatment

61 ng and monitoring disseminated intravascular coagulation, and as an aid in the identification of medi

62 rombin and other proteases involved in blood coagulation, and ATIII misfolding can thus lead to throm

63 Increases in inflammation, coagulation, and CD8(+) T-cell numbers are associated wi

64 Inflammation, coagulation, and cell stress contribute to atheroscleros

65 sive study of the crucial role of platelets, coagulation, and flow in arterial thrombosis, little att

66 ose metabolism, complement activation, blood coagulation, and inflammation.

67 urthermore, proteins associated with immune, coagulation, and inflammatory pathways were over-represe

68 m of the renal, respiratory, cardiovascular, coagulation, and neurologic systems by day 7 after surge

69 n F, hemoglobin polymerization and sickling, coagulation, and platelet activation.

70 ates the efficiency of dust and planetesimal coagulation, and the formation of comets, ice giants and

71 ts controlling initiation and propagation of coagulation are still incompletely understood.

72 Current pre-treatment methods, such as coagulation, are only partially effective to prevent lon

73 of the absence of disseminated intravascular coagulation (area under the curve, 72.9%; specificity, 7

74 o cleave human Factor V and deregulate blood coagulation, as the most abundant type II secreted effec

75 activated partial thromboplastin time (aPTT) coagulation assay was performed, and the viscosity, dens

76 compared with an MTP guided by conventional coagulation assays (CCA).

77 In vitro coagulation assays demonstrated a hypercoagulable state

78 ity testing prior to the hemolysis assay and coagulation assessment.

79 of patients with disseminated intravascular coagulation at admission.

80 teractions between inflammatory elements and coagulation at endothelial surfaces may play an importan

81 es not exclude the possibility of disordered coagulation at the time of stroke but suggests testing i

82 During the process of blood coagulation, BDNF is released from platelets, which has

83 nction of FV that targets the early phase of coagulation before prothrombinase assembly.

84 n and one case of disseminated intravascular coagulation (both in the Foley group); ten perinatal dea

85 odstream during infection, in inducing blood coagulation by direct proteolytic ProT activation.

86 This signified that DOM removal by coagulation can be achieved at lower mixing intensity, t

87 ensional ex vivo phenotyping of platelet and coagulation can now power multiscale computer simulation

88 monocyte activation (soluble CD14 [sCD14]), coagulation cascade activation [D-dimer], and fibrosis (

89 data suggesting that von Willebrand factor, coagulation cascade activation, and dysfunction of the p

90 Biomarkers of inflammation, coagulation cascade activation, and fibrosis predict the

91 Importance: Calcium is a key cofactor of the coagulation cascade and may play a role in the pathophys

92 ion was associated with normalization of the coagulation cascade and several systemic inflammatory bi

93 mutations in serpins or other members of the coagulation cascade can provide critical advantages duri

94 tational status of 33 genes belonging to the coagulation cascade in a panel of 29 BMs and we identifi

95 ntages for in-depth study of the role of the coagulation cascade in the developmental regulation of h

96 The coagulation cascade is designed to sense tissue injury b

97 Beside its classical role in the coagulation cascade, coagulation factor X (FX) is involv

98 rocesses involve platelet activation and the coagulation cascade, forming the basis for the use of an

99 n model with a tissue-factor/contact pathway coagulation cascade, representing the relevant biology o

100 if they are directed against enzymes of the coagulation cascade.

101 cell membrane are critical within the blood coagulation cascade.

102 in than to the other serine proteases of the coagulation cascade.

103 it components of the intrinsic and extrinsic coagulation cascades upstream of thrombin and fX.

104 e associated with disseminated intravascular coagulation: CD105-microparticles (odds ratio, 2.13) and

105 Although blood coagulation changes such as disseminated intravascular c

106 ng patients with increased kidney, brain, or coagulation Chronic Liver Failure-C-Organ Failure subsco

107 that, apart from its distinct role in blood coagulation, coagulation factor FVIIa enhances aggressiv

108 For each of these materials, critical coagulation concentrations (CCC) were determined for NaC

109 The critical coagulation concentrations (CCC) were quantified and the

110 well microplate platform to measure critical coagulation concentrations, a measure of colloidal stabi

111 activation (soluble [s]CD14 and sCD163), and coagulation (D-dimer) in HIV-infected and uninfected nev

112 r necrosis factor, interleukin-6, and -10); "coagulation" (D-dimers, thrombin-antithrombin complex);

113 Fibrinogen concentrate might partly restore coagulation defects and reduce intraoperative bleeding.

114 tative evaluations of proteolysis after milk coagulation, determined by the non-protein nitrogen cont

115 to improve early disseminated intravascular coagulation diagnosis and patient stratification.

116 ity of 80.60% for disseminated intravascular coagulation diagnosis.

117 lammation-induced disseminated intravascular coagulation (DIC) in micro-capillary circulation are poo

118 Disseminated intravascular coagulation (DIC) is a condition characterized by system

119 Disseminated intravascular coagulation (DIC)-positive kidneys have historically bee

120 ry pattern mimics disseminated intravascular coagulation (DIC).

121 ufficiency, single-ventricle physiology, and coagulation disorder.

122 ing 220 plasma samples of patients suffering coagulation disorders and 80 plasma samples of non-patie

123 This rational approach, applicable to other coagulation disorders, helps with interpreting the poor

124 ce in patients with F10 deficiency and other coagulation disorders.

125 d with increased fluid overload, hepatic and coagulation dysfunction, acute kidney injury, mortality,

126 ch has the potential to solve the problem of coagulation dysregulation in pig-to-primate xenotranspla

127 The results indicate that effective algae coagulation (e.g., up to 81 % algae removal efficiency)

128 for treating primary wastewater and overall coagulation efficiency was determined.

129 Factor XIa (FXIa) is a blood coagulation enzyme that is involved in the amplification

130 llent selectivity against the relevant blood coagulation enzymes.

131 (TFPI), the main inhibitor of initiation of coagulation, exerts an important anticoagulant role thro

132 ) may be linked to specific mutations in the coagulation factor 12 (FXII) gene (HAE-FXII) or function

133 390-396A) mice appeared to be independent of coagulation factor 13 (FXIII) transglutaminase, as ANIT

134 Recipients of continuous coagulation factor administration experienced either sta

135 y expressing 2 reporter proteins (a chimeric coagulation factor and MGP) in HEK293 cells.

136 's GGCX D153G mutant significantly decreased coagulation factor carboxylation and abolished MGP carbo

137 in K concentrations can restore up to 60% of coagulation factor carboxylation but do not ameliorate M

138 tration of platelet concentrates, plasma, or coagulation factor concentrates should be considered.

139 r XI deficiency is one of the rare inherited coagulation factor deficiencies.

140 Here we show that the coagulation factor fibrinogen activates the bone morphog

141 from its distinct role in blood coagulation, coagulation factor FVIIa enhances aggressive behaviors o

142 ation levels (M values) of cg03636183 in the coagulation factor II (thrombin) receptor-like 3 gene (F

143 ing the thrombin receptors on platelets F2R (coagulation factor II (thrombin) receptor; PAR1) and GP5

144 safety of recombinant fusion protein linking coagulation factor IX (FIX) with albumin (rIX-FP) which,

145 haemophilia B (</=2 IU/dL [</=2%] endogenous coagulation factor IX [FIX] activity).

146 of pegnivacogin, an RNA aptamer inhibitor of coagulation factor IXa, and anivamersen, a complementary

147 The changes in coagulation factor levels matched the changes in activit

148 The coagulation factor prothrombin has a complex spatial org

149 acids connects kringle-1 to kringle-2 in the coagulation factor prothrombin.

150 ion, which endocytoses fluorescently labeled coagulation factor V (FV) from the media into alpha-gran

151 binase assembly by directly interacting with coagulation factor V (FV), which has been activated by F

152 of the method to a tryptic digest of bovine coagulation factor V resulted in identification of sulfa

153 Here we demonstrate that coagulation factor VIIa (FVIIa) elicits TF cytoplasmic d

154 bleeding disorder caused by a deficiency in coagulation factor VIII (fVIII) that affects 1 in 5,000

155 Using available genomic sequence data on coagulation factor VIII and predictive models of molecul

156 23/26del) which cannot bind platelets, blood coagulation factor VIII, or collagen, causing VWD throug

157 Coagulation factor X (FX) binding to HAdV-5 mediates liv

158 s classical role in the coagulation cascade, coagulation factor X (FX) is involved in several major b

159 r class A member I (SR-AI) as a receptor for coagulation factor X (FX), mediating the formation of an

160 Coagulation factor XI (FXI) has become increasingly inte

161 aused by mutation in the C1 inhibitor or the coagulation Factor XII gene.

162 creased thrombus formation and activation of coagulation factor XII.

163 activity of platelets with the activation of coagulation factor XII.

164 Coagulation Factor XIII (FXIII) plays an important role

165 eover, we observed that the transglutaminase coagulation factor XIIIA (FXIIIA) was one of the most ab

166 models of hemostasis, we show that a variant coagulation factor, FXa(I16L), rapidly restores hemostas

167 After LXT, baboons received no coagulation factors (historical control, n = 1), bolus a

168 Emerging evidence has shown that coagulation factors can directly mediate cancer-associat

169 Vitamin K-dependent coagulation factors deficiency is a bleeding disorder ma

170 Elevation of multiple coagulation factors in Mrc1(-/-)Asgr2(-/-) mice may acco

171 models have implicated an integral role for coagulation factors in neuroinflammatory diseases such a

172 In patients who died, coagulation factors involved in the common pathway were

173 Our study demonstrates that coagulation factors may be key mediators in neuroinflamm

174 geneity in the surface distribution of major coagulation factors on the surface of procoagulant plate

175 Spatial distribution of blood coagulation factors on the surface of procoagulant plate

176 cal side effects, while use of fibrinogen or coagulation factors provides only partial mechanisms for

177 tatic components (platelets, fibrinogen, and coagulation factors).

178 ulation involves activation of platelets and coagulation factors.

179 the catalytic surface for the activation of coagulation factors.

180 a progestin, without increasing the level of coagulation factors.

181 We screened a panel of proteases in the coagulation, fibrinolytic, and inflammatory cascades to

182 ligands include components of complement and coagulation-fibrinolytic systems, as well as plasma lipo

183 ith UV-treatment and (2) a more conventional coagulation, filtration, UV, and chlorination treatment

184 Conventional water treatment involving coagulation-flocculation-sedimentation may be impeded by

185 tsurgery, characterized by reduced levels of coagulation FXI in plasma.

186 liary dysfunction/disseminated intravascular coagulation group included patients with only hepatobili

187 histone proteins, and neutrophil enzymes on coagulation have been characterized, the mechanism by wh

188 n changes such as disseminated intravascular coagulation have been recognized since the 1970s, recent

189 xpected role of eosinophils during plasmatic coagulation, hemostasis, and thrombosis.

190 ntity with fever, disseminated intravascular coagulation, hepatobiliary dysfunction, cytopenias, and

191 ortal islet transplantation by mitigation of coagulation in IBMIR and suppression of cytokine-induced

192 es related to cytokine storm, oxidation, and coagulation in lung microvascular endothelium.

193 g leakage and can sustainably regulate blood coagulation in response to thrombin.

194 sion to target disorders of inflammation and coagulation in severely injured patients.

195 opriate biocatalyst was based on the time of coagulation in successive batches, the concentration of

196 and subsequently releases heparin to prevent coagulation in the blood flow.

197 act NETs do not directly initiate or amplify coagulation in vitro.

198 n significant improvement in liver function, coagulation, incidence of encephalopathy, and creatinine

199 The extent of coagulation increased with growing terrestrial influence

200 ntribute to host-defense responses including coagulation, inflammation, and fibrinolysis.

201 found that the extrinsic tissue factor (TF) coagulation initiation complex can selectively activate

202 The coagulation initiation complex induced rapid and prolong

203 ctivate the MASP matriptase, thus connecting coagulation initiation to epithelial proteolysis and sig

204 mic inflammatory responses and levels of the coagulation intermediary plasminogen activator inhibitor

205 Blood coagulation involves activation of platelets and coagula

206 Blood coagulation is a finely regulated physiological process

207 Early activation of coagulation is an important factor in the initiation of

208 by NOM appears to be the mechanism by which coagulation is disrupted.

209 Blood coagulation is essential for physiological hemostasis bu

210 low rate of accumulation of cells supporting coagulation is one reason that the progress of VT is so

211 Coagulation kinetics are well established for purified b

212 impairment (P = .026), and inflammatory and coagulation markers (P < .001).

213 testing, by assessing functional pathways of coagulation, may better help manage venous thrombotic di

214 ail bleeding cessation method and an ex vivo coagulation method.

215 trast, macroscopic investigations showed the coagulation mixing energy affected floc size distributio

216 identical composition, but differing by the coagulation mode, were submitted to static in vitro gast

217 These agents can be used without regular coagulation monitoring, but the inherent risk of bleedin

218 dministration in fixed doses without routine coagulation monitoring.

219 tumorigenesis, showing a novel link between coagulation, neutrophilia and complement activation.

220 Dynamic changes in coagulation occur with progression of ALI: a pro-thrombo

221 rs ago revealed that excessive activation of coagulation occurs in the setting of inflammation.

222 Percutaneous coagulation of a post-pancreatitis pseudoaneurysm is a r

223 We found systematic iron coagulation of large (>450 Da), oxygen-rich, and highly

224 ) increase of productivity by the continuous coagulation of milk, and (ii) saving of the rennin enzym

225 g of the rennin enzyme expenses of the batch coagulation of milk.

226 No evidence of pathological activation of coagulation or detrimental animal physiology was observe

227 dysfunction, only disseminated intravascular coagulation, or neither.

228 nderstanding not only how Ca(2+) may improve coagulation outcomes, but also in predicting the conditi

229 h septic shock, alterations in inflammation, coagulation, oxidative stress, and tissue hypoxia are co

230 the development of hepatic (p < 0.0001) and coagulation (p < 0.0001) dysfunction and acute kidney in

231 Abnormal coagulation parameters and high DIC scores (primarily du

232 et count were identified as the best routine coagulation parameters for prediction of new onset of ma

233 Routine coagulation parameters were assessed, and the DIC score

234 st cancer and BMs and found mutations in the coagulation pathway genes in 5 out of 10 BM samples.

235 iciently blocked activation of the intrinsic coagulation pathway in human blood ex vivo.

236 , FVIII, triggering the hemostatic intrinsic coagulation pathway independently of thrombin feedback l

237 ications associated with blocking the common coagulation pathway remains.

238 AAT suppressed blood-mediated coagulation pathways by diminishing tissue factor produc

239 atory axis that triggers local activation of coagulation pathways to support metastatic colonization

240 liary dysfunction/disseminated intravascular coagulation patients (71.4% vs 70.8%; p = 0.88).

241 oagulation and no disseminated intravascular coagulation patients showed that a mean value of NEUT-si

242 tion characterized by systemic activation of coagulation, potentially leading to thrombotic obstructi

243 excess Fe was available for NOM removal, and coagulation proceeded according to expectations based up

244 oped in order to carry out a continuous milk coagulation process with the aim of producing soft chees

245 otein loading, caseinolytic activity and the coagulation properties of skim milk powder and cow's mil

246 e directly investigated a role for the blood-coagulation protease thrombin in regulating the adhesion

247 ted, work in mice and in vitro suggests that coagulation proteases can directly cleave complement pro

248 ssue factor (TF) from inactive precursors of coagulation proteases circulating in plasma.

249 TF is the receptor and scaffold of coagulation proteases cleaving protease-activated recept

250 We aimed to determine whether generation of coagulation proteases in vivo can activate the complemen

251 haracterised by deficiency or dysfunction of coagulation protein factors VIII and IX, respectively.

252 e time, ongoing consumption of platelets and coagulation proteins results in thrombocytopenia and low

253 similar binding measurements for three other coagulation proteins.

254 events involving activation of platelets and coagulation proteins.

255 s performed, and the viscosity, density, and coagulation rate of human blood plasma were measured alo

256 tes, platelets, and MPs that can support the coagulation reactions has a powerful influence on whethe

257 s importance in promoting membrane-dependent coagulation reactions.

258 ss the protease-activated receptor family of coagulation receptors in vivo High-concentration thrombi

259 parameters, eg, a significant improvement in coagulation, reduction in vasopressor requirements, impr

260 development of sepsis-induced intravascular coagulation regardless of the inciting bacterial stimulu

261 cytokines (IL1B, IFNG), and plasminogen- and coagulation-related molecules (SERPINB2, PLAU, PLAUR, TF

262 ients with VTE than without VTE had abnormal coagulation results (49.3% vs 35.7%; P = .02), femoral c

263 ients with VTE than without VTE had abnormal coagulation results (64.5% vs 44.4%; P = .03), femoral c

264 ative senile retinoschisis, peripheral laser coagulation scars, ora tooth, cryopexy scars (retinal te

265 ation can be optimized for algae removal via coagulation-sedimentation.

266 The backbone dynamics of the coagulation serine protease, apo-thrombin (S195M-thrombi

267 , fibrinolysis, and interactions between the coagulation system and the vascular endothelium, brain t

268 ings provide an interesting link between the coagulation system, innate immunity, LPS scavenging, and

269 he complex cross talk between platelets, the coagulation system, leukocytes, and the activated endoth

270 ne network, the vascular endothelium and the coagulation system, with the exception of antithrombin l

271 potentiate several interactions in the blood coagulation system.

272 ical states caused by a malfunctioning blood coagulation system.

273 To measure PT/INR, conventional coagulation testing (CCT) is performed, which is time-co

274 The method could extend and improve current coagulation testing.

275 with TBI have abnormalities on conventional coagulation tests at admission to the emergency departme

276 gulation and other analytical limitations of coagulation tests.

277 we explored a potential link between EMT and coagulation that may provide EMT-positive CTCs with enha

278 temporal changes in activation biomarkers of coagulation (thrombin-antithrombin [TAT]), fibrinolysis

279 es, ranging from nutrient digestion to blood coagulation, thrombosis, and beyond.

280 implicated in lung injury and repair such as coagulation/thrombosis, acute phase response signaling a

281 ), and a reduction in the pH of maximum heat coagulation time (HCT) (P<.05).

282 ely 2-fold, diminished PCA by 70%, prolonged coagulation time, and attenuated fibrin formation by 50%

283 plasma were measured along with the standard coagulation time.

284 In comparison, the coagulation times of the acoustic aPTT and PiCT yielded

285 a, applied research on circulation and blood coagulation to devise whole-body fasting and bleeding re

286 f physiological processes ranging from blood coagulation to embryo- and oncogenesis, tissue regenerat

287 rent understanding of how platelets localize coagulation to wound sites has come mainly from studies

288 proteases of the extrinsic pathway of blood coagulation transactivate the MASP matriptase, thus conn

289 geneous nucleation was studied in a particle coagulation treatment process for removing microalgae fr

290 elop a bioreactor design for continuous milk coagulation using a biocatalyst composed of immobilized

291 c and quantitative assessment of whole blood coagulation using acoustic radiation force orthogonal ex

292 stemic pathophysiological processes, such as coagulation, vascular leakiness, and reprogramming of st

293 Prediction of disseminated intravascular coagulation was also analyzed after exclusion of patient

294 NET-induced intravascular coagulation was dependent on a collaborative interaction

295 Disseminated intravascular coagulation was diagnosed according to Japanese Associat

296 utionary insights into the cellular phase of coagulation, we asked whether a functional vwf gene is p

297 ry and cytokine responses, and activation of coagulation) were largely similar between genders, femal

298 n in response to the blockade of NET-induced coagulation, which correlated with reduced markers of sy

299 mixing energy was expended than necessary in coagulation, which is typically designed at a high mixin

300 drop of whole blood following activation of coagulation with thromboplastin.