ライフサイエンスコーパス: coagulation

1 patterns (DAMPs), promoting inflammation and coagulation.

2 vs 3.4%, P < 0.0001), than those with normal coagulation.

3 nd pathogenesis associated with dysregulated coagulation.

4 sepsis-associated disseminated intravascular coagulation.

5 IIa (FVIIa) mediates the initiation of blood coagulation.

6 he release of F3, the key initiator of blood coagulation.

7 inin generation and the intrinsic pathway of coagulation.

8 otransduction, and reducing inflammation and coagulation.

9 during HFRS is associated with intravascular coagulation.

10 nflammation, transendothelial migration, and coagulation.

11 Cbs(-/-) mice show no abnormalities in blood coagulation.

12 lated neutrophils can also directly activate coagulation.

13 let aggregates and fibrin clots during blood coagulation.

14 th the inflammatory state tending to promote coagulation.

15 release, directly connecting inflammation to coagulation.

16 onocytes rapidly contribute to intravascular coagulation.

17 r VIIa and the primary cellular initiator of coagulation.

18 r, the initiator of the extrinsic pathway of coagulation.

19 during HFRS is associated with intravascular coagulation.

20 une response and inappropriate activation of coagulation.

21 in lipid binding, complement activation, and coagulation.

22 e response, inflammatory response, and blood coagulation.

23 gulation factors for active participation in coagulation.

24 ry response, dysregulated adaptive immunity, coagulation abnormalities, hemorrhage, and multiorgan fa

25 s with hepatic synthetic dysfunction-induced coagulation abnormalities.

26 s with device thrombosis exhibited a greater coagulation activation 7 days post-LAAC (P=0.038 and P=0

27 y contrast pre-LAAC associated with enhanced coagulation activation post-LAAC, which in turn increase

28 OAC significantly reduced coagulation activation within 7 days post-LAAC compared

29 elucidate the mechanism(s) of RBC-MV-induced coagulation activation, the ability of storage lesion-in

30 identified the trigger of rapid intrahepatic coagulation after PHx.

31 actor deficiency, pinpointing the trigger of coagulation after PHx.

32 CD) is associated with chronic activation of coagulation and an increased risk of venous thromboembol

33 In haemostasis and thrombosis, platelet, coagulation and anticoagulation pathways act together to

34 K's importance in human health beyond blood coagulation and bone health necessitates its further res

35 endothelial junctions, increased markers of coagulation and complement activation (including tissue

36 inflammatory reaction (IBMIR) activates the coagulation and complement cascades and leads to the des

37 ied proteins were selected and associated to coagulation and complement processes and to extracellula

38 sphatidylcholines, phosphatidylcholines, and coagulation and complement proteins.

39 Proteins involved in blood coagulation and complement/coagulation cascades represen

40 uses of these serpins for the management of coagulation and contact system disorders, respectively.

41 More severe muscle fibre coagulation and denaturation were observed in the shockw

42 s; however, only a few studies have compared coagulation and fibrinolysis across species.

43 animal species selection and optimization of coagulation and fibrinolysis translational research.

44 asmin (PG) generation is useful to assessing coagulation and fibrinolysis within the same sample.

45 the mechanisms involved in microplastic (MP) coagulation and flocculation have only been superficiall

46 r pristine PE MPs were the most resistant to coagulation and flocculation, with 82% removal observed

47 o identify the mechanisms involved during MP coagulation and flocculation.

48 events, acute-phase response signaling, and coagulation and glucometabolic signaling pathways, where

49 e oxidative stress gene signature coupled to coagulation and glutathione-pathway genes shared between

50 NVUGIB, in whom conventional electrosurgical coagulation and hemostatic clips are unsuccessful or pre

51 Ancient organisms have a combined coagulation and immune system, and although links betwee

52 the TMEM173-GSDMD-F3 pathway blocks systemic coagulation and improves animal survival in three models

53 00 patients recruited into the Activation of Coagulation and Inflammation in Trauma (ACIT) study.

54 alysis was performed using the Activation of Coagulation and Inflammation in Trauma (ACIT2) database

55 Coagulation and inflammatory parameters were compared be

56 chemia reperfusion injury is associated with coagulation and inflammatory responses.

57 h the severity of disseminated intravascular coagulation and mortality in patients with sepsis.

58 isms leading to PDEVs release, their role in coagulation and phenotypic composition are poorly unders

59 tracorporeal membrane oxygenation, plasmatic coagulation and platelet aggregation were impaired due t

60 ombination of point-of-care and conventional coagulation and platelet analyses.

61 rane oxygenation additionally contributed to coagulation and platelet defects.

62 mboembolic disease through the activation of coagulation and platelet pathways with the production of

63 xcitability and secretion to mediating blood coagulation and viral infection.

64 Furthermore, genes involved in metabolism, coagulation, and adaptive immunity were downregulated, w

65 characterizing previous G1 ACLF, with liver, coagulation, and circulatory failure posing the highest

66 all three aspects of hemostasis (platelets, coagulation, and fibrinolysis) in patients with decompen

67 nges occur, which affect primary hemostasis, coagulation, and fibrinolysis.

68 kocyte traffic, nitric oxide production, and coagulation, and harbors diverse growth and survival fac

69 istress syndrome, disseminated intravascular coagulation, and multiorgan failure, which all carry poo

70 atic pathways, such as complement, the TLRs, coagulation, and platelets.

71 rsection between inflammation, immunity, and coagulation, and soluble urokinase plasminogen activator

72 istress syndrome, disseminated intravascular coagulation, and, rarely, death).

73 al immune pathways, including complement and coagulation, as targets of coronaviruses.

74 romboelastometry (ROTEM) is a holistic blood coagulation assay.

75 y (TEG) provides a more comprehensive global coagulation assessment than routine tests (international

76 er at initial presentation was predictive of coagulation-associated complications during hospitalizat

77 d the utility of these markers in predicting coagulation-associated complications, critical illness,

78 e compared between patients with and without coagulation-associated complications.

79 sease, we identified putative complement and coagulation-associated loci including missense, eQTL and

80 the pathogenesis of CVD via a platelet/blood coagulation-based mechanism.

81 SN7-13 does not inhibit coagulation, binds Tau with low nanomolar affinity, and

82 were also greater in subgroups with baseline coagulation biomarker levels at or above median of the e

83 o 2.5 mg versus warfarin were consistent for coagulation biomarkers and clinical outcomes, providing

84 er research regarding the predictive role of coagulation biomarkers for recombinant human soluble thr

85 nded current (yellow), whereas others prefer coagulation (blue).

86 their chemical gradients and mediates blood coagulation, bone development and viral infection.

87 y to selectively block contact system-driven coagulation, both variants block vascular occlusion in a

88 vitro, CC did not directly induce plasmatic coagulation but induced neutrophil extracellular trap fo

89 c plasma glycoprotein, functions to initiate coagulation by agglutinating platelets in the blood stre

90 The lipid scramblase TMEM16F initiates blood coagulation by catalyzing the exposure of phosphatidylse

91 initiation, localization, and propagation of coagulation by ICs, is mediated through Fcgamma receptor

92 presented here indicate that SAA can affect coagulation by inducing amyloid formation in fibrin(ogen

93 the mechanisms underlying the activation of coagulation by lipopolysaccharide (LPS), the major cell-

94 ll-derived microvesicles (RBC-MVs) propagate coagulation by supporting the assembly of the prothrombi

95 onopolar hemostatic forceps with low-voltage coagulation can be an effective alternative to other mec

96 e most important natural inhibitors of blood coagulation, carries a higher risk.

97 which is both an anticoagulant in the blood coagulation cascade and an activating ligand for the imm

98 hances our understanding of this step in the coagulation cascade and highlights parallels with the pr

99 Although thrombin is a key enzyme in the coagulation cascade and is required for both normal hemo

100 in contrast to an analogous reaction in the coagulation cascade where conversion of the zymogen prot

101 he use of currently available testing of the coagulation cascade, and help practitioners use anticoag

102 Fibrinogen is a key component of the coagulation cascade, and variation in its circulating le

103 rofiles, which act at distinct points in the coagulation cascade, bleeding complications continue to

104 ctor VIII (FVIIIa) is a crucial event in the coagulation cascade.

105 -11, a cytosolic LPS receptor, activated the coagulation cascade.

106 involved in blood coagulation and complement/coagulation cascades represented a greater fraction of t

107 Following wounding in Mus the complement and coagulation cascades, PPAR signaling pathway and ECM-rec

108 pigs' immunological compatibility and blood-coagulation compatibility with humans.

109 proteases of plasma, mostly enzymes of blood coagulation, complement, and inflammatory systems.

110 NETs can serve to localize other circulating coagulation components and can also promote vessel occlu

111 ole of surface organic coatings via critical coagulation concentrations (CCCs), which were compared w

112 ith 82% removal observed even under enhanced coagulation conditions.

113 that both Plasmodium falciparum factors and coagulation contribute to endothelial activation and dys

114 dies in animal models of SCD have shown that coagulation contributes to the chronic inflammation and

115 ed in thromboinflammation through complement-coagulation cross-talk.

116 n to either a blended current (Endocut Q) or coagulation current (forced coagulation) (Erbe Inc) (sec

117 ways with alterations in patients with (anti)coagulation defects.

118 d cancer of prostate, and F11 and congenital coagulation defects.

119 increased risk of disseminated intravascular coagulation (DIC) and venous thromboembolism (VTE).

120 ad thromboses and disseminated intravascular coagulation (DIC) in patients with coronavirus disease 1

121 mbolism (VTE) and disseminated intravascular coagulation (DIC) rates, but data are limited.

122 the disease; however, it is unknown whether coagulation directly contributes to the microvascular st

123 plement-activation disorders) and history of coagulation disorders (thrombocytopenia, thrombosis and

124 using blood samples from patients with (anti)coagulation disorders indicated characteristic defects i

125 n to ApoE (-/-) mice increased intravascular coagulation during AAA development.

126 ere observed including petechial rash, blood coagulation dysfunction, and various biochemistry and bl

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

128 e first time, we describe cardiovascular and coagulation effects of thermal burn and smoke inhalation

129 Accordingly, the activation of coagulation (eg, as measured with plasma D-dimer) and th

130 We hypothesized that organ microcirculation coagulation environment predisposes to tumor cell retent

131 excellent selectivity against relevant blood coagulation enzymes and displayed antithrombotic efficac

132 implicated in allosteric networks in related coagulation enzymes.

133 Specifically, through activating coagulation, eoxPL either promoted or inhibited AAA depe

134 t (Endocut Q) or coagulation current (forced coagulation) (Erbe Inc) (secondary intervention and focu

135 wild-type mice triggered rapid intrahepatic coagulation, evidenced by intrahepatic fibrin(ogen) depo

136 F expression were associated with markers of coagulation exacerbation as fibrinogen and D-dimers, and

137 von Willebrand factor multimeric strings and coagulation factor (F) VIII.

138 DIL3 and MFGE8 proteins possess EGF-like and coagulation factor 5/8 (F5/8C) domains, and their 3D str

139 brium dissociation constants (K(d)) for each coagulation factor binding to Nanodiscs with unique comp

140 rates that synergy is effective in promoting coagulation factor binding under physiological lipid com

141 uced rise of factor levels or by infusion of coagulation factor concentrates at the time of delivery.

142 blood coagulation in vivo and the only blood coagulation factor for which a human genetic defect has

143 Prothrombin, or coagulation factor II, is a multidomain zymogen precurso

144 This occurs even if coagulation factor levels are normalized, either due to

145 Here, we show that selective expression of coagulation factor V (FV) by resident peritoneal macroph

146 lia A (AHA) is due to autoantibodies against coagulation factor VIII (FVIII) and most often presents

147 h haemophilia A of all ages with and without coagulation factor VIII (FVIII) inhibitors.

148 Coagulation factor VIII deficient (FVIII(-/-)) mice deve

149 ciated with plasma von Willebrand factor and coagulation factor VIII levels in GWAS, suggesting that

150 closed an important gap in our knowledge of coagulation factor X activation by the intrinsic Xase co

151 otent tick salivary anticoagulant that binds coagulation factor Xa (FXa) and zymogen FX, with formati

152 No adverse side effects were found for coagulation factor XI, apolipoprotein(a), and SCARA5.

153 Coagulation factor XII (FXII) drives production of the i

154 promising solution may be the inhibition of coagulation factor XII (FXII), because its knock-out or

155 (T859A, resulting in p.W268R) which encodes coagulation factor XII (FXII).

156 ce of tissue factor and platelets but not on coagulation factor XII and circulating neutrophils.

157 specifically degrade the human glycoprotein coagulation factor XII and not its deglycosylated form,

158 nvestigate the involvement of tissue factor, coagulation factor XII, platelets, and neutrophils.

159 hesis of selective inhibitors of human blood coagulation factor XIIa and thrombin exhibiting a 1,2,4-

160 Coagulation factor XIII (FXIII) is the main stabilizer o

161 n vitro, adhesion depended on fibrinogen and coagulation factor XIII (FXIII), and supraphysiological

162 The activated form of coagulation factor XIII (FXIII-A2B2), FXIII-A*, is a hem

163 Activated coagulation factor XIIIa (FXIIIa) covalently cross-links

164 Vitamin K activates both hepatic coagulation factors and extrahepatic endothelial anticoa

165 is not currently known if ECs produce other coagulation factors for active participation in coagulat

166 cerning coagulation, the reduced activity of coagulation factors is counterbalanced by an increase in

167 er-specific promoter-1 encoding either human coagulation factors IX (hFIX) or X (hFX) into Macaca fas

168 nderstanding of the roles that platelets and coagulation factors play in atherothrombosis and review

169 We conclude that human ECs produce their own coagulation factors that can activate cell surface FX wi

170 Coagulation factors were analyzed using immunostaining,

171 Coagulation factors were analyzed via immunostaining, en

172 s high-level, and in some cases hyperactive, coagulation factors were employed.

173 the hemostatic system, including platelets, coagulation factors, and regulatory proteins.

174 ng serine protease/endopeptidase inhibitors, coagulation factors, complement proteins, carbonic anhyd

175 electin, and soluble CD40 ligand, as well as coagulation factors, endogenous anticoagulants, and fibr

176 Regarding coagulation factors, factor VIII was higher, whereas pro

177 utant is also activated effectively by other coagulation factors, suggesting that the acidic cluster

178 Elevated expression levels of coagulation factors, von Willebrand factor (vWF), and ti

179 t imposed by flow-mediated washout of active coagulation factors.

180 t or eliminate inhibitory antibodies against coagulation factors.

181 r some of the serine proteases that serve as coagulation factors.

182 nvestigated using lake water collected after coagulation, flocculation, and filtration at pH 6.5 and

183 In this study, coagulation, flocculation, and settling performances wer

184 Hc and platelets, independently of coagulation formed complexes, were shown by antibody blo

185 Like aPC, activated coagulation FVIIa can also bind to EPCR.

186 Despite the faster onset of coagulation, global thrombin levels were unaffected.

187 ntervention, compared with 11% in the forced coagulation group (P = .006).

188 6% in the Endocut group vs 95% in the forced coagulation group) or the proportion of polyps found to

189 cut group and 7.9% of patients in the forced coagulation group, with no significant differences in th

190 Patients with intravascular coagulation had significantly higher peak EVTF activity

191 hed in biological pathways involved in blood coagulation, hemostasis and tissue repair.

192 nregulation of genes involved in metabolism, coagulation, hormone synthesis, and angiogenesis; upregu

193 lution (n = 23 of 40), platelet function and coagulation improved to levels observed in patients with

194 plasma-based assays reveal gC1qR stimulates coagulation in a FXII-dependent manner.

195 is no doubt that activated monocytes trigger coagulation in a tissue factor-dependent manner, it rema

196 ntal thrombosis in mice and suppresses blood coagulation in an extracorporeal membrane oxygenation (E

197 173 occupies an essential role in regulating coagulation in bacterial infections through a mechanism

198 ate the current data on mechanism of altered coagulation in patients with cirrhosis, provide guidance

199 was used to assess their ability to initiate coagulation in plasma.

200 actor (TF) is the primary initiator of blood coagulation in vivo and the only blood coagulation facto

201 s with DIC and VTE (grouped as intravascular coagulation) in HFRS patients.

202 s with DIC and VTE (grouped as intravascular coagulation) in HFRS patients.

203 The calculated coagulation index was hypercoagulable in 50% of patients

204 east 1 in 25,000 individuals and could limit coagulation initiation in undiagnosed individuals with a

205 capture the contribution of endogenous TF to coagulation initiation, the extent to which reduced TF a

206 these multiple and complex effects of SAA on coagulation invite further mechanistic analyses.

207 rior history of HSIL treatment with infrared coagulation (IRC).

208 Activation of coagulation is a hallmark of SCD.

209 Given that coagulation is involved in the thrombus formation stage

210 Blood coagulation is regulated through protein-protein and pro

211 are also compared with the fitting of dimer coagulation, isolation, and coalescence (DCIC) measureme

212 Despite VKOR's pivotal role in coagulation, its structure and active site remain poorly

213 vary proteins which interact with the host's coagulation machinery to facilitate the acquisition and

214 oembolism and the degree of inflammatory and coagulation marker elevation associated with venous thro

215 This study sought to compare changes in coagulation markers associated with short-term oral anti

216 models of thrombosis have demonstrated that coagulation may be enhanced by direct NET-dependent acti

217 critical to unleashing the full potential of coagulation models as tools for drug development and per

218 fied into groups of those with intravascular coagulation (n = 27) and those who did not (n = 61).

219 lar adhesion and resident macrophage-induced coagulation operate independently and cooperatively to m

220 h coatings are effective in preventing blood coagulation or bacterial attachment, but their chain con

221 rhages, bacterial deposition, and markers of coagulation or complement were absent or markedly lower.

222 alysis shows elevated homocysteine, hypoxia, coagulation, Osteoclast differentiation and endochondral

223 quency of organ failures (liver [P = 0.004], coagulation [P < 0.001], kidney [P = 0.004], and respira

224 Coagulation parameters analysed by CCT were outside the

225 It is characterized by individual changes of coagulation parameters and platelets and is aggravated b

226 h liver cirrhosis typically exhibit abnormal coagulation parameters in conventional coagulation tests

227 rrent study investigated early lipidomic and coagulation pathway protein signatures of later PEs in s

228 lower global and specific inhibition of the coagulation pathway than Hp.

229 the rate of clot formation via the intrinsic coagulation pathway.

230 tem activation and prolongation of the blood coagulation pathway.

231 factor-enhanced activation of the intrinsic coagulation pathway; (4) a local, suppressive role of th

232 nriched for platelet degranulation and blood coagulation pathways and the other for complement and im

233 s in vivo crosstalk between inflammation and coagulation pathways, and is a critical vascular checkpo

234 FIX) and extrinsic (tissue factor [TF]-FVII) coagulation pathways, as well as prothrombin.

235 s in robust engagement of the complement and coagulation pathways.

236 An upregulation of genes involved in blood coagulation, platelet activation was characteristic of t

237 amic forces that contribute significantly to coagulation, platelet function and fibrin formation.

238 ed, allowing for the accurate measurement of coagulation, platelets and fibrin content.

239 se that RAGE is involved in modulating blood coagulation presumably in conditions of lung injury.

240 ve shown that NMP liver grafts return better coagulation profiles intraoperatively, which could be at

241 In patients with abnormal coagulation profiles, an increased in vitro clot strengt

242 ion of tissue factor (TF) and the downstream coagulation proteases factor Xa and thrombin significant

243 Targeting individual coagulation proteases induces specific cellular response

244 ncy on FXIa, enhanced selectivity over other coagulation proteases, and a preclinical pharmacokinetic

245 he key protease in thrombus formation, other coagulation proteases, such as fXa (factor Xa) or aPC (a

246 bind human neutrophil elastase or the blood coagulation protein factor IXa.

247 ing process; it activates platelets, cleaves coagulation proteins within feedback loops, and cleaves

248 EC surfaces without the addition of external coagulation proteins, proteolytic enzymes, or phospholip

249 and sQTL variants of critical complement and coagulation regulators.

250 branes, is essential for the amplified blood coagulation response.

251 combination of normal and slightly deranged coagulation screens and FIBTEM results with the absence

252 cal and pathological processes such as blood coagulation, skeletal development, viral infection, cell

253 ronavirus disease 2019 to characterize their coagulation states.

254 Coagulation status was assessed using thromboelastograph

255 unophenotyping, analysis of plasma proteins, coagulation studies, and gene analysis for changes in im

256 A simulated coagulation study has shown that pressure-treated comple

257 ere inflammation (negative association), the coagulation system (negative association), and liver X r

258 The impact of antithrombotic therapy on coagulation system activation after left atrial appendag

259 associated with a significant attenuation of coagulation system activation post-LAAC.

260 ulting chronic inflammation and an activated coagulation system implicated in tumorigenesis.

261 uggested to provide a better overview of the coagulation system in liver cirrhosis.

262 ssociated with an enhanced activation of the coagulation system post-LAAC (144 [48-192] versus 52 [24

263 sis, and inflammation; it also activates the coagulation system through direct interaction with tissu

264 The Coagulation System was affected stronger in CBS(-/-) hum

265 Patients with HFRS have an activated coagulation system with increased risk of disseminated i

266 cting blood to tissues, interacting with the coagulation system, and modulating resistance to blood f

267 ces in these processes, in particular in the Coagulation System, could account for the thrombotic phe

268 romoting cardiovascular instability; and the coagulation system, leading to thromboembolism.

269 tribute to the development of a pathological coagulation system, with resulting chronic inflammation

270 rotein VI on platelets and factor XIa of the coagulation system.

271 elements of the bradykinin, angiotensin and coagulation systems are co-expressed with ACE2 in alveol

272 s associated with dysregulated complement or coagulation systems impact disease, we performed a retro

273 Therefore, the coagulation technique for larger vessels may play a mino

274 Coagulation test screening, including the measurement of

275 thromboelastometry (ROTEM) and conventional coagulation testing in patients with Crimean-Congo haemo

276 ormal coagulation parameters in conventional coagulation tests (CCTs).

277 ally ill patients with deranged conventional coagulation tests are often perceived to have an increas

278 says for platelet, neutrophil functions, and coagulation tests, as well.

279 tometry/platelet aggregometry), conventional coagulation tests, whole blood counts, and platelet flow

280 Concerning coagulation, the reduced activity of coagulation factors

281 r rapid, low-cost, portable testing of blood coagulation time or prothrombin time (PT).

282 RP101075 did not significantly affect coagulation time, bleeding time, heart rate, and blood p

283 Unexpectedly, the primary host initiator of coagulation, tissue factor, was found to be dispensable

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

285 us suturing, cutting, dissection, and vessel coagulation) using an avian tissue model (transfer-test)

286 to compare venous thromboembolism events and coagulation variables in patients requiring venovenous e

287 We showed that specific inhibition of coagulation via direct oral anticoagulants had different

288 ecently, the contact system, which initiates coagulation via the intrinsic pathway, has been implicat

289 has also been reported that RBC-MVs initiate coagulation via the intrinsic pathway.

290 EVTF activity value predicting intravascular coagulation was 0.51 ng/L with 63% sensitivity and 61% s

291 This inhibition of coagulation was accompanied by decreased levels of alani

292 f large colorectal polyps (Endocut vs forced coagulation), we found no difference in risk of serious

293 nd aggregation, and complement activation or coagulation were analyzed.

294 restoring oxygen-carrying capacity (OCC) and coagulation with blood products.

295 leak syndrome and disseminated intravascular coagulation, with a cytokine signature similar to that o

296 nal dysbiosis and impairs liver function and coagulation, with a potential negative impact on HIV/SIV

297 nistically link immune recognition of LPS to coagulation, with implications for the treatment of DIC.

298 PAI-1 mediates post-traumatic malfunction of coagulation, with inhibition or genetic depletion of PAI

299 triggers deep vein thrombosis by activating coagulation, yet its effects on the fibrinolytic system

300 by genetic or pharmacologic reduction of the coagulation zymogen prothrombin in mice.