ライフサイエンスコーパス: blood clotting

1 iates tissue factor induction and subsequent blood clotting.

2 wth by obstructing tumor circulation through blood clotting.

3 depleted protein production and inefficient blood clotting.

4 way inhibitor (TFPI) is a major regulator of blood clotting.

5 uid flow in the regulation of propagation of blood clotting.

6 ments lacking nuclei that play a key role in blood clotting.

7 sed by blood-sucking insects to inhibit host blood clotting.

8 sed inflammation, microvascular density, and blood clotting.

9 ccessful at representing the biochemistry of blood clotting.

10 h those involved in mammalian complement and blood clotting.

11 nd pharmacological role in the modulation of blood clotting.

12 posure of anionic phospholipids that support blood clotting.

13 genic effects on bone, lipid metabolism, and blood clotting.

14 and the mice have no overt abnormalities in blood clotting.

15 enzyme gene (ACE) may be related to abnormal blood clotting.

16 ivity of tissue factor that is distinct from blood clotting.

17 ial for in vivo biological processes such as blood clotting.

18 S) is essential for phagocytic clearance and blood clotting.

19 ed in medical procedures to prevent unwanted blood clotting.

20 ssfrogs has potential implications for human blood clotting.

21 roles in the maintenance of haemostasis via blood clotting.

22 ing to reduced protein function and abnormal blood clotting.

23 ts are anuclear cells that are essential for blood clotting.

24 for designing new antithrombotics disrupting blood clotting.

25 ndent thrombus formation, and agonist-driven blood clotting.

26 , interaction which is central to preventing blood clotting.

27 erto undiscovered, shape that contributes to blood clotting.

28 mechanical regulation of vWF activity during blood clotting.

29 a activation of FV is pivotal for plasma and blood clotting.

30 ctor IX and prolonged human plasma and whole blood clotting.

31 uclear cell fragments that are essential for blood clotting.

32 by partial loss of pigmentation and impaired blood clotting.

33 platelet stimulation and platelet-activated blood clotting.

34 siologic activator of the contact pathway of blood clotting.

35 identified as a regulatory driving force in blood clotting.

36 shown to be a crucial step in the process of blood clotting.

37 These hemo-compatible NPs showed good blood-clotting ability by reducing clotting time (6 min

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

39 During human blood clotting, alpha2-antiplasmin (alpha2AP) becomes co

40 , serving to activate the contact pathway of blood clotting and accelerate factor V activation.

41 ng from cellular signaling and regulation to blood clotting and bacterial pathogenesis.

42 e activation of various proteins involved in blood clotting and bone metabolism.

43 the roles that polyP plays in modulating the blood clotting and complement systems in health and dise

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

45 r events such as ferroptosis, apoptosis, and blood clotting and diseases such as arthritis, diabetes,

46 The importance of factors influencing blood clotting and fibrinolysis in preventing coronary e

47 gulatory actions is its ability to influence blood clotting and fibrinolysis.

48 ns is critical for platelet aggregation upon blood clotting and for leukocyte extravasation to inflam

49 We suggest that the exuberant blood clotting and immune hyper-reaction seen in patient

50 being involved in signalling, vasodilation, blood clotting and immunity and as an intermediate in mi

51 rtant roles in vivo, ranging from regulating blood clotting and inflammation to directly counteractin

52 ear polymers of orthophosphate that modulate blood clotting and inflammation.

53 protein, binds fibrinogen to induce abnormal blood clotting and interferon-induced proteins to evade

54 the rate of mixing, and surface chemistry in blood clotting and its chemical model.

55 by lipopolysaccharide (LPS) induced systemic blood clotting and massive thrombosis in tissues.

56 ny important biological responses, including blood clotting and pain perception.

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

58 Furthermore, anomalous blood clotting and structural changes in blood component

59 pread endothelial damage, complement-induced blood clotting and systemic microangiopathy - in disease

60 s may exhibit unique properties analogous to blood clotting and thereby be useful in self-healing app

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

62 lation reverses the prometastatic effects of blood clotting and tumor cell integrin alphavbeta3.

63 eosinophils, mast cells, mononuclear cells), blood clotting, and microvascular density within the tum

64 f the VKOR gene extends our understanding of blood clotting, and should facilitate development of new

65 ogical processes, including viral infection, blood clotting, and signal transduction, and as such, th

66 ed release of drugs for cancer therapy, anti-blood clotting, and the design of autonomous insulin-del

67 omposition changes, with clinical metrics of blood clotting, and with the sharp transition between mi

68 o physiological processes such as digestion, blood clotting, and wound healing.

69 extracellular processes such as virus entry, blood clotting, antibody-mediated immune response, infla

70 Substances released by platelets during blood clotting are essential participants in events that

71 generated in a tissue factor-initiated whole blood clotting assay unless exogenous FV was added, cons

72 n by in vitro fluorogenic activity and whole blood clotting assays.

73 CPC capacitance response to blood clotting at 1.3 MHz provided three sensing paramet

74 Blood clotting at the vascular injury site is a complex

75 Blood clotting at wound sites is critical for preventing

76 and has roles in platelet activation during blood clotting, bone formation and T cell activation.

77 ons to hemostasis appear to be to accelerate blood clotting but are not required for blood clotting t

78 a potent hemostatic regulator, accelerating blood clotting by activating the contact pathway and pro

79 owed that fibrin(ogen) polymerisation during blood clotting can be affected strongly by LPS.

80 ted allosteric enzyme involved in vertebrate blood clotting, can be converted into a K+-specific enzy

81 integral membrane protein that triggers the blood clotting cascade and for which membrane anchoring

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

83 , the cell-surface protein that triggers the blood clotting cascade in hemostasis and thrombotic dise

84 The blood clotting cascade is selectively involved in lung m

85 ension, dyslipidemia, and alterations of the blood clotting cascade that accentuate thrombosis.

86 ctor VIII (FVIII), an important co-factor in blood clotting cascade, elicits unwanted anti-FVIII anti

87 our cascades are: the complement system, the blood clotting cascade, the fibrinolytic system, and the

88 mbin is a dual action serine protease in the blood clotting cascade.

89 hat is exposed upon injury and initiates the blood clotting cascade.

90 iginally well characterized in the mammalian blood clotting cascade.

91 ptidomimetic drugs such as inhibitors of the blood clotting cascade.

92 malian serpin antithrombin in localizing the blood-clotting cascade, suggesting that serpin inhibitio

93 n is a dual-action protein that mediates the blood-clotting cascade.

94 erations in physiological pathways including blood clotting cascades (seminal plasma) and both actin

95 ty of 4% to 20% of normal and improved whole blood clotting compared with factor VIII-deficient mice.

96 ecretory pathway (receptors, growth factors, blood-clotting components, and even many viral envelope

97 s of inverse lag times and maximal slopes of blood clotting curves in buffers containing Na+ and Cl-

98 polyphosphate exerts differential effects on blood clotting, depending on polymer length.

99 ase is widely recognized to be a form of the blood clotting disorder hemophilia, its molecular basis

100 Two genes implicated in blood-clotting disorders, von Willebrand factor (vWA) an

101 lasminogen activator widely used in treating blood-clotting disorders.

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

103 Structures of the blood clotting enzyme thrombin complexed with hirugen an

104 dividual biological components contribute to blood clotting events in the presence of influenza infec

105 Early detection of such blood clotting events is crucial for timely intervention

106 e propose a framework for early detection of blood clotting events utilizing a deep neural network mo

107 py has the potential to maintain therapeutic blood clotting factor IX (FIX) levels in patients with h

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

109 ed by peptides of +3 to +5 net charge and by blood clotting factor V.

110 idues (gamma-carboxyglutamic acid domain) of blood clotting factor VII was carried out to identify si

111 Active site-inhibited blood clotting factor VIIa (fVIIai) binds to tissue fact

112 Blood clotting factor VIIa is involved in the first step

113 Hemophilia A is a monogenic disease with a blood clotting factor VIII (FVIII) deficiency caused by

114 VWF also is a carrier protein for blood clotting factor VIII, and this interaction is requ

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

116 s covalently linked to fibrin when activated blood clotting factor XIII (FXIIIa) catalyzes the format

117 he basis of orthologs of genes for mammalian blood clotting factors being present in its genome.

118 ified factor VIIa and to active site-blocked blood clotting factors Xa or IXa was studied.

119 ential for efficient bloodmeals such as anti-blood clotting factors, exhibits circadian expression.

120 amin K cycle, activating vitamin K-dependent blood clotting factors.

121 e lectins and to membrane-binding domains of blood-clotting factors V and VIII.

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

123 here complement the current understanding of blood clotting from the molecular to the physiological l

124 rge in patients, among whom the incidence of blood clotting has been observed.

125 Also, the blood-clotting, hemolytic, antioxidant, bactericidal and

126 telets are known primarily for their role in blood clotting; however, it is becoming clear that they

127 e to release tryptase, and thrombin mediates blood clotting in early wounds.

128 K epoxide reductase, a protein required for blood clotting in humans, as part of a disulfide bond fo

129 ompted by previous observations of defective blood clotting in rabbits deficient in the sixth compone

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

131 the spatiotemporal dynamics of initiation of blood clotting in the complex network of hemostasis.

132 The extensive blood clotting in the eotaxin-transfected tumors was ass

133 n of SNs to the hydrogels facilitated faster blood clotting in vitro without increasing hemolysis.

134 long been considered dispensable for normal blood clotting in vivo because hereditary deficiencies i

135 Blood clotting in vivo is catalyzed by thrombin, which s

136 egrates the key components in the process of blood clotting, including hemodynamics, transport of coa

137 wound healing is a complex process involving blood clotting, inflammation, migration of keratinocytes

138 Systems as varied as blood clotting, intracellular calcium signaling, and tis

139 Hemostasis and thrombosis (blood clotting) involve fibrinogen binding to integrin a

140 Mammalian blood clotting involves numerous components, most of whi

141 Pathologic blood clotting is a leading cause of morbidity and morta

142 phosphate (S1P) released by platelets during blood clotting is a potent, specific, and selective endo

143 Blood clotting is a process by which a haemostatic plug

144 Our data reveal that blood clotting is the major cause of host death followin

145 Blood clotting is triggered in hemostasis and thrombosis

146 Thrombosis, or malignant blood clotting, is associated with numerous cardiovascul

147 Tissue factor, the physiologic trigger of blood clotting, is the membrane-anchored protein cofacto

148 o a cohesive modelling framework to show how blood clotting may be connected to influenza virus infec

149 expression of the principal initiator of the blood clotting mechanism, tissue factor (TF), and blocki

150 such as dyslipidemia, oxidative stress, and blood clotting mechanisms, we hereby report the synthesi

151 For blood clotting on collagen/tissue factor (1 TF-molecule/

152 suggest that the previously noted effects of blood clotting on lung metastasis might be mediated in p

153 ding vasoconstriction, platelet aggregation, blood clotting, pain, and itching.

154 vity and inhibit activators of the intrinsic blood clotting pathway, such as polyphosphate (polyP) an

155 unexplored problem, despite applications in blood clotting, plasmonics, industrial packaging and tra

156 rich in bioactive compounds that counteract blood clotting, platelet aggregation, complement activat

157 from inverse lag times and maximal slopes of blood clotting plots, which are also anion and cation de

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

159 ed plasma levels of FVIII and restoration of blood clotting properties in a dose-dependent manor for

160 he expression of a cellular receptor for the blood-clotting protease factor Xa, designated effector c

161 reas the second version is responsive to the blood-clotting protease, thrombin.

162 serpin, antithrombin, to inhibit its target blood-clotting proteases by generating new protease inte

163 is an X-linked bleeding disorder caused by a blood clotting protein factor VIII deficiency.

164 significantly elevated circulating levels of blood clotting protein fibrin(ogen).

165 Here, Petersen et al. (2017) show that the blood clotting protein fibrinogen inhibits nerve repair

166 t the worms are capable of cleaving the host blood clotting protein fibronectin and that this activit

167 The blood-clotting protein fibrinogen has been implicated in

168 Proteolysis of the blood-clotting protein von Willebrand factor (VWF) obser

169 Here, we show that fibrinogen, a blood-clotting protein, plays a central role in impairin

170 n; 5) assess the role of insulin resistance, blood clotting, protein kinase C isoforms, and signal tr

171 in addition to its known role in regulating blood clotting, protein S may also be an important autoc

172 Exosite I of the blood clotting proteinase, thrombin, mediates interactio

173 in activates the primary serpin inhibitor of blood clotting proteinases, antithrombin, both by an all

174 49 of antithrombin, the primary inhibitor of blood clotting proteinases, has previously been implicat

175 antithrombin, the principal inhibitor of the blood-clotting proteinases factor Xa and thrombin, is ac

176 ontaining regions of the vitamin K-dependent blood-clotting proteins.

177 ing of many protein-lipid interactions among blood-clotting proteins.

178 onal assays, such as endotoxin-induced whole blood clotting, prothrombin time, as well as factor X an

179 platelets is very efficient at accelerating blood clotting reactions but is less efficient at initia

180 mechanisms by which polyphosphate modulates blood clotting reactions remain to be elucidated.

181 e platelet aggregation, vasoconstriction and blood clotting; saliva of these organisms also has anti-

182 ny of these biomolecules inhibit the central blood-clotting serine proteinase thrombin that is also t

183 activation, and phosphatidylserine exposure, blood clotting simulations require prediction of platele

184 ndividuals who participated in the Genes and Blood Clotting Study (GABC) or the Trinity Student Study

185 these responses lead to profound defects in blood clotting, such as disseminated intravascular coagu

186 onse to infection includes activation of the blood clotting system, leading to extravascular fibrin d

187 tion of thrombin, which enhances the overall blood-clotting system, both by accelerating fibrin gener

188 ry agent and a potent modulator of the human blood-clotting system.

189 SNPs initiate the contact pathway of the blood-clotting system; short-chain polyP accelerates the

190 tamin K2 is a critical nutrient required for blood clotting that also plays an important role in bone

191 h nonspecific binding and adverse effects on blood clotting that limit their use.

192 sphate, and when activated, platelets induce blood clotting (the first step in wound healing) in part

193 role, including the ectoenzyme that triggers blood clotting, the plasma serine protease, factor VIIa,

194 rin alpha(IIb)beta3 initiates the process of blood clotting through binding fibrinogen.

195 ied inflammasome activation as a trigger for blood clotting through pyroptosis.

196 fficacy was based on correction of the whole blood clotting time (WBCT) at multiple timepoints over 2

197 to 2.5 months and normalization of the whole blood clotting time (WBCT) for about a month.

198 njury in HemA mice, and fully corrects whole blood clotting time (WBCT) in HemA dogs immediately afte

199 ing times were half that of the manual whole blood clotting time (WBCT, legacy method) and exhibited

200 Coagulation tests (whole blood clotting time [WBCT], activated clotting time [ACT

201 Whole blood clotting time analysis confirmed that hemostasis w

202 st, siRNA-mediated knockdown of KLF2 reduced blood clotting time and flow rates.

203 rombin time, partial correction of the whole blood clotting time and thromboelastography parameters,

204 Despite normalization of blood clotting time and thrombus stability after r-FVIII

205 se-dependent partial correction of the whole blood clotting time and, at higher doses, of the activat

206 nfected cells, KLF2 overexpression increased blood clotting time as well as flow rates under basal an

207 Whole blood clotting time in FIX-deficient mice was corrected

208 unction were normal; however, when the whole blood clotting time was measured at 25 degrees C in plas

209 sed onto a factor VIIInull background, whole blood clotting time was partially corrected, equivalent

210 Whole-blood clotting times and FeCl3 carotid artery injury cor

211 Activated clotting times and whole blood clotting times were normalized, activated partial

212 creased levels of liver function enzymes and blood clotting times, decreased levels of platelets, mul

213 rate blood clotting but are not required for blood clotting to happen.

214 Willebrand factor receptor, functions during blood clotting to promote platelet adhesion and activati

215 that the threshold response of initiation of blood clotting to the size of a patch of stimulus is a r

216 nd tortuous arteriolar vessels would analyze blood clotting under flow, while requiring a small blood

217 ial phosphatidylserine (PS) in apoptosis and blood clotting using annexin V.

218 rnover, deubiquitination, tissue remodeling, blood clotting, virulence, defense, and cell wall remode

219 ther design, thrombin, an enzyme involved in blood clotting, was captured by thrombin-AR-modified cel

220 Here, inspired by blood clotting, we show that polymer-colloid composite a

221 ries of biochemical reactions that initiates blood clotting when plasma factors XII (FXII) and XI (FX

222 acial fluids such as whole blood and promote blood clotting, while the infused liquids facilitate int

223 arteriolar vessels, permitting evaluation of blood clotting within small sample volumes under pathoph

224 MV-dependent plasmatic coagulation and whole blood clotting without affecting thrombocyte aggregation