ライフサイエンスコーパス: clotting factor

1 with hemophilia who have antibodies to human clotting factor.

2 the development of neutralizing Ab's to the clotting factor.

3 ic delivery of proteins such as hormones and clotting factors.

4 d some mice developed autoantibodies against clotting factors.

5 of therapeutic proteins such as hormones and clotting factors.

6 es blood products such as factor VIII and IX clotting factors.

7 oteins, including CR/regulatory proteins and clotting factors.

8 ion of a small number of proteins, including clotting factors.

9 nerals, and synthesizing plasma proteins and clotting factors.

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

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

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

13 lational modification of vitamin K-dependent clotting factors.

14 for the gamma-glutamyl carboxylation of many clotting factors.

15 understanding and engineering of artificial clotting factors.

16 cycle, phase I and II metabolic enzymes, and clotting factors.

17 hage, soft clot dissolution, and dilution of clotting factors.

18 evelopment through complex interactions with clotting factors.

19 oteins, blood pressure, glycemic status, and clotting factors.

20 nce of thrombin in combination with cellular clotting factors.

21 een porcine coagulation proteins and primate clotting factors.

22 ontact with the maternal circulation and its clotting factors.

23 e find that murine deficiency of prothrombin clotting factor 2 (Cf2) was associated with the death of

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

25 In contrast, although clotting factor activation was seen in the blood of CM p

26 ble and persistent expression of circulating clotting factor activity, associated with decreased clin

27 ween 2000 and 2010 and collected data on all clotting-factor administration for up to 75 exposure day

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

29 We measured endothelium-derived clotting factors and assayed platelet aggregation in 64

30 scular disease include effects on platelets, clotting factors and endothelium.

31 inding to thrombin and are relevant to other clotting factors and enzymes allosterically activated by

32 patients who develop inhibitors to deficient clotting factors and in whom bypassing agents are requir

33 mapheresis was utilized to replace deficient clotting factors and mitigate the inflammatory response.

34 mbosis in the context of intact vasculature, clotting factors, and blood cells.

35 s (LSECs), hepatocytes, scavenger receptors, clotting factors, and immunoglobulins were analyzed.

36 C virus treatment response, plasma levels of clotting factors, and late-onset Alzheimer disease, has

37 e inhibition of thrombin and other activated clotting factors, antithrombin may also down-regulate th

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

39 er, but it does not disrupt hemostasis until clotting factors are completely depleted, at an 8-fold h

40 at EC surface expression of TF and extrinsic clotting factors are critical in augmenting capillary le

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

42 In general, deficiency of clotting factors as a result of poor hepatic synthetic f

43 ved the FVIII inhibitory effect of HA IgG in clotting factor assays.

44 II expressed poor FVIII cofactor activity in clotting factor assays.

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

46 is of orthologs of genes for mammalian blood clotting factors being present in its genome.

47 itory antibodies, replacement of the missing clotting factor by infusion of factor VIII becomes less

48 genase, alpha toxin (LH2/PLAT); (iv) Limulus clotting factor C, Coch-5b2 and Lgl1 (LCCL).

49 atients with AH, which included hepatokines, clotting factors, complement cascade components, and hep

50 rs, who received prior bypassing agent (BPA)/clotting factor concentrate (CFC) prophylaxis.

51 nhibitors and with documented treatment with clotting factor concentrate in the 24 weeks before scree

52 p 4 contained patients who received previous clotting factor concentrate prophylaxis or on-demand tre

53 ve fitusiran prophylaxis (n=80) or on-demand clotting factor concentrates (n=40).

54 alised bleeding rate compared with on-demand clotting factor concentrates and no bleeding events in a

55 th inherited bleeding disorders who received clotting factor concentrates before 1987 have high rates

56 axis once per month or to continue on-demand clotting factor concentrates for a total of 9 months.

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

58 (3.1 [95% CI 2.3-4.3]) than in the on-demand clotting factor concentrates group (31.0 [21.1-45.5]; ra

59 and five (13%) participants in the on-demand clotting factor concentrates group (gastroenteritis, pne

60 two (5%) of 40 participants in the on-demand clotting factor concentrates group.

61 ipants) was the most common in the on-demand clotting factor concentrates group.

62 up and 7.8 months (7.8-7.8) in the on-demand clotting factor concentrates group.

63 n group and 21.8 (8.4-41.0) in the on-demand clotting factor concentrates group.

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

65 atment mainly consists of the transfusion of clotting factor concentrates prepared from human blood o

66 increasing risk of HCV, particularly before clotting factor concentrates were licensed in the 1970s.

67 In this randomized clinical trial, clotting factor concentrates were not superior to FP for

68 These samples were supplemented with clotting factor concentrates, procoagulant lipid vesicle

69 odeficiency virus, and viral inactivation of clotting factor concentrates, were needed to reduce tran

70 o had previously been treated on-demand with clotting factor concentrates, were randomly assigned in

71 sion of either recombinant or plasma-derived clotting factor concentrates.

72 emophilia can experience from treatment with clotting factor concentrates.

73 cute bleeding consists of the transfusion of clotting-factor concentrates prepared from human blood a

74 and from blood products (factor VIII and IX clotting-factor concentrates, immunoglobulin preparation

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

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

77 ormation may occur in the treatment of other clotting factor deficiencies (eg, against von Willebrand

78 es arise when a patient who has a congenital clotting factor deficiency is infused with a blood produ

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

80 nsfusion of blood products in the setting of clotting factor deficiency or inhibition, platelet defic

81 f platelets, has the advantage of delivering clotting factors directly to the site of an injury, wher

82 ubstituting for the procoagulant function of clotting factors (eg, emicizumab) or targeting the natur

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

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

85 e involvement of GATA-4 in the regulation of clotting factor expression.

86 ive oxygen species (ROS) levels, influencing clotting factor expression.

87 Thrombin, an important clotting factor, extravasates at sites of blood-retina b

88 Here, we report that the clotting factor fibrin is a critical regulator of neutro

89 Blood levels of the clotting factor fibrinogen and tissue plasminogen activa

90 he binding of bacteria to ECM components and clotting factors (fibronectin and fibrinogen, respective

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

92 ther vertebrates, even though genes for some clotting factors found in mammals are absent and some ot

93 lotting factor, promote rapid clearance of a clotting factor from the blood, or alter the clotting fa

94 lucanases from two species of bacteria and a clotting factor from the horseshoe crab.

95 Nonspecific interference by E-FVIII in clotting factor function was not evident.

96 romosome 13 of the fetal genome and contains clotting factor genes PROZ, F7, and F10.

97 Notably, mRNA levels of several clotting factor genes, including coagulation factor 5 (f

98 eceive no prophylaxis and continue on-demand clotting factor (group 1) or concizumab prophylaxis (gro

99 Antithrombotic and clotting factors have long been targets for drug discove

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

101 g coagulopathy by depleting a tumor-produced clotting factor improves survival of tumor-bearing flies

102 clotting factor from the blood, or alter the clotting factor in such a way that the protein-antibody

103 r control windows, controlling for levels of clotting factor in the blood.

104 ustained expression of therapeutic levels of clotting factors in small animals, and some of these str

105 Factor XIII and fibrinogen are unusual among clotting factors in that neither is a serine protease.

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

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

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

109 Acidosis impaired coagulation by depleting clotting factors, inhibiting thrombin generation, and af

110 We have generated a mouse where the clotting factor IX (FIX) gene has been disrupted by homo

111 the potential to maintain therapeutic blood clotting factor IX (FIX) levels in patients with hemophi

112 bleeding disorder caused by a deficiency of clotting factor IX (FIX).

113 l fully gamma-carboxylated recombinant human clotting factor IX (r-hFIX), cell lines stably overexpre

114 tion of mice with AAV vectors encoding human clotting factor IX after gamma-irradiation resulted in s

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

116 resulted in synthesis of low levels of human clotting factor IX for the 5-month period of observation

117 Mice generated by disrupting the clotting factor IX gene exhibit severe bleeding disorder

118 a structure identical to that found on human clotting factor IX: Sia-alpha2,3-Gal-beta1, 4-GlcNAc-bet

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

120 nctional activity of the vitamin K-dependent clotting factors IX, X, and prothrombin.

121 For every 1% increase in clotting factor level, bleeding incidence was lower by 2

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

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

124 ms that might have a reduced set of the many clotting factors observed in higher vertebrates.

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

126 erally associated with deficiencies of other clotting factors, our findings demonstrate the primary r

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

128 ell lines overexpressing vitamin K-dependent clotting factors produce only a fraction of the recombin

129 hese antibodies may neutralize function of a clotting factor, promote rapid clearance of a clotting f

130 idrug antibodies (ADAs) may form against the clotting factor protein drugs used in replacement therap

131 atic control without exposure to immunogenic clotting factor proteins.

132 ibodies that inhibit the function of infused clotting factor remains a major challenge and is conside

133 lotting factor VIII (FVIII) DNA would ensure clotting factor replacement at constant circulating leve

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

135 HA consists of preventing joint bleeding by clotting factor replacement, and in extreme cases, ortho

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

137 progresses despite standard intravenous (IV) clotting factor replacement.

138 ticularly strategies to prolong half-life of clotting factor replacements, the management of inhibito

139 peptide sequences of the vitamin K-dependent clotting factors serve as a recognition site for the enz

140 Experiments using purified clotting factors showed that heparin enhanced by fourfol

141 onsists of the administration of recombinant clotting factors, such as factor VIII (FVIII).

142 , and gene therapies that facilitate in vivo clotting factor synthesis.

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

144 es prepared from human blood and recombinant clotting factors that are currently in clinical trials.

145 Similar to other clotting factors, thrombin is mainly present in the bloo

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

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

148 Clotting factor transfusions are vital for people with d

149 no-associated viral (AAV) vectors delivering clotting factor transgenes into hepatocytes has shown mu

150 n, coagulopathy types and severity, types of clotting factor treatment, and sex were not associated w

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

152 metabolism (hepatic lipase, APOE, PON1) and clotting (factor V Leiden, fibrinogen).

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

154 ins and to membrane-binding domains of blood-clotting factors V and VIII.

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

156 dial lipids, glucose, insulin, and activated clotting factor VII (FVIIa) concentrations.

157 e cellular receptor for an activated form of clotting factor VII (VIIa) and the binding of factor VII

158 (gamma-carboxyglutamic acid domain) of blood clotting factor VII was carried out to identify sites th

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

160 Extracellular interactions of plasma clotting factor VIIa (FVIIa) with tissue factor (TF) on

161 sue factor (TF) is the cellular receptor for clotting factor VIIa (FVIIa), and the formation of TF-FV

162 actor (TF), the cellular receptor for plasma clotting factor VIIa (FVIIa).

163 sue factor (TF) is the cellular receptor for clotting factor VIIa (FVIIa).

164 Active site-inhibited blood clotting factor VIIa (fVIIai) binds to tissue factor (TF

165 Blood clotting factor VIIa is involved in the first step of th

166 tissue factor (TF), a cellular receptor for clotting factor VIIa.

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

168 ophilia, as continuous expression of donated clotting factor VIII (FVIII) DNA would ensure clotting f

169 ed disorders caused by lack or deficiency of clotting factor VIII (FVIII) or IX (FIX), respectively.

170 epatocytes to express B domain deleted (BDD) clotting factor VIII (FVIII) to permit viral encapsidati

171 bleeding disorder caused by a deficiency in clotting factor VIII (FVIII).

172 Since 1984, unheated porcine clotting factor VIII (Hyate:C) has been used to treat se

173 Clotting factor VIII activity increased significantly du

174 ent 1+2, and soluble P-selectin and also for clotting factor VIII and the thrombin generation potenti

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

176 VWF also is a carrier protein for blood clotting factor VIII, and this interaction is required f

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

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

179 platelet copper, glutathione peroxidase, and clotting factor VIII.

180 ing disorders resulting from deficiencies in clotting factors VIII (haemophilia A) and IX (haemophili

181 on studies as well as pro- and anticoagulant clotting factors were measured.

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

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

184 Bioengineered clotting factors with enhanced pharmacokinetic profiles

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

186 ers of Kupffer cells and LSECs, the level of clotting factor X, and hepatocyte infectibility did not

187 The cDNA encoding clotting factor X, which participates in the middle stag

188 the epidermal growth factor (EGF) domain of clotting Factor X.

189 ant (CP), a cysteine protease that activates clotting factor X.

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

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

192 Clotting factor XII (Hageman factor) contains epidermal

193 Taken together, these data (i) confirm that clotting factor XII functions as a mitogenic growth fact

194 lently linked to fibrin when activated blood clotting factor XIII (FXIIIa) catalyzes the formation of