ライフサイエンスコーパス: clotting factor

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

2 with hemophilia who have antibodies to human clotting factor.

3 of therapeutic proteins such as hormones and clotting factors.

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

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

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

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

8 lational modification of vitamin K-dependent clotting factors.

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

10 understanding and engineering of artificial clotting factors.

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

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

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

14 nce of thrombin in combination with cellular clotting factors.

15 een porcine coagulation proteins and primate clotting factors.

16 ontact with the maternal circulation and its clotting factors.

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

18 d some mice developed autoantibodies against clotting factors.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

47 emophilia can experience from treatment with clotting factor concentrates.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 Clotting factor transfusions are vital for people with d

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

119 Clotting factor VIII activity increased significantly du

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

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

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

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

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

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

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

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

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

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

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

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

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

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

134 Clotting factor XII (Hageman factor) contains epidermal

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

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