ライフサイエンスコーパス: aPTT

1 aPTTs were collected 6, 12, and 24 hours after thromboly

2 rison, the coagulation times of the acoustic aPTT and PiCT yielded an excellent correlation with the

3 Finally, the acoustic aPTT assay is the ''gold standard'' for a dose administr

4 The antibody-activated aPTT allows for standardization of particulate aPTT reag

5 Before drug administration, ACTs, aPTTs, and hemodynamics were similar among the groups.

6 in were significantly more likely to have an aPTT measurement in the target range (P < .0001).

7 en glycosidase-treated FV was analyzed in an aPTT (activated partial thromboplastin time)-based APC s

8 ected by routine clinical evaluation with an aPTT assay.

9 The ACT and aPTT are sensitive to IV dalteparin at clinically releva

10 and 30 minutes after drug infusion, ACT and aPTT were slightly higher in those receiving rPF4, but t

11 After plasma transfusion, the median INR and aPTT changes were -0.2 and -5, respectively.

12 of a year in the three animals studied, and aPTT mixing studies showed no evidence for neutralizing

13 lant activity in an in vitro clotting assay (aPTT EC1.5x = 0.27 muM) and excellent selectivity agains

14 Although the relationship between aPTT and clinical outcome was confounded to some degree

15 ticoagulant activity measured by whole blood aPTT.

16 Both aPTT and anti-factor Xa increased with escalating doses

17 had weak anticoagulant activities as seen by aPTT and inhibitory assays using purified cofactors.

18 ence of baseline prognostic characteristics, aPTTs higher than 70 seconds were found to be associated

19 icient plasma when assessed by the classical aPTT coagulation assay.

20 For aPTT we report for the first time that a QCM-D (Quartz C

21 For aPTT, previously reported associations with KNG1, HRG, F

22 identified a new independent association for aPTT in F5 (rs2239852, P-value = 1.9 x 10(-8)), which cl

23 reliable than the standard coagulometer for aPTT range of upper limits of coagulation times.

24 The GWAS for aPTT was conducted in 9,240 individuals of European ance

25 d meta-analysis to identify genetic loci for aPTT and PT.

26 tudy (GWAS) has been reported previously for aPTT, but no GWAS has been reported for PT.

27 s that have not been previously reported for aPTT.

28 onducted a genome-wide association study for aPTT and identified significant associations with SNPs i

29 We conducted a genetic association study for aPTT in 9719 EAs and 2799 AAs from the Atherosclerosis R

30 Markedly high aPTTs were associated with increased risk of TIMI major

31 Markedly high aPTTs were more likely in patients who were older (adjus

32 Higher aPTT at 24 hours was strongly related to lower patient w

33 The present study aimed to identify aPTT-related gene variants in both European Americans (E

34 m has the potential to significantly improve aPTT control of intravenous heparin compared with curren

35 unt for approximately 29% of the variance in aPTT and two loci that account for approximately 14% of

36 approximately 18% of phenotypic variance in aPTT in the Lothian Birth Cohorts.

37 e, and 11 studies used a range that included aPTT values 1.5 times the control value.

38 Genetic factors influencing aPTT are not well understood, especially in populations

39 d a fibrin-specific lytic and had an initial aPTT drawn within 4 to 8 hours of starting therapy.

40 to recommended dosing, only 33.8% of initial aPTTs were therapeutic (1.50 to 2.00 times control); 13.

41 rs (odds ratio, 2.11; P=0.004); markedly low aPTTs tended to be associated with increased risk of fat

42 hrombosis was higher in patients with a mean aPTT of less than or equal to 50 seconds (odds ratio, 1.

43 rol value are subtherapeutic for most modern aPTT reagents.

44 r IX resulted in normalization of a modified aPTT in mouse plasma.

45 Most aPTT values were above therapeutic range or beyond measu

46 rombin (for anti-Xa), and baseline levels of aPTT and ACT, respectively.

47 ted in concentration-related prolongation of aPTT and decreased FXI clotting activity.

48 TT allows for standardization of particulate aPTT reagents and for sensitive monitoring of coagulatio

49 Of the 344 end-point aPTT measurements, 78% were within +/-10 seconds of the

50 NP antibodies prolonged aPTT compared to control tissue antibodies at 400 ug/mL

51 ion with evidence of coagulopathy (prolonged aPTT and INR, decreased platelet count), hepatic injury

52 d the viability at concentrations prolonging aPTT, while at higher concentrations their cytotoxicity

53 ticoagulation than that of dabigatran in PT, aPTT, and TT assays.

54 LT, cholesterol, triglyceride, HDL, LDL, PT, aPTT, INR, HbA1C, and CRP within all groups were signifi

55 icted massive RBC transfusion better than PT/aPTT or INR (P < 0.001).

56 This is the first study to report aPTT-related genetic variants in AAs.

57 /h, with dose adjustment to achieve a target aPTT of 60 to 85 seconds.

58 The time to achieve a target aPTT was 93 minutes without and 150 minutes with an init

59 usted the heparin infusion to reach a target aPTT.

60 The aPTT levels in the OHEP/SNAC group peaked at 30 minutes

61 The aPTT, anti-Xa and anti-IIa activities, and TFPI concentr

62 al and analyzed the relationship between the aPTT and both baseline patient characteristics and clini

63 n unexpected direct relationship between the aPTT and the risk of subsequent reinfarction.

64 til proven otherwise, we should consider the aPTT range of 50 to 70 seconds as optimal with intraveno

65 At 12 hours, the aPTT associated with the lowest 30-day mortality, stroke

66 By contrast, prolongation of the aPTT requires neither antithrombin nor heparin cofactor

67 in-antithrombin reaction and may prolong the aPTT by interfering with activation of factor VIII, ther

68 ar with heparin dose and correlates with the aPTT value (Pearson's r = 0.99).

69 h the activated partial thromboplastin time (aPTT) (r = 0.99).

70 i-Xa, activated partial thromboplastin time (aPTT) and activated clotting time (ACT); (2) other facto

71 The activated partial thromboplastin time (aPTT) and anti-factor X (anti-Xa) levels were measured.

72 Activated partial thromboplastin time (aPTT) and prothrombin time (PT) are clinical tests commo

73 o the activated partial thromboplastin time (aPTT) as well as the activated clotting time (ACT).

74 in an activated partial thromboplastin time (aPTT) assay and was activated by factor XIa more slowly

75 y the activated partial thromboplastin time (aPTT) assay.

76 ty in activated partial thromboplastin time (aPTT) assays.

77 on of activated partial thromboplastin time (aPTT) before and after the treatment.

78 stage activated partial thromboplastin time (aPTT) clotting assay (36% +/- 9.6% of FVIII WT) and a va

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

80 d the activated partial thromboplastin time (aPTT) in 29,656 patients in the Global Utilization of St

81 duced activated partial thromboplastin time (aPTT) is a risk marker for incident and recurrent venous

82 Activated partial thromboplastin time (aPTT) is associated with risk of thrombosis and coagulat

83 ified activated partial thromboplastin time (aPTT) measured on an optical-mechanical coagulometer.

84 ) and activated partial thromboplastin time (aPTT) obtained before elective surgery with initial PT a

85 arget activated partial thromboplastin time (aPTT) of 55 to 85 seconds and were administered for 96 h

86 lets, activated partial thromboplastin time (aPTT) reagent and prothrombin time reagent and reduces t

87 f the activated partial thromboplastin time (aPTT) therapeutic range is required to ensure administra

88 ) and activated partial thromboplastin time (aPTT) values were 1.5 and 48, respectively.

89 with activated partial thromboplastin time (aPTT) was tested for the top SNPs.

90 d the activated partial thromboplastin time (aPTT) when added to normal plasma, and alter the kinetic

91 f the activated partial thromboplastin time (aPTT), and that injection of 10(11) particles of an aden

92 ECT), activated partial thromboplastin time (aPTT), and thrombin time (TT) were secondary endpoints a

93 es in activated partial thromboplastin time (aPTT), anti-factors IIa and Xa, and tissue factor pathwa

94 (PT)/activated partial thromboplastin time (aPTT), international normalized ratio (INR), platelet co

95 f the activated partial thromboplastin time (aPTT), over controls (P < 0.05).

96 ron), activated partial thromboplastin time (aPTT), plasma anti-Xa and anti-IIa levels, tissue factor

97 (PT), activated partial thromboplastin time (aPTT), thrombin time (TT), as well as thrombin generatio

98 s for activated partial thromboplastin time (aPTT).

99 ) and activated partial thromboplastin time (aPTT).

100 , and activated partial thromboplastin time [aPTT]) have remained at the upper limits of the normal r

101 y ''activated Partial Thromboplastin Time'' (aPTT) and ''Prothrombinase complex-induced Clotting Test

102 ving activated partial thromboplastin times (aPTTs) within a range of 55 to 85 seconds in recent tria

103 ored activated partial thromboplastin times (aPTTs).

104 ction to less than 30 000 U/d in response to aPTT results.

105 Only 3 studies used a validated aPTT therapeutic range, and 11 studies used a range that

106 R(2)=0.98 in calibration curves) along with aPTT from frequency and dissipation shifts together in a

107 rs710446 and rs4253417) also associated with aPTT.

108 Anti-Xa, aPTT, and ACT all showed good discrimination between UFH

109 urred in anti-factor IIa and anti-factor Xa. aPTT rose from 28+/-0.5 to 42.2+/-6.3 seconds 2 hours af