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1 fibrinogen depletion, and elevated levels of thrombin-antithrombin complexes).
2 easing baseline prothrombin fragment 1.2 and thrombin-antithrombin complex.
3 higher baseline prothrombin fragment 1.2 or thrombin-antithrombin complex.
4 role in the recognition and clearance of the thrombin-antithrombin complex.
5 ating levels of prothrombin fragment 1+2 and thrombin-antithrombin complexes.
6 e was no difference in levels of circulating thrombin-antithrombin complexes.
7 ble occlusion times and comparable levels of thrombin.antithrombin complexes.
8 ombin fragment 1.2 (F1.2) (1.36-2.4 microM), thrombin-antithrombin complex (14.5-50 microg/L), and D-
9 oup had increased local thrombin generation (thrombin antithrombin complex: 8.5 +/- 7.6 ng/ml to 33.2
10 aric and normobaric exposure was 0 ng/mL for thrombin-antithrombin complex (95% CI, -0.30 to 0.30 ng/
11 hat native clotting times were shortened and thrombin-antithrombin complex and soluble CD40 ligand le
12 e parallel with dramatic increases in plasma thrombin-antithrombin complex and tissue factor levels.
13 it exchange were less frequent and levels of thrombin-antithrombin complexes and C-reactive protein w
14 pG DNA on bleeding time and plasma levels of thrombin-antithrombin complexes and tissue factor were m
15 X, plasminogen activator inhibitor, d-dimer, thrombin antithrombin complex), and lymphocyte cell surf
16 tissue plasminogen activator (tPA), d-dimer, thrombin-antithrombin complex, and cytokines (IL-1beta,
17 variation in concentrations of fragment 1+2, thrombin-antithrombin complex, and D-dimer, respectively
20 in increased platelet activation, increased thrombin/antithrombin complex, and decreased bleeding ti
21 identified by measuring: thrombin activity; thrombin-antithrombin complexes; and the prothrombin fra
22 vation/inhibition (prothrombin fragment 1.2, thrombin/antithrombin complex, antithrombin, protein C,
23 hrombin activation fragment 1+2 (F1+2), TAT (thrombin-antithrombin complex), APC, and D-dimer were mo
24 rombin and undergo formation of the covalent thrombin-antithrombin complex at modestly different rate
25 ns of prothrombin, prothrombin fragment 1+2, thrombin-antithrombin complex, crosslinked fibrin degrad
26 The systemic levels of fibrinopeptide A, thrombin-antithrombin complex, D-dimer, and both local a
27 rmation as evidenced by the increased plasma thrombin-antithrombin complexes, endogenous thrombin pot
28 vels of prothrombin activation peptide F1.2, thrombin-antithrombin complex, fibrinopeptide A, and sol
29 ticoagulation with 14E11 suppressed systemic thrombin- antithrombin complex formation, IL-6, and TNF-
30 (prothrombin fragment F(1+2) production and thrombin-antithrombin complex formation), fibrinogen dep
33 nal antibody (M27), raised against the human thrombin-antithrombin complex, has been identified and c
34 um glutamic pyruvic transaminase, anion gap, thrombin-antithrombin complex, IL-6, IL-8, and soluble t
35 cted increased circulating tissue factor and thrombin-antithrombin complexes in patients with NEC.
37 deposition in the liver and elevated plasma thrombin-antithrombin complexes, indicating activation o
38 ng tissue factor production, reducing plasma thrombin-antithrombin complex levels and fibrinogen depo
39 easing baseline prothrombin fragment 1.2 and thrombin-antithrombin complex levels in the placebo grou
40 ar coagulation (bronchoalveolar lavage fluid thrombin-antithrombin complex levels) and PAR-1 immunost
41 , plasminogen activator inhibitor (PAI), and thrombin-antithrombin complex levels, whereas LT and ET
42 ntly attenuated prothrombin fragment 1.2 and thrombin:antithrombin complex levels (P<.001, 2-sample t
43 ncomitant with inactivation of thrombin, the thrombin-antithrombin complex may be irreversibly releas
44 v/TM injected after endotoxin did not reduce thrombin/antithrombin complexes; nor did antibodies that
45 changes detected when vitronectin binds the thrombin-antithrombin complex or associates with the ter
46 leukin-6, and -10); "coagulation" (D-dimers, thrombin-antithrombin complex); "oxidative stress" (urin
47 ocyte tissue factor expression, formation of thrombin-antithrombin complexes (p < 0.001), and formati
48 stasis (endogenous thrombin potential [ETP], thrombin-antithrombin complex, plasmin-alpha2-antiplasmi
49 red conventional coagulation biomarkers plus thrombin-antithrombin complex, plasmin-antiplasmin compl
50 in-8, elastase-alpha1-antitrypsin complexes, thrombin-antithrombin complexes, plasminogen activator a
53 72 hours postinfection, decreased levels of thrombin-antithrombin complexes, reflecting inhibition o
54 M27 does not block binding and uptake of the thrombin-antithrombin complex, suggesting that this regi
56 al measure of thrombin generation in vitro), thrombin/antithrombin complexes (TAT; a measure of throm
57 eration (prothrombin fragment 1+2 [F1+2] and thrombin-antithrombin complex [TAT]) and platelet activa
59 by a statistically significant reduction in thrombin-antithrombin complexes (TATc), was noted in the
60 ion molecule-1, E-selectin, P-selectin, TAT (thrombin/antithrombin complex), tumor necrosis factor-al
61 the affinity of the peptides for the stable thrombin-antithrombin complex was undetectable (>/=200-f
62 a and bronchoalveolar lavage fluid levels of thrombin-antithrombin complexes were enhanced in transfu
63 arterial hypotension induced E-selectin and thrombin-antithrombin complex, whereas concomitant expos