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