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1 domain, which is able to effectively prolong thrombin time.
2 y of bleeding, is characterized by prolonged thrombin time, abnormal fibrin polymerization, and incre
3 Among 68 patients with an elevated dilute thrombin time and 81 with an elevated ecarin clotting ti
4 dabigatran plasma concentration and diluted thrombin time and ecarin clotting time, and a non-linear
6 late (DE) dose-dependently prolonged diluted thrombin time and tail-vein bleeding time, which were re
7 to exosite II of thrombin, prolong both the thrombin time and the activated partial thromboplastin t
10 21 patients (97.5%) with an elevated diluted thrombin time at presentation and 95 of 131 patients (72
13 l thromboplastin time, prothrombin activity, thrombin time, fibrinogen, d-dimer, platelet count, were
14 time, activated partial thromboplastin time, thrombin time, fibrinogen, D-dimer, von Willebrand facto
15 a monoclonal IgG to exosite II prolongs the thrombin time indirectly by accelerating the thrombin-an
16 f purified VN to VN -/- plasma prolonged the thrombin time into the normal range, suggesting that VN
17 brinogen conversion to fibrin as assessed by thrombin time measurements, and thrombin exosite binding
24 of the commonly used tests, such as PT, PTT, thrombin time, platelet count, fibrinogen, and the prese
27 ated partial thromboplastin time (aPTT), and thrombin time (TT) were secondary endpoints assessed by
28 ctivated partial thromboplastin time (aPTT), thrombin time (TT), as well as thrombin generation assay
30 function, median reversal measured by dilute thrombin time was 100% within 4 h of idarucizumab admini
32 ed activated partial thromboplastin time and thrombin time, while reducing fibrinogen, coagulation fa