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1 ected after hemostatic resuscitation without tranexamic acid.
2 understanding of the mechanism of action of tranexamic acid.
3 Thrombolysis was suppressed with tranexamic acid.
4 izumab 1% (4 mg/d), estriol 0.1% (0.4 mg/d), tranexamic acid 10% (40 mg/d), or placebo (0.9% saline).
5 use mortality was significantly reduced with tranexamic acid (1463 [14.5%] tranexamic acid group vs 1
6 tranexamic acid/cryoprecipitate (11.6%) and tranexamic acid (18.2%) groups compared with the cryopre
9 .03; 95% confidence interval, 0.80-1.33) nor tranexamic acid (65 deaths among 442 patients [14.7%]; a
10 1295 patients], aminocaproic acid [883], and tranexamic acid [822]) as compared with no agent (1374 p
12 atment of AD mice with the plasmin inhibitor tranexamic acid aggravated pathology, whereas removal of
14 cologic inhibitor of plasminogen activation, tranexamic acid, also delays the onset of neuroinflammat
15 ient mice and in wild-type mice treated with tranexamic acid, an inhibitor of plasminogen activation.
20 -Pg contributed to cell adhesion inasmuch as tranexamic acid and epsilon-aminocaproic acid inhibited
22 ) for acute swelling attacks and progestins, tranexamic acid, and danazol for the prevention of attac
26 ical community by increasing awareness about tranexamic acid-associated seizures and by translating s
32 ll requirements, mortality was lowest in the tranexamic acid/cryoprecipitate (11.6%) and tranexamic a
34 nexamic acid (mean [SD], 23.0 [19.2]) and no tranexamic acid/cryoprecipitate (mean [SD], 21.2 [18.5])
35 cryoprecipitate (mean [SD], 28.3 [15.7]) and tranexamic acid/cryoprecipitate (mean [SD], 26 [14.9]) g
36 c acid (n = 148), cryoprecipitate (n = 168), tranexamic acid/cryoprecipitate (n = 258), and no tranex
38 ation, a levonorgestrel intrauterine system, tranexamic acid (during menstrual flow), high-dose proge
39 er discontinuing eOC (16 women), 93.8% under tranexamic acid (four women), and 100% under danazol (th
40 ble outcomes data; 2311 were assigned to the tranexamic acid group and 2320 to the placebo group.
41 fused during hospitalization was 4331 in the tranexamic acid group and 7994 in the placebo group (P<0
42 tion occurred in 1.4% of the patients in the tranexamic acid group and in 2.8% of the patients in the
43 vent occurred in 386 patients (16.7%) in the tranexamic acid group and in 420 patients (18.1%) in the
44 y reduced with tranexamic acid (1463 [14.5%] tranexamic acid group vs 1613 [16.0%] placebo group; rel
45 h due to bleeding (198/3747 [5.3%] events in tranexamic acid group vs 286/3704 [7.7%] in placebo grou
46 e estriol group, 7.5 (IQR, 3.0-11.0) for the tranexamic acid group, and 8.0 (IQR, 3.0-14.0) for the p
47 0 138 patients from two randomised trials of tranexamic acid in acute severe bleeding (traumatic and
49 independently add to the survival benefit of tranexamic acid in the seriously injured requiring trans
52 trauma patients admitted late after injury, tranexamic acid is less effective and could be harmful.
54 fferent therapies among different countries, tranexamic acid is widely available, and is an effective
55 he most commonly used antifibrinolytic drug, tranexamic acid, is associated with an increased inciden
56 omly assigned within 8 h of injury to either tranexamic acid (loading dose 1 g over 10 min followed b
57 omly assigned within 8 h of injury to either tranexamic acid (loading dose 1 g over 10 min then infus
59 an [SD], 26 [14.9]) groups compared with the tranexamic acid (mean [SD], 23.0 [19.2]) and no tranexam
60 vonorgestrel-IUS or usual medical treatment (tranexamic acid, mefenamic acid, combined estrogen-proge
61 ood cells and composed the following groups: tranexamic acid (n = 148), cryoprecipitate (n = 168), tr
63 recorded strong evidence that the effect of tranexamic acid on death due to bleeding varied accordin
64 We recorded no evidence that the effect of tranexamic acid on death due to bleeding varied by systo
65 ssess the effects of early administration of tranexamic acid on death, vascular occlusive events, and
66 of early administration of a short course of tranexamic acid on death, vascular occlusive events, and
67 al (which originally evaluated the effect of tranexamic acid on mortality in trauma patients) was con
72 dysfunction in patients receiving aprotinin, tranexamic acid, or no antifibrinolytic treatment in the
73 rly, inhibiting endogenous fibrinolysis with tranexamic acid reduced retraction of fibrin polymers in
75 ion of plasmin activation and/or activity by tranexamic acid reversed both the accelerated fibrin cle
82 ental biofilms and whether the lysine analog tranexamic acid (TA) inhibits LDC activity, biofilm accu
83 log antifibrinolytics (aminocaproic acid and tranexamic acid), the serine protease inhibitor aprotini
85 zed trials have demonstrated the efficacy of tranexamic acid (TXA) in reducing blood loss and transfu
87 currently available antifibrinolytics, e.g., tranexamic acid (TXA, 1) and aprotinin, has been challen
90 patients undergoing coronary-artery surgery, tranexamic acid was associated with a lower risk of blee
93 ors, including epsilon-aminocaproic acid and tranexamic acid, were effective in treating and preventi
94 equally or more effective than aprotinin or tranexamic acid, which have been used as antifibrinolyti
95 re aprotinin, epsilon-aminocaproic acid, and tranexamic acid with placebo and head to head on 8 clini
96 o increase in vascular occlusive events with tranexamic acid, with no heterogeneity by site of bleedi
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