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1 olling the concentration of the initiator (6-aminocaproic acid).
2 pients of aprotinin than among recipients of aminocaproic acid.
3 of benzenesulfonic acid and 45 mmol L(-1) of aminocaproic acid.
4 responds well to outpatient care and topical aminocaproic acid.
5 ous iron, erythropoietin, G-CSF, and epsilon aminocaproic acid.
6 rotein, and binding was inhibited by epsilon-aminocaproic acid.
7 absence and presence of the ligand, epsilon-aminocaproic acid.
8 This process is inhibited by epsilon-aminocaproic acid.
9 ce can be reduced by the presence of epsilon-aminocaproic acid.
10 analysis based on an electrolyte of epsilon-aminocaproic acid.
11 idence interval, 1.19-1.85), whereas neither aminocaproic acid (132 deaths among 834 patients [15.8%]
12 t reduction in total blood loss over epsilon-aminocaproic acid (-184 mL; 95% CI, -256 to -112) and tr
13 ytic agents such as tranexamic acid, epsilon-aminocaproic acid, 4-aminomethylbenzoic acid, and aproti
14 or the use of aprotinin (33,517 patients) or aminocaproic acid (44,682 patients) on the day CABG was
17 otal postoperative transfusions with epsilon-aminocaproic acid (61% reduction versus placebo, P<0.010
18 butyric acid, 5-aminopentanoic acid, epsilon-aminocaproic acid, 7-aminoheptanoic acid, and t-4-aminom
19 sed three agents (aprotinin [1295 patients], aminocaproic acid [883], and tranexamic acid [822]) as c
21 directed against t-PA and u-PA, and epsilon-aminocaproic acid, a lysine analog that inhibits Plg act
22 745,870, a dopamine receptor antagonist, and aminocaproic acid, a protease inhibitor that reduce drus
27 er animal plasma in the presence of epsilon -aminocaproic acid, an active-site inhibitor that stabili
28 ve hemorrhage after cardiac surgery, epsilon-aminocaproic acid, an alternative antifibrinolytic, is c
31 reductions in total blood loss with epsilon-aminocaproic acid and low-dose aprotinin (each with a 35
32 rast, the less expensive generic medications aminocaproic acid and tranexamic acid are safe alternati
34 e safer and less expensive alternatives (ie, aminocaproic acid and tranexamic acid) are available.
35 to use of 2 lysine analog antifibrinolytics (aminocaproic acid and tranexamic acid), the serine prote
36 Fibrinolysis inhibitors, including epsilon-aminocaproic acid and tranexamic acid, were effective in
37 ed aprotinin, 6776 patients (66.8%) received aminocaproic acid, and 2029 patients (20.0%) received no
38 e colony-stimulating factor, erythropoietin, aminocaproic acid, and phytonadione was administered.
39 meta-analysis to compare aprotinin, epsilon-aminocaproic acid, and tranexamic acid with placebo and
41 ntrate, recombinant factor VIIa, and epsilon-aminocaproic acid, as potential therapeutic options.
42 mice with the fibrinolytic inhibitor epsilon-aminocaproic acid before endotoxin increased both the nu
43 The plasminogen-specific inhibitor epsilon-aminocaproic acid blocked the tv-rENO1-plasminogen assoc
46 antiserum, by low concentrations of epsilon-aminocaproic acid, by methylation of lysine residues in
48 hese data suggest that aprotinin and epsilon-aminocaproic acid differ in their effects on the inflamm
50 plasminogen (Klpg) with the ligands epsilon-aminocaproic acid (EACA) and trans-4-(aminomethyl)cycloh
51 ytic drugs tranexamic acid (TXA) and epsilon-aminocaproic acid (EACA) are structurally similar to the
52 atient received a loading dose of 5 grams of aminocaproic acid (EACA) intravenously 3 hours prior to
53 E) method containing high amounts of epsilon-aminocaproic acid (EACA) provides a detailed and robust
58 riant) in its unliganded and ligand [epsilon-aminocaproic acid (EACA)] bound modes and the structure
61 4% higher in the aprotinin group than in the aminocaproic acid group (relative risk, 1.64; 95% confid
62 inolytic drugs such as aprotinin and epsilon-aminocaproic acid have been effective in reducing fibrin
64 and the presence of a lysine analog, epsilon-aminocaproic acid, inhibited the ErpP-plasminogen intera
65 ies, the considerably less-expensive epsilon-aminocaproic acid may be preferred over aprotinin for re
66 n 1985 and 1998 involving the use of epsilon-aminocaproic acid (n=9) or aprotinin (n=46) in patients
67 vent (n = 54 unique subjects; n = 18 epsilon aminocaproic acid, n = 35 tranexamic acid, and n = 1 bot
69 xamined the effects of aprotinin and epsilon-aminocaproic acid on plasma levels of proinflammatory [i
71 is by the indirect plasmin inhibitor epsilon-aminocaproic acid or by alpha2AP restored thrombosis in
74 ransfused was similarly reduced with epsilon-aminocaproic acid (OR, 0.32; 95% CI, 0.15 to 0.69) and h
80 activation by CRT were inhibited by epsilon-aminocaproic acid, suggesting that an internal lysine re
81 nificantly inhibited by the lysine analog xi-aminocaproic acid, suggesting that the lysine-binding si
84 fewer data are available for tranexamic and aminocaproic acid, we support their use as alternatives
85 hyl)cadaverdine, but not N6-(1-iminoethyl)-6-aminocaproic acid, were NADPH-dependent, irreversible in
86 -4-Cpa-Gln-D-Phe-Pro-Asp-Aca) (Aca = epsilon-aminocaproic acid), which did not contain tyrosine, was
87 in the presence of the lysine analog epsilon-aminocaproic acid, which precludes apo(a)-B100 associati