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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
15                          Adipic acid (AA), 6-aminocaproic acid (6-ACA) and 1,6-hexamethylenediamine (
16                       This is applied to a 6-aminocaproic acid (6-ACA) pathway in Escherichia coli co
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
20                                      epsilon-Aminocaproic acid, a Lys analogue, effectively blocks an
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
23 tandard dipeptide with a linker derived from aminocaproic acid (Aca).
24 a modified method that involves N-acryloyl-6-aminocaproic acid (ACA).
25  the reductions in IL-6 and IL-10 by epsilon-aminocaproic acid achieved statistical significance.
26  higher mortality than patients who received aminocaproic acid alone.
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
29                                      epsilon-Aminocaproic acid and aprotinin had no effect on risks o
30               Both the lysine analog epsilon-aminocaproic acid and L-proline inhibited the binding of
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
33                                 Both epsilon-aminocaproic acid and tranexamic acid inhibit clot disso
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
40                    Aprotinin but not epsilon-aminocaproic acid appears to attenuate the rise in the p
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
44                    The lysine analog epsilon-aminocaproic acid blocks Plm-catalyzed BK generation.
45               [Lys3]Bombesin ([Lys3]BBN) and aminocaproic acid-bombesin(7-14) (Aca-BBN(7-14)) were la
46  antiserum, by low concentrations of epsilon-aminocaproic acid, by methylation of lysine residues in
47                   Both aprotinin and epsilon-aminocaproic acid decreased blood loss compared with sal
48 hese data suggest that aprotinin and epsilon-aminocaproic acid differ in their effects on the inflamm
49 ifibrinolytic medication (tranexamic acid or aminocaproic acid) during the bleeding event.
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
54             The binding constants of epsilon-aminocaproic acid (EACA), 7-aminoheptanoic acid (7-AHpA)
55 ibited plasminogen activation, e.g., epsilon-aminocaproic acid (EACA), or plasminogen antiserum.
56                       Treatment with epsilon-aminocaproic acid (EACA), which inhibits plasmin activat
57 nhibited by lysine analogues such as epsilon-aminocaproic acid (EACA).
58 riant) in its unliganded and ligand [epsilon-aminocaproic acid (EACA)] bound modes and the structure
59          The binding is inhibited by epsilon-aminocaproic acid (epsilonACA), indicating the requireme
60                         In contrast, epsilon-aminocaproic acid, fibrin, and fibrinogen, which induce
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
63 sion inasmuch as tranexamic acid and epsilon-aminocaproic acid inhibited cell adhesion.
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
68                                      Neither aminocaproic acid nor tranexamic acid was associated wit
69 xamined the effects of aprotinin and epsilon-aminocaproic acid on plasma levels of proinflammatory [i
70                      The presence of epsilon-aminocaproic acid only slightly inhibited binding of apo
71 is by the indirect plasmin inhibitor epsilon-aminocaproic acid or by alpha2AP restored thrombosis in
72                  As compared with the use of aminocaproic acid or no antifibrinolytic agent, aprotini
73 um creatinine levels than those who received aminocaproic acid or no antifibrinolytic agent.
74 ransfused was similarly reduced with epsilon-aminocaproic acid (OR, 0.32; 95% CI, 0.15 to 0.69) and h
75 tudy to receive high-dose aprotinin, epsilon-aminocaproic acid, or saline placebo.
76 ) for the comparison with patients receiving aminocaproic acid (P=0.004).
77 nin recipients (4.5%) and 1101 of the 44,682 aminocaproic acid recipients (2.5%) died.
78                 Saturating levels of epsilon-aminocaproic acid reduced the affinity of SK for labeled
79       Pretreatment with the lysine analog, e-aminocaproic acid, significantly increased platelet-deri
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
82 from human serum in the presence of epsilon -aminocaproic acid was also developed.
83                                              Aminocaproic acid was not statistically associated with
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