ライフサイエンスコーパス: aminocaproic acid

1 olling the concentration of the initiator (6-aminocaproic acid).

2 pients of aprotinin than among recipients of aminocaproic acid.

3 responds well to outpatient care and topical aminocaproic acid.

4 ous iron, erythropoietin, G-CSF, and epsilon aminocaproic acid.

5 rotein, and binding was inhibited by epsilon-aminocaproic acid.

6 absence and presence of the ligand, epsilon-aminocaproic acid.

7 This process is inhibited by epsilon-aminocaproic acid.

8 ce can be reduced by the presence of epsilon-aminocaproic acid.

9 idence interval, 1.19-1.85), whereas neither aminocaproic acid (132 deaths among 834 patients [15.8%]

10 t reduction in total blood loss over epsilon-aminocaproic acid (-184 mL; 95% CI, -256 to -112) and tr

11 or the use of aprotinin (33,517 patients) or aminocaproic acid (44,682 patients) on the day CABG was

12 This is applied to a 6-aminocaproic acid (6-ACA) pathway in Escherichia coli co

13 otal postoperative transfusions with epsilon-aminocaproic acid (61% reduction versus placebo, P<0.010

14 butyric acid, 5-aminopentanoic acid, epsilon-aminocaproic acid, 7-aminoheptanoic acid, and t-4-aminom

15 sed three agents (aprotinin [1295 patients], aminocaproic acid [883], and tranexamic acid [822]) as c

16 epsilon-Aminocaproic acid, a Lys analogue, effectively blocks an

17 directed against t-PA and u-PA, and epsilon-aminocaproic acid, a lysine analog that inhibits Plg act

18 a modified method that involves N-acryloyl-6-aminocaproic acid (ACA).

19 tandard dipeptide with a linker derived from aminocaproic acid (Aca).

20 the reductions in IL-6 and IL-10 by epsilon-aminocaproic acid achieved statistical significance.

21 higher mortality than patients who received aminocaproic acid alone.

22 er animal plasma in the presence of epsilon -aminocaproic acid, an active-site inhibitor that stabili

23 ve hemorrhage after cardiac surgery, epsilon-aminocaproic acid, an alternative antifibrinolytic, is c

24 epsilon-Aminocaproic acid and aprotinin had no effect on risks o

25 Both the lysine analog epsilon-aminocaproic acid and L-proline inhibited the binding of

26 reductions in total blood loss with epsilon-aminocaproic acid and low-dose aprotinin (each with a 35

27 rast, the less expensive generic medications aminocaproic acid and tranexamic acid are safe alternati

28 e safer and less expensive alternatives (ie, aminocaproic acid and tranexamic acid) are available.

29 to use of 2 lysine analog antifibrinolytics (aminocaproic acid and tranexamic acid), the serine prote

30 Fibrinolysis inhibitors, including epsilon-aminocaproic acid and tranexamic acid, were effective in

31 ed aprotinin, 6776 patients (66.8%) received aminocaproic acid, and 2029 patients (20.0%) received no

32 e colony-stimulating factor, erythropoietin, aminocaproic acid, and phytonadione was administered.

33 meta-analysis to compare aprotinin, epsilon-aminocaproic acid, and tranexamic acid with placebo and

34 Aprotinin but not epsilon-aminocaproic acid appears to attenuate the rise in the p

35 ntrate, recombinant factor VIIa, and epsilon-aminocaproic acid, as potential therapeutic options.

36 mice with the fibrinolytic inhibitor epsilon-aminocaproic acid before endotoxin increased both the nu

37 The plasminogen-specific inhibitor epsilon-aminocaproic acid blocked the tv-rENO1-plasminogen assoc

38 [Lys3]Bombesin ([Lys3]BBN) and aminocaproic acid-bombesin(7-14) (Aca-BBN(7-14)) were la

39 antiserum, by low concentrations of epsilon-aminocaproic acid, by methylation of lysine residues in

40 Both aprotinin and epsilon-aminocaproic acid decreased blood loss compared with sal

41 hese data suggest that aprotinin and epsilon-aminocaproic acid differ in their effects on the inflamm

42 plasminogen (Klpg) with the ligands epsilon-aminocaproic acid (EACA) and trans-4-(aminomethyl)cycloh

43 ytic drugs tranexamic acid (TXA) and epsilon-aminocaproic acid (EACA) are structurally similar to the

44 atient received a loading dose of 5 grams of aminocaproic acid (EACA) intravenously 3 hours prior to

45 The binding constants of epsilon-aminocaproic acid (EACA), 7-aminoheptanoic acid (7-AHpA)

46 ibited plasminogen activation, e.g., epsilon-aminocaproic acid (EACA), or plasminogen antiserum.

47 nhibited by lysine analogues such as epsilon-aminocaproic acid (EACA).

48 riant) in its unliganded and ligand [epsilon-aminocaproic acid (EACA)] bound modes and the structure

49 The binding is inhibited by epsilon-aminocaproic acid (epsilonACA), indicating the requireme

50 In contrast, epsilon-aminocaproic acid, fibrin, and fibrinogen, which induce

51 4% higher in the aprotinin group than in the aminocaproic acid group (relative risk, 1.64; 95% confid

52 inolytic drugs such as aprotinin and epsilon-aminocaproic acid have been effective in reducing fibrin

53 sion inasmuch as tranexamic acid and epsilon-aminocaproic acid inhibited cell adhesion.

54 and the presence of a lysine analog, epsilon-aminocaproic acid, inhibited the ErpP-plasminogen intera

55 ies, the considerably less-expensive epsilon-aminocaproic acid may be preferred over aprotinin for re

56 n 1985 and 1998 involving the use of epsilon-aminocaproic acid (n=9) or aprotinin (n=46) in patients

57 Neither aminocaproic acid nor tranexamic acid was associated wit

58 xamined the effects of aprotinin and epsilon-aminocaproic acid on plasma levels of proinflammatory [i

59 The presence of epsilon-aminocaproic acid only slightly inhibited binding of apo

60 As compared with the use of aminocaproic acid or no antifibrinolytic agent, aprotini

61 um creatinine levels than those who received aminocaproic acid or no antifibrinolytic agent.

62 ransfused was similarly reduced with epsilon-aminocaproic acid (OR, 0.32; 95% CI, 0.15 to 0.69) and h

63 tudy to receive high-dose aprotinin, epsilon-aminocaproic acid, or saline placebo.

64 ) for the comparison with patients receiving aminocaproic acid (P=0.004).

65 nin recipients (4.5%) and 1101 of the 44,682 aminocaproic acid recipients (2.5%) died.

66 Saturating levels of epsilon-aminocaproic acid reduced the affinity of SK for labeled

67 nificantly inhibited by the lysine analog xi-aminocaproic acid, suggesting that the lysine-binding si

68 from human serum in the presence of epsilon -aminocaproic acid was also developed.

69 Aminocaproic acid was not statistically associated with

70 fewer data are available for tranexamic and aminocaproic acid, we support their use as alternatives

71 hyl)cadaverdine, but not N6-(1-iminoethyl)-6-aminocaproic acid, were NADPH-dependent, irreversible in

72 -4-Cpa-Gln-D-Phe-Pro-Asp-Aca) (Aca = epsilon-aminocaproic acid), which did not contain tyrosine, was

73 in the presence of the lysine analog epsilon-aminocaproic acid, which precludes apo(a)-B100 associati