ライフサイエンスコーパス: nimesulide

1 evident even at substoichiometric levels of nimesulide.

2 ells and are 10- to 80-fold more active than nimesulide.

3 ened the time-dependent inhibitory action of nimesulide.

4 atter increases further on administration of nimesulide.

5 n PGI(2) biosynthesis indistinguishable from nimesulide.

6 fen (3512+/-407 pg/ml) or the COX2 inhibitor nimesulide (2800+/-830 pg/ml), production was decreased

7 plemented with the selective COX-2 inhibitor nimesulide (400 ppm) or a control diet.

8 was 4.1 min in the control, >10 h with added nimesulide, 48 min with flurbiprofen, and 0.8 min with d

9 In addition, treatment with nimesulide, a COX-2 selective inhibitor, dramatically su

10 We found that prophylactic administration of nimesulide, a preferential COX-2 inhibitor, in the feed

11 Adding nimesulide after ethyl peroxide led to some narrowing of

12 like that seen in PGHS-2 treated with TNM or nimesulide alone.

13 sis and biological evaluation of a series of nimesulide analogues as potential selective aromatase ex

14 Previously, the COX-2 selective inhibitor nimesulide and analogs decreased aromatase expression an

15 or (TP) reduces the hyperplastic response to nimesulide and carotid ligation, despite further augment

16 so important in time-dependent inhibition by nimesulide and piroxicam.

17 The COX-2-selective inhibitors NS-398 and nimesulide and the TXA(2) receptor antagonist BMS 180,29

18 based on cyclooxygenase-2 (COX-2) inhibitor nimesulide as a lead compound.

19 of PGI2 with the selective COX-2 inhibitor, nimesulide, both augment intimal hyperplasia while prese

20 end, mice were treated with indomethacin and nimesulide continuously from 8 months of age until they

21 demonstrated that COX-2 selective inhibitor nimesulide decreased aromatase activity from the transcr

22 we found that the selective COX-2 inhibitor nimesulide delays the progression of pancreatic cancer p

23 plied to evaluate the concentration of APIs (nimesulide, dexketoprofen, deflazacort) handled by the p

24 S-2 in a time-dependent fashion, and all but nimesulide did the same for the V509A mutant.

25 reported to be selective for PGHS-2 (NS398, nimesulide, DuP697, and SC58125).

26 ent of atherosclerosis by 55 +/- 4%, whereas nimesulide failed to increase the rate of atherogenesis.

27 Ten percent of all pancreatic ducts in the nimesulide-fed animals showed PanIN-2 or PanIN-3 lesions

28 ic prostaglandin E(2) levels were reduced in nimesulide-fed animals.

29 the effects of three competitive inhibitors (nimesulide, flurbiprofen, and diclofenac) on the proport

30 By contrast, nimesulide had no effect on both A beta peptides and NF-

31 ll as provides platform for synthesis of the nimesulide-imprinted polymer.

32 sensor was also applied for the detection of nimesulide in real samples like human blood serum, plasm

33 In vivo, nimesulide increased VEGF production by cancer cells in

34 In COX-2-positive pancreatic cancer, the nimesulide-induced increase of VEGF production by the ca

35 SC-560, and two selective COX-2 inhibitors, nimesulide (NIM) and dimethylfuranone (DFU), on the febr

36 th either of the selective COX-2 inhibitors, nimesulide or DuP 697, prevents the delayed increase in

37 Moreover, nimesulide or IP deletion augments the reduction in bloo

38 Nimesulide or NS-398 did not alter arachidonic acid-indu

39 treatment with the cyclooxygenase inhibitor nimesulide or the aromatase inhibitor formestane.

40 at are partially corrected by in vivo A-779, nimesulide, or L-NAME.

41 th the Mas antagonist A-779, COX-2 inhibitor nimesulide, or Sirt1 inhibitor splitomicin lowers plasma

42 Nimesulide pretreatment of Y504F and the quadruple mutan

43 treated with COX inhibitors such as NS-398, nimesulide, SC-58125, and sulindac sulfide.

44 L-NAME (NG-mono-methyl-L-arginine ester) or nimesulide shortens the thrombosis time.

45 stently, mice receiving indomethacin, but no nimesulide, showed a significant reduction in the amyloi

46 Addition of a cyclooxygenase inhibitor, nimesulide, similarly resulted in a narrow PGHS-2 radica

47 BKB2R(-/-) mice also correct with L-NAME and nimesulide therapy.

48 Addition of nimesulide to ASA-treated PGHS-2 inhibited the lipoxygen

49 Indomethacin-treated PGHS-1 and nimesulide-treated PGHS-2 rapidly formed narrow singlet

50 For nimesulide-treated PGHS-2, radical formed in concert wit

51 In vivo A-779 or combined L-NAME and nimesulide treatment corrects it.

52 Acetaminophen and nimesulide were tolerated in 60% and 88.8% of the study

53 address this hypothesis, we used dosing with nimesulide, which inhibited COX-2 ex vivo, depressed uri

54 ry good selectivity towards the detection of nimesulide with a limit of detection as low as 6.65ngL(-