ライフサイエンスコーパス: meloxicam

1 bserved and were dose-dependently reduced by meloxicam.

2 nd 17 days after the first administration of meloxicam.

3 A versus shams, with a significant effect of meloxicam.

4 acilitate local dissolution and diffusion of meloxicam.

5 ing premature precipitation of fast-released meloxicam.

6 over two weeks and was used as a carrier of meloxicam.

7 acoxib is proposed compared to celecoxib and meloxicam.

8 ib (10 mg/kg BW), mavacoxib (4 mg/kg BW) and meloxicam (1 mg/kg BW) were determined following single

9 ly intraperitoneal injection of 0.9% NaCl or meloxicam 3 mg/kg, respectively, for 7 consecutive days.

10 Animals treated with meloxicam (5 mg/kg) exhibited a dose-dependent decrease

11 Meloxicam (5), an NSAID in the enol-carboxamide class, w

12 veloped a polymeric implant that can release meloxicam, a selective cyclooxygenase (COX)-2 inhibitor,

13 trasted with selective COX-2 inhibition with meloxicam, administered alone and in combination with AL

14 udy was to determine the effects of repeated meloxicam administration on the feline plasma and urine

15 The repeated administration of meloxicam altered the feline plasma and urine lipidome a

16 This study investigated whether the use of meloxicam alters bone repair via downregulation of VEGF

17 n that might occur during concomitant use of meloxicam and esomeprazole, which are commonly prescribe

18 xpression of CD11a, CD11b, and CD18, whereas meloxicam and etanercept did not.

19 ion in CSCs we utilized the COX-2 inhibitors meloxicam and mavacoxib.

20 The variation of solid meloxicam and Mg(OH)(2) quantities allowed for flexible

21 Two selective COX-2 inhibitors, meloxicam and NS398, decreased HIF-1alpha levels and nuc

22 platform is crucial to continuous release of meloxicam and the drug release rate can be controlled by

23 t of nonselective (Piroxicam), preferential (Meloxicam), and selective COX-2 inhibitors (Parecoxib).

24 Notably, aspirin, meloxicam, and etanercept did not change retinal vascula

25 n given with rofecoxib, celecoxib, sulindac, meloxicam, and indometacin but not when given with ibupr

26 that the oxicam-type NSAIDs tenoxicam (TNX), meloxicam, and piroxicam, but not other types of NSAIDs,

27 eri and either treated with dexamethasone or meloxicam (anti-inflammatory drugs) or left untreated.

28 roidal anti-inflammatories (NSAIDs), such as meloxicam, are the mainstay for treating painful and inf

29 g release from PLGA MPs for two weeks, using meloxicam as a model compound.

30 Alternatively, encapsulating meloxicam as solid helped reduce the initial burst relea

31 crystal complexes of COX-2 with isoxicam and meloxicam at 2.0 and 2.45 angstroms, respectively, and a

32 ctively, and a crystal complex of COX-1 with meloxicam at 2.4 angstroms.

33 Aspirin and meloxicam both lowered retinal TNF-alpha levels.

34 Sustained local delivery of meloxicam by polymeric structures is desirable for preve

35 In addition, a detailed study of meloxicam.COX-2 interactions revealed that mutation of V

36 saline solution or 0.3 mg/kg body weight of meloxicam daily for up to 31 days.

37 In rat alveolar bone repair, meloxicam did not affect VEGF expression but downregulat

38 lective inhibitor of COX-1 and COX-2 whereas meloxicam displays some selectivity for COX-2.

39 cross-over non-steroidal anti-inflammatory (meloxicam) drug trial.

40 4 to Ile significantly reduces inhibition by meloxicam due to subtle changes around Phe-518, giving r

41 High-dose aspirin, etanercept, and high-dose meloxicam each reduced leukocyte adhesion and suppressed

42 High-dose aspirin, etanercept, and high-dose meloxicam each reduced retinal ICAM-1 expression.

43 High-dose aspirin, etanercept and high-dose meloxicam, each suppressed the retinal expression of eNO

44 2 by two commonly used NSAIDs, ibuprofen and meloxicam, had no effect on ACE2 expression, viral entry

45 indicated that the PCL matrices encapsulated meloxicam in crystalline clusters, which dissolved in aq

46 Only Meloxicam in histidine-tryptophan-ketoglutarate was demo

47 The subcutaneously implanted meloxicam-loaded PCL matrices in rats showed pharmacokin

48 Meloxicam-loaded polymer matrices were produced by hot-m

49 L matrices were produced with a fixed 30 wt% meloxicam loading and variable Mg(OH)(2) loadings from 2

50 oxib, diclofenac, indomethacin, lumiracoxib, meloxicam, naproxen, rofecoxib, sodium salicylate, and S

51 those animals receiving analgesia (20 mg/kg meloxicam or 5 mg/kg bupivacaine) or saline post-operati

52 roach vasectomy) and either received saline, meloxicam or bupivacaine.

53 pirin, a cyclooxygenase 2 (COX-2) inhibitor (meloxicam), or a soluble tumor necrosis factor alpha (TN

54 pirin, celecoxib, indomethacin, lumiracoxib, meloxicam, or SC560, against COX-1 (human platelets) inc

55 PCL allowed for sustained release of meloxicam over two weeks and was used as a carrier of me

56 Our previous study demonstrated that meloxicam release from hot-melt extruded (HME) poly(epsi

57 ought an alternative approach to control the meloxicam release from the PCL matrices.

58 The image analysis indicated that meloxicam release from the PCL matrix was primarily driv

59 The meloxicam release increased in proportion to the Mg(OH)(

60 ) quantities allowed for flexible control of meloxicam release, yielding MPs with distinct in vitro r

61 However, the MPs that rapidly released meloxicam showed an attenuated in vivo absorption, sugge

62 l as with the PTGS inhibitor indomethacin or Meloxicam synergistically blocks ovulation.

63 contrast to celecoxib (T1/2el = 0.88 h) and meloxicam (T1/2el = 0.90 h), mavacoxib has a prolonged e

64 hown, with Parecoxib the least effective and Meloxicam the most effective treatment.

65 re altered by the repeated administration of meloxicam to cats (p < 0.05).

66 ided into a control group (CG; n = 60) and a meloxicam-treated group (TG; n = 60) that received eithe

67 d pain behavior in animals, without and with meloxicam treatment.

68 Meloxicam use was associated with remission in 11 (64.7%

69 stration of the preferential COX-2 inhibitor Meloxicam via histidine-tryptophan-ketoglutarate showed

70 vity patterns were seen dogs receiving drug (meloxicam) vs. placebo, suggestive of improved nighttime

71 In contrast, the F% of meloxicam was low (F% = 11%).

72 In contrast, selective COX-2 inhibition with meloxicam was without effect on MNCV, NBF, or MI content

73 eroidal antiinflammatory drugs (NSAIDs), and meloxicam, were prescribed to a larger proportion of ost