ライフサイエンスコーパス: 5-ASA

1 ed the ability of these enzymes to acetylate 5-ASA.

2 The 5-aminosalicylic acid (5-ASA) agents and oral steroids remain the first-line ap

3 the anti-inflammatory 5-aminosalicylic acid (5-ASA) and one group untreated), with results showing si

4 he PPAR-gamma agonist 5-aminosalicylic acid (5-ASA) functionally replaced Clostridia species to resto

5 el disease (IBD) drug 5-aminosalicylic acid (5-ASA) has been attributed, in part, to its acetylation

6 ecently reported that 5-aminosalicylic acid (5-ASA) inhibits TNFalpha-regulated IkappaB degradation a

7 bowel disease (IBD), 5-aminosalicylic acid (5-ASA) is still the key medication, particularly for ulc

8 ne expression whereas 5-aminosalicylic acid (5-ASA) or indomethacin had no effect.

9 etic acid (4-APAA) or 5-aminosalicylic acid (5-ASA) with peptides, including an antibiotic peptide te

10 ulfapyridine (SP) and 5-aminosalicylic acid (5-ASA), on components of angiogenesis, namely, endotheli

11 elivering mesalazine (5-aminosalicylic acid, 5-ASA) to the colon were compared in an advanced in vitr

12 d on 5 main drug classes: 5-aminosalicylate (5-ASA), corticosteroids, immunosuppressants, anti-tumor

13 an increased risk of treatment failure among 5-ASA users.

14 on, assessing the impact of inflammation and 5-ASA on the gut microbiota is not feasible in a clinica

15 inflammation affects the gut microbiota and 5-ASA can change the severity of inflammation, assessing

16 SSZ, SP, and 5-ASA were assayed for their effects on basic fibroblast

17 l study to demonstrate a causal link between 5-ASA administration and alterations of the intestinal m

18 Further, both 5-ASA and sulfasalazine significantly reduced the growth

19 observed that the gut microbiota altered by 5-ASA affected host mucosal immunity and decreased susce

20 cells or cellular extracts is not blocked by 5-ASA.

21 ions in the intestinal microbiota induced by 5-ASA directed the host immune system towards an anti-in

22 S-transferase-IkappaBalpha are inhibited by 5-ASA.

23 cells treated with TNFalpha is inhibited by 5-ASA.

24 se state and ileal pH variability on colonic 5-ASA delivery.

25 ith CDI using either of the CDI definitions, 5-ASA use was associated with CDI using DAD but not labo

26 o-bond releasing the 5-ASA or a pH-dependent 5-ASA packaging system that permitted release in the dis

27 st 6 months prior to and 12 months following 5-ASA initiation (index date).

28 These findings suggest a novel role for 5-ASA in the management of IBD by disrupting TNFalpha ac

29 However, the mechanism of action of 5-ASA remains unclear.

30 fic non-pharmacy claims, at least 30 days of 5-ASA treatment and at least one corticosteroid prescrip

31 a number of alternative forms of delivery of 5-ASA were developed consisting of either a similar sulf

32 ntal confounders and excluding the effect of 5-ASA itself with a vertical transmission model, we obse

33 ich promotes the anti-inflammatory effect of 5-ASA.

34 ts were LTR without any medication except of 5-ASA.

35 tory state, which underlies the mechanism of 5-ASA efficacy.

36 To determine the mechanism of 5-ASA inhibition of IkappaB degradation, we studied youn

37 proaches resulted in a similar percentage of 5-ASA recovery under healthy conditions.

38 strategy resulted in a higher proportion of 5-ASA delivery to the colonic region as compared to the

39 In general, women on 5-ASA, thiopurine, or anti-tumor necrosis factor (TNF) m

40 to moderate disease flare while on optimized 5-ASA or thiopurine therapy should be managed with syste

41 duced by incubation with either SSZ (19%) or 5-ASA (23%) (P<0.05; [n = 6]).

42 w prescription for either corticosteroids or 5-ASA medications following an interval of at least 4 mo

43 ctiveness and tolerability of different oral 5-ASA therapies (sulfalsalazine vs diazo-bonded 5-ASAs v

44 adherent with their prescribed doses of oral 5-ASA.

45 005 for a UC diagnosis and at least one oral 5-ASA prescription on or after the first observed UC dia

46 Oral and rectal 5-ASA are recommended first-line therapy for mild to mod

47 ive effectiveness and tolerability of rectal 5-ASA and corticosteroid formulations in patients with d

48 t utilised pH and bacteria-mediated release (5-ASA, Octasa(R) 1600 mg).

49 As a result, 5-ASA-containing medications continue to provide a valua

50 ds) and those using only 5-amino-salicylate (5-ASA) treatment (LTR) for the past 3 years.

51 antibacterial agent, and 5-amino-salicylate (5-ASA), an anti-inflammatory agent.

52 We show 5-ASA inhibits TNFalpha-stimulated phosphorylation of Ik

53 In summary, 5-ASA inhibits TNFalpha-stimulated IKKalpha kinase activ

54 ophysiology of IBD, and we hypothesized that 5-ASA alters the intestinal microbiota, which promotes t

55 to target a therapeutic concentration of the 5-ASA component of the medication primarily in the colon

56 nal destruction of an azo-bond releasing the 5-ASA or a pH-dependent 5-ASA packaging system that perm

57 inclusion criteria: 72% were nonadherent to 5-ASA treatment (n=1,217) and 28% were adherent (n=476)

58 l corticosteroid therapy, with transition to 5-ASA, thiopurine, anti-TNF (with or without thiopurine

59 P decreased basal HMVEC proliferation, while 5-ASA increased proliferation (P<0.05; [n = 5]).

60 racterized microbial acetyltransferases with 5-ASA inactivation, belonging to two protein superfamili

61 treated cells (but not in cells treated with 5-ASA or indomethacin) for up to 24 h after treatment.