ライフサイエンスコーパス: acute colitis

1 egrity in vivo during experimentally induced acute colitis.

2 conds were well tolerated, even in mice with acute colitis.

3 thereby contributing to the pathogenesis of acute colitis.

4 susceptibility of F11r(-/-)Rag1(-/-) mice to acute colitis.

5 as highly protective at treating established acute colitis.

6 estinal epithelium, and infections result in acute colitis.

7 ontributing factors to the resulting typical acute colitis.

8 d treating DSS-induced intestinal injury and acute colitis.

9 arly striking when Dkk1 was inhibited during acute colitis.

10 of a dextran sulfate sodium-induced model of acute colitis.

11 persists in the PVN despite resolution of an acute colitis.

12 the intestinal mucosa and the development of acute colitis.

13 this study, we examined the role of MMP-2 in acute colitis.

14 sal ulceration and apoptosis in experimental acute colitis.

15 the outcome of inflammatory response during acute colitis.

16 xamined this possibility in a mouse model of acute colitis.

17 mpairs epithelial regeneration in a model of acute colitis.

18 chronic colitis and in the recovery phase of acute colitis.

19 nificantly increased (P < .001) in mice with acute colitis (173.8 arbitrary units [au] +/- 134.8 [sta

20 ults demonstrate an important role for NT in acute colitis and adipose tissue inflammation associated

21 Typhimurium colonization in mouse models of acute colitis and chronic persistent infection.

22 ame result was observed in alphaCD40-induced acute colitis and during peritonitis, suggesting an alte

23 62L and beta7 integrin is required to induce acute colitis and facilitate entry of CD4+ donor T cells

24 ed confirmation of inflammation in mice with acute colitis and high expression levels of P- and E-sel

25 nduced in myenteric plexus neurons (MPNs) in acute colitis and may protect cells from nitric oxide to

26 teinase (MMP)-9 mediates inflammation during acute colitis and the cleavage and activation of the tra

27 Acute colitis and TNF-alpha decrease Phex mRNA and prote

28 e synthase (iNOS) regulation was examined in acute colitis, and MnSOD and iNOS were examined in prima

29 rse of Clostridium difficile toxin A-induced acute colitis, and NTR1 antagonism attenuates the severi

30 n of epimorphin partially protects mice from acute colitis, associated with an increase in crypt cell

31 colonic mucosa promotes inflammation during acute colitis but inhibits inflammation during chronic c

32 L-33 have been described in murine models of acute colitis, but its contribution to chronic inflammat

33 the enhancement of recovery from DSS-induced acute colitis by directly stimulating CEC proliferation.

34 extravasation in the setting of DSS-induced acute colitis, consistent with decreased intestinal dise

35 nockout mice were generated and subjected to acute colitis followed by a short recovery period.

36 Conversely, IL-6 treatment protects against acute colitis in a manner dependent on STAT3 signaling a

37 eropathogenic Escherichia coli (EPEC) caused acute colitis in CTTs, which was associated with ulcerat

38 Such MCMV infection did not induce acute colitis in either wild-type mice or IL-10(-/-) mic

39 ed susceptibility to spontaneous and induced acute colitis in mice lacking either the COX-1 or COX-2

40 Thus, Tyk2 protects against acute colitis in part by amplifying inflammation-induced

41 Acute colitis in rats was induced with 5% acetic acid.

42 V1 receptors in the urinary bladder prior to acute colitis increased the number of bladder neurons re

43 le of conventional dendritic cells (cDCs) in acute colitis induced by a single cycle of dextran sodiu

44 In acute colitis induced by dextran sodium sulfate (DSS), V

45 cterium Bacillus subtilis protects mice from acute colitis induced by the enteric pathogen Citrobacte

46 d quantification of inflammation in a murine acute colitis model, leveraging the natural pathway of l

47 In an in vivo murine acute colitis model, platelet count significantly correl

48 By utilizing HIF reporter mice in an acute colitis model, we investigated the relative contri

49 In a dextran sodium sulfate-induced acute colitis model, WT mice lost more weight, had highe

50 ) development using a CAC mouse model and an acute colitis mouse model.

51 assay and in vivo with a chemically induced acute colitis murine model.

52 s study examined the long-term effects of an acute colitis on central corticotropin-releasing factor

53 ould be discussed after colectomy for severe acute colitis, or in patients naive to IS and anti-TNF.

54 Acute colitis sensitized lumbosacral spinal neurons rece

55 LR4 mice displayed greater susceptibility to acute colitis than singly housed WT mice did.

56 at reducing inflammation in a mouse model of acute colitis than the bioactive peptide alone, and show

57 shes susceptibility of these mice to induced acute colitis, through a mechanism that is not fully und

58 for adaptive immune-mediated protection from acute colitis under conditions of intestinal epithelial

59 nflammatory and proangiogenic effects during acute colitis via a NTR1-prolyl hydroxylase 2/HIF-1alpha

60 Conversely, colectomy for severe acute colitis was associated with decreased risk of IRA

61 ium (DSS), and the severity of the inflicted acute colitis was determined.

62 Acute colitis was induced by administration of Citrobact

63 Acute colitis was induced in some mice by addition of 2.

64 Acute colitis was induced using 4% dextran sodium sulfat

65 g responses of bladder spinal neurons during acute colitis was significantly reduced by RTX from 52.9

66 extran sodium sulfate-induced mouse model of acute colitis, we observed an IL-23-dependent up-regulat

67 Clostridium difficile toxin A induces acute colitis with neutrophil infiltration and up-regula

68 Treg cell transfer, they developed a severe acute colitis with poor body condition that was not obse