ライフサイエンスコーパス: acute colitis

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

2 mpairs epithelial regeneration in a model of acute colitis.

3 egrity in vivo during experimentally induced acute colitis.

4 thereby contributing to the pathogenesis of acute colitis.

5 ible to dextran sodium sulfate (DSS)-induced acute colitis.

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

7 as highly protective at treating established acute colitis.

8 estinal epithelium, and infections result in acute colitis.

9 ontributing factors to the resulting typical acute colitis.

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

11 arly striking when Dkk1 was inhibited during acute colitis.

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

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

14 the intestinal mucosa and the development of acute colitis.

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

16 sal ulceration and apoptosis in experimental acute colitis.

17 the outcome of inflammatory response during acute colitis.

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

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

20 IECs targets Nos2 expression and aggravates acute colitis.

21 he initiation, progression and resolution of acute colitis.

22 activated to mediate re-epithelialization in acute colitis.

23 for anti-IBD properties in a mouse model of acute colitis.

24 an cell-based assays and in a mouse model of acute colitis.

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

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

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

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

29 62L and beta7 integrin is required to induce acute colitis and facilitate entry of CD4+ donor T cells

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

31 ia O-acetylation was observed in mice during acute colitis and in colon biopsies from patients with i

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

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

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

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

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

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

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

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

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

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

42 ) demonstrate that Th17 responses induced by acute colitis contribute to increased disease severity d

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

44 In response to acute colitis, hepatic Slc39a8 mRNA (gene encoding the M

45 +) T cells expressing IL-26, which attenuate acute colitis in a humanized IL-26 transgenic mouse mode

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

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

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

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

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

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

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

53 Acute colitis induced a transient increase in the produc

54 inflammation were also reduced after either acute colitis induced by 5% DSS or repeat 2% DSS induced

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

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

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

58 anti-inflammatory and can protect mice from acute colitis induced by the enteric pathogen Citrobacte

59 The role of Gasdermin C was analyzed in acute colitis, infection and colitis-associated cancer.

60 yed the dextran sodium sulfate (DSS)-induced acute colitis model in mice with (WT) or without Lgals2

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

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

63 In the dextran sodium sulfate-induced acute colitis model, systemic treatment with MVs prevent

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

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

66 ells appear in the colon in murine tumor and acute colitis models.

67 In an acute colitis mouse model, this therapeutic system ameli

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

69 oborated in a dextran sodium sulfate-induced acute colitis mouse model.

70 gical features in a delayed treatment of the acute colitis mouse model.

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

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

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

74 Acute colitis sensitized lumbosacral spinal neurons rece

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

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

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

78 No changes were found in models of acute colitis, type 2 intestinal infection and colitis-a

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

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

81 Acute colitis was associated with an increase in aldehyd

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

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

84 Acute colitis was induced by administration of Citrobact

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

86 Acute colitis was induced using 4% dextran sodium sulfat

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

88 Here, using a mouse model of acute colitis, we found that enteric glia contribute to

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

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

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