ライフサイエンスコーパス: intestinal disease

1 ive colitis, and 45 control subjects without intestinal disease).

2 igella flexneri from developing inflammatory intestinal disease.

3 testinalis causes both a disseminated and an intestinal disease.

4 l intestinal pathobionts that can exacerbate intestinal disease.

5 the formation of A/E lesions in vivo and in intestinal disease.

6 gamma-glutamyl transferase activity without intestinal disease.

7 ch a cholestasis phenotype in the absence of intestinal disease.

8 determinants that confer virulence in extra-intestinal disease.

9 tial reservoir for bacteria that can promote intestinal disease.

10 iarrhea and colitis, a healthcare-associated intestinal disease.

11 erning pathophysiology in multiple models of intestinal disease.

12 mmatory commensals that preferentially drive intestinal disease.

13 ssion and could help elucidate mechanisms of intestinal disease.

14 ced acute colitis, consistent with decreased intestinal disease.

15 have greatly increased our understanding of intestinal disease.

16 therapeutic strategy to prevent or alleviate intestinal disease.

17 y initiated during acute infection prevented intestinal disease.

18 kittens euthanized for reasons unrelated to intestinal disease.

19 herapeutic decoys to ameliorate CPE-mediated intestinal disease.

20 red to sustain bacterial adhesion and incite intestinal disease.

21 ffer against the fitness-reducing effects of intestinal disease.

22 is essential for the development of maximal intestinal disease.

23 ive therapy for treatment of immune-mediated intestinal disease.

24 red susceptibility to the development of the intestinal disease.

25 ologic conditions and the pathophysiology of intestinal diseases.

26 e central to the pathogenesis of a number of intestinal diseases.

27 o mediate the effects of bacterial toxins in intestinal diseases.

28 helial barrier is a hallmark of inflammatory intestinal diseases.

29 e therapeutic potential for the treatment of intestinal diseases.

30 utic implications of targeting HIF-2alpha in intestinal diseases.

31 ostridium difficile causes potentially fatal intestinal diseases.

32 ry factor in the development of upper gastro-intestinal diseases.

33 eld insight into strategies to prevent these intestinal diseases.

34 ommon feature of functional and inflammatory intestinal diseases.

35 n increasingly common heterogeneous group of intestinal diseases.

36 ells show promise for therapy in a number of intestinal diseases.

37 th ALP levels may point to genes for bone or intestinal diseases.

38 oteins and their role in the pathogenesis of intestinal diseases.

39 e benefit of these molecules in treatment of intestinal diseases.

40 at they also prevent C. rodentium-associated intestinal disease after a single injection.

41 nover in the body and has been implicated in intestinal disease and cancer; understanding the regulat

42 Spontaneous intestinal disease and death occurred with low penetranc

43 est in establishing in vitro models of human intestinal disease and in developing drug-screening plat

44 hia coli (EPEC) is a leading cause of severe intestinal disease and infant mortality in developing co

45 to illuminate how amoebic trophozoites cause intestinal disease and liver abscess, and have expanded

46 stigated the use of MSCs in the treatment of intestinal disease and modeled abnormal repair by creati

47 tamin D absorption, resulting from extensive intestinal disease and resection of duodenum and jejunum

48 It may mimic various intestinal diseases and be confused with certain nonisch

49 stem for studies in a broad context of human intestinal diseases and treatments.

50 cells were preserved in LSI animals without intestinal disease, and levels of CD3 staining in all LS

51 Numerous intestinal diseases are characterized by immune cell act

52 uman liver disorders, whereas their roles in intestinal diseases are unclear.

53 more than five decades to treat a variety of intestinal diseases associated with pathological imbalan

54 difficile spo0A mutant derivatives can cause intestinal disease but are unable to persist within and

55 nction is insufficient to cause experimental intestinal disease but can broadly activate mucosal immu

56 din-3 was reduced in LSI animals with severe intestinal disease but did not correlate with increased

57 l for pathogen colonization and induction of intestinal disease, but the mechanisms by which host imm

58 intestinal epithelial barrier occurs in many intestinal diseases, but neither the mechanisms nor the

59 tential source of cells for the treatment of intestinal diseases, but strategies to increase the numb

60 ntial pathogen that induces NEC and triggers intestinal disease by modulating enterocyte intracellula

61 etter utilize beneficial microbes to prevent intestinal disease caused by pathogenic bacteria, ultima

62 The intestinal disease coccidiosis, caused by protozoan para

63 c role in rheumatoid arthritis, inflammatory intestinal disease, colitis-associated cancer, and lipop

64 g better depicted the extent and severity of intestinal disease compared with single-shot fast SE ima

65 o evaluate the association between extent of intestinal disease determined at operation and outcome m

66 he impact of norovirus-associated infectious intestinal disease, especially in children aged <5 years

67 hylogeny of the commonest protozoal agent of intestinal disease, Giardia, is unclear.

68 LSI animals that did not develop intestinal disease had increased T-cell intracytoplasmic

69 l organoids offer great promise for modeling intestinal diseases; however, harvesting intestinal tiss

70 ing estimates of the incidence of infectious intestinal disease (IID) caused by norovirus are based o

71 rge-scale, prospective studies of infectious intestinal disease (IID) in developed countries are unco

72 hese mutations develop inflammatory skin and intestinal disease in addition to ectodermal dysplasia w

73 were ascertained in the Study of Infectious Intestinal Disease in England (1993-1996), and stool spe

74 on of England during the Study of Infectious Intestinal Disease in England (1993-1996).

75 coli (ETEC) strains are important causes of intestinal disease in humans and lead to severe producti

76 ay contribute to the relatively low level of intestinal disease in patients with CF.

77 ion may reduce the incidence and severity of intestinal disease in patients with CF.

78 infection associated with hepatobiliary and intestinal disease in simian immunodeficiency virus (SIV

79 1993-1996 and the Second Study of Infectious Intestinal Disease in the Community (IID2) in 2008-2009.

80 fic rates of norovirus-associated infectious intestinal disease in the United Kingdom.

81 diseases (CIBD), are common causes of gastro-intestinal disease in the Western world, with a combined

82 cholera toxin, or CD40 triggering can induce intestinal disease in transgenic mice.

83 Rotavirus is a major cause of infectious intestinal disease in young children; a substantial prev

84 progression of several intestinal and extra-intestinal diseases, including childhood asthma developm

85 Caspase dysfunction has been associated with intestinal diseases, including inflammatory bowel diseas

86 l translational targets for the treatment of intestinal diseases, including inflammatory bowel diseas

87 lated to be a central predisposing factor to intestinal diseases, including inflammatory bowel diseas

88 genetically-determined chronic inflammatory intestinal disease induced by an environmental precipita

89 nd that Atg16L1 mutant mice are resistant to intestinal disease induced by the model bacterial pathog

90 Cystic fibrosis (CF) intestinal disease is associated with the pathological m

91 LIGHT-mediated intestinal disease is dependent on both of its identifie

92 Stem cell therapy for intestinal diseases is an emerging area in clinical gast

93 ssed protein whose expression or function in intestinal diseases is not known.

94 n the role of intestinal epithelial cells in intestinal diseases, it is now clear that this cell laye

95 ncern because of its ability to cause severe intestinal disease leading to complications such as rela

96 al treatment failure, the presence of stable intestinal disease made them eligible for surgery.

97 In contrast to the approach to intestinal disease, many centers are advocating a more a

98 rough the same route as rotavirus infectious intestinal disease: person-to-person contact.

99 olecular mechanisms for the action of ROS in intestinal diseases remain poorly defined.

100 with IL-33 or transfer of ILC2s ameliorated intestinal disease severity in an AREG-dependent manner.

101 Idiopathic intestinal disease states characterized by active inflam

102 similarly important when type A and C human intestinal disease strains attach to Caco-2 cells.

103 contribute to host cell attachment of human intestinal disease strains, since a nanI null mutant con

104 ducted in the United Kingdom: the Infectious Intestinal Disease Study in England (IID1) in 1993-1996

105 n effective treatment for acute inflammatory intestinal diseases such as acute flare of inflammatory

106 erapeutic role for NOD2 in the protection of intestinal diseases such as NEC.

107 could play an important role in Th1-mediated intestinal diseases, such as Crohn's disease, where incr

108 the treatment and prevention of inflammatory intestinal diseases, such as IBD and colitis-associated

109 otizing enterocolitis (NEC) is a devastating intestinal disease that has been associated with Cronoba

110 e compromised (Myd88(-/-)) leads to a severe intestinal disease that is often fatal.

111 this space is extended to less-well-studied intestinal diseases that may also have an important micr

112 review focuses on how the microbiota drives intestinal disease through alterations in microbial comm

113 ducing E. coli strains in the progression of intestinal disease to more severe systemic complications

114 Histologic evidence of intestinal disease was observed in only half of infected

115 ether analogous changes might occur in human intestinal disease, we established a three-dimensional i

116 Clostridium difficile causes chronic intestinal disease, yet little is understood about how t