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 ffer against the fitness-reducing effects of intestinal disease.

3 is essential for the development of maximal intestinal disease.

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

5 red susceptibility to the development of the intestinal disease.

6 igella flexneri from developing inflammatory intestinal disease.

7 testinalis causes both a disseminated and an intestinal disease.

8 an gut and how these might affect health and intestinal disease.

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

10 cell tropism, and the role of tuft cells in intestinal disease.

11 t can cause nosocomial antibiotic-associated intestinal disease.

12 nterobacteriaceae may be useful in resolving intestinal disease.

13 ed fungal antigens in the context of chronic intestinal disease.

14 tractive target to modulate ILC3 function in intestinal disease.

15 can induce nosocomial antibiotic-associated intestinal disease.

16 tial reservoir for bacteria that can promote intestinal disease.

17 y initiated during acute infection prevented intestinal disease.

18 l intestinal pathobionts that can exacerbate intestinal disease.

19 gamma-glutamyl transferase activity without intestinal disease.

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

21 determinants that confer virulence in extra-intestinal disease.

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

23 erning pathophysiology in multiple models of intestinal disease.

24 mmatory commensals that preferentially drive intestinal disease.

25 ssion and could help elucidate mechanisms of intestinal disease.

26 ced acute colitis, consistent with decreased intestinal disease.

27 have greatly increased our understanding of intestinal disease.

28 therapeutic strategy to prevent or alleviate intestinal disease.

29 kittens euthanized for reasons unrelated to intestinal disease.

30 herapeutic decoys to ameliorate CPE-mediated intestinal disease.

31 red to sustain bacterial adhesion and incite intestinal disease.

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

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

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

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

36 ly)phenols contributing to the prevention of intestinal diseases.

37 echanisms that govern the pathophysiology of intestinal diseases.

38 nt of colon cancer and colitis, two types of intestinal diseases.

39 iver abscess, and is associated with chronic intestinal diseases.

40 rotect against environmental hazards-induced intestinal diseases.

41 nd modulation of inflammatory and infectious intestinal diseases.

42 may provide new clues for the prevention of intestinal diseases.

43 es has been associated with inflammation and intestinal diseases.

44 egulation of the severity of T cell-mediated intestinal diseases.

45 potential therapeutic target in inflammatory intestinal diseases.

46 ure studies on infection- or allergen-driven intestinal diseases.

47 ppressive strategy to mitigate T cell-driven intestinal diseases.

48 t provides a platform for discovery in other intestinal diseases.

49 of new targets for drug development to treat intestinal diseases.

50 a prerequisite for elucidating their role in intestinal diseases.

51 tion may have therapeutic potential in human intestinal diseases.

52 rtunities for improved mouse models of human intestinal diseases.

53 ologic conditions and the pathophysiology of intestinal diseases.

54 helial barrier is a hallmark of inflammatory intestinal diseases.

55 e therapeutic potential for the treatment of intestinal diseases.

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

57 ostridium difficile causes potentially fatal intestinal diseases.

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

59 eld insight into strategies to prevent these intestinal diseases.

60 ommon feature of functional and inflammatory intestinal diseases.

61 n increasingly common heterogeneous group of intestinal diseases.

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

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

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

65 (NEC) is a common, potentially catastrophic intestinal disease among very low birthweight premature

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

67 Spontaneous intestinal disease and death occurred with low penetranc

68 to contain pro-inflammatory immunity during intestinal disease and highlight the utility of mycobiot

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

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

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

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

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

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

75 st associations between chronic inflammatory intestinal diseases and pancreatic ductal adenocarcinoma

76 ics to the GI tract for treating challenging intestinal diseases and potentially other conditions.

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

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

79 adults (aged >=18 years) without history of intestinal disease, antibiotic treatment, or hospital ad

80 Numerous intestinal diseases are characterized by immune cell act

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

82 unction and biological processes involved in intestinal diseases as well as gastrointestinal and dono

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

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

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

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

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

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

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

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

91 Thus, we demonstrate that an extra-intestinal disease can trigger an ILC2/IL-9 immune circu

92 Coccidiosis, an intestinal disease caused by Eimeria parasites, is respo

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

94 The intestinal disease coccidiosis, caused by protozoan para

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

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

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

98 t bowel syndrome (SBS) and potentially other intestinal diseases (e.g., IBD).

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

100 omeostasis and modulating the progression of intestinal diseases from both metabolic and immunologica

101 abundance of microorganisms associated with intestinal diseases from Eubacteriales, Desulfovibrional

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

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

104 ompared to two control groups without active intestinal disease, HC and CM, which may suggest a role

105 atory differentiation cascade, and associate intestinal disease heritability with specific cell types

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

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

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

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

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

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

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

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

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

115 The intestinal disease in patients with TTC7A deficiency is

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

117 1993-1996 and the Second Study of Infectious Intestinal Disease in the Community (IID2) in 2008-2009.

118 Furthermore, the intestinal disease in the LckP440S/P440S mice is prevent

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

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

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

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

123 or the onset of several immune-related extra-intestinal diseases including coeliac disease, diabetes

124 s and differences with other immune-mediated intestinal diseases, including a common upregulation of

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

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

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

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

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

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

131 inks between bacterial metabolites and human intestinal disease is a significant challenge.

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

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

134 ever, the mechanism by which Cdx2 influences intestinal disease is not clear.

135 epithelial integrity and the development of intestinal disease is of increasing interest.

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

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

138 en gut barrier integrity and inflammation in intestinal diseases is well established, we review here

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

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

141 IL-10 signaling increases susceptibility to intestinal diseases like inflammatory bowel disease, we

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

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

144 nd modulate immune pathways, contributing to intestinal diseases, metabolic syndrome, and chronic inf

145 s (<32 weeks' gestation) who did not develop intestinal disease or sepsis over a study period of 10 y

146 ic toxin-producing bacterium associated with intestinal diseases, particularly in neonatal humans and

147 unding variants associated with inflammatory intestinal diseases, particularly, ulcerative colitis, C

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

149 distinct from the core symptom group: gastro-intestinal disease, productive cough, confusion, and pau

150 insights into dietary lipid contribution to intestinal disease progression and identify new potentia

151 ighlight that oral commensals can exacerbate intestinal disease, providing pathways to design therape

152 ium difficile infections (CDIs), which cause intestinal disease ranging from mild diarrhea to pseudom

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

154 iarrhea and colitis, a healthcare-associated intestinal disease resulting in a significant fatality r

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

156 Implicated as regulators in intestinal diseases, sphingolipids are a potential corne

157 Idiopathic intestinal disease states characterized by active inflam

158 changes in O-glycan structure in a number of intestinal disease states.

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

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

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

162 enzyme which is closely associated with the intestinal disease such as ulcerative colitis (UC).

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

164 l homeostasis and protecting against various intestinal diseases such as colitis and intestinal tumor

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

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

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

168 nes for neuropathic, inflammatory, and extra-intestinal diseases, suggesting neuronal contributions t

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

170 Crohn's disease is a chronic inflammatory intestinal disease that is frequently accompanied by abe

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

172 chsprung disease (HSCR) is a rare congenital intestinal disease that occurs in 1 in 5,000 live births

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

174 nd colorectal cancer (CRC) are heterogeneous intestinal diseases that threaten the health of an incre

175 eric glia modulate immune responses in other intestinal diseases, their interaction with the colorect

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

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

178 ermogenic fat-epithelial cell axis regulates intestinal disease tolerance during experimental colitis

179 We find that intestinal disease tolerance is a metabolically expensiv

180 tified an unexpected mechanism that controls intestinal disease tolerance with implications for colit

181 drug delivery is particularly promising for intestinal disease treatment.

182 antitumor and anti-inflammation efficacy for intestinal disease treatment.

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

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

185 o a large proportion of chronic inflammatory intestinal diseases, we hypothesize that the genomic reg

186 ivity and they even precede the onset of the intestinal disease, while episcleritis are common define

187 ol group comprised individuals without known intestinal disease who were referred for colorectal canc

188 eline to study host-microbe interactions and intestinal disease will enable the generation of hypothe

189 and Crohn's disease are chronic inflammatory intestinal diseases with perplexing heterogeneity in dis

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