ライフサイエンスコーパス: colitis

1 litis patients are suggested to diagnose CMV colitis.

2 nts can induce Th1 cell responses to promote colitis.

3 L/6 mice with dextran sodium sulfate-induced colitis.

4 cal blockade of OSM significantly attenuates colitis.

5 dominal perforation resulting from stercoral colitis.

6 y patients 18 years or older with ulcerative colitis.

7 ) in evaluating the presence and severity of colitis.

8 el homing receptor for T-cells implicated in colitis.

9 nts with Clostridium difficile or ulcerative colitis.

10 ) and dextran sodium sulfate (DSS) models of colitis.

11 imals, blocking IL23 reduces the severity of colitis.

12 SP-miR-31-3p-RhoA pathway that protects from colitis.

13 r new neurons in infectious and inflammatory colitis.

14 sa among associations stronger in ulcerative colitis.

15 lic acid or dextran sodium sulfate to induce colitis.

16 patients with moderate to severe ulcerative colitis.

17 lve intestinal inflammation in patients with colitis.

18 cells, we used an adoptive-transfer model of colitis.

19 ogical inhibition of ILK during experimental colitis.

20 anagement of stercoral colitis with ischemic colitis.

21 gut microbiota developed markedly increased colitis.

22 state for up to 12 weeks, thereby preventing colitis.

23 ics-associated diarrhea and pseudomembranous colitis.

24 an from the diet increases susceptibility to colitis.

25 ble for preventing the development of murine colitis.

26 iciency protected against the development of colitis.

27 d susceptibility to an experimental model of colitis.

28 in mice with dextran sodium sulfate-induced colitis.

29 were highly susceptible to chemical-induced colitis.

30 f IL-10, Helicobacter hepaticus (Hh) induces colitis.

31 (odds ratio 1.75; 1.44-2.13) for ulcerative colitis.

32 pithelium of patients with IBD and mice with colitis.

33 ing mediates microglial activation following colitis.

34 fects were also measured in a mouse model of colitis.

35 G mice protect non-TG mice from induction of colitis.

36 9 studies) of Crohn's disease and ulcerative colitis.

37 reases the efficacy of anti-TNF in mice with colitis.

38 cted of acute gastroenteritis, enteritis, or colitis.

39 increased susceptibility to mouse models of colitis.

40 h infection or in the gut after induction of colitis.

41 assess the mitochondria in a mouse model of colitis.

42 ofacitinib therapy in adults with ulcerative colitis.

43 ine producers, and were powerful inducers of colitis.

44 ecent data also suggest a protective role in colitis.

45 nic fat, which were suggestive for stercoral colitis.

46 as the gold standard in treating ulcerative colitis.

47 rity of autoimmune diseases and experimental colitis.

48 stercoral colitis complicated with ischemic colitis.

49 k of colorectal cancer related to ulcerative colitis.

50 erent types of normal LNs or in animals with colitis.

51 given dextran sodium sulfate (DSS) to induce colitis.

52 ways in a chemically induced murine model of colitis.

53 d to determine the fate of these cells after colitis.

54 riasis, rheumatoid arthritis, and ulcerative colitis.

55 1-3p ameliorated the severity of DSS-induced colitis.

56 given dextran sulfate sodium (DSS) to induce colitis.

57 rons increase from 1-2% to an average 14% in colitis.

58 inflammatory infiltrate in human and murine colitis.

59 in ADCY7 that doubles the risk of ulcerative colitis.

60 ars who were newly diagnosed with ulcerative colitis.

61 nted intestinal inflammation in experimental colitis.

62 iota on intestinal health and development of colitis.

63 sensitized infant mice to the development of colitis.

64 and displayed intermediate susceptibility to colitis.

65 s, which were strongly detected in mice with colitis.

66 were well tolerated, even in mice with acute colitis.

67 [6%] of 362 patients in the 3 mg/kg group), colitis (19 [5%] vs nine [2%]), increased alanine aminot

68 group), dyspnoea (29 [8%] vs 24 [13%]), and colitis (24 [6%] vs none).

69 oup), diarrhoea (58 [15%] vs one [<1%]), and colitis (26 [7%] vs none).

70 00 in Germany) and North America (ulcerative colitis 286 per 100 000 in the USA; Crohn's disease 319

71 prevalence values were in Europe (ulcerative colitis 505 per 100 000 in Norway; Crohn's disease 322 p

72 testinal samples of patients with ulcerative colitis, a condition associated with increased risk for

73 Guided by the Pediatric Ulcerative Colitis Activity Index (PUCAI), patients received initia

74 egulated in the thoracolumbar spinal cord of colitis-affected mice.

75 l as Stat1IEC-KO mice, developed more severe colitis after administration of dextran sulfate sodium t

76 Mice given hgd40 did not develop colitis after administration of oxazolone or 2,4,6-trini

77 essing hREG3A were monitored for DSS-induced colitis after cohousing or feeding feces from control mi

78 GFR from myeloid cells developed more severe colitis after DSS administration, characterized by incre

79 xhibit severe dextran sodium sulfate-induced colitis, ameliorated by TNF inhibition.

80 controls proliferation of IECs in mice with colitis and accelerates mucosal healing by activating ST

81 e high production of IL10 and have increased colitis and adenomatous polyps in chemical and genetic m

82 Here, we showed that miR-19a can promote colitis and colitis-associated colon cancer (CAC) develo

83 it has been implicated in the suppression of colitis and colon cancer.

84 be valuable for studying diseases including colitis and colon cancer.

85 mice are strongly resistant to experimental colitis and colorectal cancer; this is mainly through a

86 nd MAPT for rheumatoid arthritis, ulcerative colitis and Crohn disease.

87 ncluded in the systematic review, ulcerative colitis and Crohn's disease needed to be reported separa

88 f the inflammatory bowel diseases ulcerative colitis and Crohn's disease, we sequenced the whole geno

89 itochondrial iron chelation therapy improved colitis and demonstrated an essential role of mitochondr

90 signature that indicated the development of colitis and discriminated between inflammations of vario

91 P9, has shown promise in treating ulcerative colitis and gastric cancer.

92 disease, multiple sclerosis, and ulcerative colitis and hereby elucidate the molecular mechanisms un

93 ns alleviated pathological conditions in rat colitis and hypertension models via the endogenous opioi

94 TEAP4) was highly induced in mouse models of colitis and in IBD patients.

95 inhibitor exacerbated TNBS- and DSS-induced colitis and increased colonic TNF-alpha, CXCL10, and che

96 o cigarette smoke accelerated development of colitis and increased expression of interferon gamma in

97 ate damaged mitochondria in a mouse model of colitis and inflammatory bowel disease patients, and thi

98 Susceptibility to colitis and influenza A virus infection occurring upon c

99 trafficking in chemically induced models of colitis and investigate the therapeutic potential of BAR

100 biting OXPHOS reduces the severity of murine colitis and psoriasis.

101 Fx-/- mice developed colitis and serrated-like lesions.

102 ared with patients with quiescent ulcerative colitis and that colitis was attenuated in IL-19-deficie

103 ation is the central pathological feature of colitis and the inflammatory bowel diseases.

104 However, the role of miR-31-3p in colitis and the underlying mechanisms has not been eluci

105 l-specific deletion of GATA3 did not develop colitis and their colonic tissues did not produce inflam

106 elial inflammatory signaling pathways during colitis and, as a consequence, targeting M-ILK could pro

107 iated with diseases such as Crohn's disease, colitis, and colon cancer, but mechanistic insights into

108 ty, intestinal inflammation, the severity of colitis, and colon tumorigenesis.

109 e of host-parasite interaction during amebic colitis, and highlights a potential immunomodulatory tar

110 , alkaline phosphatase increase (five [1%]), colitis, and muscle weakness (both four [1%]).

111 from bone marrow transplantation, ulcerative colitis, and partial hepatectomy.

112 pathogenesis of Crohn's disease, ulcerative colitis, and pouchitis.

113 enuated the wasting syndrome and severity of colitis ( approximately 70% reduction in the Colitis Dis

114 Here we show that although signs of colitis are absent in IL10R-deficient mice during the fi

115 Crohn's disease and ulcerative colitis are heterogeneous inflammatory bowel diseases, a

116 (IBD), such as Crohn disease and ulcerative colitis, are chronic relapsing conditions that affect a

117 Dysbiosis and susceptibility to colitis associated with Nlrp12 deficency were reversed e

118 myeloid AC protects from tumor incidence in colitis-associated cancer (CAC) and inhibits the expansi

119 myeloid cells contributes to development of colitis-associated cancer and Apc(Min)-dependent intesti

120 dence for their roles in the pathogenesis of colitis-associated cancer and sporadic colorectal cancer

121 e intestine, where it helps protects against colitis-associated cancer by regulating HMOX-1 expressio

122 of colorectal cancer gave rise to the term "colitis-associated cancer" and the concept that inflamma

123 arthritis, inflammatory intestinal disease, colitis-associated cancer, and lipopolysaccharide (LPS,

124 showed that miR-19a can promote colitis and colitis-associated colon cancer (CAC) development using

125 ochondrial iron chelation were assessed in a colitis-associated colon cancer model (CAC).

126 In colitis-associated colon cancer models, epithelial HIF-2

127 Genetic ablation of IRE1alpha prevented the colitis-associated colonic tumorigenesis in mice.

128 to colitis-prone mice-protected them against colitis-associated death.

129 is associated with subsequent development of colitis-associated dysplasia after in situ fluorination

130 nflammation and site-specific development of colitis-associated dysplasia in the descending colon sho

131 The signal intensity in mice with colitis-associated dysplasia was compared with that in c

132 methane and dextran sulfate sodium to induce colitis-associated dysplasia.

133 positive correlation with the development of colitis-associated dysplasia.

134 Chronic trinitrobenzene sulfonic acid (TNBS) colitis-associated intestinal fibrosis mouse model with

135 yers revealed that barrier disruption by the colitis-associated Th2-type cytokines, IL-4 and IL-13, d

136 d for the treatment of IBD and prevention of colitis-associated tumorigenesis.

137 time that baicalein attenuated TNBS-induced colitis, at least in part, via inhibition of TLR4/MyD88

138 susceptible to a more aggressive infectious colitis caused by Citrobacter rodentium.

139 dium sulfate (DSS) and Citrobacter rodentium colitis (CC) was induced in adult mice and colonic neuro

140 mice, as well as the severity of DSS-induced colitis; changes in 1 ingredient could be offset by chan

141 different IBD subtypes, including ulcerative colitis, colonic Crohn's disease and ileal Crohn's disea

142 TA3 by lamina propria T cells from mice with colitis compared with controls.

143 d in establishing the diagnosis of stercoral colitis complicated with ischemic colitis.

144 Mice with bacterial colitis demonstrated a temporally associated increase in

145 had moderately to severely active ulcerative colitis despite previous conventional therapy or therapy

146 re collected at different time points during colitis development and analyzed by histology, immunohis

147 The role of Cd14 in colitis development was determined using dextran sulfate

148 rotein and fiber had the strongest effect on colitis development.

149 colitis ( approximately 70% reduction in the Colitis Disease Activity Index).

150 MSC-Ex reduced colitis, disease activity index (DAI), and histological

151 era mice with chronic dextran sodium sulfate colitis exhibited delayed ulcer healing, more mucosal in

152 stinal tissues from patients with ulcerative colitis expressed significantly lower levels of SIRT1 mR

153 who did not receive antiviral treatment had colitis flare-ups after the index admission.

154 h; these mice developed less-severe forms of colitis following DSS administration.

155 prevalence of Crohn's disease or ulcerative colitis from 1990 or later.

156 ed between inflammations of various origins (colitis from arthritis).

157 s of colorectal cancer related to ulcerative colitis from Asia vary.

158 s related to colorectal cancer in ulcerative colitis from inception to July 1, 2016.

159 NF in colon tissues, compared with mice with colitis given siRNA against Tnf mRNA without ultrasound

160 Conversely, patients with ulcerative colitis had an increased risk of liver disease progressi

161 tissues of patients with IBD, and mice with colitis, had increased expression of IL28 compared with

162 itional gp96-null mice developed spontaneous colitis, had increased levels of systemic and fecal IgA,

163 trospective studies of paediatric ulcerative colitis have had limited ability to describe disease pro

164 Patients with ulcerative colitis have mucosal inflammation starting in the rectum

165 hazard ratio 2.19; 1.44-3.34) and ulcerative colitis (hazard ratio 1.63; 1.18-2.27) was significantly

166 ciated with diarrhea, dysentery, hemorrhagic colitis (HC) and hemolytic uremic syndrome (HUS).

167 ory symptoms, including wasting, dermatitis, colitis, hypereosinophilia, and high IgE levels.

168 In mice with colitis, hypo-fucosylated anti-TNF significantly increas

169 in patients with Crohn disease or ulcerative colitis, identifying that expression correlates with dis

170 hat Ccdc88b inactivation in T cells prevents colitis in a transfer model, and detect high colonic lev

171 Following colitis in adult Sox2CreER:YFP mice, YFP initially expre

172 used dextran sulphate sodium (DSS) to induce colitis in C57BL/6 N mice.

173 sents a severe form of antibiotic-associated colitis in critically ill patients signified by microbio

174 Two associated factors for CMV colitis in hospitalized IBD patients were that they were

175 the prevalence and clinical features of CMV colitis in hospitalized IBD patients.

176 Attenuated colitis in IL-19-deficient animals was associated with r

177 contrast, the same TSO treatment exacerbates colitis in immunosuppressed animals.

178 insic IL10R signaling is required to prevent colitis in infancy is unknown.

179 me that prevents expression of GATA3 reduces colitis in mice, independently of TNF, and reduces level

180 liorated the clinical course of experimental colitis in mice, resulting in improved weight gain and s

181 e of its metabolites reduces the severity of colitis in mice, whereas removing tryptophan from the di

182 stigated the role of GATA3 in development of colitis in mice.

183 genitor cells that overexpress MFSD2A reduce colitis in mice.

184 30c to significantly improve the outcome of colitis in mice.

185 tly increases susceptibility to experimental colitis in mice.

186 fecal microbiota and affects development of colitis in mice.

187 Stat1IEC-KO mice also developed more severe colitis in response to oxazolone than control mice.

188 and cellulose fiber reduced the severity of colitis in SPF mice, whereas methylcellulose increased s

189 olon inflammation over 3 days; hgd40 reduced colitis in TNFR double-knockout mice.

190 small intestinal obstruction in one patient; colitis in two patients, and neuritis and skin ulcer in

191 Treatments for ulcerative colitis include 5-aminosalicylic acid drugs, steroids, a

192 he selected lead to alleviate the effects of colitis induced by 2,4-dinitrobenzenesulfonic acid in ra

193 the epithelial inflammatory signaling during colitis induced by dextran sodium sulfate.

194 re, we demonstrate in a preclinical model of colitis-induced colorectal cancer that regular consumpti

195 in mucus gut microbiota composition preceded colitis-induced inflammation and stool microbial differe

196 In analyses of intestinal tissues, colitis induction, and gut microbiota in mice with intes

197 during sensitization and challenge phase of colitis induction.

198 Ulcerative colitis is a chronic inflammatory disease affecting the

199 Stercoral colitis is a rare inflammatory process involving the col

200 Colitis is exacerbated in patients with concurrent cytom

201 patients with Crohn's disease or ulcerative colitis is necessary for their total care and should be

202 One of the hallmarks of amoebic colitis is the detection of Entamoeba histolytica (Eh) t

203 Dextran sodium sulfate-induced colitis model was established in C57BL/6 mice, and MSC-E

204 tion in a mouse dextran sulfate sodium (DSS) colitis model, and we demonstrate that the epithelium is

205 unities exhibited differential survival in a colitis model.

206 s examined in murine airway inflammation and colitis models, and the role of Neu5Gc in regulating imm

207 roscopic symptoms of IBD in the TNBS-induced colitis mouse model, indicating the potential of FOLH1/G

208 lopment using a CAC mouse model and an acute colitis mouse model.

209 lications, including hypothyroidism (n = 3), colitis (n = 2), and hepatitis (n = 1).

210 es from age-matched patients with ulcerative colitis (n=10) vs without IBD (n=8, controls).

211 xpression of miR-223 attenuated experimental colitis, NLRP3 levels, and IL-1beta release.

212 testinal tissues were collected; severity of colitis, numbers and size of tumors, and intestinal barr

213 ciency (one [3%] and two [5%] patients), and colitis (one [3%] and two [5%] patients).

214 atheter-related blood stream infections, two colitis, one extracorporeal membrane oxygenation cannula

215 in rhesus macaques also resembles ulcerative colitis, one form of human inflammatory bowel disease.

216 icrobial differences only became apparent at colitis onset.

217 s from human subjects with active ulcerative colitis or Crohn's disease, implicating the loss of this

218 atients with Crohn's disease (CD)-associated colitis or without inflammatory bowel disease (IBD), and

219 younger and had Crohn's disease, ulcerative colitis, or IBD-unclassified with 24,543.0 patient-years

220 e discussed after colectomy for severe acute colitis, or in patients naive to IS and anti-TNF.

221 s a diagnosis of Crohn's disease, ulcerative colitis, or inflammatory bowel disease unclassified befo

222 r degeneration (P=1.4 x 10(-12)), ulcerative colitis (P<1.0 x 10(-20)), type 2 diabetes (P=2.8 x 10(-

223 opathology studies and/or PCR for refractory colitis patients are suggested to diagnose CMV colitis.

224 The CMV colitis patients' demographic data, clinical information

225 Compared to CD patients without CMV colitis, patients with CMV colitis were more often older

226 ants with exogenous creatine ameliorated the colitis phenotype.

227 its absence on T cells results in attenuated colitis progression.

228 These results suggest that colitis promotes rapid enteric neurogenesis in adult mic

229 olic profiles did, however, discriminate the colitis-prone mdr1a (-/-) genotype from controls.

230 from this family, that-when administered to colitis-prone mice-protected them against colitis-associ

231 ral treatment is recommended to decrease the colitis relapse rate.

232 ology in the IL-10-deficient murine model of colitis relative to mice fed a low salt diet.

233 e and 15 (83.3%) of 18 studies on ulcerative colitis reported stable or decreasing incidence of infla

234 h1) were exclusively identified in mice with colitis, revealing changes in the peptidome associated w

235 d type 1 diabetes, Crohn disease, ulcerative colitis, rheumatoid arthritis, celiac disease, psoriasis

236 the effects of anti-TNF: their histological colitis scores were as severe as those from FcgammaR(-/-

237 sease activity index (DAI), and histological colitis scores, and increased the body weight.

238 Chemically induced osmotic diarrhea reduced colitis severity and C. rodentium burden in claudin-2-de

239 anti-TNF and was more effective in reducing colitis severity as measured by histology.

240 Colitis significantly altered the stability of mucosal R

241 In human colitis, Sox2-expressing neurons increase from 1-2% to a

242 ity; especially if complicated with ischemic colitis, stercoral ulcer formation and subsequent perfor

243 beta-gal reporter to show that inflammatory colitis suppresses the activity of the St14 gene promote

244 Among 27 colitis susceptibility phenotypes identified and mapped,

245 hn's disease patients and causally linked to colitis susceptibility.

246 nths of age, and did not develop more severe colitis than control mice at 4-6 months.

247 Mefv-/- mice developed more severe colitis than control mice, with a greater extent of epit

248 fective gut microbiota developed more severe colitis than control mice.

249 rovides superior protection from DSS-induced colitis than curcumin alone, highlighting the anti-infla

250 ucing inflammation in a mouse model of acute colitis than the bioactive peptide alone, and showed enh

251 stinal inflammation, compared with mice with colitis that did not receive MFSD2A-overexpressing endot

252 o delineate mechanisms regulating ulcerative colitis, the role of acid ceramidase (AC) in intestinal

253 t report of an effect of NAMPT inhibitors in colitis, this result paves the way for novel application

254 inal homeostasis and protects against murine colitis through interactions with its receptor AdipoR1 a

255 Psyllium fiber reduced the severity of colitis through microbiota-dependent and microbiota-inde

256 del of dextran sodium sulphate (DSS) induced colitis to study the efficacy, mechanisms and safety of

257 ith moderately to severely active ulcerative colitis, tofacitinib was more effective as induction and

258 In mice with colitis, transplanted endothelial progenitor cells that

259 31-3p mimics may be a promising approach for colitis treatment.

260 ardiac failure (one [<1%] vs one [<1%]), and colitis (two [<1%] vs none).

261 uncertain origin, which includes ulcerative colitis (UC) and Crohn's disease (CD).

262 risk for Crohn's disease (CD) and ulcerative colitis (UC) in a case-only study of patients and in mou

263 The odds of having ulcerative colitis (UC) or Crohn disease (CD) were elevated in carr

264 tudy with Crohn's disease (CD) or ulcerative colitis (UC) patients initiating anti-integrin therapy (

265 and IBD, Crohn's disease (CD), or ulcerative colitis (UC) were investigated.

266 ncluding Crohn's disease (CD) and ulcerative colitis (UC), are complex chronic inflammatory condition

267 e response in the pathogenesis of ulcerative colitis (UC)-few data are available from treatment-naive

268 pathway has been associated with ulcerative colitis (UC).

269 (IRA) failure after colectomy for ulcerative colitis (UC).

270 Crohn's disease (CD) and 361 with ulcerative colitis (UC).

271 with Crohn's disease (n = 61) or ulcerative colitis (UC, n = 74) or from patients without inflammato

272 ith Crohn's disease [CD], 23 with ulcerative colitis [UC]), and 30 children without IBD (controls).

273 utive patients with IBD (211 with ulcerative colitis [UC], 234 with Crohn's disease [CD]; 236 male),

274 In mice with colitis, ultrasound delivery of unencapsulated siRNA aga

275 Ulcerative colitis usually presents with bloody diarrhoea and is di

276 fference between individuals with ulcerative colitis vs Crohn's disease.

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

278 s with quiescent ulcerative colitis and that colitis was attenuated in IL-19-deficient mice.

279 CMV colitis was diagnosed as having positive inclusion bodie

280 Once colitis was established, mice were treated with solvent,

281 biopsies of patients with active ulcerative colitis was increased compared with patients with quiesc

282 Colitis was induced by administration of oxazolone or 2,

283 Experimental chronic colitis was induced by oral administration of dextran so

284 Colitis was induced in another set of control and hREG3A

285 Colitis was induced in mice by transfer of CD4+CD45RB(hi

286 Acute colitis was induced in some mice by addition of 2.5% dex

287 tal cancer in Asian patients with ulcerative colitis was similar to recent estimates in Europe and No

288 robiota on mice with and without DSS-induced colitis, we found complex mixtures of nutrients affect i

289 In studies with DSS-induced colitis, we found that pyrin (MEFV) is required for infl

290 ongitudinal study of various mouse models of colitis, we identified a serum miRNA signature that indi

291 ients without CMV colitis, patients with CMV colitis were more often older (p < 0.005).

292 ohn's disease and no IBD (both vs ulcerative colitis) were associated with a lower risk of LTD (unadj

293 with clodronate inhibited the development of colitis, while the absence of IL10R specifically on macr

294 ture identified in mice predicted ulcerative colitis with 83.3% accuracy.

295 d a total of 31 287 patients with ulcerative colitis with a total of 293 reported colorectal cancers.

296 with exacerbated myeloid-driven experimental colitis with heightened clinical, histopathological, and

297 in the diagnosis and management of stercoral colitis with ischemic colitis.

298 predominant feature during the initiation of colitis with miR-223 deficiency.

299 k factor for the development of diarrhea and colitis with varying severity.

300 ude mice with dextran sodium sulfate-induced colitis, with or without oral administration of DHA.

301 glia becomes expressed by neurons following colitis, without observable DNA replication.