ライフサイエンスコーパス: large intestine

1 ct) but detrimental in the main habitat (the large intestine).

2 om spreading from the small intestine to the large intestine.

3 al tissues such as the related mucosa of the large intestine.

4 hable bacterial populations in the small and large intestine.

5 pism compared to MNV-1 by replicating in the large intestine.

6 mptoms, including intermittent bleeding from large intestine.

7 evolve as a noninvasive imaging test of the large intestine.

8 s, diagnosis, and treatment of polyps in the large intestine.

9 nded clones to evenly seed the small but not large intestine.

10 identify stem cells throughout the small and large intestine.

11 of secretory cells throughout the small and large intestine.

12 parallel in different segments of small and large intestine.

13 entional culture techniques in the small and large intestine.

14 etary polysaccharide substrates in the human large intestine.

15 place the normal microbiota of the small and large intestine.

16 in self-limiting mucosal inflammation of the large intestine.

17 st Dra expression in the jejunum relative to large intestine.

18 easing in frequency in a gradient toward the large intestine.

19 cid may have an antineoplastic effect in the large intestine.

20 s the growth of mucosa in both the small and large intestine.

21 ntestinal tumorigenesis, particularly in the large intestine.

22 ntified only in minute quantities within the large intestine.

23 nthesized biotin and pantothenic acid in the large intestine.

24 s largely restricted to moderate staining of large intestine.

25 not in the myenteric plexus of the small and large intestine.

26 e majority of NeuN-li cells in the small and large intestine.

27 the esophagus, stomach, small intestine, and large intestine.

28 pression in the mucosa of both the small and large intestine.

29 ne exhibited higher activity levels than the large intestine.

30 are synthesized by normal microflora of the large intestine.

31 , lymph nodes, spleen, thymus, and small and large intestine.

32 nd in the submucosal plexus of the small and large intestine.

33 ouse and found high levels of 15-PGDH in the large intestine.

34 al mucus, it is unable to colonize the mouse large intestine.

35 SDS and fed to mice, it colonized the mouse large intestine.

36 acterized epithelial malignant tumors of the large intestine.

37 yenteric plexus of the stomach and small and large intestine.

38 actalkine in human skin, the tonsil, and the large intestine.

39 aning, then quickly retreat to the cecum and large intestine.

40 stomach and was overlapping in the small and large intestine.

41 at high levels for at least 8 months in the large intestine.

42 rat liver, pancreas, stomach, and small and large intestine.

43 even though apoptotic MCs were common in the large intestine.

44 l membranes of epithelial cells in small and large intestine.

45 sulfide generation by bacteria in the human large intestine.

46 ntestine and a very robust resistance in the large intestine.

47 lamydia from the small intestine but not the large intestine.

48 infiltration into the lamina propria of the large intestine.

49 l ileum, the ileocecal valve, and all of the large intestine.

50 mice develop an inflammatory disease of the large intestine.

51 ) isoforms, PKC-alpha and -betaII in the rat large intestine.

52 y lamina propria lymphocytes in the small or large intestine.

53 . muridarum to reach but not to colonize the large intestine.

54 reflective of the distal region of the human large intestine.

55 lls reside at crypt bottoms of the small and large intestine.

56 ithelial architecture in larger areas of the large intestine.

57 kidneys, spleen, descending aorta, and upper large intestine.

58 ed expression of inflammatory markers in the large intestine.

59 reflective of the distal region of the human large intestine.

60 nal (GI) tract, and then colonization of the large intestine.

61 represents different anatomical areas of the large intestine.

62 e, tunneling through epithelial cells of the large intestine.

63 lant fiber: those of the rumen and the human large intestine.

64 nciple mechanism of Mphi accumulation in the large intestine.

65 the serosa and lamina propria region of the large intestine.

66 T(4) receptors were present in the small and large intestines.

67 ghout the different regions of the small and large intestines.

68 eosinophils and macrophages in the small and large intestines.

69 ects of purified CPB in the rabbit small and large intestines.

70 adenomas to develop throughout the small and large intestines.

71 feration in the crypts of both the small and large intestines.

72 ght to cause infection in both the small and large intestines.

73 cts of the Mom1 locus, in both the small and large intestines.

74 lso found in the epithelium of the small and large intestines.

75 ithelium and lamina propria of the small and large intestines.

76 d colonic cell hyperplasia in both small and large intestines.

77 c islet, the hypothalamus, and the small and large intestines.

78 ntial gene expression in the mouse small and large intestines.

79 el with deleterious effects to the small and large intestines.

80 the neutral-pH environment of the small and large intestines.

81 biota and bile acid profile of the small and large intestines.

82 elated with that found in the small, but not large, intestine.

83 ighest for gallbladder (0.27 mSv/MBq), upper large intestine (0.19 mSv/MBq), and small intestine (0.1

84 mCi +/- 0.168 [0.068 mSv/MBq +/- 0.046]) and large intestine (0.529 rem/mCi +/- 0.236 [0.143 mSv/MBq

85 brain (5-10%); heart (1-10%); kidney (1-5%); large intestine (1-10%) and liver (5-10%).

86 e; brain (5%); heart (1-10%); kidney (1-5%); large intestine (1-10%) and liver (5-10%).

87 intestine (1.43 +/- 0.19 rad/mCi) and upper large intestine (1.20 +/- 0.38 rad/mCi).

88 ion; the dose-critical organs were the lower large intestine (1.43 +/- 0.19 rad/mCi) and upper large

89 roid, 5 lacrimal gland, 3 small intestine, 2 large intestine, 1 kidney, 1 paraspinal region and 1 ski

90 ral surgery: 5.0%; upper GI: 6.9%; small and large intestine: 12.6%; HPB: 15.8%; vascular: 11.9%; tho

91 [0.849 rad/mCi]), followed by the small and large intestines (161.26 muGy/MBq [0.597 rad/mCi] and 18

92 (general surgery: 2; upper GI: 3; small and large intestine: 2; HPB: 3; vascular: 3; thoracic: 3; P

93 l intestine 47, stomach 41, pancreas 45, and large intestine 25.

94 (general surgery: 0; upper GI: 2; small and large intestine: 5; HPB: 6; vascular: 2; thoracic: 4; P

95 In the large intestine, aberrant DNA methylation arises very ea

96 the rate of epithelial cell turnover in the large intestine acts like an "epithelial escalator" to e

97 S2215Y was identified in large intestine adenocarcinoma whereas R2505P was identi

98 y cytokines and chemokines were found in the large intestine after intraperitoneal challenge.

99 soflavone daidzein, which is produced in the large intestine after soy intake in 30% of Western popul

100 f Bacteroidetes, and lower Firmicutes in the large intestine, along with lower levels of circulating

101 ly, many of the expanded clones found in the large intestine also were found in the spleen and elsewh

102 ient Chlamydia sp. still failed to reach the large intestine, although similarly inoculated plasmid-f

103 RNA phylotypes detected in the healthy human large intestine and belongs to the Ruminococcaceae famil

104 Clostridium difficile can infect the large intestine and cause colitis when the normal intest

105 bset resides within the normal mucosa of the large intestine and expands in response to inflammation.

106 yenteric plexus of the stomach and small and large intestine and in the submucosal plexus of the smal

107 adulteration with beef brain, heart, kidney, large intestine and liver tissues and chemometric analys

108 obic bacterium that infects the lumen of the large intestine and produces toxins.

109 subdivided into domains -- small intestine, large intestine and rectum -- each characterized by a sp

110 c2(-/-) mice develop tumors in the small and large intestine and the rectum, but in contrast to tumor

111 l studies revealed necrosis in the small and large intestines and livers of infected IL-10-/- mice.

112 (including esophagus, stomach, and small and large intestine) and nerves projecting to the GIT and su

113 inal tract), excretion (lung, urinary tract, large intestine), and reproduction (reproductive tract).

114 al tissues of mice, mainly kidney, small and large intestine, and brain.

115 lt levels, and urobilinogen levels in cecum, large intestine, and feces.

116 artery, blood, muscle, lungs, bone, spleen, large intestine, and heart at 2 h after injection and 10

117 ns, including the skin, esophagus, air sacs, large intestine, and kidney.

118 ents ileus primarily affects the stomach and large intestine, and most patients who are diagnosed wit

119 heart, stomach, mesentery, small intestine, large intestine, and muscle) in wild-type and SCID mice.

120 ium, histopathologic changes in the trachea, large intestine, and pancreas, and abnormalities in the

121 pression in the prospective small intestine, large intestine, and rectum of genes encoding cell signa

122 e morphological subdomains: small intestine, large intestine, and rectum.

123 propionate, are generated in the caecum and large intestine, and when absorbed may elicit localised

124 dult heart, brain, thymus, spleen, small and large intestines, and peripheral blood leukocytes.

125 ells in the salivary gland, small intestine, large intestine, appendix, and tonsils.

126 The esophagus, stomach, small intestine, and large intestine are sites of infection for viruses, bact

127 Bacterial infections of the small and large intestine are widespread and continue to be topics

128 The small and large intestines are tubular organs composed of several

129 the nematode parasite Trichuris muris in the large intestine around the time of oral prion exposure d

130 anding the fate of the dietary fibres in the large intestine as it was shown that degradation of a di

131 n UGT1A1 was markedly increased in small and large intestines as well as in liver.

132 ogical damage to the mucosa of the small and large intestine, as well as a 20% reduction of the intes

133 t changes to the microbiota in the small and large intestines, as well as a significant shift in the

134 We also obtained small and large intestine biopsies from 8 adults and 10 newborn in

135 s found in crypts and villi of the small and large intestine, bronchiolar epithelial cells, the epide

136 replication and histological changes in the large intestine, bursa of Fabricius, and cecal tonsil.

137 Ras and Wnt pathways tend to co-occur in the large intestine but are mutually exclusive in cancers of

138 elop predominantly in the distal part of the large intestine but the biological basis of this intrigu

139 ent in myenteric neurons along the small and large intestines but are rare in the gastric corpus.

140 ed in the fetal bowel (stomach and small and large intestine), but that encoding the 5-HT(2C) recepto

141 estine and superficial lamina propria of the large intestine, but distinct from the intraepithelial c

142 OX-2) is not normally expressed in the human large intestine, but its levels are increased in the maj

143 ts are associated with carcinogenesis of the large intestine, but no prospective study has examined m

144 s oral vaccine delivery system to target the large intestine, but not the small intestine, may repres

145 y eliminated enteric glia from the small and large intestines, but caused no defects in epithelial pr

146 nd goblet cell hyperplasia were found in the large intestine by 24 hours post-intraperitoneal Shigell

147 lonization of the streptomycin-treated mouse large intestine by Escherichia coli MG1655, a human comm

148 Butyrate, produced by fermentation in the large intestine by gut microbiota, and its synthetic der

149 sion to, and subsequent colonization of, the large intestine by oral microbes is common and extensive

150 cted in villous enterocytes of the small and large intestines by immunohistochemistry.

151 colorectal adenomas and no previous invasive large intestine carcinoma.

152 rhagic Escherichia coli (EHEC) colonizes the large intestine, causing attaching and effacing (AE) les

153 ferentially in the small (CCL25 and CCL5) or large intestine (CCL19, CCL21, and CXCL5).

154 omains of the small intestine (duodenum) and large intestine (cecum).

155 ry arteries, thyroid and parathyroid glands, large intestine, colon, bladder, testes, and prostate.

156 osa-associated microbiota, between small and large intestine, concordant with differences in regional

157 llustrate isolated lymphoid follicles in the large intestine, consisting of B cells interspersed with

158 dimethylhydrizene-treated Sprague Dawley rat large intestine containing a suspect growth.

159 ifferences were observed in the liver, upper large intestine contents, and small intestine contents b

160 Radiologic imaging of the large intestine continues to evolve and expand the poten

161 al muscle, heart, lung, small intestine, and large intestine despite large differences in hyaluronan

162 ped by evaluating histopathologic lesions in large intestine detected 16 days after a 5-day period of

163 The terminal part of the small intestine and large intestine did not to contribute to this projection

164 ohistochemistry following infection with the large intestine dwelling helminth parasite Trichuris mur

165 After colonizing the large intestine, EHEC forms attaching and effacing (AE)

166 nished mesoderm and overproliferation of the large intestine endoderm, leading to stenosis of the lum

167 s also govern the initial recognition of the large intestine environment and attachment to the host c

168 Wnt-dependent tumorigenesis, whereas in the large intestine epithelial HuR indirectly downregulates

169 In contrast, S. flexneri invades the large intestine epithelium at the basolateral membrane,

170 1WAF-1/CIP1 immunoreactivity was detected in large intestine epithelium up to 6 days after irradiatio

171 of the bacterially synthesized folate in the large intestine exists in the form of folate monoglutama

172 -deficient Chlamydia sp. failed to reach the large intestine, explaining the lack of live pGP3-defici

173 tudy of polyphenols after in vitro simulated large intestine fermentation was carried out on edible n

174 and, as a consequence, delivering PAs to the large intestine for fermentation and metabolism by gut b

175 e in the genital tract, but persisted in the large intestine for long periods.

176 jecting the probe into the lumen of small or large intestine fragments, robust phosphorescence intens

177 ells isolated from the lamina propria of the large intestine from wild type or CerS6-deficient groups

178 plexus, the stomachs, small intestines, and large intestines from 3-, 12-, 21-, 24- and 27-month-old

179 ; expression in the colon indicates that the large intestine has a mechanism for luminal di- and trip

180 ity of E. coli strains to colonize the mouse large intestine has been correlated with their ability t

181 eral, upper gastrointestinal (GI), small and large intestine, hepatopancreatobiliary (HPB), vascular,

182 , high viral loads in the spleen, liver, and large intestine, histological changes in the liver and s

183 (-/-) Treg were significantly reduced in the large intestine, however, compared with wild-type Treg,

184 rplasia and adenocarcinomas in the small and large intestines; however, no differences were noted in

185 junum, upper ileum, and lower ileum) and the large intestine (i.e., cecum and mid-colon/rectum).

186 munities' compositions of terminal ileum and large intestine in 5 healthy individuals.

187 ing in the developing gizzard, duodenum, and large intestine in chick were tested by viral misexpress

188 sm for increasing energy uptake by the human large intestine in obese persons.

189 recently identified as an inhabitant of the large intestine in young domestic cats with chronic diar

190 Here we show by imaging the murine small and large intestines in steady-state that intestinal CX3CR1(

191 ain fatty acid formed by fermentation in the large intestine, in the regulation of insulin sensitivit

192 28 was detected in all IECs of the small and large intestine, including in cells expressing leucine r

193 ease-like pathogenesis in both the small and large intestine, including segmental inflammatory cell i

194 ctious progenies were eventually detected in large intestine, indicating a critical role of the plasm

195 lamydia from the small intestine but not the large intestine, indicating that chlamydial colonization

196 cient mice were prone to develop more severe large intestine inflammation, which was rescued by the t

197 nfection by Salmonella, whereas those of the large intestine inhibit invasion.

198 The large intestine is a major site of infection and disease

199 These data indicate that the large intestine is a major viral reservoir in LTNPs, whi

200 The large intestine is capable of absorbing water-soluble vi

201 Whether the large intestine is covered by the same lymphatic system

202 his study suggests that drug exposure in the large intestine is essential for generating a superior i

203 Propulsion in both small and large intestine is largely mediated by the peristaltic r

204 ning of the hindgut into small intestine and large intestine is likely required for its correct morph

205 lminating in the expulsion of worms from the large intestine is not known.

206 The human large intestine is populated by a high density of microo

207 show that the frequency of Th17 cells in the large intestine is significantly elevated in the absence

208 Leukocyte trafficking to the small and large intestines is tightly controlled to maintain intes

209 crobial fermentation of dietary fiber in the large intestine, is a physiological regulator of major p

210 ne mucin normally expressed in the small and large intestine, is differentially expressed during infl

211 FOXP3(+) regulatory T cells (Tregs), to the large intestine lamina propria (LILP).

212 Phenotypic analysis of large intestine lamina propria lymphocytes revealed a la

213 efine the major APC subsets in the small and large intestine lamina propria.

214 ology disrupt the microbial ecosystem in our large intestine leading to disease.

215 od, which permits for early detection of the large intestine lesions with specificity and sensitivity

216 refractory to bacterial colonization and the large intestine less susceptible to the onset of colitis

217 T cells in the small intestine (SI), but not large intestine (LI), including an almost complete absen

218 ate<--urinary bladder contents) and S (lower large intestine [LLI] wall<--urinary bladder contents) a

219 f bacterial metabolite concentrations in the large intestine luminal content, notably after changes i

220 vely with the HYDIN, KRAS, and PTEN genes in large intestine, lung, and endometrial cancers respectiv

221 ichuriasis relates to an inflammation of the large intestine manifested in bloody diarrhea, and chron

222 For EA treatment, large intestine meridian points LI4 and LI11 and stomach

223 Lef1 is expressed in the chick duodenum and large intestine mesoderm.

224 ed whether pathology specifically within the large intestine might influence prion pathogenesis.

225 g new questions on the impact of HPDs on the large intestine mucosa homeostasis.

226 a composition and metabolic activity and for large intestine mucosal homeostasis.

227 In the small and large intestines, myenteric cell loss occurred by 12 mon

228 , increased uptake of D-FAC in the small and large intestine occurred at an earlier stage of disease

229 colonoscopy in detection of focal lesions in large intestine of 10 mm or more diameter.

230 ut were present in the lung, spleen, BM, and large intestine of beta7 integrin-deficient mice (on the

231 TCRbeta repertoire of the cells found in the large intestine of diseased mice revealed a population w

232 Finally, the identification in the large intestine of efficient and specialized carrier-med

233 with the one prevalent in isolates from the large intestine of healthy individuals.

234 ow that inflammatory Mphis accumulate in the large intestine of mice during the local inflammatory re

235 ng parasitic nematode Trichuris muris in the large intestine of mice is dependent on microflora and c

236 commensal bacterium Escherichia coli in the large intestine of mice.

237 g the K1 polysaccharide capsule colonize the large intestine of newborn infants, and are the leading

238 lamydia from the small intestine but not the large intestine of recipient mice.

239 The large intestine of these mice contained an increase in C

240 Gata6 throughout the epithelium of small and large intestines of adult mice.

241 The spirochetes inhabiting the large intestines of humans and animals consist of a dive

242 icrobial parasite Blastocystis colonizes the large intestines of numerous animal species and increasi

243 eling indices of adenomas from the small and large intestines of omeprazole-treated mice were increas

244 amina propria compartments of both small and large intestines of SCID recipients.

245 MD42 initially grew in the large intestines of streptomycin-treated mice but then f

246 hat V. cholerae colonizes both the small and large intestines of the mouse in a distribution that doe

247 We investigated the importance of the large intestine on the bioavailability of anthocyanins f

248 inal tissue substitutes, such as segments of large intestine or skin, which are not anatomically or f

249 gastrointestinal organs (stomach, small and large intestine) or liver of rats.

250 uring fermentation of prebiotic fiber in the large intestine), or high prebiotic fiber diets.

251 e oral cavity, esophagus, stomach, small and large intestines, pancreas, and liver.

252 one patient in the experimental group (<1%; large intestine perforation) and two patients in the sta

253 eated with pembrolizumab (unspecified cause, large intestine perforation, malignant neoplasm progress

254 ardiac arrest, cardiac failure, myocarditis, large intestine perforation, pneumonia, and pulmonary em

255 In the large intestine, prebiotics, in addition to their select

256 A dense mucus layer in the large intestine prevents inflammation by shielding the u

257 ant increase in tumors in the small, but not large, intestine relative to their BALB-Min counterparts

258 ectable in the mucosa of the human small and large intestine, respectively.

259 Mucus production by goblet cells of the large intestine serves as a crucial antimicrobial protec

260 w- and high-grade dysplastic adenomas in the large intestine, similar to the precancerous lesions tha

261 estimated organ-absorbed doses to the upper large intestine, small intestine, gallbladder wall, and

262 pancreas, prostate, brain, heart, small and large intestine, stomach, and epididymis.

263 ydia sp. was no longer able to spread to the large intestine, suggesting that pGP3-deficient Chlamydi

264 Therefore, we designed a large intestine-targeted oral delivery with pH-dependent

265 xocrine cells found throughout the small and large intestine that have a characteristic morphology du

266 bacterium in the streptomycin-treated mouse large intestine that respires nitrate.

267 ma membrane of the enterocytes of the normal large intestine, the reaction being most intense in the

268 ut there is little known about homing to the large intestine, the site most commonly affected in infl

269 reatment reduces epithelial apoptosis in the large intestine, thereby protecting the integrity of the

270 e from the vast microbial populations in the large intestine, thereby reducing conflict between host

271 ice had FDC-containing GALT throughout their large intestines, these tissues were not early sites of

272 entially elicited more IgA production in the large intestine through the T cell-dependent B cell-acti

273 Large intestine tissue showed minimal to mild inflammati

274 ized at high levels (10(8) CFU/g of stool or large intestine tissue) followed by clearance after seve

275 ative contributions of GALT in the small and large intestines to oral prion pathogenesis were unknown

276 bers in the lamina propria of both small and large intestines under both steady-state and inflammator

277 In the large intestine, very few adenomas were found in Msh2(-/

278 ses were the kidneys (0.0830 mSv/MBq), upper large intestine wall (0.0267 mSv/MBq), small intestine (

279 The lungs, upper large intestine wall, small intestine, urinary bladder w

280 The large intestine was the most consistently colonized site

281 At necropsy, the small, and occasionally the large, intestine was dilated and gas filled in most mice

282 th the goal of modeling human disease of the large intestine, we sought to develop an effective proto

283 idium infection, these concentrations in the large intestine were the sole predictors of the observed

284 small intestine, gallbladder wall, and lower large intestines were 0.082, 0.043, 0.042, and 0.035 mSv

285 r all mice, frontal cortex, liver, and small/large intestines were collected.

286 The cecums and large intestines were studied for numbers of dysplasias/

287 resulting acute inflammatory response in the large intestine, were all prevented by intestinal-specif

288 The remainder transits the large intestine where it becomes food for the commensal

289 sted flavan-3-ols pass from the small to the large intestine where the action of the microbiota resul

290 and the majority of the flavanols reach the large intestine where they may be metabolized by residen

291 ides fragilis is a commensal organism in the large intestine, where it utilizes both dietary and host

292 The latter function is most evident in the large intestine, where the inner mucus layer separates t

293 ng in epithelial cells of both the small and large intestine whereas no staining was seen with Hyb213

294 ed in a partially intracellular niche in the large intestine, whereas A. lumbricoides larvae penetrat

295 induced moderate inflammation mainly in the large intestine, whereas the Th17 cells induced with opt

296 However, a source for Ang4 in the large intestine, which is devoid of Paneth cells, has no

297 pithelial cells and lengthened crypts in the large intestine, which was associated with increased tra

298 bacterial number was noted in the cecum and large intestine with 10x LD(50) S. enterica serovar Typh

299 are expressed in similar patterns within the large intestine, with greatest staining near the epithel

300 The large intestine, with its array of crypts lining the epi