ライフサイエンスコーパス: intestinal

1 We blocked intestinal absorption of cholesterol in milk fed to newb

2 Intestinal absorption of mercury is influenced by intera

3 d that citrus pectin encapsulation increased intestinal accessibility during passage through the smal

4 us pectin influences the bioavailability and intestinal accessibility of anthocyanins in humans.

5 ssion and fusion could provide insights into intestinal adaptation to altered environmental condition

6 redominantly macrophages) in human and mouse intestinal adenomas.

7 One patient assigned to placebo reported intestinal adhesions with obstruction as a severe and se

8 the formation and/or proliferation of adult intestinal adult stem cells during postembryonic develop

9 lerated the molecular aging and clearance of intestinal alkaline phosphatase (IAP).

10 .This study aimed to accurately characterize intestinal alpha-carotene cleavage and its relative cont

11 d carbohydrate release to simulated gastric, intestinal and colonic fluids, and thus largely enriched

12 Survival, bacterial dissemination, and intestinal and systemic pathology of wild-type and CCR7-

13 interfering with secretion and compromising intestinal antimicrobial defense.

14 ute lethality due to bone marrow failure and intestinal atrophy featuring stem and progenitor cell de

15 Patients with CD have extra-intestinal autoimmune comorbid conditions more frequentl

16 Interestingly, intestinal bacteria can promote infection of several mam

17 bacillus plantarum and its interactions with intestinal bacteria in mice undergoing switches between

18 ses vs controls, we found that reactivity to intestinal bacteria is a normal property of the human CD

19 chain fatty acids (SCFA) are metabolites of intestinal bacteria resulting from fermentation of dieta

20 al stimulation that can functionally replace intestinal bacteria.

21 ia, which also involved in the impairment of intestinal barrier after FMT.

22 ptides should be absorbed intact through the intestinal barrier and reach the blood stream to exert t

23 ndependent cell death, ATG16L1 maintains the intestinal barrier by inhibiting necroptosis in the epit

24 Immunity, intestinal barrier function, host metabolism and host-mi

25 tective role in IBD development by enhancing intestinal barrier function.

26 of colitis, numbers and size of tumors, and intestinal barrier integrity were assessed by histologic

27 reflect the important relevance of an intact intestinal barrier.

28 d by a marked augmentation of pancreatic and intestinal BF responses.

29 Importantly, intestinal bile acid sequestration with cholestyramine w

30 Human intestinal biopsies were used in clinical data analysis.

31 Intestinal biopsy specimens of patients with CD were sco

32 orescence microscopy to optically access the intestinal bulb of the larval zebrafish, a model vertebr

33 nthocyanins and vitamin C contents, on human intestinal Caco-2 cells exposed to hydrogen peroxide (H2

34 Similarly, increased intestinal cAMP and PKA phosphorylation were demonstrate

35 h are crucial gatekeepers in common forms of intestinal cancer.

36 Deletion of Tgfbr1 results in markedly fewer intestinal CD103(+)CD11b(+) DCs and a reciprocal increas

37 heir potential to induce IL-22 expression by intestinal CD4(+) T cells.

38 hanges in cancer-related signaling networks, intestinal cell metabolism, and physiology in a three-di

39 aid in wound healing and the maintenance of intestinal cell populations in particular compartments.

40 Intestinal cell suspensions and ILC3s sorted from gut bi

41 modulate endocytic and secretory systems in intestinal cells.

42 o measured using a 70% Caco2/30% HT-29 human intestinal co-culture layer.

43 high-affinity inhibitory mannoside, reduces intestinal colonization of genetically diverse UPEC isol

44 Intestinal colonization with V. cholerae results in expe

45 onstitutively challenged environment keeping intestinal commensal microbiota at bay and defending aga

46 n six edible greens during simulating gastro-intestinal conditions has been investigated.

47 ity and digestibility under simulated gastro-intestinal conditions were studied.

48 n competent CS/DNA NPs occurred in simulated intestinal conditions with CS/DNA NP cores successfully

49 compounds, constituted the bulk of the large-intestinal core microbiota where topologically distinct

50 p21-independent mechanisms that radioprotect intestinal crypts and that ATM inhibition promotes GI sy

51 ools of free virions were present in 10% of intestinal crypts by 10-12 days.

52 We isolated intestinal crypts from C57BL/6 mice, cultured enteroids,

53 Intestinal crypts from Cd44(-/-) mice did not expand to

54 iting chemicals results in severe defects in intestinal development.

55 orphins was evaluated during in vitro gastro-intestinal digestion (GID) of six sterilised model syste

56 ermined in vitro under simulated stomach and intestinal digestion conditions.

57 After intestinal digestion, 77% carotenoids and 67% tocols wer

58 After intestinal digestion, antioxidant capacity increased reg

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

60 tial reservoir for bacteria that can promote intestinal disease.

61 ologic conditions and the pathophysiology of intestinal diseases.

62 loss of fluid, is not normally stimulated by intestinal distension as the meal passes through the gas

63 oss of colonization resistance can result in intestinal domination with vancomycin-resistant Enteroco

64 ox9(flox/flox)-vil-cre mice had evidence for intestinal dysbiosis of the microbiota, characterized by

65 of the host urinary metabolomics profile and intestinal energy absorption.

66 We recapitulated normal intestinal ENS development by combining human-PSC-derive

67 advantage occurs at the expense of resident intestinal enterococci.

68 n therefore appears to promote overgrowth of intestinal Enterococcus, which promotes liver disease, b

69 cuss how a dietary-induced disruption of the intestinal environment may influence transplantation out

70 ome P450 3A4 (CYP3A4) is a major hepatic and intestinal enzyme that oxidizes more than 60% of adminis

71 ese increases were correlated with increased intestinal epithelial apoptosis.

72 rolein exposure in mice caused damage to the intestinal epithelial barrier, resulting in increased pe

73 esized that TNF exerts beneficial effects on intestinal epithelial cell (IEC) responses to injury.

74 Intestinal epithelial cells (Caco-2 and IEC-6 lines) wer

75 ation patterns and transcriptomes of primary intestinal epithelial cells (IEC) of children newly diag

76 immune signalling pathway that functions in intestinal epithelial cells and may present useful targe

77 xpression of a transgene increased growth of intestinal epithelial cells and organoids.

78 NLR Nlrp9b that is specifically expressed in intestinal epithelial cells and restricts rotavirus infe

79 Deletion of EGFR from intestinal epithelial cells did not affect tumor growth.

80 t, analysis of genomic architecture in mouse intestinal epithelial cells disclosed that microbiota co

81 ragweed did not affect the integrity of the intestinal epithelial cells.

82 is methodology can be applied to interrogate intestinal epithelial dynamics and characterize situatio

83 Intestinal epithelial HIF-2alpha-overexpressing mice dem

84 cellular toxins that eliminate glia in mice, intestinal epithelial permeability and proliferation inc

85 mozygous-knockout animals have reduced adult intestinal epithelial stem cell proliferation at the end

86 l segregation between these bacteria and the intestinal epithelial surface.

87 cells from both mice and humans into robust intestinal epithelial tissue.

88 In studies of intestinal epithelial tissues from patients with CD and

89 with disruption of Sirt1 specifically in the intestinal epithelium (SIRT1 iKO, villin-Cre+, Sirt1(flo

90 use "TEM-17" cells to be enriched within the intestinal epithelium and among lamina propria lymphocyt

91 his allowed visualization of areas where the intestinal epithelium had been compromised and demonstra

92 The intestinal epithelium is a major site for the conversion

93 , the in vivo roles of TFEB in the mammalian intestinal epithelium were not known.

94 ed Campylobacter must translocate across the intestinal epithelium, spread systemically in the circul

95 or SATB2+ domain in developing and postnatal intestinal epithelium.

96 formation: the hematopoietic lineage and the intestinal epithelium.

97 In light of recent studies identifying intestinal factors, such as the microbiota, that alter e

98 Children with intestinal failure (IF) depend on parenteral nutrition (

99 whole organ-scale technology needed to treat intestinal failure patients.There is a need for humanise

100 atients with short bowel syndrome (SBS) with intestinal failure, increasing intestinal wet weight abs

101 for humanised grafts to treat patients with intestinal failure.

102 dentify a neuronal mechanism for controlling intestinal fat stores and organismal behavioral states i

103 Intestinal fibrosis resulting in (sub)obstruction is a c

104 a locally acting ROCK inhibitor (AMA0825) on intestinal fibrosis.

105 termined that purified chymotrypsin or mouse intestinal fluids can also activate NanI activity.

106 exposure to simulated salivary, gastric and intestinal fluids.

107 ), procedure type (eg, laparoscopic vs open, intestinal, foregut, hepatopancreaticobiliary vs abdomin

108 sis, glucose regulation, satiety, and gastro-intestinal function, as well as pain transmission.

109 fecal biomarkers studied, 2 that related to intestinal function-AAT and myeloperoxidase-were associa

110 or that is highly potent in vitro and delays intestinal glucose absorption in vivo to improve glycemi

111 ett's oesophagus in terms of the presence of intestinal goblet cells.

112 was to evaluate management of patients with intestinal graft failure with special reference to indic

113 e reactivity are needed to improve long-term intestinal graft outcomes.

114 dietary macronutrients and the microbiota on intestinal health and development of colitis.

115 These results suggest that intestinal HIF-2alpha could be a viable target for hepat

116 of RNA-Seq experiments with mouse models of intestinal HIF-2alpha or Yes-associated protein 1 (YAP1)

117 hyl-N-nitrosourea-mutagenized grandsires for intestinal homeostasis abnormalities after oral administ

118 we found HGF receptor signaling to regulate intestinal homeostasis and regeneration, as well as aden

119 ese findings provide a mechanism of NCoR1 in intestinal homeostasis during development and provide a

120 Cdx1 and Cdx2 also regulate intestinal homeostasis throughout life.

121 MET-deficient mice did not have defects in intestinal homeostasis.

122 Megacystis microcolon intestinal hypoperistalsis syndrome (MMIHS) is a congeni

123 Megacystis microcolon intestinal hypoperistalsis syndrome (MMIHS) is a congeni

124 mans; however, whether CD6 plays any role in intestinal I/R-induced injury and, if so, the underlying

125 Some studies detected infected intestinal immune cells (8-12) , other studies detected

126 Evidence suggests that enteric neurons and intestinal immune cells share common regulatory mechanis

127 e discovered that it can nonetheless disrupt intestinal immune homeostasis at inductive and effector

128 ociations may reflect impaired maturation of intestinal immunity and integrity in boys with a risk of

129 D in mice increased susceptibility to severe intestinal inflammation and epithelial dysregulation, ac

130 were remarkably unaffected by development of intestinal inflammation and there were no differences in

131 se activity reduced PD1n-3 DPA and augmented intestinal inflammation in experimental colitis.

132 orescence to delineate pancreatic, liver, or intestinal inflammation in living mice.

133 This pathway might be induced to resolve intestinal inflammation in patients with colitis.

134 Intestinal inflammation is associated with low levels of

135 Intestinal inflammation is the central pathological feat

136 P nick-end labeling assay was performed, and intestinal inflammation severity was evaluated histologi

137 th no endoscopic or radiological evidence of intestinal inflammation) in patients with treatment-refr

138 ed the ability of the endothelium to resolve intestinal inflammation, compared with mice with colitis

139 In an animal model of anti-TNF-resistant intestinal inflammation, genetic deletion or pharmacolog

140 Blimp1CKO mice) spontaneously develop severe intestinal inflammation, indicating a crucial role for B

141 r how ILC3s could be manipulated to regulate intestinal inflammation.

142 of ATIs in various foods and their effect on intestinal inflammation.

143 t endothelial cells to promote resolution of intestinal inflammation.

144 regulating the innate immune response during intestinal inflammation.

145 gene networks contributing to the underlying intestinal inflammation.

146 rally administered fluorophores can identify intestinal injury in a rat model.

147 nt modality for gastrointestinal tumors, but intestinal injury is a common side effect.

148 rotected mice from ethanol-induced liver and intestinal injury.

149 tylase, senses environmental stress to alter intestinal integrity.

150 eneral condition, showed jejunal dilatation, intestinal intramural gas, portomesenteric vein gas, ext

151 controls systemic iron levels by inhibiting intestinal iron absorption and iron recycling.

152 expansion, hypercoagulability, and increased intestinal iron absorption.

153 Intestinal ischemia followed by reperfusion leads to loc

154 esent in pancreatic alpha and beta cells and intestinal L and K cells, secreting glucagon, insulin, a

155 rmone glucagon-like peptide 1 (GLP-1) by the intestinal L cell is essential for the incretin effect a

156 ry T cell induction among lymphocytes in the intestinal lamina propria (LPL) and cervical lymph nodes

157 bset, as residual cells persist in the small intestinal lamina propria (siLP) of adult and neonatal I

158 CX3CR1(+) macrophages in the intestinal lamina propria contribute to gut homeostasis

159 ive mononuclear cells was higher in skin and intestinal lesions of BD patients than in those of HCs.

160 ulation of Lgr5+ ISCs that contribute to all intestinal lineages with distinct kinetics.

161 ted robust secretion of cholesterol into the intestinal lumen via the sterol-exporting heterodimer ad

162 esumably caused by excess fatty acids in the intestinal lumen.

163 These abnormalities include intestinal lymphangiectasia, mesenteric lymph node lymph

164 The levels of cannabinoids recovered in the intestinal lymphatic system, but not in plasma, were sub

165 However, intestinal lymphatic transport of cannabinoids in immuno

166 Exposure to BAR501 shifted intestinal macrophages from a classically activated (CD1

167 Microbial-driven expression of IL-19 by intestinal macrophages may contribute to the pathogenesi

168 Occurrence of extra-intestinal manifestations was similar in elderly and adu

169 g MCs and the effects of gliadin peptides on intestinal MCs indicated an increase in proinflammatory

170 ctice as well as the diverse presentation of intestinal melanoma metastases and the diagnostic and th

171 The treatment of intestinal melanoma metastases has changed due to the in

172 d adjacent mucosa with atrophic gastritis or intestinal metaplasia (AG/IM GC+), as well as in atrophi

173 remalignant lesions gastric atrophy (GA) and intestinal metaplasia (IM) influence gastric cancer risk

174 IM GC+), as well as in atrophic gastritis or intestinal metaplasia mucosa of patients without GC (AG/

175 a timely diagnosis and optimal treatment of intestinal metastases.

176 Median overall survival after detection of intestinal metastasis in patients receiving systemic tre

177 ation and intestinal tissues that respond to intestinal microbes and determined their clonal diversit

178 pulation genetics of previously inaccessible intestinal microbes, providing a comprehensive strain-le

179 in their pregnant mother can affect how the intestinal microbiome develops, so we asked whether the

180 s aureus and Staphylococcus epidermidis) and intestinal microbiota (Lactobacillus reuteri, Enterococc

181 he complex interactions between diet and the intestinal microbiota affect development of mucosal infl

182 recede arthritis, and that modulation of the intestinal microbiota after the onset of arthritis may o

183 e association between the composition of the intestinal microbiota and clinical features of irritable

184 ew of the interactions occurring between the intestinal microbiota and the immune system, and we will

185 ed on geographic and cultural differences in intestinal microbiota are necessary to define applicabil

186 gA(-/-) and wild-type mice disappeared after intestinal microbiota equalization.

187 BACKGROUND & AIMS: Dysbiosis of the intestinal microbiota has been associated with developme

188 The intestinal microbiota has been identified as an environm

189 The study of the intestinal microbiota has begun to shift from cataloging

190 licated in changes in the composition of the intestinal microbiota in Crohn's disease, but its role o

191 The intestinal microbiota of finishing pigs, fed with 16%, 1

192 Our observations suggest that intestinal microbiota perturbations precede arthritis, a

193 ause accumulating evidence has revealed that intestinal microbiota play an important role in human he

194 The intestinal microbiota provides colonization resistance a

195 ngs provide mechanistic insight into how the intestinal microbiota regulates body composition and est

196 AIMS: It might be possible to manipulate the intestinal microbiota with prebiotics or other agents to

197 pplicability of new strategies targeting the intestinal microbiota.

198 ould turn to the role of antibiotics and the intestinal microflora in the rising obesity epidemic.

199 oton laser scanning microscopy in an ex vivo intestinal model.

200 ilation of the urinary bladder and defective intestinal motility.

201 y several Clostridiales members that utilize intestinal mucins.

202 rched for T-UCRs that regulate growth of the intestinal mucosa and investigated the mechanism by whic

203 cyclase C (GUCY2C), a receptor expressed by intestinal mucosa and universally expressed by metastati

204 ociated with a type 2 immune response in the intestinal mucosa are up-regulated in treatment-naive pe

205 cant numbers in their tissues, including the intestinal mucosa.

206 ific treatment for IgA nephropathy targeting intestinal mucosal immunity upstream of disease manifest

207 IgA Ab-mediated system in the protection of intestinal mucosal surface.

208 The intestinal mucous layer provides a critical host defense

209 isolate F11 that are important for growth in intestinal mucus, which is thought to be a major source

210 We analyzed intestinal mycobiomes of patients with IBS and a rat mod

211 In this study, we report that deletion of intestinal nuclear receptor corepressor 1 (NCoR1) comple

212 According to the anti-incretin theory, intestinal nutrients should also cause a reduction of in

213 ne patient, intestinal perforation and small intestinal obstruction in one patient; colitis in two pa

214 Nopal modified gut microbiota and increased intestinal occludin-1 in the HFS + N group.

215 In human intestinal organ cultures, microbial activation of Vgamm

216 In studies of intestinal organoid cultures and mice with inducible del

217 rate potential applications in imaging human intestinal organoids (HIOs), colon mucosa, and retina.

218 ural crest cells (NCCs) and developing human intestinal organoids (HIOs).

219 of human pluripotent stem-cell-derived human intestinal organoids is globally similar to the immature

220 t to promote maintenance of Lgr5(+) IESCs in intestinal organoids, an effect mainly mediated by Greml

221 YAMC cells, and mouse and human intestinal organoids, died rapidly in response to TNF.

222 heroids were pre-organoids that matured into intestinal organoids.

223 Entamoeba histolytica is an intestinal parasite that infects 50-100 million people a

224 sm utilized by C. jejuni, and possibly other intestinal pathogens, to survive in the presence of bile

225 development of therapeutic interventions in intestinal pathologies.

226 vates lipopolysaccharides (LPS), and induces intestinal pathology, as indicated by inflammation, barr

227 MAP-altered gut microbial community leads to intestinal pathology.

228 of death were lung infection in one patient, intestinal perforation and small intestinal obstruction

229 The role of CB1 in intestinal permeability and inflammation.

230 s of exposure to a bacteriophage cocktail on intestinal permeability and relative abundance of taxono

231 Increased intestinal permeability and translocation of gut bacteri

232 We investigated whether impaired intestinal permeability contributes to these symptoms.

233 cts with celiac disease might have increased intestinal permeability in early life.

234 Intestinal permeability was quantified by the Confocal L

235 se strains and was associated with augmented intestinal permeability, an altered microbiome and activ

236 l disease (IBD) is associated with increased intestinal permeability, which involves paracellular pas

237 opment of diseases associated with increased intestinal permeability.

238 s with IBD in mucosal healing have increased intestinal permeability.

239 and increases in whole gut transit time and intestinal permeability.

240 ncy impairs epithelial integrity, increasing intestinal permeability.

241 endritic cells resulted in the regulation of intestinal phagocytes.

242 d bioaccessibility were monitored during the intestinal phase.

243 bulin A (IgA) are constitutively secreted by intestinal plasma cells to coat and contain the commensa

244 Strikingly, vasoactive intestinal polypeptide (VIP), a neuropeptide critical fo

245 nd colocalization of the peptides vasoactive intestinal polypeptide (VIP), calcitonin-gene related pe

246 frontal cortex that originates in vasoactive intestinal polypeptide (VIP)-expressing interneurons.

247 Then, active contraction along the anterior intestinal portal generates tension to elongate the fore

248 Together, our findings show that intestinal PPARdelta is important in maintaining metabol

249 ate that CD34(+) Gp38(+) cells are the major intestinal producers of the niche factors Wnt2b, Gremlin

250 animal disease, these findings suggest that intestinal proteases may enhance NanI activity, which in

251 in modern wheat and were highly resistant to intestinal proteolysis.

252 cids decreased 2.8-fold, suggesting enhanced intestinal reabsorption due to induction of ileal transp

253 ation by Rancimat, and simulation of gastric/intestinal release.

254 structed using molecular data generated from intestinal samples isolated from three populations of pa

255 of Interleukin (IL)-33 has been detected in intestinal samples of patients with ulcerative colitis,

256 The individual small intestinal segments studied revealed comparable staining

257 in vivo microrheological measurements of the intestinal space in living animals, and we comment on it

258 ining metabolic homeostasis and suggest that intestinal-specific activation of PPARdelta could be a t

259 Human intestinal stem cell-derived enteroid monolayers co-cult

260 cells and quiescent Bmi1(+) cells behave as intestinal stem cells (ISCs) in vivo.

261 hieved by Pol III inhibition specifically in intestinal stem cells.

262 The current study first showed that human intestinal strains of C. perfringens can grow by utilizi

263 Just a decade ago, intestinal strictures were considered to be an inevitabl

264 celiac disease or wheat allergy but who have intestinal symptoms, extraintestinal symptoms, or both,

265 Furthermore, intestinal targeting of Baf180 renders mice susceptible

266 imilar gene expression profile in CT-induced intestinal Th17 cells and endogenous intestinal Th17 cel

267 induced intestinal Th17 cells and endogenous intestinal Th17 cells at homeostasis, with upregulated e

268 Here we show that intestinal Th2 responses against Trichuris muris worms a

269 y based on the reduction of EndoMT mitigates intestinal tissue damage.

270 We mounted isolated intestinal tissue from C57BL/6 (wild-type) and Cftr(-/-)

271 NF greatly increased levels of cell death in intestinal tissue of cIAP1-null mice, compared with wild

272 rin receptor (TfR) colocalization in ex vivo intestinal tissue sections, despite blocking of the rece

273 is of peripheral blood mononuclear cells and intestinal tissues from patients with inflammatory bowel

274 Intestinal tissues from patients with ulcerative colitis

275 pathway molecules are increased in inflamed intestinal tissues of patients with IBD.

276 the abundance of T cells in circulation and intestinal tissues that respond to intestinal microbes a

277 Intestinal tissues were collected; severity of colitis,

278 proliferation and ultrastructure from their intestinal tissues.

279 influence the bacterial colonisation of the intestinal tract and can be visualised non-destructively

280 emia initiated from translocation across the intestinal tract in an immunocompromised host is substan

281 The intestinal tract is a site of intense immune cell activi

282 The preferential expression of DPP4 in the intestinal tract of insectivorous bats, suggests that tr

283 community structure along the length of the intestinal tract.

284 ning, potentially indicating prolonged trans-intestinal transfer of IgG.

285 arrier to improving long-term outcomes after intestinal transplantation.

286 contributions to the understanding of human intestinal transport in normal physiologic conditions an

287 , glucose absorption, another representative intestinal transport process, did not differ in Cftr(-/-

288 of V33 with Apc (Min/+) mice, had increased intestinal tumor burden compared with littermate Apc (Mi

289 ecific Sirt1 heterozygous mice have enhanced intestinal tumor formation, whereas intestine-specific S

290 while having no discernable effect on small intestinal tumor formation.

291 of EGFR from epithelial cells of established intestinal tumors in mice given AOM and DSS did not redu

292 ignificantly decreased protein expression of intestinal types I and II IFNRs.

293 erbilirubinemia in hUGT1 neonates because of intestinal UGT1A1 gene derepression.

294 -) neonatal mice because of ROS induction of intestinal UGT1A1.

295 , disrupted lung alveolarization, atrophy of intestinal villus and colon-resident lymphoid follicle,

296 In primary intestinal villus cells, we identified hundreds of tissu

297 Intestinal viromes of case subjects were less diverse th

298 me (SBS) with intestinal failure, increasing intestinal wet weight absorption and reducing diarrhea.

299 igated the effects and mechanism of AS II on intestinal wound healing in both in vitro and in vivo mo

300 ntributes to cell adhesion regulation during intestinal wound repair and the development of IBD.