ライフサイエンスコーパス: small intestinal

1 cidence of critical illness was greatest for small intestinal (17.2% [95% CI, 13.3%-21.8%]) and color

2 e the impact of delayed enteral nutrition on small intestinal absorption of 3-O-methyl-glucose.

3 arance and clearance in plasma indicative of small intestinal absorption.

4 rily in the colon, largely avoiding proximal small intestinal absorption.

5 ficantly reduced both the number and size of small intestinal adenomas arising in this model, and it

6 intestinal-specific Bmi1 deletion suppressed small intestinal adenomas in a manner that was indisting

7 ired for both progression and maintenance of small intestinal adenomas.

8 omal macrophage Cox-2 in colorectal (but not small intestinal) adenomas from cLys-Cox-2 x Apc (Min/+)

9 y discrete colonization factors that mediate small intestinal adhesion.

10 B-cell homing to the intestine, rejection of small intestinal allografts, and recruitment of mast cel

11 nflammation and oxidative stress that limits small intestinal alpha-tocopherol absorption and/or impa

12 gulation of genes encoding components of the small intestinal (alpha-defensins Defa24 and Defa-rs1) a

13 Surprisingly, the ischemically damaged small intestinal and ascending colonic tissue showed a c

14 ntal localization of the two proteins in the small intestinal and ascending colonic tissue.

15 nohistochemical approach in normal adult rat small intestinal and ascending colonic tissue.

16 Gal1-R knockout) with RRV or vehicle, closed small intestinal and colon loops were constructed.

17 ts of genes in these two DC subsets, both in small intestinal and colon-draining LNs.

18 transgenic mice that overexpress Cdx2 in the small intestinal and colonic epithelium to investigate t

19 EPEC had a significantly greater severity of small intestinal and colonic lesions and were significan

20 re beta-catenin(+) early lesions and visible small intestinal and colonic tumors relative to Apc(+/De

21 f the present study was to describe gastric, small intestinal and colorectal motility and transit in

22 Liver, small intestinal, and kidney exposure were slightly, but

23 as expressed strongly in epithelial cells of small intestinal as well as ascending colonic tissue.

24 = 2.68), diaphragmatic hernia (aOR = 2.58), small intestinal atresia/stenosis (aOR = 2.97) including

25 40331]), gastrostomy (5.8% [$21227436]), and small-intestinal atresia (5.1% [$18840546]).

26 Gastroschisis and small-intestinal atresia may be particularly high-yield

27 Small intestinal bacteria exhibit distinct gluten metabo

28 y is to summarize the recent developments in small intestinal bacterial infections.

29 Small intestinal bacterial overgrowth (SIBO) and changes

30 pathogenesis of IBS is not well-understood, small intestinal bacterial overgrowth (SIBO) or other ab

31 To critically review recent literature on small intestinal bacterial overgrowth (SIBO).

32 Additionally, small intestinal bacterial overgrowth and Helicobacter p

33 Small intestinal bacterial overgrowth is one of the caus

34 charides (e.g., lactose or fructose) and for small intestinal bacterial overgrowth.

35 Hepatic fat accumulation, small intestinal barrier impairment and components of th

36 tryptophan supplementation had no impact on small intestinal barrier or fatty liver disease.

37 The small intestinal BB Na(+)/H(+) antiporter NHE3 accounts

38 infusion decreased pancreatic but increased small intestinal BF similarly in all groups both before

39 Endoscopic small intestinal biopsies was recommended for all POCT-

40 with HIV status and morphometric analysis of small intestinal biopsies.

41 lular TG2 in cryosections of human and mouse small intestinal biopsies.

42 and February 12, 2008, we collected data on small-intestinal biopsies performed at Sweden's 28 patho

43 Lnc13 levels are significantly decreased in small intestinal biopsy samples from patients with celia

44 ve qualified for a diagnosis of CD without a small intestinal biopsy, according to the new ESPGHAN pr

45 CD was mainly diagnosed from small intestinal biopsy, available in all centers.

46 the same area could be identified without a small intestinal biopsy.

47 s) for future ASDs in individuals undergoing small intestinal biopsy.

48 We have constructed a small intestinal bioreactor using 3-D printing and polym

49 he present study we examined the role of the small intestinal brush-border enzyme, intestinal alkalin

50 MGAM and SI are anchored to the small intestinal brush-border epithelial cells, and each

51 -out mice exhibited a significantly impaired small intestinal calcium absorption that resulted in sec

52 d us to define a functional role for 4.1R in small intestinal calcium absorption through regulation o

53 Hereditary small intestinal carcinoid has not been recognized and g

54 tion was detected in all 11 individuals with small intestinal carcinoids and in 17 of 35 family membe

55 Small intestinal carcinoids are rare and difficult to di

56 We found that small intestinal carcinoids can occur as an inherited au

57 erformed a genetic analysis of families with small intestinal carcinoids to establish a hereditary ba

58 tudy of 33 families with at least 2 cases of small intestinal carcinoids.

59 nces between pancreatic tumor cell lines and small intestinal cell lines, the different gene expressi

60 lishes feeding-induced OEA production in rat small-intestinal cells.

61 Gastric and small intestinal circular smooth muscle layers have a tr

62 (150min) of digestion under simulated gastro-small intestinal conditions that decreased to approximat

63 Homeostatic adult small intestinal crypt cell proliferation, survival, and

64 we find no (15)N label retention by dividing small intestinal crypt cells after a four-week chase.

65 The epithelium of the small intestinal crypt, which has a vital role in protec

66 Paneth cells residing at the base of the small intestinal crypts contribute to the mucosal intest

67 the pyloric glands of the stomach and in the small intestinal crypts differ in their differentiation

68 d2 function in nonhematopoietic cells of the small intestinal crypts is critical for protecting mice

69 Cell proliferation within small intestinal crypts is the principal driving force f

70 Paneth cells at the base of small intestinal crypts of Lieberkuhn secrete host defen

71 We found that small intestinal crypts of Villin(Cre);Dclk1(f/f) mice w

72 Paneth cells at the base of small intestinal crypts secrete microbicidal alpha-defen

73 Small intestinal crypts were isolated and subsequently c

74 a lineage normally confined to the bottom of small intestinal crypts), elevated expression of the Wnt

75 s of quiescent and cycling stem cells in the small intestinal crypts, respectively.

76 elf-regenerating human epithelial cells from small intestinal crypts, which contain both intestinal s

77 demonstrate that Pnn plays a crucial role in small intestinal development by influencing expression o

78 of Wnt signaling and Cdx2 expression during small intestinal development.

79 lipid-mucin interactions were evident in all small intestinal digesta.

80 ry proteins and peptides were present in the small intestinal digesta.

81 fold decrease in the IC50 value of FVJ after small intestinal digestion (p<0.05).

82 cs of glucose release during in vitro gastro-small intestinal digestion of freshly cooked and refrige

83 al IRI with pentobarbital led to significant small intestinal dysfunction with increased mucosal inju

84 nutrient exposure to the brush border due to small intestinal dysmotility.

85 B and R-SFB showed host-specific adhesion to small intestinal ECs, accompanied by host-specific induc

86 t views of the integrative physiology of the small intestinal electrolyte transport.

87 fat that might be responsible for triggering small-intestinal endocannabinoid signaling.

88 nt sera, is required for efficient access to small intestinal enterocytes and for the optimal deliver

89 T1 localized in the brush border membrane of small intestinal enterocytes, it is unclear whether func

90 sorptive microvilli (MV) from the surface of small intestinal enterocytes.

91 vitro observations, the results suggest that small intestinal enterocytic epithelial differentiation

92 nd that these effects may be specific to the small intestinal enterocytic phenotype as opposed to tha

93 We used human small intestinal enteroids to study neutral Na(+) absorp

94 in protein were not significantly altered in small intestinal epithelia from Apc(mNLS/mNLS) mice.

95 asured in human colonic epithelial cells and small intestinal epithelial cells after knockdown of MIR

96 a illustrate that dietary adjustments affect small intestinal epithelial cells and can be used to mod

97 Viral antigen was detected in small intestinal epithelial cells but not in colon.

98 owed that the expression levels of RALDH1 in small intestinal epithelial cells correlated with the ac

99 Deficiency of either UPR or autophagy in small intestinal epithelial cells promotes each other's

100 In infected mice, proliferation of small intestinal epithelial cells was compromised in an

101 veral tissues, including apical membranes of small intestinal epithelial cells.

102 Intestinal stem cells (ISCs) drive small intestinal epithelial homeostasis and regeneration

103 physically separates the microbiota from the small intestinal epithelial surface.

104 x vivo and to infect polarized monolayers of small-intestinal epithelial cells derived from DAF trans

105 t its physiologic functions in the mammalian small intestinal epithelium remain poorly defined.

106 cohabitate in the crypts and rejuvenate the small intestinal epithelium.

107 reased via suppressed Notch signaling in the small intestinal epithelium.

108 absorptive enterocyte gene expression in the small intestinal epithelium.

109 ocarcinoma and have similar functions to the small intestinal epithelium.

110 neth cells mediate immunity and maintain the small intestinal epithelium; defects in activities of th

111 , we identified several abnormalities in the small-intestinal epithelium of Nod2(-/-) mice including

112 critically ill patients on insertion of the small intestinal feeding catheter and examined for disac

113 cies corresponding to major chymotrypsin- or small intestinal fluid-generated NanI fragments possesse

114 t (corresponding to esophageal, gastric, and small intestinal function evaluation, respectively) befo

115 ing gastric emptying, although its impact on small intestinal function is unknown.

116 We show that the small intestinal GALT are the essential early sites of p

117 Together, these data demonstrate that the small intestinal GALT are the major early sites of prion

118 ity was dramatically reduced in mice lacking small intestinal GALT.

119 nd is associated with significant changes in small intestinal gene expression.

120 Erythromycin increased small intestinal glucose absorption [3-OMG AUC360: 105.2

121 After gavage of d-glucose, small intestinal glucose absorption across the brush-bor

122 ute administration of erythromycin increases small intestinal glucose absorption in the critically il

123 al feeding is associated with a reduction in small intestinal glucose absorption, consistent with the

124 on these data, we conclude that the rate of small intestinal glucose exposure (i.e., glucose load) i

125 dulate Asc bioavailability via inhibition of small intestinal GLUT2 and GLUT8.

126 Ammonia was generated through increased small intestinal glutaminase activity with concomitantly

127 ts the evidence that biomarkers of sustained small intestinal growth or mucosal healing and evaluatio

128 All subjects had normal small intestinal histology.

129 s were correlated with significantly reduced small intestinal HRV IgA Ab responses in EcN-colonized c

130 and directly obtaining control and infected small intestinal human tissue.

131 R, MAdCAM-1, and chemokines in PP and lowers small intestinal IgA compared with chow.

132 we found that NOD2 was required for optimal small intestinal IL-10 production, in particular from CD

133 Paneth cell numbers significantly decreased small intestinal IL-17A release and plasma IL-17A levels

134 acologic depletion of Paneth cells decreased small intestinal IL-17A secretion and plasma IL-17A leve

135 Here, we show that small-intestinal ILC3s had lower Ikaros expression than

136 human microbiota (HMb) to determine whether small intestinal immune maturation depends on a coevolve

137 targeted to the small intestine induced only small intestinal immunity and provided no rectal or vagi

138 Ingestion of wheat, barley, or rye triggers small intestinal inflammation in patients with celiac di

139 These findings demonstrate that small intestinal inflammation in Rc3h1(san/san) and Rc3h

140 TL1A in transgenic mice was associated with small intestinal inflammation, which was accompanied by

141 y patients remain symptomatic and still have small intestinal inflammation.

142 Celiac disease is a common small intestinal inflammatory condition induced by wheat

143 CKGROUND & AIMS: Celiac disease is a chronic small intestinal inflammatory disorder mediated by an im

144 assigned randomly to groups that were given small intestinal infusions of allogenic or autologous mi

145 soflurane post-conditioning protects against small intestinal injury and hepatic and renal dysfunctio

146 in modulating genotoxic chemotherapy-induced small intestinal injury in vitro and in vivo.

147 njury but also developed significant AKI and small intestinal injury.

148 cerbated inflammation in Nod2(-/-) mice upon small-intestinal injury.

149 NKT cells (iNKT), CD8alphaalphaTCRalphabeta small intestinal intraepithelial lymphocytes, and innate

150 lls: hepatic iNKT, CD8alphaalphaTCRalphabeta small intestinal intraepithelial lymphocytes, and innate

151 found in five puppies, of which two also had small intestinal intussusception.

152 t (March 2010 to September 2011) advances in small intestinal ion transport, with particular emphasis

153 high demands of iron during erythropoiesis, small intestinal iron absorption is increased through an

154 at IL as opposed to IP microdialysis detects small intestinal ischemia with higher sensitivity and sp

155 perfusion generally has a milder course than small intestinal ischemia-reperfusion.

156 ILC subset, as residual cells persist in the small intestinal lamina propria (siLP) of adult and neon

157 otected against endothelial apoptosis in the small intestinal lamina propria and facilitated recovery

158 quired for optimal steady-state migration of small intestinal lamina propria CD103(+) DCs into the ML

159 rance) rely on the steady-state migration of small intestinal lamina propria dendritic cells (DCs) in

160 ted from the spleen, mesenteric lymph nodes, small intestinal lamina propria, and colonic lamina prop

161 re activated CD8(+) alphabeta T cells in the small intestinal lamina propria, this increase was absen

162 igen expression was observed in cells of the small intestinal lamina propria.

163 mals reflected a loss of Th17 cells from the small intestinal lamina propria.

164 l-characterized network of phagocytes in the small intestinal lamina propria.

165 helper cell type 17 (Th17) population in the small-intestinal lamina propria (SI-LP) of the mouse gut

166 ) weeks, birth weight of 1423 (895, 2445) g, small intestinal length of 41.0 (24.0, 65.0) cm, and pre

167 derwent transplant or died, the median (IQR) small intestinal length was 55.0 (28.0, 75.0) cm in wean

168 Small intestinal length was found to be the primary pred

169 stress responses and implicates this unique small intestinal lineage in inflammatory bowel disease p

170 there was a tendency for the drug to reduce small intestinal lipid absorption and slow transit.

171 ed three small mesenteric LNs, distinct from small intestinal LNs, which drain lymph specifically fro

172 he study was repeated in vivo using a rabbit small intestinal loop assay, preincubation or coincubati

173 amage and luminal fluid accumulation in both small intestinal loops and colonic loops after as little

174 mulation and severe tissue damage in ligated small intestinal loops of rabbits and other animals.

175 nts to cause necrotizing enteritis in rabbit small intestinal loops or enterotoxemic lethality in mic

176 ns caused enteropathogenic effects in rabbit small intestinal loops, which is significant since CPE i

177 and STa toxin-induced fluid accumulation in small intestinal loops, with IC50 down to 0.1 mg/kg.

178 ccumulation and histologic lesions in rabbit small intestinal loops.

179 lso acted together synergistically in rabbit small intestinal loops; however, only higher doses of ei

180 Small intestinal LPLs had increased numbers of CD44(hi),

181 ere shed back from intestinal villi into the small intestinal lumen and reinfected the Peyer's patche

182 rodialysis and metabolic parameters from the small intestinal lumen indicate onset of ischemia earlie

183 d by sporulating C. perfringens cells in the small intestinal lumen, where it then causes epithelial

184 gical methods to the characterization of the small intestinal microbiome will tell us, once and for a

185 ha-defensins modulate the composition of the small intestinal microflora, that development of crypt o

186 ice, accompanied by significant increases in small intestinal microsomal lovastatin-hydroxylase activ

187 apidly than large droplets using a simulated small intestinal model (pH stat), which was attributed t

188 the many advantages of using TC-7 cells as a small intestinal model to study host-pathogen interactio

189 s such as Caco-2 - the most extensively used small intestinal model.

190 from pluripotent stem cells and demonstrate small intestinal morphology and physiology, could be use

191 th groups with exenatide, but suppression of small intestinal motility and flow was observed even in

192 study aimed to evaluate the effect of SNS on small intestinal motility in IBS patients.

193 The gastric emptying time and small intestinal motility were evaluated by MTS-1, and t

194 The inhibition of small intestinal motor function represents a novel mecha

195 compared these data to RNA-Seq from both the small intestinal mucosa and colonic mucosa of healthy co

196 impact on the structure and function of the small intestinal mucosa and suggest signaling through th

197 Growth inhibition of the small intestinal mucosa by fasting in mice was associate

198 29b-reduced endogenous miR-29b levels in the small intestinal mucosa increases cyclin-dependent kinas

199 studies reveal that growth inhibition of the small intestinal mucosa is associated with increased exp

200 G2 can be activated by dietary gluten in the small intestinal mucosa of celiac sprue patients, our fi

201 n (GFP)-tagged gammadelta T cells within the small intestinal mucosa of mice infected with DsRed-labe

202 messenger RNA targeting relationships in the small intestinal mucosa provides insight into the molecu

203 , dramatic, and reversible remodeling of the small intestinal mucosa with significant villus shorteni

204 me closely mirrored the transcriptome of the small intestinal mucosa.

205 ease in mice, likely by a dysfunction of the small intestinal mucosal barrier.

206 We examined 26 small intestinal mucosal biopsies (AR/NR group; 15/11) o

207 y Nod2 is an important mechanism to regulate small intestinal mucosal damage following acute T cell a

208 ctivation with anti-CD3 mAb induced stronger small intestinal mucosal damage in NOD2(-/-) mice compar

209 However, recent data suggest that altered small intestinal mucosal function may be a contributing

210 tients, possibly indicating an impairment of small intestinal mucosal function.

211 Gluten ingestion leads to small intestinal mucosal injury in patients with celiac

212 e ALV003 appears to attenuate gluten-induced small intestinal mucosal injury in patients with celiac

213 AIMS: Gluten ingestion leads to symptoms and small intestinal mucosal injury in patients with celiac

214 Gluten ingestion leads to symptoms and small intestinal mucosal injury in patients with celiac

215 free diet continue to have symptoms and have small intestinal mucosal injury.

216 , with lactulose/rhamnose ratio, a marker of small intestinal mucosal permeability.

217 t the direct impact of high-fat (HF) diet on small-intestinal mucosal defenses and spatial distributi

218 performance of antibody tests in predicting small-intestinal mucosal status in diagnosis vs. follow-

219 ading MUC2, the major protein present in the small intestinal mucous layer, and that removal of this

220 In contrast, small intestinal neoplasia development significantly cor

221 Small intestinal neuroendocrine tumors (SI-NETs) are ser

222 analysis of pancreatic endocrine tumors with small intestinal neuroendocrine tumors in clinical studi

223 ROUND & AIMS: Paneth cells contribute to the small intestinal niche of Lgr5(+) stem cells.

224 e the effects of intravenous erythromycin on small intestinal nutrient absorption and transit in the

225 ients during intragastric feeding to augment small intestinal nutrient delivery.

226 Common serious adverse events included small intestinal obstruction (10 [5%] of 204 patients),

227 n in one patient, intestinal perforation and small intestinal obstruction in one patient; colitis in

228 ng pancreatic tumor cell lines as models for small intestinal or 'carcinoid' tumor biology are consid

229 Gastric and small intestinal organoids differentiated from human plu

230 dult Lgr5-positive stem cells, isolated from small intestinal organoids, require Cdx2 to maintain the

231 ed to the more promiscuous transformation of small intestinal organoids.

232 Current knowledge suggests that small intestinal overgrowth participates in the pathogen

233 Hepatic IR induced small intestinal Paneth cell degranulation and increased

234 cKit marks small intestinal Paneth cells and a subset of colonic go

235 chemia-reperfusion or bilateral nephrectomy, small intestinal Paneth cells increased the synthesis an

236 Small intestinal Paneth cells supply Wnt3, EGF, and Notc

237 t-defense peptide, expressed and released by small intestinal Paneth cells, that exhibits antibacteri

238 Giardia duodenalis is a small intestinal parasite responsible for diarrheal dise

239 The macrohemodynamics and small intestinal pCO(2) gap changes were recorded and pe

240 o 0.5, consistent with values encountered in small intestinal permeability tests.

241 itro model to simulate the oral, gastric and small intestinal phases of the gastrointestinal tract.

242 ystokinin (CCK), a physiological agonist for small intestinal propulsion in mice.

243 normal conditions, the vast majority of the small intestinal pTreg cells are induced by dietary anti

244 Extensive small intestinal resection was the major predictor for l

245 esponse durability correlated with increased small intestinal rotavirus-specific, immunoglobulin A-pr

246 Proximal small intestinal samples were harvested for molecular bi

247 of dietary fat stimulates production of the small-intestinal satiety factors oleoylethanolamide (OEA

248 gesting that sympathetic activity may engage small-intestinal satiety signals such as OEA and NPPE.

249 o retard diffusion and mixing in a simulated small intestinal segment.

250 The individual small intestinal segments studied revealed comparable st

251 as assessed using everted rings of different small intestinal segments.

252 erein, we demonstrate that fasting preserves small intestinal (SI) architecture by maintaining SI ste

253 ed the difference between WT and LCN mice in small intestinal (SI) CYP3A levels at 6 hours after the

254 and COX-2-derived prostaglandins and caused small intestinal (SI) damage.

255 e dependent on migration of T cells into the small intestinal (SI) lamina propria.

256 Small intestinal (SI) neuroendocrine tumors (NETs) have

257 To summarize our current understanding of small intestinal stem cell biology and the current tools

258 In particular, the small intestinal stem cell populations identified as the

259 However, the population of putative small intestinal stem cells (ISCs) at position +4 from t

260 n intestinal tissues of mice, PRC2 maintains small intestinal stem cells by promoting proliferation a

261 Clonal descendants of Cdx2(null) small intestinal stem cells enter the gastric differenti

262 For the first time mouse small intestinal stem cells in intact live crypts are id

263 iferation and lineage-generating capacity of small intestinal stem cells, disrupting the supply of di

264 9H is not responsible for the differences in small intestinal sterol transporter expression.

265 performed a high-resolution analysis of the small intestinal stroma and determined that lacteals res

266 Porcine small intestinal submucosa (SIS) has been widely used in

267 Small intestinal submucosa-derived extracellular matrix

268 ead caused villus destruction with a loss of small intestinal surface epithelium and death.

269 s assessed by proliferation assays of celiac small intestinal T cells/interferon-gamma (IFN-gamma) an

270 No eYFP expression was detected in small intestinal Th17 cells, and they did not expand in

271 activation and proliferation in response to small intestinal tissue damage induced by the chemothera

272 pression in RAJ tissue compared with that in small intestinal tissue from the same calves.

273 pitated hypersecretion in morphine-dependent small intestinal tissue.

274 To extend this work, we examined small-intestinal tissue sections at various time points

275 Small-intestinal tissue was harvested for analysis of ti

276 onversely, TLR2 activation failed to protect small intestinal tissues genetically deficient in MDR1A

277 e fatty acid and lipophilic nutraceutical in small intestinal tissues was highest when they were enca

278 rodialysate metabolites in depicting ex vivo small intestinal total ischemia during GI-tract surgery.

279 Lrig1-null mice had significant delays in small intestinal transit compared with control mice.

280 Slowed small intestinal transit observed in Lrig1-null mice may

281 nd mixed IBS, it has no detectable effect on small intestinal transit patterns.

282 ock intestinal cholesterol absorption caused small intestinal transit time to return to normal.

283 ction with Helicobacter hepaticus, influence small intestinal transit time.

284 a combined manometry-impedance catheter and small intestinal transit using scintigraphy.

285 by gavage did not alter gastric emptying or small intestinal transit, but luminal AITC inhibited col

286 eflect reduced absorption and/or accelerated small intestinal transit.

287 mation while having no discernable effect on small intestinal tumor formation.

288 P and colon cancer, diminished the number of small intestinal tumors generated.

289 y impairs the progression and maintenance of small intestinal tumors in a cell autonomous and highly

290 Neuroendocrine tumors, particularly small intestinal tumors, also grouped as 'carcinoids', a

291 ouse tumor model that normally only develops small intestinal tumors.

292 therapy, highlighting the aspects unique to small intestinal tumors.

293 ucing antioxidant power was increased in the small intestinal vessel for PM09.960 and in the ascendin

294 ore anthocyanin species were detected in the small intestinal vessel relative to other vessels for ac

295 CoV antigen was found in epithelial cells of small intestinal villi in all puppies and the colon in 2

296 cteria were eliminated in the liver, whereas small intestinal villi provided a niche for bacterial re

297 Proteobacteria and Firmicutes penetrated small intestinal villi, and flagellated bacteria breache

298 uncovered drainage of absorbed molecules in small intestinal villus lacteals and the involvement of

299 roteins led to Neu5Gc incorporation into the small intestinal wall, appearance in circulation at a st

300 Small intestinal wash fluid was collected and IgA was qu