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1 cidence of critical illness was greatest for small intestinal (17.2% [95% CI, 13.3%-21.8%]) and color
4 ficantly reduced both the number and size of small intestinal adenomas arising in this model, and it
5 intestinal-specific Bmi1 deletion suppressed small intestinal adenomas in a manner that was indisting
7 omal macrophage Cox-2 in colorectal (but not small intestinal) adenomas from cLys-Cox-2 x Apc (Min/+)
8 nflammation and oxidative stress that limits small intestinal alpha-tocopherol absorption and/or impa
9 gulation of genes encoding components of the small intestinal (alpha-defensins Defa24 and Defa-rs1) a
17 EPEC had a significantly greater severity of small intestinal and colonic lesions and were significan
19 pounds significantly reduced accumulation in small intestinal and hepatic microsomes, which influence
22 as expressed strongly in epithelial cells of small intestinal as well as ascending colonic tissue.
25 t terminals along the entire proximal-distal small intestinal axis had similar morphology to those pr
32 to ready access to hydrogen breath testing, small intestinal bacterial overgrowth (SIBO) is now comm
39 Primary outcomes were changes in VH, in vivo small intestinal barrier dysfunction assessed by confoca
42 infusion decreased pancreatic but increased small intestinal BF similarly in all groups both before
45 and February 12, 2008, we collected data on small-intestinal biopsies performed at Sweden's 28 patho
46 Lnc13 levels are significantly decreased in small intestinal biopsy samples from patients with celia
47 ve qualified for a diagnosis of CD without a small intestinal biopsy, according to the new ESPGHAN pr
52 he present study we examined the role of the small intestinal brush-border enzyme, intestinal alkalin
53 -out mice exhibited a significantly impaired small intestinal calcium absorption that resulted in sec
54 ere similar in magnitude to WT mice, whereas small intestinal cAMP DeltaI(sc) responses were reduced.
56 tion was detected in all 11 individuals with small intestinal carcinoids and in 17 of 35 family membe
59 erformed a genetic analysis of families with small intestinal carcinoids to establish a hereditary ba
61 c treatment of neonates restored LPS-induced small intestinal cell shedding, whereas adult fecal micr
62 (150min) of digestion under simulated gastro-small intestinal conditions that decreased to approximat
66 the pyloric glands of the stomach and in the small intestinal crypts differ in their differentiation
71 elf-regenerating human epithelial cells from small intestinal crypts, which contain both intestinal s
77 cs of glucose release during in vitro gastro-small intestinal digestion of freshly cooked and refrige
79 B and R-SFB showed host-specific adhesion to small intestinal ECs, accompanied by host-specific induc
81 nt sera, is required for efficient access to small intestinal enterocytes and for the optimal deliver
83 T1 localized in the brush border membrane of small intestinal enterocytes, it is unclear whether func
86 vitro observations, the results suggest that small intestinal enterocytic epithelial differentiation
87 nd that these effects may be specific to the small intestinal enterocytic phenotype as opposed to tha
91 hesion molecules (CEACAMs) on the surface of small intestinal epithelia, where they serve as critical
93 asured in human colonic epithelial cells and small intestinal epithelial cells after knockdown of MIR
94 a illustrate that dietary adjustments affect small intestinal epithelial cells and can be used to mod
95 owed that the expression levels of RALDH1 in small intestinal epithelial cells correlated with the ac
97 are three-dimensional structures of primary small intestinal epithelial cells that contain all diffe
99 impaired cAMP generation in acutely isolated small intestinal epithelial cells, and significantly imp
102 x vivo and to infect polarized monolayers of small-intestinal epithelial cells derived from DAF trans
103 plain why Giardia trophozoites adhere to the small intestinal epithelium during human and animal infe
108 neth cells mediate immunity and maintain the small intestinal epithelium; defects in activities of th
109 , we identified several abnormalities in the small-intestinal epithelium of Nod2(-/-) mice including
110 critically ill patients on insertion of the small intestinal feeding catheter and examined for disac
111 cies corresponding to major chymotrypsin- or small intestinal fluid-generated NanI fragments possesse
112 t (corresponding to esophageal, gastric, and small intestinal function evaluation, respectively) befo
115 Together, these data demonstrate that the small intestinal GALT are the major early sites of prion
117 Resistant starch escapes digestion by host small intestinal glucoamylases and transits the colon wh
118 on these data, we conclude that the rate of small intestinal glucose exposure (i.e., glucose load) i
120 Ammonia was generated through increased small intestinal glutaminase activity with concomitantly
122 us preferentially infects actively secreting small intestinal goblet cells, specialized epithelial ce
124 s were correlated with significantly reduced small intestinal HRV IgA Ab responses in EcN-colonized c
126 ce in addition to anoctamin-1 may develop in small intestinal ICC with ageing and contribute to pacem
128 we found that NOD2 was required for optimal small intestinal IL-10 production, in particular from CD
134 CKGROUND & AIMS: Celiac disease is a chronic small intestinal inflammatory disorder mediated by an im
136 aPC) mice also showed high susceptibility to small intestinal injury induced by indomethacin, a nonst
138 NKT cells (iNKT), CD8alphaalphaTCRalphabeta small intestinal intraepithelial lymphocytes, and innate
139 lls: hepatic iNKT, CD8alphaalphaTCRalphabeta small intestinal intraepithelial lymphocytes, and innate
142 ILC subset, as residual cells persist in the small intestinal lamina propria (siLP) of adult and neon
143 quired for optimal steady-state migration of small intestinal lamina propria CD103(+) DCs into the ML
144 rance) rely on the steady-state migration of small intestinal lamina propria dendritic cells (DCs) in
145 re activated CD8(+) alphabeta T cells in the small intestinal lamina propria, this increase was absen
147 ) weeks, birth weight of 1423 (895, 2445) g, small intestinal length of 41.0 (24.0, 65.0) cm, and pre
148 derwent transplant or died, the median (IQR) small intestinal length was 55.0 (28.0, 75.0) cm in wean
150 ed three small mesenteric LNs, distinct from small intestinal LNs, which drain lymph specifically fro
151 he study was repeated in vivo using a rabbit small intestinal loop assay, preincubation or coincubati
152 amage and luminal fluid accumulation in both small intestinal loops and colonic loops after as little
153 mulation and severe tissue damage in ligated small intestinal loops of rabbits and other animals.
154 ns caused enteropathogenic effects in rabbit small intestinal loops, which is significant since CPE i
155 and STa toxin-induced fluid accumulation in small intestinal loops, with IC50 down to 0.1 mg/kg.
157 lso acted together synergistically in rabbit small intestinal loops; however, only higher doses of ei
159 rodialysis and metabolic parameters from the small intestinal lumen indicate onset of ischemia earlie
160 ratching, caused expansion and activation of small intestinal MCs, increased intestinal permeability,
162 riggered FGID-related symptoms and decreased small intestinal microbial diversity while increasing sm
163 SIBO is our limited understanding of normal small intestinal microbial populations-progress in sampl
164 gical methods to the characterization of the small intestinal microbiome will tell us, once and for a
165 Our findings demonstrate that characterizing small intestinal microbiomes in patients with gastrointe
166 ps in the literature, particularly regarding small intestinal microbiota abundance and diversity, hig
167 etween growth stunting and components of the small intestinal microbiota and enteropathy and offer a
169 ice, accompanied by significant increases in small intestinal microsomal lovastatin-hydroxylase activ
170 apidly than large droplets using a simulated small intestinal model (pH stat), which was attributed t
171 the many advantages of using TC-7 cells as a small intestinal model to study host-pathogen interactio
173 from pluripotent stem cells and demonstrate small intestinal morphology and physiology, could be use
175 th groups with exenatide, but suppression of small intestinal motility and flow was observed even in
178 i-diabetic agent metformin, while inhibiting small intestinal mTOR alone lowers plasma glucose levels
179 econd, we found that molecular activation of small intestinal mTOR blunts the glucose-lowering effect
180 se findings illustrate that inhibiting upper small intestinal mTOR is sufficient and necessary to low
181 per small intestine is sufficient to inhibit small intestinal mTOR signaling and lower glucose produc
183 compared these data to RNA-Seq from both the small intestinal mucosa and colonic mucosa of healthy co
184 d by the difficulty in directly sampling the small intestinal mucosa and microbial community (microbi
185 impact on the structure and function of the small intestinal mucosa and suggest signaling through th
187 studies reveal that growth inhibition of the small intestinal mucosa is associated with increased exp
189 n (GFP)-tagged gammadelta T cells within the small intestinal mucosa of mice infected with DsRed-labe
191 M d-glucose, hSGLT1-mediated AMG uptake into small intestinal mucosa was decreased by 40% to 50%.
192 on's terminals and their distribution in the small intestinal mucosa were examined by quantitatively
193 , dramatic, and reversible remodeling of the small intestinal mucosa with significant villus shorteni
194 tandard for successful treatment is a healed small intestinal mucosa, and therefore, the outcome meas
197 y Nod2 is an important mechanism to regulate small intestinal mucosal damage following acute T cell a
198 ctivation with anti-CD3 mAb induced stronger small intestinal mucosal damage in NOD2(-/-) mice compar
200 ed by combining coeliac disease serology and small intestinal mucosal histology during a gluten-conta
201 AIMS: Gluten ingestion leads to symptoms and small intestinal mucosal injury in patients with celiac
204 e ALV003 appears to attenuate gluten-induced small intestinal mucosal injury in patients with celiac
209 t the direct impact of high-fat (HF) diet on small-intestinal mucosal defenses and spatial distributi
210 performance of antibody tests in predicting small-intestinal mucosal status in diagnosis vs. follow-
211 ading MUC2, the major protein present in the small intestinal mucous layer, and that removal of this
213 y used to simulate difficult-to-obtain human small intestinal mucus for investigating the intramucus
215 ability characteristics of human and porcine small intestinal mucus secretions to sub-micron sized pa
216 t GI tract integrity or the thickness of the small-intestinal mucus layer but, in contrast to P9 wild
217 ntagonists in inhibiting slow waves in adult small intestinal muscles suggest that a conductance in a
218 tagonists on muscles from juvenile and adult small intestinal muscles suggests that conductances in a
223 eatment-emergent serious adverse events were small intestinal obstruction (34 [7%] of 463 patients),
224 n in one patient, intestinal perforation and small intestinal obstruction in one patient; colitis in
228 n polymerase chain reaction and RNAscope) of small intestinal organoids incubated with the Notch inhi
229 PTMs in >1 million single cells derived from small intestinal organoids reveals cell-type- and cell-s
230 dult Lgr5-positive stem cells, isolated from small intestinal organoids, require Cdx2 to maintain the
233 icient in intestinal epithelial TLR9 develop small intestinal Paneth cell hyperplasia and higher Pane
240 mature ILC2s can enter the circulation after small intestinal perturbation by migratory helminths and
241 follicular dendritic cells (FDC) within the small intestinal Peyer's patches is essential to establi
245 normal conditions, the vast majority of the small intestinal pTreg cells are induced by dietary anti
246 of patients with IBS, we found that neither small-intestinal-release nor ileocolonic-release pepperm
248 and placebo groups: 29 of 62 patients in the small-intestinal-release peppermint oil group had a resp
250 ere randomly assigned to groups given 182 mg small-intestinal-release peppermint oil, 182 mg ileocolo
252 esponse durability correlated with increased small intestinal rotavirus-specific, immunoglobulin A-pr
255 erein, we demonstrate that fasting preserves small intestinal (SI) architecture by maintaining SI ste
256 ed the difference between WT and LCN mice in small intestinal (SI) CYP3A levels at 6 hours after the
261 To summarize our current understanding of small intestinal stem cell biology and the current tools
262 n intestinal tissues of mice, PRC2 maintains small intestinal stem cells by promoting proliferation a
264 iferation and lineage-generating capacity of small intestinal stem cells, disrupting the supply of di
266 performed a high-resolution analysis of the small intestinal stroma and determined that lacteals res
267 vides a spatially-resolved cell atlas of the small intestinal stroma and exposes Lgr5+ villus tip tel
268 sue engineered vessels (A-TEVs) comprised of small intestinal submucosa (SIS) immobilized with hepari
270 we show that combinatory transplantation of small intestinal submucosa-extracellular matrix (SIS-ECM
271 e corrected UABCs on an FDA-approved porcine small intestinal submucosal membrane (pSIS), and they re
272 the effects of teas and tea catechins on the small intestinal sugar transporters, SGLT1 and GLUTs (GL
274 (SFB), pentanoate inhibits the generation of small-intestinal Th17 cells and ameliorates SFB-promoted
275 activation and proliferation in response to small intestinal tissue damage induced by the chemothera
279 onversely, TLR2 activation failed to protect small intestinal tissues genetically deficient in MDR1A
280 e fatty acid and lipophilic nutraceutical in small intestinal tissues was highest when they were enca
282 Administration of IL1B to mice increased small intestinal TJ permeability, compared with mice giv
283 antigen and RNA are detected throughout the small intestinal tract in jejunal and ileal tissue from
288 measured total GI transit, gastric emptying, small intestinal transit, and propulsive colorectal moti
289 al levels of succinate, increased numbers of small intestinal tuft cells, and evidence for activation
292 y impairs the progression and maintenance of small intestinal tumors in a cell autonomous and highly
294 ucing antioxidant power was increased in the small intestinal vessel for PM09.960 and in the ascendin
295 ore anthocyanin species were detected in the small intestinal vessel relative to other vessels for ac
296 CoV antigen was found in epithelial cells of small intestinal villi in all puppies and the colon in 2
297 Proteobacteria and Firmicutes penetrated small intestinal villi, and flagellated bacteria breache
298 eliac disease was defined by the presence of small intestinal villus atrophy on histopathology specim
299 uncovered drainage of absorbed molecules in small intestinal villus lacteals and the involvement of