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1 nd decreased HuC/D protein expression in the small intestine.
2 edly reduced mast cell infiltration into the small intestine.
3  kidneys, adrenal glands, spleen, liver, and small intestine.
4 hat is abundantly expressed in the liver and small intestine.
5 ation of the protective mucus barrier in the small intestine.
6 mmunity showed chlamydial persistence in the small intestine.
7  gastrointestinal tract, particularly in the small intestine.
8  in vitro digestion in simulated stomach and small intestine.
9 nd oral tolerance to dietary antigens in the small intestine.
10 n T cells did not reduce T(reg) cells in the small intestine.
11 D4(+) T cells in clearing Chlamydia from the small intestine.
12 s found on the absorptive enterocytes of the small intestine.
13 unsaturated fatty acids in three segments of small intestine.
14 NA expression of interleukin (IL)-17A in the small intestine.
15 inked tuft cells with type 2 immunity in the small intestine.
16  iNOS expression and MDA accumulation in the small intestine.
17 hways rescued chlamydial colonization in the small intestine.
18 es from the intramuscular type of ICC in the small intestine.
19 ides, suggestive of a role for TM6SF2 in the small intestine.
20 l role in looping morphogenesis of the avian small intestine.
21 then contrasted with what is known about the small intestine.
22 differentiation into infectious particles in small intestine.
23  TG2 as its principal protein partner in the small intestine.
24 mbling the segmentation motor pattern of the small intestine.
25 ate of delivery of nutrients to the proximal small intestine.
26 he primary site of injury, namely the distal small intestine.
27 y intact anthocyanins were absorbed from the small intestine.
28 tes along the proximal-to-distal axis of the small intestine.
29 mposition of the bacterial population in the small intestine.
30 g glucose-induced GLP-1 secretion from human small intestine.
31 er cholesterol transporters, in the proximal small intestine.
32 laughter age, but reduces clearance from the small intestine.
33 ed information on survivin expression in the small intestine.
34 , and cholecystokinin (CCK), secreted by the small intestine.
35 irectly by modulation of BMP activity in the small intestine.
36 ction of polyphenol could be absorbed by the small intestine.
37 s immune-mediated inflammatory damage to the small intestine.
38  T cells (T(EM)) found only in the lungs and small intestine.
39 mportantly, no adenomas were observed in the small intestine.
40  in the apical surface of enterocytes in the small intestine.
41  YY (PYY), from enteroendocrine cells in the small intestine.
42 nd food crops was found to be highest in the small intestine.
43 eferentially enzymatically hydrolyzed in the small intestine.
44 not previously demonstrated in the mammalian small intestine.
45 dification in wild-type and Apc(Min/+) mouse small intestine.
46 ess this GPCR, such as the lung, testes, and small intestine.
47  regulation of tuft-ILC2 circuits within the small intestine.
48 le to IR-induced tissue injury than the male small intestine.
49 nes to amplify anti-helminth immunity in the small intestine.
50 litis, using conditions that mimic the human small intestine.
51 ped with a triple-lumen sampling tube in the small intestine.
52 ts with the host innate immune system in the small intestine.
53  clonally related IgA(+) plasma cells in the small intestine.
54 c emptying; modest changes were noted in the small intestine.
55  cholera by releasing cholera toxin into the small intestine.
56 and is abundantly expressed in the liver and small intestine.
57 nd Pb and galena were the main phases in the small intestines.
58 ite impaired Mn export into the lumen of the small intestines.
59  paramount for Mn excretion in the liver and small intestines.
60 ducing microbiota and SCFA production in the small intestines.
61 were to the right colon (0.167 +/- 0.04) and small intestine (0.153 +/- 0.03).
62 lso found in the subepithelial region of the small intestine 24h after pollens were gavaged to mice.
63 (45.9%), liver (60.2%), gallbladder (76.3%), small intestine (88.7%), and colon (93.6%), while mainta
64 ential homing of the engineered cells to the small intestine, a site of intense early AIDS virus repl
65                 However, whether mTOR in the small intestine affects glucose homeostasis in vivo rema
66  We showed that upregulation of SGLT1 in the small intestine after glucose ingestion is promoted by g
67 monstrated that microcapsules released Lf in small intestine allowing 6.5 times higher concentration
68 ia failed to produce infectious progenies in small intestine, although infectious progenies were even
69  in primary cultures of enteroids from human small intestine and anion current in enteroid monolayers
70            Survivin could be detected in the small intestine and ascending colon of the normoxia grou
71 vin was detected in the ischemically damaged small intestine and ascending colon.
72 ed by mesenteric ischemia/reperfusion in the small intestine and by dextran sulfate sodium in the col
73 b/p53(DeltaIEC) mice spontaneously developed small intestine and colon carcinomas.
74 uanylin promoter was observed throughout the small intestine and colon in goblet and Paneth(-like) ce
75 on intestinal epithelial cells (IECs) in the small intestine and colon is required for enteric IFN-la
76 nd significantly increased cell death in the small intestine and colon of VDR(DeltaIEC) mice.
77                        We used 3-dimensional small intestine and colon organoids, along with RNA-Seq
78 ghly analogous biochemical profiles of human small intestine and colon scaffolds, indicating that the
79 C) mice and ex vivo organoids generated from small intestine and colon tissues.
80 PS significantly elevated neutrophils in the small intestine and colon, but LPS was not detected in s
81                              In contrast, in small intestine and colon, the fraction of alpha4 integr
82  to result in the development of adenomas in small intestine and colon.
83 hitosan that subsequently release NPs in the small intestine and colon.
84 n the membrane, damaging epithelial cells in small intestine and colon.
85 lter the microbial community residing in the small intestine and colon.
86 oung woman and affected the stomach, sparing small intestine and colon.
87 -driven FAO program was highest in the upper small intestine and declined distally.
88 y localizing PBMC-derived CD8 T cells to the small intestine and enables the direct experimental ACT-
89 thelial surfaces in the distal region of the small intestine and exploit an intracellular route acros
90  the intestinal epithelial cells in the host small intestine and has evolved strategies to antagonize
91 ice elevated trophozoite colonization in the small intestine and impaired weight gain.
92 ties by inhibiting sugar transporters in the small intestine and improving insulin sensitivity.
93 ients we found along the length of the mouse small intestine and in tumours contrast with previous re
94  of H2-T3/TL and H2-Q10 is restricted to the small intestine and liver, respectively, yet CD8alphaalp
95 , although is involved in clearance from the small intestine and longer-term clearance from the ceca.
96 regulator of macronutrient absorption in the small intestine and may be a viable therapeutic option t
97 he enzyme transits through the length of the small intestine and measured in the terminal ileum, and
98 nal accessibility during passage through the small intestine and modulated the formation of the degra
99 the effects of HFD on bacterial flora in the small intestine and NSAID-induced enteropathy.
100  53,193 individual epithelial cells from the small intestine and organoids of mice, which enabled the
101     MSC therapy reduced crypt dropout in the small intestine and promoted elevated expression of grow
102 y to regulate GI stem cell function in adult small intestine and stomach.
103 ed [(11)C]biotin was rapidly absorbed in the small intestine and swiftly distributed to the same orga
104 e colonizes mainly the medial portion of the small intestine and that both the abundance and localiza
105 ersed throughout the enterocyte layer of the small intestine and that modulates systemic metabolism.
106 on of infection, including both the proximal small intestine and the colon.
107 e cell differentiation in both the mammalian small intestine and the Drosophila midgut, yet how Notch
108 d to the parental strain was observed in the small intestine and the liver.
109 s are one of 4 secretory cell linages in the small intestine and the source of IL-25, a critical init
110  enterocyte surface in the mid-region of the small intestine and translocate through the epithelial c
111 E mutant RVs replicated at low levels in the small intestine and were shed less in the feces of wild-
112 ntibiotic-induced dysbiosis caused elongated small intestines and ceca, and B16-F10 melanoma and Lewi
113 collected from the duodenum, jejunum, ileum (small intestine) and colon at six weeks post-term age an
114 s spectrometry of serum, gallbladder, liver, small intestine, and colon of wild-type, Cyp7a1(-/-) , C
115 ed in the duodenum, jejunum and ileum of the small intestine, and in human intestinal tumours from th
116  2 (FATP2) is highly expressed in the liver, small intestine, and kidney, where it functions in both
117 art, spleen, liver, kidneys, stomach, colon, small intestine, and pancreas, respectively.
118 i were most highly expressed in lung, blood, small intestine, and spleen.
119 r suppressor in the mouse colon, but not the small intestine, and that invasive ARID1A-deficient aden
120 elate in aquatic reservoirs and in the human small intestine, and therefore that phages may quench ch
121 e proteomics on the brains, spleens, hearts, small intestines, and colons of conventionally raised an
122 -PCR did not detect viral RNA in the wall of small intestine, appendix, gallbladder, bile, liver, and
123 d EW RV replication and IFN induction in the small intestine are accompanied by significant decreases
124                       In vitro models of the small intestine are crucial tools for the prediction of
125  GALT and of T cells and plasmablasts to the small intestine are well described.
126 that CS5 + CS6 ETEC use NaGCH present in the small intestine as a signal to initiate colonization of
127 b particles were detected in the stomach and small intestine at 4 and 8 h, respectively.
128 cation of the colonizing bacteria across the small intestine, bacteremia, and invasion of the meninge
129 nter relatively high levels of oxygen in the small intestine before transit to the oxygen-limited env
130 ept studies should be based on evaluation of small intestine biopsies.
131              Since DGAT1 is expressed in the small intestine, both 1 and 9 can suppress postprandial
132 radually to facilitate its absorption in the small intestine, both citrate cleavage in hepatocytes an
133 he lung, airways, lamina propria (LP) of the small intestine, brain, visceral adipose tissue, bone ma
134 ased expression of Cldn2 and Cldn4 in murine small intestine but increased only CLDN2 expression in T
135 ufficient for eliminating Chlamydia from the small intestine but not the large intestine of recipient
136  Th1 immunity in clearing Chlamydia from the small intestine but not the large intestine, indicating
137 s sufficient for clearing Chlamydia from the small intestine but not the large intestine.
138 t Chlamydia produced infectious progenies in small intestine but was 530-fold less infectious than pl
139  provides a noninvasive option to assess the small intestine, but its use with respect to endoscopic
140 s been extensively studied in the guinea pig small intestine, but less is known about colonic circuit
141 s study, we studied PC dynamics in the human small intestine by cell-turnover analysis in organ trans
142 l chlamydial organisms were cleared from the small intestine by day 28, paralleling their infection c
143                   L. plantarum adapts to the small intestine by expressing genes required for tolerat
144  analyzed 58,067 immune cells from the mouse small intestine by single-cell RNA sequencing (scRNA-seq
145 e number and tightness of loops in the chick small intestine can be increased or decreased directly b
146 erial tyrosine decarboxylase in the proximal small intestine can explain the increased dosage regimen
147 ing abnormalities in immune responses in the small intestine can trigger chronic type 2 inflammation
148 microbiome, while age is a driving force for small intestine cancer.
149 hesis that pathology specifically within the small intestine caused by a helminth co-infection would
150     Thus, HFD-induced microbial dysbiosis in small intestine caused microinflammation through the ind
151 iscovered that Giardia's colonization of the small intestine causes a systemic dysbiosis of aerobic a
152 iral infection and subsequent replication in small intestine CD4 T cells.
153 x-Aire-expressing medullary thymic cells and small-intestine cells that mediate tissue remodeling in
154                                       In the small intestine, chemosensing by epithelial tuft cells r
155 or primordial germ cell-like cells and E18.5 small intestine, combined with functional annotation ana
156 eria were present in higher abundance in the small intestine compared to the colon.
157 reased expression of interferon gamma in the small intestine compared to wild-type mice exposed to sm
158  the derived COs represent colon rather than small intestine, containing stem cells, transit-amplifyi
159                                          The small intestine contains CD4(+)CD8alphaalpha(+) double-p
160                          Bacteria invade the small intestine, crossing the intestinal epithelium from
161 )Atg7 (Delta/Delta) mice died rapidly due to small intestine damage, which was not rescued by p53 cod
162                          Pancreas, large and small intestines demonstrated lower segmentation accurac
163       Analysis of ileal effluents (at end of small intestine) demonstrated that 30% of ingested antho
164                            We also show that small intestine dendritic cells from pregnant, but not f
165                           Enteropathy of the small intestine developed in gnotobiotic mice that had b
166 ocytes, but mice with Slc30a10 deficiency in small intestines developed minimal Mn excess despite imp
167 , mice with Slc30a10 deficiency in liver and small intestines developed Mn excess that was less sever
168           The major iron transporters in the small intestine divalent metal-ion transporter 1 (DMT1)
169 tigen differ between gLNs, with the proximal small intestine-draining gLNs preferentially giving rise
170 duction of this key cytokine by ILC3s in the small intestine during development and under basal condi
171 nutrient delivery to the proximal and distal small intestine elicits different outcomes.
172 that loss of Tff2 in the developing neonatal small intestine enables the opportunistic neonatal patho
173 lated transcriptional signature is shared in small intestine enterocytes among coronavirus receptors
174 gulates the expression of CCL20 and CCL25 by small intestine enterocytes, while it increases the expr
175  at the slightly alkaline pHs simulating the small intestine environment, suggesting a potential of t
176 gene expression (GE) in nontransformed human small intestine epithelial cells (FHs 74 Int) after expo
177 lly differentiated T(RM) cells isolated from small intestine epithelium exhibited the potential to di
178                                              Small intestine expression of enzymes involved in lipid
179 d by an in vitro digestion model using a Rat Small Intestine Extract (RSIE).
180 re most highly expressed in skin, blood, and small intestine; genes at the adult onset-specific loci
181  with the OA patients, more AYA patients had small-intestine GISTs (139 [35.5%] vs 1465 [27.3%], P =
182      Unbiased analyses revealed that, in the small intestine, group-3 innate lymphoid cells (ILC3s) a
183 at the site of levodopa absorption, proximal small intestine, had a significant impact on levels of l
184 g extensive anatomical or functional loss of small intestine, has debilitating long-term consequences
185  starch (RS), which is not hydrolyzed in the small intestine, has proposed health benefits.
186                         While studies in the small intestine have addressed the lineage identity of t
187 chemical and immunohistochemical staining of small intestine, heart, liver and spleen as well as in s
188 -/-) animals showed lower muscle mass of the small intestine, higher abundance of Bacteroidetes, and
189  are dually targeted by IgA1 and IgA2 in the small intestine, IgA1+IgA2+ and IgA1-IgA2+ bacteria coex
190 lammatory drugs (NSAIDs) cause damage in the small intestine in a bacteria-dependent manner.
191 ls in stool as a means to surveil the distal small intestine in a murine model of NSAID enteropathy.
192 gulated autophagy-related gene expression in small intestine in mice.
193 oming receptor redirected CD8 T cells to the small intestine in rhesus macaque ACT experiments.
194 ne surveillance is distinct from that of the small intestine in terms of draining LNs, and identify p
195 T cells showed chlamydial persistence in the small intestine, indicating a critical role for CD4(+) T
196 he following variables were addressed in the small intestine: intraepithelial lymphocyte (IEL) and la
197                  The ability to colonize the small intestine is essential for enterotoxigenic Escheri
198 ic cells (FDC) in the Peyer's patches in the small intestine is essential for the efficient spread of
199                                          The small intestine is highly enriched in these activating e
200                                          The small intestine is maintained by actively cycling intest
201                     Replication of RV in the small intestine is restricted to homologous host species
202 e acting mTOR-mutated protein into the upper small intestine is sufficient to inhibit small intestina
203 er, oral anti-CD3 promotes XCL1 secretion by small intestine lamina propria gammadelta T cells that,
204 anifested an increase in the length of their small intestines, likely to compensate for challenges in
205 gan disease affecting the ileum and jejunum (small intestine), liver, skeletal muscle, and lung clini
206 h tumors of the stomach and small intestine, small-intestine location was associated with improved su
207 cantly increased apoptosis in the esophagus, small intestine, mesenteric lymph nodes, and kidney in m
208 ems TM6SF2 deficiency resulted in defects in small intestine metabolism in response to dietary lipids
209 l effects of diet on each taxon in stool and small-intestine mucosa samples.
210  are necessary for doxorubicin (DXR)-induced small intestine mucosal damage.
211 stasis, and basic functions performed by the small intestine need to be tightly preserved to maintain
212  levels of alpha-defensin (Defa) mRNA in the small intestine of C57BL/6 mice through an optimized set
213  observed an enlarged Th17 population in the small intestine of C57BL/6.IgA(-/-) mice compared with w
214 ells collected from the proximal half of the small intestine of Hnf4alphagamma(DKO) and control mice.
215 reased segmented filamentous bacteria in the small intestine of IgA(-/-) mice.
216 ndividual operational taxonomic units in the small intestine of mice fed HFD for 8 weeks.
217 NS progenitors from tunica muscularis of the small intestine of newborn (postnatal day 0) wild-type C
218 -2 by ILC3s was significantly reduced in the small intestine of patients with Crohn's disease, and th
219 iardia colonization and proliferation in the small intestine of the host may, however, disrupt the ec
220                                Moreover, the small intestine of treated animals show reduced hypoxic
221 A cytosine modifications by LC/MS, in normal small intestines of C57BL/6J wild-type mice, and in norm
222  only small decreases were observed in their small intestine or esophagus.
223 correlated with linear position in the mouse small intestine or intestinal tumours.
224 -specific RNA-sequencing data from pancreas, small intestine, ovary, kidney, and heart with existing
225  tissues, including blood, lungs, liver, and small intestines (P < 0.001-0.05).
226  pulmonary embolism (n=2), sepsis (n=1), and small intestine perforation (n=1).
227 rajejunally coinoculated into the same mouse small intestine, plasmid-free Chlamydia sp. was no longe
228 er the compromised mucus layer in the distal small intestine prior to systemic invasion and infection
229                           Macrophages in the small intestine produce IL-1beta, and activation of this
230 uction of the radioprotective WR-1065 in the small intestine, providing protective benefits without t
231 stinct CD4(+) T cell subsets in SLOs and the small intestine, respectively (C.
232  (SLOs) and within the lamina propria of the small intestine, respectively (C.
233               Here we used the natural mouse small intestine-restricted helminth pathogen Heligmosomo
234     Our data suggest that co-infections with small intestine-restricted helminth pathogens may be imp
235 atures, such as granzyme B expression in the small intestine, revealing tissue-specific and migration
236                             The human female small intestine seems less susceptible to IR-induced tis
237                            Tuft cells in the small intestine sense and direct the immune response aga
238 t favoured tumour initiation in the proximal small intestine (SI) and blocked tumour growth in the co
239          Food allergens are sampled by using small intestine (SI) epithelial secretory cells (termed
240                       M s that reside in the small intestine (SI) have been previously shown to be re
241 rovide effective protective responses in the small intestine (SI) in mice.
242                Throughout a 24-h period, the small intestine (SI) is exposed to diurnally varying foo
243                             The lumen of the small intestine (SI) is filled with particulates: microb
244 , and single-cell RNA-sequencing analyses on small intestine (SI) MMC9s were performed to illuminate
245             Gels from decellularized porcine small intestine (SI) mucosa/submucosa enable formation a
246      The development and physiologic role of small intestine (SI) vasculature is poorly studied.
247 ied four distinct Mf subpopulations in human small intestine (SI).
248  hydrolyzed in crude human-stomach and human-small-intestine simulations and may therefore meet the p
249 6SF2 is expressed predominantly in liver and small intestine, sites for triglyceride-rich lipoprotein
250  AYA patients with tumors of the stomach and small intestine, small-intestine location was associated
251 ed in the deep muscular plexus region of the small intestine, suggesting there are functional similar
252 f TM6SF2 protein being 10-fold higher in the small intestine than in the liver, dietary lipid absorpt
253  that are more representative of the in vivo small intestine than the widely used 2D transwell model.
254 ediators of host-microbe interactions in the small intestine that contribute to host defense and home
255 nction (EED) is an enigmatic disorder of the small intestine that is postulated to play a role in chi
256       The development of in vitro artificial small intestines that realistically mimic in vivo system
257          Here we show that, in the mammalian small intestine, the expression of Hmgcs2 (3-hydroxy-3-m
258 eracts with the developing microbiome of the small intestine, the major site for nutrient metabolism
259 ts pro-apoptotic activity in mouse thymi and small intestines, the chromosomal instability caused by
260 bility to indomethacin-induced damage in the small intestine; this phenotype was observed in normal d
261 grams diurnal metabolic rhythms in the mouse small intestine through histone deacetylase 3 (HDAC3).
262 lood via inhibition of its absorption in the small intestine, thus protecting against heart attack an
263 y free polyphenols, could be absorbed by the small intestine; thus, reducing their effective antioxid
264 3 to -607 of the proximal Npc1l1 promoter in small intestine tissues from 24-week-old offspring fed e
265                       Histologic analysis of small intestine tissues from IDO1-TG mice revealed incre
266                                              Small intestine tissues were collected and intestinal in
267 l forces in the functional response of human small intestine to a virulence factor of a pathogenic in
268   We find that peptide YY is required in the small intestine to maintain normal electrophysiology in
269 gh the delivery of nutrients into the distal small intestine to promote satiety and suppress food int
270 . might be prevented from spreading from the small intestine to the large intestine.
271  used stem cell-derived enteroids from human small intestines to study enterovirus infections of the
272 ptosis in the myenteric ganglia of the adult small intestine, total myenteric neuronal numbers remain
273 gative enteropathogens presumably invade the small intestine via Peyer's patches to initiate dissemin
274 (IEC) proliferation, and decreased growth of small intestine villi and colon crypts.
275 s were observed to retain integrity of their small intestine villi and had reduced eosinophilic infil
276 hnology, the elemental distribution of Zn in small intestine villi of mice subjected to a Zn-enriched
277 ffectors and (ii) chlamydial colonization in small intestine was highly dependent on plasmid.
278 tagenicity in site-of-contact tissues (e.g., small intestine) was generally more than dose-additive a
279 nses during infection of the skin, lung, and small intestine, we assessed the role of CGRP receptor s
280 erification of OATP1B3-1B7 expression in the small intestine, we determined in microsomes whether SER
281       Next, focusing on the developing chick small intestine, we determined that Bmp2 expressed in th
282 nes in tibia and barrier marker genes in the small intestine were analyzed by quantitative PCR.
283                                              Small intestines were perfused with, and stored in, pres
284 d lungs before returning to the lumen of the small intestine, where adult worms dwell.
285 s expressed at the crypt base throughout the small intestine, where it is enriched in crypt base colu
286 es lactose into glucose and galactose in the small intestine, where they are absorbed.
287 neration of T(RM) at some sites (such as the small intestine), whereas CD69 was critical for establis
288 b(+)CD103(+) DCs induce Th2 responses in the small intestine, whereas CD11b(+)CD103(-) DCs perform th
289          Lactose is mostly hydrolysed in the small intestine, whereas lactulose, recognised prebiotic
290                         One exception is the small intestine, which is unique in expressing exclusive
291 nin-gamma1 was significantly depleted in the small intestines, which showed crypt hyperplasia and dis
292 eria inhibit viral infection of the proximal small intestine while simultaneously stimulating the inf
293 ericutes and Verrucomicrobia compared to the small intestine, while Actinobacteria, and superphylum P
294 Streptococcus) were found in the stomach and small intestine, while anaerobic Lachnospiraceae and Rum
295 genesis, is expressed by Paneth cells in the small intestine, while group X sPLA2 is expressed by Pan
296 tion showed a more pronounced release in the small intestine with a vitamin bioaccessibility of 56%.
297 tein-free, elemental diet led to an atrophic small intestine with low numbers of activated T cells, i
298 ocrine cells in both crypts and villi of the small intestine, with no changes observed in goblet or P
299 , permitting proper placement of the lengthy small intestine within the confines of the body cavity.
300 ganisms immotile, thus they pass through the small intestine without colonizing.

 
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