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1 ct) but detrimental in the main habitat (the large intestine).
2 etary polysaccharide substrates in the human large intestine.
3 place the normal microbiota of the small and large intestine.
4 in self-limiting mucosal inflammation of the large intestine.
5 st Dra expression in the jejunum relative to large intestine.
6 easing in frequency in a gradient toward the large intestine.
7 cid may have an antineoplastic effect in the large intestine.
8 s the growth of mucosa in both the small and large intestine.
9 reflective of the distal region of the human large intestine.
10 ntestinal tumorigenesis, particularly in the large intestine.
11 ntified only in minute quantities within the large intestine.
12 nthesized biotin and pantothenic acid in the large intestine.
13 s largely restricted to moderate staining of large intestine.
14 not in the myenteric plexus of the small and large intestine.
15 e majority of NeuN-li cells in the small and large intestine.
16 the esophagus, stomach, small intestine, and large intestine.
17 pression in the mucosa of both the small and large intestine.
18 ne exhibited higher activity levels than the large intestine.
19  are synthesized by normal microflora of the large intestine.
20 , lymph nodes, spleen, thymus, and small and large intestine.
21 nd in the submucosal plexus of the small and large intestine.
22 ouse and found high levels of 15-PGDH in the large intestine.
23 al mucus, it is unable to colonize the mouse large intestine.
24 lls reside at crypt bottoms of the small and large intestine.
25  SDS and fed to mice, it colonized the mouse large intestine.
26 acterized epithelial malignant tumors of the large intestine.
27 yenteric plexus of the stomach and small and large intestine.
28 actalkine in human skin, the tonsil, and the large intestine.
29 aning, then quickly retreat to the cecum and large intestine.
30 stomach and was overlapping in the small and large intestine.
31  at high levels for at least 8 months in the large intestine.
32  rat liver, pancreas, stomach, and small and large intestine.
33 even though apoptotic MCs were common in the large intestine.
34 l membranes of epithelial cells in small and large intestine.
35  sulfide generation by bacteria in the human large intestine.
36 ithelial architecture in larger areas of the large intestine.
37 ntestine and a very robust resistance in the large intestine.
38  infiltration into the lamina propria of the large intestine.
39 l ileum, the ileocecal valve, and all of the large intestine.
40  mice develop an inflammatory disease of the large intestine.
41 ) isoforms, PKC-alpha and -betaII in the rat large intestine.
42 kidneys, spleen, descending aorta, and upper large intestine.
43 y lamina propria lymphocytes in the small or large intestine.
44  small intestine, and almost undetectable in large intestine.
45  lethal mutations which manifest only in the large intestine.
46 lonization of the streptomycin-treated mouse large intestine.
47 ed bleeding from ulcerations in the small or large intestine.
48 e against infection of the biliary tract and large intestine.
49 ed expression of inflammatory markers in the large intestine.
50 reflective of the distal region of the human large intestine.
51 nal (GI) tract, and then colonization of the large intestine.
52 represents different anatomical areas of the large intestine.
53 e, tunneling through epithelial cells of the large intestine.
54 lant fiber: those of the rumen and the human large intestine.
55 nciple mechanism of Mphi accumulation in the large intestine.
56  the serosa and lamina propria region of the large intestine.
57 al tissues such as the related mucosa of the large intestine.
58 hable bacterial populations in the small and large intestine.
59 pism compared to MNV-1 by replicating in the large intestine.
60 mptoms, including intermittent bleeding from large intestine.
61  evolve as a noninvasive imaging test of the large intestine.
62 s, diagnosis, and treatment of polyps in the large intestine.
63 nded clones to evenly seed the small but not large intestine.
64 identify stem cells throughout the small and large intestine.
65  of secretory cells throughout the small and large intestine.
66  parallel in different segments of small and large intestine.
67 entional culture techniques in the small and large intestine.
68 ghout the different regions of the small and large intestines.
69 eosinophils and macrophages in the small and large intestines.
70 ects of purified CPB in the rabbit small and large intestines.
71 adenomas to develop throughout the small and large intestines.
72 feration in the crypts of both the small and large intestines.
73 ght to cause infection in both the small and large intestines.
74 cts of the Mom1 locus, in both the small and large intestines.
75 lso found in the epithelium of the small and large intestines.
76 ithelium and lamina propria of the small and large intestines.
77 d colonic cell hyperplasia in both small and large intestines.
78 c islet, the hypothalamus, and the small and large intestines.
79  the neutral-pH environment of the small and large intestines.
80 biota and bile acid profile of the small and large intestines.
81 ntial gene expression in the mouse small and large intestines.
82 T(4) receptors were present in the small and large intestines.
83 elated with that found in the small, but not large, intestine.
84 ighest for gallbladder (0.27 mSv/MBq), upper large intestine (0.19 mSv/MBq), and small intestine (0.1
85 mCi +/- 0.168 [0.068 mSv/MBq +/- 0.046]) and large intestine (0.529 rem/mCi +/- 0.236 [0.143 mSv/MBq
86  intestine (1.43 +/- 0.19 rad/mCi) and upper large intestine (1.20 +/- 0.38 rad/mCi).
87 ion; the dose-critical organs were the lower large intestine (1.43 +/- 0.19 rad/mCi) and upper large
88 roid, 5 lacrimal gland, 3 small intestine, 2 large intestine, 1 kidney, 1 paraspinal region and 1 ski
89 ral surgery: 5.0%; upper GI: 6.9%; small and large intestine: 12.6%; HPB: 15.8%; vascular: 11.9%; tho
90  [0.849 rad/mCi]), followed by the small and large intestines (161.26 muGy/MBq [0.597 rad/mCi] and 18
91  (general surgery: 2; upper GI: 3; small and large intestine: 2; HPB: 3; vascular: 3; thoracic: 3; P
92 l intestine 47, stomach 41, pancreas 45, and large intestine 25.
93  (general surgery: 0; upper GI: 2; small and large intestine: 5; HPB: 6; vascular: 2; thoracic: 4; P
94                                       In the large intestine, aberrant DNA methylation arises very ea
95  the rate of epithelial cell turnover in the large intestine acts like an "epithelial escalator" to e
96                     S2215Y was identified in large intestine adenocarcinoma whereas R2505P was identi
97 y cytokines and chemokines were found in the large intestine after intraperitoneal challenge.
98 soflavone daidzein, which is produced in the large intestine after soy intake in 30% of Western popul
99 ly, many of the expanded clones found in the large intestine also were found in the spleen and elsewh
100 RNA phylotypes detected in the healthy human large intestine and belongs to the Ruminococcaceae famil
101         Clostridium difficile can infect the large intestine and cause colitis when the normal intest
102 bset resides within the normal mucosa of the large intestine and expands in response to inflammation.
103 yenteric plexus of the stomach and small and large intestine and in the submucosal plexus of the smal
104 obic bacterium that infects the lumen of the large intestine and produces toxins.
105  subdivided into domains -- small intestine, large intestine and rectum -- each characterized by a sp
106 c2(-/-) mice develop tumors in the small and large intestine and the rectum, but in contrast to tumor
107 l studies revealed necrosis in the small and large intestines and livers of infected IL-10-/- mice.
108 inal tract), excretion (lung, urinary tract, large intestine), and reproduction (reproductive tract).
109 al tissues of mice, mainly kidney, small and large intestine, and brain.
110 lt levels, and urobilinogen levels in cecum, large intestine, and feces.
111  artery, blood, muscle, lungs, bone, spleen, large intestine, and heart at 2 h after injection and 10
112 ns, including the skin, esophagus, air sacs, large intestine, and kidney.
113 ents ileus primarily affects the stomach and large intestine, and most patients who are diagnosed wit
114  heart, stomach, mesentery, small intestine, large intestine, and muscle) in wild-type and SCID mice.
115 pression in the prospective small intestine, large intestine, and rectum of genes encoding cell signa
116 e morphological subdomains: small intestine, large intestine, and rectum.
117  propionate, are generated in the caecum and large intestine, and when absorbed may elicit localised
118 dult heart, brain, thymus, spleen, small and large intestines, and peripheral blood leukocytes.
119 ells in the salivary gland, small intestine, large intestine, appendix, and tonsils.
120 The esophagus, stomach, small intestine, and large intestine are sites of infection for viruses, bact
121        Bacterial infections of the small and large intestine are widespread and continue to be topics
122                                The small and large intestines are tubular organs composed of several
123 the nematode parasite Trichuris muris in the large intestine around the time of oral prion exposure d
124 anding the fate of the dietary fibres in the large intestine as it was shown that degradation of a di
125 n UGT1A1 was markedly increased in small and large intestines as well as in liver.
126 ogical damage to the mucosa of the small and large intestine, as well as a 20% reduction of the intes
127 t changes to the microbiota in the small and large intestines, as well as a significant shift in the
128 s found in crypts and villi of the small and large intestine, bronchiolar epithelial cells, the epide
129  replication and histological changes in the large intestine, bursa of Fabricius, and cecal tonsil.
130 Ras and Wnt pathways tend to co-occur in the large intestine but are mutually exclusive in cancers of
131 elop predominantly in the distal part of the large intestine but the biological basis of this intrigu
132 ent in myenteric neurons along the small and large intestines but are rare in the gastric corpus.
133 ed in the fetal bowel (stomach and small and large intestine), but that encoding the 5-HT(2C) recepto
134 estine and superficial lamina propria of the large intestine, but distinct from the intraepithelial c
135 OX-2) is not normally expressed in the human large intestine, but its levels are increased in the maj
136 ts are associated with carcinogenesis of the large intestine, but no prospective study has examined m
137 s oral vaccine delivery system to target the large intestine, but not the small intestine, may repres
138 y eliminated enteric glia from the small and large intestines, but caused no defects in epithelial pr
139 nd goblet cell hyperplasia were found in the large intestine by 24 hours post-intraperitoneal Shigell
140 lonization of the streptomycin-treated mouse large intestine by Escherichia coli MG1655, a human comm
141    Butyrate, produced by fermentation in the large intestine by gut microbiota, and its synthetic der
142 cted in villous enterocytes of the small and large intestines by immunohistochemistry.
143 colorectal adenomas and no previous invasive large intestine carcinoma.
144 rhagic Escherichia coli (EHEC) colonizes the large intestine, causing attaching and effacing (AE) les
145 ferentially in the small (CCL25 and CCL5) or large intestine (CCL19, CCL21, and CXCL5).
146 omains of the small intestine (duodenum) and large intestine (cecum).
147 ry arteries, thyroid and parathyroid glands, large intestine, colon, bladder, testes, and prostate.
148 osa-associated microbiota, between small and large intestine, concordant with differences in regional
149 llustrate isolated lymphoid follicles in the large intestine, consisting of B cells interspersed with
150 dimethylhydrizene-treated Sprague Dawley rat large intestine containing a suspect growth.
151 ifferences were observed in the liver, upper large intestine contents, and small intestine contents b
152                    Radiologic imaging of the large intestine continues to evolve and expand the poten
153 al muscle, heart, lung, small intestine, and large intestine despite large differences in hyaluronan
154 ped by evaluating histopathologic lesions in large intestine detected 16 days after a 5-day period of
155 The terminal part of the small intestine and large intestine did not to contribute to this projection
156 ohistochemistry following infection with the large intestine dwelling helminth parasite Trichuris mur
157                         After colonizing the large intestine, EHEC forms attaching and effacing (AE)
158 nished mesoderm and overproliferation of the large intestine endoderm, leading to stenosis of the lum
159 s also govern the initial recognition of the large intestine environment and attachment to the host c
160 ed S. typhi vaccine strains induce small and large intestine epithelial cells to secrete IL-6, and ki
161  Wnt-dependent tumorigenesis, whereas in the large intestine epithelial HuR indirectly downregulates
162         In contrast, S. flexneri invades the large intestine epithelium at the basolateral membrane,
163 1WAF-1/CIP1 immunoreactivity was detected in large intestine epithelium up to 6 days after irradiatio
164 of the bacterially synthesized folate in the large intestine exists in the form of folate monoglutama
165 tudy of polyphenols after in vitro simulated large intestine fermentation was carried out on edible n
166 and, as a consequence, delivering PAs to the large intestine for fermentation and metabolism by gut b
167 ells isolated from the lamina propria of the large intestine from wild type or CerS6-deficient groups
168  plexus, the stomachs, small intestines, and large intestines from 3-, 12-, 21-, 24- and 27-month-old
169 ; expression in the colon indicates that the large intestine has a mechanism for luminal di- and trip
170 ity of E. coli strains to colonize the mouse large intestine has been correlated with their ability t
171 eral, upper gastrointestinal (GI), small and large intestine, hepatopancreatobiliary (HPB), vascular,
172 , high viral loads in the spleen, liver, and large intestine, histological changes in the liver and s
173 (-/-) Treg were significantly reduced in the large intestine, however, compared with wild-type Treg,
174 junum, upper ileum, and lower ileum) and the large intestine (i.e., cecum and mid-colon/rectum).
175 ing in the developing gizzard, duodenum, and large intestine in chick were tested by viral misexpress
176 sm for increasing energy uptake by the human large intestine in obese persons.
177 TNBS) in 50% ethanol induced inflammation of large intestine in susceptible (C3H/HeJ and BALB/c) but
178 bit the peristaltic reflex in the guinea pig large intestine in vitro.
179  recently identified as an inhabitant of the large intestine in young domestic cats with chronic diar
180 ain fatty acid formed by fermentation in the large intestine, in the regulation of insulin sensitivit
181 28 was detected in all IECs of the small and large intestine, including in cells expressing leucine r
182 ease-like pathogenesis in both the small and large intestine, including segmental inflammatory cell i
183 cient mice were prone to develop more severe large intestine inflammation, which was rescued by the t
184 nfection by Salmonella, whereas those of the large intestine inhibit invasion.
185                                          The large intestine is a major site of infection and disease
186                 These data indicate that the large intestine is a major viral reservoir in LTNPs, whi
187                                          The large intestine is capable of absorbing water-soluble vi
188                                  Whether the large intestine is covered by the same lymphatic system
189 gesting that the distinct niche in the mouse large intestine is defined by the presence of gluconate.
190 his study suggests that drug exposure in the large intestine is essential for generating a superior i
191                 Propulsion in both small and large intestine is largely mediated by the peristaltic r
192 ning of the hindgut into small intestine and large intestine is likely required for its correct morph
193 lminating in the expulsion of worms from the large intestine is not known.
194                                    The human large intestine is populated by a high density of microo
195 show that the frequency of Th17 cells in the large intestine is significantly elevated in the absence
196       Leukocyte trafficking to the small and large intestines is tightly controlled to maintain intes
197 crobial fermentation of dietary fiber in the large intestine, is a physiological regulator of major p
198 ne mucin normally expressed in the small and large intestine, is differentially expressed during infl
199  FOXP3(+) regulatory T cells (Tregs), to the large intestine lamina propria (LILP).
200                       Phenotypic analysis of large intestine lamina propria lymphocytes revealed a la
201 efine the major APC subsets in the small and large intestine lamina propria.
202 od, which permits for early detection of the large intestine lesions with specificity and sensitivity
203 refractory to bacterial colonization and the large intestine less susceptible to the onset of colitis
204 T cells in the small intestine (SI), but not large intestine (LI), including an almost complete absen
205 ate<--urinary bladder contents) and S (lower large intestine [LLI] wall<--urinary bladder contents) a
206 f bacterial metabolite concentrations in the large intestine luminal content, notably after changes i
207 vely with the HYDIN, KRAS, and PTEN genes in large intestine, lung, and endometrial cancers respectiv
208 ichuriasis relates to an inflammation of the large intestine manifested in bloody diarrhea, and chron
209                            For EA treatment, large intestine meridian points LI4 and LI11 and stomach
210  Lef1 is expressed in the chick duodenum and large intestine mesoderm.
211 ed whether pathology specifically within the large intestine might influence prion pathogenesis.
212 g new questions on the impact of HPDs on the large intestine mucosa homeostasis.
213 a composition and metabolic activity and for large intestine mucosal homeostasis.
214                             In the small and large intestines, myenteric cell loss occurred by 12 mon
215 , increased uptake of D-FAC in the small and large intestine occurred at an earlier stage of disease
216 colonoscopy in detection of focal lesions in large intestine of 10 mm or more diameter.
217 ut were present in the lung, spleen, BM, and large intestine of beta7 integrin-deficient mice (on the
218  inflammation developed spontaneously in the large intestine of C.B-17 scid mice restored with the CD
219 TCRbeta repertoire of the cells found in the large intestine of diseased mice revealed a population w
220           Finally, the identification in the large intestine of efficient and specialized carrier-med
221  with the one prevalent in isolates from the large intestine of healthy individuals.
222 f chronic inflammatory bowel diseases in the large intestine of human patients.
223 ow that inflammatory Mphis accumulate in the large intestine of mice during the local inflammatory re
224 ng parasitic nematode Trichuris muris in the large intestine of mice is dependent on microflora and c
225  commensal bacterium Escherichia coli in the large intestine of mice.
226 g the K1 polysaccharide capsule colonize the large intestine of newborn infants, and are the leading
227                           The changes in the large intestine of these mice are similar to those seen
228                                          The large intestine of these mice contained an increase in C
229 Gata6 throughout the epithelium of small and large intestines of adult mice.
230               The spirochetes inhabiting the large intestines of humans and animals consist of a dive
231 eling indices of adenomas from the small and large intestines of omeprazole-treated mice were increas
232 amina propria compartments of both small and large intestines of SCID recipients.
233                   MD42 initially grew in the large intestines of streptomycin-treated mice but then f
234 hat V. cholerae colonizes both the small and large intestines of the mouse in a distribution that doe
235        We investigated the importance of the large intestine on the bioavailability of anthocyanins f
236 inal tissue substitutes, such as segments of large intestine or skin, which are not anatomically or f
237  gastrointestinal organs (stomach, small and large intestine) or liver of rats.
238 e oral cavity, esophagus, stomach, small and large intestines, pancreas, and liver.
239                                       In the large intestine, prebiotics, in addition to their select
240                   A dense mucus layer in the large intestine prevents inflammation by shielding the u
241 ant increase in tumors in the small, but not large, intestine relative to their BALB-Min counterparts
242 ectable in the mucosa of the human small and large intestine, respectively.
243      Mucus production by goblet cells of the large intestine serves as a crucial antimicrobial protec
244 w- and high-grade dysplastic adenomas in the large intestine, similar to the precancerous lesions tha
245  estimated organ-absorbed doses to the upper large intestine, small intestine, gallbladder wall, and
246  pancreas, prostate, brain, heart, small and large intestine, stomach, and epididymis.
247                     Therefore, we designed a large intestine-targeted oral delivery with pH-dependent
248 xocrine cells found throughout the small and large intestine that have a characteristic morphology du
249  bacterium in the streptomycin-treated mouse large intestine that respires nitrate.
250 ma membrane of the enterocytes of the normal large intestine, the reaction being most intense in the
251 ut there is little known about homing to the large intestine, the site most commonly affected in infl
252 reatment reduces epithelial apoptosis in the large intestine, thereby protecting the integrity of the
253 e from the vast microbial populations in the large intestine, thereby reducing conflict between host
254 ice had FDC-containing GALT throughout their large intestines, these tissues were not early sites of
255                                              Large intestine tissue showed minimal to mild inflammati
256 ized at high levels (10(8) CFU/g of stool or large intestine tissue) followed by clearance after seve
257 ative contributions of GALT in the small and large intestines to oral prion pathogenesis were unknown
258 bers in the lamina propria of both small and large intestines under both steady-state and inflammator
259                                       In the large intestine, very few adenomas were found in Msh2(-/
260 ses were the kidneys (0.0830 mSv/MBq), upper large intestine wall (0.0267 mSv/MBq), small intestine (
261                             The lungs, upper large intestine wall, small intestine, urinary bladder w
262                                          The large intestine was the most consistently colonized site
263 At necropsy, the small, and occasionally the large, intestine was dilated and gas filled in most mice
264 th the goal of modeling human disease of the large intestine, we sought to develop an effective proto
265 In this patient, the crypts of the small and large intestine were clonal, but at least 76 percent of
266 e parasite loads in the common bile duct and large intestine were not significantly reduced, there we
267 idium infection, these concentrations in the large intestine were the sole predictors of the observed
268 small intestine, gallbladder wall, and lower large intestines were 0.082, 0.043, 0.042, and 0.035 mSv
269                               The cecums and large intestines were studied for numbers of dysplasias/
270 the bone marrow, the small intestine and the large intestine, were free of silver grains (i.e., no DN
271                   The remainder transits the large intestine where it becomes food for the commensal
272 sted flavan-3-ols pass from the small to the large intestine where the action of the microbiota resul
273  and the majority of the flavanols reach the large intestine where they may be metabolized by residen
274 ides fragilis is a commensal organism in the large intestine, where it utilizes both dietary and host
275 ng in epithelial cells of both the small and large intestine whereas no staining was seen with Hyb213
276 ricted to the crypt regions of the small and large intestine, whereas cyclin D1 immunoreactivity was
277  induced moderate inflammation mainly in the large intestine, whereas the Th17 cells induced with opt
278            However, a source for Ang4 in the large intestine, which is devoid of Paneth cells, has no
279 pithelial cells and lengthened crypts in the large intestine, which was associated with increased tra
280  bacterial number was noted in the cecum and large intestine with 10x LD(50) S. enterica serovar Typh
281 are expressed in similar patterns within the large intestine, with greatest staining near the epithel

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