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1 53-/- mice (P < 0.004, esophagus; P < 0.001, forestomach).
2 licle, nail, oral mucosa, tongue, esophagus, forestomach).
3 fferentiated epithelium in the esophagus and forestomach.
4 tion of squamous cell carcinoma (SCC) in the forestomach.
5 genitor population in both the esophagus and forestomach.
6 mors (both papillomas and carcinomas) of the forestomach.
7 mous epithelia of the tongue, esophagus, and forestomach.
8 to that occurring in the mouse esophagus and forestomach.
9 MP signaling in the developing esophagus and forestomach.
10 ed the restored epithelia of FHIT transduced forestomachs.
11 ne content was reduced in NMBA-treated ZD:AZ forestomachs.
12 and NMBA-treated ZD:AZ than respective ZD:Wt forestomachs.
13 RNA expression in ZD:p53-/- versus ZS:p53-/- forestomach, a result showing gene-modulating effects of
14                                       In the forestomach, a singular concentration of orthogonally cr
15 ed specifically in the tongue, esophagus and forestomach, all sharing a stratified squamous epitheliu
16 ly 80% of the glandular portion, leaving the forestomach almost intact (glandular gastrectomy [GG]) a
17 isting of long, rectilinear processes in the forestomach, along the greater curvature, and in limited
18 interleukin 1 beta in esophagus and squamous forestomach and are used as a model of BE).
19 id cells, and the squamous epithelium of the forestomach and epithelium of the glandular stomach.
20  between the keratinized, squamous esophagus/forestomach and glandular hindstomach.
21                                           In forestomach and glandular stomach, reverse-transcription
22 lts indicate a difference in potency between forestomach and midgut precursor endodermal cells.
23           IMAs were most concentrated in the forestomach and sphincters in mice, as in rats, but the
24 ted tumors (average 3.3 tumors/mouse) of the forestomach and squamocolumnar junction; half of the -/-
25  diet enhances cellular proliferation in the forestomach and susceptibility to N-nitrosomethylbenzyla
26 enhances cellular proliferation in esophagus/forestomach and susceptibility to NMBA-induced carcinoge
27 he boundary between the squamous epithelium (forestomach) and the proximal glandular epithelium.
28 % of mutants had developed papillomas of the forestomach, and 89% of mutants older than 14 months had
29  liver, mammary gland, Zymbal gland, kidney, forestomach, and bladder, as well as intestine and lung,
30 emically induced carcinogenesis in the skin, forestomach, and colon when it is administered during in
31 skin, including the mouth palate, esophagus, forestomach, and exocervix.
32 ressing tissues, including the skin, vagina, forestomach, and odontogenic epithelium.
33 pecific expression in the tongue, esophagus, forestomach, and skin, all sharing stratifying squamous
34 the epithelium of the tongue, esophagus, and forestomach, and the kidney, bladder, and hippocampus).
35  mucosa, salivary glands, tongue, esophagus, forestomach, and uterine cervix within just 10 to 20 day
36  branch carries sensory information from the forestomach, antrum, pylorus, duodenum, and cecum.
37  with keratinocyte hyperactivation in normal forestomachs as early as 2 months of age.
38  27% of Wwox+/- mice had invasive SCC in the forestomach, as compared with 0% of wild-type controls (
39 amous papillomas, invasive carcinomas of the forestomach, as well as tumors of sebaceous glands.
40  cell carcinomas of the distal esophagus and forestomach at a much higher frequency and speed (~90 to
41 umors and by 84 days approximately 10 tumors/forestomach; b) mice receiving FHIT virus at 2 or 42 day
42  and invasive squamous cell carcinoma of the forestomach, both associated with an increased abundance
43 type, consisting of relatively proportionate forestomach but disproportionately reduced glandular sto
44 ZD) mice and reduced their susceptibility to forestomach carcinogenesis by N-nitrosomethylbenzylamine
45  more susceptible to NMBA-induced esophageal/forestomach carcinogenesis.
46                Zinc deficiency increased the forestomach cell proliferation in Wt mice, but this effe
47                                              Forestomach CEs also use trichohyalin as a novel cross-b
48 he three major gastric regions in the mouse, forestomach, corpus and antrum, we first describe the ex
49 ric juice with the exclusion of the body and forestomach developed adenocarcinoma, showing a progress
50    Ulcers were observed in the esophagus and forestomach during endoscopic examination in two of the
51 on of Jag1/2 in mice disrupts esophageal and forestomach epithelial homeostasis.
52  recombination results in the development of forestomach epithelium at ectopic sites in pericaecal ar
53 sion targeted to the basal cell layer of the forestomach epithelium by the keratin 5 promoter were us
54                           The restored ZD:AZ forestomach epithelium displayed strong expression of Ba
55       We have investigated the epidermis and forestomach epithelium of these mice by electron microsc
56 a more rostral endodermal phenotype, such as forestomach epithelium that does not express Cdx2 during
57                                       Murine forestomach epithelium undergoes particularly rigorous m
58  of acute ulceration with destruction of the forestomach epithelium was extremely low at 8.7% in the
59 lymphoid cells, haematopoietic cells and the forestomach epithelium.
60 el of periostin-expressing distal esophageal/forestomach ESCC.
61  of the tumor suppressor function of WWOX in forestomach/esophageal carcinogenesis and suggest that i
62  that tea consumption protects against lung, forestomach, esophagus, duodenum, pancreas, liver, breas
63 -)) mice develop squamous cell tumors of the forestomach, esophagus, oral mucosa, tongue, and skin.
64 roliferation was greatest in ZD:TG esophagus/forestomach, followed by ZD:WT, and then ZS:TG>/=ZS:WT.
65                                Intriguingly, forestomachs from Wwox+/- mice displayed moderately stro
66 ar features similar to those observed at the forestomach/glandular junction.
67 studied included an alpha class isoenzyme of forestomach (GST 9.5), alpha class hepatic isoenzymes mG
68               In all hypomorphic embryos the forestomach has an abnormal phenotype, with reduced kera
69 are important for maintaining esophageal and forestomach homeostasis and the onset of foregut SCC.
70 l for maintaining foregut (the esophagus and forestomach) homeostasis.
71 tologically with overt hyperkeratosis of the forestomach, hyperkeratosis and acanthosis of the epider
72 o target cat reporter gene expression to the forestomach in transgenic mice.
73       These results indicate that GST 9.5 of forestomach is different among mammalian alpha class GST
74 gastric juice with exclusion of the body and forestomach (n = 51); esophagoduodenostomy plus total ga
75 (GST) isoenzymes purified from the liver and forestomach of female A/J mouse has been investigated.
76 f Lactobacillus reuteri densely colonize the forestomach of mice and possess several genes whose pred
77 n addition, genetically restoring ADA to the forestomach of otherwise ADA-deficient mice prevented ad
78  cellular proliferation in the esophagus and forestomach of p53-/- mice.
79 g cat reporter gene expression mainly to the forestomach of transgenic mice, with a level comparable
80 ene used also directed ADA expression to the forestomach postnatally, producing adult animals that la
81 eport the identification of the first murine forestomach regulatory element using the murine adenosin
82             In contrast, proliferative ZD:Wt forestomach showed strong expression of Bcl-2, an antiap
83 0% of Fhit +/- mice exhibiting tumors of the forestomach/squamocolumnar junction vs. 25% of Fhit +/+
84 ctopically expressed in the developing mouse forestomach, the tissue emerges as columnar-like rather
85 sequence of tissue types between the ectopic forestomach tissue and the surrounding colon.
86                                   Cardia and forestomach tissues from mice were cultured as organoids
87 ining cell proliferation, thereby inhibiting forestomach tumor development.
88 zinc intake, AZ mice had significantly lower forestomach tumor incidence and tumor multiplicity than
89                   ZD substantially increased forestomach tumor incidence in TG mice: 85% of ZD:TG ver
90  Wwox gene might lead to enhanced esophageal/forestomach tumorigenesis induced by N-nitrosomethylbenz
91 e: 85% of ZD:TG versus 14% of ZS:TG mice had forestomach tumors (P < 0.001), with progression to mali
92 sus 29% (10 of 34) of Wwox+/+ mice developed forestomach tumors (P = 1.3 x 10(-7)).
93  100% (21 of 21) of ZD:p53-/- mice developed forestomach tumors and 38% showed esophageal tumors vers
94 or retards development of carcinogen-induced forestomach tumors and reverses development of establish
95 , sulforaphane blocked benzo[a]pyrene-evoked forestomach tumors in ICR mice.
96 cy, with 10% of esophageal tumors and 38% of forestomach tumors presenting as carcinomas.
97                                              Forestomach tumors were first detected in a ZD:p53-/- mo
98 of N-nitrosomethylbenzylamine-induced murine forestomach tumors.
99 of N-nitrosomethylbenzylamine (NMBA)-induced forestomach tumors.
100              The order of tumor incidence in forestomach was as follows: naught incidence in ZS:p53+/
101 se in the number of myenteric neurons in the forestomach was noted at 27 months.
102                     The number of tumors per forestomach was significantly greater in Wwox+/- than in
103                The only fibers on the dorsal forestomach were distal branches and terminals that wrap
104 ignificantly, carcinoma only develops in the forestomach, where pathological progression correlates w
105 wer esophageal sphincter and coursing to the forestomach, where they branched into distinct terminal
106 + mice developed adenoma or papilloma of the forestomach, whereas 100% of the +/- mice developed mult
107 t the development of the mouse esophagus and forestomach, which are composed of a stratified squamous
108               Hepatic afferents supplied the forestomach with both intraganglionic laminar endings (I

 
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