ライフサイエンスコーパス: forestomach

1 53-/- mice (P < 0.004, esophagus; P < 0.001, forestomach).

2 licle, nail, oral mucosa, tongue, esophagus, forestomach).

3 genitor population in both the esophagus and forestomach.

4 mous epithelia of the tongue, esophagus, and forestomach.

5 mors (both papillomas and carcinomas) of the forestomach.

6 MP signaling in the developing esophagus and forestomach.

7 fferentiated epithelium in the esophagus and forestomach.

8 to that occurring in the mouse esophagus and forestomach.

9 ed the restored epithelia of FHIT transduced forestomachs.

10 ne content was reduced in NMBA-treated ZD:AZ forestomachs.

11 and NMBA-treated ZD:AZ than respective ZD:Wt forestomachs.

12 RNA expression in ZD:p53-/- versus ZS:p53-/- forestomach, a result showing gene-modulating effects of

13 In the forestomach, a singular concentration of orthogonally cr

14 ed specifically in the tongue, esophagus and forestomach, all sharing a stratified squamous epitheliu

15 ly 80% of the glandular portion, leaving the forestomach almost intact (glandular gastrectomy [GG]) a

16 isting of long, rectilinear processes in the forestomach, along the greater curvature, and in limited

17 id cells, and the squamous epithelium of the forestomach and epithelium of the glandular stomach.

18 between the keratinized, squamous esophagus/forestomach and glandular hindstomach.

19 In forestomach and glandular stomach, reverse-transcription

20 lts indicate a difference in potency between forestomach and midgut precursor endodermal cells.

21 IMAs were most concentrated in the forestomach and sphincters in mice, as in rats, but the

22 ted tumors (average 3.3 tumors/mouse) of the forestomach and squamocolumnar junction; half of the -/-

23 diet enhances cellular proliferation in the forestomach and susceptibility to N-nitrosomethylbenzyla

24 enhances cellular proliferation in esophagus/forestomach and susceptibility to NMBA-induced carcinoge

25 he boundary between the squamous epithelium (forestomach) and the proximal glandular epithelium.

26 % of mutants had developed papillomas of the forestomach, and 89% of mutants older than 14 months had

27 liver, mammary gland, Zymbal gland, kidney, forestomach, and bladder, as well as intestine and lung,

28 emically induced carcinogenesis in the skin, forestomach, and colon when it is administered during in

29 skin, including the mouth palate, esophagus, forestomach, and exocervix.

30 ressing tissues, including the skin, vagina, forestomach, and odontogenic epithelium.

31 pecific expression in the tongue, esophagus, forestomach, and skin, all sharing stratifying squamous

32 the epithelium of the tongue, esophagus, and forestomach, and the kidney, bladder, and hippocampus).

33 mucosa, salivary glands, tongue, esophagus, forestomach, and uterine cervix within just 10 to 20 day

34 branch carries sensory information from the forestomach, antrum, pylorus, duodenum, and cecum.

35 with keratinocyte hyperactivation in normal forestomachs as early as 2 months of age.

36 27% of Wwox+/- mice had invasive SCC in the forestomach, as compared with 0% of wild-type controls (

37 amous papillomas, invasive carcinomas of the forestomach, as well as tumors of sebaceous glands.

38 umors and by 84 days approximately 10 tumors/forestomach; b) mice receiving FHIT virus at 2 or 42 day

39 and invasive squamous cell carcinoma of the forestomach, both associated with an increased abundance

40 type, consisting of relatively proportionate forestomach but disproportionately reduced glandular sto

41 ZD) mice and reduced their susceptibility to forestomach carcinogenesis by N-nitrosomethylbenzylamine

42 more susceptible to NMBA-induced esophageal/forestomach carcinogenesis.

43 Zinc deficiency increased the forestomach cell proliferation in Wt mice, but this effe

44 Forestomach CEs also use trichohyalin as a novel cross-b

45 he three major gastric regions in the mouse, forestomach, corpus and antrum, we first describe the ex

46 ric juice with the exclusion of the body and forestomach developed adenocarcinoma, showing a progress

47 Ulcers were observed in the esophagus and forestomach during endoscopic examination in two of the

48 recombination results in the development of forestomach epithelium at ectopic sites in pericaecal ar

49 sion targeted to the basal cell layer of the forestomach epithelium by the keratin 5 promoter were us

50 The restored ZD:AZ forestomach epithelium displayed strong expression of Ba

51 We have investigated the epidermis and forestomach epithelium of these mice by electron microsc

52 a more rostral endodermal phenotype, such as forestomach epithelium that does not express Cdx2 during

53 Murine forestomach epithelium undergoes particularly rigorous m

54 of acute ulceration with destruction of the forestomach epithelium was extremely low at 8.7% in the

55 lymphoid cells, haematopoietic cells and the forestomach epithelium.

56 el of periostin-expressing distal esophageal/forestomach ESCC.

57 of the tumor suppressor function of WWOX in forestomach/esophageal carcinogenesis and suggest that i

58 that tea consumption protects against lung, forestomach, esophagus, duodenum, pancreas, liver, breas

59 -)) mice develop squamous cell tumors of the forestomach, esophagus, oral mucosa, tongue, and skin.

60 roliferation was greatest in ZD:TG esophagus/forestomach, followed by ZD:WT, and then ZS:TG>/=ZS:WT.

61 Intriguingly, forestomachs from Wwox+/- mice displayed moderately stro

62 ar features similar to those observed at the forestomach/glandular junction.

63 studied included an alpha class isoenzyme of forestomach (GST 9.5), alpha class hepatic isoenzymes mG

64 In all hypomorphic embryos the forestomach has an abnormal phenotype, with reduced kera

65 tologically with overt hyperkeratosis of the forestomach, hyperkeratosis and acanthosis of the epider

66 o target cat reporter gene expression to the forestomach in transgenic mice.

67 These results indicate that GST 9.5 of forestomach is different among mammalian alpha class GST

68 gastric juice with exclusion of the body and forestomach (n = 51); esophagoduodenostomy plus total ga

69 (GST) isoenzymes purified from the liver and forestomach of female A/J mouse has been investigated.

70 f Lactobacillus reuteri densely colonize the forestomach of mice and possess several genes whose pred

71 n addition, genetically restoring ADA to the forestomach of otherwise ADA-deficient mice prevented ad

72 cellular proliferation in the esophagus and forestomach of p53-/- mice.

73 g cat reporter gene expression mainly to the forestomach of transgenic mice, with a level comparable

74 ene used also directed ADA expression to the forestomach postnatally, producing adult animals that la

75 eport the identification of the first murine forestomach regulatory element using the murine adenosin

76 In contrast, proliferative ZD:Wt forestomach showed strong expression of Bcl-2, an antiap

77 0% of Fhit +/- mice exhibiting tumors of the forestomach/squamocolumnar junction vs. 25% of Fhit +/+

78 sequence of tissue types between the ectopic forestomach tissue and the surrounding colon.

79 ining cell proliferation, thereby inhibiting forestomach tumor development.

80 zinc intake, AZ mice had significantly lower forestomach tumor incidence and tumor multiplicity than

81 ZD substantially increased forestomach tumor incidence in TG mice: 85% of ZD:TG ver

82 Wwox gene might lead to enhanced esophageal/forestomach tumorigenesis induced by N-nitrosomethylbenz

83 e: 85% of ZD:TG versus 14% of ZS:TG mice had forestomach tumors (P < 0.001), with progression to mali

84 sus 29% (10 of 34) of Wwox+/+ mice developed forestomach tumors (P = 1.3 x 10(-7)).

85 100% (21 of 21) of ZD:p53-/- mice developed forestomach tumors and 38% showed esophageal tumors vers

86 or retards development of carcinogen-induced forestomach tumors and reverses development of establish

87 , sulforaphane blocked benzo[a]pyrene-evoked forestomach tumors in ICR mice.

88 cy, with 10% of esophageal tumors and 38% of forestomach tumors presenting as carcinomas.

89 Forestomach tumors were first detected in a ZD:p53-/- mo

90 of N-nitrosomethylbenzylamine-induced murine forestomach tumors.

91 of N-nitrosomethylbenzylamine (NMBA)-induced forestomach tumors.

92 The order of tumor incidence in forestomach was as follows: naught incidence in ZS:p53+/

93 se in the number of myenteric neurons in the forestomach was noted at 27 months.

94 The number of tumors per forestomach was significantly greater in Wwox+/- than in

95 The only fibers on the dorsal forestomach were distal branches and terminals that wrap

96 ignificantly, carcinoma only develops in the forestomach, where pathological progression correlates w

97 wer esophageal sphincter and coursing to the forestomach, where they branched into distinct terminal

98 + mice developed adenoma or papilloma of the forestomach, whereas 100% of the +/- mice developed mult

99 t the development of the mouse esophagus and forestomach, which are composed of a stratified squamous

100 Hepatic afferents supplied the forestomach with both intraganglionic laminar endings (I