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2 r persistent changes in mucosal immunocytes, enterochromaffin and mast cells, enteric nerves, and the
4 e populations, and identify Lmx1a as a novel enterochromaffin cell marker that is also essential for
6 er RNA, encoding the rate-limiting enzyme in enterochromaffin cell serotonin (5-hydroxytryptamine [5H
8 biota promote 5-HT biosynthesis from colonic enterochromaffin cells (ECs), which supply 5-HT to the m
9 onstrated that 5-HT released from intestinal enterochromaffin cells activates 5-HT3 receptors on vaga
10 5-Hydroxytryptamine (5-HT) released from enterochromaffin cells activates secretory and peristalt
11 5-Hydroxytryptamine (5-HT) is released from enterochromaffin cells and activates neural reflex progr
12 e of 5-hydroxytryptamine (5-HT) from mucosal enterochromaffin cells and activation of 5-HT(3) recepto
13 e transcription factor Lmx1a is expressed in enterochromaffin cells and functions downstream of Nkx2.
15 sis, consistent with localization of TGR5 to enterochromaffin cells and intrinsic primary afferent ne
17 vious results showing guanylin expression in enterochromaffin cells appear to be a consequence of ant
20 tion to neurons, a subset of 5-HT-containing enterochromaffin cells expressed 5-HT1A immunoreactivity
22 onsistent with the hypothesis that 5-HT from enterochromaffin cells in response to mucosal stimuli in
27 g kg-1) indicating that endogenous 5-HT from enterochromaffin cells is not essential for transduction
30 , it is unclear whether they act directly on enterochromaffin cells or indirectly through an intermed
31 kx2.2 mutant conditions, serotonin-producing enterochromaffin cells were the most severely reduced en
34 release serotonin (5-hydroxytryptamine) from enterochromaffin cells, and stretch reflexes that determ
35 erotonin (5-HT), which abounds in intestinal enterochromaffin cells, is released in response to vario
36 athematical modeling, we show that, in human enterochromaffin cells, Myrip (1) inhibits a class of SG
38 release of endogenous 5-HT from the mucosal enterochromaffin cells, which acts on the 5-HT3 receptor
43 sults suggest that mechanical stimulation of enterochromaffin-derived BON cells directly or indirectl
47 KEY POINTS: The gastrointestinal epithelial enterochromaffin (EC) cell synthesizes the vast majority
50 In the gastrointestinal (GI) epithelium, enterochromaffin (EC) cells are enteroendocrine cells re
53 , whereas the number of serotonin-expressing enterochromaffin (EC) cells is decreased dramatically.
54 esis that the secretion of 5-HT from mucosal enterochromaffin (EC) cells is essential for the manifes
55 used by the secretion of serotonin (5-HT) by enterochromaffin (EC) cells of the mucosal epithelium.
56 hat 5-hydroxytryptamine (5-HT) released from enterochromaffin (EC) cells plays an important role in t
60 s localized to subpopulations of G cells and enterochromaffin (EC) cells; neither was found in antral
61 reotide was infused for 72 hours to suppress enterochromaffin-like (ECL) cell and gastrin cell functi
65 een three major gastric endocrine cells: the enterochromaffin-like (ECL) cell, the gastrin or G cell,
67 PYY inhibits histamine release from isolated enterochromaffin-like (ECL) cells by stimulation of a se
68 to isolate enriched serotonin-secreting and enterochromaffin-like (ECL) cells from the stomach and t
69 ecretion and in vitro histamine release from enterochromaffin-like (ECL) cells in responses to tumor
70 and II) involve the transformation of naive enterochromaffin-like (ECL) cells to the neoplastic stat
71 ucing parietal cells and histamine-secreting enterochromaffin-like (ECL) cells, and the expression of
72 Gastrin, from G-cells, and histamine, from enterochromaffin-like (ECL) cells, are two of the hormon
76 rboxylase, releasing histamine, and inducing enterochromaffin-like cell hypertrophy and hyperplasia.
77 , parietal and zymogenic, but not for pit or enterochromaffin-like cell lineages in the oxyntic gastr
78 INS-GAS mice showed no evidence of increased enterochromaffin-like cell number, but instead exhibited
80 s, including the role of hypergastrinemia on enterochromaffin-like cell proliferation and its relatio
81 for VMAT2 in the transport of histamine into enterochromaffin-like cell secretory vesicles, and with
82 tic atrophy were sustained while chief cell, enterochromaffin-like cell, and somatostatin cell popula
83 e, with a decrease in number of parietal and enterochromaffin-like cells and an increase in number of
84 hormone-like hormone in histamine-secreting enterochromaffin-like cells and hepcidin in acid-secreti
85 irculating gastrin leads to proliferation of enterochromaffin-like cells and to the development of ga
86 n, acting via cholecystokinin-2 receptors on enterochromaffin-like cells coupled to an increase in in
87 MAT2 alone is expressed in histamine-storing enterochromaffin-like cells of the oxyntic mucosa of the
91 the stomach of mutant animals, parietal and enterochromaffin-like cells were decreased, providing a
93 ance of the gastric mucosa, proliferation of enterochromaffin-like cells, and neoplastic transformati
94 ctivity was localized to the cell surface of enterochromaffin-like cells, and of myenteric and submuc
95 y regulating the secretion of histamine from enterochromaffin-like cells, gastrin from G cells, and s
96 ric neuroendocrine tumours (NETs) arise from enterochromaffin-like cells, which are located in oxynti
100 per was to define physiological responses of enterochromaffin-like, gastrin, and somatostatin cells i
103 l root ganglion neurons from rats and in the enterochromaffin model cell line QGP-1, from which serot
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