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1 , crypt perimeter, and relative densities of enterochromaffin and enteroendocrine cells in small inte
3 r persistent changes in mucosal immunocytes, enterochromaffin and mast cells, enteric nerves, and the
5 cts as an in vivo sensor for shear forces in enterochromaffin and Paneth cells of the small intestine
6 of serotonin signaling in a newly developed enterochromaffin cell (ECC)-enriched gut organoid model.
7 e populations, and identify Lmx1a as a novel enterochromaffin cell marker that is also essential for
8 human carcinoid BON cells, an in vitro human enterochromaffin cell model, to understand the mechanism
10 er RNA, encoding the rate-limiting enzyme in enterochromaffin cell serotonin (5-hydroxytryptamine [5H
14 biota promote 5-HT biosynthesis from colonic enterochromaffin cells (ECs), which supply 5-HT to the m
15 onstrated that 5-HT released from intestinal enterochromaffin cells activates 5-HT3 receptors on vaga
16 5-Hydroxytryptamine (5-HT) released from enterochromaffin cells activates secretory and peristalt
17 5-Hydroxytryptamine (5-HT) is released from enterochromaffin cells and activates neural reflex progr
18 e of 5-hydroxytryptamine (5-HT) from mucosal enterochromaffin cells and activation of 5-HT(3) recepto
19 e transcription factor Lmx1a is expressed in enterochromaffin cells and functions downstream of Nkx2.
21 sis, consistent with localization of TGR5 to enterochromaffin cells and intrinsic primary afferent ne
23 vious results showing guanylin expression in enterochromaffin cells appear to be a consequence of ant
27 tion to neurons, a subset of 5-HT-containing enterochromaffin cells expressed 5-HT1A immunoreactivity
29 iven by ammoniagenesis in the gut, sensed by enterochromaffin cells in a TRPA1-dependent fashion and
30 onsistent with the hypothesis that 5-HT from enterochromaffin cells in response to mucosal stimuli in
35 g kg-1) indicating that endogenous 5-HT from enterochromaffin cells is not essential for transduction
37 the central nervous system (CNS) as well as enterochromaffin cells of the gastrointestinal tract.
39 Factors that control secretion of 5-HT from enterochromaffin cells or BON cells are important as par
40 , it is unclear whether they act directly on enterochromaffin cells or indirectly through an intermed
41 phils, platelets, histaminergic neurons, and enterochromaffin cells produce varying amounts of histam
42 Most RET(+) epithelial cells were either enterochromaffin cells that release serotonin or L-cells
43 mulated serotonin biosynthesis in intestinal enterochromaffin cells via a mechanism involving activat
44 kx2.2 mutant conditions, serotonin-producing enterochromaffin cells were the most severely reduced en
45 of the cells expressed SOX9 (duct), SLC18A1 (enterochromaffin cells), and CDX2 (gut cells), respectiv
48 release serotonin (5-hydroxytryptamine) from enterochromaffin cells, and stretch reflexes that determ
49 ceptor OR51E1 was notably expressed in ileal enterochromaffin cells, and the glucose-sensing sodium g
50 le cells in the gut, including immune cells, enterochromaffin cells, gut microbiota and the derived l
51 erotonin (5-HT), which abounds in intestinal enterochromaffin cells, is released in response to vario
52 athematical modeling, we show that, in human enterochromaffin cells, Myrip (1) inhibits a class of SG
53 eptor FFAR2 was highest in ileal L-cells and enterochromaffin cells, olfactory receptor OR51E1 was no
55 release of endogenous 5-HT from the mucosal enterochromaffin cells, which acts on the 5-HT3 receptor
64 sults suggest that mechanical stimulation of enterochromaffin-derived BON cells directly or indirectl
65 ntiation toward secretory lineages including enterochromaffin (EC) and Paneth cells, leading to EC hy
66 (TET2) protected against colitis by limiting enterochromaffin (EC) cell differentiation and subsequen
70 KEY POINTS: The gastrointestinal epithelial enterochromaffin (EC) cell synthesizes the vast majority
74 In the gastrointestinal (GI) epithelium, enterochromaffin (EC) cells are enteroendocrine cells re
80 , whereas the number of serotonin-expressing enterochromaffin (EC) cells is decreased dramatically.
81 esis that the secretion of 5-HT from mucosal enterochromaffin (EC) cells is essential for the manifes
83 used by the secretion of serotonin (5-HT) by enterochromaffin (EC) cells of the mucosal epithelium.
84 ory system of the gut, in which serotonergic enterochromaffin (EC) cells play an important part(1,2).
85 hat 5-hydroxytryptamine (5-HT) released from enterochromaffin (EC) cells plays an important role in t
87 Serotonin (5-HT), produced predominantly by enterochromaffin (EC) cells via tryptophan hydroxylase 1
88 invariant natural killer T (iNKT) cells with enterochromaffin (EC) cells, a subset of intestinal epit
94 s localized to subpopulations of G cells and enterochromaffin (EC) cells; neither was found in antral
95 eroendocrine cells (EECs) secrete serotonin (enterochromaffin [EC] cells) or specific peptide hormone
96 reotide was infused for 72 hours to suppress enterochromaffin-like (ECL) cell and gastrin cell functi
100 een three major gastric endocrine cells: the enterochromaffin-like (ECL) cell, the gastrin or G cell,
102 d stimulates the secretion of histamine from enterochromaffin-like (ECL) cells and subsequently acid
103 PYY inhibits histamine release from isolated enterochromaffin-like (ECL) cells by stimulation of a se
104 to isolate enriched serotonin-secreting and enterochromaffin-like (ECL) cells from the stomach and t
105 ecretion and in vitro histamine release from enterochromaffin-like (ECL) cells in responses to tumor
106 and II) involve the transformation of naive enterochromaffin-like (ECL) cells to the neoplastic stat
108 ucing parietal cells and histamine-secreting enterochromaffin-like (ECL) cells, and the expression of
109 Gastrin, from G-cells, and histamine, from enterochromaffin-like (ECL) cells, are two of the hormon
113 rboxylase, releasing histamine, and inducing enterochromaffin-like cell hypertrophy and hyperplasia.
114 , parietal and zymogenic, but not for pit or enterochromaffin-like cell lineages in the oxyntic gastr
115 INS-GAS mice showed no evidence of increased enterochromaffin-like cell number, but instead exhibited
117 s, including the role of hypergastrinemia on enterochromaffin-like cell proliferation and its relatio
118 for VMAT2 in the transport of histamine into enterochromaffin-like cell secretory vesicles, and with
119 tic atrophy were sustained while chief cell, enterochromaffin-like cell, and somatostatin cell popula
121 e, with a decrease in number of parietal and enterochromaffin-like cells and an increase in number of
122 hormone-like hormone in histamine-secreting enterochromaffin-like cells and hepcidin in acid-secreti
123 irculating gastrin leads to proliferation of enterochromaffin-like cells and to the development of ga
124 n, acting via cholecystokinin-2 receptors on enterochromaffin-like cells coupled to an increase in in
125 t the difference between beta cells and awry enterochromaffin-like cells is a gradient of cell states
126 MAT2 alone is expressed in histamine-storing enterochromaffin-like cells of the oxyntic mucosa of the
130 the stomach of mutant animals, parietal and enterochromaffin-like cells were decreased, providing a
132 ance of the gastric mucosa, proliferation of enterochromaffin-like cells, and neoplastic transformati
133 ctivity was localized to the cell surface of enterochromaffin-like cells, and of myenteric and submuc
134 y regulating the secretion of histamine from enterochromaffin-like cells, gastrin from G cells, and s
135 ric neuroendocrine tumours (NETs) arise from enterochromaffin-like cells, which are located in oxynti
140 per was to define physiological responses of enterochromaffin-like, gastrin, and somatostatin cells i
143 l root ganglion neurons from rats and in the enterochromaffin model cell line QGP-1, from which serot