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2 alpha) levels in the gastric fundus leads to oxyntic atrophy and massive foveolar hyperplasia in both
6 ng over 3-6 months, foveolar hyperplasia and oxyntic atrophy were sustained while chief cell, enteroc
7 s of parietal cells from the gastric mucosa (oxyntic atrophy) is a critical step in the pathogenesis
9 and characterized by progressive gastritis, oxyntic atrophy, hyperplasia, intestinal metaplasia, and
10 d progressive gastritis, epithelial defects, oxyntic atrophy, marked foveolar hyperplasia, dysplasia,
11 sion of Dcamkl1(+) cells, and progression to oxyntic atrophy, metaplasia, hyperplasia, and high-grade
12 ers, including chronic gastritis followed by oxyntic atrophy, mucous neck cell hyperplasia, spasmolyt
23 GERD as follows: the presence of any squamo-oxyntic gap defines GERD; the length of the gap is a mea
30 anges in pH and levels of histamine over the oxyntic glands of guinea pig stomach have been investiga
32 distributed along much of the length of the oxyntic glands, with highest density in the neck and bas
35 Gastrin is trophic for the normal gastric oxyntic mucosa and exerts a growth-promoting action on g
37 enotype, but the cellular composition of the oxyntic mucosa of the gastric corpus is altered, with pa
39 m amidated gastrin, marked thickening of the oxyntic mucosa, and an increased BrdU labeling index (LI
40 cted to the chief cell compartment in normal oxyntic mucosa, rare in established metaplastic lesions,
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