ライフサイエンスコーパス: oxyntic

1 n esophageal squamous epithelium and gastric oxyntic (acid secreting) mucosa.

2 alpha) levels in the gastric fundus leads to oxyntic atrophy and massive foveolar hyperplasia in both

3 The emergence of oxyntic atrophy and metaplastic cell lineages in respons

4 Oxyntic atrophy is the hallmark of chronic gastritis.

5 SPEM and oxyntic atrophy occurred independently of lymphocytes.

6 We evaluated the gastric mucosal response to oxyntic atrophy using cell lineage-specific markers.

7 ng over 3-6 months, foveolar hyperplasia and oxyntic atrophy were sustained while chief cell, enteroc

8 s of parietal cells from the gastric mucosa (oxyntic atrophy) is a critical step in the pathogenesis

9 d onset of spontaneous gastric inflammation, oxyntic atrophy, and spasmolytic polypeptide-expressing

10 ies have sought to develop animal models for oxyntic atrophy, but none of them are reversible.

11 and characterized by progressive gastritis, oxyntic atrophy, hyperplasia, intestinal metaplasia, and

12 d progressive gastritis, epithelial defects, oxyntic atrophy, marked foveolar hyperplasia, dysplasia,

13 sion of Dcamkl1(+) cells, and progression to oxyntic atrophy, metaplasia, hyperplasia, and high-grade

14 ers, including chronic gastritis followed by oxyntic atrophy, mucous neck cell hyperplasia, spasmolyt

15 iregulin (AR) promotes SPEM induced by acute oxyntic atrophy.

16 gence of metaplasia after induction of acute oxyntic atrophy.

17 ication in the induction of SPEM after acute oxyntic atrophy.

18 d the rapid emergence of SPEM in response to oxyntic atrophy.

19 ligands regulate the metaplastic response to oxyntic atrophy.

20 creased parietal cell mucous metaplasia with oxyntic atrophy.

21 high doses of DMP 777 demonstrate reversible oxyntic atrophy.

22 lated acid and pepsin outputs were measured, oxyntic biopsy samples were obtained.

23 here is no evidence of a premeal decrease in oxyntic cell ghrelin.

24 Oxyntic cells coexpress ghrelin and the circadian clock

25 GERD as follows: the presence of any squamo-oxyntic gap defines GERD; the length of the gap is a mea

26 severity of GERD, indicating that the squamo-oxyntic gap is a marker for chronic GERD.

27 The squamo-oxyntic gap is zero or very small in autopsies performed

28 tion of a new histologic concept: the squamo-oxyntic gap.

29 Prior to cancer development, the oxyntic gastric glands atrophy and are replaced by metap

30 r enterochromaffin-like cell lineages in the oxyntic gastric mucosa.

31 We conclude that oxyntic gland cells of the stomach contain FEOs, which p

32 anges in pH and levels of histamine over the oxyntic glands of guinea pig stomach have been investiga

33 ochromaffin-like cells, which are located in oxyntic glands within the stomach.

34 distributed along much of the length of the oxyntic glands, with highest density in the neck and bas

35 rs rather then the ECL cell receptors of the oxyntic glands.

36 r migration and differentiation into pit and oxyntic lineages.

37 Gastrin is trophic for the normal gastric oxyntic mucosa and exerts a growth-promoting action on g

38 physiological differences between antral and oxyntic mucosa contribute to spatial partitioning of H.

39 cell-rich basal mucosa of the antrum and the oxyntic mucosa of the corpus.

40 enotype, but the cellular composition of the oxyntic mucosa of the gastric corpus is altered, with pa

41 e-storing enterochromaffin-like cells of the oxyntic mucosa of the stomach.

42 m amidated gastrin, marked thickening of the oxyntic mucosa, and an increased BrdU labeling index (LI

43 cted to the chief cell compartment in normal oxyntic mucosa, rare in established metaplastic lesions,

44 ute to specific adaptation to the antral and oxyntic mucosa.

45 f both acid secretion and differentiation of oxyntic mucosal cells of the stomach.