ライフサイエンスコーパス: gastric gland

1 ulovesicles and luminal (TV/L) spaces of the gastric gland.

2 arietal cell, the acid secretory cell of the gastric gland.

3 usion, VacA was detected in association with gastric glands.

4 spo3 in the stroma clears H. pylori from the gastric glands.

5 gr5-positive stem cell population in pyloric gastric glands.

6 microenvironment, or microniche, deep in the gastric glands.

7 h MUC6 secreted in concert with TFF2 by deep gastric glands.

8 clusters of Dcamkl1(+) cells at the base of gastric glands.

9 n and acid trapping, as measured in isolated gastric glands.

10 iple gastric cell lineages that populate the gastric glands.

11 id secretion in streptolysin-O-permeabilized gastric glands.

12 ad significantly reduced numbers of infected gastric glands.

13 gestive enzyme pepsinogen into the lumina of gastric glands.

14 hanisms involved in the injury and repair of gastric glands; (2) to present a hypothesis on the devel

15 2(+)Lgr5(-) stem cells in the isthmus of the gastric gland and finally gastric gland hyperplasia.

16 y were studied using freshly isolated rabbit gastric glands and cultured parietal cells.

17 at cell-associated H pylori can colonize the gastric glands and directly affect precursor and stem ce

18 In the stomach, inflammation damages the gastric glands and drives the development of potentially

19 stem cells are located in the isthmus of the gastric glands and give rise to epithelial progenitors t

20 rved consistently in epithelial cells of the gastric glands and in gastric surface cells.

21 ers initially establish colonies deep in the gastric glands and then expand to colonize adjacent glan

22 ype and DeltaF508-deficient mice in isolated gastric glands and whole stomach preparations.

23 e ablation of parietal cells, dissolution of gastric glands, and loss of chief and mucus-producing ce

24 Organoids formed primitive gastric gland- and pit-like domains, proliferative zones

25 nd stem cell origin of normal and neoplastic gastric glands are uncertain.

26 We find that gastric glands are units of monoclonal cell populations

27 Prior to cancer development, the oxyntic gastric glands atrophy and are replaced by metaplastic c

28 ymogenic) chief cells (ZCs) in the mammalian gastric gland base are believed to arise from descending

29 ](i) in ECL and parietal cells of superfused gastric glands, but only the parietal cell signal was in

30 Activation of SCAR in the intact rat gastric gland by divalent cations (Ca(2+) or Mg(2+)) or

31 ue-induced acid secretion in wild-type mouse gastric glands could be significantly reduced with eithe

32 the nucleus in vitro and in a novel ex vivo gastric gland culture system.

33 Furthermore, we show that gastric gland development occurs close to hatching, acco

34 values; and (d) no channels carrying primary gastric gland fluid through the mucus were observed.

35 Gastric glands from animals expressing mutant beta subun

36 KCNQ1 exhibited abnormal distribution in gastric glands from kcne2 (-/-) mice, with increased exp

37 rexpression of several STAT3 target genes in gastric glands from the TFF1-KO mice.

38 Organ cultures of gastric glands from wild-type or IL-1R1 null mice were t

39 Yet another group (e.g. gastric glands), have stem cells with well characterized

40 lls exposed to hostile environments, such as gastric glands, have no demonstrable permeability to the

41 results demonstrate that microniches in the gastric glands house a persistent H. pylori reservoir, w

42 the isthmus of the gastric gland and finally gastric gland hyperplasia.

43 arp contrast, they infiltrated deep into the gastric glands in Gal3-deficient mice.

44 ing were, however, unaffected in Trpml1(-/-) gastric glands, indicating that Trpml1 does not function

45 Methods: Isolated rabbit gastric glands (intact or permeabilized with S. aureus a

46 In parietal cells in isolated gastric glands, intracellular levels of Ca2+ responded t

47 Although physiologically low MYC levels in gastric glands limit beta-catenin transcriptional activi

48 y marginal reactions to bacterial infection, gastric gland lineages mounted a strong inflammatory res

49 or the generation of concentrated HCl in the gastric gland lumen.

50 ithelium, including moderate dilation of the gastric gland lumens and a reduction in the number of pa

51 t acidity within the TV/L compartment of the gastric gland may be regulated, at least in part, by its

52 the stomach epithelium before completion of gastric gland morphogenesis.

53 calpha1-->4Gal from glycans expressed in the gastric gland mucous cell-type mucin.

54 Klotho expression was detected in gastric glands, myenteric neurons and smooth muscle cell

55 pylori had successfully colonized within the gastric glands of both WT and Gal3-deficient mice, altho

56 specifically express either lineages of the gastric gland, or the gastric pit, by addition of nicoti

57 We utilized in vitro assays, 3D gastric gland organoid cultures, mouse models, and human

58 protein in human gastric cancer cells and 3D gastric glands organoids from TFF1-KO mice abrogates IL6

59 g immunohistochemistry, both mouse and human gastric glands overexpressed Cldn7 in dysplastic but not

60 55(+) cells strategically positioned beneath gastric glands promote epithelial expansion in the absen

61 Both components of the gastric gland secretome associate non-covalently and sho

62 These data provide evidence that gastric gland specification and progenitor cell maintena

63 lture surface cells and surgically dissected gastric glands, staining was observed consistently in ep

64 After 1 year, gastric glands that contained green fluorescent protein-

65 y and 3-dimensional reconstruction of entire gastric glands to determine the localizations of H pylor

66 Light microscopy indicated that gastric glands were dilated, and electron micrographs di

67 +)](i) and histamine release; its effects on gastric glands were examined by confocal microscopy of [

68 is limited to the base and lower isthmus of gastric glands, where the stem cells reside.

69 ibroblasts leads to hypercolonization of the gastric glands with H. pylori, including the stem cell c

70 Studies of the clonal architecture of gastric glands with intestinal metaplasia are important

71 Double labeling of gastric glands with rab3D and pepsinogen antibodies conf

72 Gastric glands with such lineage confusion (mixed incomp

73 Atrophic gastritis is defined as the loss of gastric glands, with or without metaplasia, in the setti