ライフサイエンスコーパス: atrophic gastritis

1 entations (peptic ulcer, gastric cancer, and atrophic gastritis).

2 redominantly in tissues showing gastritis or atrophic gastritis.

3 strains isolated from patients with chronic atrophic gastritis.

4 sually occurs in stomachs containing chronic atrophic gastritis.

5 important role in the development of chronic atrophic gastritis.

6 s associated with the development of chronic atrophic gastritis.

7 re not significantly associated with chronic atrophic gastritis.

8 te to tumorigenesis in patients with chronic atrophic gastritis.

9 amin B12 remains intact in older people with atrophic gastritis.

10 of hypergastrinemia associated with chronic atrophic gastritis.

11 secretors of acid, most had serum markers of atrophic gastritis.

12 otential concern in patients with autoimmune atrophic gastritis.

13 circumvent the pH alteration resulting from atrophic gastritis.

14 c superficial gastritis that may progress to atrophic gastritis, a premalignant process.

15 otic transgenic mouse model of human chronic atrophic gastritis, a preneoplastic condition.

16 as an efficient model for the development of atrophic gastritis after infection and to determine the

17 Gastric premalignant conditions, atrophic gastritis (AG) and intestinal metaplasia (IM) a

18 biopsy specimens from 74 patients, including atrophic gastritis (AG) cases without aspirin use (contr

19 ly related to a higher prevalence of chronic atrophic gastritis and a lower prevalence of smoking.

20 e associated with hypergastrinaemia, chronic atrophic gastritis and achlorhydria.

21 NS-GAS and B6 wild-type mice had both severe atrophic gastritis and corpus dysplasia, while GAS-KO mi

22 d characteristictly found in assciation with atrophic gastritis and gastric cancer consistent with Bh

23 The high incidence of atrophic gastritis and gastric cancer suggest the phylog

24 ze the human stomach and have been linked to atrophic gastritis and gastric carcinoma.

25 ting gastrin levels, and develop spontaneous atrophic gastritis and gastrointestinal intraepithelial

26 The presence of chronic atrophic gastritis and Helicobacter pylori infection was

27 min malabsorption, which usually arises from atrophic gastritis and hypochlorhydria but other mechani

28 Decreased Bcl-2 gene expression signified atrophic gastritis and IM in presence of cancer, as well

29 hanges in the gastric mucosa, beginning with atrophic gastritis and leading in some patients to pepti

30 the investigation of a patient with chronic atrophic gastritis and multiple large gastric carcinoid

31 To examine the association between chronic atrophic gastritis and other gastric cancer risk factors

32 how helminth coinfection may protect against atrophic gastritis and T helper type 1 responses.

33 We evaluated 19 superficial gastritis, 18 atrophic gastritis, and 18 intestinal metaplasia from ca

34 range of pathology, including peptic ulcer, atrophic gastritis, and gastric cancer.

35 tis, has been associated with a high risk of atrophic gastritis, and is considered a gastric tumor pr

36 Individuals with chronic atrophic gastritis are considered to be at increased ris

37 adenocarcinoma rests on the assumption that atrophic gastritis can be correctly identified and repro

38 on host biology-the transition from chronic atrophic gastritis (ChAG) to gastric adenocarcinoma-and

39 er, a subset of individuals develops chronic atrophic gastritis (ChAG), a condition characterized in

40 Chronic atrophic gastritis (ChAG), a Helicobacter pylori-associa

41 hat develop an antecedent condition, chronic atrophic gastritis (ChAG).

42 ; 2) gastric IM adjacent to a GU but with no atrophic gastritis changes; 3) patients receiving H. pyl

43 sia (SPEM) develops in patients with chronic atrophic gastritis due to infection with Helicobacter py

44 rent study tests the hypothesis that chronic atrophic gastritis from hypochlorhydria in the gastrin-d

45 ed with reduced pepsin output independent of atrophic gastritis, H. pylori infection, and smoking.

46 The atrophic gastritis in the infected wild-type mice, parti

47 n the elderly, owing to a high prevalence of atrophic gastritis in this age group.

48 included, of which 37 were cases of chronic atrophic gastritis, intestinal metaplasia, or dysplasia.

49 ive once preneoplastic lesions of multifocal atrophic gastritis (MAG) and intestinal metaplasia (IM)

50 postulated to initiate a progression through atrophic gastritis, metaplasia and dysplasia to cancer,

51 ces gastric cancer risk in patients with non-atrophic gastritis (NAG), and is ineffective once preneo

52 alt diet groups developed moderate to marked atrophic gastritis of the corpus in response to H. pylor

53 psinogen ratios of less than 2.9, indicating atrophic gastritis, only 2 (5%) of 44 consistent or inte

54 gastric cancer (GC) and adjacent mucosa with atrophic gastritis or intestinal metaplasia (AG/IM GC+),

55 stinal metaplasia (AG/IM GC+), as well as in atrophic gastritis or intestinal metaplasia mucosa of pa

56 gnificantly increases the risk of developing atrophic gastritis, peptic ulcer disease, and gastric ad

57 topic, and the terms "gastric atrophy" and "atrophic gastritis" remain imprecisely defined and, ther

58 Atrophic gastritis results in a low acid-pepsin secretio

59 Furthermore, hypochlorhydria in atrophic gastritis results in bacterial overgrowth of th

60 Atrophic gastritis was defined as a ratio of serum pepsi

61 ssion, the significant predictors of chronic atrophic gastritis were age over 50 years, H. pylori inf

62 resulted in chronic diffuse lymphofollicular atrophic gastritis with areas of mucosal dysplasia in th