ライフサイエンスコーパス: gastric ulcer

1 uodenal ulcers; 4% vs. 59% for patients with gastric ulcers).

2 aken to establish a rat model of ICH-induced gastric ulcer.

3 rtery pseudoaneurysm caused by a penetrating gastric ulcer.

4 drinking, history of general anesthesia, or gastric ulcers.

5 with Helicobacter pylori are major causes of gastric ulcers.

6 al pain, two of whom had microsphere-induced gastric ulcers.

7 examined their modulation after induction of gastric ulcers.

8 Helicobacter pylori, the causative agent of gastric ulcers.

9 tric ulcers was similar to that found in rat gastric ulcers.

10 n of solid tumors, rheumatoid arthritis, and gastric ulcers.

11 e is involved in the healing of experimental gastric ulcers.

12 ylori infection in patients with duodenal or gastric ulcers.

13 Three subjects developed gastric ulcers, 1 while taking 10 mg/day of aspirin.

14 552 in 1993 vs. 60,029 in 2006, -37.2%) than gastric ulcers (106,987 in 1993 vs. 86,064 in 2006, -19.

15 ears (range 17-73), 95 had gastritis, 92 had gastric ulcers, 108 had duodenal ulcers, and 65 had gast

16 inal lesions were esophagitis (23 patients), gastric ulcer (14), gastritis (12), and duodenal ulcer (

17 g 50 patients with simple gastritis, 40 with gastric ulcer, 35 with duodenal ulcer, and 30 with gastr

18 A total of 150 men with gastric ulcer, 65 with duodenal ulcer, and 14 with both

19 This study compared the incidence of gastric ulcers after treatment with risedronate, a pyrid

20 Gastric ulcers altered the properties of acid-elicited c

21 (95% confidence interval (CI): 1.9, 8.5) for gastric ulcer and 2.5 (95% CI: 0.8, 7.4) for duodenal ul

22 odds ratios were 1.4 (95% CI: 0.9, 2.4) for gastric ulcer and 2.6 (95% CI: 1.1, 5.8) for duodenal ul

23 an odds ratio of 4.4 (95% CI: 1.8, 10.5) for gastric ulcer and 5.8 (95% CI: 1.1, 30.0) for duodenal u

24 ce of chronic hyperacidity, the mice develop gastric ulcers and a hypertrophic gastropathy resembling

25 gastric mucosa, is strongly associated with gastric ulcers and adenocarcinoma.

26 with Helicobacter pylori, causing gastritis, gastric ulcers and an increased incidence of gastric ade

27 ism that is implicated in the development of gastric ulcers and cancer.

28 ld's most successful human pathogens causing gastric ulcers and cancers.

29 blesome dyspepsia led to impaired healing of gastric ulcers and did not affect the rate of peptic ulc

30 tion is a risk factor for developing chronic gastric ulcers and gastric cancer.

31 the role of H. cetorum in the development of gastric ulcers and gastritis of cetaceans.

32 ly linked to the development of duodenal and gastric ulcers and stomach cancer.

33 fense mechanisms, leading to duodenal ulcer, gastric ulcer, and gastroesophageal reflux disease.

34 d a higher gastric pH, a higher incidence of gastric ulcers, and a higher incidence of fecal occult b

35 se gastritis using iodoacetamide or creating gastric ulcers by injecting 60% acetic acid for 45 secon

36 ignificantly increased 10-19 years after the gastric ulcer diagnosis (RR, 2.89; 95% CI, 1.26-6.64).

37 ri infection is associated with duodenal and gastric ulcer disease, gastric cancer, and gastric mucos

38 of jhp0945 was significantly associated with gastric ulcer, duodenal ulcer, and gastric cancer (odds

39 luded esophageal inflammation and stricture, gastric ulcer, duodenal ulcer, suspected Barrett's esoph

40 tivities in the ulcer margin of experimental gastric ulcer during healing.

41 Gastritis and gastric ulcers enhanced the visceromotor responses to in

42 es gastritis and is strongly associated with gastric ulcers, gastric adenocarcinomas, and mucosa-asso

43 In patients with gastric ulcer (GU) and IM, the GU may have a different h

44 itis, 140 with duodenal ulcer (DU), 110 with gastric ulcer (GU), and 130 with gastric cancer.

45 report of no peptic ulcer disease, men with gastric ulcer had an increased risk of pancreatic cancer

46 amotidine with patients assigned to placebo, gastric ulcers had developed in seven (3.4%) of 204 pati

47 Fewer baseline gastric ulcers healed among eradication-treatment patien

48 h SRF significantly accelerated experimental gastric ulcer healing and promoted re-epithelialization

49 n this study, we examined the role of SRF in gastric ulcer healing and the mechanisms involved.

50 of IGF-1 in gastric ulcer margin accelerates gastric ulcer healing by promoting cell re-epithelizatio

51 These findings indicate that experimental gastric ulcer healing involves activation of EGF-R-ERK s

52 ndings indicate that Raf-1 activation during gastric ulcer healing is Ras mediated, involves Shc-Grb2

53 ole of insulin-like growth factor (IGF)-1 in gastric ulcer healing is unknown.

54 nd cyclooxygenase-2 (COX-2) selective, delay gastric ulcer healing.

55 t gene expression, significantly accelerates gastric ulcer healing.

56 teins Shc, Grb2, and Sos during experimental gastric ulcer healing.

57 d in 50.0% (40 vs 27 in the CG, P = .04) and gastric ulcers in 10.0% (8 vs 3 in the CG, P = .13); 20.

58 on, two clinicohistologic patterns appeared: gastric ulcers in 32% and hyperplastic polyps in 68% of

59 ion of SRF antisense expression plasmid into gastric ulcers in rats significantly inhibited in vivo a

60 Gastric ulcer increases the risk of pancreatic cancer, w

61 s from S. paniculatum were evaluated against gastric ulcer induced by ethanol in rats.

62 The up-regulation of IGF-1 in gastric ulcer margin accelerates gastric ulcer healing b

63 nal pain and salivary VZV DNA had perforated gastric ulcers, necessitating a wedge gastrectomy.

64 ere significantly associated with absence of gastric ulcer or duodenal ulcer (0.21 [0.05 to 0.94] and

65 ut the higher proportion of TPM-A strains in gastric ulcer patients merits further investigation.

66 The time trends of gastric ulcer preceded those of duodenal ulcer by 10-30

67 pylori as a causative agent in duodenal and gastric ulcer, respectively, vs. 68% and 68% of family p

68 Diagnosis of gastric ulcer rose by 22 %, and that of duodenal ulcer f

69 ing diets with a high salt content developed gastric ulcers significantly more frequently than gerbil

70 levance, we examined SRF expression in human gastric ulcer specimens.

71 Gastric ulcer strain B128 induced more severe gastritis,

72 Fourteen duodenal ulcer and five gastric ulcer studies satisfied requisite inclusion crit

73 t significantly [P = 0.071]) associated with gastric ulcer than with duodenal ulcer (86 versus 56%).

74 ated with a significantly lower incidence of gastric ulcers than alendronate.

75 sk was highest for those with a diagnosis of gastric ulcer that was close in time to the cancer diagn

76 duodenal ulcer, the corresponding value for gastric ulcer was 8.7 percent.

77 SRF up-regulation in human gastric ulcers was similar to that found in rat gastric

78 ive agent of gastric cancer and duodenal and gastric ulcers, was early associated with gastric diseas

79 In experimental rat gastric ulcers, we examined expression of IGF-1 mRNA and

80 After 1-2 weeks, gastric ulcers were induced by 45 s of luminal exposure

81 Gastric ulcers were induced in rats by acetic acid appli

82 Gastric ulcers were induced in rats by serosal applicati

83 Gastric ulcers were observed during the treatment period

84 with gastritis, 3 with duodenal ulcer and 1 gastric ulcer, were studied.

85 gh significance) in mucus from patients with gastric ulcer, when compared with that in mucus from ind

86 jects receiving naproxen (6 of 32) developed gastric ulcers, whereas no ulcers occurred in subjects r