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 useful use in the treatment or prevention of gastric ulcer.

3 erest in research new drugs for treatment of gastric ulcer.

4 rtery pseudoaneurysm caused by a penetrating gastric ulcer.

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

6 significantly associated with gastritis and gastric ulcer.

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

8 with Helicobacter pylori are major causes of gastric ulcers.

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

10 examined their modulation after induction of gastric ulcers.

11 Helicobacter pylori, the causative agent of gastric ulcers.

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

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

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

15 ylori infection in patients with duodenal or gastric ulcers.

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

17 552 in 1993 vs. 60,029 in 2006, -37.2%) than gastric ulcers (106,987 in 1993 vs. 86,064 in 2006, -19.

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

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

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

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

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

23 Gastric ulcers altered the properties of acid-elicited c

24 (95% confidence interval (CI): 1.9, 8.5) for gastric ulcer and 2.5 (95% CI: 0.8, 7.4) for duodenal ul

25 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

26 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

27 meta-analysis and the effect of homB gene on gastric ulcer and gastric cancer diseases was evaluated

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

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

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

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

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

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

34 imited treatment of acute disorders, such as gastric ulcers and esophagitis, PPIs are now commonly us

35 ead to gastric pathologic conditions such as gastric ulcers and gastric adenocarcinomas.

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

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

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

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

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

41 UD in Africa, its patterns (duodenal ulcers, gastric ulcers, and coexisting ulcers), and its associat

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

43 ensing and detection, circuit repairing, and gastric ulcer coating, respectively.

44 and to explore the underlying mechanism for gastric ulcer development.

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

46 ple develop more adverse outcomes, including gastric ulcer disease, gastric adenocarcinoma, or gastri

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

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

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

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

51 Gastritis and gastric ulcers enhanced the visceromotor responses to in

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

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

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

55 Gastric ulcers (GU) were diagnosed in 2095 (8%) cases, d

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

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

58 Fewer baseline gastric ulcers healed among eradication-treatment patien

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

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

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

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

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

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

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

66 t gene expression, significantly accelerates gastric ulcer healing.

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

68 tion filtrate, in a model of ethanol-induced gastric ulcer in mice, suggesting its possible useful us

69 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.

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

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

72 extracts of khambir alleviated cold-induced gastric ulcers in the animal model as it exhibited histo

73 Gastric ulcer increases the risk of pancreatic cancer, w

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

75 Pharmacologic prophylaxis for gastric ulcer is commonly prescribed in patients hospita

76 80% to 100% of patients within 4 weeks, but gastric ulcers larger than 2 cm may require 8 weeks of t

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

78 We found that history of gastric ulcer may be a risk factor for gastric ulceratio

79 Patients with history of gastric ulcer might benefit from higher than standard do

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

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

82 Gastric ulcer or peptic ulcer is a common disease worldw

83 nt between cases and controls was history of gastric ulcer (p = 0.04) with OR 3.8 (95% CI 1.1-12.5; p

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

85 e abiraterone acetate plus prednisone group (gastric ulcer perforation, sudden death, and cerebrovasc

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

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

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

89 ee duodenal ulcer, three gastritis, and four gastric ulcer samples), 10 for H. felis (one gastritis,

90 (four duodenal ulcer, five gastritis, and 11 gastric ulcer samples), 13 for H. heilmannii (three gast

91 one gastritis, three duodenal ulcer, and six gastric ulcer samples), 20 for H. salomonis (four duoden

92 ree gastritis, five duodenal ulcer, and five gastric ulcer samples), and 7 for H. bizzozeronii (zero

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

94 wed bilateral hypermetabolic adrenal masses, gastric ulcer, small hypermetabolic adenopathies, multip

95 tory of H. pylori, NSAIDs, family history of gastric ulcer, smoking, and fruit intake were considered

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

97 Gastric ulcer strain B128 induced more severe gastritis,

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

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

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

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

102 er samples), and 7 for H. bizzozeronii (zero gastric ulcer, two duodenal ulcer, and five gastritis sa

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

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

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

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

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

108 Gastric ulcers were induced in rats by acetic acid appli

109 Gastric ulcers were induced in rats by serosal applicati

110 Gastric ulcers were observed during the treatment period

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

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

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