ライフサイエンスコーパス: gastroduodenal

1 as expanded into the nonsurgical therapy for gastroduodenal and colorectal obstructions.

2 , right postceliac arteries (common hepatic, gastroduodenal, and right gastroepiploic arteries; score

3 PHA) was the first branch of the SMA and the gastroduodenal artery (GDA) was a branch of the celiac a

4 Perfusion inflow was through the gastroduodenal artery and outflow was from a cannula pos

5 the contribution of the portal vein and the gastroduodenal artery to the bile ducts is unknown.

6 mine the contribution of the hepatic artery, gastroduodenal artery, and portal vein to the microvascu

7 te plasma concentrations were obtained (ie., gastroduodenal artery, portal vein, hepatic vein, and fe

8 Gastroduodenal bicarbonate secretion is mediated by pros

9 All had at least two follow-up endoscopic gastroduodenal biopsies at Memorial Sloan-Kettering Canc

10 Primary outcomes were hospitalizations for gastroduodenal bleeding and serious cardiovascular disea

11 Adjusted incidence of hospitalization for gastroduodenal bleeding in concurrent PPI users was 50%

12 28.5 (CI, 11.7 to 36.9) hospitalizations for gastroduodenal bleeding per 1000 person-years.

13 th reduced incidence of hospitalizations for gastroduodenal bleeding.

14 roximal small intestine is innervated by the gastroduodenal branch of the vagus nerve, the transectio

15 43/57 (75%) gastroduodenal convergent neurons had low-threshold (< o

16 In addition, 34/40 (85%) gastroduodenal convergent neurons had somatic receptive

17 Of 57 gastroduodenal convergent neurons, 41 (72%) had excitato

18 Gastroduodenal convergent spinal neurons might contribut

19 ensive mechanisms, with the expectation that gastroduodenal damage will be minimized.

20 Enhanced understanding of the mechanisms of gastroduodenal defense and injury provides new insight i

21 Enhanced understanding of the mechanisms of gastroduodenal defense and injury provides new insight i

22 s contribute to our overall understanding of gastroduodenal defense and suggest innovative avenues of

23 s contribute to our overall understanding of gastroduodenal defense and suggest innovative avenues of

24 s contribute to our overall understanding of gastroduodenal defense and suggest innovative avenues of

25 addition, a great deal can be learned about gastroduodenal defense by studying the effects of ulcero

26 The field of gastroduodenal defense can be subdivided into the follow

27 anti-inflammatory drugs (NSAIDs) compromise gastroduodenal defense mechanism including blood flow an

28 mpacting on these properties contributing to gastroduodenal defense since the prior review article on

29 The results showed that during gastroduodenal digestion alpha-DCs react with digestive

30 Gastroduodenal digestion conditions do not disrupt the 3

31 enriched extracts before and after simulated gastroduodenal digestion inhibited enzymes associated wi

32 olyphenols enriched extract with and without gastroduodenal digestion inhibited enzymes associated wi

33 After gastroduodenal digestion, the human fluids gave less num

34 Rather, we propose that gastroduodenal disease associated with H. pylori infecti

35 nsmission of H. pylori and the expression of gastroduodenal disease caused by this infection.

36 BabA adhesin correlates with development of gastroduodenal disease in adults.

37 e role H. pylori plays in the development of gastroduodenal disease in children.

38 thogenesis of Helicobacter pylori associated gastroduodenal disease remains poorly understood.

39 C5AC mucin in mucus from individuals without gastroduodenal disease was very high, suggesting that th

40 bacterial infections in the pathogenesis of gastroduodenal disease, which triggered an avalanche of

41 with that in mucus from individuals without gastroduodenal disease.

42 ogenesis of gastric mucosal inflammation and gastroduodenal disease.

43 nce markers, was associated with more severe gastroduodenal disease.

44 practice of medicine or our understanding of gastroduodenal disease.

45 nfection and prevention of H. pylori-induced gastroduodenal disease.

46 s human stomachs and sometimes causes severe gastroduodenal disease.

47 i infection has been linked to a spectrum of gastroduodenal diseases of broad public health impact, y

48 an important etiologic agent in a variety of gastroduodenal diseases, produces large amounts of ureas

49 in the pathogenesis of H. pylori-associated gastroduodenal diseases.

50 Helicobacter pylori causes several gastroduodenal diseases.

51 ri as a significant causative factor in many gastroduodenal diseases.

52 and tnpB (no cagA) with H. pylori associated gastroduodenal diseases.

53 humans and is implicated in a wide range of gastroduodenal diseases.

54 in women than men, functional esophageal and gastroduodenal disorders do not appear to vary by gender

55 diagnosis and effective intervention in most gastroduodenal disorders of childhood can alter natural

56 The gastroduodenal epithelium is protected from acid-peptic

57 We have previously shown that gastroduodenal-esophageal reflux (GDER) together with N-

58 Rats underwent surgical placement of a gastroduodenal feeding catheter and were randomly assign

59 Luminal lipid in the duodenum modulates gastroduodenal functions via the release of gut hormones

60 cag+ strains may be instrumental in inducing gastroduodenal inflammation, ulceration, and neoplasia.

61 central role in the development of H. pylori gastroduodenal inflammation.

62 Esophageal and gastroduodenal injury assessed by endoscopy scores was a

63 SAIDs) are probably the most common cause of gastroduodenal injury in the United States today.

64 of the involvement of Helicobacter pylori in gastroduodenal injury, the mechanism by which the organi

65 Too much acid can induce gastroduodenal injury.

66 pact on cure of the infection and healing of gastroduodenal lesions.

67 nvironmental or host factors converge in the gastroduodenal milieu and control the final outcome of i

68 lity, (2) noninvasive techniques to evaluate gastroduodenal motility, and (3) the pathophysiology and

69 es emerged over the past year in the area of gastroduodenal motility.

70 The defensive mechanism of the gastroduodenal mucosa comprises a series of physical, ch

71 The mechanisms by which the gastroduodenal mucosa maintains viability and normal fun

72 idal antiinflammatory drug toxicity than the gastroduodenal mucosa.

73 e have summarized recent findings related to gastroduodenal mucosal defense as well as factors contri

74 Research in the field of gastroduodenal mucosal defense has focused on continued

75 Research in the field of gastroduodenal mucosal defense has focused on continued

76 Gastroduodenal mucosal defense is a dynamic process, and

77 RECENT FINDINGS: Research in the field of gastroduodenal mucosal defense is shifting from animal m

78 Aging weakens gastroduodenal mucosal defense mechanisms.

79 highlighted the recent findings relating to gastroduodenal mucosal defense, including elements that

80 o review recent developments in the field of gastroduodenal mucosal defense.

81 o review recent developments in the field of gastroduodenal mucosal defense.

82 o review recent developments in the field of gastroduodenal mucosal defense.

83 There is a wide array of pathways leading to gastroduodenal mucosal injury in addition to protective

84 The effect of H. pylori on NSAID-related gastroduodenal mucosal injury may be best established by

85 oidal anti-inflammatory drug (NSAID)-related gastroduodenal mucosal injury.

86 s stimulates pancreatic enzyme secretion via gastroduodenal mucosal vagal afferent fibres in the rat.

87 Helicobacter pylori is a human gastroduodenal pathogen that leads to active chronic inf

88 While the majority of patients with gastroduodenal pathology (12 of 14) were seropositive fo

89 valence (35%) to determine the prevalence of gastroduodenal pathology and its relationship to serolog

90 mphocytes may be required for the genesis of gastroduodenal pathology.

91 lts underwent gastroduodenoscopy, and 14 had gastroduodenal pathology.

92 Both LTPs are initially cleaved during gastroduodenal proteolysis at three major sites between

93 They are highly resistant to simulated gastroduodenal proteolysis, a property that may play a r

94 Gastroduodenal reflux may cause symptoms such as chronic

95 rate, 76-100%; complication rate, 4-28%) and gastroduodenal stenting (success rate, 81-92%; complicat

96 t preparation, endoscopic mucosal resection, gastroduodenal stenting, and endoscopic placement of ent

97 he major visceral (celiac, hepatic, splenic, gastroduodenal, superior mesenteric) and small pancreati

98 fection in 30 sequential adult patients with gastroduodenal symptoms by three biopsy-based methods (r

99 Clinically, the overlap of gastroduodenal symptoms, such as visceral pain or hypers

100 No change in the gastroduodenal tissue levels of EGF was observed.

101 e aim of this study was to determine whether gastroduodenal tissue levels of TGF-alpha and EGF protei

102 years the role of food derived alpha-DCs in gastroduodenal tract is under investigation to understan

103 of conditions, including those found in the gastroduodenal tract.

104 One patient (4.3%) developed a gastroduodenal ulcer (grade 2).

105 ter pylori is a major cause of gastritis and gastroduodenal ulcer disease and can cause cancer.

106 new capillary blood vessels, is crucial for gastroduodenal ulcer healing because it enables delivery

107 noscopy was performed because of a suspected gastroduodenal ulcer.

108 which Helicobacter pylori infection leads to gastroduodenal ulceration remain poorly understood.

109 of osteoarthritis, caused significantly less gastroduodenal ulceration than ibuprofen, with ulcer rat

110 Gastroduodenal ulceration was assessed by endoscopy at 6

111 scular events, renal failure or dysfunction, gastroduodenal ulceration, and wound-healing complicatio

112 The cumulative incidence of gastroduodenal ulcers >/=3 mm with rofecoxib (25 or 50 m

113 There was an increased incidence of gastroduodenal ulcers and elevated levels of alanine tra

114 so been recognized as a pathogen that causes gastroduodenal ulcers and gastric cancer.

115 d secondary end points were the incidence of gastroduodenal ulcers at 12 and 24 weeks, respectively.

116 However, NSAIDs produce gastroduodenal ulcers in about 25% of users (often with

117 The incidence of endoscopically determined gastroduodenal ulcers in placebo-treated patients was 4

118 ite of overt or occult bleeding, symptomatic gastroduodenal ulcers or erosions, obstruction, or perfo

119 tients with osteoarthritis would cause fewer gastroduodenal ulcers than an equally effective dose of

120 inhibits cyclooxygenase 2, would cause fewer gastroduodenal ulcers than ibuprofen (in a multicenter t

121 Gastroduodenal ulcers were detected endoscopically in 33

122 est known risk factor for the development of gastroduodenal ulcers, with infection being present in 6

123 ngly, common branch hepatic vagotomy (unlike gastroduodenal vagotomy) entirely blocked these fat-indu