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 (4.3%) died within 30 days due to sepsis and gastroduodenal artety (GDA) stump blowout.

9 the effects of an acute aspirin challenge on gastroduodenal barrier function with or without prophyla

10 Gastroduodenal bicarbonate secretion is mediated by pros

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

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

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

14 Although gastroduodenal bleeding or superinfection showed no clea

15 28.5 (CI, 11.7 to 36.9) hospitalizations for gastroduodenal bleeding per 1000 person-years.

16 e of the most common adverse events, namely, gastroduodenal bleeding, superinfection, and hyperglycem

17 th reduced incidence of hospitalizations for gastroduodenal bleeding.

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

19 43/57 (75%) gastroduodenal convergent neurons had low-threshold (< o

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

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

22 Gastroduodenal convergent spinal neurons might contribut

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

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

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

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

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

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

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

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

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

32 teases involved in primary hydrolysis during gastroduodenal digestion and exopeptidases that hydrolys

33 Gastroduodenal digestion conditions do not disrupt the 3

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

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

36 After gastroduodenal digestion, the human fluids gave less num

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

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

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

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

41 common in H. pylori strains in patients with gastroduodenal disease in Vietnam, and the complete clus

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

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

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

45 with that in mucus from individuals without gastroduodenal disease.

46 ogenesis of gastric mucosal inflammation and gastroduodenal disease.

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

48 practice of medicine or our understanding of gastroduodenal disease.

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

50 s human stomachs and sometimes causes severe gastroduodenal disease.

51 e relationship between virulence factors and gastroduodenal diseases among patients.

52 ction is the main cause of the most frequent gastroduodenal diseases and gastric atrophy, with or wit

53 lete cluster of tfs3 ICE was associated with gastroduodenal diseases in Vietnam.

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

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

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

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

58 Helicobacter pylori causes several gastroduodenal diseases.

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

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

61 lved in the etiology and severity of several gastroduodenal diseases; however, plasticity of the H. p

62 tional dyspepsia (FD) is a common functional gastroduodenal disorder with a high socioeconomic burden

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

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

65 The gastroduodenal epithelium is protected from acid-peptic

66 Only gastroduodenal erosions were associated with symptom sub

67 On UGIE, gastroduodenal erosions were seen in 250 (60.8%), GORD-a

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

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

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

71 with gastric outlet obstruction secondary to gastroduodenal IgG4-related disease.

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

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

74 Esophageal and gastroduodenal injury assessed by endoscopy scores was a

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

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

77 Too much acid can induce gastroduodenal injury.

78 terizing the abnormal motor functions at the gastroduodenal junction are discussed.

79 trointestinal tract with a simulation of the gastroduodenal junction, and demonstrate using video mic

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

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

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

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

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

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

86 idal antiinflammatory drug toxicity than the gastroduodenal mucosa.

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

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

89 Gastroduodenal mucosal defense is a dynamic process, and

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

91 Aging weakens gastroduodenal mucosal defense mechanisms.

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

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

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

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

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

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

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

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

100 onic gastritis, which can progress to severe gastroduodenal pathologies, including peptic ulcer, gast

101 determine possible progression to different gastroduodenal pathologies.

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

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

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

105 lts underwent gastroduodenoscopy, and 14 had gastroduodenal pathology.

106 ive ileus which develop after laparotomy for gastroduodenal perforations.

107 Gastroduodenal permeability increased with aspirin chall

108 Gastroduodenal permeability was assessed by urinary excr

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

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

111 Gastroduodenal reflux may cause symptoms such as chronic

112 ia is a complex of symptoms referable to the gastroduodenal region of the gastrointestinal tract and

113 g localized most capsule stimulations to the gastroduodenal segments.

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

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

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

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

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

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

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

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

122 cute or chronic inflammatory diseases of the gastroduodenal tract.

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

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

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

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

127 noscopy was performed because of a suspected gastroduodenal ulcer.

128 itor omeprazole is administered to dogs with gastroduodenal ulceration or oesophagitis, whereas the n

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

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

131 Gastroduodenal ulceration was assessed by endoscopy at 6

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

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

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

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

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

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

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

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

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

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

142 Gastroduodenal ulcers were detected endoscopically in 33

143 r age, sex, anemia, obesity, low hemoglobin, gastroduodenal ulcers, rehospitalization, critical illne

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

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