ライフサイエンスコーパス: gastric acid

1 The duodenum absorbs nearly all secreted gastric acid.

2 on of duodenal epithelial cells from luminal gastric acid.

3 of excess ammonia, some of which neutralizes gastric acid.

4 using a formulation which protects them from gastric acid.

5 owing for cell injury from back diffusion of gastric acid.

6 in L. reuteri is mainly devoted to overcome gastric acid.

7 s of PPIs that are independent of effects on gastric acid.

8 se for low-pH simulants containing nitric or gastric acid.

9 despite continuous exposure to concentrated gastric acid.

10 re exposed to postprandial concentrations of gastric acid (0.15N HCl) for 7 days, and radiographs wer

11 Urease is an essential component of gastric acid acclimation by Helicobacter pylori.

12 Gastric acid aids protein digestion; facilitates the abs

13 rganisms to the potential killing effects of gastric acid, allows several logarithmic increases in gr

14 ssociated with intrasphincteric extension of gastric acid and cardiac mucosal lengthening.

15 lia in the gastric antrum decreased, whereas gastric acid and circulating gastrin increased.

16 so also in humans, reflux of an admixture of gastric acid and duodenal juice in a high-pH environment

17 Esophageal reflux of an admixture of gastric acid and duodenal juice induces Barrett's esopha

18 n is the only hormone capable of stimulating gastric acid and is thus required to maintain functional

19 consistent with their resisting digestion by gastric acid and pancreatic enzymes in vivo.

20 The aims of this study were to measure gastric acid and pepsin output in 206 health Americans (

21 Gastric acid and pepsin output rates were similar in you

22 Simulated gastric acid and pepsin were used to mimic human digesti

23 ese motors can safely and rapidly neutralize gastric acid and simultaneously release payload without

24 tagonists (H2RAs) suppress the production of gastric acid and thus may lead to malabsorption of vitam

25 e stable in water and buffers, in artificial gastric acid, and even in blood serum.

26 ecretion of airway mucus, antibody, insulin, gastric acids, and ions.

27 ng injury, including influenza infection and gastric acid aspiration.

28 Lung injury (LI) due to gastric-acid aspiration is associated with poor posttran

29 g and surfactant administration on LI due to gastric-acid aspiration.

30 Enteric bacteria circumvent the gastric acid barrier by activating extreme acid-resistan

31 iofilm once the organisms have traversed the gastric acid barrier of the stomach.

32 aquatic environment and passage through the gastric acid barrier of the stomach.

33 ronments and aids in the passage through the gastric acid barrier to allow access to the small intest

34 not increase V. cholerae passage through the gastric acid barrier.

35 rvival of E. coli during passage through the gastric acid barrier.

36 ences numerous cellular processes, including gastric acid/bicarbonate secretion, mucus secretion, and

37 Nocturnal gastric acid breakthrough was not a useful predictor of

38 ce (controls), with or without inhibition of gastric acid by omeprazole.

39 dogenous and exogenous substances, including gastric acid, carbon dioxide, and foodstuffs.

40 To examine the molecular sensor(s) of gastric acid chemonociception, we characterized acid-eli

41 Aspiration of gastric acid commonly injures airway epithelium and, if

42 cellular composition of the gastric mucosa, gastric acid content, and plasma levels of gastrin.

43 Gastric acid contributes to dyspeptic symptoms, includin

44 experiment was determined using a simulated gastric acid extraction.

45 Gastric acid facilitates the digestion of protein and th

46 Gastric acid facilitates the digestion of protein as wel

47 Gastric acid facilitates the digestion of protein as wel

48 The mechanism of gastric acid hypersecretion by NGASP was investigated in

49 Parenteral control of gastric acid hypersecretion in conditions such as Zollin

50 In a cohort of patients with gastric acid hypersecretion in whom acid secretion statu

51 llinger-Ellison syndrome (ZES) or idiopathic gastric acid hypersecretion is necessary perioperatively

52 og-interacting protein-1 had lower levels of gastric acid (hypochlorhydria), reduced production of so

53 In contrast, secretion of gastric acid in adult Nkcc1(-/-) stomachs and enterotoxi

54 hout known risk factors for iron deficiency, gastric acid inhibitor use for >/=2 years was associated

55 Previous and current gastric acid inhibitor use was significantly associated

56 contact with poultry animals; and the use of gastric acid inhibitors.

57 uced during Helicobacter infection inhibited gastric acid, intracellular calcium, and Shh expression

58 Use of drugs that inhibit gastric acid is associated with an increased risk of hip

59 hanisms and causing injury, the secretion of gastric acid is precisely regulated by a variety of cent

60 Because gastric acid may exacerbate postbanding ulcers and delay

61 Drugs that inhibit gastric acid might increase the risk of hip fracture.

62 o avoid damage under these harsh conditions, gastric acid must be finely regulated by overlapping neu

63 Gastric acid neutralization increases infectivity, but 3

64 ous release of the encapsulated payload upon gastric-acid neutralization by the motors.

65 m intrinsic and extrinsic factors, including gastric acid, nonsteroidal anti-inflammatory drugs, and

66 be caused by the caustic effects of refluxed gastric acid on esophageal epithelial cells.

67 n a twofold increase in basal and stimulated gastric acid output and an undetectable serum gastrin le

68 Helicobacter pylori alterations in gastric acid output and mucosal proliferation may involv

69 Vagal secretory function was measured by gastric acid output and pancreatic polypeptide response

70 0 microg/kg IV) or saline was then given and gastric acid output collected for another 2 hours.

71 toprazole in maintaining adequate control of gastric acid output during the switch from oral to intra

72 on of the vagi, as evident by an increase in gastric acid output, a rise in serum pancreatic polypept

73 pylori-infected subjects with low or absent gastric acid output.

74 more potent and longer-acting inhibitors of gastric acid production than intravenous histamine-2-rec

75 comparable to OPGV in decreasing stimulated gastric acid production without significantly altering g

76 mine-2 receptor antagonists (H2RAs) suppress gastric acid production, which can inhibit iron absorpti

77 mine-2 receptor antagonists (H2RAs) suppress gastric acid production, which can inhibit iron absorpti

78 redominant factor in mediating resistance to gastric acid production.

79 n is involved in the endocrine regulation of gastric acid production.

80 of ATPase activity and acid transport by the gastric acid pump.

81 Of note, exposure to gastric acid-reducing agents, such as H2 blockers and pr

82 effective for the treatment of allergic and gastric acid-related conditions.

83 p inhibitors (PPIs) are widely used to treat gastric acid-related disorders.

84 upper gastrointestinal tract to concentrated gastric acid remains one of the biggest unsolved mysteri

85 upper gastrointestinal tract to concentrated gastric acid remains one of the biggest unsolved mysteri

86 patterns have been associated with different gastric acid responses to H. pylori infection.

87 Caffeine, generally known as a stimulant of gastric acid secretion (GAS), is a bitter-tasting compou

88 Slc26a9 deletion resulted in the loss of gastric acid secretion and a moderate reduction in the n

89 ers, paracrine agents, and hormones regulate gastric acid secretion and are themselves regulated.

90 esults demonstrate that AE2 is essential for gastric acid secretion and for normal development of sec

91 Epidermal growth factor (EGF) stimulates gastric acid secretion and H(+)/K(+)-ATPase alpha-subuni

92 In vivo, gastric acid secretion and in vitro histamine release fr

93 w emphasizes the importance and relevance of gastric acid secretion and its regulation in health and

94 mpairments in basal and histamine-stimulated gastric acid secretion and markedly reduced levels of th

95 disease.Proton pump inhibitors (PPIs) reduce gastric acid secretion and modulate gut microbiota compo

96 the vagus (DMV) has been shown to stimulate gastric acid secretion and motility, respectively, via v

97 ons into the DMV may mediate the increase in gastric acid secretion and motor activity associated wit

98 rin receptor is one of several regulators of gastric acid secretion and mucosal growth.

99 t analysis of its role during organogenesis, gastric acid secretion and neoplastic transformation.

100 biological processes including inflammation, gastric acid secretion and neuromodulation.

101 potassium channel beta subunit gene ablates gastric acid secretion and predisposes to gastric neopla

102 ine alone showed partial suppression of both gastric acid secretion and progression to neoplasia.

103 g cellular restitution as well as inhibiting gastric acid secretion and reactive oxygen species (ROS)

104 ent strategies including improved control of gastric acid secretion and role for surgery, and new app

105 lly linked to epithelial processes including gastric acid secretion and thyroid hormone biosynthesis.

106 Recent milestones in the understanding of gastric acid secretion and treatment of acid-peptic diso

107 prove our understanding of the regulation of gastric acid secretion at the central, peripheral, and i

108 buting to understanding of the regulation of gastric acid secretion at the central, peripheral, and i

109 ovides direct evidence for the regulation of gastric acid secretion by a TRP channel; TRPML1 is an im

110 Endotoxemia from LPS inhibits gastric acid secretion by an unknown mechanism.

111 e hypothesized that LPS causes inhibition of gastric acid secretion by down-regulating the H/K-ATPase

112 These data suggest that inhibition of gastric acid secretion by LPS is due to inhibition of H/

113 contributes to galanin-induced inhibition of gastric acid secretion by means of the suppression of en

114 Gastric acid secretion by parietal cells is precisely re

115 Gastric acid secretion by parietal cells requires traffi

116 Inhibition of gastric acid secretion by proton pump inhibitors like om

117 ass of protein may account for inhibition of gastric acid secretion by PYY released from the small in

118 Our understanding of the regulation of gastric acid secretion continues to advance.

119 es central neurotensin-induced inhibition of gastric acid secretion does not appear to be the high-af

120 RECENT FINDINGS: Gastric acid secretion facilitates the digestion of prot

121 nd 2c (L-736,380) dose-dependently inhibited gastric acid secretion in anesthetized rats (ID(50), 0.0

122 edge, the understanding of the regulation of gastric acid secretion in health and disease is far from

123 es in our understanding of the regulation of gastric acid secretion in health and disease, as well as

124 ss in our understanding of the regulation of gastric acid secretion in health and disease.

125 d distal renal tubular acidosis or decreased gastric acid secretion in humans.

126 ociated with any significant change in basal gastric acid secretion in monkeys and occurred despite a

127 Helicobacter pylori infection increases gastric acid secretion in patients with duodenal ulcers

128 esis that inhibition of gastric emptying and gastric acid secretion in response to dietary lipid is d

129 Secretagogues that stimulate gastric acid secretion induce Shh gene expression throug

130 The regulation of gastric acid secretion is achieved in the periphery by i

131 Gastric acid secretion is mediated by the H/K-ATPase of

132 fluence of central and peripheral stimuli on gastric acid secretion is mediated via activation of his

133 Gastric acid secretion is regulated by biologic agents p

134 Gastric acid secretion is tightly regulated by overlappi

135 histamine H3 receptors in the regulation of gastric acid secretion is unclear.

136 ar target for peptide YY (PYY) inhibition of gastric acid secretion is unknown.

137 ng of the pathways and mechanisms regulating gastric acid secretion may lead to the development of ne

138 Gastric acid secretion must be precisely controlled at a

139 more potent and longer-lasting inhibition of gastric acid secretion provided by proton pump inhibitor

140 After excision of the tumor, WDS ceased and gastric acid secretion returned.

141 ng of the pathways and mechanisms regulating gastric acid secretion should lead to improved managemen

142 ng of the pathways and mechanisms regulating gastric acid secretion should lead to the development of

143 ed into the cisterna magna potently inhibits gastric acid secretion stimulated by intravenous infusio

144 licobacter pylori interaction with the human gastric acid secretion system.

145 minant gastritis and profound suppression of gastric acid secretion that is partially reversible with

146 Reduction of gastric acid secretion therefore appears to promote over

147 nal role of Akt appears to be stimulation of gastric acid secretion through induction of H(+)/K(+)-AT

148 e whereby endogenous somatostatin suppresses gastric acid secretion through inhibition of gastrin act

149 the VLRF to inhibit pentagastrin-stimulated gastric acid secretion through spinal pathways, suggesti

150 re, we identified a novel pathway modulating gastric acid secretion through the stomach calcium-sensi

151 actor (EGF) inhibits secretagogue-stimulated gastric acid secretion via an EGF receptor located on pa

152 pose that Slc26a9 plays an essential role in gastric acid secretion via effects on the viability of t

153 ction of this amidated peptide in regulating gastric acid secretion via the CCK2 receptor is now well

154 naesthetized A-IV(+/+) mice, meal-stimulated gastric acid secretion was 59% inhibited by intestinal l

155 Decreased gastric acid secretion was associated with cholera but n

156 Gastric acid secretion was blocked and stimulated by ML1

157 A rat model to study gastric acid secretion was created.

158 enervated rats with a gastric fistula, basal gastric acid secretion was depressed 3-fold, and plasma

159 When gastric acid secretion was measured after maximal stimul

160 art of an intravenous pentagastrin infusion; gastric acid secretion was monitored every 10 min for 20

161 la oblongata where bombesin acts to suppress gastric acid secretion were investigated in urethane-ane

162 rticularly the gastrin (G) cell, co-ordinate gastric acid secretion with the arrival of food in the s

163 ximal tubular and intestinal Na+ absorption, gastric acid secretion, and cAMP-induced jejunal Cl- sec

164 siological vagal control of gastrin release, gastric acid secretion, and gastric motility.

165 wed mild hypergastrinemia, increased maximal gastric acid secretion, and increased parietal cell numb

166 ocin, which acts within the DMV to stimulate gastric acid secretion, but inhibits gastric motor funct

167 heir ability of immune defense responses and gastric acid secretion, consistent with their ability to

168 exchanger, is important for normal levels of gastric acid secretion, gastric epithelial cell differen

169 ed vascular permeability, and stimulation of gastric acid secretion, histamine plays important roles

170 detectable tissue histamine levels, impaired gastric acid secretion, impaired passive cutaneous anaph

171 h advancing age has no independent effect on gastric acid secretion, it is associated with reduced pe

172 ical processes including allergic reactions, gastric acid secretion, neurotransmitter release, and in

173 ished the stimulatory effect of histamine on gastric acid secretion, providing evidence for the regul

174 ists for the treatment of allergy and excess gastric acid secretion, respectively.

175 data demonstrate that KCNE2 is essential for gastric acid secretion, the first genetic evidence that

176 agents have been implicated as regulators of gastric acid secretion, their site and mechanism of acti

177 mmunoreactivity, and pentagastrin-stimulated gastric acid secretion, were similar in both infected an

178 n in the somatostatin pathway have increased gastric acid secretion, which confirms an important nega

179 onal, and paracrine pathways finely regulate gastric acid secretion.

180 g a gene-dose effect and a primary defect in gastric acid secretion.

181 n made in understanding of the regulation of gastric acid secretion.

182 sight into the complex regulation of in vivo gastric acid secretion.

183 ponses, inflammation, neurotransmission, and gastric acid secretion.

184 ation of proliferation and downregulation of gastric acid secretion.

185 ward an understanding of the cell biology of gastric acid secretion.

186 lead to new insights into the regulation of gastric acid secretion.

187 ased numbers of parietal cells and decreased gastric acid secretion.

188 n kinase Akt, we explored the role of Akt in gastric acid secretion.

189 lary VLRF area in the sympathetic control of gastric acid secretion.

190 mmatory cytokine and a powerful inhibitor of gastric acid secretion.

191 r to play a role in inhibition of stimulated gastric acid secretion.

192 t (CWR) and also inhibits gastrin-stimulated gastric acid secretion.

193 astric parietal cell that is responsible for gastric acid secretion.

194 100-23 contribute to tolerance towards host gastric acid secretion.

195 tric environment may be its ability to alter gastric acid secretion.

196 e, hormonal, and intracellular regulation of gastric acid secretion.

197 ameters and mechanism of P-CAB inhibition of gastric acid secretion.

198 e, hormonal, and intracellular regulation of gastric acid secretion.

199 estigate the requirement for this protein in gastric acid secretion.

200 e2 channel facilitates its essential role in gastric acid secretion.

201 mulation-associated membrane recruitment and gastric acid secretion.

202 Gastrin is a key regulator of gastric acid secretion.

203 e regarding the regulation and assessment of gastric acid secretion.

204 een performed on colonic fluid transport and gastric acid secretion.

205 gulatory role for the CFTR protein in normal gastric acid secretion.

206 cial hemodynamic effects, has prokinetic and gastric acid secretory functions in the stomach, and may

207 Proton pump inhibitors (PPIs) are gastric acid-suppressing agents widely prescribed for th

208 ay not be appropriate, however, both because gastric acid suppression by PPIs might benefit EoE patie

209 To assess the role of gastric acid suppression in the prevention of stress ulc

210 icile acquisition while antibiotic exposure, gastric acid suppression, and immunosuppression increase

211 Proton pump inhibitors, commonly used for gastric acid suppression, have been shown to have an ass

212 Simultaneously, use of gastric acid suppressive medications is increasing.

213 Recent increases in the use of gastric acid-suppressive medications might contribute to

214 h can autonomously and temporally neutralize gastric acid through efficient chemical propulsion in th

215 Presence of basal unstimulated gastric acid was evaluated noninvasively by having subje

216 Gastric acid with a pH lower than 3.5 releases quinine,

217 (2) >200 mm Hg due to the luminal mixture of gastric acid with secreted bicarbonate, which augments m