ライフサイエンスコーパス: gastric acid

1 despite continuous exposure to concentrated gastric acid.

2 The duodenum absorbs nearly all secreted gastric acid.

3 on of duodenal epithelial cells from luminal gastric acid.

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

5 using a formulation which protects them from gastric acid.

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

7 rial defenses in the upper GI tract, such as gastric acid.

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

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

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

11 gainst dehydration, pathogen penetration, or gastric acids.

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

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

14 Gastric acid aids protein digestion; facilitates the abs

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

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

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

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

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

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

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

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

23 Gastric acid and pepsin output rates were similar in you

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

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

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

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

28 of probiotics, resistance to antibiotics and gastric acid, and potential benefits in reducing postope

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

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

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

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

33 ibed proton pump inhibitors (PPIs) to reduce gastric acid associated damage to esophageal and airway

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

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

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

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

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

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

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

41 Nocturnal gastric acid breakthrough was not a useful predictor of

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

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

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

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

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

47 Gastric acid contributes to dyspeptic symptoms, includin

48 n gut and in healthy volunteers demonstrates gastric acid-dependent phage resilience, safety, and via

49 sophageal reflux disease (GERD) is caused by gastric acid entering the esophagus.

50 experiment was determined using a simulated gastric acid extraction.

51 Gastric acid facilitates the digestion of protein and th

52 Gastric acid facilitates the digestion of protein as wel

53 Gastric acid facilitates the digestion of protein as wel

54 , found in fortified foods, does not require gastric acid for its absorption and could thus be benefi

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

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

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

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

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

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

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

62 Previous and current gastric acid inhibitor use was significantly associated

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

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

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

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

67 Because gastric acid may exacerbate postbanding ulcers and delay

68 physiological stressor in tumor development, gastric acid-mediated regional microscopic injury in for

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

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

71 Gastric acid neutralization increases infectivity, but 3

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

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

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

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

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

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

78 0 microg/kg IV) or saline was then given and gastric acid output collected for another 2 hours.

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

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

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

82 t not plasmid mutant while mice deficient in gastric acid production rescued the plasmid mutant but n

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

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

85 s), which are commonly used as inhibitors of gastric acid production, also have anti-inflammatory pro

86 ly deficient in gastrin, a key regulator for gastric acid production, or pharmacologically treated wi

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

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

89 redominant factor in mediating resistance to gastric acid production.

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

91 contributes to airway surface hydration and gastric acid production.

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

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

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

95 pump inhibitors (PPIs) are commonly used for gastric acid-related disorders, but their safety profile

96 for gastroesophageal reflux disease or other gastric acid-related disorders, namely PPIs, histamine 2

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

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

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

100 a Gram-negative, facultative intracellular, gastric acid-resistant bacterium of the Enterobacteriace

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

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

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

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

105 Morphine treatment also increases gastric acid secretion and causes delays in gastric empt

106 tion of acid in the stomach due to increased gastric acid secretion and delayed gastric emptying.

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

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

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

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

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

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

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

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

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

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

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

118 limited to allergic reactions, wakefulness, gastric acid secretion and neurotransmission.

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

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

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

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

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

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

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

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

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

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

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

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

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

132 Gastric acid secretion by parietal cells is precisely re

133 Gastric acid secretion by parietal cells requires traffi

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

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

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

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

138 Stimulation of gastric acid secretion during P. yoelii infection restor

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

140 Different aspects of regulation of gastric acid secretion have been focused either in terms

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

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

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

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

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

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

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

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

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

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

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

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

153 Gastric acid secretion is regulated by biologic agents p

154 Gastric acid secretion is tightly regulated by overlappi

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

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

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

158 Gastric acid secretion must be precisely controlled at a

159 onse to counteract infection-related damage, gastric acid secretion or gastrointestinal motility for

160 Gastric acid secretion plays a pivotal role in the physi

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

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

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

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

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

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

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

168 Reduction of gastric acid secretion therefore appears to promote over

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

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

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

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

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

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

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

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

177 Decreased gastric acid secretion was associated with cholera but n

178 Gastric acid secretion was blocked and stimulated by ML1

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

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

181 When gastric acid secretion was measured after maximal stimul

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

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

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

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

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

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

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

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

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

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

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

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

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

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

196 Global Kcne2 deletion, which inhibits gastric acid secretion, reduced the relative abundance o

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

198 oltage-dependent K(+) channel that regulates gastric acid secretion, salt and glucose homeostasis, an

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

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

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

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

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

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

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

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

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

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

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

210 ation of proliferation and downregulation of gastric acid secretion.

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

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

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

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

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

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

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

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

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

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

221 d following a rise in gastric pH, leading to gastric acid secretion.

222 limiting food-stimulated gastrin release and gastric acid secretion.

223 axis, a neurotransmitter, and a regulator of gastric acid secretion.

224 100-23 contribute to tolerance towards host gastric acid secretion.

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

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

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

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

229 mulation-associated membrane recruitment and gastric acid secretion.

230 Gastrin is a key regulator of gastric acid secretion.

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

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

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

234 This study demonstrates the association of gastric acid stress with Cyclooxygenase-2-dependent tumo

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

236 gulant, antihypertensive, antirheumatic, and gastric acid-suppressing medications.

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

238 be particularly vulnerable to the effects of gastric acid suppression during infancy.

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

240 e of proton pump inhibitors (PPIs) result in gastric acid suppression that can impair the absorption

241 sms that are vs are not associated with less gastric acid suppression were associated with 1.72-fold

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

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

244 d before mice were immunized with or without gastric acid-suppression medication.

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

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

247 ctor in the pathogenesis of peptic ulcers is gastric acid, the secretion of which is controlled by th

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

249 Parietal cells (PCs) produce gastric acid to kill pathogens and aid digestion.

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

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

252 (2) >200 mm Hg due to the luminal mixture of gastric acid with secreted bicarbonate, which augments m