ライフサイエンスコーパス: gastric

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

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

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

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

5 Gastric acid neutralization increases infectivity, but 3

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

7 Reduction of gastric acid secretion therefore appears to promote over

8 Gastric acid secretion was blocked and stimulated by ML1

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

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

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

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

13 synthesized, and their inhibitory effects on gastric adenocarcinoma (AGS) and esophageal squamous cel

14 characteristics of six cases containing both gastric adenocarcinoma and GIST.

15 nt total gastrectomy for stage I through III gastric adenocarcinoma between 2009 and 2012.

16 rgoing curative-intent total gastrectomy for gastric adenocarcinoma between January 2009 and December

17 Gastric adenocarcinoma is the third leading cause of can

18 model offers a valuable tool to investigate gastric adenocarcinoma subtypes where RAS/MAPK pathway a

19 t of a genetically engineered mouse model of gastric adenocarcinoma tumorigenesis based on Kras(G12D)

20 most important in both cases of synchronous gastric adenocarcinoma with GIST and GIST alone.

21 cter pylori is the strongest risk factor for gastric adenocarcinoma, yet only a minority of infected

22 be a precursor to intestinal metaplasia and gastric adenocarcinoma.

23 CD117, CD34 and Dog1 in all six synchronous gastric adenocarcinomas with GIST, and in GIST alone.

24 pecific Odc deletion significantly increased gastric and colonic inflammation, respectively, and enha

25 ive adjuvant radiochemotherapy for high risk gastric and gastroesophageal junction adenocarcinoma: De

26 ined from wheat (2.12CI/mL and 3.78CI/mL for gastric and intestinal dialysate respectively) and rye b

27 and rye breads (4.16CI/mL and 2.46CI/mL for gastric and intestinal dialysate respectively).

28 n sequential exposure to simulated salivary, gastric and intestinal fluids.

29 Higher rutin contents were found in both gastric and intestinal phases than in fresh leaves.

30 nostic marker for detection of patients with gastric and lung cancer.

31 ycoforest was tested on two data sets (human gastric and salmon mucosa O-linked glycomes) for which M

32 e age-adjusted incident rate ratios by lung, gastric, and colorectal cancers, with manufacturing used

33 ad higher relative mortality risks for lung, gastric, and colorectal cancers.

34 signaling in subsets of pancreatic, ovarian, gastric, and colorectal tumors.

35 Case studies of colon, gastric, and kidney cancers were also implemented, and t

36 Results The left gastric artery, with or without the gastroepiploic arter

37 um (IS) sample, compared with a single IS or gastric aspirate (GA) sample, is not well known.

38 eral studies have shown premalignant lesions gastric atrophy (GA) and intestinal metaplasia (IM) infl

39 pplication for active drug delivery to treat gastric bacterial infection in a mouse model using clari

40 open Roux-en-Y gastric bypass, laparoscopic gastric band placement, or laparoscopic sleeve gastrecto

41 ed reoperations occurring after laparoscopic gastric band surgery as well as the associated payments

42 Among Medicare beneficiaries undergoing gastric band surgery, device-related reoperation was com

43 of this study was to analyze the adjustable gastric banding (AGB) natural history on a national basi

44 Adjustable gastric banding represented the most common bariatric pr

45 f psoriasis and psoriatic arthritis, whereas gastric banding was not.

46 rgoing bariatric surgery (gastric bypass and gastric banding).

47 3 (95% CI, 0.08-3.56) for gastric bypass and gastric banding, respectively.

48 3 (95% CI, 0.40-3.75) for gastric bypass and gastric banding, respectively.

49 Overall, simulated gastric bioaccessibility was higher than duodenal bioacc

50 Six standard gastric biopsies were taken.

51 approximately 4.5-fold in H. pylori-infected gastric biopsy specimens.

52 rformed in H. pylori-infected and uninfected gastric biopsy specimens.

53 st as often in Europe as laparoscopic Roux-Y-Gastric Bypass (LRYGB).

54 Roux-en-Y gastric bypass (RYGB) and sleeve gastrectomy (SG) accoun

55 drug use among patients undergoing Roux-en-Y gastric bypass (RYGB) surgery and a matched population-b

56 e markers for T2DM remission after Roux-en-Y gastric bypass (RYGB).

57 patients who sought and underwent Roux-en-Y gastric bypass (surgery group), 417 patients who sought

58 is in patients undergoing bariatric surgery (gastric bypass and gastric banding).

59 0.12-0.71) and 0.53 (95% CI, 0.08-3.56) for gastric bypass and gastric banding, respectively.

60 0.33-0.81) and 1.23 (95% CI, 0.40-3.75) for gastric bypass and gastric banding, respectively.

61 ts who have undergone laparoscopic Roux-en-Y gastric bypass and to develop decision tree models to op

62 Bariatric surgeries, such as Roux-en-Y gastric bypass and vertical sleeve gastrectomy, produce

63 ely 11 % of patients who underwent Roux-en-Y gastric bypass develop symptomatic gallstone disease.

64 people aged 13-21 years underwent Roux-en-Y gastric bypass for clinically severe obesity at a paedia

65 ssure occurred in 41 of 49 patients from the gastric bypass group (83.7%) compared with 6 of 47 patie

66 nts with severe obesity undergoing Roux-en-Y gastric bypass had substantial weight loss over 5 years,

67 y, 2007, 74 young people underwent Roux-en-Y gastric bypass in the FABS study.

68 tive patients scheduled to undergo Roux-en-Y gastric bypass or sleeve gastrectomy in three bariatric

69 Patients were randomized to Roux-en-Y gastric bypass plus medical therapy or medical therapy a

70 In this nationwide study, gastric bypass resulted in large improvements in obesity

71 The gastric bypass subset was composed of 9480 (76.7%) women

72 We hypothesized that gastric bypass surgery leads to a lower incidence of hea

73 INTERPRETATION: Roux-en-Y gastric bypass surgery resulted in substantial and durab

74 year Framingham risk score were lower in the gastric bypass than in the control group.

75 bservational, prospective study of Roux-en-Y gastric bypass that was conducted in the United States.

76 Gastric bypass was associated with a significantly reduc

77 adolescent surgical patients after Roux-en-Y gastric bypass with those of conservatively treated adol

78 and 22 of 48 (45.8%) patients randomized to gastric bypass, considering office and 24-hour ambulator

79 olescents and of adults undergoing Roux-en-Y gastric bypass, in the Adolescent Morbid Obesity Surgery

80 pic Roux-en-Y gastric bypass, open Roux-en-Y gastric bypass, laparoscopic gastric band placement, or

81 ity and who underwent laparoscopic Roux-en-Y gastric bypass, open Roux-en-Y gastric bypass, laparosco

82 years, changes from baseline observed in the gastric-bypass and sleeve-gastrectomy groups were superi

83 t to body weight (-23%, -19%, and -5% in the gastric-bypass, sleeve-gastrectomy, and medical-therapy

84 and 49% vs 46% in Scotland, respectively) or gastric cancer (58% vs 57% in England and 59% vs 55% in

85 proliferation and apoptosis-related genes in gastric cancer (GC) and adjacent mucosa with atrophic ga

86 Gastric cancer (GC) has a poor prognosis with wide varia

87 sis of some cancers, but the role of FPR2 in gastric cancer (GC) has not yet been elucidated.

88 The molecular mechanism underlying gastric cancer (GC) invasion and metastasis is still poo

89 onstrate that the invasion and metastasis of gastric cancer (GC) is closely associated with a multi-s

90 Gastric cancer (GC) is the second leading cause of cance

91 the gastric mucosa associated with increased gastric cancer (GC) risk.

92 ons, it is currently unknown for its role in gastric cancer (GC).

93 led adjusted HR, 1.03; 95% CI, 0.85-1.25) or gastric cancer (pooled adjusted HR, 1.06; 95% CI, 0.85-1

94 reviously treated for HER2-positive advanced gastric cancer (unresectable, locally advanced, or metas

95 Helicobacter pylori, the causative agent of gastric cancer and duodenal and gastric ulcers, was earl

96 We observe that Claudin-4 is up-regulated in gastric cancer and is associated with poor prognosis.

97 se of the high risk of invasive diffuse-type gastric cancer and lack of reliable surveillance options

98 Eligible patients had HER2-positive advanced gastric cancer and progressed during or after first-line

99 stablished therapeutic targets in breast and gastric cancer but agents targeting Her2 have not yet de

100 discovered in primary leukemia/lymphoma and gastric cancer by human cancer genome sequencing efforts

101 By continuously exposing the gastric cancer cell line MKN45 to 5-FU for >100 passages

102 e metastatic models using the SGC-7901/sFRP1 gastric cancer cell line.

103 CR2 were highly expressed in a high invasive gastric cancer cell model and in gastric cancer tissues.

104 ong anti-proliferative activity on other two gastric cancer cells (HGC27 and SGC7901), but less cytot

105 dy demonstrates that sFRP1 overexpression in gastric cancer cells leads to increased cell proliferati

106 S17 potently killed gastric cancer cells with causing modulation of Bcl-2 fa

107 tively regulated by prolyl isomerase PIN1 in gastric cancer cells.

108 ay suppress disease relapse after 5-FU-based gastric cancer chemotherapy.

109 sive generations should be weighed in future gastric cancer control programs.

110 A prospective gastric cancer database identified 41 patients with CDH1

111 viduals might affect disease progression and gastric cancer development.

112 and determine the overall incidence rate of gastric cancer for patients with these premalignant lesi

113 r more foci of intramucosal signet ring cell gastric cancer in the examined specimen.

114 e the roles of CXCR4 and CXCR2 signalings in gastric cancer metastasis.

115 XCR4 and CXCR2 is more effective in reducing gastric cancer metastasis.

116 This feedforward ACh-NGF axis activates the gastric cancer niche and offers a compelling target for

117 Similar experiments performed in 4 different gastric cancer patient-derived xenograft models showed l

118 terminal loop of pri-mir-30c-1 in breast and gastric cancer patients had been previously described to

119 GA) and intestinal metaplasia (IM) influence gastric cancer risk.

120 ective analysis of a prospectively collected gastric cancer surgery database at a single National Can

121 gh invasive gastric cancer cell model and in gastric cancer tissues.

122 ffect of MMRD and MSI in curatively resected gastric cancer treated with perioperative chemotherapy i

123 e the authors reveal a regulatory network in gastric cancer whereby claudin-4 expression is reduced b

124 So far, stomach-specific biomarkers, gastric cancer(GC)-related environmental factors, and ca

125 sophageal adenocarcinoma, erosive gastritis, gastric cancer, diarrhea, colonic diverticular disease,

126 ith esophageal cancer and 3833 patients with gastric cancer, including 3240 and 2392 cancer-specific

127 nresectable, locally advanced, or metastatic gastric cancer, including adenocarcinoma of the gastro-o

128 rst-line treatment of HER2-positive advanced gastric cancer, there is no established therapy in the s

129 nvestigation for prevention and treatment of gastric cancer.

130 One example is Helicobacter pylori and gastric cancer.

131 as associated with an improved prognostic in gastric cancer.

132 assay could improve diagnostic accuracy for gastric cancer.

133 ng, esophageal, and hepato-pancreato-biliary/gastric cancer.

134 nd worse outcomes in people with lung and/or gastric cancer.

135 patients responding to treatment in advanced gastric cancer.

136 ontributed to EMT, migration and invasion of gastric cancer.

137 e population of Asian patients with advanced gastric cancer.

138 n promise in treating ulcerative colitis and gastric cancer.

139 tional; however, these models rarely develop gastric cancer.

140 e discover a network regulating Claudin-4 in gastric cancer.

141 r consumption and the risk of esophageal and gastric cancers and their different subtypes.In this stu

142 strated in bladder, liver, lung, breast, and gastric cancers.

143 h carcinogenesis including breast, renal and gastric cancers.

144 effect of nut consumption on esophageal and gastric cancers.The objective was to evaluate the associ

145 e mechanisms by which H pylori might promote gastric carcinogenesis (persisting despite constant infl

146 comparison of SBA with colorectal cancer and gastric carcinoma.

147 , B16F10 melanoma, WT-GBM glioma and MKN45-P gastric carcinoma.

148 kes of nuts or peanut butter and the risk of gastric cardia adenocarcinoma, esophageal adenocarcinoma

149 esiding for prolonged periods of time in the gastric cavity have transformed our ability to diagnose

150 injections of 5-fluorouracil, which blocked gastric cell proliferation, plus tamoxifen to induce SPE

151 gene expression patterns among primary human gastric cells, uninfected or infected with H pylori P12

152 transferase (encoded by cgt) is required for gastric colonization and T-cell activation.

153 ium sources were almost fully soluble in the gastric compartment, and then became insoluble in the in

154 he irreversible inactivated myrosinase under gastric conditions caused no further GR hydrolysis.

155 rose esters induced an unstable system after gastric conditions leading to coalesced oil droplets, wh

156 stabilized by proteins coalesced under human gastric conditions.

157 utive patients undergoing esophagectomy with gastric conduit reconstruction were studied preoperative

158 For any given gastric content volume, self-reported postprandial fulln

159 columnar metaplasia of the lower esophagus, gastric corpus and antrum.

160 Lineage tracing experiments of the gastric corpus in mice have not established whether SPEM

161 was observed for most of the products after gastric digestion (maximum registered for sweet biscuits

162 e the impact of human milk pasteurization on gastric digestion (particularly for proteins and lipids)

163 e second aim was to investigate the in vitro gastric digestion behavior of whey and casein proteins i

164 higher enzyme concentrations of young child gastric digestion conditions compared to infant conditio

165 ons greatly affected the antioxidants, while gastric digestion led to slight additional losses.

166 Overall, pasteurization had no impact on the gastric digestion of lipids and some proteins from human

167 ree objectives were addressed: the impact of gastric digestion on acrylamide content of French Fries,

168 (var. Granny Smith) behavior during in vitro gastric digestion was investigated.

169 ral changes of protein gels during simulated gastric digestion.

170 ly hydrophilic molecules were solubilised by gastric digestion.

171 uence of processing on apple behavior during gastric digestion.

172 ples, this approach was used during in vitro gastric digestions of a model of complex food containing

173 lithium chloride (LiCl), a salt that creates gastric discomfort, and lipopolysaccharide (LPS), a bact

174 nd gastric ulcers, was early associated with gastric disease, but it has also been proposed that the

175 Despite the global prevalence of gastric disease, there are few adequate models in which

176 ntributes to H. pylori persistence and overt gastric disease.

177 The expression of CDX2 and TCTP in gastric diseases was measured by immunohistochemistry.

178 ake and attenuates the hypophagic effects of gastric distension.

179 ance of CagA and CagA-signaling molecules in gastric DLBCL remains unexplored.

180 n 63 patients with stage IE/IIE1 HP-positive gastric DLBCL who received HPE as frontline treatment.

181 can be detected in the malignant B cells of gastric DLBCL, and the expression of these molecules is

182 on of SOX6 to be required for development of gastric dopamine neurons.

183 Pasteurization did not affect gastric emptying ( approximately 30-min half time) or pH

184 er 180 min, appetite (visual analog scales), gastric emptying (3-dimensional ultrasonography), and bl

185 n gastric emptying of solids; measurement of gastric emptying (eg, at 5 weeks of treatment) may be a

186 n, whey-protein drinks load-dependently slow gastric emptying and alter gut hormone secretion compare

187 Delayed gastric emptying and bile reflux are common concerns in

188 AN have slower gastric emptying and heightened visceral perception comp

189 A relationship between body weight and gastric emptying as well as self-reported feelings of sa

190 l (180-210 min; energy intake, appetite, and gastric emptying in the men have been published previous

191 While gastric emptying is probably the most significant compon

192 Delayed gastric emptying occurs in critically ill patients and i

193 Compared with placebo, liraglutide delayed gastric emptying of solids at 5 weeks (median 70 min [IQ

194 on weight loss are associated with delay in gastric emptying of solids; measurement of gastric empty

195 intragastric meal distribution (IMD) during gastric emptying scintigraphy (GES) allows for a simple

196 Gastric emptying, antral contractions and oro-cecal tran

197 asting, and to search for a correlation with gastric emptying.

198 elate symptoms of gastroparesis with IMD and gastric emptying.

199 The highly acidic gastric environment creates a physiological barrier for

200 This study describes a large animal model of gastric eosinophil in peanut-sensitized piglets.

201 PE orally for 10 days, a sequence leading to gastric eosinophilia assessed by endoscopy.

202 n on the DNA damage response sensor, ATM, in gastric epithelial cells and in biopsy specimens from pa

203 We investigated how cgt affects gastric epithelial cells and the host immune response.

204 901), but less cytotoxicity to non-malignant gastric epithelial cells GES1.

205 By in vitro infection of gastric epithelial cells with wild-type and VacA-deficie

206 Gastric epithelial hyper-proliferation was reported in p

207 ssion, and in turn NGF overexpression within gastric epithelium expanded enteric nerves and promoted

208 Cholinergic stimulation of the gastric epithelium induced nerve growth factor (NGF) exp

209 ss the neural activity to detect hypoxic and gastric extension events from the glossopharyngeal and v

210 ely colonizing the mesogleal axis inside the gastric filaments.

211 ange significantly following HP eradication, Gastric findings on VCE were not impacted by HP eradicat

212 0.7%) and inhibited BSA release in simulated gastric fluid (SGF) to a greater extent.

213 DNA release profiles in simulated gastric fluid (SGF) were improved compared to un-encapsu

214 lease of protein from the beads in simulated gastric fluid (SGF, pH 3) and simulated intestinal fluid

215 showed slow release of lycopene in simulated gastric fluid at acidic pH and faster release in simulat

216 through efficient chemical propulsion in the gastric fluid by rapidly depleting the localized protons

217 nt stability and digestibility properties in gastric fluid due to their structural differences which

218 not released (<3.5% during 6h) in simulated gastric fluids (pH 1.2 and 4); while, a sustained releas

219 raditionally used as a mild agent to support gastric function and to stimulate the stomach's proteoly

220 esigned to assess modified retro colic retro gastric gastrojejunostomy in reducing macro and microsco

221 rrhage (eight [4%]), pneumonia (seven [3%]), gastric haemorrhage (six [3%]), and gastrointestinal hae

222 Gastric half-emptying time (t50) was slower in AN than H

223 ale Lepr(db/db) mice, GE was accelerated and gastric ICC and phasic cholinergic responses were increa

224 Patient with gastric IM change may have a higher GU healing rate than

225 a higher GU healing rate than those without gastric IM.

226 We found that recurrent nonlethal gastric infections of Gram-negative Salmonella enterica

227 Coro1A(-/-) mice, resulting in an attenuated gastric inflammation.

228 apy in the Medical Research Council Adjuvant Gastric Infusional Chemotherapy (MAGIC) trial.

229 e, glucagon, glucagon-like peptides 1 and 2, gastric inhibitory peptide, acetaminophen, and 3-O-methy

230 gut hormones including GLP-1, glucagon, and gastric inhibitory peptide.

231 associated with lower fasting and stimulated gastric inhibitory polypeptide (GIP) levels.

232 ), and the target of clinical investigation, gastric inhibitory polypeptide (GIP), as proof-of-princi

233 insulin, glucagon, ghrelin, cholecystokinin, gastric inhibitory polypeptide (GIP), glucagon-like pept

234 near transcription factor 7-like 2 (TCF7L2), gastric inhibitory polypeptide receptor (GIPR), caveolin

235 controlled carbohydrate release to simulated gastric, intestinal and colonic fluids, and thus largely

236 ted oxidation by Rancimat, and simulation of gastric/intestinal release.

237 sample negative had MABSC isolated in their gastric juice or PEG tube.

238 rees C) sequentially with artificial saliva, gastric juice, and intestinal juice while continuously m

239 F4/80(hi)CD64(+)CX3CR1(+) macrophages in the gastric lamina propria.

240 tumors, K-Ras(G12V) induced lung tumors and gastric lesions.

241 lineages: albumin (ALB) in liver carcinoma, gastric lipase (LIPF) in stomach carcinoma, and thyroglo

242 c proton pump H(+),K(+)-ATPase acidifies the gastric lumen, and thus its inhibitors, including the im

243 pecies may represent a novel animal model of gastric lymphomagenesis.

244 d with chronic gastritis, peptic disease and gastric malignancies.

245 hows that metatranscriptomic analysis of the gastric microbiota is feasible and can provide new insig

246 ter pylori, the dominant member of the human gastric microbiota, elicits immunoregulatory responses i

247 ths (CV = 0.4) and branching patterns in the Gastric Mill (GM) neuron, an identified neuron type with

248 urface of peritoneal carcinoma cell lines of gastric (MKN-45P), ovarian (SKOV-3), and colon (CT-26) o

249 ring GES can yield additional information on gastric motility to help explain patients' symptoms.

250 red effects of liraglutide versus placebo on gastric motor functions, satiation, satiety, and weight

251 s of virus-like particles (VLPs) against pig gastric mucin (PGM) using 4 VLPs that represent differen

252 in control biopsy samples of non-transformed gastric mucosa (Control).

253 sia (IM) is a pre-malignant condition of the gastric mucosa associated with increased gastric cancer

254 < .01, respectively, active vs placebo) and gastric mucosa eosinophils counts (239 eosinophils/mm(2)

255 onse, Helicobacter pylori can persist in the gastric mucosa for decades.

256 ted to the severity of inflammation in human gastric mucosa in either a synchronous or metachronous m

257 e infection model, PMN infiltration into the gastric mucosa is dramatically reduced in Coro1A(-/-) mi

258 transcriptase PCR in infected and uninfected gastric mucosa obtained from Bhutan and from the Dominic

259 ith Helicobacter pylori (H. pylori)-infected gastric mucosa with intestinal metaplasia (IM) changes.

260 in sources of acetylcholine (ACh) within the gastric mucosa.

261 e strong acidic/enzymatic environment of the gastric mucosa.

262 Active EPIT significantly reduced gastric mucosal lesions induced by PPE oral intake (macr

263 ly coupled to smooth muscle cells within the gastric musculature.

264 and induce carcinogenic consequences in the gastric niche.

265 sumption (C3) had a lower risk of developing gastric noncardia adenocarcinoma [C3 compared with C0, H

266 n were inversely associated with the risk of gastric noncardia adenocarcinoma.

267 unresectable locally advanced or metastatic gastric or gastro-oesophageal junction adenocarcinoma, a

268 ability in patients with advanced breast and gastric or gastro-oesophageal tumours.

269 Purpose After curative resection of gastric or gastroesophageal junction adenocarcinoma, Int

270 Conclusion After a curative resection of gastric or gastroesophageal junction adenocarcinoma, pos

271 deficiency, resulting from a failure of the gastric or ileal phase of physiological B12 absorption,

272 ed human pluripotent stem cells (hPSCs) into gastric organoids containing fundic epithelium by first

273 tivation of E-cadherin (Cdh1) and p53 in the gastric parietal cell lineage.

274 in H. pylori-host interaction with links on gastric pathogenesis.

275 first time that arginase of all Helicobacter gastric pathogens utilizes a unique non-catalytic triad

276 xclusively in arginase of other Helicobacter gastric pathogens, which may have similar function.

277 esidues in the homolog of other Helicobacter gastric pathogens.

278 nzymes and bile salts, as well as the higher gastric pH in the infant model.

279 he others because the caseins clotted at the gastric pH.

280 Bioavailable phenolics after the gastric-phase, intestinal-phase and in dialysable fracti

281 rinegic signaling is important in regulating gastric physiological functions, it is currently unknown

282 uman fundus and the molecular bases of human gastric physiology and pathophysiology, and also represe

283 In comparison, gastric Pi loading elicited similar but delayed phosphat

284 Intravenous but not gastric Pi loading in parathyroidectomized rats also led

285 Gastric premalignant conditions, atrophic gastritis (AG)

286 The gastric proton pump H(+),K(+)-ATPase acidifies the gastr

287 There was no association between type of gastric resection (ie, anatomic v partial/wedge) and EFS

288 In histologic analyses of gastric resection specimens from 10 patients with adenoc

289 and fed patients or between the high and low gastric residual volume groups.

290 erefore identified for the first time from a gastric sample in a minority of patients.

291 s), nausea (8%), ascites (3%), fatigue (3%), gastric stenosis (3%), hepatic failure (3%), liver absce

292 Gastric stump carcinoma is an exceptional and poorly kno

293 pulations according to the 5-FU dose, and in gastric submucosal orthotopic xenografts of MKN45/5FU ce

294 h bethanechol caused relaxation of wild type gastric tissues and these were inhibited by the nitric o

295 In WT-infected mice, infiltrates in gastric tissues were predominantly composed of T cells,

296 Stimulation of the SNpc increased gastric tone and motility via activation of dopamine 1 r

297 Gastric tone and motility were recorded after N-methyl-d

298 t ginger constituents ameliorate ASA-induced gastric ulceration.

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

300 llness, satiety, or fasting and postprandial gastric volumes at week 16.