ライフサイエンスコーパス: gastric

1 A total of 7934 gastric, 15,908 pancreatic, and 21,354 rectal cancer pat

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

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

4 metric analysis of circulating MDSCs from 20 gastric adenocarcinoma (GAC) patients found that >=80% A

5 he primary outcome was a diagnosis of distal gastric adenocarcinoma 30 days or more after detection o

6 2011 through 2015 to estimate incidences of gastric adenocarcinoma in specific anatomic sites for no

7 lack of precise, contemporary information on gastric adenocarcinoma incidence in specific anatomic si

8 a decision analysis, screening for noncardia gastric adenocarcinoma might be cost-effective for non-W

9 ag PAI) are associated with a higher risk of gastric adenocarcinoma or peptic ulcer disease than cag

10 ts 50 years and older, the risk of noncardia gastric adenocarcinoma was 1.8-fold (95% CI, 1.37-2.31)

11 l and ethnic differences in the incidence of gastric adenocarcinoma worldwide and in the US.

12 One of these deaths was due to gastric adenocarcinoma, which was assessed by the invest

13 ng to disease progression that may result in gastric adenocarcinoma.

14 develop targeted risk reduction programs for gastric adenocarcinoma.

15 en, had a significantly lower risk of cardia gastric adenocarcinoma.

16 ncidence of and risk factors for nonproximal gastric adenocarcinomas after detection of H pylori.

17 ple esophagogastroduodenoscopies with normal gastric and duodenal biopsies findings and a normal colo

18 case of OLE-MD, OE was partially degraded in gastric and intestinal conditions; whereas in OLE-IN, OE

19 at designated timepoints throughout in vitro gastric and intestinal digestion for differences in pept

20 Regardless of species, in vitro gastric and intestinal digestion released a higher conce

21 of both compounds was evaluated by studying gastric and intestinal digestion.

22 ocolate through in vitro simulation of oral, gastric and intestinal digestions.

23 ulation might be induced by a combination of gastric and intestinal effectors and (ii) chlamydial col

24 f the two in vitro protocols at the level of gastric and intestinal endpoints.

25 o release of phenolic compounds in simulated gastric and intestinal mediums were 96.02 +/- 0.96% and

26 e strong interactions between vancomycin and gastric and intestinal mucins, resulting in very large a

27 ons increased in oral phase and decreased in gastric and intestinal phases.

28 cacy of these ADCs were further evaluated in gastric and lung cancer xenograft models in mice.

29 a common but underdiagnosed complication of gastric and oesophageal surgery.

30 s, compared with normal tissues (esophageal, gastric, and duodenum; controls) from the same patients

31 ve types of pain and discomfort (esophageal, gastric, and rectal distension, cutaneous thermal stimul

32 ct of increased ST6Gal-I, we generated human gastric antral organoids from epithelial stem cells and

33 We show that a +4 stem cell (SC) in the gastric antrum, marked by expression of Cck2r (a GPCR) a

34 catheter bariatric embolotherapy of the left gastric artery is well-tolerated and promotes clinically

35 ght in Severe Obesity by Embolization of the Gastric Artery Trial [LOSEIT]; NCT03185949).

36 1:1 to either sham or TBE targeting the left gastric artery using an occlusion balloon microcatheter

37 er bariatric embolotherapy (TBE) of the left gastric artery, has been reported to promote weight loss

38 We tested patient sera, stool, and gastric aspirates using mouse bioassay for BoNT and/or c

39 uggestion of an additive interaction between gastric atrophy and poor oral health was observed (relat

40 We aimed to test whether gastric atrophy and, further, its interaction with poor

41 Previous findings concerning gastric atrophy as a potential risk factor for esophagea

42 To investigate whether gastric BA changes were regulated by hepatic BA synthesi

43 ence interval (CI) 0.86-0.99) and adjustable gastric band (AGB; 33.6%; RR 0.45, CI 0.34-0.60; p < 0.0

44 e gastrectomy, and 50% of patients following gastric banding (P=0.004).

45 n intrajejunal inoculation that bypasses the gastric barrier, plasmid-deficient Chlamydia produced in

46 The study included 428 gastric biopsies form dyspeptic patients, who did not re

47 We obtained gastric biopsies from 30 patients in Australia.

48 Gastric biopsies of 814 H. pylori infected patients naiv

49 Multiple gastric biopsies showed a small-sized lymphoid infiltrat

50 sceptibility test results from pre-treatment gastric biopsies was a pre-condition for matching 52 aiH

51 be applied on regular whole slide images of gastric biopsies.

52 receptor gamma rearrangement present in the gastric biopsies.

53 ith symptoms of gastritis, routinely undergo gastric biopsies.

54 Gastric biopsy samples taken at baseline and 3, 6, 12, 1

55 Using cultured cell lines, gastric biopsy specimens, primary cells, and human enter

56 Danish patients undergoing laparoscopic gastric bypass (BMI >35-50) from January 1, 2005 to Dece

57 Roux-en-Y gastric bypass (RYGB) was associated with a higher rate

58 ore for internal hernia (IH) after Roux-en-Y gastric bypass (RYGB).

59 he beneficial effect of bariatric (Roux-en-Y gastric bypass [RYGB]) surgery on insulin resistance.

60 lusively open operations in 1993 (n = 8,631; gastric bypass and vertical banded gastroplasty, 49% eac

61 rior studies comparing sleeve gastrectomy to gastric bypass are limited by low sample size (in random

62 nificantly higher in the first 5 years after gastric bypass compared with a matched nonsurgical refer

63 ty Surgery Registry, 509 patients (Roux-en-Y gastric bypass n=465; sleeve gastrectomy n=44) could be

64 e, and any type of cardiovascular event than gastric bypass patients.

65 years, operated with a primary laparoscopic gastric bypass procedure from 2010 until 2015 were ident

66 atients who underwent laparoscopic Roux-en-Y gastric bypass procedure, in which comprehensive video d

67 all bowel obstruction after the laparoscopic gastric bypass procedure.

68 d without T2D (n = 9) subjected to Roux-en-Y gastric bypass surgery (RYGB).

69 d type 2 diabetes, the metabolic benefits of gastric bypass surgery and diet were similar and were ap

70 morbidly obese subjects undergoing Roux-en-Y gastric bypass surgery compared to lean controls undergo

71 ppear to be the greatest in those undergoing gastric bypass surgery.

72 eve gastrectomy (VSG) has recently surpassed gastric bypass to become the most popular surgical inter

73 gastrectomy had a superior safety profile to gastric bypass up to 2 years from surgery, even when acc

74 162,969; 69.8% sleeve gastrectomy and 27.8% gastric bypass) in 2016.

75 F type occurred in 71% of patients following gastric bypass, 56% of patients who underwent sleeve gas

76 al patients (cholecystectomy, hernia repair, gastric bypass, and hysterectomy) who developed perioper

77 Compared to gastric bypass, other types of bariatric surgery had low

78 ageal squamous cell carcinoma (n = 267), and gastric cancer (cardia: n = 603; noncardia: n = 631) amo

79 otein on cancer cells are found in 10-26% of gastric cancer (GC) and esophagogastric junction cancer

80 Targeted treatments for advanced gastric cancer (GC) are needed, particularly for HER2-ne

81 anisms of UHMK1 in the pathogenesis of human gastric cancer (GC) are unclear.

82 Gastric cancer (GC) is a world health problem and it is

83 Gastric cancer (GC) is the third leading cause of cancer

84 Gastric cancer (GC) patients with metastasis had limited

85 signaling pathway is critically involved in gastric cancer (GC) progression.

86 rett's oesophagus (n=4) or stage I oesophago-gastric cancer (n=5) in the intervention group, whereas

87 eradication after treatment reduced risk of gastric cancer (SHR, 0.24; 95% CI, 0.15-0.41; P < .001).

88 ori infection still had an increased risk of gastric cancer (SHR, 1.16; 95% CI, 0.74-1.83; P = .51) b

89 Han Chinese individuals, of whom 10 254 had gastric cancer and 10 914 geographically matched control

90 as 2 L chemotherapy for advanced/metastatic gastric cancer and a third received doublets.

91 aimed to establish a genetic risk model for gastric cancer and assess the benefits of adhering to a

92 Family history of gastric cancer and Helicobacter pylori treatment.

93 c/Latino patients have a higher incidence of gastric cancer and worse cancer-related outcomes compare

94 The relative and absolute risk of incident gastric cancer associated with healthy lifestyle factors

95 ecognition of a potential hereditary diffuse gastric cancer can provide a substantial health benefit

96 that accounts for approximately 1-3% of all gastric cancer cases.

97 as investigated using exosomes isolated from gastric cancer cell lines MKN-28, MKN-45, and SGC-7901.

98 exposed to exosomes isolated from all three gastric cancer cell lines when the mice were injected wi

99 The drug sensitivity of human BGC823 gastric cancer cells toward different drugs, paclitaxel

100 l, this study provides new insights into how gastric cancer derived exosomes modulate the immune resp

101 ontribution of pyloric LGR5(+) stem cells to gastric cancer following dysregulation of the WNT pathwa

102 L) chemotherapies for advanced or metastatic gastric cancer have shown improved survival but there is

103 Gastric cancer in Hispanic/Latino patients has unique ge

104 ation of the WNT pathway-a frequent event in gastric cancer in humans(3)-is unknown.

105 tion, we found significantly higher risks of gastric cancer in racial and ethnic minorities and smoke

106 the association between genetic variants and gastric cancer in six independent genome-wide associatio

107 as to identify the best strategies to combat gastric cancer in the AN population through prevention a

108 l leaders together to evaluate issues around gastric cancer in the AN population.

109 ies (p(trend)<0.0001), with a higher risk of gastric cancer in those with an unfavourable lifestyle t

110 There was a uniform decrease in gastric cancer incidence, but an increasing incidence of

111 Targeted therapies licensed to treat gastric cancer include trastuzumab (HER2-positive patien

112 Hereditary diffuse gastric cancer is a rare condition that accounts for app

113 Gastric cancer is associated with chronic inflammation (

114 Gastric cancer is the fifth most common cancer and the t

115 Advanced gastric cancer is treated with sequential lines of chemo

116 Non-early operable gastric cancer is treated with surgery, which should inc

117 ing homeostatic epithelial cell apoptosis in gastric cancer pathogenesis, suggesting a mechanism for

118 and function of the Cag T4SS and its role in gastric cancer pathogenesis.

119 with poor overall survival (OS) for lung and gastric cancer patients and hence led to the conclusion

120 sociated with improved long-term survival in gastric cancer patients and merits further focus in surg

121 Hispanic/Latino patients with gastric cancer possess unique genomic landscapes, includ

122 tformin increases acid secretion and reduces gastric cancer risk in humans.

123 strectomy remains the recommended option for gastric cancer risk management in pathogenic CDH1 varian

124 lifestyle factors have been associated with gastric cancer risk, but the extent to which an increase

125 ersely, epithelial monolayers generated from gastric cancer stem cells retained high levels of ST6Gal

126 ar increase in the relative risk of incident gastric cancer was observed across the lifestyle categor

127 GI cancers combined, esophageal cancer, and gastric cancer were lower when biomass was burned using

128 ataset of lung cancer and another dataset of gastric cancer with FSSEM inferred differential GRNs in

129 ource for deciphering the early formation of gastric cancer, and for isolating and characterizing hum

130 regulated in several malignancies, including gastric cancer, and is an important biomarker in drug di

131 APC mutations in colorectal cancer, KRAS in gastric cancer, and pancreatic cancer were mostly associ

132 In one gastric cancer, both aneuploid and euploid cells contain

133 of signal transduction pathway mutations in gastric cancer, liver cancer, colorectal cancer, and pan

134 the main risk factor for the development of gastric cancer, the third leading cause of cancer death

135 al in patients with HER2-positive metastatic gastric cancer.

136 gnostic marker for the detection of lung and gastric cancer.

137 H. pylori is the main risk factor for distal gastric cancer.

138 a patient diagnosed with hereditary diffuse gastric cancer.

139 most important of them i.e. peptic ulcer and gastric cancer.

140 substantially reduce their risk of incident gastric cancer.

141 perative treatment in patients with operable gastric cancer.

142 d cancers, such as nasopharyngeal cancer and gastric cancer.

143 on of H. pylori-infected individuals develop gastric cancer.

144 ered as one of the principal risk factors of gastric cancer.

145 bacter pylori eradication therapy to prevent gastric cancer: systematic review and meta-analysis.

146 study, EBV-infected cell lines derived from gastric cancers and Burkitt lymphomas were incubated wit

147 onstitutive pS-STAT3 in Helicobacter-induced gastric carcinogenesis.

148 an important role in inflammation-associated gastric carcinogenesis.

149 receiving the diagnosis of undifferentiated gastric carcinoma from the biopsy taken from the ulcerat

150 EtHOBA inhibited gastric carcinoma in infected INS-GAS mice and gerbils a

151 tyrosine kinase inhibitor pazopanib in MKN45 gastric carcinoma xenografts and the combination of tubu

152 rointestinal (GI)-related cancers, including gastric carcinoma.

153 TICE ADVICE 11: Intestinal metaplasia of the gastric cardia (without residual columnar epithelium in

154 f NF-kappaB and regulates differentiation of gastric cardia progenitor cells in a mouse model of BE.

155 arcated by the top of the gastric folds (ie, gastric cardia) using focal ablation in a circumferentia

156 us mucosal and retroflexed inspection of the gastric cardia.

157 ma eotaxin-3 levels strongly associated with gastric CCL26 expression (r = 0.81, P < .0001).

158 ce and immunohistochemical analyses to study gastric cell proliferation, differentiation, and turnove

159 Deletion of Trp53 in gastric cells confers a selective advantage and promotes

160 nt in causing vacuolation of HeLa cells, AGS gastric cells, and AZ-521 duodenal cells and had reduced

161 trointestinal cancers, including esophageal, gastric, colorectal, and pancreatic cancers.

162 ns; whereas in OLE-IN, OE was released under gastric conditions and partially degraded under intestin

163 ents and that they are resistant to oral and gastric conditions that were tested in vitro.

164 olecular lipolysis mechanisms under in vitro gastric conditions.

165 Gastric conjugated BAs could become a panel of biomarker

166 and extent of betacyanin degradation in the gastric content, as well as the intensity of absorption,

167 the profile and level of betacyanins in the gastric content, blood (portal and main veins) and urine

168 ngle-cell RNA-sequencing (scRNA-seq) data of gastric corpus epithelium to define transcriptomes of in

169 Gkn3 mRNA was undetectable in healthy gastric corpus; its expression in chronically inflamed s

170 The rate of gastric degree of hydrolysis of gliadin was greater (P <

171 The gastric degree of hydrolysis of gluten proteins was infl

172 of beta-lactoglobulin increase in particular gastric digestibility and the translocation efficiency a

173 lease of trans-Res from GSP was ~ 45% during gastric digestion and the total release in the intestina

174 While gastric digestion did not promote the release of insolub

175 a model that illustrate the significance of gastric digestion in influencing the release of curcumin

176 aper we report the importance of swelling on gastric digestion of protein gels, which is rarely recog

177 ere increased significantly (p < 0.05) after gastric digestion regardless of the treatment.

178 olid coagula that were persistent throughout gastric digestion, which caused a delay in nutrient empt

179 ples were digested within the early phase of gastric digestion.

180 exotoxin that is epidemiologically linked to gastric disease in humans.

181 inking (fully recapitulating the symptoms of gastric distension) in part via signalling to the parave

182 sgust to habituation, putatively by reducing gastric dysrhythmias during incentivized engagement with

183 rical rhythms in the stomach,(9-13) inducing gastric dysrhythmias that correlate with neural signatur

184 etic, at a dose (10 mg) that acts to convert gastric dysrhythmias to normal rhythms.(9) In a preregis

185 have been conflicting results from trials of gastric electrical stimulation (GES) for treatment of re

186 emorrhage (9.1% vs 5.1%, P = 0.352), delayed gastric emptying (21.2% vs 22.4%, P = 0.930), bile leaka

187 operative pancreatic fistula (POPF), delayed gastric emptying (DGE), postpancreatectomy hemorrhage (P

188 volume was linearly correlated to increased gastric emptying rate as well as increased GLP-1 respons

189 dard (99m)Tc-sulfur colloid ((99m)Tc-SC) for gastric emptying scintigraphy (GES).

190 odified oral glucose tolerance test, but not gastric emptying testing, is useful for diagnosis.

191 Gastric emptying was not accelerated during the ON perio

192 equency, impaired glucose tolerance, delayed gastric emptying, and increased body weight compared to

193 Gastroparesis, a condition of abnormal gastric emptying, is most commonly observed in diabetic

194 functions, which include insulin secretion, gastric emptying, satiety, and the hedonic aspects of fo

195 eurons are reflected functionally in delayed gastric emptying, slowed colonic motility, and prolonged

196 ater-only gastric emptying, water-with-solid gastric emptying, small-bowel transit, and colonic trans

197 obtained for esophageal transit, water-only gastric emptying, water-with-solid gastric emptying, sma

198 effect on postprandial glucose, insulin, and gastric emptying.

199 tiatives should in addition focus on delayed gastric emptying.

200 is a clinicopathologic disorder with marked gastric eosinophilia and clinical symptoms.

201 n vitro studies indicate that VacA modulates gastric epithelial and immune cells, but the in vivo con

202 We show increased isoLG adducts in gastric epithelial cell nuclei in patients with gastriti

203 described bacterial oncoprotein, CagA causes gastric epithelial cell transformation by promoting an e

204 to H. pylori's ability to delay apoptosis in gastric epithelial cells by actively driving the degrada

205 ression levels of ST6GAL-I and SOX9 in human gastric epithelial cells correlated positively with one

206 dings suggest that promoting the survival of gastric epithelial cells has implications not only for H

207 The effect of EtHOBA on mutations in gastric epithelial cells of H pylori-infected INS-GAS mi

208 wever, its role has not been investigated in gastric epithelial cells or gastric tumorigenesis.

209 Exposure of gastric epithelial cells to the bacterial carcinogen Hel

210 ll as nonprotein bacterial constituents into gastric epithelial cells.

211 Gastric epithelial stem cells strongly expressed ST6Gal-

212 as used to predict differentiation of normal gastric epithelium to metaplastic epithelium in chronica

213 w cytokines made by T lymphocytes impact the gastric epithelium, especially during Helicobacter pylor

214 proteins were rapidly digested in simulated gastric fluid and their enzymatic activity was inhibited

215 ted a promising stability in both plasma and gastric fluid.

216 al junction, as demarcated by the top of the gastric folds (ie, gastric cardia) using focal ablation

217 petite-stimulating hormone secreted from the gastric fundus.

218 ymogenic) chief cells (ZCs) in the mammalian gastric gland base are believed to arise from descending

219 % confidence interval (CI): 1.02, 3.50], and gastric HR: 1.83; 95% CI: 1.01, 3.31) cancers, whereas u

220 on with H felis, Nlrc5(mo-KO) mice developed gastric hyperplasia (P < .0001), splenomegaly (P < .0001

221 Gastric hyperplastic polyps (GHPs) have a potential risk

222 ndicates that persistent Helicobacter pylori gastric infection influences immune responses to oral en

223 e histopathology of HP group showed moderate gastric inflammation and many HP colonization.

224 aged with H pylori (PMSS1) to induce chronic gastric injury.

225 cile inoculum, and pre-exposure to simulated gastric intestinal fluid (SGF) and simulated intestinal

226 In this study, gastric juice was collected from patients clinically dia

227 read khambir is nutritious and can alleviate gastric lesions related to acute mountain sickness.

228 Macroscopic disease: Gastric lesions were multiple: 38%, single: 62%, submuco

229 ximately four-fold enhanced retention in the gastric lining compared to monocompartment motors, while

230 Furthermore, a mechanistic gastric lipolysis model was established based on a react

231 t only from PDAC, but also bladder, ovarian, gastric, lung, and basal-like breast cancers.

232 tions between group 2 innate lymphocytes and gastric microbes that enhance IgA production.

233 ro-intestinal digestion using a semi-dynamic gastric model, a static intestinal model and an ex vivo

234 s resulted in a profound insight in in vitro gastric molecular lipolysis mechanisms.

235 duced gastric retention in an acute model of gastric motility that traces the passage of a food bolus

236 ac, considering the pH gradient found in the gastric mucosa (3 < pH < 7.4).

237 Once the micromotor penetrates the gastric mucosa (pH >= 6.0), its pH-responsive cap dissol

238 H. pylori colonizes the human gastric mucosa and persists for decades.

239 ic the protective phospholipid layers of the gastric mucosa and to describe the interactions with dic

240 s in close proximity to S-phase cells in the gastric mucosa of gastritis patients.

241 In the gastric mucosa of mice and patients with gastritis, pS-S

242 The IF pattern was composed of liver and gastric mucosa staining on rat kidney/liver/stomach sect

243 iferative potential of infected Stat3(SA/SA) gastric mucosa.

244 or the protective phospholipid layers of the gastric mucosa.

245 Stomach weight and gastric mucosal thickness were also reduced in infected

246 tility in the management and surveillance of gastric NET disease.

247 y assessed utility of the NETest to diagnose gastric neuroendocrine neoplasms (GNENs) and identify mi

248 ression and nitrergic relaxation of circular gastric neuromuscular strips were assessed.

249 nNOS) expression and nitrergic relaxation in gastric neuromuscular tissues exposed to in-vitro hyperg

250 o analysis of HER2 status in tumor tissue in gastric or esophagogastric junction cancers.

251 ritis and intestinal metaplasia and in human gastric organoids infected with H pylori.

252 ta-catenin activation was confirmed in human gastric organoids that were treated with a novel SMOX in

253 tion in H. pylori-infected Smox(-/-) mice or gastric organoids, compared to infected wild-type animal

254 nd differentiated epithelial monolayers from gastric organoids.

255 -positive H. pylori in the lumen of infected gastric organoids.

256 observed also in primary cells derived from gastric organoids.

257 In the gastric pathogen Helicobacter pylori we identify six dis

258 ve assessment of the ulcer-causing H. pylori gastric pathogen.

259 We observed similar evolutions of gastric peptide distribution and duodenal proteolysis be

260 foodstuffs (declared vitamin C fortified) at gastric pH 1.5 and 4, respectively.

261 from 1.3 to 53.8%, and from 0.3 to 26.3% at gastric pH 1.5 and 4, respectively.

262 min C in baby foodstuffs is very low in both gastric pH conditions.

263 nts in pigs key digestive parameters such as gastric pH, stomach emptying kinetics, and intestinal tr

264 also suggest the size of fat and protein in gastric phase to be smaller than in intestinal phase.

265 aglycone (3,4-DHPEA-EDA) in the salivary and gastric phase, beyond luteolin in the gastric phase.

266 titative LC-MS/MS; none were detected in the gastric phase, but rapidly peaked in the intestinal phas

267 ry and gastric phase, beyond luteolin in the gastric phase.

268 amples increased antioxidant capacity in the gastric phase.

269 fs by an in vitro digestion model at varying gastric pHs.

270 multicompartment micromotors display strong gastric-powered propulsion with tunable lifetime dependi

271 n2a, were upregulated by p53 inactivation in gastric premalignancy, serving as a barrier to disease p

272 transcriptional and functional evaluation of gastric premalignancy.

273 In AIG, the gastric proton pump, H(+)/K(+) ATPase, is the major auto

274 This work shows the key role of the gastric restructuring for the overall digestive mechanis

275 PDE4 inhibitors induced gastric retention at similar or below doses commonly use

276 Indeed, PDE4 inhibition induced gastric retention in an acute model of gastric motility

277 We thus explored the abnormal gastric retention induced by PDE4 inhibition in mice und

278 bitor-induced gastroparesis, indicating that gastric retention may result from the concurrent inhibit

279 In humans, abnormal gastric retention of food is known as gastroparesis, a s

280 of disgust.(11) However, the causal role of gastric rhythm in disgust avoidance is unknown.

281 We manipulated gastric rhythm using domperidone, a peripheral dopamine

282 levels may mediate the beneficial effects of gastric sleeve surgery in improving insulin sensitivity

283 cient mice exhibit significant reductions of gastric spermidine levels and H. pylori-induced inflamma

284 Gastric (stage II/III), pancreatic (stage I/II/III), and

285 (2020) compare intra-gastric sugar and non-caloric sweetener to investigate h

286 Staining of healthy and diseased human gastric tissue samples paralleled these results.

287 ired, and this most likely requires excising gastric tissue.

288 We collected gastric tissues and performed immunofluorescence and imm

289 essenger RNA were significantly increased in gastric tissues from patients with H pylori infection, c

290 The results highlight the essential role of gastric treatments and the presence of bile salts in the

291 and is associated with the ability to induce gastric tumor.

292 c host and bacterial factors responsible for gastric tumorigenesis.

293 investigated in gastric epithelial cells or gastric tumorigenesis.

294 nal endovascular procedures in patients with gastric variceal bleeding have changed after the emergen

295 Nonetheless, gastric variceal bleeding is more severe and associated

296 e led to an improvement in the management of gastric variceal disease through newer modalities of tre

297 to the small bowel, on the role of decreased gastric volume capacity and release of glucagon-like pep

298 is begs the question whether less aggressive gastric volume reduction may provide sufficient efficacy

299 Gastric volume was linearly correlated to increased gast

300 ight loss and was logarithmically related to gastric volume.