ライフサイエンスコーパス: peptic

1 Additionally, the HX-MS data of peptic A beta fragments suggest that the C-terminal segm

2 at 120 degrees C significantly improved both peptic and pancreatic digestion attributed to structural

3 3% of total beta-carotene was released after peptic and pancreatic digestion, respectively.

4 measured as evidence of T cell activation by peptic and tryptic (PT) digests of gliadins from 2 monoc

5 of potentially toxic epitopes released after peptic and tryptic digestion, showing inefficiency as a

6 Signature product ions of this peptic BChE nonapeptide (FGES*AGAAS) offer a route to br

7 rable in maize processing, and resistance to peptic degradation in simulated gastric fluid digests, a

8 An examination of the peptic digest of insulin provides an example of the appl

9 without calcium crosslinking displayed rapid peptic digestion in less than 30 min.

10 cm, 260-690kJ/kg) treatments on the in vitro peptic digestion of ovomucin-depleted egg white was inve

11 Peptic digestion of selected proteins was used to provid

12 disulfide-linked peptide dimers produced by peptic digestion of the 80 kDa glycoprotein transferrin

13 Release of zinc during peptic digestion was lower for WPH-Ever-zinc, and over 5

14 levels unheated beta-lg showed resistance to peptic digestion with high antigenic value while it was

15 he mixtures of ions generated by tryptic and peptic digestions of lysozyme and insulin, respectively,

16 ssHDX of peptic digests further indicated that these protective e

17 ve at basic residues that are "forbidden" in peptic digests.

18 pylori (Hp)--the pathogen that produces acid-peptic disease (gastritis, ulcers) in humans.

19 n, and is associated with chronic gastritis, peptic disease and gastric malignancies.

20 be regarded as a proof of an underlying acid peptic disorder such as gastroesophageal reflux disease

21 wledge is crucial for the management of acid-peptic disorders and the development of novel medication

22 of new strategies to prevent and treat acid peptic disorders as well as circumvent the adverse effec

23 of novel therapies to prevent and treat acid-peptic disorders as well as circumvent the adverse effec

24 gastric acid secretion and treatment of acid-peptic disorders include the (1) discovery of histamine

25 lifelong problem that can be complicated by peptic esophageal stricture and adenocarcinoma of the es

26 However, in peptic fluid, NLC loading and citric acid crosslinking b

27 sidue-level resolution is demonstrated for a peptic fragment of a 37 kDa recombinant protein (N-lobe

28 High quality peptic fragments covering approximately 63% of the entir

29 ionization mass spectrometry analysis of the peptic fragments derived from alphaTS labeled at 3 M ure

30 ESI-MS analysis of the peptic fragments derived from alphaTS mass-labeled and q

31 Of the 47 peptic fragments monitored by HXMS, 15 showed significan

32 etermined from the deuterium levels found in peptic fragments of the labeled protein.

33 or ions were identified that corresponded to peptic fragments of three TGase cross-linked species: Ab

34 ddition, the HDX results for two overlapping peptic fragments suggest that a segment of the polypepti

35 stributions of deuterium were found for most peptic fragments, indicating that regions represented by

36 nderstanding the mechanisms of action of the peptic HIV-1 fusion inhibitors and for rational design o

37 activities; however, the functions of these peptic hydrolases are still under investigation.

38 ous report showed that yam dioscorin and its peptic hydrolysates exhibit radical scavenging activitie

39 pepsin digestion yields a large diversity of peptic N-glycosylated peptides that can be difficult to

40 zyme PNGase A for deglycosylation of labeled peptic N-linked glycopeptides at HDX quench conditions,

41 y was determined using an in vitro simulated peptic-pancreatic digestion, followed by measurement of

42 mained bound in both peptide complexes after peptic-pancreatic digestion.

43 On the basis of peptic peptide data, exchange was localized to specific

44 ft time distributions (XIDTDs) of deuterated peptic peptides are mobility-matched to corresponding XI

45 pe labeling simplified identification of the peptic peptides by providing partial amino acid composit

46 For 119 peptic peptides covering 74.1% of VP55, the extent of HD

47 HX-MS analysis of the peptic peptides derived from the pulse-labeled product o

48 tinctive isotope patterns in mass spectra of peptic peptides from the labeled protein.

49 hodology, which includes easy recognition of peptic peptides from the protein(s) of interest during h

50 were localized by mass determination of the peptic peptides of Rho.

51 g steps, the analysis of deuterium levels in peptic peptides produced after labeling was accomplished

52 When dopamine is bound, three peptic peptides show significantly slower deuterium inco

53 ched to corresponding XIDTDs of undeuterated peptic peptides that were identified using collision-ind

54 Peptic peptides undergoing either more or less HDX than

55 was increased and reproducibly produced more peptic peptides versus digestion at 1000 psi.

56 Decreased local HDX in peptic peptides was mapped on the tubulin structure and

57 erated cytochrome c and its fully deuterated peptic peptides were used to evaluate deuterium recovery

58 Broadly, across VP55's peptic peptides, a mild negative correlation was noted b

59 The rate and extent of H/D exchange of 26 peptic peptides, spanning 91% of the primary structure,

60 ed complications (ie, erosive esophagitis or peptic stricture) should take a PPI for short-term heali

61 Treatments for Barrett esophagus, peptic strictures, and esophageal adenocarcinoma still a

62 considered in patients with lung cancer with peptic symptoms.

63 tro for 48 h in the presence or absence of a peptic-tryptic digest (P-T digest) of gliadin.

64 ied by the enzyme transglutaminase 2) or the peptic-tryptic digest of gliadin (in native and deamidat

65 BCC sequence was more frequently observed in peptic ulcer (64.1%, 25/39) and gastric cancer patients

66 patients who had bleeding associated with a peptic ulcer (hazard ratio, 0.70; 95% CI, 0.26 to 1.25)

67 ing triple treatment or being diagnosed with peptic ulcer (HR 2.24; CI 95% 1.16:4.35) after adjustmen

68 However, the risks of peptic ulcer (OR = 7.0, 95% CI = 3.3-15.1; p < 0.001) an

69 ith laparoscopic surgery (LS) for perforated peptic ulcer (PPU) disease using a National dataset BACK

70 obstruction or gangrene (PEH) and perforated peptic ulcer (PPU) was analyzed, independent of HV esoph

71 Fifty-one patients had peptic ulcer and 56 were diagnosed as functional dyspeps

72 thogen responsible, with acid secretion, for peptic ulcer and a 20-fold increase in the risk of gastr

73 derwent emergent laparotomy for a perforated peptic ulcer and died from sepsis.

74 vacA s2/m2 strains are associated with lower peptic ulcer and gastric cancer risk and are non-toxic.

75 variety of pathological sequelae, including peptic ulcer and gastric cancer, resulting in significan

76 s work has shown which features of vacA make peptic ulcer and gastric cancer-associated type s1/m1 an

77 ssociation of cagA EPIYA motif patterns with peptic ulcer and gastric cancer.

78 world's population and is a leading cause of peptic ulcer and gastric cancer.

79 r pylori (Hp) infection is the main cause of peptic ulcer and gastric cancer.

80 particular, the most important of them i.e. peptic ulcer and gastric cancer.

81 and high-dose PPI groups who had a high risk peptic ulcer bleeding (n = 104 in each group), and these

82 ifferent stages of cirrhosis following acute peptic ulcer bleeding (PUB).

83 all patients (n = 271,030) hospitalized for peptic ulcer bleeding between January 1997 and December

84 association between cirrhosis and recurrent peptic ulcer bleeding by analyzing the Taiwan National H

85 pump inhibitor after endoscopic therapy for peptic ulcer bleeding has been recommended as adjuvant t

86 Peptic ulcer bleeding leads to substantial morbidity and

87 Mortality in peptic ulcer bleeding remains high, especially in patien

88 d forty-seven patients presenting with major peptic ulcer bleeding were randomized to heater probe pl

89 associated with long-term risk of recurrent peptic ulcer bleeding, although the risk declines with a

90 surgery regarding prognosis after refractory peptic ulcer bleeding, and the shorter length of hospita

91 apy has become the mainstay of treatment for peptic ulcer bleeding, with current consensus guidelines

92 nagement of hospitalized patients with acute peptic ulcer bleeding.

93 6), myocardial infarction (1.34; 1.07-1.69), peptic ulcer disease (1.27; 1.03-1.58), peripheral vascu

94 y was oesophageal varices (57%), followed by peptic ulcer disease (18%) and gastritis (10%).

95 cluded diverticulitis (5), pancreatitis (4), peptic ulcer disease (4), and cholecystitis (2).

96 by paralysis (90% increase), dementia (60%), peptic ulcer disease (53%), other neurological disorders

97 in patients developing the complications of peptic ulcer disease (eg, obstruction and perforation),

98 m2) was associated with an increased risk of peptic ulcer disease (PUD) (P = 0.003).

99 Gastric biopsy specimens of 68 peptic ulcer disease (PUD) and 327 chronic gastritis (CG

100 udy was to analyse the risk of uncomplicated peptic ulcer disease (PUD) in a cohort of new users of l

101 Despite progress in diagnosis and treatment, peptic ulcer disease (PUD) remains a common reason for h

102 tion in 1994 of guidelines for management of peptic ulcer disease (PUD), trends in physician practice

103 astrointestinal bleeding (UGIB) secondary to peptic ulcer disease (PUD).

104 71 (36%), intestinal obstruction 11 (6%) and peptic ulcer disease 9 (5%).

105 phenotypic subgroup has been associated with peptic ulcer disease and an increased bleeding tendency.

106 lori varies in severity from asymptomatic to peptic ulcer disease and cancer.

107 ylori is the strongest known risk factor for peptic ulcer disease and distal gastric adenocarcinoma,

108 s and is the strongest known risk factor for peptic ulcer disease and distal gastric cancer, yet only

109 er pylori infection is the leading cause for peptic ulcer disease and gastric adenocarcinoma.

110 n that may contribute to the pathogenesis of peptic ulcer disease and gastric adenocarcinoma.

111 A (CagA) into host cells are associated with peptic ulcer disease and gastric adenocarcinoma.

112 Peptic ulcer disease and gastric cancer are caused most

113 Helicobacter pylori, the main cause of peptic ulcer disease and gastric cancer in adult populat

114 Gastric diseases, including peptic ulcer disease and gastric cancer, affect 10% of t

115 an cells, contributes to the pathogenesis of peptic ulcer disease and gastric cancer, and is a candid

116 tomach and contributes to the development of peptic ulcer disease and gastric cancer.

117 ects half of the world population and causes peptic ulcer disease and gastric cancer.

118 acter pylori infection of the stomach causes peptic ulcer disease and gastric cancer.

119 cells and contributes to the pathogenesis of peptic ulcer disease and gastric cancer.

120 tant virulence factor in the pathogenesis of peptic ulcer disease and gastric cancer.

121 ch and may contribute to the pathogenesis of peptic ulcer disease and gastric cancer.

122 use of most gastric diseases, including both peptic ulcer disease and gastric cancer.

123 ) that may contribute to the pathogenesis of peptic ulcer disease and gastric cancer.

124 tence increases the risk of diseases such as peptic ulcer disease and gastric cancer.

125 to persistence of the bacterium and risk for peptic ulcer disease and gastric cancer.

126 tant virulence factor in the pathogenesis of peptic ulcer disease and gastric cancer.

127 tients is known to prevent the occurrence of peptic ulcer disease and gastric cancer.

128 tric epithelial cells and has been linked to peptic ulcer disease and gastric carcinoma.

129 the human stomach and increases the risk for peptic ulcer disease and gastric carcinoma.

130 oton pump inhibitor used in the treatment of peptic ulcer disease and gastrosophageal reflux disease

131 class it is fraught with the risk of serious peptic ulcer disease and its complications.

132 isms by which H pylori increases the risk of peptic ulcer disease and noncardia gastric adenocarcinom

133 rove to lessen the morbidity associated with peptic ulcer disease and other benign conditions.

134 ploratory laparotomy and gastric surgery for peptic ulcer disease approximately 10 years ago.

135 A small proportion of patients have peptic ulcer disease as cause and this can be treated em

136 Peptic ulcer disease has been associated with an increas

137 pylori in the pathogenensis of gastritis and peptic ulcer disease has been shown in adults and childr

138 roscopic surgery for treatment of perforated peptic ulcer disease has now been validated, with subseq

139 H. pylori-induced peptic ulcer disease is associated with inadequate regul

140 he risk for development of gastric cancer or peptic ulcer disease is higher among humans infected wit

141 Upper gastrointestinal bleeding from peptic ulcer disease is not a new clinical problem.

142 Gastric surgery for benign peptic ulcer disease is not a risk factor for either sho

143 greatest effect on surgical intervention in peptic ulcer disease is the Centers for Disease Control

144 lly asymptomatic but sometimes progresses to peptic ulcer disease or gastric adenocarcinoma.

145 ommon in strains isolated from patients with peptic ulcer disease or gastric cancer, rather than asym

146 face, evade host immune clearance, and cause peptic ulcer disease or gastric neoplasia in a significa

147 in the pathogenesis of chronic gastritis or peptic ulcer disease remain unclear.

148 h a higher risk of gastric adenocarcinoma or peptic ulcer disease than cag PAI-negative strains.

149 g(+)/type s1-vacA strains from patients with peptic ulcer disease than in cag-negative/s2-vacA strain

150 ri causes diseases ranging from gastritis to peptic ulcer disease to gastric cancer.

151 History of peptic ulcer disease was assessed at baseline in 1986 an

152 Peptic ulcer disease was believed to be caused by acid a

153 ergency operation for bleeding or perforated peptic ulcer disease was performed to determine the asso

154 Prevalences of heart or peptic ulcer disease were not significantly higher.

155 an early proponent of an infectious cause of peptic ulcer disease were recently discovered.

156 Peptic ulcer disease, although declining in prevalence,

157 Peptic ulcer disease, although declining in prevalence,

158 ion, psychiatric disorders, anemia, obesity, peptic ulcer disease, and cancer but a lower prevalence

159 s the risk of developing atrophic gastritis, peptic ulcer disease, and gastric adenocarcinoma.

160 its etiologic role in symptomatic gastritis, peptic ulcer disease, and gastric adenocarcinoma.

161 elium is strongly associated with gastritis, peptic ulcer disease, and gastric cancer.

162 major role in the development of gastritis, peptic ulcer disease, and gastric cancer.

163 estive diseases including chronic gastritis, peptic ulcer disease, and gastric cancer.

164 can lead to gastroesophageal reflux disease, peptic ulcer disease, and stress-related erosion/ulcer d

165 nificant association observed in vacA s1 and peptic ulcer disease, as well as vacA s1/m2 and gastric

166 e human stomach and induces acute gastritis, peptic ulcer disease, atrophic gastritis, and gastric ad

167 edical history (smoking, diabetes, bleeding, peptic ulcer disease, cancer, chronic liver disease, chr

168 In patients with bleeding related to peptic ulcer disease, combination therapy (epinephrine i

169 tic significance among CAD patients, whereas peptic ulcer disease, connective tissue disease, and lym

170 ns of the PCSK9 T allele were also seen with peptic ulcer disease, depression, asthma, chronic kidney

171 chronic active gastritis, which can lead to peptic ulcer disease, gastric adenocarcinoma, and mucosa

172 a resultant decline in H. pylori-associated peptic ulcer disease, gastric cancer remains the second

173 acterial pathogens, often causing gastritis, peptic ulcer disease, gastric mucosa-associated lymphati

174 s, in whom it is a key etiological factor in peptic ulcer disease, gastric mucosa-associated lymphoid

175 ndications for PPI use, including history of peptic ulcer disease, gastroesophageal reflux disease, o

176 on, cholecystectomy, operative management of peptic ulcer disease, lysis of peritoneal adhesions, app

177 Compared with those with report of no peptic ulcer disease, men with gastric ulcer had an incr

178 nistering therapy include active or inactive peptic ulcer disease, mucosa-associated lymphoid tissue

179 intestinal tract, such as chronic gastritis, peptic ulcer disease, mucosa-associated lymphoid tissue

180 at a variety of gastric disorders, including peptic ulcer disease, neoplasia, and autoimmune gastriti

181 Peptic ulcer disease, present in 56% of patients, was th

182 d contraindication to aspirin use, including peptic ulcer disease, renal insufficiency, and use of no

183 cobacter pylori, implicated in gastritis and peptic ulcer disease, Streptococcus agalactiae, implicat

184 ding after successful hemostasis of bleeding peptic ulcer disease, the following questions should be

185 refractory NVUGIB, the etiology of bleeding (peptic ulcer disease, unknown source, post surgical); pa

186 s1m1, and s2m1 genotypes and development to peptic ulcer disease.

187 ndrome, gastroesophageal reflux disease, and peptic ulcer disease.

188 nfected congenital anomalies, and perforated peptic ulcer disease.

189 tes to the development of gastric cancer and peptic ulcer disease.

190 d areas: morbid obesity, gastric cancer, and peptic ulcer disease.

191 or for the development of gastric cancer and peptic ulcer disease.

192 the bacterium in pathogenesis and relapse of peptic ulcer disease.

193 IDA regardless of the presence or absence of peptic ulcer disease.

194 and that contributes to the pathogenesis of peptic ulcer disease.

195 es to the pathogenesis of gastric cancer and peptic ulcer disease.

196 ggest a relationship between lung cancer and peptic ulcer disease.

197 superior result for H. pylori eradication in peptic ulcer disease.

198 s requiring emergency surgery for perforated peptic ulcer disease.

199 ction is a major cause of chronic gastritis, peptic ulcer diseases and cancer.

200 ing triple treatment or being diagnosed with peptic ulcer during the following 33 months more than tw

201 nducted on 235 cirrhotic patients with acute peptic ulcer hemorrhage who underwent therapeutic endosc

202 Among 20,294 GBP patients, diabetes and peptic ulcer history entailed statistically significantl

203 Diabetes and peptic ulcer history seem to be risk factors for MU, but

204 We studied peptic ulcer hospitalizations in a cohort of Tennessee M

205 ctive cotherapy had an adjusted incidence of peptic ulcer hospitalizations of 5.65 per 1000 person-ye

206 h 363,037 person-years of follow-up and 1223 peptic ulcer hospitalizations.

207 1m1, s1m2, s2m1 and s2m2) and development to peptic ulcer in Iranian population.

208 A total of 121 peptic ulcer incidents were recorded within 33 months of

209 Perforated peptic ulcer is a common emergency condition worldwide,

210 Among causes, peptic ulcer is the casuistic one.

211 We summarise the evidence for perforated peptic ulcer management and identify directions for futu

212 ing triple treatment or being diagnosed with peptic ulcer of approximately 0.4%, whereas the highest

213 Upper gastrointestinal endoscopy revealed peptic ulcer of the duodenal bulb.

214 Patients with peptic ulcer or functional dyspepsia infected by H. pylo

215 proposed regimen in Brazilian patients with peptic ulcer or functional dyspepsia showed no significa

216 ulcer complications (age 75 years or older, peptic ulcer or gastrointestinal bleeding in the past ye

217 Subgroup analysis of diagnosed peptic ulcer patients revealed the same pattern as the m

218 chronic gastritis patients, 73.6% (39/53) in peptic ulcer patients, and 78.6% (11/14) in gastric canc

219 perforation (OR 6.97, 95% CI 6.60-7.37), and peptic ulcer perforation (OR 3.67, 95% CI 3.40-3.96).

220 perforation (OR 4.33, 95% CI 4.12-4.56), and peptic ulcer perforation (OR 4.63, 95% CI 4.27-5.02).

221 with Roux-en-Y reconstruction for nonhealing peptic ulcer presented to the emergency department and r

222 cirrhosis was significantly associated with peptic ulcer rebleeding (adjusted hazard ratio, 3.19; 95

223 d assess whether the most recent behavior of peptic ulcer still fits the overall pattern governed by

224 ry, 127 (2.8%) versus 2033 (2.4%), P > 0.05; peptic ulcer surgery, 22 (0.5%) versus 277 (0.3%), P > 0

225 tion and produces a variety of diseases from peptic ulcer to cancer.

226 nued to influence the temporal variations of peptic ulcer until most recently.

227 The optimal management of bleeding peptic ulcer with adherent clot is controversial and may

228 SAIDs) prescribed to those with a history of peptic ulcer without co-prescription of a proton-pump in

229 non-selective NSAID if they had a history of peptic ulcer without gastroprotection (OR 0.58, 95% CI 0

230 of these, 402 had chronic gastritis, 77 had peptic ulcer, and 20 had gastric cancer.

231 ection is associated with chronic gastritis, peptic ulcer, and gastric cancer.

232 ticosteroid or anticoagulant use, history of peptic ulcer, and high average daily dose of NSAIDs.

233 wide range of diseases, including gastritis, peptic ulcer, and two forms of gastric cancer.

234 ociated with a range of pathology, including peptic ulcer, atrophic gastritis, and gastric cancer.

235 ment or being diagnosed in a hospital with a peptic ulcer, in relation to quintiles of stress levels.

236 elicobacter pylori strain is associated with peptic ulcer, it is uncertain whether the risk is greate

237 Pseudoachalasia, peptic ulcer, normal gastric emptying scintigraphy (GES)

238 duodenal wall of the patient with perforated peptic ulcer, real time reverse transcriptase polymerase

239 suppression status and acid-related disease (peptic ulcer, reflux esophagitis).

240 section, appendicitis, perforated esophagus, peptic ulcer, small bowel or large bowel, and incarcerat

241 section, appendicitis, perforated esophagus, peptic ulcer, small bowel or large bowel, and incarcerat

242 itor (PPI) therapies for patients with acute peptic ulcer-related bleeding of sufficient severity to

243 % in these cases, so that 33.65% of whom had peptic ulcer.

244 astric adenocarcinoma, gastric lymphoma, and peptic ulcer.

245 placebo as endoscopic treatment for bleeding peptic ulcer.

246 tting in patients at risk of rebleeding from peptic ulcer.

247 g after hemostasis in patients with bleeding peptic ulcer.

248 tion of esophagus, small or large bowel, and peptic ulcer.

249 a triple treatment or being diagnosed with a peptic ulcer.

250 ith Helicobacter pylori is the main cause of peptic-ulcer disease.

251 ons for the divergent trends in incidence of peptic ulceration and apparent trends in diagnosis of up

252 ylori is the strongest known risk factor for peptic ulceration and distal gastric cancer, and adheren

253 lonizes the human stomach and contributes to peptic ulceration and gastric adenocarcinoma.

254 confers risk of serious diseases, including peptic ulceration and gastric neoplasia.

255 lly underlies the perceived relative lack of peptic ulceration in patients affected by cystic fibrosi

256 clinical outcomes (i.e., gastric cancer and peptic ulceration).

257 egative bacterium associated with gastritis, peptic ulceration, and gastric adenocarcinoma in humans,

258 Helicobacter pylori is the main cause of peptic ulceration, distal gastric adenocarcinoma, and ga

259 the host environment, increasing the risk of peptic ulceration, gastric adenocarcinoma, and possibly

260 osa, which is associated with development of peptic ulceration, gastric atrophy, and gastric adenocar

261 ers an increased risk for the development of peptic ulceration, noncardia gastric adenocarcinoma, and

262 ith Helicobacter pylori is a risk factor for peptic ulceration, noncardia gastric adenocarcinoma, and

263 te to the pathogenesis of gastric cancer and peptic ulceration.

264 to be a major cause of gastric carcinoma and peptic ulceration.

265 9.3-18.0] per 1000 person-years; P = .40) or peptic ulcers (10.9 [95% CI, 7.7-15.5] vs 11.4 [95% CI,

266 (HR, 1.14 [CI, 1.06 to 1.22]; P < 0.001) and peptic ulcers (HR, 1.17 [CI, 1.09 to 1.27]; P < 0.001) o

267 ensive care unit at risk for rebleeding from peptic ulcers after hemostasis.

268 Patients with high-risk bleeding peptic ulcers after successful endoscopic therapy were r

269 er-related bleeding or prevent rebleeding in peptic ulcers after successful hemostasis?

270 current hemorrhage in patients with bleeding peptic ulcers and adherent clots.

271 2)-receptor antagonist, in the prevention of peptic ulcers and erosive oesophagitis in patients recei

272 PIYA-ABCC motif patterns are associated with peptic ulcers and gastric cancer.

273 in a spectrum of gastric diseases, including peptic ulcers and gastric cancer.

274 disorders ranging from chronic gastritis to peptic ulcers and gastric cancer.

275 ic mucosa by Helicobacter pylori can lead to peptic ulcers and gastric cancer.

276 ontrolled cell proliferation, and eventually peptic ulcers and gastric cancer.

277 nce and forming a recognized risk factor for peptic ulcers and gastric cancer.

278 pathogen to survive in the stomach and cause peptic ulcers and gastric cancer.

279 d between the number of EPIYA-C segments and peptic ulcers and gastric cancer.

280 shed as the etiologic agent of gastritis and peptic ulcers and is a major risk factor for gastric ade

281 It is responsible for most peptic ulcers and is an important risk factor for gastri

282 The association between stress and peptic ulcers has been questioned since the discovery of

283 with an increased risk of gastric cancer and peptic ulcers in adults.

284 of Helicobacter pylori, the leading cause of peptic ulcers in humans.

285 copy in 105 of the 158 patients (66.4%) with peptic ulcers in the urgent-endoscopy group and in 76 of

286 be associated with disease symptoms such as peptic ulcers or cardiovascular disorders, and epidemiol

287 is found more commonly in strains that cause peptic ulcers or gastric cancer, rather than asymptomati

288 Upper gastrointestinal bleeding from peptic ulcers or other nonvariceal causes generally stop

289 Long before the cause was discovered, peptic ulcers were known to occur preferentially in indi

290 robe plus placebo injection as treatment for peptic ulcers with active bleeding or nonbleeding visibl

291 anxiety, dementia, migraine, heart disease, peptic ulcers, and arthritis are up to eight times more

292 infections are known to cause gastritis and peptic ulcers, and dramatically enhance the risk of gast

293 spectrum of disease that includes gastritis, peptic ulcers, and gastric adenocarcinoma.

294 rious gastric diseases, including gastritis, peptic ulcers, and gastric cancer.

295 Gastrointestinal bleeding, peptic ulcers, and polyps were self-reported during exte

296 ponsible for severe gastric diseases such as peptic ulcers, gastric adenocarcinoma, and gastric lymph

297 reduced despite the decreasing incidence of peptic ulcers, strategies to eradicate Helicobacter pylo

298 (H2) receptor agonist commonly used to treat peptic ulcers, would be effective against lung adenocarc

299 The main side-effect of aspirin is peptic ulcers; therefore coadministration of aspirin wit

300 l hypertension (PH) in 99 (63%) patients and peptic/vascular lesions in 57 (37%).