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

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

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

8 obtained at the residue-specific level using peptic digestion and mass spectrometry.

9 By using peptic digestion in combination with high-resolution Fou

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 The results of the peptic digestion show that residues A13 to A21 and B11 t

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

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

16 the protected amides was carried out using a peptic-digestion protocol at low pH.

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

18 ssHDX of peptic digests further indicated that these protective e

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

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

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

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

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

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

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

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

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

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

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

30 from isotope patterns in the mass spectra of peptic fragments derived from aldolase incubated in 3 M

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

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

33 light mass spectrometry was used to identify peptic fragments from protein complexes that retained de

34 s spectra of both the intact protein and its peptic fragments had multiple envelopes of isotope peaks

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

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

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

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

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

40 ass spectra of either intact aldolase or its peptic fragments, were used to determine the abundances

41 , and determining the deuterium level in the peptic fragments.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

59 Peptic peptides undergoing either more or less HDX than

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

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

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

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

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

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

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

67 considered in patients with lung cancer with peptic symptoms.

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

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

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

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

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

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

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

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

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

77 us disease and was proximal in patients with peptic ulcer and Crohn disease.

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

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

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

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

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

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

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

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

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

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

88 Peptic ulcer bleeding leads to substantial morbidity and

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

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

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 i to activate neutrophils is associated with peptic ulcer disease (PUD).

104 (s1a) allele of the underlying vacA gene to peptic ulcer disease (PUD).

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

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

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

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

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

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

113 Peptic ulcer disease and gastric cancer are caused most

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

137 Peptic ulcer disease has been associated with an increas

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

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

140 Incidence and risk factors for peptic ulcer disease in the United States have not been

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

142 ts for children in whom H. pylori-associated peptic ulcer disease is diagnosed.

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

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

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

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

147 Dumping, bile gastritis, or peptic ulcer disease occurred in three patients after PP

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

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

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

151 ns of Helicobacter pylori from patients with peptic ulcer disease or intestinal-type gastric cancer c

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

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

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

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

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

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

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

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

160 Peptic ulcer disease, although declining in prevalence,

161 Peptic ulcer disease, although declining in prevalence,

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

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

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

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

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

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

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

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

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

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 ic gastritis and leading in some patients to peptic ulcer disease, mucosa-associated lymphomas, and g

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

182 Of patients with peptic ulcer disease, nine of 37 (24%) had stigmata of r

183 lays an etiologic role in the development of peptic ulcer disease, only a small number of these child

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

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

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

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

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

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

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

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

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

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

194 oeconomic status, added salt, and history of peptic ulcer disease.

195 episodes of acute distress that can lead to peptic ulcer disease.

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

197 s requiring emergency surgery for perforated peptic ulcer disease.

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

199 nfected congenital anomalies, and perforated peptic ulcer disease.

200 Using solid state NMR methods, a peptic ulcer drug analogue has been described at atomic

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

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

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

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

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

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

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

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

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

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

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

223 g in severity from superficial gastritis and peptic ulcer to gastric cancer and mucosal-associated ly

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

225 pulmonary disease, perinatal conditions, and peptic ulcer was relatively underfunded.

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

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

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

229 f 75 patients with gastric IM (30 cancer, 26 peptic ulcer, and 19 chronic gastritis patients) and was

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 Alcohol consumption, smoking, prior peptic ulcer, and history of gastric cancer in parents w

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

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

236 ients with different clinical presentations (peptic ulcer, gastric cancer, and atrophic gastritis).

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

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

239 for murine atherosclerosis and that, unlike peptic ulcer, Koch's postulates cannot be fulfilled for

240 ption presumably due to over-distention from peptic ulcer, pyloric stenosis, annular pancreas, and ev

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

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

243 astric adenocarcinoma, gastric lymphoma, and peptic ulcer.

244 a triple treatment or being diagnosed with a 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 ith Helicobacter pylori is the main cause of peptic-ulcer disease.

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

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

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

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

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

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

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

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

257 ication in patients with current or previous peptic ulceration, dyspepsia, or both who continued to u

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

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

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

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

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

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

264 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,

265 (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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

285 pancreas and, if untreated, can cause severe peptic ulcers or metastatic disease.

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

287 Hospitalization for bleeding peptic ulcers was identified by hospital claims and veri

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

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

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

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

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

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

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

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

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

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

298 such markers and can identify patients with peptic ulcers.

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%).