ライフサイエンスコーパス: gastritis

1 potential role for HIF in H. pylori-mediated gastritis.

2 lls or promote the development of autoimmune gastritis.

3 tly in tissues showing gastritis or atrophic gastritis.

4 ted mild gastritis and 51.3% moderate/severe gastritis.

5 e younger than patients with moderate/severe gastritis.

6 s, DSS-induced colitis, and H. felis-induced gastritis.

7 es of leak, stricture, cholangitis, and bile gastritis.

8 ylori and are involved in the development of gastritis.

9 associated with increased antral and corpus gastritis.

10 rophage chemoattractant during initiation of gastritis.

11 terations during Helicobacter pylori-induced gastritis.

12 on of its promoter in patients with H pylori gastritis.

13 ereas Treg from CD73-/- mice did not inhibit gastritis.

14 a, and GAS-KO mice had only mild to moderate gastritis.

15 hey progress to metaplasia mice with chronic gastritis.

16 s gastric adenocarcinoma in rodent models of gastritis.

17 10(6) H. pylori CFU/gram without associated gastritis.

18 autoimmunity in a murine model of autoimmune gastritis.

19 patterns of H pylori and thus the extent of gastritis.

20 tic ulcer disease, neoplasia, and autoimmune gastritis.

21 ed BAs are associated with human bile reflux gastritis.

22 ria can develop gastric inflammation, termed gastritis.

23 thological changes especially chronic active gastritis.

24 l vacA mixed genotypes showed chronic active gastritis.

25 l compared with normal mucosa or nonatrophic gastritis.

26 concern in patients with autoimmune atrophic gastritis.

27 nt the pH alteration resulting from atrophic gastritis.

28 by metaplastic cells in response to chronic gastritis.

29 , followed by peptic ulcer disease (18%) and gastritis (10%).

30 % with normal endoscopy results and 46% with gastritis), 18% had GERD and 13% had ulcers (duodenal in

31 We evaluated 19 superficial gastritis, 18 atrophic gastritis, and 18 intestinal meta

32 One hundred-twenty patients; 116 with gastritis, 3 with duodenal ulcer and 1 gastric ulcer, we

33 7BL/6J T cells or T-bet KO T cells developed gastritis 4 or 8 weeks after adoptive transfer.

34 % of juvenile patients showed some degree of gastritis (45.3% of patients with mild gastritis and 54.

35 cause, followed by varices [52 (18.1%)] and gastritis [51 (17.1%)].

36 the gastric mucosa of patients with H pylori gastritis (69.7%) than in those without (28.6%, P = .022

37 ents were studied; of these, 402 had chronic gastritis, 77 had peptic ulcer, and 20 had gastric cance

38 average age 42.1 years (range 17-73), 95 had gastritis, 92 had gastric ulcers, 108 had duodenal ulcer

39 the U.S. and Colombian populations (126 with gastritis, 96 with duodenal ulcer, and 64 with gastric c

40 ally all infected persons develop coexisting gastritis, a signature feature of which is the capacity

41 tigen, H(+)K(+)-ATPase, to induce autoimmune gastritis after transfer to immunodeficient recipients.

42 Gastric premalignant conditions, atrophic gastritis (AG) and intestinal metaplasia (IM) are charac

43 ecimens from 74 patients, including atrophic gastritis (AG) cases without aspirin use (control), AG c

44 Autoimmune gastritis (AIG) is an increasingly prevalent, organ-spec

45 e, chronic inflammation caused by autoimmune gastritis (AIG) is associated with an increased risk of

46 all three subpopulations induced autoimmune gastritis (AIG) upon transfer into nu/nu recipients.

47 carcinoma are serious sequelae of autoimmune gastritis (AIG).

48 cancer precursor lesions versus persons with gastritis alone.

49 ociated with autoimmune metaplastic atrophic gastritis (AMAG).

50 Among adults, 48.7% presented mild gastritis and 51.3% moderate/severe gastritis.

51 ee of gastritis (45.3% of patients with mild gastritis and 54.7% with moderate/severe gastritis) and

52 Second, we sought to determine whether gastritis and achlorhydria cause negative iron balance.

53 ted with hypergastrinaemia, chronic atrophic gastritis and achlorhydria.

54 ll regulator SOX9 in bacteria-infected human gastritis and cancer samples, paralleling increased leve

55 Gastritis and colonic crypt distortion were present in t

56 D73 in regulating Helicobacter felis-induced gastritis and colonization.

57 d B6 wild-type mice had both severe atrophic gastritis and corpus dysplasia, while GAS-KO mice had se

58 Arg2(-/-) mice had increased histologic gastritis and decreased bacterial colonization compared

59 Eosinophilic gastritis and duodenitis are characterized by gastrointe

60 nimal models as a treatment for eosinophilic gastritis and duodenitis.

61 with Gln was shown to temper H. suis induced gastritis and epithelial (hyper)proliferation in Mongoli

62 erged as key elements in the pathogenesis of gastritis and epithelial cell damage.

63 critical step in the pathogenesis of chronic gastritis and gastric adenocarcinoma.

64 eristictly found in assciation with atrophic gastritis and gastric cancer consistent with Bhutanese s

65 ter infection, as well as the development of gastritis and gastric cancer precursor lesions, using a

66 The high incidence of atrophic gastritis and gastric cancer suggest the phylogeographic

67 man stomach and have been linked to atrophic gastritis and gastric carcinoma.

68 ciation between Helicobacter pylori-positive gastritis and gastric MALT lymphoma.

69 re protected against Helicobacter-associated gastritis and gastric preneoplasia as a result of their

70 The upper endoscopy showed gastritis and gastric stenosis in the gastric antrum.

71 ceA genes were significantly associated with gastritis and gastric ulcer.

72 Helicobacter pylori is a major cause of gastritis and gastroduodenal ulcer disease and can cause

73 rin levels, and develop spontaneous atrophic gastritis and gastrointestinal intraepithelial neoplasia

74 ent of these complications include radiation gastritis and gastrointestinal ulcers, cholecystitis, ra

75 H pylori monoassociation accelerated gastritis and GIN but caused less severe gastric lesions

76 m a patient who developed corpus-predominant gastritis and hypochlorhydia over a 6-year interval.

77 sed Bcl-2 gene expression signified atrophic gastritis and IM in presence of cancer, as well as intes

78 Deleting Egfr in myeloid cells attenuated gastritis and increased H. pylori burden in infected mic

79 cells, including in intestinal metaplastic, gastritis and inflammatory cells.

80 at IFN-gamma overexpression failed to induce gastritis and instead inhibited gastric carcinogenesis i

81 tric epithelial cell nuclei in patients with gastritis and intestinal metaplasia and in human gastric

82 icobacter pylori and signs of chronic active gastritis and intestinal metaplasia in gastric biopsy sa

83 associated disorders, such as chronic active gastritis and intestinal metaplasia, are inversely assoc

84 3 represents a critical link between chronic gastritis and intestinalizing metaplasia that may serve

85 n gastric tissue from patients with H pylori gastritis and investigated the effects of H pylori infec

86 eles between the isolates from subjects with gastritis and isolates from subjects with IM or GC; 12 o

87 of humans, causing severe illnesses such as gastritis and malignancies.

88 We conclude that sulindac enhances H. pylori gastritis and may promote inflammation-mediated gastric

89 copy of the gastrointestinal tract has shown gastritis and non-specific inflammation whereas laparosc

90 lvement of NHPGHs in patients suffering from gastritis and nonexistence of mixed H. pylori infection,

91 Helicobacter pylori in the pathogenensis of gastritis and peptic ulcer disease has been shown in adu

92 acterial pathogen Helicobacter pylori causes gastritis and predisposes infected individuals to gastri

93 d at 6 and 11 months postinfection (mpi) for gastritis and premalignant lesions.

94 control) AKR mice were assessed for baseline gastritis and progression to metaplasia.

95 idence and character of bacterial-associated gastritis and related disorders.

96 ter pylori is a major cause of acute chronic gastritis and the development of stomach and duodenal ul

97 scopy was used to extract biopsies to assess gastritis and the presence of gastric H. pylori using Gi

98 e of physical health problems, such as acute gastritis and vomiting, road accident, high fever, or ca

99 Progressive gastritis and, ultimately, intestinalized spasmolytic po

100 ild gastritis and 54.7% with moderate/severe gastritis) and patients with mild gastritis were younger

101 for H. salomonis (four duodenal ulcer, five gastritis, and 11 gastric ulcer samples), 13 for H. heil

102 luated 19 superficial gastritis, 18 atrophic gastritis, and 18 intestinal metaplasia from cancer-free

103 10 for H. suis (three duodenal ulcer, three gastritis, and four gastric ulcer samples), 10 for H. fe

104 te gastritis, peptic ulcer disease, atrophic gastritis, and gastric adenocarcinoma.

105 (Nod1-/-) mice acutely developed more severe gastritis, and INS-GAS (Nod1-/-) mice developed gastric

106 H pylori infection, chronic active gastritis, and intestinal metaplasia had similar epidemi

107 atients; only three events (drug inefficacy, gastritis, and reflux esophagitis) in two patients were

108 re of Treg engraftment, that Treg ameliorate gastritis, and that the proinflammatory response is attr

109 ossess Treg that suppress AOD and autoimmune gastritis as efficiently as adult cells.

110 pylori-infected mice led to additive corpus gastritis associated with inflammatory cytokine expressi

111 nfected mice at 6 and 11 mpi had less severe gastritis, atrophy, mucous metaplasia and hyperplasia (P

112 agnosed as an infectious disease and chronic gastritis, based on clinical and laboratory findings.

113 s were collected from patients with H pylori gastritis before and after eradication and from H pylori

114 ion was examined in human H. pylori-positive gastritis biopsies.

115 d in macrophages of human H. pylori-positive gastritis biopsies.

116 enosine receptors decreases inflammation and gastritis but leads to persistent Helicobacter pylori in

117 on (IFN-gamma) is essential for induction of gastritis but showed that IFN-gamma-producing CD4 T cell

118 noculation, C57BL/6J mice developed moderate gastritis but T-bet KO mice and SCID mice did not.

119 Interleukin 17A (IL-17A) also contributed to gastritis, but to a lesser extent than IFN-gamma.

120 foperazone alone was not sufficient to cause gastritis, C. albicans colonization was also needed.

121 Chronic atrophic gastritis can lead to gastric metaplasia and increase ri

122 infection in patients with chronic atrophic gastritis, can cause metaplasia, characterized by gastri

123 Thirteen chronic erosive gastritis (CEG) patients with typical yellow tongue coat

124 the respective roles of H pylori, autoimmune gastritis, celiac disease, and genetic defects in the pa

125 8 peptic ulcer disease (PUD) and 327 chronic gastritis (CG) patients with a positive histological dia

126 solates; a total of 74 patients with chronic gastritis (CG, N = 37), intestinal metaplasia (IM, N = 2

127 biology-the transition from chronic atrophic gastritis (ChAG) to gastric adenocarcinoma-and defined t

128 Chronic atrophic gastritis (ChAG), a Helicobacter pylori-associated risk

129 op an antecedent condition, chronic atrophic gastritis (ChAG).

130 ric IM adjacent to a GU but with no atrophic gastritis changes; 3) patients receiving H. pylori eradi

131 Despite disparate effects on gastritis, colonization levels of gastric H. pylori were

132 f PPE, sensitized piglets developed moderate gastritis compared to naive piglets (1.5 vs 1.0, median

133 nd protein levels in patients with H. pylori gastritis compared to those of uninfected controls.

134 erbated the severity of H. pylori-associated gastritis despite decreased gastric prostaglandin E(2) l

135 was sufficient to prevent the development of gastritis, despite being ineffective at conferring colon

136 We suggest that gastritis due to H. pylori is associated with loss of im

137 FN-gamma are both essential for induction of gastritis due to H. pylori, IFN-gamma production by T ce

138 use models to elucidate the role of T-bet in gastritis due to H. pylori.

139 ) develops in patients with chronic atrophic gastritis due to infection with Helicobacter pylori; it

140 Eosinophilic gastritis (EG) is a clinicopathologic disorder with mark

141 The definition of eosinophilic gastritis (EG) is currently limited to histologic EG bas

142 trointestinal tract and include eosinophilic gastritis (EG), eosinophilic gastroenteritis (EGE), and

143 gned adults who had symptomatic eosinophilic gastritis, eosinophilic duodenitis, or both conditions i

144 H pylori monoassociation caused progressive gastritis, epithelial defects, oxyntic atrophy, marked f

145 hyperresponsiveness, as well as eosinophilic gastritis; esophagitis and other organ damage occurred i

146 PC-Shh(KO) mice did not develop gastritis, even after 6 months of infection with H pylor

147 ulcer samples), 13 for H. heilmannii (three gastritis, five duodenal ulcer, and five gastric ulcer s

148 of human gastric cancers, including chronic gastritis followed by oxyntic atrophy, mucous neck cell

149 is the etiological agent of diseases such as gastritis, gastric and duodenal ulcers, and two types of

150 genotypes were significantly associated with gastritis, gastric and duodenal ulcers.

151 gastroesophageal reflux disease, autoimmune gastritis, gastric cancer, and functional dyspepsia.

152 sophagus, esophageal adenocarcinoma, erosive gastritis, gastric cancer, diarrhea, colonic diverticula

153 ukin-10-deficient (IL-10(-/-)) T(R) cells on gastritis, gastric cytokines, and H. pylori colonization

154 of the autoantigen recognized in autoimmune gastritis, gastric H(+)/K(+) ATPase, which is naturally

155 as proinflammatory T cells (Th1 and Th17) in gastritis, gastric T cell engraftment, and gastric cytok

156 determine the development and progression of gastritis, gastric ulceration, and gastric cancer, this

157 y infected with Helicobacter pylori, causing gastritis, gastric ulcers and an increased incidence of

158 R) cells reduced morbidity, H. pylori corpus gastritis, gastroduodenitis, and inflammatory cytokine e

159 Using the gastritis group as a reference a significantly aberrant

160 Patients with chronic gastritis had excess fecal loss of isotopically tagged p

161 Patients with gastritis had significantly higher number of D and M tha

162 DA, screening for celiac disease, autoimmune gastritis, Helicobacter pylori, and hereditary forms of

163 ounts of acid; those with antral predominant gastritis, however, are hypergastrinemic and produce inc

164 All infected gerbils developed gastritis; however, inflammation was significantly atten

165 ted with H. pylori develop only asymptomatic gastritis; however, some develop ulcers or gastric adeno

166 Stratification by age cohorts in autoimmune gastritis implies a disease presenting as IDA many years

167 cobacter bilis modulates Helicobacter pylori gastritis in C57BL/6 mice.

168 H. muridarum-mediated attenuation of gastritis in coinfected mice was associated with signifi

169 Gastritis in H. felis-infected CD73-/- mice was signific

170 Enhanced gastritis in H. pylori-infected mmp-7-/- mice is strongl

171 h17 responses in Helicobacter pylori-induced gastritis in humans.

172 r T cells (T(E)) promote Helicobacter pylori gastritis in mice, and CD4(+) CD45RB(lo) CD25(+) regulat

173 s1bm2, s1a1b and s2 m2 showed chronic active gastritis in percentages of 90.0, 81, and 84.2%, respect

174 hat IL-21 is required for the development of gastritis in response to infection.

175 upport published data indicating that severe gastritis in T cell recipient mice is due to failure of

176 ratio (<5), indicating more advanced corpus gastritis, increased the odds of seroconversion of IgG S

177 that DNA repair is disrupted during H pylori gastritis, increasing mutagenesis in H pylori-infected g

178 Chronic gastritis induced by Helicobacter pylori is the stronges

179 Persistent gastritis induced by Helicobacter pylori is the stronges

180 iologic studies supports the hypothesis that gastritis-induced achlorhydria can be an independent cau

181 We re-evaluated the old hypothesis that gastritis-induced achlorhydria is a cause of iron defici

182 , of which 37 were cases of chronic atrophic gastritis, intestinal metaplasia, or dysplasia.

183 tory IDA have celiac disease, and autoimmune gastritis is encountered in 20% to 27% of patients.

184 a from Helicobacter(+) patients with chronic gastritis is enriched in IL-17 and BAFF, whereas the two

185 itic cell regulation in Helicobacter-induced gastritis is poorly understood.

186 Helicobacter pylori-induced gastritis is the strongest risk factor for gastric adeno

187 Helicobacter pylori-induced gastritis is the strongest singular risk factor for gast

188 s to duodenal ulceration; corpus-predominant gastritis leads to hypochlorhydria and predisposes to ga

189 preneoplastic lesions of multifocal atrophic gastritis (MAG) and intestinal metaplasia (IM) have occu

190 inflammation, leading to a worsening of the gastritis, measured by an increased epithelial cell prol

191 ) is protective against Helicobacter-induced gastritis, mediated by the suppression of proinflammator

192 Along the gastritis-metaplasia-carcinoma sequence, we observed a b

193 trointestinal tract is a hallmark within the gastritis-metaplasia-carcinoma sequence.

194 troduodenitis and H. pylori-dependent corpus gastritis more effectively than IL-10(-/-) T(R) cells.

195 sed in Helicobacter(-) patients with chronic gastritis; moreover, the expression of both BAFF and IL-

196 ic cancer risk in patients with non-atrophic gastritis (NAG), and is ineffective once preneoplastic l

197 ion that an axis BAFF/Th17 exists in chronic gastritis of Helicobacter(+) patients and that its prese

198 e increased predominantly in tissues showing gastritis or atrophic gastritis.

199 In patients with eosinophilic gastritis or duodenitis, AK002 reduced gastrointestinal

200 odenitis but did not reduce H. pylori corpus gastritis or impact T(E) cell inhibition of colonization

201 ancer (GC) and adjacent mucosa with atrophic gastritis or intestinal metaplasia (AG/IM GC+), as well

202 taplasia (AG/IM GC+), as well as in atrophic gastritis or intestinal metaplasia mucosa of patients wi

203 a, while B6 wild-type mice had either severe gastritis or metaplasia, and GAS-KO mice had only mild t

204 e found no credible evidence that IDA caused gastritis or that IDA preceded the development of achlor

205 29), type 2 diabetes mellitus (OR: 1.59) and gastritis (OR: 0.47).

206 lated complications (leak, cholangitis, bile gastritis, or stricture), and the secondary end points w

207 ifferences between patients with and without gastritis, oral H. pylori and gastric H. pylori in the p

208 gastritis, when compared with those without gastritis (p < 0.05, p < 0.001, p < 0.01, and p < 0.05,

209 erate/severe gastritis than in cases of mild gastritis (p = 0.026).

210 gher number of D and M than patients without gastritis (P = 0.03).

211 of 64 patients reporting rash, and colitis, gastritis, pancreatitis and arthritis, and diabetic keto

212 H pylori gastritis, particularly in patients infected with H pylo

213 tern was more frequently observed in chronic gastritis patients (79.3%, 130/164), while the EPIYA-ABC

214 ression in gastric mucosa from 31 HP chronic gastritis patients and 12 controls.

215 juvenile gastritis patients, 69.2% of adult gastritis patients and 88% of GC patients.

216 ed in 0% of normal mucosa, 58.5% of juvenile gastritis patients, 69.2% of adult gastritis patients an

217 ive H. pylori was 74.6% (164/220) in chronic gastritis patients, 73.6% (39/53) in peptic ulcer patien

218 ty to S-phase cells in the gastric mucosa of gastritis patients.

219 l population, and is associated with chronic gastritis, peptic disease and gastric malignancies.

220 ly increases the risk of developing atrophic gastritis, peptic ulcer disease, and gastric adenocarcin

221 stric epithelium is strongly associated with gastritis, peptic ulcer disease, and gastric cancer.

222 and plays a major role in the development of gastritis, peptic ulcer disease, and gastric cancer.

223 severe digestive diseases including chronic gastritis, peptic ulcer disease, and gastric cancer.

224 olonizes the human stomach and induces acute gastritis, peptic ulcer disease, atrophic gastritis, and

225 pper gastrointestinal tract, such as chronic gastritis, peptic ulcer disease, mucosa-associated lymph

226 ylori) infection is a major cause of chronic gastritis, peptic ulcer diseases and cancer.

227 chronic infection is associated with chronic gastritis, peptic ulcer, and gastric cancer.

228 d causes a spectrum of disease that includes gastritis, peptic ulcers, and gastric adenocarcinoma.

229 ion with various gastric diseases, including gastritis, peptic ulcers, and gastric cancer.

230 id HIF-1 is protective in H. pylori-mediated gastritis, pointing to the complex counterbalancing role

231 Helicobacter pylori-induced gastritis predisposes to the development of gastric canc

232 tors that have a role in determining whether gastritis progresses to gastric cancer.

233 production was assessed, and the presence of gastritis, proinflammatory cytokine expression, or colon

234 ecific antigen targeted by autoantibodies in gastritis-prone mice lacking thymic expression of aire a

235 nflammation and gastric carcinogenesis using gastritis-prone SAMP1/YitFc (SAMP) mice.

236 the gastric mucosa of mice and patients with gastritis, pS-STAT3 was constitutively expressed irrespe

237 ically, patients presenting with symptoms of gastritis, routinely undergo gastric biopsies.

238 gastric ulcer, two duodenal ulcer, and five gastritis samples).

239 bserved in intestinal metaplasia compared to gastritis samples.

240 Increased gastritis scores correlated with decreased colonization

241 out infection (P < .01), and correlated with gastritis severity (P < .05).

242 Notably, the Th2 responses and gastritis severity are significantly ameliorated in IL-4

243 educed both H pylori colonization levels and gastritis severity.

244 of p73 protein in vitro and in vivo in human gastritis specimens and H pylori-infected mice.

245 s specific for a major self-Ag in autoimmune gastritis suppress inflammation and associated pathology

246 Patients with gastritis tend to have a higher number of decayed and mi

247 as more frequent in cases of moderate/severe gastritis than in cases of mild gastritis (p = 0.026).

248 , HP infection was more common in those with gastritis than in normal samples (p = 0.004).

249 immunized mice induced significantly greater gastritis than that of infected mice, preceding signific

250 ngival bleeding, mean PPD, AL, F, and either gastritis, the presence of oral or gastric H. pylori.

251 gastric ulcer samples), 10 for H. felis (one gastritis, three duodenal ulcer, and six gastric ulcer s

252 C were increased in mouse and human H pylori gastritis tissues and localized to macrophages.

253 DNA damage was assessed in H pylori-infected gastritis tissues from humans, gerbils, and both wild-ty

254 Principal component analysis separated gastritis tissues from patients with cancer vs those wit

255 g human in vivo data from H. pylori-positive gastritis tissues indicated that the mir-124 gene loci a

256 OS were measured in macrophages and H pylori gastritis tissues.

257 thus favoring diseases ranging from chronic gastritis to adenocarcinoma.

258 , leading to disease conditions ranging from gastritis to cancer.

259 rrays containing each stage of disease, from gastritis to carcinoma, and gastric biopsy specimens fro

260 erved throughout the histologic cascade from gastritis to carcinoma.

261 eradication in preventing the progression of gastritis to gastric cancer in H. pylori-infected transg

262 ents of distinct disease types, ranging from gastritis to gastric cancer, and geographic origins, cov

263 trum of the gastric mucosa, progressing from gastritis to hyperplasia, low-grade dysplasia, high-grad

264 in a spectrum of pathologies that range from gastritis to invasive adenocarcinoma.

265 study was to use a mouse model of H. pylori gastritis to investigate the roles of regulatory T cells

266 cobacter pylori causes diseases ranging from gastritis to peptic ulcer disease to gastric cancer.

267 ients infected with Helicobacter pylori from gastritis to precancerous intestinal metaplasia, in huma

268 cer is associated with chronic inflammation (gastritis) triggered by persistent Helicobacter pylori (

269 ylori persistently colonizes humans, causing gastritis, ulcers, and gastric cancer.

270 cobacter pylori infection is associated with gastritis, ulcers, and gastric cancer.

271 ses a spectrum of gastric diseases including gastritis, ulcers, and gastric carcinoma.

272 olerated in some individuals while it causes gastritis, ulcers, or cancer in others.

273 H. pylori-induced gastritis was accompanied by an acute and dramatic decre

274 Chronic gastritis was induced in B6 mice by Helicobacter pylori

275 analyses of inflammatory genes revealed that gastritis was markedly suppressed in infected Stat3(SA/S

276 Gastritis was not evident until after day 7 in cefoperaz

277 Although gastritis was protective against SIBO, results show that

278 he dual-therapy arm, one of which (a case of gastritis) was reported as possibly or probably related

279 e a prominent component of H. pylori-induced gastritis, we investigated microbial and host mechanisms

280 Because coinfections can alter helicobacter gastritis, we investigated whether enterohepatic Helicob

281 ate/severe gastritis) and patients with mild gastritis were younger than patients with moderate/sever

282 in human gastric biopsies displaying severe gastritis, when compared with those without gastritis (p

283 ns, including Helicobacter pylori-associated gastritis, where its production of hydrogen peroxide con

284 pulation worldwide and causes chronic active gastritis, which can lead to peptic ulcer disease, gastr

285 accumulation of adenosine and attenuation of gastritis, which may favor persistent infection.

286 cobacter pylori infection results in chronic gastritis, which may progress to gastric cancer.

287 H. pylori-infected mice increased histologic gastritis, which was associated with enhanced M1/Th1/Th1

288 al metaplasia (IM), in patients with chronic gastritis who had taken aspirin for more than 3 years.

289 We evaluated five patients with autoimmune gastritis, who showed high serum thyrotropin (TSH) level

290 sed tests to evaluate H. pylori infection in gastritis with atrophy are not well known.

291 opsy-based test decreased when the degree of gastritis with atrophy increased regardless of biopsy si

292 Gastritis with atrophy was significantly higher at the a

293 In moderate to severe antrum or body gastritis with atrophy, additional corpus biopsy resulte

294 In moderate to severe gastritis with atrophy, biopsy-based test should include

295 site (for normal, mild, moderate, and severe gastritis with atrophy, the sensitivity of histology Gie

296 of biopsy-based tests in terms of degree of gastritis with atrophy.

297 d body were calculated in terms of degree of gastritis with atrophy.

298 ach type of effector cell induced autoimmune gastritis with distinct histological patterns.

299 rpus dysplasia, while GAS-KO mice had severe gastritis with mild gastric atrophy, but no corpus dyspl

300 lected from patients clinically diagnosed as gastritis with/without bile reflux and healthy subjects