ライフサイエンスコーパス: gastritis

1 cancer = 0.42, 95% CI: 0.2-0.9 compared with gastritis).

2 0 wild without gastritis and 23 captive with gastritis).

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

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

5 ylori and are involved in the development of gastritis.

6 associated with increased antral and corpus gastritis.

7 rophage chemoattractant during initiation of gastritis.

8 terations during Helicobacter pylori-induced gastritis.

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

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

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

12 s gastric adenocarcinoma in rodent models of gastritis.

13 10(6) H. pylori CFU/gram without associated gastritis.

14 autoimmunity in a murine model of autoimmune gastritis.

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

16 tic ulcer disease, neoplasia, and autoimmune gastritis.

17 on of the infection and the degree of corpus gastritis.

18 concern in patients with autoimmune atrophic gastritis.

19 chronic persistence of Helicobacter-induced gastritis.

20 with Helicobacter felis (H. felis) to induce gastritis.

21 antibodies and may be a model for autoimmune gastritis.

22 for gastric malignancy, and acute H. pylori gastritis.

23 nt the pH alteration resulting from atrophic gastritis.

24 asia and adenocarcinoma in a rodent model of gastritis.

25 er infection and the presence or severity of gastritis.

26 isolated from patients with chronic atrophic gastritis.

27 tal cell antibodies suggestive of autoimmune gastritis.

28 n (C57BL/6 x 129SvEv)F1 mice induces chronic gastritis.

29 lonal nTreg on the development of autoimmune gastritis.

30 e histopathology demonstrated mild to severe gastritis.

31 by metaplastic cells in response to chronic gastritis.

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

33 lls or promote the development of autoimmune gastritis.

34 tly in tissues showing gastritis or atrophic gastritis.

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

36 e younger than patients with moderate/severe gastritis.

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

38 t Asia and South America, including 120 with gastritis, 140 with duodenal ulcer (DU), 110 with gastri

39 % with normal endoscopy results and 46% with gastritis), 18% had GERD and 13% had ulcers (duodenal in

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

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

42 7BL/6J T cells or T-bet KO T cells developed gastritis 4 or 8 weeks after adoptive transfer.

43 % of juvenile patients showed some degree of gastritis (45.3% of patients with mild gastritis and 54.

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

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

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

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

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

49 sgenic mouse model of human chronic atrophic gastritis, a preneoplastic condition.

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

51 dupA was present in 42% of DU vs. 21% of gastritis (adjusted odds ratio [OR] = 3.1, 95% confidenc

52 icient model for the development of atrophic gastritis after infection and to determine the processes

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

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

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

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

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

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

59 cancer precursor lesions versus persons with gastritis alone.

60 with Helicobacter organisms (10 wild without gastritis and 23 captive with gastritis).

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

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

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

64 ted with hypergastrinaemia, chronic atrophic gastritis and achlorhydria.

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

66 Gastritis and colonic crypt distortion were present in t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

92 i is an important human pathogen that causes gastritis and is strongly associated with gastric ulcers

93 Helicobacter pylori induces chronic gastritis and is the strongest known risk factor for pep

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

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

96 "Helicobacter heilmannii" is associated with gastritis and mucosa-associated lymphoid tissue lymphoma

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

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

99 s been established as the etiologic agent of gastritis and peptic ulcers and is a major risk factor f

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

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

102 Wild-type C. jejuni caused moderately severe gastritis and proximal duodenitis in 3X mice that were m

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

104 elicobacter infection in the pathogenesis of gastritis and support the premise that host factors acco

105 nth coinfection may protect against atrophic gastritis and T helper type 1 responses.

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

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

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

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

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

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

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

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

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

115 e hypochlorhydric mouse stomach, the chronic gastritis, atrophy, metaplasia, dysplasia paradigm can b

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

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

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

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

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

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

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

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

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

125 ellular responses and possibly contribute to gastritis by phosphorylation-dependent pathways.

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

127 Chronic gastritis causes significant morbidity and mortality in

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

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

130 hylation index increased from normal/chronic gastritis (CG) mucosa (0.09) to intestinal metaplasia (I

131 8 peptic ulcer disease (PUD) and 327 chronic gastritis (CG) patients with a positive histological dia

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

133 set of individuals develops chronic atrophic gastritis (ChAG), a condition characterized in part by d

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

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

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

137 The role of TFF2 in the development of gastritis, colitis, and inflammatory cytokine responses

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

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

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

141 rated prominent nuclear staining in SPEM and gastritis cystica profunda.

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

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

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

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

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

147 Gastritis due to Helicobacter pylori is induced by a Th1

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

149 After chart review, gastritis/duodenitis was not significantly associated wi

150 Before chart review, only 1 diagnosis, gastritis/duodenitis, was more likely to occur in the 14

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

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

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

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

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

156 y tests the hypothesis that chronic atrophic gastritis from hypochlorhydria in the gastrin-deficient

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

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

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

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

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

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

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

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

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

166 Using the gastritis group as a reference a significantly aberrant

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

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

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

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

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

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

173 (LPS) O-chain polysaccharide contributes to gastritis in a mouse model.

174 hannel, which very rapidly establish chronic gastritis in a pathogen-exposed environment.

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

176 licobacter species that were associated with gastritis in captive cheetahs but are apparently commens

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

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

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

180 tion, CD4+ T cells from T-bet KO mice induce gastritis in H. pylori-infected recipient SCID mice.

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

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

183 licobacter pylori produces acute superficial gastritis in nearly all of its human hosts.

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

185 The atrophic gastritis in the infected wild-type mice, particularly t

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

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

188 Chronic gastritis induced by Helicobacter pylori is the stronges

189 Persistent gastritis induced by Helicobacter pylori is the stronges

190 Persistent gastritis induced by Helicobacter pylori is the stronges

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

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

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

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

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

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

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

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

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

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

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

202 d to initiate a progression through atrophic gastritis, metaplasia and dysplasia to cancer, and has b

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

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

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

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

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

208 Bacterial colonization, gastric lesions (gastritis, neutrophilic infiltration, and gastric epithe

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

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

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

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

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

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

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

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

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

218 nt severity and characterized by progressive gastritis, oxyntic atrophy, hyperplasia, intestinal meta

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

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

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

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

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

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

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

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

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

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

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

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

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

232 prevalent bacterial pathogens, often causing gastritis, peptic ulcer disease, gastric mucosa-associat

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

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

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

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

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

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

239 Patients developing nonatrophic gastritis present a Th1 response without developing prot

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

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

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

243 bserved in intestinal metaplasia compared to gastritis samples.

244 Increased gastritis scores correlated with decreased colonization

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

246 educed both H pylori colonization levels and gastritis severity.

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

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

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

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

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

252 nfection of the human stomach causes chronic gastritis that can lead to gastric cancer.

253 H. pylori induces gastritis through production of a variety of antigens, v

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

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

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

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

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

259 thus favoring diseases ranging from chronic gastritis to adenocarcinoma.

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

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

262 erved throughout the histologic cascade from gastritis to carcinoma.

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

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

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

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

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

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

269 sociated with disorders ranging from chronic gastritis to peptic ulcers and gastric cancer.

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

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

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

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

274 cells but not recipients of T-bet KO cells, gastritis was associated with a delayed-type hypersensit

275 Gastritis was not evident until after day 7 in cefoperaz

276 Although gastritis was protective against SIBO, results show that

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

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

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

280 eployed veterans, and migraine headaches and gastritis were associated with CMI among nondeployed vet

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 increased susceptibility to H. felis-induced gastritis, with enhanced gastric inflammation.