ライフサイエンスコーパス: gastric mucosa

1 e strong acidic/enzymatic environment of the gastric mucosa.

2 icant increase in IL-17C expression in human gastric mucosa.

3 modulating effector T cell responses at the gastric mucosa.

4 in CD25+Foxp3+ Treg from peripheral blood or gastric mucosa.

5 ch as the Lewis(b) antigens in human primate gastric mucosa.

6 ella that live near the surface of the human gastric mucosa.

7 ghly specialized organelles and cells in the gastric mucosa.

8 OX on inducible NOS (iNOS) expression in the gastric mucosa.

9 ritical regulators of differentiation in the gastric mucosa.

10 and increased neutrophil accumulation at the gastric mucosa.

11 stablish a persistent infection in the human gastric mucosa.

12 nd the role of DAF within H. pylori-infected gastric mucosa.

13 is synthesized in the exocrine pancreas and gastric mucosa.

14 blood cells and inflammatory cells into the gastric mucosa.

15 approximately 25 kDa complex in normal human gastric mucosa.

16 to the ABO blood group antigen-glycosylated gastric mucosa.

17 nses to maintain chronic colonization of the gastric mucosa.

18 common and persistent human pathogen of the gastric mucosa.

19 uclear leukocyte neutrophils (PMNs) into the gastric mucosa.

20 metastases when compared with that in normal gastric mucosa.

21 cteria and PMNs act in concert to damage the gastric mucosa.

22 hat activates sensory neurons located in the gastric mucosa.

23 rmal pattern of E-cadherin expression in the gastric mucosa.

24 TFIZ1 is expressed and secreted in normal gastric mucosa.

25 the disappearance of HEV-like vessels in the gastric mucosa.

26 H. pylori to persistently colonize the human gastric mucosa.

27 on of total RNA directly from infected human gastric mucosa.

28 gen species, and oxidative DNA damage in the gastric mucosa.

29 t free radioiodine by Na/I symporters in the gastric mucosa.

30 in the relatively hostile environment of the gastric mucosa.

31 arietal cells in the fundic glands of normal gastric mucosa.

32 oproteinases (MMPs) in cell lines and in the gastric mucosa.

33 ression was increased by 3.3-fold vs. normal gastric mucosa.

34 d in response to interactions with mammalian gastric mucosa.

35 ed primarily in the mucous neck cells of the gastric mucosa.

36 11c(+) dendritic cells (DCs) with PCs in the gastric mucosa.

37 hly restricted ecological niche in the human gastric mucosa.

38 have been developed to reduce erosion of the gastric mucosa.

39 ation of inducible NO synthase (iNOS) in the gastric mucosa.

40 asis for the impaired mucosal healing in PHT gastric mucosa.

41 w therapeutic modality for protection of PHT gastric mucosa.

42 -induced ERK2 activation is defective in PHT gastric mucosa.

43 led to rapid loss of parietal cells from the gastric mucosa.

44 lin D1 expression, and cell proliferation in gastric mucosa.

45 pylori to specific cell lineages within the gastric mucosa.

46 rostaglandin synthesis and do not damage the gastric mucosa.

47 equal to the H+, K+-ATPase purified from hog gastric mucosa.

48 eased by 43% compared with the sham-operated gastric mucosa.

49 1B transcripts are more important than 1A in gastric mucosa.

50 he impaired angiogenesis after injury of PHT gastric mucosa.

51 the liver, large bowel, urinary bladder, and gastric mucosa.

52 and the density of T cells recruited to the gastric mucosa.

53 , which is essential for colonization of the gastric mucosa.

54 between H pylori and progenitor cells in the gastric mucosa.

55 duced levels of myeloperoxidase (MPO) in the gastric mucosa.

56 ere is no experimental model of normal human gastric mucosa.

57 ase, for efficient colonization of the human gastric mucosa.

58 he target for bacterial binding to the human gastric mucosa.

59 . pylori-infected, compared with uninfected, gastric mucosa.

60 in sources of acetylcholine (ACh) within the gastric mucosa.

61 portant for in vivo colonization of the host gastric mucosa.

62 ant for colonization and survival within the gastric mucosa.

63 n of bcl-2 and up-regulation of bax genes in gastric mucosa.

64 lso expedites the healing of already damaged gastric mucosa.

65 ced activation of caspase-9 and caspase-3 in gastric mucosa.

66 ssion, Leb-binding activity, and adhesion to gastric mucosa.

67 emical analysis of human biopsies and rodent gastric mucosa.

68 hanced infiltration of inflammatory cells in gastric mucosa.

69 increasing mutagenesis in H pylori-infected gastric mucosa.

70 chromaffin-like cell lineages in the oxyntic gastric mucosa.

71 d the vertical "pit and crypt" morphology of gastric mucosa, (2) disorganized architecture with inhom

72 vivin expression and extent of injury in rat gastric mucosa; (2) the effects of indomethacin, NS-398,

73 with histological finding of non-transformed gastric mucosa, 20 patients with AG or IM (AG/IM GC-), a

74 In PHT gastric mucosa 6 h after injury, PTEN protein levels wer

75 d can establish a long-term infection of the gastric mucosa, a condition that affects the relative ri

76 ylori establishes lifelong infections of the gastric mucosa, a niche considered hostile to most micro

77 The epithelial cell kinetics in AG and IM in gastric mucosa adjacent to gastric cancer is still uncle

78 sa (p < 0.0001) but not compared to AG/IM in gastric mucosa adjacent to GC.

79 The expression of AM in PHT gastric mucosa after ethanol-induced injury is significa

80 ly demonstrated impaired angiogenesis of PHT gastric mucosa after ethanol-induced injury.

81 ation and inhibits dysplastic changes in the gastric mucosa after infection of mice with H pylori or

82 to the stomach and in the protection of the gastric mucosa against H. felis infection.

83 Infection of the gastric mucosa AGS cells by H. pylori, the gastric cance

84 PHT gastric mucosa also has excessive nitric oxide (NO) prod

85 intimately associated with the cells of the gastric mucosa, although there was not a strict correlat

86 of key growth signalling pathways within the gastric mucosa and as such lead to growth alterations.

87 Increased MMP-1 mRNA levels in the gastric mucosa and epithelial cells were observed in H.

88 n enhanced the expression of iNOS in the rat gastric mucosa and exacerbated gastric injury in the pre

89 expression in normal and H. pylori -infected gastric mucosa and gastric epithelial cells was determin

90 calized with HDC-immunoreactivity within the gastric mucosa and gastric submucosa and also within the

91 pylori-induced gastritis with that in normal gastric mucosa and in non-H. pylori gastritis.

92 etion was significantly impaired in isolated gastric mucosa and in the intact organ.

93 f innate immunity, is expressed in the human gastric mucosa and is capable of aggregating H. pylori.

94 nstitutive and regulated expression by human gastric mucosa and its bactericidal activity against the

95 AM is involved in the impaired repair of PHT gastric mucosa and its microvasculature after damage.

96 ved in IL-18 induction in H. pylori-infected gastric mucosa and may contribute to gastric injury.

97 al potential of CD4(+) and CD8(+) T cells in gastric mucosa and peripheral blood to produce cytokines

98 n protein levels and caused severe injury of gastric mucosa and RGM-1 cells.

99 s revealed a relationship between changes in gastric mucosa and risk of esophageal squamous cell carc

100 TFIZ1 mRNA was cloned from gastric mucosa and sequenced.

101 e TFF1 complex was immunopurified from human gastric mucosa and shown to comprise two proteins joined

102 severe gastritis involving 50 to 100% of the gastric mucosa and strong DTH responses not present in C

103 cterized by eosinophilic infiltration of the gastric mucosa and Th2 differentiation of transgenic T c

104 ein family, is expressed in the normal human gastric mucosa and that its levels decrease in the mucos

105 naling mechanisms for eNOS activation in PHT gastric mucosa and the role of TNF-alpha in this signali

106 contributes to their clearance in the human gastric mucosa and this is associated with anti-inflamma

107 ogenitor cells induces transformation of the gastric mucosa and tumorigenesis in the antrum in mice.

108 Because activated lymphocytes persist in the gastric mucosa, and because a high multiplicity of infec

109 ction results in chronic inflammation of the gastric mucosa, and progression of chronic inflammation

110 ter pylori, bacteria that colonize the human gastric mucosa, are naturally competent for transformati

111 lymphoid tissue (MALT) may accumulate within gastric mucosa as a result of long standing Helicobacter

112 ter taste receptors in the antral and fundic gastric mucosa as well as in the lining of the duodenum.

113 sia (IM) is a pre-malignant condition of the gastric mucosa associated with increased gastric cancer

114 ten causing gastritis, peptic ulcer disease, gastric mucosa-associated lymphatic tissue lymphoma, or

115 Gastric mucosa-associated lymphoid tissue (MALT) lymphom

116 The development of gastric mucosa-associated lymphoid tissue (MALT) lymphom

117 BALB/c mice has been described as a model of gastric mucosa-associated lymphoid tissue (MALT) lymphom

118 hed as the standard of care in patients with gastric mucosa-associated lymphoid tissue (MALT) lymphom

119 tion induces remission in most patients with gastric mucosa-associated lymphoid tissue lymphoma (GML)

120 etiological factor in peptic ulcer disease, gastric mucosa-associated lymphoid tissue lymphoma, and

121 e most studied, gastrointestinal lymphoma is gastric mucosa-associated lymphoid tissue lymphoma, whic

122 cobacter pylori eradication in patients with gastric mucosa-associated lymphoid tissue lymphoma.

123 sound in treatment planning in patients with gastric mucosa-associated lymphoid tissue lymphoma.

124 s strong association with gastric cancer and gastric mucosa-associated lymphoid tissue lymphoma.

125 c relationship to gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue lymphoma.(2) I

126 This is important as early-stage gastric mucosa-associated lymphoid tissue lymphomas can

127 s to modulate the risk of lymphomagenesis in gastric mucosa-associated lymphoid tissue.

128 fection initiates a series of changes in the gastric mucosa, beginning with atrophic gastritis and le

129 uppressed the expression of ER chaperones at gastric mucosa both with and without administration of i

130 e associated with H. pylori infection of the gastric mucosa but may also limit the host's ability to

131 lori infection, T cells are recruited to the gastric mucosa, but the host T-cell response is not suff

132 e initiation of intestinal metaplasia in the gastric mucosa, but the role of CDX2 in established gast

133 prostaglandin E2 (PGE2) production in rats' gastric mucosa by 33% following a dose of 100 mg/kg.

134 astric prostaglandin E2 (PGE2) production in gastric mucosa by 77% but caused minimal GI damage.

135 the density of CCK-A receptor fibers in the gastric mucosa by approximately 50%, whereas celiac/supe

136 It is upregulated in the gastric mucosa by chronic Helicobacter infection; howeve

137 Colonization of gastric mucosa by Helicobacter pylori leads to epithelia

138 essential for successful colonization of the gastric mucosa by Helicobacter pylori.

139 MMP-7 was detected in human gastric mucosa by immunohistochemistry and in H. pylori/

140 ration of spirochetes in diffusely inflammed gastric mucosa by staining with a fluorescent monoclonal

141 acterial infection and carcinogenesis in the gastric mucosa by suppressing putative gastric progenito

142 terized bacterial diversity within the human gastric mucosa by using a small subunit 16S rDNA clone l

143 Helicobacter pylori infection of the gastric mucosa can be found in approximately 50% of the

144 Inflammation of the gastric mucosa can progress to metaplastic changes in th

145 Helicobacter pylori infection of the gastric mucosa causes an active-chronic inflammation tha

146 ncer and HFE-145 immortalized non-neoplastic gastric mucosa cell lines.

147 nd vastly increased numbers of proliferating gastric mucosa cells, suggesting a role of SET-CAN in pr

148 s were enriched approximately 10-fold in the gastric mucosa compared with peripheral blood (P<0.0001)

149 at HLA-DR(+) mononuclear phagocytes in human gastric mucosa contain cytokeratin-positive and TUNEL-po

150 Importantly, we show that H. pylori-infected gastric mucosa contained significantly higher numbers of

151 in control biopsy samples of non-transformed gastric mucosa (Control).

152 In immune mice, T-cell recruitment to the gastric mucosa correlated with a continuous rise in IL-1

153 acteria that persistently colonize the human gastric mucosa despite the recruitment of immune cells.

154 ver, neoplastic transformation of the antral gastric mucosa does not require gastrin.

155 n increase in CD4(+) T cells occurred in the gastric mucosa during acute H. pylori infection as early

156 Myeloid cells recruited to the gastric mucosa during H. pylori infection have been dire

157 < .01, respectively, active vs placebo) and gastric mucosa eosinophils counts (239 eosinophils/mm(2)

158 Here we show that in PHT gastric mucosa, ERK2 activation by oxidative stress is i

159 In SO gastric mucosa, ERK2 phosphorylation and activity were s

160 and pathology of the Deltafur strain in the gastric mucosa even after comparable levels of colonizat

161 In contrast, in PHT gastric mucosa following alcohol injury, neither ERK2 ph

162 ted whether ERK activation is altered in PHT gastric mucosa following alcohol injury.

163 onse, Helicobacter pylori can persist in the gastric mucosa for decades.

164 p53, cyclin D1, and ki67 immunoexpression in gastric mucosa from 31 HP chronic gastritis patients and

165 induction of MMP-7 may serve to protect the gastric mucosa from pathophysiologic processes that prom

166 ssue morphology, cellular composition of the gastric mucosa, gastric acid content, and plasma levels

167 In mice, ectopic expression of CDX2 in the gastric mucosa gives rise to intestinal metaplasia and i

168 contrast, extracts prepared from neoplastic gastric mucosa had reduced levels of pepsin A and did no

169 Portal hypertensive (PHT) gastric mucosa has impaired injury healing, but the unde

170 Aging gastric mucosa has impaired mucosal defense and increase

171 Portal hypertensive (PHT) gastric mucosa has increased susceptibility to injury an

172 PHT gastric mucosa has numerous abnormalities such as reduce

173 PHT gastric mucosa has significantly increased (1) eNOS phos

174 epithelial cell line derived from normal rat gastric mucosa), HGF caused an increase in COX-2 mRNA an

175 of the parietal cell, and metaplasia of the gastric mucosa; however, the absence of the pump appears

176 hrough both T2-weighted MR imaging and Raman gastric mucosa imaging using functionalized MGNs.

177 on triggers neoplastic transformation of the gastric mucosa in a small subset of patients, but the ri

178 ted to the severity of inflammation in human gastric mucosa in either a synchronous or metachronous m

179 t may serve to maintain the integrity of the gastric mucosa in older animals.

180 rol mice had an influx of macrophages to the gastric mucosa in response to H pylori infection; this w

181 in the superficial mucosa, compared with the gastric mucosa in sham-operated rats.

182 as the small intestine, thus implicating the gastric mucosa in the metabolism of dietary glutamate.

183 interactions between NOS and COX in the rat gastric mucosa in the presence and absence of lipopolysa

184 s critical for H. pylori colonization of the gastric mucosa include urease, flagella, adhesins, and d

185 s indicate that, in contrast to normotensive gastric mucosa, inhibition of COX-1 alone is sufficient

186 his detection seeks to sense ischemia in the gastric mucosa inside the stomach, an event indicative o

187 two conditions known to oscillate within the gastric mucosa: iron limitation and low pH.

188 Adhesion of Helicobacter pylori to the gastric mucosa is a necessary prerequisite for the patho

189 Helicobacter pylori infection of the gastric mucosa is a significant cause of morbidity and m

190 e infection model, PMN infiltration into the gastric mucosa is dramatically reduced in Coro1A(-/-) mi

191 ated whether impaired healing of injured PHT gastric mucosa is due to abnormal PTEN expression/activa

192 een growth factors and prostaglandins in the gastric mucosa is not well characterized.

193 h H. pylori induces RANTES expression in the gastric mucosa is unknown.

194 , flagellated bacteria that adheres to human gastric mucosa, is strongly associated with gastric ulce

195 which does not damage normal (normotensive) gastric mucosa, is sufficient to cause PHT gastric damag

196 microaerophilic bacterium that colonizes the gastric mucosa, leading to disease conditions ranging fr

197 synthase (eNOS) in portal hypertensive (PHT) gastric mucosa leads to hyperdynamic circulation and inc

198 The gastric mucosa maintains structural integrity and functi

199 , entry of proinflammatory proteins into the gastric mucosa may contribute to the induction of a muco

200 In PHT gastric mucosa, MKP-1 mRNA and protein expression were i

201 cavenger, reduces the oxidative state in PHT gastric mucosa, normalizes MKP-1 expression, and thereby

202 transcriptase PCR in infected and uninfected gastric mucosa obtained from Bhutan and from the Dominic

203 tological abnormalities were observed in the gastric mucosa of 9-week-old NHE4-/- mice, including sha

204 Gastric mucosa of aging (vs young) rats has a 60% reduct

205 The down-regulation of PTEN in gastric mucosa of aging rats completely reversed its inc

206 (1) Gastric mucosa of aging rats has significantly reduced b

207 ighly successful pathogen that colonizes the gastric mucosa of approximately 50% of the world's popul

208 were found at an increased frequency in the gastric mucosa of biopsy specimens from H. pylori-infect

209 The gastric mucosa of cyclooxygenase-1 knockout mice was mor

210 ed the roles of transcription factors in the gastric mucosa of H pylori-infected gerbils over the cou

211 T cells have been detected infiltrating the gastric mucosa of H. pylori-infected patients, which con

212 nt with the mouse data, DCs infiltrating the gastric mucosa of human H. pylori carriers exhibited a s

213 gram-negative bacterium, which colonizes the gastric mucosa of humans and is implicated in a wide ran

214 > 0.7) between the H. pylori density of the gastric mucosa of humans and mice when using the same H.

215 Neutrophil numbers in the gastric mucosa of immune Kitl(Sl)/Kitl(Sl-d) mice were l

216 valuating the immunodominant antigens at the gastric mucosa of infected persons and possibly in deter

217 terferon-gamma were markedly elevated in the gastric mucosa of infected TFF2(-/-) mice at both 6 and

218 H. pylori infection induced mutations in the gastric mucosa of male and female gpt delta C57BL/6 mice

219 We found that hydrogen is available in the gastric mucosa of mice and that its use greatly increase

220 With regard to H. pylori, the gastric mucosa of mice deficient in the tyrosine phospha

221 feoB mutants were unable to colonize the gastric mucosa of mice, indicating that FeoB makes an im

222 H. pylori colonization in the gastric mucosa of OLFM4 KO mice was significantly lower

223 Premalignant and malignant lesions from the gastric mucosa of patients had increased levels of AURKA

224 By contrast, very few PNAd were found in the gastric mucosa of patients with chemical gastritis cause

225 y normal appearing, non-polypoid colonic and gastric mucosa of patients with familial juvenile polypo

226 methylation of MGMT was more frequent in the gastric mucosa of patients with H pylori gastritis (69.7

227 ssion of MAP kinase phosphatase-1 (MKP-1) in gastric mucosa of PHT and sham-operated (SO) normal rats

228 In contrast, gastric mucosa of recipient SCID mice colonized by H. py

229 ase E (CPE) and Interleukin 1B (IL1B) in the gastric mucosa of same patient.

230 ecrosis factor-alpha and inflammation in the gastric mucosa of Tff1(-/-) mice (r = 0.62; P = .0001).

231 Tff1-/- mice was compared to that of normal gastric mucosa of wild-type mice.

232 nstrated that C. fetus could also infect the gastric mucosa of wild-type, outbred ICR mice.

233 We also examined susceptibility of gastric mucosa of young and aging rats to ethanol injury

234 t of the intrinsic neural innervation to the gastric mucosa originates in the myenteric plexus.

235 We conclude that, in injured PHT gastric mucosa, overexpressed/activated PTEN leads to th

236 The loss of parietal cells from the gastric mucosa (oxyntic atrophy) is a critical step in t

237 cantly increased compared to not transformed gastric mucosa (p < 0.0001) but not compared to AG/IM in

238 stric tumors as compared with that in normal gastric mucosa (P < 0.0001), which was significantly ass

239 ter pylori, bacteria that colonize the human gastric mucosa, possess a large number of genes for rest

240 s is the loss of glandular structures in the gastric mucosa, presumably as the consequence of increas

241 logical changes in the pyloric antrum of the gastric mucosa, progressing from gastritis to hyperplasi

242 gical processes including maintenance of the gastric mucosa, proliferation of enterochromaffin-like c

243 The gastric mucosa provides a stringent epithelial barrier a

244 In aging human gastric mucosa, PTEN expression was significantly increa

245 versed all of the above abnormalities in PHT gastric mucosa, reduced mucosal injury, and enhanced hea

246 ption factor activation in H pylori-infected gastric mucosa remain unclear.

247 concentration of purines present within the gastric mucosa remains unknown.

248 Ultrastructural analysis of AE2(-/-) gastric mucosa revealed abnormal parietal cell structure

249 Gastric mucosa samples were collected at 35, 50, or 80 w

250 gastric cancer samples and 113 nonneoplastic gastric mucosa samples.

251 ow how mutations expand in normal mucosa and gastric mucosa showing intestinal metaplasia.

252 that PNAd on HEV-like vessels present in the gastric mucosa subsequent to H. pylori infection is simi

253 ge mutants proficiently colonized the murine gastric mucosa, suggesting that the amino acid compositi

254 zation of the LabA target, restricted to the gastric mucosa, suggests a plausible explanation for the

255 Stromal factors in gastric mucosa suppressed H pylori-stimulated DC activat

256 which is increased in the H. pylori-infected gastric mucosa, synergizes with H. pylori in downregulat

257 r capacity to colonize and/or persist in the gastric mucosa than did strain J99.

258 e leads to a chronic inflammation within the gastric mucosa that actually promotes the development of

259 2 (TFF2)-a protein expressed by PDGs and the gastric mucosa that are involved in epithelial repair an

260 fection triggers chronic inflammation of the gastric mucosa that may progress to gastric cancer.

261 f an increase in the opioid signaling within gastric mucosa that may results in a shift to proinflamm

262 infection causes chronic inflammation of the gastric mucosa that results from an ineffective immune r

263 er, with the cytokine environment within the gastric mucosa the strongest predictor of disease risk.

264 Despite a vigorous immune response by the gastric mucosa, the bacterium survives in its ecological

265 though T cells are recruited to the infected gastric mucosa, they have been reported to be hyporespon

266 Heat shock protein 70 (HSP70) protects the gastric mucosa through inhibition of apoptosis, proinfla

267 conclusion, these findings show that in PHT gastric mucosa, TNF-alpha stimulates eNOS phosphorylatio

268 ulation of MDSCs that predict a shift in the gastric mucosa to a metaplastic phenotype.

269 reverses the increased susceptibility of PHT gastric mucosa to alcohol injury.

270 obacter pylori interacts intimately with the gastric mucosa to avoid the microbicidal acid in the sto

271 g, RX 77368, increased the resistance of the gastric mucosa to ethanol injury through vagal pathways

272 ociated with increased susceptibility of the gastric mucosa to injury by a variety of factors, includ

273 d i.c. TRH to increase the resistance of the gastric mucosa to injury caused by 45% ethanol.

274 tion of PTEN affects susceptibility of aging gastric mucosa to injury.

275 ese changes increase susceptibility of aging gastric mucosa to injury.

276 vity of Akt, and eNOS phosphorylation in PHT gastric mucosa to normal levels.

277 cyclin D1, and ki67 immunoreactivity in the gastric mucosa to the level of controls.

278 Bacterial colonisation of the gastric mucosa triggers lymphoid infiltration and the fo

279 ogic features and recruitment of BMDC to the gastric mucosa using immunohistochemistry and fluorescen

280 Metaplastic gastric mucosa was analyzed by dual immunostaining for T

281 The gastric mucosa was examined at early, mid, and late inte

282 was reduced in Hip1r-deficient mice, and the gastric mucosa was grossly transformed, with fewer parie

283 thetized mice were exteriorized, and exposed gastric mucosa was imaged by confocal microscopy.

284 ol administration, AM mRNA expression in PHT gastric mucosa was significantly decreased by 81%, espec

285 In PHT gastric mucosa we studied (1) eNOS phosphorylation (at s

286 evelopment, maintenance, and function of the gastric mucosa, we used gene targeting to prepare mice l

287 transcription 1 (STAT1) levels in the antral gastric mucosa were measured by enzyme-linked immunosorb

288 IL-18 levels in H. pylori-infected gastric mucosa were well correlated with the severity of

289 Helicobacter pylori inhabits the gastric mucosa where it senses and responds to various s

290 bacterial pathogens of humans, colonizes the gastric mucosa, where it appears to persist throughout t

291 Helicobacter pylori chronically infects the gastric mucosa, where it can be found free in mucus, att

292 le report of the chronically infected murine gastric mucosa, where the BM origin of the stem cells ca

293 FoxM1b protein in the mucous neck region of gastric mucosa, whereas we observed strong staining for

294 evels of sonic hedgehog are expressed in the gastric mucosa, which has served to direct analysis of i

295 esults in a low acid-pepsin secretion by the gastric mucosa, which in turn results in a reduced relea

296 on induces chronic inflammation in the human gastric mucosa, which is associated with development of

297 nsing of dietary glutamate in the developing gastric mucosa, which is poorly developed in premature i

298 revealed the presence of inflammation in the gastric mucosa with both A. lwoffii and H. pylori infect

299 ith Helicobacter pylori (H. pylori)-infected gastric mucosa with intestinal metaplasia (IM) changes.

300 e injection, in the glandular portion of the gastric mucosa with penetration of red blood cells and i