ライフサイエンスコーパス: gastric mucosa

1 iferative potential of infected Stat3(SA/SA) gastric mucosa.

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

3 emical analysis of human biopsies and rodent gastric mucosa.

4 hanced infiltration of inflammatory cells in gastric mucosa.

5 increasing mutagenesis in H pylori-infected gastric mucosa.

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

7 ited limited Th1 and Th17 responses in their gastric mucosa.

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

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

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

11 ghly specialized organelles and cells in the gastric mucosa.

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

13 ritical regulators of differentiation in the gastric mucosa.

14 optic atrophy 1 (OPA1) and mitofusins in rat gastric mucosa.

15 stablish a persistent infection in the human gastric mucosa.

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

17 is synthesized in the exocrine pancreas and gastric mucosa.

18 blood cells and inflammatory cells into the gastric mucosa.

19 approximately 25 kDa complex in normal human gastric mucosa.

20 nses to maintain chronic colonization of the gastric mucosa.

21 common and persistent human pathogen of the gastric mucosa.

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

23 or the protective phospholipid layers of the gastric mucosa.

24 metastases when compared with that in normal gastric mucosa.

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

26 hat activates sensory neurons located in the gastric mucosa.

27 TFIZ1 is expressed and secreted in normal gastric mucosa.

28 lineage expansion within H. pylori-infected gastric mucosa.

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

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

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

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

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

34 in the relatively hostile environment of the gastric mucosa.

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

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

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

38 d in response to interactions with mammalian gastric mucosa.

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

40 11c(+) dendritic cells (DCs) with PCs in the gastric mucosa.

41 hly restricted ecological niche in the human gastric mucosa.

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

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

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

45 w therapeutic modality for protection of PHT gastric mucosa.

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

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

48 pylori to specific cell lineages within the gastric mucosa.

49 rostaglandin synthesis and do not damage the gastric mucosa.

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

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

52 modulating effector T cell responses at the gastric mucosa.

53 and increased neutrophil accumulation at the gastric mucosa.

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

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

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

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

58 1B transcripts are more important than 1A in gastric mucosa.

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

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

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

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

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

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

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

66 ant for colonization and survival within the gastric mucosa.

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

68 lso expedites the healing of already damaged gastric mucosa.

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

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

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

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

73 ac, considering the pH gradient found in the gastric mucosa (3 < pH < 7.4).

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

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

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

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

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

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

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

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

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

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

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

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

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

92 n essential role in keeping the integrity of gastric mucosa and its barrier function.

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

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

95 H. pylori colonizes the human gastric mucosa and persists for decades.

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

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

98 Helicobacter pylori colonizes the gastric mucosa and secretes a pore-forming toxin (VacA).

99 TFIZ1 mRNA was cloned from gastric mucosa and sequenced.

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

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

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

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

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

105 ic the protective phospholipid layers of the gastric mucosa and to describe the interactions with dic

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

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

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

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

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

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

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

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

114 Gastric mucosa-associated lymphoid tissue (MALT) lymphom

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

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

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

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

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

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

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

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

123 ic ulcer disease, gastric adenocarcinoma, or 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 uppressed the expression of ER chaperones at gastric mucosa both with and without administration of i

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

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

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

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

133 Lifelong infection of the gastric mucosa by Helicobacter pylori can lead to peptic

134 Colonization of gastric mucosa by Helicobacter pylori leads to epithelia

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

136 d CXCL1, which increased infiltration of the gastric mucosa by immune cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

155 < .01, respectively, active vs placebo) and gastric mucosa eosinophils counts (239 eosinophils/mm(2)

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

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

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

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

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

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

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

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

164 The gastric mucosa from the double KO mice did not show phos

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

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

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

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

169 Aging gastric mucosa has impaired mucosal defense and increase

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

171 PHT gastric mucosa has numerous abnormalities such as reduce

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

188 The human gastric mucosa is the most active layer of the stomach w

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

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

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

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

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

194 The gastric mucosa maintains structural integrity and functi

195 s of the external phospholipid layers of the gastric mucosa may constitute an additional toxicity mec

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

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

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

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

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

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

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

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

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

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

206 s in close proximity to S-phase cells in the gastric mucosa of gastritis patients.

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

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

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

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

211 > 0.7) between the H. pylori density of the gastric mucosa of humans and mice when using the same H.

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

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

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

215 In the gastric mucosa of mice and patients with gastritis, pS-S

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

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

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

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

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

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

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

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

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

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

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

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

228 The gastric mucosa of the stomach is continually exposed to

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

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

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

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

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

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

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

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

237 Once the micromotor penetrates the gastric mucosa (pH >= 6.0), its pH-responsive cap dissol

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

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

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

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

242 The gastric mucosa provides a stringent epithelial barrier a

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

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

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

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

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

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

249 gastric cancer samples and 113 nonneoplastic gastric mucosa samples.

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

251 The IF pattern was composed of liver and gastric mucosa staining on rat kidney/liver/stomach sect

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

285 ough primarily associated with the mammalian gastric mucosa, we conclude that loss of Tff2 in the dev

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

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

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

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

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

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

296 rmaceutical ingredients directly through the gastric mucosa while avoiding perforation.

297 , miR-124a-3, miR-129-2, and miR-137, in the gastric mucosa with and without GC, i.e., in atrophic mu

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