ライフサイエンスコーパス: esophagus

1 iatus are arranged like a "noose" around the esophagus.

2 rticularly in the squamous epithelium of the esophagus.

3 cetate, using applied tension, to an ex vivo esophagus.

4 ribed expression pattern in sporadic Barrett esophagus.

5 n medical therapy in patients with Barrett's esophagus.

6 ignant to malignant progression in Barrett's esophagus.

7 should be managed as nondysplastic Barrett's esophagus.

8 a, inflammatory bowel diseases and Barrett's Esophagus.

9 ng from the muscularis propria of the distal esophagus.

10 iagnosed with LGD vs nondysplastic Barrett's esophagus.

11 egorization of lichenoid inflammation in the esophagus.

12 tion, and values increased axially along the esophagus.

13 EoE that might allow pathogens to invade the esophagus.

14 ine lungs via an optical fiber placed in the esophagus.

15 or the diagnosis and management of Barrett's esophagus.

16 well as on the phrenic nerve and within the esophagus.

17 n to GERD, and the complication of Barrett's esophagus.

18 astric corpus microbiota in ESCC with normal esophagus.

19 patients with biopsy-proven carcinoma of the esophagus.

20 homeostasis and EoE development in the adult esophagus.

21 ues that are constantly replenished like the esophagus.

22 for those who treat patients with Barrett's esophagus.

23 or epithelial morphogenesis in the embryonic esophagus.

24 a differs in early ESCC and ESD from healthy esophagus.

25 rcinomas and squamous cell carcinomas of the esophagus.

26 bese patients and for long-segment Barrett's esophagus.

27 associated with a reduced risk of Barrett's esophagus.

28 303 primary care controls without Barrett's esophagus.

29 iation between statins and risk of Barrett's esophagus.

30 to severe esophagitis and 7% with Barrett's esophagus.

31 se is an underappreciated risk for Barrett's esophagus.

32 phagus and inactive in squamous-lined, adult esophagus.

33 ous cell carcinoma and adenocarcinoma of the esophagus.

34 pithelia, including the paw skin, tongue and esophagus.

35 select patients for screening for Barrett's esophagus.

36 out their effect on development of Barrett's esophagus.

37 embryonic esophagus compared with postnatal esophagus.

38 oncern is the reported relation to Barrett's esophagus.

39 r, SERPINB genes are highly expressed in the esophagus.

40 safe modality for catheter ablation near the esophagus.

41 afe and effective in patients with Barrett's esophagus.

42 were included in the definition of Barrett's esophagus.

43 gn, each of which forms a "noose" around the esophagus.

44 ocarcinoma (EAC) in patients with LGD of the esophagus.

45 ate the association between IP and Barrett's esophagus.

46 here is reversion to nondysplastic Barrett's esophagus.

47 gs (IGLEs) were identified in the stomach or esophagus.

48 patients undergoing endoscopy for Barrett's esophagus.

49 e observed excess deaths from cancers of the esophagus (100 observed vs. 93.1 expected), stomach (182

50 columnar cell metaplasia, 5.8% in Barrett's esophagus, 19.0% in low grade dysplasia, 35.7% in high g

51 ients, 506 (83.5%) had adenocarcinoma of the esophagus, 323 (53%) died within 5 years of surgery, and

52 ery for squamous cell carcinoma (SCC) of the esophagus, adenocarcinomas of the esophagogastric juncti

53 with a significantly lower risk of Barrett's esophagus (adjusted OR = 0.57; 95% CI: 0.38-0.87) compar

54 We report that Pirb is upregulated in the esophagus after inducible overexpression of IL-13 (CC10-

55 segment of columnar metaplasia in the distal esophagus, also called an irregular Z line, are encounte

56 segment of columnar metaplasia in the distal esophagus, also called an irregular Z line, are encounte

57 lence of gastric heterotopia in the cervical esophagus, also termed inlet patch (IP), varies substant

58 tics, 1 case of adenocarcinoma of the distal esophagus and 1 case of gastric lymphoma.

59 us tissue in a further 12 patients (3 cancer esophagus and 9 cancer stomach) involving 175 measuremen

60 is randomized trial of patients with Barrett esophagus and a confirmed diagnosis of low-grade dysplas

61 s to potentiate the development of Barrett's esophagus and adenocarcinoma.

62 of chronic acid biliary reflux to Barrett's esophagus and cancer.

63 ole-genome sequencing on 23 paired Barrett's esophagus and EAC samples, together with one in-depth Ba

64 uxate is a noxious material that injures the esophagus and elicits symptoms.

65 ma and Barrett's esophagus from the Barretts Esophagus and Esophageal Adenocarcinoma Consortium (BEAC

66 and environmental architecture of Barrett's esophagus and esophageal adenocarcinoma.

67 sive esophagitis and eventually by Barrett's esophagus and esophageal adenocarcinoma.

68 cible model for the development of Barrett's esophagus and esophageal adenocarcinoma.

69 l maturation and the pathogenesis of Barrett esophagus and esophageal adenocarcinoma.

70 s in particular, in development of Barrett's esophagus and esophageal carcinoma.

71 equencing from 25 pairs of EAC and Barrett's esophagus and from 5 patients whose Barrett's esophagus

72 icacy of surveillance programs for Barrett's esophagus and gastric intestinal metaplasia.

73 All adenocarcinomas (ADC) of the esophagus and GEJ-patients undergoing primary resection

74 cells generated from patients with Barrett's esophagus and human esophageal specimens, we found that

75 aling is active in columnar-lined, embryonic esophagus and inactive in squamous-lined, adult esophagu

76 ent of HGD or EAC in patients with Barrett's esophagus and LGD.

77 lated to obesity alter the risk of Barrett's esophagus and may work synergistically with gastroesopha

78 ance endoscopy among patients with Barrett's Esophagus and no or low-grade dysplasia.

79 no significant association between Barrett's esophagus and nonstatin lipid-lowering medications (P =

80 Mucosal biopsy from esophagus and rectus confirmed amyloidosis by Congo red

81 rging data on the risk factors for Barrett's esophagus and risk stratification tools.

82 found that ARID3B expression is decreased in esophagus and stomach tumors compared to normal correspo

83 to the hypothesis that to prevent Barrett's esophagus and subsequent esophageal adenocarcinoma in hu

84 t Practice Advice 3: Patients with Barrett's esophagus and symptomatic GERD should take a long-term P

85 The relationship between the esophagus and the left atrial posterior wall is variable

86 sophagus and from 5 patients whose Barrett's esophagus and tumor were extensively sampled.

87 affected by MMP were examined apart from the esophagus (and larynx in a subset).

88 ined as intestinal metaplasia in the tubular esophagus) and dysplastic BE recurrence among patients w

89 cluding 7 studies of patients with Barrett's esophagus, and 2 studies comparing EAC risk after antire

90 evelopment of esophageal strictures, Barrett esophagus, and esophageal adenocarcinoma.

91 w measurements of 'k' (W/m.K) of porcine PV, esophagus, and phrenic nerve, all needed for PV cryoabal

92 d by in vivo imaging of a mouse colon, a rat esophagus, and small airways in sheep.

93 alimentary canal; these included the tongue, esophagus, and stomach in addition to the small intestin

94 MUC2, an intestinal mucin found in Barrett's esophagus, and the MUC2-processing protein AGR2.

95 urgery may halt the progression of Barrett's esophagus, and this might reduce the risk of cancer deve

96 nuclei innervate jaw, facial, pharynx/larynx/esophagus, and tongue muscles, respectively.

97 e overlap between EAC and adjacent Barrett's esophagus; and (iii) despite differences in specific cod

98 ay 7, all densities had disappeared, and all esophaguses appeared completely normalized.

99 Cancers of the stomach and esophagus are among the most challenging cancers of the

100 f radiofrequency ablation (RFA) in Barrett's esophagus are highlighted in this review.

101 Newer forms of management of Barrett esophagus are showing significant promise as potentially

102 nic effects of this new energy source on the esophagus are unknown.

103 t non-transformed squamous epithelium of the esophagus, as well as in control biopsy samples from eso

104 ed of concomitant disease and 2 of Barrett's esophagus-associated cancer.

105 Barrett's esophagus-associated high-grade dysplasia is commonly tr

106 with biopsies from noneroded areas of distal esophagus at baseline (taking PPIs) and at 1 week and 2

107 s that occur during progression of Barrett's esophagus, based on findings from clinical studies and m

108 ic factors that determine risk for Barrett's esophagus (BE) and progression to esophageal adenocarcin

109 of patients with reflux to detect Barrett's esophagus (BE) and surveillance of BE to detect early EA

110 A proportion of patients with Barrett's esophagus (BE) are diagnosed with esophageal adenocarcin

111 Barrett's esophagus (BE) increases the risk of esophageal adenocar

112 Barrett's esophagus (BE) is a common disease in which the lining o

113 Barrett's esophagus (BE) is a commonly undiagnosed condition that

114 Complete eradication of Barrett's esophagus (BE) often requires multiple sessions of radio

115 ensive models to determine risk of Barrett's esophagus (BE) or esophageal adenocarcinoma (EAC) based

116 Barrett's esophagus (BE) patients are routinely screened for high

117 ay accelerate the progression from Barrett's esophagus (BE) to esophageal adenocarcinoma (EA) are not

118 s for the rate of progression from Barrett's esophagus (BE) to esophageal adenocarcinoma (EAC) vary.

119 efficacy of antireflux surgery on Barrett's esophagus (BE) using BRAVO wireless pH monitoring.

120 Evaluation of patients with Barrett's esophagus (BE) using dye-based chromoendoscopy, optical

121 & AIMS: The goal of treatment for Barrett's esophagus (BE) with dysplasia is complete eradication of

122 Barrett's esophagus (BE) with low-grade dysplasia (LGD) can progre

123 imulated interest in screening for Barrett's esophagus (BE), a precursor to esophageal cancer.

124 oesophageal reflux disease (GERD), Barrett's esophagus (BE), and non-steroidal anti-inflammatory drug

125 often referred to as patients with Barrett's esophagus (BE), are enrolled in surveillance programs.

126 (HGD), low grade dysplasia (LGD), Barrett's esophagus (BE), columnar cell metaplasia (CM), squamous

127 and premalignant tissues, such as Barrett's esophagus (BE), have the potential to improve the assess

128 Screening for Barrett's esophagus (BE), the only known precursor lesion of EAC,

129 arise in a metaplastic epithelium, Barrett's esophagus (BE), which is associated with greatly increas

130 The incidence of Barrett's esophagus (BE)-associated esophageal adenocarcinoma (EAC

131 nocarcinoma (EAC) in patients with Barrett's esophagus (BE).

132 gement decisions for patients with Barrett's esophagus (BE).

133 on (RFA) is commonly used to treat Barrett's esophagus (BE).

134 th erosive reflux disease (ERD) or Barrett's esophagus (BE).

135 e dysplasia (LGD) in patients with Barrett's esophagus (BE).

136 e dysplasia (LGD) in patients with Barrett's esophagus (BE).

137 ides a surgical solution for a foreshortened esophagus but has been associated with postoperative dys

138 ntrolled before the development of Barrett's esophagus by methods other than acid-suppression therapy

139 d Barrett esophagus, termed familial Barrett esophagus, by using high-throughput sequencing in affect

140 re patients with bladder, lung, pancreas, or esophagus cancer who were diagnosed in 2001 to 2007 and

141 r (20.3%; 95% CI, 8.9% to 31.6%) and stomach/esophagus cancers (21.2%; 95% CI, 12.8% to 29.6%).

142 amples, together with one in-depth Barrett's esophagus case study sampled over time and space, we hav

143 d the growth rate of nondysplastic Barrett's esophagus cells.

144 en-mediated clinicopathologic disease of the esophagus characterized by an eosinophil-predominant inf

145 tive mortality after operations for bladder, esophagus, colon, lung, pancreas, and stomach cancers.

146 is more highly expressed in murine embryonic esophagus compared with postnatal esophagus.

147 tients with a confirmed diagnosis of Barrett esophagus containing low-grade dysplasia at 9 European s

148 Barrett esophagus containing low-grade dysplasia is associated w

149 d intolerance and 10 patients with Barrett's esophagus (controls) without IBS symptoms were examined

150 tis (EoE) is an inflammatory disorder of the esophagus defined by eosinophil infiltration and tissue

151 mmatory, genetically impacted disease of the esophagus, defined clinically by symptoms of esophageal

152 to evaluate whether different definitions of esophagus (DEs) impact on the esophageal toxicity predic

153 during a 10-year period before the Barrett's esophagus diagnosis date for patients and study endoscop

154 Many patients with Barrett's esophagus do not adhere to guideline-recommended endosco

155 entilation (32 degrees C within 5 min in the esophagus) dramatically attenuated the post-cardiac arre

156 onary vein (PV) junction, phrenic nerve, and esophagus during PV isolation (PVI) using the second-gen

157 flux disease, erosive esophagitis, Barrett's esophagus, esophageal adenocarcinoma, erosive gastritis,

158 cluded age and sex-matched subjects with mid-esophagus esophagitis (diseased-control), and histologic

159 owever, 3 out 4 patients present with distal esophagus exposure to WAR.

160 ultiplex, multigenerational familial Barrett esophagus family to identify candidate disease susceptib

161 ic acid and duodenal juice induces Barrett's esophagus followed by adenocarcinoma.

162 ronment induces the development of Barrett's esophagus followed by esophageal adenocarcinoma.

163 The esophagus for 21 patients diagnosed with primary EC were

164 etermine the risk of patients with Barrett's esophagus for progression to high-grade dysplasia (HGD)

165 r a lichenoid pattern of inflammation in the esophagus for which a precise histologic diagnosis canno

166 for esophageal adenocarcinoma and Barrett's esophagus from the Barretts Esophagus and Esophageal Ade

167 cancer of the bladder, breast, colon/rectum, esophagus, gallbladder, kidney, liver, lung, skin (melan

168 to the IP, columnar metaplasia of the lower esophagus, gastric corpus and antrum.

169 Purpose The Cancer Esophagus Gefitinib trial demonstrated improved progress

170 cified, blinded molecular analysis of Cancer Esophagus Gefitinib trial tumors was conducted to compar

171 nocarcinoma and its precursor lesion Barrett esophagus have seen a dramatic increase in incidence ove

172 diseased-control), and histologically normal esophagus (healthy-control).

173 The correlation of IP with Barrett's esophagus hints to a partly common pathogenesis.

174 is knowledge to identify high-risk Barrett's esophagus in a new non-endoscopic test.

175 The involvement of esophagus in morphea has been studied very scarcely.

176 ter than 98% of eosinophils infiltrating the esophagus in patients with EoE demonstrate morphologic a

177 positioned incorrectly, either ending in the esophagus, in the stomach but too close to the esophagus

178 efined in the following four ways: the whole esophagus, including the tumor (ESOwhole); ESOwhole with

179 variants have been associated with Barrett's esophagus, involving pathways in esophageal development.

180 ent in GERD patients without known Barrett's esophagus (IRR 0.98, 95% CI 0.72-1.33).

181 Barrett's esophagus is a squamous-to-columnar epithelial metaplasi

182 Barrett's esophagus is associated with increased risk of esophagea

183 propriate histologic definition of Barrett's esophagus is debated.

184 Because the esophagus is easily accessible with endoscopy, early dia

185 f care for the treatment of batteries in the esophagus is emergent endoscopic removal.

186 t atrial posterior wall is variable, and the esophagus is most susceptible to injury where it is clos

187 ed the following new insights: (i) Barrett's esophagus is polyclonal and highly mutated even in the a

188 understanding of risk factors for Barrett's esophagus is shifting the clinical guidelines to a nuanc

189 Esophagus is the most frequently affected part of the ga

190 Barrett's esophagus is the presumed precursor lesion for this canc

191 Barrett's esophagus is thought to progress to esophageal adenocarc

192 ma (EAC) and its precursor lesion, Barrett's esophagus, is poorly understood.

193 Some of the LM fascicles of the esophagus leave the esophagus to enter into the crural d

194 ominal obesity, is associated with Barrett's esophagus, likely because of both mechanical effects pro

195 s, such as cancers of the stomach, pancreas, esophagus, liver, and anus.

196 sue types (columnar cell metaplasia, Barrett esophagus, low- and high-grade dysplasia, esophageal ade

197 affolds of a wide range of intricate organs (esophagus, lung, liver and small intestine) were imaged

198 c treatment of mucosal adenocarcinoma of the esophagus (mAC).

199 HGD of the esophagus may be managed by surgical resection or EMR-RF

200 tients with esophagitis (n = 8) or Barrett's esophagus (n = 6); median age was 56 years and median bo

201 The duplication cysts were identified in the esophagus (n=2), stomach (n=5), duodenum (n=1), terminal

202 enign metaplastic never-dysplastic Barrett's esophagus (NDBE; n=66) and high-grade dysplasia (HGD; n=

203 rtions which appeared to originate in normal esophagus (NE) or BE and were later clonally expanded in

204 Although proposed as a model for Barrett esophagus, no large studies have examined the molecular

205 y gastroesophageal reflux disease, Barrett's esophagus, obesity, and tobacco smoking.

206 m the upper, middle, and lower thirds of the esophagus of 18 patients with EoE and 21 individuals und

207 endoscopy, 6 allergens were injected in the esophagus of 8 patients with EoE and 3 patients without

208 f type VII collagen in the skin, tongue, and esophagus of genetically altered mice that express type

209 idence of chronic inflammation in the distal esophagus on histopathology, including 22% with moderate

210 In the esophagus, only IGVEs were identified in myenteric gangl

211 entially curable adenocarcinoma of the lower esophagus or gastroesophageal junction were reviewed.

212 e patients with adenocarcinoma of the distal esophagus or GEJ who underwent transthoracic esophagecto

213 EGFP+ neurons in the nAmb projecting to the esophagus or laryngeal muscles, (b) EGFP+ neurons in the

214 n device for circumferential ablation of the esophagus or the focal device for targeted ablation, wit

215 smoking (cancers of the lung, head and neck, esophagus, or any metastatic cancer) were excluded.

216 ophagus, in the stomach but too close to the esophagus, or too far into the stomach or duodenum.

217 histopathology, particularly in the proximal esophagus (P </= .0049).

218 A smaller proportion of Barrett's esophagus patients filled statin prescriptions (57.4%) t

219 Carcinoma esophagus patients require some form of palliation becau

220 ment of dysplasia and early EAC in Barrett's esophagus patients today.

221 Practice Advice 5: In Barrett's esophagus patients with confirmed LGD (based on expert g

222 nd efficacious in most but not all Barrett's esophagus patients with dysplasia and esophageal adenoca

223 c resection should be performed in Barrett's esophagus patients with LGD with endoscopically visible

224 nt of low-grade dysplasia (LGD) in Barrett's esophagus patients.

225 No damage was observed in the tissues of the esophagus, phrenic nerves, or trachea.

226 ial and maximal extent of the columnar lined esophagus (Prague classification) with a clear descripti

227 mutations often occurred early in Barrett's esophagus progression, including in non-dysplastic epith

228 lowly (32 degrees C within 90-120 min in the esophagus), providing none of the above-mentioned system

229 with food bolus impaction due to Jackhammer esophagus referred to emergency department.

230 ter and a pathologically confirmed Barrett's esophagus registry.

231 actice Advice 13: In patients with Barrett's esophagus-related LGD undergoing ablative therapy, radio

232 scopist with expertise in managing Barrett's esophagus-related neoplasia practicing at centers equipp

233 ologist with a special interest in Barrett's esophagus-related neoplasia who is recognized as an expe

234 Barrett's esophagus remains a particularly important disease entit

235 n in multiple gastrointestinal segments; the esophagus represented the most common secondary site.

236 ction-susceptible P2 animals, suggesting the esophagus represents a portal of entry for E. coli K1 in

237 o the DEJ of multiple skin sites, tongue and esophagus, restored anchoring fibrils, improved dermal-e

238 d a scoring system (Progression in Barrett's Esophagus score) based on male sex, smoking, length of B

239 oughout the length of the original Barrett's esophagus segment and any visible columnar mucosa is sug

240 A Barrett's esophagus segment of at least 3 cm and evidence of intes

241 I: 0.09-0.71), as was the risk for Barrett's esophagus segments >/= 3 cm (OR = 0.13; 95% CI: 0.06-0.3

242 Practice Advice 1: The extent of Barrett's esophagus should be defined using a standardized grading

243 LGD is downgraded to nondysplastic Barrett's esophagus should be managed as nondysplastic Barrett's e

244 vice 4: Asymptomatic patients with Barrett's esophagus should consider a long-term PPI.

245 The middle portion of the esophagus showed a 9 cm longitudinal ulcer situated 12 c

246 Inflammatory parameters were assessed in the esophagus, skin, and lungs after allergen challenge.

247 ts with EoE revealed 39 rare mutations in 18 esophagus-specific differentially expressed genes.

248 ority of transcriptional changes observed in esophagus-specific genes were reproduced in vitro in eso

249 ncing was performed to identify mutations in esophagus-specific genes.

250 eptidase inhibitors as the most dysregulated esophagus-specific protein families in patients with EoE

251 We interrogated the pattern of expression of esophagus-specific signature genes derived from the Huma

252 We found that approximately 39% of the esophagus-specific transcripts were altered in patients

253 coupling power from outside the body to the esophagus, stomach, and colon, respectively.

254 tenna inside the body endoscopically, at the esophagus, stomach, and colon.

255 odenal pneumatosis is the presence of air in esophagus, stomach, and duodenum simultaneously, which h

256 impairment of the UGI system, including the esophagus, stomach, and small intestine.

257 digestive system including the oral cavity, esophagus, stomach, small and large intestines, pancreas

258 mpassing the digestive tract (mouth, throat, esophagus, stomach, small intestine, and colorectum) and

259 ter in Netherlands enrolled in the Barrett's Esophagus Study database from 1985 through 2014.

260 ents VSIG10L as a candidate familial Barrett esophagus susceptibility gene, with a putative role in m

261 ome of esophageal adenocarcinoma and Barrett esophagus, termed familial Barrett esophagus, by using h

262 al and mucosal microenvironment of Barrett's esophagus that promote, in a small proportion of patient

263 In patients with Barrett's esophagus, the corresponding IRR was 0.46 (95% CI 0.20-1

264 For patients with Barrett's esophagus, the diagnosis of low-grade dysplasia (LGD) is

265 CKGROUND & AIMS: For patients with Barrett's esophagus, the diagnosis of low-grade dysplasia (LGD) is

266 m is molecularly similar to sporadic Barrett esophagus, thereby confirming suitability as a research

267 oral and lingual epithelia, salivary gland, esophagus, thymus, and bladder.

268 Molecular monitoring in Barrett's esophagus to avoid overdiagnosis/treatment highlights an

269 ti-reflux barrier and reduced ability of the esophagus to clear and buffer the refluxate, leading to

270 the LM fascicles of the esophagus leave the esophagus to enter into the crural diaphragm and the rem

271 dual progression from premalignant Barrett's esophagus to esophageal adenocarcinoma (EAC) provides an

272 oscopic biopsy of the mucosa lining from the esophagus to the duodenum was performed on day 45.

273 d exocrine glands in tissues including skin, esophagus, trachea, tongue, eye, bladder, testis and ute

274 a common disease in which the lining of the esophagus transitions from stratified squamous epitheliu

275 investigated radiosensitivity in the normal esophagus using an imaging biomarker of radiation-respon

276 gitis (18%), pneumonia (7%), hemobilia (7%), esophagus variceal hemorrhage (3%), and vascular disease

277 The risk of Barrett's esophagus was especially lower with statin use among obe

278 After euthanasia at day 60, the esophagus was evaluated visually and histologically.

279 The distal esophagus was examined by high definition endoscopy and

280 S AND In 8 pigs (+/-70 kg), the suprasternal esophagus was surgically exposed.

281 ly reported association of IP with Barrett's esophagus was weak, statistically significant only when

282 sophageal adenocarcinoma and 11 with Barrett esophagus) was identified, and whole-exome sequencing id

283 CAPN14 was specifically expressed in the esophagus, was dynamically upregulated as a function of

284 dy of patients with esophagitis or Barrett's esophagus, we found belt compression increased acid refl

285 segments of cardia-type mucosa of the lower esophagus were included in the definition of Barrett's e

286 y, mice were euthanized, and the stomach and esophagus were removed, fixed, and stained for calcitoni

287 odes of palliation of dysphagia in carcinoma esophagus were studied, which were mainly randomized and

288 Different definitions of Barrett's esophagus were tested for an association with IP.

289 ial-PV junction, phrenic nerve, and internal esophagus) were monitored.

290 EoE) is a severe inflammatory disease of the esophagus which is characterized histologically by an eo

291 -segment and 519 with long-segment Barrett's esophagus) who presented at a tertiary care center from

292 We compared 303 patients with Barrett's esophagus with 2 separate sex-matched control groups: 60

293 E) is a chronic, inflammatory disease of the esophagus with a rapidly increasing incidence.

294 ently recognized inflammatory disease of the esophagus with clinical symptoms derived from esophageal

295 ation (EMR-RFA) for the treatment of Barrett esophagus with high-grade dysplasia (HGD).

296 ice 10: In patients with confirmed Barrett's esophagus with LGD by expert GI pathology review that pe

297 ong pathologists, the diagnosis of Barrett's esophagus with LGD should be confirmed by an expert gast

298 exhibited high expression in normal squamous esophagus with marked loss of expression in Barrett-asso

299 t (TRAIL(-/-)) mice and targeted MID1 in the esophagus with small interfering RNA.

300 en VII was observed in the skin, tongue, and esophagus, with a half-life of about 1 month.