ライフサイエンスコーパス: esophagus

1 t damage the phrenic nerve, vessels, and the esophagus.

2 es aberrant stratification of the developing esophagus.

3 enitor cells (EPCs) in the developing murine esophagus.

4 ith mucosal biopsies along any aspect of the esophagus.

5 and p53 mutant cells in the transgenic mouse esophagus.

6 ients with BORN and non-dysplastic Barrett's esophagus.

7 gus, (3) distal esophagus, and (4) Barrett's esophagus.

8 tenance of high turn-over organs such as the esophagus.

9 on presence of the key precursor, Barrett's esophagus.

10 or occurs with other diseases involving the esophagus.

11 carcinoma, rheumatoid arthritis, and Barrett esophagus.

12 tissue biopsies along various points of the esophagus.

13 during endoscopy over a long segment of the esophagus.

14 es were observed in their small intestine or esophagus.

15 measurements were low in all segments of the esophagus.

16 an in vitro cell culture model of Barrett's esophagus.

17 n were dysregulated in the adult Foxp1 (+/-) esophagus.

18 GERD) is caused by gastric acid entering the esophagus.

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

20 patients with biopsy-proven carcinoma of the esophagus.

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

22 rticularly in the squamous epithelium of the esophagus.

23 including 10 discrete histological sections/esophagus.

24 egorization of lichenoid inflammation in the esophagus.

25 rcinomas and squamous cell carcinomas of the esophagus.

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

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

28 safe modality for catheter ablation near the esophagus.

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

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

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

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

33 here is reversion to nondysplastic Barrett's esophagus.

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

35 patients undergoing endoscopy for Barrett's esophagus.

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

37 ribed expression pattern in sporadic Barrett esophagus.

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

39 healthy subjects and patients with achalasia esophagus.

40 d with marked eosinophil accumulation in the esophagus.

41 tion, and (3) PF delivered directly atop the esophagus.

42 nferior vena cava onto a forcefully deviated esophagus.

43 ) is a chronic inflammatory condition of the esophagus.

44 ysfunction in patients with achalasia of the esophagus.

45 of PPI use on the microbial community of the esophagus.

46 d its acute effects on the phrenic nerve and esophagus.

47 diaphragm muscle in patients with achalasia esophagus.

48 of high power in the region neighboring the esophagus.

49 or re-operation, and potential for Barrett's esophagus.

50 e cancer of the middle or lower third of the esophagus.

51 Throughout the esophagus, 17 bacterial genera were detected from the sa

52 geal mucosa were taken from the (1) proximal esophagus, (2) mid-esophagus, (3) distal esophagus, and

53 ken from the (1) proximal esophagus, (2) mid-esophagus, (3) distal esophagus, and (4) Barrett's esoph

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

55 23 [21-25] applications) to the approximated esophagus (6 [4.5-14] mm) produced transmural lesions wi

56 nts with severe GERD (esophagitis or Barrett esophagus) after surgery [SIR 6.09 (95% CI 4.39-8.23) 1-

57 17 patients with Barrett's esophagus agreed to participate in the study.

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

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

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

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

62 nounced muscular atrophy was detected in the esophagus and colon, caused by reduced muscle cell proli

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

64 us-columnar junction, a site where Barrett's esophagus and esophageal adenocarcinoma often arise clin

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

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

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

68 Worldwide data for adenocarcinoma of the esophagus and esophagogastric junction demonstrate that

69 oadjuvant) therapy for adenocarcinoma of the esophagus and esophagogastric junction using Worldwide E

70 food bolus across the oropharynx towards the esophagus and flips the epiglottis over the laryngeal in

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

72 ex vivo videos of a methylene blue dyed pig esophagus and images of different disease stages in the

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

74 atify the patient with nondysplastic Barrett esophagus and may form the basis of a future surveillanc

75 with GERD, MI values were low in the distal esophagus and normalized along the proximal esophagus, w

76 ice (which overexpress interleukin 1 beta in esophagus and squamous forestomach and are used as a mod

77 Esophagectomy involves resection of the esophagus and surrounding lymph nodes, which are commonl

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

79 genic assay to follow cell division in mouse esophagus and the epidermis at multiple body sites.

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

81 The esophagus and trachea arise from the dorsal and ventral

82 ls (24 with no disease and 16 with Barrett's esophagus and/or EAC).

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

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

85 mal esophagus, (2) mid-esophagus, (3) distal esophagus, and (4) Barrett's esophagus.

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

87 the brain (specifically for HHV-6A), testis, esophagus, and adrenal gland.

88 ory diseases develop over time in the heart, esophagus, and colon of some patients.

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

90 esophagitis, esophageal strictures, Barrett esophagus, and esophageal adenocarcinoma.

91 ect of cold storage on fresh healthy spleen, esophagus, and lung from >= 5 donors over 72 h.

92 We found that sun-exposed skin, esophagus, and lung have a higher mutation burden than o

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

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

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

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

97 owing, burning, choking, and pressure in the esophagus appearing within 5 minutes of ingesting a prov

98 grams that specify the mammalian trachea and esophagus are unknown.

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

100 The trachea and esophagus arise from the separation of a common foregut

101 ng the neoplastic precursor lesion Barrett's esophagus as an exemplar(5).

102 We found that full thickness human esophagus as well as the individual layers of circular a

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

104 x disease (GERD), esophagitis, and Barrett's esophagus (BE) after sleeve gastrectomy (SG) through a s

105 e and is the major risk factor for Barrett's esophagus (BE) and esophageal adenocarcinoma (EA).

106 uals who are at increased risk for Barrett's esophagus (BE) and esophageal adenocarcinoma.

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

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

109 Barrett's esophagus (BE) can progress to dysplasia and esophageal

110 Barrett's esophagus (BE) is a precursor to esophageal adenocarcino

111 Barrett's esophagus (BE) is a precursor to esophageal adenocarinom

112 Barrett's esophagus (BE) is associated with reflux and is implicat

113 Barrett's esophagus (BE) is most commonly seen as the condition in

114 ween metabolic syndrome (MetS) and Barrett's esophagus (BE) is still a challenging issue, and inconsi

115 Barrett's esophagus (BE) is the only known precursor to esophageal

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

117 Barrett's esophagus (BE) predisposes for the malignant condition o

118 o determine the mechanism by which Barrett's esophagus (BE) progresses to esophageal adenocarcinoma (

119 contribute to the progression from Barrett's esophagus (BE) to esophageal adenocarcinoma (EA).

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

121 pic therapy (BET) in patients with Barrett's esophagus (BE) with dysplasia and/or early cancer and ap

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

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

124 (EA) and its premalignant lesion, Barrett's esophagus (BE), are characterized by a strong and yet un

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 In patients with Barrett's esophagus (BE), metaplastic columnar mucosa containing e

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

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

131 patients with EAC and nonmalignant Barrett's esophagus (BE), with or without dysplasia.

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

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

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

135 eterogeneous and often preceded by Barrett's esophagus (BE).

136 f early neoplasia in patients with Barrett's esophagus (BE).

137 ble to lyse ingested immune cells within the esophagus before passing them into the gut.

138 s tool might improve management of Barrett's esophagus by general endoscopists.

139 mutant cells can be depleted from the normal esophagus by redox manipulation, showing that external i

140 gnaling is conserved in the developing human esophagus by utilizing 3D human pluripotent stem cell (h

141 -signaling-associated receptors in Barrett's esophagus, by showing variations of the Fzd- and co-rece

142 flat areas of columnar mucosa in the tubular esophagus can be treated with mucosal ablation.

143 skin epidermis and the epithelium lining the esophagus cells are constantly shed from the tissue surf

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

145 atic samples from individuals with Barrett's Esophagus, CNValidator provided feedback on the correctn

146 For instance, within the esophagus cohort, the lowest-spending hospitals had an a

147 larynx and for the constricted, muscularized esophagus, crucial for transport and powered swallowing

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

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

150 In cases of true short esophagus diagnosed intraoperatively with an endoscopic-

151 amage to vagus nerves as well as evidence of esophagus dilation occurred at sites associated with IRF

152 ESCC-free, Zn-deficient miR-31(-/-) rat esophagus displayed no genome instability and limited me

153 vert lesions in the pancreas, liver, kidney, esophagus, duodenum, and ileum of RCO-treated mice.

154 yocardium selective, potentially sparing the esophagus during left atrial ablation.

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

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

157 o as "food-induced immediate response of the esophagus" (FIRE), observed in EoE patients.

158 The esophagus for 21 patients diagnosed with primary EC were

159 cer evolution within patients with Barrett's esophagus for a more personalized screening design.

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

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

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

163 Purpose The Cancer Esophagus Gefitinib trial demonstrated improved progress

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

165 hageal caustic injuries: Grade I show normal esophagus; Grade IIa display internal enhancement of the

166 PFA on block durability, phrenic nerve, and esophagus >=2 weeks.

167 midline from anterior to posterior until the esophagus-gut boundary.

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

169 and skeletal muscle of the crural diaphragm (esophagus hiatus) provide the sphincter mechanisms at th

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

171 treat solid tumors of the breast, lung, and esophagus; however, the heart is an unintentional target

172 which allows the drug to be delivered to the esophagus in adults with active EoE.

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

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

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

176 Food-induced immediate response of the esophagus is a novel syndrome frequently reported in EoE

177 Food-induced immediate response of the esophagus is an unpleasant/painful sensation, unrelated

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

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

180 the normal squamous epithelium lining of the esophagus is replaced by goblet cells.

181 Although malignant involvement of the esophagus is the most common cause of pseudoachalasia, b

182 (GERD), which leads to acid reflux into the esophagus, is a common gastrointestinal disorder.

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

184 Esophagus, LES, stomach, right and left crus of the diap

185 inically detected cancers of the colorectum, esophagus, liver, lung, ovary, pancreas, breast, or stom

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

187 diaphragmatic hiatus after maximal thoracic esophagus mobilization was measured.

188 nasal airway epithelial cells and MROH3P in esophagus mucosa.

189 When performing microflora studies of the esophagus, mucosal biopsies should be used for analysis.

190 signaling for antero-posterior migration of esophagus muscle progenitors, where Hgf ligand is expres

191 et genetic hierarchy that uniquely regulates esophagus myogenesis and identify distinct genetic signa

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

193 sis of tissues from both distal and proximal esophagus; n = 21), or non-GERD (normal results from eso

194 s associated with MTV and with IMH.Keywords: Esophagus, Neoplasms-Primary, PET/CT, Tumor Response (C)

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

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

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

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

199 bsence of columnar epithelium in the tubular esophagus on high-definition white-light endoscopy and p

200 of 3859 patients with adenocarcinoma of the esophagus or esophagogastric junction received neoadjuva

201 ry after completed nCRT for carcinoma of the esophagus or esophagogastric junction, is not of major i

202 th esophageal cancer localized in the distal esophagus or gastroesophageal junction undergoing McKeow

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

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

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

206 t in serious complications if they reach the esophagus or phrenic nerve, for instance-structures that

207 rnia (OR 2.06, 95% CI 1.97-2.15), perforated esophagus (OR 1.71, 95% CI 1.31-2.24), small and large b

208 rnia (OR 3.49, 95% CI 3.29-3.70), perforated esophagus (OR 4.06, 95% CI 3.03-5.44), small and large b

209 ive pH study, erosive esophagitis, Barrett's esophagus, or esophageal ulcer), and pH impedance testin

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

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

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

213 aortic dissection, appendicitis, perforated esophagus, peptic ulcer, small bowel or large bowel, and

214 aortic dissection, appendicitis, perforated esophagus, peptic ulcer, small bowel or large bowel, and

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

216 Ablation at the vicinity of the esophagus predicts risk of EI.

217 ctivation has been reported during Barrett's esophagus progression, but with rarely detected mutation

218 criteria were: fish bone located beyond the esophagus, radiological diagnosis by CT and confirmation

219 sus TRG3-4 using SUL(max), SUL(max) tumor-to-esophagus ratio, and Delta%SUL(max) was performed to def

220 l tumor recurrence after nCRT as soon as the esophagus recovers from radiation-induced esophagitis.

221 Endoscopic detection of early Barrett's esophagus-related neoplasia (BORN) is a challenge.

222 egulating these progenitor activities in the esophagus remain to be elucidated.

223 ion and resolution into distinct trachea and esophagus requires endosome-mediated epithelial remodeli

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

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

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

227 residual columnar epithelium in the tubular esophagus) should not warrant additional ablation therap

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

229 Biopsies from the esophagus showed an eosinophilic inflammation (65 eosino

230 h severe GERD (reflux esophagitis or Barrett esophagus) showed similar results.

231 hibit defects in axial skeleton, kidneys and esophagus, similar to the affected individuals, supporti

232 ion durability and concerns of damage to the esophagus-situated behind the LAPW.

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

234 ved significantly increased apoptosis in the esophagus, small intestine, mesenteric lymph nodes, and

235 trangulated abdominal hernia, perforation of esophagus, small or large bowel, and peptic ulcer.

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

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

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

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

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

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

242 t potentially fatal complication of proximal esophagus stenting.

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

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

245 scuss these new findings with a focus on the esophagus, stomach, and intestine.

246 on of various portions of the GIT (including esophagus, stomach, and small and large intestine) and n

247 treatment of diseases in hollow-organs; the esophagus, stomach, colon, uterus and the bladder.

248 Data on primary cancers of the esophagus, stomach, colorectum, liver, and pancreas were

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

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

251 Masticatory and esophagus striated muscles (ESM) share a common cardioph

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

253 ere survived to 25 days, sacrificed, and the esophagus submitted for pathological examination, includ

254 psies, sampled from 88 patients in Barrett's esophagus surveillance over a period of up to 15 years,

255 Food-induced immediate response of the esophagus symptoms included narrowing, burning, choking,

256 ggin (NOG) expression, resulting in immature esophagus that contains respiratory glands.

257 o discriminate between nondysplastic Barrett esophagus that either progress to adenocarcinoma or rema

258 antigen-mediated eosinophilic disease of the esophagus that involves fibroblast activation and progre

259 composed of muscularized jaws linked to the esophagus that permits food ingestion and swallowing.

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

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

262 that this network is activated in Barrett's esophagus, the putative precursor state to EAC, thereby

263 As a case study in Barrett's esophagus, these methods were applied for a model of eso

264 zes the motility of the entire gut, from the esophagus through the rectosigmoid colon.

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

266 ted changes in gene expression in muscle and esophagus tissue.

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

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

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

270 d a conveniently long segment of the tubular esophagus to obtain an efficient fundoplication should b

271 The close proximity of esophagus to the left atrial posterior wall predisposes

272 mechanical deviation model approximating the esophagus to the right atrium (n=4) and by direct ablati

273 o the left atrial posterior wall predisposes esophagus to thermal injury during catheter ablation for

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

275 3 compared the effects of PFA and RFA on the esophagus using a mechanical deviation model approximati

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

277 mperature was monitored in all patients; the esophagus was also mechanically deviated in 10 patients.

278 , an overlap between the ablation lesion and esophagus was an independent predictor of EI (odds ratio

279 After 8 weeks the stent was removed and the esophagus was considered healed.

280 animals, under general anesthesia, the lower esophagus was deflected toward the inferior vena cava us

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

282 achalasia due to vascular compression of the esophagus was found.

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

284 The esophagus was visualized by oral soluble contrast during

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

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

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

288 Mucosal biopsies of the distal esophagus were analyzed using a customized esophageal mi

289 with "nonprogressive" nondysplastic Barrett esophagus were analyzed via methylation array.

290 ges of different disease stages in the human esophagus were analyzed, showing spatially distinct colo

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

292 cancers of the middle or lower third of the esophagus were randomized to undergo either transthoraci

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

294 esophagus and normalized along the proximal esophagus, whereas in patients with EoE, measurements we

295 array of patients with nondysplastic Barrett esophagus who either develop adenocarcinoma or remain st

296 ntifying patients with nondysplastic Barrett esophagus who progress to invasive adenocarcinoma remain

297 ls of esophageal acid exposure in the distal esophagus with absence of reflux-symptom association (ie

298 ocarcinoma or squamous cell carcinoma of the esophagus with an initial staging (18)F-FDG PET/CT.

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

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