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Gastrointestinal Function and Toxicology in Canines
Published in Shayne C. Gad, Toxicology of the Gastrointestinal Tract, 2018
The following lesions can be noted in the esophagus. Dilatation of the esophagus itself. Mild dilatation of the esophageal gland ducts. Hypertrophy or inflammation of the esophageal walls, arising as a result of mechanical irritation or reflux esophagitis.
Diseases and Parasites of Pufferfish and Their Management
Published in Ramasamy Santhanam, Biology and Ecology of Toxic Pufferfish, 2017
Diagnosis of the parasite: The new taxon is distinguishable by the presence of esophageal glands, teguments covered by ciliated papillae, and the position and shape of the hermaphroditic duct. Body of this species is slightly longer than wide, narrow at the posterior region. Tegument is with small papillae distributed irregularly throughout the entire body. Adhesive disc is occupying the entire ventral region composed of 29 rows of transverse alveoli separated by two longitudinal septa. Pharynx is oval and large, surrounded by pharyngeal glands ((Giese et al., 2015).
Oesophagus
Published in Paul Ong, Rachel Skittrall, Gastrointestinal Nursing, 2017
The epithelial tissue lining the oesophagus is of ectoderm origin, developing as ciliated epithelial cells in week 10 and maturing to stratified squamous epithelium by week 25. Any remaining ciliated cells develop into oesophageal glands.
Schistosome proteomics: updates and clinical implications
Published in Expert Review of Proteomics, 2022
William Castro-Borges, R Alan Wilson
Unlike internal schistosome proteins many of the exposed or secreted proteins proved to be poorly reactive and some were virtually silent (e.g. Cathepsin D from the gastrodermis). It was previously suggested that many secreted MEGs and VALs had been subjected to selective pressure by the immune system during evolution of the Genus Schistosoma [92]. Two tegument surface proteins, tetraspanin TSP-2 and Sm29, also appear to have been subjected to the same pressures. Overall, the esophageal gland MEGs (4.1, 4.2, 8.1, 8.2, 12) were the most and tegument surface proteins the least reactive with murine serum on the arrays [23]. Nevertheless, tegument surface Sm25, ADP-ribosyl cyclase and carbonic anhydrase did show reactivity above background. The expression library of 96 soluble proteins was used for direct vaccination experiments in mice, followed by cercarial challenge to pinpoint potential vaccine candidates, but without success [93].
Long-term outcomes of the randomized controlled trial comparing 5-aminolaevulinic acid and Photofrin photodynamic therapy for Barrett’s oesophagus related neoplasia
Published in Scandinavian Journal of Gastroenterology, 2018
Darina Kohoutova, Rehan Haidry, Matthew Banks, Mohammed Adil Butt, Jason Dunn, Sally Thorpe, Laurence Lovat
Our data show that patients treated with ALA PDT which led to reversal of dysplasia had a significantly better long-term outcome when compared to those who failed PDT originally. This finding is not replicated in the Photofrin group. This is a crucial finding and confirms the fact, that BE is not just one disease, which responds to any ablative therapy in a uniform way. Our original study allowed up to three consecutive PDT treatments. We previously reported that if dysplasia was not cleared after the first treatment, subsequent PDT was less likely to lead to remission [8]. Prasad et al. looked at the biomarkers of patients with HGD or IMC in BE who underwent PDT with Photofrin. Loss of biomarkers related to progression of neoplasia in BE was associated with histologic downgrading of dysplasia after PDT; those patients with persistent positivity of biomarkers were at higher risk of recurrent HGD [19]. They confirmed in another study, that p16 allelic loss predicted decreased response to PDT [20]. Recently, Timmer et al. reported that genetic biomarkers can predict achievement of CR-D after endoscopic therapy and that patients with multiple genetic alterations may have a lower response rate [21]. Investigation of biomarkers could therefore help in the management of dysplastic BE. We have similarly demonstrated that relapse is related to persistence of aneuploidy after treatment within the residual Barrett’s segment [22]. We have also demonstrated that pro-tumorigenic mutations can be found in post-ablation squamous mucosa as well as in mutant deep oesophageal glands; both are associated with dysplasia recurrence [23]. These findings all suggest that the genetic milieu of the residual Barrett’s segment is more complex and other abnormalities occur prior to the onset of dysplasia, a phenomenon that has been described in detail by a number of groups [24,25].