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Glial Cell Line-Derived Neurotrophic Factor, S-100 Protein and Synaptophysin Expression in Biliary Atresia Gallbladder Tissue

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dc.contributor.author Gürünlüoğlu, S.
dc.contributor.author Ceran, C.
dc.contributor.author Gürünlüoğlu, K.
dc.contributor.author Koçbiyik, A.
dc.contributor.author Gül, M.
dc.contributor.author Yıldız, T.
dc.contributor.author Bağ, H.G.
dc.contributor.author Gül, S.
dc.contributor.author Taşçi, A.
dc.contributor.author Bayrakçi, E.
dc.contributor.author Akpinar, N.
dc.contributor.author Çin, E.S.
dc.contributor.author Ateş, H.
dc.contributor.author Demircan, M.
dc.date.accessioned 2022-10-06T12:49:56Z
dc.date.available 2022-10-06T12:49:56Z
dc.date.issued 2021
dc.identifier.issn 22348646 (ISSN)
dc.identifier.uri http://hdl.handle.net/11616/71581
dc.description.abstract Purpose: Biliary atresia (BA) is a disease that manifests as jaundice after birth and leads to progressive destruction of the ductal system in the liver. The aim of this study was to investigate histopathological changes and immunohistochemically examine the expression of glial cell line-derived neurotrophic factor (GDNF), synaptophysin, and S-100 protein in the gallbladder of BA patients. Methods: The study included a BA group of 29 patients and a control group of 41 children with cholecystectomy. Gallbladder tissue removed during surgery was obtained and examined immunohistochemically and histopathologically. Tissue samples of both groups were immunohistochemically assessed in terms of GDNF, S-100 protein, and synaptophysin expression. Expression was classified as present or absent. Inflammatory activity assessment with hematoxylin and eosin staining and fibrosis assessment with Masson's trichrome staining were performed for tissue sample sections of both groups. Results: Ganglion cells were not present in gallbladder tissue samples of the BA group. Immunohistochemically, GDNF, synaptophysin, and S-100 expression was not detected in the BA group. Histopathological examination revealed more frequent fibrosis and slightly higher inflammatory activity in the BA than in the control group. Conclusion: We speculate that GDNF expression will no longer continue in this region, when the damage caused by inflammation of the extrahepatic bile ducts reaches a critical threshold. The study's findings may represent a missing link in the chain of events forming the etiology of BA and may be helpful in its diagnosis. © 2021 by The Korean Society of Pediatric Gastroenterology, Hepatology and Nutrition
dc.source Pediatric Gastroenterology, Hepatology and Nutrition
dc.title Glial Cell Line-Derived Neurotrophic Factor, S-100 Protein and Synaptophysin Expression in Biliary Atresia Gallbladder Tissue


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