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dc.contributor.authorAshizawa, N.es
dc.contributor.authorNiigaki, M.es
dc.contributor.authorHamamoto, N.-
dc.contributor.authorKaji, T.-
dc.contributor.authorKatsube, T.-
dc.contributor.authorSato, S.-
dc.contributor.authorEndoh, H.-
dc.contributor.authorHidaka, K.-
dc.contributor.authorWatanabe, M.-
dc.contributor.authorKinoshita, Y.-
dc.date.accessioned2011-02-22T11:08:36Z-
dc.date.available2011-02-22T11:08:36Z-
dc.date.issued1999-
dc.identifier.issn0213-3911es
dc.identifier.urihttp://hdl.handle.net/10201/19177-
dc.description.abstractThe following changes were found by either light or electron microscopic observation of the pancreas in spontaneously developed chronic pancreatitis models (WBNIKob rats, spontaneously hypertensive rats, and rats with common bile-pancreatic duct stones) and in experimental models of chronic pancreatitis (alcoholic pancreatitis, ischemic pancreatitis, and obstructive pancreatitis): 1) the units of lobules, which were constituted by acinar cell deletion, ductular proliferation, and fibrosis; and 2) tortuous or helical ductal channels of pancreatic ducts with periductal fibrosis, which had many crater-like depressions and very long cilia in their inner surface. These are considered to be the results of obstructive pancreatitis, which are caused by the reactions of defensive factors against the increase of pancreatic duct pressure, including the apoptosis of acinar cells, the hyperplasia and hypertrophy of duct cells, a tighter junctional complex of duct cells, and periductal fibrosis.en_EN
dc.formatapplication/pdfes
dc.format.extent14es
dc.languageenges
dc.publisherMurcia : F. Hernándezes
dc.relation.ispartofHistology and histopathologyen_EN
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.subjectChronic pancreatitisen_EN
dc.subjectAnimal modelen_EN
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicinaes
dc.titleThe morphological changes of exocrine pancreas in chronic pancreatitisen_EN
dc.typeinfo:eu-repo/semantics/articlees
Aparece en las colecciones:Vol.14, nº 2 (1999)

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