1,721,048 research outputs found
Quality really matters: the need to improve specimen quality in biomedical research
This Editorial is being published simultaneously in both Histopathology and The Journal of Pathology.Daniel Simeon-Dubach, Alastair D Burt, and Peter A Hal
Primary hepatocellular carcinoma of the pancreas: a case report and review of the heterogeneous group of pancreatic hepatoid carcinomas
Paul J Kelly, Robert Spence, Bobby V Dasari, Alastair D Burt, Mark Taylor, Maurice B Loughre
Efavirenz induced acute liver failure requiring liver transplantation in a slow drug metaboliser
Abstract not availableAhmed M. Elsharkawy, Ulrich Schwab, Brendan McCarron, Alastair D. Burt, Ann K. Daly, Mark Hudson, Steven Masso
Pathologic diagnosis of early hepatocellular carcinoma: a report of the international consensus group for hepatocellular neoplasia
International Consensus Group for Hepatocellular Neoplasia Contributor: Alastair D. Burt for the University of AdelaideInternational Consensus Group for Hepatocellular Neoplasi
Serum immunoglobulin levels predict fibrosis in patients with non-alcoholic fatty liver disease
Abstract not availableStuart McPherson, Elsbeth Henderson, Alastair D. Burt, Christopher P. Day, Quentin M. Anste
Human liver stem cells originate from the canals of hering
Letter to the EditorNimantha De Alwis, Gavin Hudson, Alastair D. Burt, Christopher P. Day and Patrick F. Chinner
The specificity of liver inflammation in mouse models of primary biliary cirrhosis
Letter to the editorDavid E. J. Jones, Jeremy M. Palmer, Alastair D. Burt and John A. Kirb
Prospective study assessing associated factors in patients with colon polyps: interim analysis
Poster # P-0521Leonardo Zorron Tao Pu Cheng, Doreen Ching Koay Siew, Amanda Ovenden, Alastair D Burt, Rajvinder Sing
Disrupted pancreatic exocrine differentiation and malabsorption in response to chronic elevated systemic glucocorticoid
Glucocorticoids are antiinflammatory therapeutics that have potent effects on cell differentiation. The aim of this study was to establish whether systemic glucocorticoid exposure significantly affects pancreatic differentiation in vivo because hepatocyte-like cells have been documented to occur in the diseased rodent pancreas. Expression of hepatic markers was examined in pancreata from mice genetically modified to secrete elevated circulating endogenous glucocorticoid [Tg(Crh)]. Tg(Crh) mice with elevated glucocorticoid appeared cushingoid and by 21 weeks of age were obese, insulin-resistant, and had extensive areas of hepatic gene expression in exocrine tissue. Acinar cells from Tg(Crh) mice costained for both amylase and cyp2e1, suggesting direct acinar-hepatic transdifferentiation. Hepatic expression increased with age in the pancreas to such an extent that malabsorption and rapid weight loss occurred in a subset of aging mice; this effect was reversed by dietary porcine pancreatic enzyme supplementation. Indeed, pancreatic expression of hepatic markers was prevented by adrenalectomy, establishing a direct role for glucocorticoid. Elevated levels of circulating glucocorticoid therefore promote a transdifferentiation of adult exocrine pancreas into hepatocyte-like cells, and chronic exposure results in pancreatic malfunction. Glucocorticoids are thus capable of modulating the differentiation of terminally differentiated adult cells.Karen Wallace, Paul A. Flecknell, Alastair D. Burt, Matthew C. Wrigh
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