1,721,048 research outputs found

    Preface

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    Alastair D. Burt, Bernard C. Portmann, Linda D. Ferrel

    Quality really matters: the need to improve specimen quality in biomedical research

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    This Editorial is being published simultaneously in both Histopathology and The Journal of Pathology.Daniel Simeon-Dubach, Alastair D Burt, and Peter A Hal

    Pathologic diagnosis of early hepatocellular carcinoma: a report of the international consensus group for hepatocellular neoplasia

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    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

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    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

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    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

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    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

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    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

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    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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