Resource evaluation and management alternatives : Ahuriri Estuary, Napier

In 1976 the Ahuriri Estuary Steering Committee was established to examine the management of Ahuriri Estuary, Napier (Hawke's Bay, New Zealand). An advisory Technical Committee was also formed to undertake continuing research. Professor G.A. Knox of the University of Canterbury was appointed to co-ordinate the research programme, of which this work forms a part. This report presents a broad overview of the management issues which have arisen, and seeks to clarify the conflict. The estuary's present biological state is described using information received from scientists who are also studying the estuary. The report includes a descriptive evaluation of the estuary from a local, regional, national and international perspective. The effects of human interference, both in the past and today, are also outlined. Some objectives and principles for management are suggested and used to examine the implications of the various physical management alternatives that have been put forward. Recommendations are made for the consideration of the people of Napier and the management authorities. The administrative structure which relates to the estuary is described and evaluated in the light of some suggested principles for administration. Several alternative structures are suggested and evaluated, and recommendations are made

Bile acids modulate glucocorticoid metabolism and the hypothalamic-pituitary-adrenal axis in obstructive jaundice

<b>Background & Aims</b> Suppression of the hypothalamic–pituitary–adrenal axis occurs in cirrhosis and cholestasis and is associated with increased concentrations of bile acids. We investigated whether this was mediated through bile acids acting to impair steroid clearance by inhibiting glucocorticoid metabolism by 5β-reductase.<p></p> <b>Methods</b> The effect of bile acids on glucocorticoid metabolism was studied in vitro in hepatic subcellular fractions and hepatoma cells, allowing quantitation of the kinetics and transcript abundance of 5β-reductase. Metabolism was subsequently examined in vivo in rats following dietary manipulation or bile duct ligation. Finally, glucocorticoid metabolism was assessed in humans with obstructive jaundice.<p></p> <b>Results</b> In rat hepatic cytosol, chenodeoxycholic acid competitively inhibited 5β-reductase (Ki 9.19 ± 0.40 μM) and reduced its transcript abundance (in H4iiE cells) and promoter activity (reporter system, HepG2 cells).<p></p> In Wistar rats, dietary chenodeoxycholic acid (1% w/w chow) inhibited hepatic 5β-reductase activity, reduced urinary excretion of 3α,5β-tetrahydrocorticosterone and reduced adrenal weight. Conversely, a fat-free diet suppressed bile acid levels and increased hepatic 5β-reductase activity, supplementation of the fat-free diet with CDCA reduced 5β-reductase activity, and urinary 3α,5β-reduced corticosterone. Cholestasis in rats suppressed hepatic 5β-reductase activity and transcript abundance.<p></p> In eight women with obstructive jaundice, relative urinary excretion of 3α,5β-tetrahydrocortisol was significantly lower than in healthy controls.<p></p> <b>Conclusion</b> These data suggest a novel role for bile acids in inhibiting hepatic glucocorticoid clearance, of sufficient magnitude to suppress hypothalamic–pituitary–adrenal axis activity. Elevated hepatic bile acids may account for adrenal insufficiency in liver disease.<p></p&gt