The impact of floating net cages culturing the seabass, Lates calcarifer, on planktonic processes and water chemistry in two heavily used mangrove estuaries in Malaysia was examined. Concentrations of dissolved inorganic and particulate nutrients were usually greater in cage vs. adjacent (approximately 100 m) non-cage waters, although most variability in water-column chemistry related to water depth and tides. There were few consistent differences in plankton abundance, production or respiration between cage and non-cage sites. Rates of primary production were low compared with rates of pelagic mineralization reflecting high suspended loads coupled with large inputs of organic matter from mangrove forests, fishing villages, fish cages, pig farms and other industries within the catchment. Our preliminary sampling did not reveal any large-scale eutrophication due to the cages. A crude estimate of the contribution of fish cage inputs to the estuaries shows that fish cages contribute only approximately 2% of C but greater percentages of N (32-36%) and P (83-99%) to these waters relative to phytoplankton and mangrove inputs. Isolating and detecting impacts of cage culture in such heavily used waterways--a situation typical of most mangrove estuaries in Southeast Asia--are constrained by a background of large, highly variable fluxes of organic material derived from extensive mangrove forests and other human activities.
Cardiac dysfunction has an increased prevalence in diseases complicated by liver cirrhosis such as primary biliary cholangitis and primary sclerosing cholangitis. This observation has led to research into the association between abnormalities in bile acid metabolism and cardiac pathology. Approximately 50% of liver cirrhosis cases develop cirrhotic cardiomyopathy. Bile acids are directly implicated in this, causing QT interval prolongation, cardiac hypertrophy, cardiomyocyte apoptosis and abnormal haemodynamics of the heart. Elevated maternal serum bile acids in intrahepatic cholestasis of pregnancy, a disorder which causes an impaired feto-maternal bile acid gradient, have been associated with fatal fetal arrhythmias. The hydrophobicity of individual bile acids in the serum bile acid pool is of relevance, with relatively lipophilic bile acids having a more harmful effect on the heart. Ursodeoxycholic acid can reverse or protect against these detrimental cardiac effects of elevated bile acids.