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The introduction of the Manila clam into British coastal waters in the 1980s was contested by conservation agencies. While recognizing the value of the clam for aquaculture, the government decided that it posed no invasive risk, as British sea temperatures would prevent naturalization. This proved incorrect. Here we establish the pattern of introduction and spread of the species over the first 30 years of its presence in Britain. We report archival research on the sequence of licensed introductions and examine their relationship in time and space to the appearance of wild populations as revealed in the literature and by field surveys. By 2010 the species had naturalized in at least 11 estuaries in southern England. These included estuaries with no history of licensed introduction. In these cases activities such as storage of catch before market or deliberate unlicensed introduction represent the probable mechanisms of dispersal. In any event naturalization is not an inevitable consequence of introduction and the chances of establishment over the period in question were finely balanced. Consequently in Britain the species is not currently aggressively invasive and appears not to present significant risk to indigenous diversity or ecosystem function. However it is likely to gradually continue its spread should sea surface temperatures rise as predicted.
The changes in lipoprotein metabolism which follow the ingestion of a large fat load have been well described. The hypothesis was tested that similar changes in lipoprotein metabolism would occur after a relatively normal meal. Plasma and lipoprotein triacylglycerol, cholesterol and apolipoprotein concentrations were determined in twenty subjects (ten female) given a mixed meal containing approximately one-third of the daily intake of major nutrients in the typical Western diet. Fasting plasma triacylglycerol concentrations (range 0.38–2.70 mm/l) and the postprandial rise in plasma triacylglycerol varied considerably between subjects and were significantly associated (P < 0.01). The rise in plasma triacylglycerol corresponded to marked increases in the triacylglycerol concentration of the triacylglycerol-rich lipoproteins (TRL; chylomicrons and very-low-density lipoproteins). TRL cholesterol also increased after the meal. An increase in high-density-lipoprotein (HDL)-triacylglycerol following the meal was accompanied by a decrease in HDL-cholesterol concentration, presumably due to the action of the cholesteryl-ester transfer protein. The increases in HDL-triacylglycerol and in TRL- cholesterol were correlated with the postprandial rise in triacylglycerol in the TRL (P < 0.01). We conclude that potentially adverse changes occur in both triacylglycerol-rich and high-density lipoproteins following a typical mixed meal, as they do after large fat loads. The changes are exaggerated in those subjects with greater fasting plasma triacylglycerol concentrations.
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