ABSTRACT. The detailed behavioural mechanisms underlying an instance of compensation for changes in dietary nutrients are described for the first time in an insect. Nymphs of Lucustu migruturiu L. were given one of four artificial diets on the third day of the fifth instar, and their feeding patterns recorded in detail for 12 h. The diets represented combinations of two protein and two digestible carbohydrate levels (28% and 14% dry weight) presented in an otherwise complete nutrient mix. At the nutrient levels used, locusts regulated their intake of food with respect to protein but not digestible carbohydrate in the diet. They ate more of the lower protein diets by eating the same sized meals more frequently than insects fed on the higher protein diets. Compensation was not complete over the 12h observation period: insects on the lower-protein diets ingested and absorbed 72% as much nitrogen as those insects fed on the higher-protein diets. Possible physiological mechanisms underlying the behavioural mechanisms are discussed.

A recently developed framework was applied to investigate the responses of newborn pea aphids, Acyrthosiphon pisum (Harris) (Homoptera: Aphididae), to simultaneous variations in dietary suerose and amino acid levels. The location of functional 'targets' for intake and growth were determined experimentally using performance criteria. Behavioural rules employed by insects to approach these targets were investigated by reference to the geometry of arrays of intake and growth across a range of diets. First-instar aphids were fed one of thirty-one chemically-defined diets ranging in sucrose concentration from 200 to 1000 mM and amino acid concentration from 25 to 250 mM. Insect survivorship, dry weight, protein-and carbohydrate-derived growth were high for all diets except those with the lowest nutrient levels. Peaks in final dry weight and protein content identified the intake target as the point reached by larvae fed the 600mM sucrose, 7 5 m~ amino acid diet. Aphids regulated sucrose primarily by consumption (i.e. behaviourally), whereas amino acids were regulated post-ingestively (i.e. by physiological mechanisms).

We investigated whether cholecystectomy is associated with subsequent cancer and, if so, whether the association is likely to be causal, by undertaking a retrospective cohort study using linked medical statistics, comprising a cholecystectomy group (n ¼ 39 254) and a reference cohort admitted for a range of other medical and surgical conditions (n ¼ 334 813). We found a short-term significant elevation of rates of cancers of the colon, pancreas, liver, and stomach after cholecystectomy, but no long-term elevation. Excluding colon cancers within 2 years of admission to hospital, the rate ratio for colon cancer after cholecystecomy, compared with the reference cohort, was 1.01 (95% confidence interval 0.90 -1.12) and after 10 years or more follow-up it was 0.94 (0.79 -1.10). It is highly improbable that the short-term associations between cholecystectomy and gastrointestinal cancers are causal, and we conclude that cholecystectomy does not cause cancer.

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