Biomedical subjects

I M Hamilton

Publications and source records attributed to I M Hamilton.

3 recordsLinked to original sources

PubMed2001

The effects of temporal variation in predation risk on anti-predator behaviour: an empirical test using marine snails.

Foraging animals must often balance the conflicting demands of finding food and avoiding predators. Temporal variation in predation risk is expected to influence how animals allocate time to these behaviours. Counterintuitively, the proportion of time spent foraging during both high- and low-risk periods should increase with increasing time exposed to high risk. We tested this prediction using intertidal marine snails (Littorina spp.) that were exposed to temporal variation in perceived predation risk from crabs (Cancer productus and Cancer magister). Our results were consistent with those predicted for high-risk, but not low-risk, periods. During high-risk periods, a greater number of snails foraged (versus those that left the water or remained in their shells) as time at high perceived risk increased. For low-risk periods, there was no relationship between the number of snails foraging and time at high risk. This might be due to snails in all treatments foraging maximally in the low-risk periods. As a consequence, the difference in the number of snails foraging between high- and low-risk periods decreased with increasing time subject to high risk. These results indicate that the commonly used protocol of exposing foragers to a single pulse of heightened risk might tend to overestimate their typical investment in anti-predator behaviour.

Adaptation, Biological↗

PubMed2000

Interactions between vitamins C and E in human subjects.

Despite convincing in vitro evidence, a vitamin C-E interaction has not been confirmed in vivo. This study was designed to examine the effects of supplementation with either vitamin C or E on their respective plasma concentrations, other antioxidants, lipids and some haemostatic variables. Fasting blood was collected before and after intervention from thirty healthy adults in a double-blinded crossover study. Baselines for measured variables were established after 2 weeks of placebo supplementation, followed by daily supplementation with 73.5 mg RRR-alpha-tocopherol acetate or 500 mg ascorbic acid, and placebo, for 6 weeks. A 2 month washout preceded supplement crossover. Mean values showed that plasma lipid standardised alpha-tocopherol increased with ascorbic acid supplementation: from 4.09 (sem 0.51) to 4.53 (sem 0.66) micromol/mmol total cholesterol plus triacylglycerol (P < 0.05), and plasma ascorbic acid increased from 62.8 (sem 14.9) to 101.3 (sem 22. 2) micromol/l (P < 0.005). Supplementation with (RRR)-alpha-tocopherol acetate increased plasma alpha-tocopherol from 26.8 (sem 3.9) to 32.2 (sem 3.8) micromol/l (P < 0.05), and lipid-standardised alpha-tocopherol from 4.12 (sem 0.48) to 5.38 (sem 0.52) micromol/mmol (P < 0.001). Mean plasma ascorbic acid also increased with vitamin E supplementation, from 64.4 (sem 13.3) to 76. 4 (sem 18.4) micromol/l (P < 0.05). Plasma ferric reducing (antioxidant) power and glutathione peroxidase (U/g haemoglobin) increased in both groups, while urate, total cholesterol and triacylglycerol levels decreased (P < 0.05 throughout). Results are supportive of an in vivo interaction between vitamins C and E.

Adult↗

PubMed2000

Marginal copper deficiency and atherosclerosis.

Copper is an essential trace element in the maintenance of the cardiovascular system. Copper-deficient diets can elicit, in animals, structural and functional changes that are comparable to those observed in coronary heart disease. In this study, the effect of dietary-induced copper deficiency on aortic lesion development was measured by quantitative image analysis in C57BL/6 mice that are susceptible to diet-induced aortic lesions. The diets administered were severely copper deficient (0.2 mg/kg diet), marginally deficient (0.6 mg/kg diet), or copper adequate (6.0 mg/kg diet). Similarly, increased aortic lesion areas and elevated serum cholesterol were demonstrated in both deficient groups, compared with the copper-adequate group. Evidence for graded differences in copper status among the dietary groups was shown by the dose-response increase in liver copper concentration, copper-zinc superoxide dismutase and cytochrome-c oxidase activities, together with serum caeruloplasmin oxidase with increasing intakes of dietary copper. Despite the difference in copper status between the copper marginal and severely deficient groups, similar lesions found in both groups of mice suggest a threshold effect of copper deficiency on lesion formation.

Animals↗