The Role of Regret in Informed Consent

Informed consent to medical procedures tends to be construed in terms of principle-based ethics and one or other form of expected utility theory. These constructions leave problems created by imperfect communication; subjective distress and other emotions; imperfect knowledge and incomplete understanding; complexity, and previous experience or the lack of it. There is evidence that people giving consent to therapy or to research participation act intuitively and assess consequences holistically, being influenced more by the magnitude of outcomes than their probability. People avoid decisions they may regret, but modern regret theory has received little attention in discussions of informed consent. This essay suggests ways in which regret may be acknowledged in the consent process and in the assessment of the information that is an intrinsic part of it.     

Influence of photoperiod on growth changes in juvenile Atlantic salmon, Salmo salar L.

During their first 6 months sibling Atlantic salmon parr, Salmo salar L., grew larger under constant light than under natural photoperiod or simulated natural photoperiod (control). When rate of change of photoperiod was accelerated after midsummer, ×2, ×3 and ×4, there were no growth differences between the three groups, but all were smaller than the control population. Under constant autumn photoperiod of 8 h light: 16 h dark growth was less than under all other experimental photoperiod conditions. Mean length was directly correlated with total hours of daylight experienced, excluding those fish kept under constant light. Fish reared from first feeding under photoperiod regimes delayed 6 and 9 months out of phase with the natural light cycle were smaller than the controls, whereas those under a regime 3 months out of phase did not differ from the controls. The clear segregation of modal length groups within the 3, 6 and 9 months out-of-phase populations occurred 1, 4 and 4 months, respectively, after the segregation in the control group. Under constant light, and under constant 12 h light: 12 h dark (12 LD), the segregation was delayed 3 and 4 months, respectively. The proportion of the population which maintained growth (upper modal group) was significantly less in the 9 and 6 months out-of-phase and 12 LD groups (39, 40 and 42%, respectively) than in the other three groups (82.5-85%). Acceleration of photoperiod change also resulted in decreased growth. The results support a model of salmon development in which, 2-3 months after first feeding, growth is maintained if feeding opportunities at that time are above a threshold level, and in which this critical timing is influenced by photoperiod. It is suggested that the delays reflect a synchronizing effect of photoperiod on an endogenous rhythm of appetite and growth. The differences in upper modal group proportions observed in the present experiments, reflect the relative feeding opportunities available at the critical period in July-August.     

Calcium transients in human platelets monitored by aequorin, fura-2 and quin-2: effects of protein kinase C activation and inhibition

Tumour-promoting phorbol esters and 1,2-dioctanoyl-sn-glycerol both induce calcium transients in platelets. However, these can only be detected in platelets loaded with aequorin, but not in those loaded with the fluorescent probes quin-2 and fura-2 presumably because of intracellular calcium buffering. Several effects induced by phorbol esters and diacylglycerols, including the rise in (Ca2+)i, the stimulation of Na+/H+ transporter and the inhibition of the effects of thrombin alone on (Ca2+)i are potently antagonised by staurosporine, a compound known to inhibit protein kinase C. Higher concentrations of staurosporine themselves inhibit the thrombin-induced calcium transient. Staurosporine inhibits the effects of phorbol esters and dioctanoyl glycerol with equal potency although the latter does not cause enzyme translocation of cytosolic protein kinase C to membranes. These results therefore suggest that some, if not all, the effects of protein kinase C activation can occur without translocation of the enzyme.