On the evolution of misunderstandings about evolutionary psychology.

Some of the controversy surrounding evolutionary explanations of human behavior may be due to cognitive information-processing patterns that are themselves the result of evolutionary processes. Two such patterns are (1) the tendency to oversimplify information so as to reduce demand on cognitive resources and (2) our strong desire to generate predictability and stability from perceptions of the external world. For example, research on social stereotyping has found that people tend to focus automatically on simplified social-categorical information, to use such information when deciding how to behave, and to rely on such information even in the face of contradictory evidence. Similarly, an undying debate over nature vs. nurture is shaped by various data-reduction strategies that frequently oversimplify, and thus distort, the intent of the supporting arguments. This debate is also often marked by an assumption that either the nature or the nurture domain may be justifiably excluded at an explanatory level because one domain appears to operate in a sufficiently stable and predictable way for a particular argument. As a result, critiques in-veighed against evolutionary explanations of behavior often incorporate simplified--and erroneous--assumptions about either the mechanics of how evolution operates or the inevitable implications of evolution for understanding human behavior. The influences of these tendencies are applied to a discussion of the heritability of behavioral characteristics. It is suggested that the common view that Mendelian genetics can explain the heritability of complex behaviors, with a one-gene-one-trait process, is misguided. Complex behaviors are undoubtedly a product of a more complex interaction between genes and environment, ensuring that both nature and nurture must be accommodated in a yet-to-be-developed post-Mendelian model of genetic influence. As a result, current public perceptions of evolutionary explanations of behavior are handicapped by the lack of clear articulation of the relationship between inherited genes and manifest behavior.

Comparative analysis of leucine transport in temperate fish liver in vivo.

The uptake of [14C]leucine in toadfish (Opsanus tau) liver in vivo at 10 degrees C has been studied by a single pulse injection technique. Transport parameters were determined on the basis of the distribution of the amino acid and of [3H]inulin, used as a marker for extracellular space, in liver free and protein-bound fractions and in venous blood draining from the liver. Saturation analysis by the Cornish-Bowden method yielded a maximal uptake of 0.26 mumole, which was similar on a concentration basis to that at 21 degrees C when circulation rate and dilution with blood are taken into account. Isoleucine and phenylalanine competed with leucine uptake at 10 degrees C as at 21 degrees C; additional competitors at 10 degrees C included histidine, methionine and valine. Fish acclimated to 10 degrees C for 2 weeks or more showed a restoration in maximal leucine uptake and disappearance of histidine inhibition. Methionine inhibition was retained. Three transport systems in this species are discussed: 20-20, operating in 20 degrees C-acclimated fish at 20 degrees C; 20-10, in 20 degrees C-acclimated fish at 10 degrees C; and 10-10, in 10 degrees C-acclimated fish at 10 degrees C. The properties of these systems are compared with the 0-0 system of Antarctic fish and with transport systems of mammalian cells. The latter are similar to our non-acclimated system, 20-10, suggesting that the mammalian cell may not be at a state of optimal temperature adaptation.

Effects of temperature on L-leucine transport in toadfish liver in vivo.

The effect of body temperature in the 4--30 degrees C range on L-leucine uptake by toadfish liver in vivo was examined by means of a single-injection pulse technique. The ratio of [14C]leucine to [3H]mannitol or [3H]inulin in blood leaving the liver was measured as a function of time after hepatic portal vein injection. Recoveries of the two isotopes in liver and [14C]leucine incorporation into protein were determined. The Q10 value for influx was 3.8, that for efflux 2.8. At all temperatures, the leucine influx was 8--10-times higher than its incorporation into protein. The directly energy-linked reactions appear to be the main site of increased temperature sensitivity at low temperatures.

Effect of temperature on protein synthesis in fish of the Galapagos and Perlas Islands.

1. The temperature dependency of protein synthesis was studied in vivo in five species of Pacific fish collected in the Galapagos and Perlas Islands: batfish (Ogcocephalus darwini), groupers (Epinephelus labriformis), catfish (Netuma platypogan), puffers (Arothron hispidus) and triggerfish (Sufflamen verres). 2. Liver protein synthesis, assayed by a rapid pulse injection technique, showed a moderate temperature dependency (Q10 = 2-3) in the 15-30 degree C range for all species except puffers (Q10 = 10-20). Synthesis was inhibited above 32 degrees C. 3. Protein synthesis in triggerfish was measured by the constant-infusion technique. Synthetic rates (% of tissue protein synthesized per day) at 25 degrees C were 20% for liver, 10% for gill, 1.8% for red muscle and 0.6% for white muscle. Q10 in the 20 degrees-30 degrees C range was 3.0 +/- 0.5 degrees C for all tissues.

Characterization of leucine transport by toadfish liver in vivo.

Kinetic analysis of L-leucine uptake by toadfish liver at 20 degrees C in vivo has been carried out after pulse injection of L-[14C]leucine into the hepatic portal vein. D-[3H]mannitol, which is taken up slowly by toadfish liver, is used as a marker for extracellular space and space accessible by simple diffusion. At normal plasma leucine concentration (0.1 mM), leucine uptake occurs rapidly (t1/2 = 0.25 min), representing a flux of 0.6 mumol/min for the liver as a whole. Analysis of the distribution of radioactive leucine among intracellular and extracellular free pools and protein-bound form at times of 30 s to 5 min after injection is consistent with operation of a concentrative or uphill transport system accounting for 40% of uptake at normal plasma concentration. Saturation of uptake occurs at increasing leucine loads; calculation of intracellular pool dilution from protein synthesis data indicates that 20-30% of liver intracellular space is occupied by incoming leucine during the first 2 min after portal injection. Maximal flux (V max) is 4.1 mumol/min per 7-g liver as a whole with Km = 0.6 mM. Competitive inhibition of leucine uptake is afforded by isoleucine and phenylalanine with lesser effects by aspartic acid, cysteine, methionine, threonine, tyrosine, and valine. No effect is observed with alanine, glycine, histidine, lysine, and proline.