Frictional properties of cattle hooves and their conformation after trimming.

The conformation of the hooves of nine heifers obtained from an abattoir was measured and their coefficient of static friction (mu) was determined for movement in forward, backward and sideways directions. The hooves were trimmed by the Dutch method and their conformation and p were measured again. Trimming increased mu, and decreased the length of the digit and the angle between it and the floor. The value of mu was considerably greater for movement in a forward or backwards direction than sideways. The relationship between the value of mu for sideways movement and hoof conformation was examined by using 52 lower limbs from a variety of cattle breeds. Although mu was greater for Belgian blue than other cattle breeds, there were no relationships between mu and hoof conformation, including a measure of the roughness of the sole.

Prey processing in central place foragers.

The importance of prey processing as an integral part of foraging behaviour has long been acknowledged, but little theoretical consideration has been given to the optimization of the processing behaviour itself. Processing renders food down to ingestible, palatable portions, and also removes non-essential mass thus reducing transport costs. Here, several models of processing are developed for a central place forager. When the forager has to make a simple choice between processing the prey and not, a critical distance from the central place can be calculated, beyond which it is optimal to process prey. If the forager also decides on how much of the prey to remove, the optimal amount to be removed can also be calculated. Imposing a ceiling on overall metabolic expenditure is shown to reduce the distances at which processing becomes the optimal strategy. The models are tested using parameters derived for a provisioning merlin, Falco columbarius, and alternative explanations as to why observed behaviours should differ from the optimal behaviour predicted are discussed.

Incorporating rules for responding into evolutionary games.

Evolutionary game theory is concerned with the evolutionarily stable outcomes of the process of natural selection. The theory is especially relevant when the fitness of an organism depends on the behaviour of other members of its population. Here we focus on the interaction between two organisms that have a conflict of interest. The standard approach to such two-player games is to assume that each player chooses a single action and that the evolutionarily stable action of each player is the best given the action of its opponent. We argue that, instead, most two-player games should be modelled as involving a series of interactions in which opponents negotiate the final outcome. Thus we should be concerned with evolutionarily stable negotiation rules rather than evolutionarily stable actions. The evolutionarily stable negotiation rule of each player is the best rule given the rule of its opponent. As we show, the action chosen as a result of the negotiation is not the best action given the action of the opponent. This conclusion necessitates a fundamental change in the way that evolutionary games are modelled.

Urea inhibits NaK2Cl cotransport in human erythrocytes.

We examined the effect of urea on NaK2Cl cotransport in human erythrocytes. In erythrocytes from nine normal subjects, the addition of 45 mM urea, a concentration commonly encountered in uremic subjects, inhibited NaK2Cl cotransport by 33 +/- 7%. Urea inhibited NaK2Cl cotransport reversibly, and in a concentration-dependent fashion with half-maximal inhibition at 63 +/- 10 mM. Acute cell shrinkage increased, and acute cell swelling decreased NaK2Cl cotransport in human erythrocytes. Okadaic acid (OA), a specific inhibitor of protein phosphatase 1 and 2A, increased NaK2Cl cotransport by nearly 80%, suggesting an important role for these phosphatases in the regulation of NaK2Cl cotransport. Urea inhibited bumetanide-sensitive K influx even when protein phosphatases were inhibited with OA, suggesting that urea acted by inhibiting a kinase. In cells subjected to shrinking and OA pretreatment, maneuvers expected to increase the net phosphorylation, urea inhibited cotransport only minimally, suggesting that urea acted by causing a net dephosphorylation of the cotransport protein, or some key regulatory protein. The finding that concentrations of urea found in uremic subjects inhibited NaK2Cl cotransport, a widespread transport pathway with important physiological functions, suggests that urea is not only a marker for accumulation of other uremic toxins, but may be a significant uremic toxin itself.

Urea activation of K-Cl transport in human erythrocytes.

This report prompted us to examine the effect of urea on K-Cl cotransport in human erythrocytes. In human erythrocytes, urea activated K-Cl cotransport reversibly and in a concentration-dependent manner. Pretreatment with okadaic acid abolished the urea activation of transport, suggesting that exposure to urea resulted in net dephosphorylation of the transporter or a key regulator and that the action of urea was exerted proximal to the phosphorylation-dephosphorylation step. At a concentration of 200 mM, urea activated K-Cl cotransport without any delay, even in the absence of cell swelling. However, with increasing urea concentrations, an appreciable increase in lag time was observed before the final steady-state flux was reached, suggesting that urea inhibits a regulatory kinase. The latter conclusion was also supported by the finding that, at any given urea concentration, the lag time for activation was greater than the lag time for deactivation. Mg depletion activated cotransport, and urea had no additional stimulatory effect in Mg-depleted cells. In urea-pretreated cells, swelling further activated cotransport, but without any measurable delay, in contrast to a time lag of 8 min when control cells (not exposed to urea) were swollen. The latter finding suggests that urea promotes the conversion of transporters from the resting to the partially activated state. These findings raise the possibility that high concentrations of urea in the renal medulla may play a role in the decrease in cell volume that occurs during the maturation of reticulocytes and young erythrocytes, both in normal subjects and in subjects with hemoglobinopathies.