Evolving process-based models from psychological datausing genetic programming

The development of computational models to provide explanations of psychological data can be achieved using semi-automated search techniques, such as genetic programming. One challenge with these techniques is to control the type of model that is evolved to be cognitively plausible – a typical problem is that of “bloating”, where continued evolution generates models of increasing size without improving overall fitness. In this paper we describe a system for representing psychological data, a class of process-based models, and algorithms for evolving models. We apply this system to the delayed match-to-sample task. We show how the challenge of bloating may be addressed by extending the fitness function to include measures of cognitive performance

Change and Aging Senescence as an adaptation

Understanding why we age is a long-lived open problem in evolutionary biology. Aging is prejudicial to the individual and evolutionary forces should prevent it, but many species show signs of senescence as individuals age. Here, I will propose a model for aging based on assumptions that are compatible with evolutionary theory: i) competition is between individuals; ii) there is some degree of locality, so quite often competition will between parents and their progeny; iii) optimal conditions are not stationary, mutation helps each species to keep competitive. When conditions change, a senescent species can drive immortal competitors to extinction. This counter-intuitive result arises from the pruning caused by the death of elder individuals. When there is change and mutation, each generation is slightly better adapted to the new conditions, but some older individuals survive by random chance. Senescence can eliminate those from the genetic pool. Even though individual selection forces always win over group selection ones, it is not exactly the individual that is selected, but its lineage. While senescence damages the individuals and has an evolutionary cost, it has a benefit of its own. It allows each lineage to adapt faster to changing conditions. We age because the world changes.Comment: 19 pages, 4 figure

A model of force balance in Saturn's magnetodisc

We present calculations of magnetic potential associated with the perturbation of Saturn's magnetic field by a rotating, equatorially-situated disc of plasma. Such structures are central to the dynamics of the rapidly rotating magnetospheres of Saturn and Jupiter. They are `fed' internally by sources of plasma from moons such as Enceladus (Saturn) and Io (Jupiter). We use a scaled form of Euler potentials for the Jovian magnetodisc field (Caudal, 1986). In this formalism, the magnetic field is assumed to be azimuthally symmetric about the planet's axis of rotation, and plasma temperature is constant along a field line. We perturb the dipole potential by using simplified distributions of plasma pressure and angular velocity for both planets, based on observations by Cassini (Saturn) and Voyager (Jupiter). Our results quantify the degree of radial `stretching' exerted on the dipolar field lines through the plasma's rotational motion and pressure. A simplified version of the field model, the `homogeneous disc', can be used to easily estimate the distance of transition in the outer magnetosphere between pressure-dominated and centrifugally-dominated disc structure. We comment on the degree of equatorial confinement as represented by the scale height associated with disc ions of varying mass and temperature. For Saturn, we identify the principal forces which contribute to the magnetodisc current and make comparisons between the field structure predicted by the model and magnetic field measurements from Cassini. For Jupiter, we reproduce Caudal's original calculation in order to validate our model implementation. We also show that compared to Saturn, where plasma pressure gradient is, on average, weaker than centrifugal force, the outer plasmadisc of Jupiter is clearly a pressure-dominated structure.Comment: 24 pages, 15 figures, 2 tables; accepted for publication in MNRA

Discounting Climate Change

* The ideas I apply here were presented in my Plenary Lecture to the World Congress o

Modelling the regulation of telomere length: the effects of telomerase and G-quadruplex stabilising drugs

Telomeres are guanine-rich sequences at the end of chromosomes which shorten during each replication event and trigger cell cycle arrest and/or controlled death (apoptosis) when reaching a threshold length. The enzyme telomerase replenishes the ends of telomeres and thus prolongs the life span of cells, but also causes cellular immortalisation in human cancer. G-quadruplex (G4) stabilising drugs are a potential anticancer treatment which work by changing the molecular structure of telomeres to inhibit the activity of telomerase. We investigate the dynamics of telomere length in different conformational states, namely t-loops, G-quadruplex structures and those being elongated by telomerase. By formulating deterministic differential equation models we study the effects of various levels of both telomerase and concentrations of a G4-stabilising drug on the distribution of telomere lengths, and analyse how these effects evolve over large numbers of cell generations. As well as calculating numerical solutions, we use quasicontinuum methods to approximate the behaviour of the system over time, and predict the shape of the telomere length distribution. We find those telomerase and G4-concentrations where telomere length maintenance is successfully regulated. Excessively high levels of telomerase lead to continuous telomere lengthening, whereas large concentrations of the drug lead to progressive telomere erosion. Furthermore, our models predict a positively skewed distribution of telomere lengths, that is, telomeres accumulate over lengths shorter than the mean telomere length at equilibrium. Our model results for telomere length distributions of telomerase-positive cells in drug-free assays are in good agreement with the limited amount of experimental data available