Co-nutrient limitation of diatom growth under nitrogen or silicon limitation. A reply to the paper of Flynn and Martin-Jezequel

Flynn and Martin-Jézéquel (J. Plankton Res., 22,447–472, 2000) derived a mechanistic model for nitrogenand silicon physiology of diatoms. During their analysis, theycompared the output of this model with that of the co-nutrientmodel of Davidson and Gurney (J. Plankton Res., 21, 839–858,1999). They highlighted some discrepancies between the predictionsof the two models, which occurred subsequent to exhaustion ofthe yield-limiting nutrient, and suggested that the co-nutrientmodel contained technical inaccuracies in its output. Here itis shown that by simply modifying the numerical values of twoof the parameters of the co-nutrient model, while retainingexactly the same model structure, it is possible to producesimilar dynamics to those exhibited by the model of Flynn andMartin-Jézéquel.     

Genotype to phenotype: associations,errors and complexity

The Keystone Symposium on Genotype to Phenotype: Focus on Disease was held in Santa Fe, New Mexico, USA, from 19 to 24 February 2002.     

Animal signals: A reply to Hinde

Hinde has criticized articles by Dawkins & Krebs (1978) and Caryl (1979) in which supposedly traditional ethological views about agonistic display were contrasted with those arising from games theory. It is argued here that the views that we contrasted with those from games theory were not ‘straw men’: in particular, Cullen's view is completely incompatible with the predictions from games theory, and is well supported by ethological evidence (as conventionally interpreted). But an unusually detailed analysis of the ethological data, which raises many points for future studies, shows that the evidence actually favours the games theoretic view. Hinde argues that the conflict hypothesis of threat display implies that displays could not and should not carry precise information. The arguments he used in this context are not wholly satisfactory: in particular, explanations in terms of interaction are of little value unless details of the interaction can be specified. Clear hypotheses are needed in the analysis of animal communication, and ideas from games theory can be of help to ethology in this respect.     

Linking social complexity and vocal complexity: a parid perspective

The Paridae family (chickadees, tits and titmice) is an interesting avian group in that species vary in important aspects of their social structure and many species have large and complex vocal repertoires. For this reason, parids represent an important set of species for testing the social complexity hypothesis for vocal communication--the notion that as groups increase in social complexity, there is a need for increased vocal complexity. Here, we describe the hypothesis and some of the early evidence that supported the hypothesis. Next, we review literature on social complexity and on vocal complexity in parids, and describe some of the studies that have made explicit tests of the social complexity hypothesis in one parid--Carolina chickadees, Poecile carolinensis. We conclude with a discussion, primarily from a parid perspective, of the benefits and costs of grouping and of physiological factors that might mediate the relationship between social complexity and changes in signalling behaviour.     

Chemical carcinogenesis and toxicity models: Matching complexity to objectives

Mathematical models predicting tissue doses of chemical toxicants can be either highly complex or simple, depending upon the end results needed. As an example of a highly complex mathematical model, the Miller Model of the distribution of reactive gases in human and animal lungs is described. The Miller Model accounts for the convection, the radial and axial diffusion, and the chemical reactions of gases as an inhaled breath passes down the airways. The geometry and physiology of human and animal lungs are used to calculate the convection and diffusion likely in each generation or bifurcating series of airways commencing with the trachea and extending 24 generations in humans. The chemical reactivity of ozone, an air pollutant, is accounted for by simulating second-order chemical reactions with the fluid lining materials of the lung and tissue biological molecules. The flux of ozone into three compartments (pulmonary tissue, overlying liquid layer and capillary blood) in each generation of the lung is calculated to provide molecular doses of ozone reaching each region of the lung. These results of calculated molecular dose are then used to construct dose-response curves for a variety of biological endpoints. A much simpler model is also described which recognizes the saturable or Michaelis-Menten type of kinetics controlling the removal of nickelous ion (nickel) from the lung. This model is used to calculate the chronic lung burden of the human lung for occupational, environmental and cigarette smoking exposure scenarios. In both the complex Miller Model and the simpler nickel lung burden model, the results can be used to calculate molecular doses at the potential site of action of these environmental chemicals and to unify a wide variety of studies. The predictions made are more likely to be valid since multiple investigators using a variety of animal species have participated in generation of the primary data. As a methodology, mathematical modeling based on physiological, physicochemical and anatomical principles provides a means of eliminating non-scientific considerations from the important process of regulating and recognizing toxic or cancer causing chemicals in the human environment.