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William S C Gurney

Publications and source records attributed to William S C Gurney.

2 recordsLinked to original sources

Modeling the demographic effects of endocrine disruptors.

In this article we describe a series of strategic models of populations and individuals subject to challenge by endocrine disruptors. These models are not designed to be fitted to detailed data on specific species but rather are intended to provide general insights on the relative importance of different demographic mechanisms in the population context. Therefore, the models contain the minimum necessary biological detail, but in recompense they are highly accessible to mathematical analysis. We show that, over a range of models with contrasting biological detail, population viability is controlled by the number of female offspring that result from the average female's lifetime reproductive activity. Thus, male fertility changes have little effect at the population level until they become severe enough to reduce this average female output. We argue that in many circumstances endocrine disruptors are likely to produce directly deleterious effects on female fecundity at levels far below those required to reduce male fertility to dangerously low levels. Finally, we formulate a simple model of individual energetics that we argue can form the basis of a strategic discussion of the likely sensitivity of female demographic parameters to chemically induced changes in physiological function.

Animals↗

Resource allocation, hyperphagia and compensatory growth.

Organisms often shown enhanced growth during recovery from starvation, and can even overtake continuously fed conspecifics (overcompensation). In an earlier paper (Ecology 84, 2777-2787), we studied the relative role played by hyperphagia and resource allocation in producing overcompensation in juvenile (non-reproductive) animals. We found that, although hyperphagia always produces growth compensation, overcompensation additionally requires protein allocation control which routes assimilate preferentially to structure during recovery. In this paper we extend our model to cover reproductively active individuals and demonstrate that growth rate overcompensation requires a similar combination of hyperphagia and allocation control which routes the part of enhanced assimilation not used for reproduction preferentially towards structural growth. We compare the properties of our dynamic energy budget model with an earlier proposal, due to Kooijman, which we extend to include hyperphagia. This formulation assumes that the rate of allocation to reserves is controlled by instantaneous feeding rate, and one would thus expect that an extension to include hyperphagia would not predict growth overcompensation. However, we show that a self-consistent representation of the hyperphagic response in Kooijman's model overrides its fundamental dynamics, leading to preferential allocation to structural growth during recovery and hence to growth overcompensation.

Animals↗