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P Calow

Publications and source records attributed to P Calow.

30 records · Page 2Linked to original sources
PubMed1987

Ecological compensation--a complication for testing life-history theory.

Mortality, growth and birth rates cannot vary independently in stable populations, environmental change of one variable must be accompanied by compensatory variation of another. Ecological compensation is recognized if the stable populations are genetically identical. Ecological compensation, if it operates, constrains the direction of evolutionary change, and predictions that ignore it may be in error.

Adaptation, Physiological↗
PubMed1987

Acute toxicity tests on the freshwater isopod, Asellus aquaticus using FeSO4. 7H2O, with special reference to techniques and the possibility of intraspecific variation.

Techniques are described for assessing the toxicity of Fe(II), an important component of the effluent from mines, to the freshwater isopod, Asellus aquaticus. These techniques either involve buffer systems or working at low pH. Both techniques indicate that A. aquaticus is very tolerant of Fe(II). Furthermore, the low-pH technique suggests that animals from sites exposed to mine-waste pollution are more tolerant than those from sites not so exposed. This difference is masked in the buffer experiments, possibly due to the formation of less toxic buffer-Fe(II) complexes.

Journal Article↗
PubMed1985

Are patterns of growth adaptive?

Models which define fitness in terms of per capita rate of increase of phenotypes are used to analyse patterns of individual growth. It is shown that sigmoid growth curves are an optimal strategy (i.e. maximize fitness) if (Assumption 1a) mortality decreases with body size; (2a) mortality is a convex function of specific growth rate, viewed from above; (3) there is a constraint on growth rate, which is attained in the first phase of growth. If the constraint is not attained then size should increase at a progressively reducing rate. These predictions are biologically plausible. Catch-up growth, for retarded individuals, is generally not an optimal strategy though in special cases (e.g. seasonal breeding) it might be. Growth may be advantageous after first breeding if birth rate is a convex function of G (the fraction of production devoted to growth) viewed from above (Assumption 5a), or if mortality rate is a convex function of G, viewed from above (Assumption 6c). If assumptions 5a and 6c are both false, growth should cease at the age of first reproduction. These predictions could be used to evaluate the incidence of indeterminate versus determinate growth in the animal kingdom though the data currently available do not allow quantitative tests. In animals with invariant adult size a method is given which allows one to calculate whether an increase in body size is favoured given that fecundity and developmental time are thereby increased.

Adaptation, Physiological↗
PubMed1983

Pattern and paradox in parasite reproduction.

Parasites are more fecund than free-living relatives. The traditional explanation of this is that parasites have to compensate for massive mortality in the transmission phase of their life cycles, but there are neo-Darwinian problems with this interpretation. Similarly, parasites invest more resources in reproduction than free-living relatives but often live longer as adults, and yet negative correlations are expected between fecundity and longevity. These patterns and paradoxes are discussed within the context of a general life-cycle theory. The theory is also used to address questions concerning the influence of age-specific mortality on life-cycle patterns, the trade-off between gamete size and numbers, and the relative merits of gametic and non-gametic reproduction. Wherever possible, the theory is related to facts about parasites.

Animals↗
PubMed1978

Bidder's hypothesis revisited. Solution to some key problems associated with general molecular theory of ageing.

In this paper I consider three major difficulties associated with the general molecular theory of ageing, namely: (1) How can molecular damage accumulate in the face of the constellation of repair mechanisms that is found in cells? (2) How can the obvious programmatic nature of ageing be reconciled with underlying stochastic processes? (3) How do some organisms avoid ageing? As a solution to points 1 and 2, I propose that the repair mechanisms themselves deteriorate in a programmed fashion with age. However, I argue that this programming is unlikely to be a result of direct selection for life-shortening but, rather, is more likely to be a result of an indirect selection for other characters. This idea is very similar to the theory of senescence first formulated by Bidder. The solution to point 3 is that the repair mechanisms in systems which avoid ageing, in particular cellular and molecular turnover, are not impaired with age. The rejuvenating capacities of sexual and asexual reproduction are also discussed.

Aging↗
PubMedDate not supplied

Ecological risk assessment: risk for what? How do we decide?

Ecological risk assessment is defined both in theory and in practice. To do it properly, we need to know what targets we are protecting, but these targets are not always obvious and clearly defined. The pragmatic approach, used most generally in the context of environmental protection legislation, is the risk quotient method. Two other approaches involving more transparency and ecological relevance are critically assessed. One is based on species sensitivity distributions; the other is based on generalized population dynamics. Challenges for the future are considered.

Ecology↗