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M S Chesters

Publications and source records attributed to M S Chesters.

11 recordsLinked to original sources
PubMed1985

Natural and radiation-induced cataracts in man and mouse, and natural macular degeneration in man: proposed mechanisms.

A unified theory of growth and age-dependent disorders is applied to the interpretation of epidemiological data for natural and radiation-induced cataracts and natural macular degeneration in man. Using the same unified theory, mechanisms are also proposed to explain the experimental evidence for natural and radiation-induced lenticular opacities in the lens of the mouse. Epidemiological and experimental data are strikingly consistent with the hypothesis that natural cataract formation is an autoaggressive process but the details of pathogenesis differ greatly between the two species. Radiation dose-response relations reflect these contrasts. Lenticular opacities in the nuclear-bomb survivors at Hiroshima and Nagasaki were probably induced by a 'single-track' mechanism. Radiation-induced generalised opacification in the lens of the mouse results from a 'multi-track' process. The pathogenesis of natural macular degeneration in man happens to have close parallels with that of natural opacification in the mouse. We discuss some implications of these inferences for the phenomenon of radiation-induced lethal disorders in man.

Age Factors↗
PubMed1981

Mammalian cell survival and radiation quality: analysis with allowance for delta tracks.

The RBE for mammalian cell survival is analysed in relation to the distribution of LET. Complex target theory is described, together with a procedure for applying LET distributions to experimental findings in order to estimate the modes of cellular inactivation. Track segment theory is shown to have previously unrecognised limitations. The stepwise method is adopted to calculate the LET distributions for the radiations (alpha-particles, deuterons and x-rays) used by Barendsen et al (1966) in their study of the survival of T1 cells of human origin. Satisfactory fits of theory to experiment are obtained. Three distinctive modes of cellular inactivation, with independent energy transfers (direct and indirect) to complex targets comprising 2, 4 adn 6 elements respectively, appear to be involved overall. At 'low dose', no contribution from the 2-transfer-mode can be discerned; only this mode is reparable. Saturation cross-sections (at high LET) for the 2- and 4-transfer-, but not the 6-transfer-mode, are oxygen-dependent. All three modes of inactivation might entail unrepaired double strand breaks and/or some form of mutation in DNA, at 1, 2 and 3 vulnerable sections, respectively.

Alpha Particles↗
PubMed1979

A critique of Katz's 'high LET constraint on low LET survival'.

Katz's interpretation of the connexion between RBE and LET is contrasted with a version published previously by Burch. The implications of Katz's model for dose-response relations apply only at ultra-high absorbed doses in Burch's model. In the latter, the shoulder on type-C survival curves for mammalian cells is explained in terms of Haynes' repair model. Under certain conditions the repair model becomes mathematically equivalent to the 'alpha--beta' model; under some other conditions it becomes equivalent to the 'two-component' model. The formulation of a new repair hypothesis, based on the idea of an inducible repair mechanism, is also set out. It is argued that Katz's 'supralinearity index' is appropriate to the induction of (rare) mutations but inappropriate to cell survival, for which an alternative index is proposed. Certain plausible hypotheses of radiobiological action conflict with Katz's 'logical constraint' which, it is contended, is neither logical nor valid. In conclusion, although experimental findings for some radiobiological systems conform to Katz's 'constraint', the frequently observed violations should not necessarily be regarded as artefacts.

Cell Survival↗