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By F. De Matteis, E. A. Lock

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Demyelination' is, therefore, a misleading description. A number of light- and electron-microscopic studies of the degenerative process in various species have been published and critically reviewed (listed by Davis and Richardson, 1980). Recent work by Bouldin and Cavanagh (1979a,b) has clarified the details of early stages of the degeneration. It is necessary to sample in a way that takes into account the intricate structure of the nervous system and the manner in which the nervous system both degenerates and responds to degeneration; axon samples need to be taken at various distances from the cell body.

W. Deatherage), Atomic Energy Commission, USA, pp. 3-43 Staub, N. C. (1974). Pathogenesis of pulmonary oedema. Am. Rev. Respir. , 109,358-72 Staub, N. , Nagano, H. and Pearce, M. C. (1967). Pulmonary oedema in dogs, especially the sequence of fluid accumulation in lungs. J. appl. , 22, 227-40 Suttorp, N. and Simon, L. M. (1982). Lung cell oxidant injury. Enhancement of polymorphonuclear leukocyte-mediated cytotoxicity in lung cells exposed to sustained in vitro hyperoxia. J. Clin. , 70, 342-50 Suttorp, N.

Development of pulmonary artery arterial changes in rats fed Crotalania Spectabilis. Am. J. , 94, 37-50 Michaelis, L. and Hill, E. S. (1933). Potentiometric studies on semiquinones. J. Am. chem. , 55,1481-94 Minchin, R. F. and Boyd, M. R. (1983). Localisation of metabolic activation and deactivation systems in the lung: Significance to the pulmonary toxicity of xenobiotics. Ann. Rev. Pharmacol. , 23, 217-38 Minchin, R. , McManus, M. , Thorgeirsson, S. , Schwarts, D. and Boyd, M. R. (1985). Metabolism of 2-acetylaminofluorene in isolated rabbit pulmonary cells.

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