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1. The metabolism of (+/-)-norcamphor, (+)-camphor, (-)-camphor, (+)-epicamphor, (+/-)-camphorquinone, (+/-)-camphane-2,5-dione and camphane was investigated in rabbits. All the compounds except camphane-2,5-dione increased the content of glucuronide in the urine. 2. (+/-)-Norcamphor was reduced to endo-norborneol; (+)-camphor, contrary to expectation, was reduced to (+)-borneol, as well as being hydroxylated to (+)-5-endo-hydroxycamphor and (+)-3-endo-hydroxycamphor, 5-endo-hydroxycamphor being the predominant product. (+)-Epicamphor was reduced mainly to (+)-epiborneol; (+/-)-camphorquinone gave 3-endo-hydroxycamphor and 2-endo-hydroxyepicamphor, the former being the major metabolite. (+/-)-Camphane-2,5-dione was reduced to 5-endo-hydroxycamphor. Camphane was hydroxylated to borneol and epiborneol, the latter predominating. 3. An explanation of these findings is given in terms of steric hindrance and thermodynamic stability. 4. The possibility was investigated that NADH was involved in the reductions.

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SUMMARYLarvae of the small tortoiseshell butterfly, Aglais urticae (Lepidoptera: Nymphalidae), were infected orally with a nuclear polyhedrosis virus. Sections of larvae which had been killed and fixed at intervals after infection were examined by light and electron microscopy. Typical virus development was observed in the fat body cells. However, in the nuclei of infected columnar cells of the mid-gut no incorporation of the virus particles into the polyhedral inclusion body was observed although both virus particles and crystalline polyhedron protein were present. Subsequently virus particles were found in the cytoplasm of these ceils between the nucleus and the basal membrane. It is proposed that this unusual virus development is significant in the pathway of infection of a nuclear polyhedrosis virus.

SUMMARYA small iridescent virus (type 29) has been isolated from the meal worm Tenebrio molitor. The virus is distinct from a number of previous isolates of small iridescent viruses (types 2, 6, 21, 22, 23 and 28) judged by polyacrylamide gel electrophoresis of its structural polypeptides. Immunodiffusion and immunoprecipitation tests showed that iridescent virus type 29 is related to types 22 and 23 but not types 2, 6, 21 and 28. The relationships between iridescent virus types 22, 23 and 29 were further studied by complement fixation and kinetic neutralization. Complement fixation tests confirmed that these viruses were related and showed that type 29 is distantly related to types 22 and 23 (which were more closely related to each other) though type 23 shares a closer relationship with type 29 than type 22. Kinetic neutralization experiments suggested a close relationship between types 29 and 23, and that both these viruses were remotely related to type 22. Low neutralization rate constants were obtained with these sera.

1. The metabolism of cis- and trans-decalin in the rabbit has been investigated. 2. Both hydrocarbons were oxidized to racemic secondary alcohols and excreted as ether glucuronides in amounts equal to about 60% of the dose administered. The principal glucuronides were isolated as triacetyl methyl esters and as sodium salts. 3. cis-Decalin gave rise mainly to (+/-)-cis-cis-2-decalol, together with a little cis-trans-2-decalol, and trans-decalin mainly to (+/-)-trans-cis-2-decalol and a small amount of trans-trans-2-decalol. 4. These results suggest that biological oxidation of the decalins does not occur via a free-radical mechanism. An attempt is made to explain why racemic alcohols are obtained, rather than the more typical optically active products of enzymic reaction, and a mechanism is proposed. It is suggested that enzymes similar to steroid hydroxylases are involved.

SUMMARY After noting the rarity of papers describing the pathology of delayed radiation necrosis of the spinal cord, the clinical and pathological findings from four cases are presented. The main pathological features are asymmetric demyelination of the lateral columns and to a lesser degree the posterior and anterior columns of white matter, with coagulative necrosis at the level of irradiation which affected the grey matter to a lesser degree. There is ascending and descending secondary tract degeneration, and poor glial response in the lesions themselves. Vascular changes, mainly hyaline thickening of arteriolar walls, are present, but not in degree sufficient to explain the primary lesion. The discussion of the pathogenesis of the myelopathy weighs the merits of a primary vascular lesion against those of a primary effect of the radiation on neural tissue. The latter is favoured.The clinical syndrome of radiation myelopathy is well documented (Malamud, Boldrey, Welch, and Fadell, 1954; Itabashi, Bebin, and De Jong, 1957;Dynes and Smedal, 1960;Pallis, Louis, and Morgan, 1961;Atkins and Tretter, 1966;Baldus, 1966;Hughes, 1966; Kristensson, Moulin, and Sourander, 1967;Reagan, Thomas, and Colby, 1968; Van den Brenk, Richter, and Hurley, 1968;Lehmann, Zett, and Neumeister, 1968;Locksmith and Powers, 1968;Maier, Perry, Saylor, and Sulak, 1969; Philips and Buschke, 1969;Tan and Khor, 1969;Coy, Baker, and Dolman, 1969;Eyster and Wilson, 1970). It occurs invariably as an iatrogenic lesion due to irradiation of malignant tissues in the vicinity of the spinal cord. The cervical region is the commonest part of the cord to be affected, and most reports of the pathology of radiation myelopathy have been of lesions at this site.The type of malignancy irradiated seems to have no bearing on the subsequent development of myelopathy. The exact incidence of radiation myelopathy is not known. The factors which appear to be especially important in the development of the myelopathy are total dose, field size, and dose rate. The dose-incidence relationship has been given a mathematical description by Van den Brenk et al. (1968), who also suggest that treatment in hyperbaric oxygen increases 888

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