Following previous doses of local x-irradiation, the brains' subsequent cellular reaction to superficial freezing injury was reduced. The reduction in cellular response was dependent on the radiation does (200–4000 r) but was independent of the time interval between irradiation and injury (3 days to 6 months). It is suggested that radiation damage was stored up in local cells until they are stimulated to divide when they die. This hypothesis is based on the assumption that following superficial freezing injury to the cerebral cortex, the majority of brain macrophages are of local origin and are not to any large extent derived from the general circulation. This is a view supported by our autoradiographic study using H3-thymidine. It was found however that a small number of hematogenous cells did enter the lesion and that the participation of these cells was slightly increased in the lesions of previously irradiated brain.

The cerebral hemispheres of normotensive and hypertensive rats were irradiated using exposures from 1,000 R to 4,000 R. Hypertension was shown to shorten the latent period between irradiation and death for exposures of 2,000 and 3,000 R and to lower the threshold for radiation damage to 1,000 R. Following an exposure of 4,000 R no differential shortening of the latent period occurred, normotensive and hypertensive animals dying after similar lengths of time. The hypothesis is put forward that with low exposures of X rays (2,000–3,000 R) radiation death is due to sudden vascular damage while with high values of exposure (3,000–4,000 R) death is due to white matter necrosis which follows glial depletion and subependymal stem cell damage respectively. Hypertension only accelerates vascular radiation damage and reduces the effective threshold dose of radiation. The latent period and both modes of damage are explained on the basis of the known slow mitotic replacement of vascular and glial cells in the central nervous system.

Mice have been irradiated with fast neutrons (mean energy 6 MeV) under normal and hypoxic conditions. Hypoxia was induced by brief periods of nitrogen breathing. Observations of the thymus weight two days later gave an oxygen enhancement ratio of 1·7 ± 0·2. Earlier irradiations with 8 MeV electrons gave an OER of 2·7 ± 0·3. This gives a gain factor of l·6 ± 0·2. The RBE relative to 8 MeV electrons is 2·35 in air and 3·82 in nitrogen.

The Journal of Pathology and BacteriologyVolume 92, Issue 2 p. 375-384 Article The long-term survival of mice protected from 8MeV electron irradiation by combined treatment with cysteamine, hypoxia, syngeneic bone marrow and antibiotics Jennifer Shewell, Jennifer Shewell Department of Pathology, St Mary's Hospital Medical School, LondonSearch for more papers by this authorE. A. Wright, E. A. Wright Department of Pathology, St Mary's Hospital Medical School, LondonSearch for more papers by this author Jennifer Shewell, Jennifer Shewell Department of Pathology, St Mary's Hospital Medical School, LondonSearch for more papers by this authorE. A. Wright, E. A. Wright Department of Pathology, St Mary's Hospital Medical School, LondonSearch for more papers by this author First published: October 1966 https://doi.org/10.1002/path.1700920215Citations: 10AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume92, Issue2October 1966Pages 375-384 RelatedInformation

The Journal of Pathology and BacteriologyVolume 91, Issue 2 p. 613-615 Short Article The absence of effect of X-rays on the number of large nerve cells in the mouse spinal cord two years after irradiation E. A. Wright, E. A. Wright Department of Pathology, St Mary's Hospital, LondonSearch for more papers by this authorJean M. Jacobs, Jean M. Jacobs Department of Pathology, St Mary's Hospital, London Formerly Jean M. SpinkSearch for more papers by this author E. A. Wright, E. A. Wright Department of Pathology, St Mary's Hospital, LondonSearch for more papers by this authorJean M. Jacobs, Jean M. Jacobs Department of Pathology, St Mary's Hospital, London Formerly Jean M. SpinkSearch for more papers by this author First published: April 1966 https://doi.org/10.1002/path.1700910240Citations: 2 AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume91, Issue2April 1966Pages 613-615 RelatedInformation