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R D ADAMS

Publications and source records attributed to R D ADAMS.

At least 55 records · Page 3Linked to original sources

Allergic neuritis: an experimental disease of rabbits induced by the injection of peripheral nervous tissue and adjuvants.

In experimental allergic encephalomyelitis (EAE), produced by injecting rabbits with whole rabbit spinal cord together with tubercle bacilli and mineral oil, lesions comparable to those seen in the central nervous system are found in the nerve roots, spinal ganglia, and peripheral nerves. When special fractions of bovine white matter are used as antigen in rabbits, the same distribution of lesions is seen but peripheral nerve involvement is relatively less frequent. When rabbit sciatic nerve or spinal ganglia are used as antigen in rabbits, lesions occur only in the roots, ganglia, and peripheral nerves. Lesions are not produced in the central nervous system, nor is there a meningitis. This disease picture has been called experimental allergic neuritis (EAN). The antigenicity of rabbit nerve is not impaired by autoclaving. Sciatic nerve of other mammalian species produces the same disease in rabbits as does rabbit nerve. Optic nerve, used as antigen, produces the typical picture of EAE, not EAN. The optic nerves are not affected in EAN, whereas they commonly contain lesions in EAE. There are differences of symptomatology, referable to the difference in distribution of lesions, between EAE and EAN. The spinal fluid of EAE shows an increase both in the number of cells and in the total protein content. In EAN, the same changes in protein are observed, but usually the cell count remains normal. The cell count appears to be related to the involvement of cerebral and spinal meninges, which is an almost invariable accompaniment of EAE. The skin tests and serologic studies made with homologous and heterologous antigens were essentially non-contributory, apparently as a consequence of the diversity of antigens present in the inoculated materials. The similarity between EAN and certain of the human polyneuritides is indicated and discussed.

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A study of the chemical nature of components of bovine white matter effective in producing allergic encephalomyelitis in the rabbit.

Fractions of bovine white matter, prepared by the methods of Folch and Lees, were studied for chemical composition and for their ability to produce experimental allergic encephalomyelitis in rabbits. Evaluation of the disease and of the lesions in animals injected with the more active fractions at several dose levels permitted comparison of the antigenic activity of these materials. When tissue was fractionated by the methods of Folch and Lees, antigenic activity was found in the chloroform-methanol extract but not in the denatured tissue residue. This activity was traced to proteolipides A and B and to the lower phase, more specifically the ether-soluble fraction of the lower phase. Proteolipide C was inactive. Correlation of the chemistry of fractions with their antigenic activity suggested two possibilities: (a) that there might be two antigens, one proteolipide and the other non-proteolipide; or (b) that a small specific proteolipide is responsible for all the observed activity. The high concentration of acetal phosphatide in the ether-soluble lower phase suggested that compounds of this type might be the hypothetical non-proteolipide antigen, but this hypothesis was disproved by analytic study of active and inactive materials. The possibility that proteolipide might account for all the antigenic activity was strongly supported by the experimental finding that total lipide and proteolipide progressively lost activity as proteolipide was degraded by adequate processing. The use of an entirely different method for preparing total lipides free of proteolipide (the colloidal iron technique) indicated that this loss of activity did not result from incidental removal of some non-proteolipide antigen. These tentative conclusions are in agreement with those of Tal and Olitsky and provide a satisfactory interpretation of the findings of Goldstein et al. The very fact, however, that the suggested proteolipide antigen would amount to no more than 1 per cent of the total chloroform-methanol extractives leaves open the possibility that some unrecognized trace substance may be the antigen. Skin tests with the various fractions indicated some cross-reactivity between proteolipides A and B and the ether-soluble lower phase fraction and a fair correlation of positive skin reactions with disease. This finding is compatible with the suggestion that the same antigen is present in both of these types of material. When the disease produced by whole tissue or fractions was evaluated by the use of the proportion of animals developing disease, the day of onset, and the severity of the histologic lesions, it was found that fractions produced milder disease of later onset than intact tissue at all dose levels. The disease-producing activity was not enhanced by increasing the dose; i.e., it appeared to reach an asymptotic maximum below that obtainable with whole fresh tissue. This finding suggests both a quantitative loss of activity and a qualitative change during the initial chloroform-methanol extraction, a procedure which denatures all proteins in the tissue residue. A comparable change appeared to occur in whole white matter stored at -15 degrees C. for 15 months and thawed and refrozen several times during this period. The later fractionation steps resulted in no apparent loss of antigenic activity. A scoring method employing the same type of data to estimate the actual relative antigen contents of different preparations is presented in the Appendix.

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