sulphated mucopolysaccharide carragheenin as an agent to produce arthritis in rabbits and guinea pigs. Repetitive periarticular injections lead to sustained synovial inflammation, in selected microscopic fields it is found possible to locate changes indistinguishable from those commonly seen in rheumatoid av-951 Tivozanib arthritis in the human. Such changes, however, are individually not specific. Considerable interest was aroused by the description of the hydralazine syndrome, but the enthusiastic description of an experimental form of systemic lupus erythematosus has not been confirmed, and joint changes analogous with those of the human disease have not been found. The use of mustard in causing an experimental arthritis was popularized by Coutu and Selye, who injected 0 1 ml.
of a 10 per cent. mustard suspension into eighteen intact rats and eighteen adrenalectomized rats. The authors were unable to confirm the claim of Brownlee that deoxycortone and ascorbic acid were Topotecan beneficial. Teodoru, Feyal Cabanes, and Jequier, studying mustard arthritis, showed that chloramphenicol did not influence the anti inflammatory effect of cortisone in spite of its stimulating effect on the reticuloendothelial system. Ducommun and Coutu observed the effect of fasting on mustard arthritis, and Ducommun, Jacot, Coutu, Koch, and Selye compared the anti inflammatory effects of irgapyrine and phenergan on the same condition, these anti inflammatory effects could be produced in adrenalectomized rats. Coutu, Gareau, and Ducommun claimed that deoxycortone exaggerated the arthritic response which was minimized by cortisone.
It is clear from the illustrations in this and in earlier papers that the mustard arthritis induced in rats was a poor replica of rheumatoid arthritis in man. Coutu, however, emphasized that the differences were quantitative and not qualitative, a point which requires objective confirmation or refutation. Later, Radino extended her study of the effects of ultrasonics to mustard arthritis, including work on the histochemistry of the connective tissues. COMMENT Several organic and inorganic chemicals may be used to induce convenient forms of experimental arthritis in small laboratory animals. These forms of arthritis provide acceptable models for the study of the pathological physiology of joint disease, but none can be regarded as reduplicating in detail the evolution and behaviour of rheumatoid arthritis.
III. EXPERIMENTAL PRODUCTION OF ARTHRITIS BY ALTERED ENDOCRINE MECHANISMS Action of Deoxycortone Acetate in Normal Rats. The possibility that arthritic changes resembling those of rheumatic fever and of rheumatoid arthritis might be produced experimentally by altered endocrine function was suggested by Selye . The production of joint lesions in rats by giving very large amounts of deoxycortone acetate was described. In the original report three animals out of eight given deoxycortone developed arthritic changes, these changes appeared within 10 days of starting treatment, and subsided and reappeared in different joints without obvious reason. Many animals in the colony died from intercurrent infection and the possible role of infection in causing arthritis was not given sufficient consideration. From this work, whic