A survey of U.A.F.'s regarding the role and training of clinical psychologists in MR.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to D A Gordon.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
A disease in mink has been discovered that has many of the features of collagen diseases in man. Affected animals suffer from wasting with leukopenia and thrombocytopenia as well as plasma cell infiltration, hypergammaglobulinemia, glomerulonephritis, arteritis and amyloidosis. Cell-free filtrates and ultracentrifugates from diseased animals induced the disease in normal mink, and aleutian genotypes were unusually susceptible to infection. This genotype was characterized by abnormal lysosomal structures in all the granule-forming cells, resembling the Chediak-Higashi syndrome of man. Anti-gamma-globulin factors similar to human rheumatoid factors were reported, although tests for antibodies such as ANF and LE factors have been negative. Arteritis and glomerulonephritis lesions stained positively for gamma-globulin, and Coombs-type sensitized red cells have been detected in the majority of affected mink. Some mink develop a monodispersion of hypergammaglobulinemia resembling the serum protein changes in human myeloma. These studies highlight genetic, immunological and microbiological causative factors in a mink disorder resembling human collagen disease.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In 1973 we reported the beneficial effects of azathioprine in a double blind, cross-over study in 17 patients with classic rheumatoid arthritis. During subsequent follow-up over a mean period of 40 months, 4 patients had discontinued therapy because of poor therapeutic response and 1 because of nausea. Eleven of the 12 patients still taking azathioprine had maintained their initial beneficial response or showed further improvement. Adverse side effects during the follow-up period were minor. They included nausea in 1 patient and leukopenia with thrombocytopenia in another. An increased incidence of chromosomal abnormalities was detected in those patients still receiving azathioprine.
The mixed leukocyte reaction (MLR) responses of 29 patients with classic rheumatoid arthritis (RA) were compared with those of 24 age- and sex-matched healthy controls. Pools of stimulating cells were selected to include the major cross-reacting HL-A specificities. In pooled human serum the MLR response of the RA lymphocytes was significantly enhanced relative to the response controls (P less than 0.05). In autologous serum there was suppression of the MLR response in patients with RA which correlated with disease activity. The data suggest the presence of an intrinsically enhanced cellular reactivity of RA lymphocytes suppressed by serologic factor(s). The mechanisms of this enhancement of suppression are discussed.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Five patients with primary idiopathic polymyositis developed proteinuria associated with urine sediment abnormalities. Renal biopsies disclosed a focal mesangial proliferative glomerulonephritis with deposits of immunoglobulin and complement. After treatment of the polymyositis with corticosteroids, proteinuria and urine sediment changes disappeared within 4 to 8 wk along with an improvement in the muscle disease. Although the pathogenesis remains to be determined, immune complexes may be implicated in the etiology of this renal lesion.