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Biomedical subjects

R A Good

Publications and source records attributed to R A Good.

At least 541 records · Page 30Linked to original sources

Prostaglandin effect on lymphokine production in multiple sclerosis.

Production of the lymphokine LIF (leukocyte migration inhibitory factor) by normal lymphocytes on stimulation with mitogens in inhibited by E type prostaglandins (PGE). It has been reported that the leukocytes of patients with multiple sclerosis (MS) are resistant to this inhibitory effect. We have studied 10 MS patients using an indirect technique for measuring LIF activity. This allows separation of the effects of PGE on lymphocyte LIF production from the effects on the action of LIF on the target granulocytes. There was no difference between normal subjects and MS patients in the effects of prostaglandins E1 and E2 in concentrations of 2.5 and 0.25 microgram per milliliter, on LIF production, or on granulocyte response to LIF. These results do not support the hypothesis that the chronic inflammatory process in MS is the result of resistance to the normal inhibitory effects of PGE on the cellular immune response.

Humans↗

Familial herpes simplex infection associated with activation of the complement system.

A patient with severe recurrent herpes infection was evaluated for immunologic analysis including a profile of complement components. The peripheral blood lymphocytes from the patient responded by proliferation to herpes simplex antigen but failed to produce leukocyte migration inhibition factor. Herpes simplex antibody titers increased during active infection. Total hemolytic complement (TCH50), the third (C3), fifth (C5), sixth (C6) and seventh (C7) components of complement, and factor B were dramatically reduced; the first (C1), second (C2) and fourth (C4) components of complement were within normal limits. In family members with a history of recurrent herpes simplex, one or more of the later complement components (C5, C6 or C7) was reduced. This study demonstrates the activation of complement in these serums via the alternative pathway.

Adult↗

Selective IgA deficiency and circulating immune complexes containing bovine proteins in a child with chronic graft versus host disease.

We have previously shown that a selective absence of serum and secretory immunoglobulin A (IgA) may lead to the development of circulating immune complexes which appear to contain bovine milk antigens. We report here that high levels of circulating immune complexes were found in the serum of a child who was treated for severe combined immunodeficiency by bone marrow transplantation but in whom the IgA-producing cells subsequently failed. As increasing amounts of complexes appeared over a two year period, the child had a parallel progression of an apparent chronic graft versus host disease including a Sjögrens syndrome and scleroderma. Very large amounts of complexes were eventually formed but the level fell 77 per cent after milk was excluded from the diet. Chemical studies on the complexes showed that the majority of complexes did contain bovine milk proteins, and fluorescence antibody staining of skin biopsy samples showed the presence of dense deposits of bovine casein in the dermis. The relationship between bovine protein-antigen antibody complexes and the chronic graft reaction remains uncertain.

Antibodies↗

Studies on the pathogenesis of aplastic anemia.

Three assays were used to study myelopoiesis in 14 patients with aplastic anemia: (1) the soft agar colony assay for granulocyte-monocyte progenitors (CFU-c); (2) coculture of marrow from patients with normal marrows in the CFU-c assay; and (3) culture of marrow pretreated with antithymocyte globulin (ATG) in the CFU-c assay. Marrow from five patients gave low colony counts when cultured alone and suppressed colony formation by normal marrow cells in coculture. Suppressor cells may have caused the aplasia in these patients. Eight patients had low colony formation and no suppression in coculture. These patients may have absent or defective stem cells. Marrow from one patient produced normal colony formation, did not contain suppressor cells and may have a defective hematopoietic environment. Aplastic anemia thus may result from at least three different defects involving (1) the stem cells, (2) the hematopoietic environment or (3) suppressor cells.

Adolescent↗

Myasthenia gravis, thymectomy and serum thymic hormone activity.

Serum thymic hormone activity was measured in 36 patients with myasthenia gravis and in 10 control subjects from each age decade. In all 25 patients under 50 years of age results were within, or close to, the normal range. Activity at levels considered normal for juveniles was detected in 10 of the 11 older patients whereas levels normally decline in older subjects. One week after thymectomy, 13 of 17 patients (76 per cent) had no demonstrable serum thymic hormone activity. However, 10 months or longer after thymectomy only five patients (30 per cent) lacked thymic hormone activity in the serum. There was a significant correlation between clinial improvement and sustained lowering of serum thymic hormone activity after thymectomy.

Adolescent↗