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Biomedical subjects

J Watkins

Publications and source records attributed to J Watkins.

At least 181 records · Page 10Linked to original sources

A simple technique for studying immunoglobulin synthesis by normal and malignant plasma cells in vitro.

Plasma cells from human marrows are saturated with C-14 labelled amino acids, harvested and recultured in unlabelled growth medium. The appearance of radioactivity in the growth medium then provides a simple and rapid measure of protein synthesis. The secreted radio-labelled material is characterized by isoelectric focusing and autoradiography in acrylamide gels, a technique which has advantages over established serological methods.

Autoradiography↗

Immunological mechanisms in the pathogenesis of vinyl chloride disease.

Vinyl chloride (VC) disease is a multisystem disorder incorporating Raynaud's phenomenon, acro-osteolysis, thrombocytopenia, portal fibrosis, and hepatic and pulmonary dysfunction. Immunological and immunochemical investigations showed the presence of circulating immune complexes in 19 out of 28 patients with the disease and in a further two out of 30 workers exposed to VC. The immunological data were reviewed in relation to the clinical picture of the disease and to the available evidence on the metabolism of VC. The results suggest that VC disease is an immune complex disorder and that the immune response is initiated by the adsorption of VC or a metabolite on to tissue or plasma protein.

Autoantibodies↗

Identification and quantitation of hypersensitivity reactions to intravenous anaesthetic agents.

It is not possible to distinguish between direct pharmacological effects and immune-mediated hypersensitivity reactions by clinical observation alone and errors may occur in the absence of laboratory tests. A convenient and simple test is the measurement of plasma complement C3 consumption and conversion in sequential blood samples taken at intervals over the 24 h following an adverse response.

Alfaxalone Alfadolone Mixture↗

Immune-mediated reactions to althesin (alphaxalone).

Measurements of complement conversion and white cell variations were made on sequential blood samples obtained from a single volunteer following repeated administration of Althesin. The results suggest a mechanism by which a clinically significant hypersensitivity reaction to the drug might be mediated. Studies of patients receiving routine anaesthesia revealed a very high incidence of subclinical "hypersensitivity" reaction, some of which appear to be immune-mediated. These reactions occurred irrespective of whether the patients were induced with Althesin, methohexitone or propanidid.

Adult↗

Antiglobulin production to altered IgG in rheumatoid arthritis.

Conformationally altered IgG molecules have been detected in the serum of patients with rheumatoid arthritis. A hypothesis is presented that specific T-cell unresponsiveness to autologous IgG can be bypassed through the recognition of the altered IgG by competent B lymphocytes. The recognition of altered IgG is mediated through membrane Fc receptors (which may themselves be different in rheumatoid arthritis) and this favours stimulation of those cells carrying a specific receptor for an antigenic part of the molecule. A particular cellular arrangement may be required for complete antigenic stimulation and antiglobulin production. The resultant antiglobulin can have the same binding affinity for autologous and homologous IgG since the antigenic part of the molecule need not be a structurally altered site.

Animals↗

Catabolism of human IgG in mice sensitized to various IgG fragments. Similarities to the catabolism of rheumatoid IgG in mice.

Whole body elimination studies of human serum IgG have showm that C57Bl miceare tolerant to this protein at low concentrations. The present study demonstrates that tolerance to this protein may be broken by presensitization of the mouse with the pepsin-derived fragments of human IgG (F(ab)2 and pFc), in marked contrast to the papain-derived fragments (Fab and Fc). Sensitization with F(ab)2 fragments induced a distinctive elimination pattern of the intact protein which was analogousto that observed in non-sensitized mice injected with serum IgG isolated from patients with rheumatoid arthritis. Since, by circular dichroism studies, we have previouslyimplicated a structural anomaly at or near the hinge region of the 'rheumatoid' IgGmolecule, our observations are discussed in relationship to a possible immune aetiologyfor rheumatoid arthritis.

Animals↗