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Biomedical subjects

D M MacDonald

Publications and source records attributed to D M MacDonald.

At least 163 records · Page 9Linked to original sources
PubMed1983

Quantitative analysis of T-lymphocyte subsets in atopic eczema, using monoclonal antibodies and flow cytofluorimetry.

An analysis of T-lymphocyte subpopulations was performed on thirty-eight consecutive patients with atopic eczema, using monoclonal antibodies and flow cytofluorimetry. The total T-lymphocyte and helper T-cell numbers did not differ significantly from those of a matched control group, but there was a highly significant reduction in suppressor T-cell numbers among the atopic group. Both suppressor T-cell deficiency and circulating IgE elevation were found to correlate positively with disease activity. Food specific IgE levels to milk and egg were ascertained by radioallergosorbent (RAST) studies. These proved positive in seven out of thirty-five atopics (20%).

Adolescent↗
PubMed1983

Impaired lymphocyte cyclic adenosine monophosphate responses in atopic eczema.

Peripheral blood lymphocyte cyclic AMP responses to isoprenaline, prostaglandin E2 and histamine were examined in patients with atopic eczema, in the presence and absence of a potent phosphodiesterase inhibitor (PDEI). Basal cyclic AMP levels were not significantly different in atopic and control groups. In the presence of the PDEI, there were impaired cyclic AMP responses to both isoprenaline and prostaglandin E2 in the atopic group. Differences between atopic and control cyclic AMP responses were exaggerated by the omission of the PDEI, when impaired responses to all agonists were observed in lymphocytes from atopic subjects. These results imply that, in atopic eczema, lymphocytes exhibit impaired responses not only at the beta-adrenoceptor site but at unrelated sites of adenylate cyclase activation, and these observations are consistent with increased leukocyte phosphodiesterase activity.

Adult↗
PubMed1982

Genomic location and lack of phosphorylation of the HSV immediate-early polypeptide IE 12.

Herpes simplex virus type 1 (HSV-1) induces an immediate-early (IE) polypeptide IE 12. An equivalent polypeptide coded by HSV-2 which migrated slightly more slowly on SDS-polyacrylamide gels was identified and designated IE 12.3. Analysis of the serotype of the IE polypeptide induced by five HSV-1/HSV-2 intertypic recombinants when correlated with their genome structures showed that IE 12/IE 12.3 mapped in the region spanning the TRs/Us junction. Unlike four other IE polypeptides induced by HSV-1 (IEs 175, 110, 68 and 63), IE 12 was not detectably phosphorylated.

Base Sequence↗
PubMed1982

A technique for immunoultrastructural identification of T6-positive Langerhans cells and indeterminate cells in mycosis fungoides.

An immunoelectron microscopic method was developed using T6 antiserum in an immunoperoxidase technique to label the dendritic cells of the epidermis in mycosis fungoides (MF). The technique allows simultaneous identification of intracellular Birbeck granules and T6 membrane positivity. Ultrastructural examination of the epidermal infiltrate of MF, using this method, confirmed the T6-positive nature of Langerhans cells and indeterminate cells. All Sézariform and mature lymphocytes were T6-negative and a small population of T6-negative histiocytic cells were also observed.

Horseradish Peroxidase↗