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Biomedical subjects

D J Rowe

Publications and source records attributed to D J Rowe.

At least 73 records · Page 4Linked to original sources
PubMed1981

Characterization of polymyositis infiltrates using monoclonal antibodies to human leucocyte antigens.

Frozen serial sections of muscle from 15 patients with polymyositis and three normal controls were studied by indirect immunofluorescence with a panel of mouse monoclonal antibodies to various human leucocyte components. The results showed good correlation with conventional histology. In addition, large numbers of T lymphocytes were identified in those cases with a marked inflammatory infiltrate. Many of the T cells probably bear HLA-DR antigen as the anti-HLA-DR antibody stained as many cells as the anti-leucocyte antiserum. This strongly suggests that the T cells present are 'activated'. In two patients HLA-DR-positive material was identified apparently diffusing from the infiltrates into muscle fibres suggesting its release as a soluble factor. In one case, structures with the appearance of giant cells were seen. The method promises to provide new information on the nature of infiltrating leucocytes which may provide more accurate diagnostic and prognostic information than conventional histology alone.

Adult↗
PubMed1980

Comparison of digoxin analysis by EMIT with Immophase and Dac-Cel radioimmunoassay.

The results obtained by an enzyme multiplied immunoassay kit, EMIT, for the measurement of serum digoxin concentration were compared with those from two radioimmunoassay kit methods, Immophase and Dac-Cel. Patients' sera were used to study the correlation between the methods, and three quality control sera with low, intermediate, and high digoxin concentrations were used to study individual method precision. The coefficients of correlation between the three methods varied between 0.915 and 0.951 for serum drug concentrations up to 4.5 nmol/l. There were statistically significant differences between the means of the patients' samples for each method. Precision was acceptable for each method: within-batch percentage coefficient of variation (%CV) less than 8, between-batch %CV less than 10, except for Dac-Cel at low concentration %CV = 18.6. The time taken for the analysis of a batch of 10 samples was between 1.5 and 2 hours, depending on the method.

Digoxin↗
PubMed1980

The effects of calcitonin and colchicine on the cellular response to diphosphonate.

The mechanism by which diphosphonates inhibit bone resorption remains speculative; however, the osteoclast appears to be selectively affected by the drug. This study examined the effects off diphosphonate on osteoclasis in bones treated concomitantly with agents which reduce the osteoclast ruffled border, calcitonin and colchicine. Dichloromethylene diphosphonate, calcitonin, and colchicine inhibited parathyroid-hormone-stimulated bone resorption, as indicated by a significantly reduced release of 45Ca from prelabelled long bones. Quantitative and qualitative histological analyses of osteoclasts indicated differences among effects resulting from agents. Only bones treated with diphosphonate demonstrated a majority of osteoclasts with degenerative appearance; colchicine-treated bones exhibited many spherulated cells with cytoplasmic blebs. The number of normal osteoclasts in calcitonin-treated bones was the same as in controls and decreased with diphosphonate and colchicine treatment. All inhibitory agents reduced the number of nuclei per osteoclast; furthermore, colchicine effected an additional significant reduction, as compared with diphosphonate and calcitonin. The number and frequency of abnormal osteoclasts was increased by diphosphonate, but unaffected by colchicine and calcitonin. The addition of calcitonin, but not colchicine, to diphosphonate-treated bones decreased the incidence of abnormal osteoclasts. Although both calcitonin and colchicine are known to reduce the osteoclast ruffled border, this study has shown differences between the morphological effects of the 2 agents which presumably reflect differences in their mode of action and their interaction with diphosphonate.

Animals↗
PubMed1979

The effect of indomethacin on the biochemical response to fracture stress in rats.

After acclimatization to metabolic cages, groups of male Wistar rats were pretreated for 48 h with parenteral indomethacin to observe its effect on the biochemical response to femoral fracture stress. This trauma induced an average 2.3-fold rise in fibrinogen levels in all animals, which was maximal 24 h after injury. Indomethacin pretreatment caused a dose-related decrease in the plasma fibrinogen response 24 h after fracture: 1, 2, 10 or 20 mg/kg/day of drug reduced the response by approximately 3, 10, 13 and 23%. Fibrinogen levels in rats treated with high doses (10 and 20 mg/kg) of drug began to rise before fracture owing to intestinal ulceration. Plasma 11-hydroxycorticosteroids and urine total catecholamine levels did not respond to either indomethacin treatment or to fracture but levels of both compounds rose gradually during the experiment. Indomethacin is an inhibitor of prostaglandin synthesis and prostglandins may therefore be involved in the metabolic response to stress.

11-Hydroxycorticosteroids↗
PubMed1977

Quantitative analyses of osteoclast changes in resorbing bone organ cultures.

The stimulation of bone resorption, assessed by the release of 45Ca from prelabeled bones, was associated with an increase in number of osteoclasts per bone section in parathyroid hormone (PTH)-treated bones, but not in lipopolysaccharide (LPS)-treated bones. By contrast the number of nuclei per osteoclast increased following LPS treatment, but was not affected by PTH. LPS-treated bones had more multinucleated cells, some having as many as 27 nuclei per osteoclast. More osteoclasts were adjacent to the bone collar in bones treated with LPS or PTH than in control bones. In LPS-treated bones this area also contained the largest osteoclasts, as determined by the greatest number of nuclei per osteoclast. The results suggest that LPS and PTH stimulate osteoclastic resorption by different mechanisms.

Animals↗