Search PubMed⌕ Search

Biomedical subjects

M A Reed

Publications and source records attributed to M A Reed.

45 records · Page 3Linked to original sources
PubMed1980

Radioallergosorbent testing of toluene diisocyanate-reactive individuals using p-tolyl isocyanate antigen.

Serum from 26 persons shown to react to provocative inhalation challenge with low concentration of toluene diisocyanate (TDI) was tested by radioallergosorbent test (RAST) using a p-tolyl isocyanate-human serum albumin (TMI-HSA) conjugate. Results were evaluated by the RAST ratio and by the mean +3 standard deviation methods. Positive results were obtained in 15% to 19% of TDI reactors, depending on the method of evaluation. These findings suggest that TDI asthma may be a complex syndrome with several types of reaction possible, including an IgE mechanism in some individuals, but they do not support the theory that TDI asthma is based solely on an immune mechanism. However, they do not disagree with the hypothesis that TDI reactivity may be mediated by a pharmacologic mechanism.

Antigens↗
PubMed1977

In vitro metabolism of vitamin D3 by isolated liver cells.

Liver cells were prepared from rats fed a rachitogenic diet to investigate the hepatic metabolism of [alpha-1,2-3H2] vitamin D3. Rat hepatocytes suspended in Hanks medium rapidly took up labeled vitamin D3 from the incubation medium and converted this sterol to various metabolites, including 25-hydroxy vitamin D3 (25-OH-D3). There was steady increment in the cellular production of 25-OH-D3 and of the more polar metabolites of vitamin D3 over 3 hr of incubation as determined by thin layer chromatography. Neither the addition of cyclic nucleotides or dexamethasone to, nor the removal of calcium or phosphate from the medium resulted in changes in the rate of conversion of vitamin D3 to its products. Rats pretreated with sodium diphenylhydantoin converted labeled vitamin D3 to its metabolites at the same rate as control rats. These data indicate that isolated liver cells retain the capacity for vitamin D3 hydroxylation, but suggest that the rate of this process does not undergo rapid changes in response to metabolic stimulation.

Animals↗
PubMed1977

Correlation of metabolic and chemiluminescent responses of granulocytes from three female siblings with chronic granulomatous disease.

Polymorphonuclear leukocytes (PMNL) from children with atypical chronic granulomatous disease (CGD), their mother and siblings, and normal controls were studied in regard to glycolytic and hexose monophosphate shunt activities in the resting, methylene blue-stimulated, and phagocytizing states. PMNL from the patients with CGD had normal glycolytic and hexose monophophate shunt activities in the resting state and after stimulation with methylene blue. However, stimulation of the hexose monophosphate shunt after phagocytosis was greatly decreased. These data were correlated with studies of both initial rate and integral counts of chemiluminescence. The chemiluminescent response from patients with atypical CGD was also greatly decreased. This decreased response probably reflects a defect in the oxidative destruction of the phagocytized microbe and correlates well with the decreased activity of the phagocytically activated hexose monophosphate shunt. The defect in generation of radical species of oxygen, singlet oxygen, and chemiluminescence by leukocytes from patients with CGD is discussed.

Adult↗
PubMed1975

Rapid modulation of lipogenesis by clofibrate in rat and monkey hepatocytes.

Previous studies have proposed various possible mechanisms for the hypolipidemic actions of clofibrate. In the present study, isolated liver cells freshly prepared from rats and squirrel monkeys were used to investigate the acute effects of sodium clofibrate (sodium chlorophenoxyisobutyrate) on hepatic lipogenesis. Incubation of liver cells with levels of the drug (1 mM) known to lower plasma lipid level in vivo produced a rapid inhibition of [14C]acetate incorporation into cellular lipids. The degree of inhibition caused by the drug was not diminished by preincubation with an excess of unlabeled acetate. Conversion of [14C]acetate to 14CO2 was not significantly altered by sodium clofibrate at 1--3 mM levels, but was decreased at 5--10 mM levels. Incorporation of [14C]acetate into all lipid classes was suppressed by this agent, but inhibition of sterol synthesis was more pronounced than that of fatty acids. Sodium clofibrate (1 mM) reduced the synthesis of sterols from either labeled acetate or labeled mevalonate to a similar degree, but the decline was augmented in each case by a 30-min preincubation of the cells with sodium clofibrate. Addition of fatty acids to cell incubations stimulated sterol generation from [14C] acetate or from [3H] mevalonate, but did not reverse the inhibitory effects of the drug. These results suggest (a) the sodium clofibrate rapidly interferes with hepatic fatty acid and sterol synthesis by direct or indirect actions at diverse loci; (b) that these effects probably occur after acetyl-CoA formation and do not stem from precursor pool dilution; (c) that sodium clofibrate diminishes sterol production at post-mevalonic and perhaps also at pre-mevalonic sites; (d) that a similar pattern of inhibition occurs with sodium clofibrate in the presence of added fatty acids; and (e) that rat and primate livers demonstrate similar metabolic responses to the drug.

Acetates↗