Fatty acid composition of adipose tissue and blood in humans and its use as a biomarker of dietary intake.

GLUCOCORTICOSTEROID hormones of the adrenal cortex have striking pharmacologic effects on lymphoid tissues and cells. These effects form part of the basis for the widespread use of these hormones in the treatment of a variety of diseases involving immunologic, inflammatory or neoplastic processes. The subject is large and has been reviewed in the past,1 2 3 4 5 6 7 but many questions remain to be answered. The purpose of this article is to take a new look at the subject, concentrating on three aspects. The first is species differences in susceptibility to corticosteroids. (Although these differences have been noted before, they are often overlooked; they . . .

Corticosteroids and lymphoid cells.

Depletion of muscle mitochondrial DNA in AIDS patients with zidovudine-induced myopathy

It has long been recognized that certain ordinarily salutary drugs may produce an acute hemolytic anemia in some susceptible individuals. The 8-aminoquinoline antimalarial, pamaquine (plasmoquine), was such a medication. It was the investigation of the hemolytic effect of pamaquine and its derivatives which led to the recognition that hereditary red cell enzyme deficiencies could produce hemolytic disease.

Glucose-6-phosphate dehydrogenase deficiency.

The mechanism of action of glucocorticoids is reviewed from the standpoint of seeing how far current concepts of the molecular action of steroids go towards explaining the varied physiologic and metabolic effects induced. The role of plasma binding to transport proteins in modifying steroid action is considered. The interactions between glucocorticoids and other hormones, particularly those mediated by cAMP are considered along with a discussion of the mechanism of “permissive” effects. Various proposals concerning the way in which glucocorticoids induce their effects including direct interactions with enzymes, nucleic acids, lysosomes, and receptor proteins are considered in detail, and an attempt is made to consider how far each of these mechanisms can go in explaining steroid action. Those biologic effects that cannot be accounted for by currently available mechansims are mentioned. Effects of glucocorticoids on growth, differentiation, and the inflammatory response are discussed from a mechanistic point of view. Catabolic or inhibitory effects of glucocorticoids as well as enzyme induction are examined using several exemplary systems. Finally an attempt is made to summarize the current state of knowledge concerning glucocorticoid and genome interaction.

Mechanism of action of glucocorticoids.

Lipid synthesis in human leukocytes, platelets, and erythrocytes.

THE mammalian cell life cycle is determined by a series of coordinated events which reflect time-dependent gene expression, although the duration of some of these events appears to be flexible1. Examples of both cyclic2 and steady state3 activities of certain enzymes in different, synchronized mammalian cell lines have been reported; there is at least one known example3 of enzyme inducibility that is restricted to part of the cell cycle. Collagen, a protein synthesized in large amounts for export, is produced throughout the life cycles of several fibroblast lines at rates corresponding to those of overall protein synthesis4.

Programmed Synthesis and Export of Immunoglobulin by Synchronized Myeloma Cells

The initial events Involved in the regulation of RNA and protein synthesis by the hormone cortisol are rapid. This suggests that steroid hormones act as effector molecules in induction and repression.

Cortisol in the Regulation of RNA and Protein Synthesis

A Challenge to the Concept of Selection by Malaria in Glucose-6-Phosphate Dehydrogenase Deficiency

Chev Kidson

Papers

Lipid synthesis in human leukocytes, platelets, and erythrocytes.

Programmed Synthesis and Export of Immunoglobulin by Synchronized Myeloma Cells

Cortisol in the Regulation of RNA and Protein Synthesis

A challenge to the concept of selection by malaria in glucose-6-phosphate dehydrogenase deficiency.

Malaria Antibody Content of Gamma2-7S Globulin in Tropical Populations.