Biomedical subjects

E S Dye

Publications and source records attributed to E S Dye.

24 records · Page 2Linked to original sources

PubMed1980

Formation of intraperitoneal abscesses by Staphylococcus aureus.

Certain Staphylococcus aureus strains, when inoculated into the peritoneal cavity of mice, were clumped and surrounded by a thick layer of leukocytes. After being enclosed with a connective tissue capsule, the structures histologically resembled staphylococcal abscesses. Of four strains examined, all were destroyed within abscesses, although at different rates. Abscess homogenates possessed bactericidal activity toward staphylococci, and this activity was associated with the sedimentable fraction of the homogenates. Leukocytes did not appear to be responsible for the bactericidal activity. Appreciable quantities of alpha toxin accumulated in these abscesses even without multiplication of the organisms. This model infection offers opportunities for studying some aspects of staphylococcal host-parasite interactions occurring in localized lesions.

Abscess↗

PubMed1980

Macrophage accumulation in murine ascites tumors. I. Cytoxan-induced dominance of macrophages over tumor cells and the anti-tumor effect of endotoxin.

The host cellular response to i.p. growth of the SA-1 spindle cell sarcoma was studied in semisyngeneic AB6F1 hybrid mice. At progressive stages of tumor growth mice were sacrificed, their ascites were collected, and changes in the numbers of tumor cells, macrophages, lymphocytes, and granulocytes were determined. It was found that macrophages were the predominant host cell that accumulated locally in response to tumor growth. Cytoxan treatment caused a 90% reduction in tumor cells without affecting the accumulation of macrophages. Six days after treatment with cytoxan, macrophages exceeded all other cell types present in the peritoneal cavity and outnumbered tumor cells by 20:1. However, in spite of this macrophage dominance, the tumor cells ultimately regrew to kill the host. Ascites tumors could be completely regressed, however, by following cytoxan treatment with an appropriately timed intratumor injection of endotoxin. The relatively long delay before endotoxin caused the tumor to regress suggests that endotoxin acted by stimulating the generation of anti-tumor immunity, rather than by directly augmenting the tumoricidal activity of macrophages.

Animals↗

PubMed1979

Metabolism and insulin-releasing capabilities of glucosamine and N-acetylglucosamine in isolated rat islets.

The ability of glucosamine and N-acetylglucosamine to stimulate insulin secretion from perifused rat islets and the suitability of these hexoses to be metabolized in a static incubation was studied under various conditions. N-Acetylglucosamine alone stimulated insulin release with a threshold of 10 mM, with half-maximal effect at approx. 16 mM, and maximally at 20 mM. With higher concentrations stimulation was slightly diminished. Release caused by 20 mM-N-acetylglucosamine was unaffected by 30 mM-mannoheptulose, but was blocked by 2-deoxyglucose or iodoacetate (1 mM). At moderate concentrations, (2.75--20 mM), the metabolism of N-acetyl[1-3H]glucosamine was similar to that of [1-3H]glucose and secretion rates paralleled the corresponding rates of metabolism with these hexoses. Glucosamine (27.5 mM) alone weakly stimulated insulin secretion, which was unaltered by 30 mM-mannoheptulose but blocked by 2-deoxyglucose or iodoacetate. A lower rate of [1-3H]glucosamine metabolism appeared to account for its weaker stimulatory efficacy. Insulin release caused by 27.5 mM-glucosamine or 27.5 mM-N-acetylglucosamine in the presence of basal (2.75 mM) glucose was accurately predicted based on the summed metabolic rates of these compounds. The data strengthen the theory proposing that metabolites or cofactors generated during metabolism are essential for triggering insulin secretion.

Acetylglucosamine↗

PubMed1979

Nicotinamide modulation of rat pancreatic islet cell responsiveness in vitro.

The influence of nicotinamide (NA), a highly suitable precursor substrate for NAD synthesis in various tissues, on islet cell responsiveness was determined. After a 30 minute perifusion with this compound, nicotinamide, in a dose-dependent manner, potentiated glucose-induced insulin secretion. Maximal potentiation (approximately 250%) was observed at 20 mM NA and the threshold for potentiation was 3 mM. In the absence of glucose, NA did not affect basal secretion rates. Mannoheptulose blocked the primary stimulant action of glucose and the potentiating effects of NA. NA did not alter the rate of glucose usage by isolated islets. These results further underscore the possible importance of pyridine nucleotides in stimulated secretion.

Animals↗

PubMed1979

Starvation diabetes in the rat: onset, recovery, and specificity of reduced responsiveness of pancreatic beta-cells.

A 24-h starvation markedly diminished the stimulant action of 8 mM glucose on insulin secretion from isolated perifused rat islets of Langerhans. The response to a supramaximal glucose stimulus (27.5 mM) remained normal, but prolonged fasting (48 or more) also reduced its efficacy. Refeeding of 24-h fasted animals resulted in complete restoration of glucose sensitivity within 24 h. The responses to glyceraldehyde (2 mM) and alpha-ketoisocaproate (8 mM) at concentrations which elicit approximately half-maximal stimulation were unaltered by a 24-h fast, while that to a half-maximally effective dose of mannose (15 mM) was decreased. Theophylline (5 mM) could not normalize the reduced secretory response to glucose seen in this state. The islets' ability to metabolize glucose, using various in vitro pretreatment protocols and different incubation times, was not affected by a 24-h fast. Mannose and glyceraldehyde metabolism were also unaltered. Prolonged fasting (48 h) reduced glucose metabolism by 25% at both 8 and 27.5 mM. The acute adaptive changes in islet sensitivity to moderate glucose and mannose concentrations during short term fasting (24 h) cannot be explained by an altered usage of the added hexoses.

Animals↗

PubMed1978

On the biochemical nature of triose- and hexose-stimulated insulin secretion.

The differential effects of several specific inhibitors of intermediary metabolism, mannoheptulose, 2-deoxylucose, and iodoacetate, were studied with isolated perifused pancreatic islets stimulated with glucose, mannose, glyceraldehyde, dihydroxyacetone, or alpha-ketoisocaproate. Insulin release rates and/or capacities to metabolize these caloric stimuli served as indicators of the inhibitors' actions. Mannoheptulose and 2-deoxyglucose blocked hexose-stimulated hormone release and hexose metabolism concomitantly, but left the functional and metabolic actions of trioses unaltered. Iodoacetate blocked hexose- and triose-stimulated hormone release as well as their metabolism in a parallel fashion. The action of alpha-ketoisocaproate was not affected by any of these three inhibitory agents. The data are most easily explained by a theory that incorporates metabolic signals, arising during the degradation of insulin-releasing fuel molecules, as an integral component in the process of beta-cell stimulation.

Animals↗