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Biomedical subjects

G BRECHER

Publications and source records attributed to G BRECHER.

At least 19 recordsLinked to original sources
PubMed1965

THE BRAIN LESION OF GOLDTHIOGLUCOSE OBESITY.

The development of hypothalamic lesions due to goldthioglucose are described. The initial extensive necrotic lesion occurs in close to 100 per cent of animals injected with LD(50). Within 2 weeks the necrotic material has been removed and a narrow scar results. After a lapse of several months, the scar is often difficult to visualize, especially in animals that have not developed obesity. The ventromedial nucleus is not the center of the lesion. The nucleus is preserved in some instances, and partially or completely destroyed in others, depending on the extent of the lesion. The more prominent scar in the obese animals correlates with the larger initial lesion necessary for the complete bilateral destruction of the ventromedial nucleus which is known to be a prerequisite for the development of hypothalamic obesity. Thus, contrary to earlier suggestions, goldthioglucose does not localize specifically in the cells of the ventromedial nucleus.

Animals↗
PubMed1965

THE EFFECT OF HYPERGLYCEMIA ON HYPOTHALAMIC GOLD UPTAKE AND HYPERPHAGIA IN GOLDTHIOGLUCOSE-TREATED MICE.

The accumulation of gold in the hypothalamus and the development of hyperphagia and obesity were studied in mice given a single intravenous injection of goldthioglucose at various levels of blood glucose concentration. It was found that the glucose concentration prevailing at the time of goldthioglucose injection was correlated directly with the level of free and bound goldthioglucose in the blood 3 minutes later, with the hypothalamic uptake of gold, with the extent of the hypothalamic lesion, and with the severity of the subsequent hyperphagia and obesity. Hyperglycemia was associated with an increased gold deposition throughout the brain. A gold content of 88 +/- 12 microg/mg wet tissue in the hypothalamus of fasted animals was associated with clearcut lesions in all animals studied, whereas a similar gold content in the control brain lobes of hyperglycemic animals was not associated with lesions in any animal. This finding indicates that some regions in the brain (e.g. the ventral hypothalamus) are more susceptible than others to damage by goldthioglucose.

Animals↗
PubMed1964

RADIATION BLEEDING.

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Bone Marrow Diseases↗
PubMed1963

DELAYED INCORPORATION OF TRITIATED THYMIDINE INTO DNA.

Delayed utilization of tritiated thymidine by regenerating mouse liver can be almost completely suppressed by a continuous infusion of nonradioactive thymidine. In addition, as shown earlier for lymphocytes, labeled granulocytes are a potential source of the tritium marker. These observations suggest that the delayed incorporation of label into DNA must be due to the transfer of labeled nucleoside, which may be derived either from the degradation of DNA or from a long-lived intracellular pool. In either case, the transferred material probably originates from all tissues that have a high rate of cell turnover.

Animals↗