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Biomedical subjects

M Frank

Publications and source records attributed to M Frank.

At least 307 records · Page 17Linked to original sources
PubMed1970

Genetically controlled total deficiency of the fourth component of complement in the guinea pig.

Guinea pigs with a total deficiency of the fourth component of complement (C4) have been discovered. There was no evidence for the presence of a C4 inhibitor in the serum of these animals. Mating studies indicate that C4 deficiency is transmitted as a simple autosomal recessive trait. A colony of these animals is being established at the National Institutes of Health. They will provide an opportunity to more precisely define the role of complement in immune phenomena and the defense against disease.

Animals↗
PubMed1969

Taste nerve fibers: a random distribution of sensitivities to four tastes.

The numbers of rat glossopharyngeal and chorda tympani fibers responding to one, two, three, or four taste stimuli of different quality (sodium chloride, hydrochloric acid, quinine, and sucrose) and to each of the six possible pairs of these stimuli can be predicted if there are four independent sensitivities randomly distributed among innervating fibers.

Animals↗
PubMed1968

Metabolic and calcium kinetic studies in idiopathic hypercalciuria.

Calcium balances and calcium kinetic studies using (47)Ca were performed in nine male patients with idiopathic hypercalciuria and in three normal male subjects. A sharp reduction in calcium intake in eight patients with idiopathic hypercalciuria caused a decrease in urinary calcium excretion, the latter remaining elevated above that reported for normal subjects on a low calcium diet. The hypercalciuric patients had an enlarged miscible calcium pool size, an increased calcium turnover rate, increased bone formation and bone resorption rates, and an elevated true intestinal calcium absorption rate, the increase of the latter three parameters being proportional to the increase of the turnover rate. The fraction of the calcium turnover rate excreted in the urine was elevated whereas that constituted by the endogenous fecal calcium excretion was decreased. Arguments are presented for the concept that the primary abnormality in idiopathic hypercalciuria is neither renal calcium hyperexcretion nor intestinal calcium hyperreabsorption, but a more fundamental disturbance in calcium metabolism of as yet unknown cause, leading to a high calcium turnover.

Journal Article↗