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Biomedical subjects

B Starcher

Publications and source records attributed to B Starcher.

49 records · Page 3Linked to original sources
PubMed1978

Abnormal cellular copper metabolism in the blotchy mouse.

Defective copper metabolism was demonstrated in male mice bearing the blotchy (Moblo/y) allele at the mottled locus on the X-chromosome. Copper absorption from the gut was only 64% of that found in normal mice and hepatic copper levels were only 56% of the controls. Ceruloplasmin and heart cytochrome c oxidase activities were normal, yet lysyl oxidase activity from cultured fibroblasts was only 45% of control levels. Copper accumulated in fibroblasts cultured from these mutants to values that were five times normal. The accumulation of copper in the fibroblasts was associated with a protein of approximately 12,000 molecular weight.

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PubMed1971

Salmonellosis pacifarin activity of enterobactin.

Salmonellosis pacifarin activity is detected by an increased survivorship of mice, doubly infected with avirulent and virulent Salmonella typhimurium, when heretofore unknown agents, found in certain natural foodstuffs and in the supernatants of certain bacterial cultures, are fed to the infected animals as dietary supplements. We now announce the identity of one of these agents: it is enterobactin, a cyclic trimer of 2,3-dihydroxy-N-benzoyl-L-serine. Basal diets enriched with as little as 2 mg of crystalline trimer per kg of diet show pacifarin activity to a statistically significant degree. Diets supplemented with as much as 100 mg of the monomer per kg of diet show no such activity.

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PubMedDate not supplied

The kinetics of elastolysis: elastin catabolism during experimentally induced fibrosis.

Lung injury and matrix destruction result in the release into the circulation of desmosine, a product of elastin catabolism. To determine whether measurements of desmosine concentrations in the urine can provide important information about the severity of lung injury, we measured the kinetics of lung elastin catabolism following elastase-induced and fibrotic lung injury in mice. Pancreatic elastase instillation in the lung caused immediate elastin destruction, removing as much as 25% of the lung elastin within the first few hours. Peak concentrations of desmosine peptides appeared in the blood within 1-2 hours, and soluble elastin peptides in the lung and urine followed a similar course with peak levels occurring early and then declining rapidly, approaching control levels by 24 hours. More than half of the desmosine peptides removed from the lung following elastase injury were sequestered by the kidney and then slowly released over a period of several days. Lung histology and morphological measurements indicated that bleomycin, TiO2, and SiO2 instillation resulted in severely fibrotic lungs. However, the lung injuries sustained from these agents resulted in minimal elastin damage, representing less than 0.1% of the total lung elastin catabolized as estimated by desmosine analysis. The rapid accumulation of desmosine in renal tissue and its slow release into the urine keep urine concentrations low and minimize the power of urine desmosine assays for quantifying low level tissue destruction.

Animals↗
PubMedDate not supplied

Soluble beta-galactoside specific lectin is developmentally regulated in lungs of neonatal black mice and beige mice.

The beige mouse, a mutant of the C57 black mouse, is best known as a model of the Chediak-Higashi syndrome. Recently, it was found that alveolar maturation in neonatal beige mice is impaired, resulting in abnormally large alveoli. In guinea pigs, hamsters, and rats there is an elevated activity of a soluble, beta-galactoside-binding lectin in lungs at the age when alveolar maturation is in progress. Our present studies were done to find out if the temporal relationship between elevated lectin activity and alveolar maturation also occurs in mice and, further, if the impaired alveolar maturation in beige mice might be linked to the lectin. We found that the temporal relationship between lectin activity and alveolar maturation is also present in black and beige mice, with a peak in specific lectin activity occurring at about 8 days after birth. We also found that the major lectin purified from black or beige mice has essentially the same subunit molecular weight, isoelectric point, and amino acid composition. In conclusion, we found nothing abnormal about the lectin or its developmental regulation that can explain the impaired alveolar maturation in neonatal beige mice. The results do not rule out the possibility of an important role for the lectin in normal lung development or the possibility that some aspect of function or localization of the lectin or its ligands, not related to total lung lectin hemagglutinating activity, may be altered in the beige mouse.

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