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Biomedical subjects

M E Coryell

Publications and source records attributed to M E Coryell.

11 recordsLinked to original sources
PubMed1986

Increased excretion of histidyl-L-proline diketopiperazine by infants receiving Pregestimil and Nutramigen formulas.

Histidyl-L-proline diketopiperazine is excreted in increased amounts by infants receiving Nutramigen or Pregestimil. When these formulas are discontinued, its excretion becomes undetectable. The compound was isolated from Nutramigen and Pregestimil, as well as from the urine of the infants receiving these formulas, and was identified by comparison with authentic histidyl-L-proline diketopiperazine standard in various chromatographic and electrophoretic systems. A neuropeptide widely distributed in the brain and gut and having a variety of biological functions, histidyl-L-proline diketopiperazine may have as-yet-undetermined effects on infants who are receiving these formulas.

Electrophoresis↗
PubMed1984

Gamma-glutamylornithine excretion in patients with hyperornithinemia.

Gamma-glutamylornithine has been identified in urine from patients with the HHH syndrome (hyperornithinemia, hyperammonemia and homocitrullinuria) and with gyrate atrophy associated with hyperornithinemia. The amount of gamma-glutamylornithine excreted was 10-15 times higher than that excreted in normal subjects. The level of excretion was comparable in the HHH syndrome subjects and the gyrate atrophy subjects despite the fact that the gyrate atrophy subjects excreted more ornithine. A 100 mg/kg oral challenge of ornithine increased the excretion of gamma-glutamylornithine by a factor of three. This increased excretion of gamma-glutamylornithine was observed in hyperornithinemia patients with different etiologies and is therefore presumably due to the hyperornithinemic state, per se, independent of the underlying defect.

Amino Acid Metabolism, Inborn Errors↗
PubMed1982

Decreased transport of ornithine across the inner mitochondrial membrane as a cause of hyperornithinaemia.

Hyperornithinaemia due to a transport of ornithine across the inner mitochondrial membrane was demonstrated in three patients by measuring ornithine uptake by fibroblast mitochondria. Particulate compartments and soluble cytoplasm of fibroblasts were separated by a slight modification of the digitonin method of Zuurendonk and Tager. Patients' fibroblast pellet fraction contained significantly less radioactivity than control fibroblast pellet fraction after incubation of fibroblasts with [14C]-ornithine. Since neither of the patients was deficient in ornithine-delta-oxoacid aminotransferase, we concluded that in these hyperornithinaemia patients a defect exists for transport of ornithine across the inner mitochondrial membrane. The exact nature of this transport defect remains to be elucidated.

Amino Acid Metabolism, Inborn Errors↗
PubMed1979

Hydroxyproline metabolism in two sisters with hydroxyprolinemia.

Hydroxyproline metabolism was evaluated in two sisters with hydroxyprolinemia and their mother. 33 and 21% of an oral hydroxyproline load (200 mg/kg) was excreted by the sisters, 5.4% by the mother, and 1.3% by normal subjects. Plasma and erythrocyte values in the sisters and their mother were elevated, indicating that extra- and intracellular hydroxyproline pools were increased. Analysis for urinary glycolate and oxalate (metabolic products of hydroxyproline) showed no increased excretion by the two sisters, although the mother's excretion was normal. A deficiency of hydroxyproline oxidase in the two sisters was indicated by the lack of delta 1-pyrroline-3-hydroxy-5-carboxylic acid excretion.

Adult↗