Biomedical subjects
L A Barness
Publications and source records attributed to L A Barness.
Calcium mobilization in osteopetrosis.
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Vitamin E deficiency: a previously unrecognized cause of hemolytic anemia in the premature infant.
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Vitamin B12 deficiency with emphasis on methylmalonic acid as a diagnostic aid.
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New studies in infant anemias.
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Citrullinemia with defective urea production.
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Isovaleric acidemia with promyelocytic myeloproliferative syndrome.
Isovaleric acidemia, an autosomal recessive disorder, is due to isovaleryl-coenzyme A dehydrogenase deficiency and is one of the branched-chain aminoacidopathies. Isovaleric acidemia may present in the neonatal period with an acute episode of severe metabolic acidosis, ketosis, and vomiting and may lead to coma and death in the first 2 months of life. This report concerns an infant who presented at 10 days of age because of lethargy, poor feeding, hypothermia, cholestasis, and thrombocytopenia, leukopenia, and profound pancytopenia. Death occurred at 19 days of age. Autopsy showed mild fatty change in the liver and extramedullary hematopoiesis, generalized Escherichia coli sepsis, and myelodysplasia of the bone marrow with arrest of the myeloid series at the promyelocytic stage. The appearance resembled promyelocytic leukemia, but the diagnostic 15:17 translocation was not present. The maturation arrest in granulopoiesis in isovaleric acidemia appears to be most likely due to a direct metabolic effect on granulocyte precursor cells.
Nonmalformative cardiovascular pathology in infants and children.
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Lysine and potassium supplementation of wheat protein.
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Dietary nucleotide effects upon murine natural killer cell activity and macrophage activation.
Weanling mice fed chow or chow plus water supplemented with 3.5 mg of nucleotides per 100 ml of water for 6 weeks exhibited increased natural killer cell (NK) activity and lower macrophage activation compared to mice fed chow plus nonsupplemented water. In a dose-response study, NK activity, macrophage activation and spleen weight (as a percentage of body weight) were higher in mice fed up to 0.035% w/w nucleotides, however macrophage activation was decreased by feeding over 0.35% w/w compared to those receiving basal purified diet (BPD). Nucleotides in human milk may affect the immune response in breast-fed infants.
Dietary nucleotides affect hepatic growth and composition in the weanling mouse.
The effect of dietary nucleotides upon hepatic growth and composition was examined in weanling mice. For 5 weeks, mice were fed either Purina Rat Chow, a nucleotide-free diet (NT-), a nucleotide-free diet supplemented with a mixture of five nucleotides (0.21% w/w), (NT+) or a nucleotide-free diet supplemented with adenosine 5'-monophosphate (0.0425% w/w) (NTA). Hepatic cholesterol and lipid phosphorous were significantly higher, whereas liver weight (expressed as a percentage of body weight), and glycogen were lower in animals fed NT- vs all other groups. NTA-fed animals presented a greater contrast to the NT- group than did animals fed the mixture of nucleotides. Liver fatty acid composition and distribution of phospholipid subclasses were not affected by dietary nucleotide supplementation. Dietary nucleotide supplementation in weanling mice affects hepatic growth and composition; adenosine 5'-monophosphate may play a unique role in these effects.
Postnatal inositol levels in preterm infants.
OBJECTIVE: To measure plasma inositol levels in preterm infants fed formula containing inositol at levels close to those in human milk. STUDY DESIGN: Plasma inositol levels were measured in 72 preterm infants fed formula containing 1110 mumol/L inositol and in cord blood of 12 healthy term infants. Preterm infant plasma levels were measured four times: (1) within the first 7 days of life, (2) intermediate enteral feeding, (3) at hospital discharge, and (4) 2 months after hospital discharge. RESULTS: Inositol concentrations in term cord blood samples were significantly lower than in preterm initial feeding, intermediate feeding, and discharge samples. Initial concentrations in blood of preterm infants were higher than in all other groups, and were significantly lower among infants with gestational ages of 31 to 33 weeks compared with those of 28 to 30 or 31 to 33 weeks. Days of parenteral nutrition were a significant predictor of inositol levels in the full feeding sample, with lower levels associated with prolonged parenteral nutrition. Clinical outcomes were not related to plasma inositol levels. CONCLUSIONS: Feeding preterm formula with inositol levels close to those reported for human milk may not prevent the postnatal decline in preterm infant plasma inositol levels.