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R E Morton

Publications and source records attributed to R E Morton.

76 records · Page 5Linked to original sources
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Iron status in the first year of life.

The iron status of babies of different race born at term to mothers in an inner city area was studied at birth and during the first year of life and related to maternal iron status. Haemoglobin and ferritin were measured in the mother at term (n = 81) and in the baby in cord blood (n = 81), at 6 months (n = 55), and at 1 year (n = 51). No relationship was found between the iron status of mothers and their babies at birth. However, iron stores at birth did affect later iron status, cord ferritin being significantly related to ferritin at 6 months (r = 0.42, p less than 0.01) and 1 year (r = 0.55, p less than 0.01) but not to haemoglobin at these ages. No relationship was found between haemoglobin iron at birth and subsequent iron status. Introduction of full cow's milk before the age of 6 months was associated with iron deficiency at this age and at 1 year. By the age of 1 year, iron deficiency was also associated with feeding greater than 900 ml whole cow's milk a day, inadequate feeding with solids, and higher weight gain. No stool parasites were found at the age of 1 year, and the presence of occult blood in stools did not significantly affect iron status at this age. At 1 year of age, 49% of these infants had low iron stores, including 20% with iron deficiency anaemia. Considerable improvement could result from simple changes in dietary practices.

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Cholesterol esterification in macrophages. Stimulation by lipoproteins containing apo B isolated from human aortas.

A lipoprotein fraction possessing many of the characteristics of plasma low density lipoproteins (P-LDL) was isolated from homogenates of lesioned human aortas by affinity chromatography. In contrast to P-LDL, this fraction, termed A-LP, was found to be more electronegative than P-LDL and to stimulate cholesterol esterification in mouse peritoneal macrophages (MPM). This stimulation tended toward saturation at approximately 100 micrograms/ml lipoprotein cholesterol. Cholesterol esterification was partially inhibited by fucoidin, a competitive inhibitor of the scavenger receptor on MPM. These results suggest that A-LP is recognized by a high affinity binding site on MPM. Stimulation of cholesterol esterification in MPM by A-lP was inhibited by the lysosomotropic agent, chloroquine, indicating that degradation in lysosomes was a prerequisite for cholesterol esterification. Substantial degradation of apo B within the intact A-LP was demonstrated by SDS-PAGE and immunoblotting. This degradation could be responsible for the increased negative charge on A-LP, and the enhanced recognition of A-LP by a receptor on MPM. Stimulation of cholesterol esterification increased linearly over a 48-hour time period, suggesting that the receptor on MPM recognizing A-LP was not down-regulated. This unabated increase in cholesterol esterification resulted in massive accumulation of intracellular cholesteryl esters and a gradual increase in oil red O-positive droplets, giving the MPM the characteristic morphology of foam cells. If these mechanisms demonstrated in vitro also occur in the intact artery, they could explain how foam cells are formed within the fatty streak lesion.

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