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Biomedical subjects

K D Foote

Publications and source records attributed to K D Foote.

11 recordsLinked to original sources

Effect of early introduction of formula vs fat-free parenteral nutrition on essential fatty acid status of preterm infants.

Previous studies have used relative (%) values of plasma 18:2n-6 (18:2 omega-6) and the ratio of 20:3n-9 to 20:4n-6 (triene/tetrene) to indicate the essential fatty acid (EFA: 18:2n-6 and 18:3n-3) status of preterm infants. The extent to which these indices reflect milligrams per liter quantities of n-6 and n-3 long-chain polyunsaturated derivatives of EFA (LCPs), required for cell membrane accretion, is unknown. Thus, 18:2n-6, the triene-tetrene ratio, and n-6 and n-3 LCPs were measured in plasma phospholipid of preterm infants' cord blood (n = 22) and of preterm infants fed formula (n = 12) or of preterm infants who received fat-free parenteral nutrition (n = 15) on postnatal day 3. Whether expressed as percent or milligrams per liter, 18:2n-6 was markedly higher and the triene-tetrene ratio lower in infants fed formula than in infants who had received no lipid. However, concentrations of n-6 and n-3 LCPs were similar in the two groups of infants and significantly higher than cord values. In the absence of an exogenous lipid source, it is suggested that tissue stores of LCPs are released in response to birth.

Birth Weight

Brain synaptosomal, liver, plasma, and red blood cell lipids in piglets fed exclusively on a vegetable-oil-containing formula with and without fish-oil supplements.

Clinical studies showed that a decrease in red blood cell 22:6n-3 caused by feeding infants formula (F) can be prevented by supplementation with fish oil (F + O). It is not known whether fish-oil supplementation is able to support normal accretion of fatty acids with greater than or equal to 20 carbons (LCPs) in the brain. Therefore piglets were fed exclusively F + O, F, or sow milk (SM) for 15 d and their liver and brain synaptosomal fatty acids were determined. Feeding F + O corrected the low n-3 LCP in the liver phospholipid (PL) and synaptosomal phosphatidylethanolamine (PE) of piglets fed F compared with SM. An apparent compensatory increase in n-6 LCPs in liver PL and synaptosomal PE of piglets fed F compared with SM was suppressed by feeding F + O. F + O also reduced the ratio of plasma PL 20:4n-6 to 20:5n-3, important for eicosanoid metabolism. Supplementation of F with n-3 LCPs as fish oil, without n-6 LCPs, at levels giving normal brain n-3 LCP, may alter n-6 LCP accretion.

Animals

Plasma and red blood cell fatty acids of low-birth-weight infants fed their mother's expressed breast milk or preterm-infant formula.

The fatty acid composition of plasma phospholipids, red blood cell (RBC) phosphatidylcholine (PC), and phosphatidylethanolamine (PE) was determined for low-birth-weight (LBW) infants when full oral feeding commenced (day 0) and after a further 28 d (day 28). They were fed their mother's expressed breast milk (PTM, n = 9), formula (SCF, n = 16) with 2% 18:3n-3 fatty acids, 20% 18:2n-6 fatty acids, or a combination of SCF and PTM (n = 11). Concentrations of all 20- and 22-carbon n-6 and n-3 fatty acids were similar among the infant groups on days 0 and 28 (mean postnatal age 42 +/- 1.3 d). The results suggest that formula with greater than or equal to 2% 18:3n-3 and a ratio of 18:2n-6 to 18:3n-3 similar to that of human milk may permit incorporation of n-3 fatty acids in LBW infant tissues equivalent to that from human milk.

Erythrocytes

Peak inspiratory pressure requirements in infants born weighing less than 750 g.

The possibility that peak inspiratory pressure requirements or the arterial:alveolar oxygen ratio can predict the clinical outcome in infants weighing less than 750 g at birth was explored in a consecutive series. Nine of 10 infants (90%) with a peak inspiratory pressure requirement of more than 18 cm H2O at 48 hours or more than 16 cm H2O at 72 hours from age subsequently died later of respiratory causes (defined as death after 72 hours of pulmonary interstitial emphysema, bronchopulmonary dysplasia, or cor pulmonale). Twenty of 21 remaining infants (95%) survived until discharge. Using these data a 95th centile for peak inspiratory pressure requirement during the first 72 hours of life was constructed. The potential value of this centile in predicting later death of respiratory causes was examined in a separate series. Twelve of 15 infants (80%) whose peak inspiratory pressure requirements remained below the 95th centile, or were not ventilated (n = 6), survived. In contrast, 11 of 12 (92%) infants whose requirements crossed the 95th centile died later of respiratory causes. The infants who died had more radiological changes and higher mean arterial carbon dioxide pressure than survivors suggesting that the severity of the initial lung disease rather than the way that ventilation was managed determined prognosis. Peak inspiratory pressure requirement was more useful than arterial:alveolar oxygen ratio in clearly distinguishing between survivors and infants who died later of respiratory causes.

Birth Weight

Height attainment in children with steroid-responsive nephrotic syndrome.

The heights of 80 patients with steroid-responsive nephrotic syndrome (SRNS) were measured 5-24 years after diagnosis. During childhood most patients had received repeated courses of high-dose corticosteroids and prolonged maintenance therapy. Although at the time of taking corticosteroids growth was suppressed, those who had completed growth had a mean height standard deviation score (SDS) of -0.22, equivalent to a height on the 40th centile. Total corticosteroid dose prescribed was correlated only weakly with height SDS; there was no correlation between total dose and height when the post-pubertal patients were studied separately, indicating that their ultimate height attainment was not affected significantly.

Adolescent