SUMMARY Metabolisable energy intake, determined by bomb calorimetry of food, vomit, stool and urine, and resting metabolism, assessed by respiratory gas exchange, were studied in 21 infants with congenital heart disease and nine control infants. Weight for age, growth rates, and daily metabolisable energy intake per kg tended to be lower in infants with heart disease than in control infants. Resting oxygen consumption was high in those infants with pulmonary hypertension and persistent cardiac failure. Energy intake, as a percentage of that recommended for age, correlated with weight gain, and resting oxygen consumption correlated inversely with both percentage body mass index and relative fatness. Failure to thrive in infants with congenital heart disease may be due to a combination of low energy intakes and, in some cases, high energy requirements allowing insufficient energy for normal growth. Increasing the energy intakes of infants with congenital heart disease may be a way of improving their growth.Many children with congenital heart disease are small.' Their failure to thrive usually dates from early infancy, and postmortem studies suggest infants dying with congenital heart disease and failure to thrive are malnourished.2 There are several possible explanations for this: hypoxia and breathlessness may lead to feeding problems; anoxia or venous congestion of the bowel may result in malabsorption; peripheral anoxia and acidosis may lead to inefficient utilisation of nutrients; and increased metabolic rate may mean that recommended energy intakes are insufficient for normal growth and nutrition.Many of the studies investigating failure to thrive and congenital heart disease review children over wide age ranges.1 3 The findings in children of school age or adolescents will not necessarily indicate causes of poor growth that date from infancy. We have compared total energy intake, metabolisable energy intake (total energy ingested minus energy losses in stool, urine, and vomit), resting oxygen consumption, and growth rates of infants with congenital heart disease and normal infants to try to determine the causes of failure to thrive in infants with congenital heart disease.

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A mother's expressed breast milk (MEBM) is overall the best feed for her preterm baby during the neonatal period, and is associated with improved short-term and long-term outcomes. Neonatal services should commit the resources needed to optimise its use. The place of banked donor expressed breast milk (DEBM) is less clear, but it probably has a role in reducing the risk of necrotising enterocolitis and sepsis in preterm infants at particularly high risk. There is considerable variation in the composition of human milk and nutrient fortification is often needed to achieve intrauterine growth rates. Human milk can transmit potentially harmful micro-organisms, and pasteurisation, which denatures some of the bioactive factors, is the only known way of preventing this. This is carried out for DEBM but not MEBM in the UK. Future research on human milk should focus on (a) critical exposure periods, (b) understanding better its bioactive properties, (c) the role of DEBM and (d) nutritional quality assurance.

SummaryA double-blind, placebo-controlled, cross-over clinical trial was performed to assess the effect of betahistine hydrochloride (Serc) in M6niere's disease. The diagnosis was based on paroxysmal attacks of rotational vertigo, with tinnitus, and a fluctuating sensori-neural deafness, together with the results of auditory and vestibular tests. Twenty-eight patients were admitted to the trial over 3 years. Twenty-two patients completed the trial. In total, they received betahistine 32 mg daily, for a period of 16 weeks, and placebo also for the same length of time, preceded in every case by a 4-week pre-treatment period. Daily symptom score cards were kept. There was a statistically significant improvement in favour of the drug with regard to vertigo, tinnitus and deafness. Vertigo was the most responsive symptom. No adverse reactions were observed.

Morphine delays the attainment of full enteral feeds, partly by delaying the start of feeding, but does not discernibly increase gastrointestinal complications. The attainment of full feeds is influenced by morphine dose, but other factors seem to be important, including birth weight and neonatal morbidity.

A posttranslational modification site in natural and recombinant urinary-type plasminogen activators (urokinases; EC 3.4.21.31) has been localized to Thr-18, in the growth factor domain of the molecule. This is the region of urinary plasminogen activator responsible for its specific receptor binding. An unusual carbohydrate-protein linkage, a single monosaccharide, fucose, covalently attached directly to threonine in the peptide, is described here. The glycan moiety and the site of modification have been identified with mass spectrometry and confirmed by carbohydrate composition analysis, Edman degradation, and one-and two-dimensional NMR studies. This type of modification is normally not detected without mass spectrometry because the fucose-threonine bond is hydrolyzed under standard acidic conditions of the amino acid analysis and Edman sequencing. This modification may be widely found in other proteins.

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