Prophylaxis of early adrenal insufficiency did not improve survival without BPD in the overall study population; however, treatment of chorioamnionitis-exposed infants significantly decreased mortality and improved survival without BPD. Low-dose hydrocortisone therapy did not suppress adrenal function or compromise short-term growth. The combination of indomethacin and hydrocortisone should be avoided.

The novel chlorhexidine-impregnated dressing, replaced weekly, was as effective as cutaneous disinfection with 10% PI and redressing the site every 3 to 7 days for preventing CRBSI and BSI without a source in critically ill neonates requiring prolonged central venous access. The risk of local contact dermatitis under the chlorhexidine dressing limits its use in low birth weight infants who require prolonged central access during the first 2 weeks of life.

A simple model, in which deposition is limited by diffusion through a thin laminar film of water, has successfully described the deposition of several gases to the sea. However, the deposition velocity of ozone to seawater is 10–30 times greater than this model predicts. This enhancement is attributed to significant reactions of ozone with halides and other components of seawater within the laminar surface layer, and a modified version of the model for ozone, and possibly other reactive gases, is proposed. To test the model, comparisons were made of predicted and observed deposition velocities for ozone to solutions of sodium sulphite and nitrite. Measurements of the rate constants for the reaction of ozone with these solutions and with some components of seawater were made with a stopped flow apparatus. The reaction with iodide was too rapid for direct observation, but the rate constant was inferred from measurements of the deposition of ozone to iodide solutions. According to the model, iodide makes a substantial contribution to the deposition of ozone to seawater, but an additional, unidentified reaction is necessary to explain fully the deposition rate. A surfactant species may well be involved. The model indicates that the ozone is destroyed and the oxidation products produced in the top few microns of the sea. The production of molecular iodine at the surface may have significant geochemical consequences.

Leptin is a 16-kD protein encoded by the ob/ob (obesity) gene. In rodents it plays a role in obesity, diabetes, fertility, and neuroendocrine function. In humans serum concentrations of leptin correlate with total body fat in both adults and children. We measured cord blood leptin in 186 neonates that included 82 appropriate for gestational age (AGA), 47 large for gestational age (LGA), 20 infants of diabetic mothers, 52 preterm infants, and 15 intrauterine growth-retarded (IUGR) infants. There were 16 pairs of twins. The mothers of 17 preterm infants were treated with steroids before delivery. Leptin (mean +/- SD) concentration in term, AGA infants (39.4 +/- 1.1 wk) with birth weight (BW) of 3.2 +/- 0.3 kg, body mass index (BMI) of 12.6 +/- 1.1 was 4.01 +/- 3.5 ng/mL. BW correlated with cord leptin (p = 0.002) in a multivariate analysis controlling for potential confounders. Both LGA infants and infants of diabetic mothers had higher cord leptin concentration 7.3 +/- 3.8 and 6.1 +/- 4.8 ng/mL, respectively, compared with AGA infants (p < 0.05). Preterm infants had a mean leptin level of 1.8 +/- 0.97 ng/mL and a 3-fold elevation was seen if mothers received steroids antenatally (p = 0.006). IUGR infants had increased leptin (6.5 +/- 3.9 ng/mL, p = 0.03). Concerning the twin pairs, the smaller had a higher leptin level compared with larger twin (4.1 +/- 9.51 versus 2.8 +/- 5.14, p = NS). Neonatal cord leptin concentrations correlate well with BW and BMI. No gender differences were found in cord blood leptin. Maternal obesity had no effect on cord leptin, whereas exogenous maternal steroids increased neonatal leptin concentrations.

Iodine‐132 was used as a tracer to demonstrate that ozone causes iodine vapor to be released from the sea surface. This rate of release was porportional to ozone concentration in the range 0–100 ppb and depended on mixing of the water phase. At the mean ozone concentration existing at the sea surface the rate of iodine release was equivalent to an annual contribution of 6 to 12 × 1010 g to the atmosphere. This estimate is subject to uncertainties arising from inadequate knowledge of the mean concentration of iodide at the sea surface and the effect of mixing of the surface sea water on the rate of release of iodine. The significance of such a contribution to the iodine budget of the atmosphere is discussed.