New evidence for the involvement of oxygen radicals in triggering neonatal chronic lung disease.

We measured the plasma concentration of allantoin, an oxidation product of uric acid and an "in vivo" marker of free radical generation, within 24-48 h after birth in 10 premature infants who subsequently developed chronic lung disease (CLD) and 9 infants without CLD (non-CLD). The plasma allantoin level (mean +/- SD, 25.9 +/- 9.8 microM for CLD versus 11.0 +/- 5.7 microM for non-CLD, p < 0.01) and the allantoin/urate ratio (5.8 +/- 2.0% for CLD infants versus 2.4 +/- 0.9% for non-CLD infants, p < 0.01) were significantly higher in the CLD group than those in the non-CLD group. These observations suggest the possible involvement of oxygen radicals in triggering CLD. In addition, the plasma allantoin concentration and the allantoin/urate ratio may be useful early predictors of the development of CLD.

Plasma levels of retinol, retinol-binding protein, all-trans beta-carotene and cryptoxanthin in low birth weight infants.

In neonatal medicine, it is thought that retinol is useful for preventing CLD and for fetal development. However, beta-carotene had other vitamin A precursors have not been studied in neonates with CLD or others disorders. Cord blood of neonates including ELBW and VLBW infants was assayed for plasma levels of retinol, RBP, beta-carotene and cryptoxanthin. Plasma beta-carotene levels in ELBW and VLBW were lower than that in term infants, but plasma cryptoxanthin levels in ELBW and VLBW were about the same as in term infants. Plasma retinol and RBP levels showed almost same levels during 23-41 gestational weeks. Maternal smoking reduced plasma beta-carotene but not cryptoxanthin, retinol, or RBP levels. IUGR was associated with increased cryptoxanthin levels in cord blood. Serious neonatal diseases, including CLD and ROP manifested no significant effects on the cord blood vitamin levels. Thus, the occurrence of these diseases at birth could not be predicted by examination of vitamin levels in cord blood.

Congenital myotonic dystrophy: molecular diagnosis and clinical study.

Recently, an unstable DNA fragment specific to myotonic dystrophy (MyD) was discovered. In affected individuals, a DNA fragment is found that is larger than in normal siblings. Our objectives were to show whether the results of DNA analysis agree with the disease severity and prognosis in congenital myotonic dystrophy (CMyD) by DNA analysis. We investigated three pregnancies (two studied retrospectively) in three families. We genotyped the family members with the Southern blots and the polymerase chain reaction (PCR) analysis. In one case a prenatal diagnosis was carried out using chorionic villus sampling. This report also presents the three cases of affected mothers and CMyD babies with their growth courses. We clarify four main problems in CMyD, namely, respiratory distress, delayed motor development, feeding difficulty, and delayed mental development. The allele size in the range of 10 to 13 kb tended to be present as the adult form of MyD, and 14 to 15 kb as the CMyD. The three CMyD cases whose alleles size in the range of 14 to 15 kb showed various forms of disease and prognosis. We reached the following conclusions: the disease severity and prognosis in babies with CMyD did not correlate with the result of DNA analysis. The DNA analysis is a useful test for prenatal diagnosis. However, it is impossible to predict the disease severity and prognosis in babies with CMyD.