At school entrance, VP/VLBW children are more likely to have behavioural and emotional problems that are detrimental for academic functioning. Targeted and timely help is needed to support them and their parents in overcoming these problems and in enabling them to be socially successful.

A total of 12.6% of young adults who were born very preterm and/or with a very low birth weight had moderate or severe problems in cognitive or neurosensory functioning. Compared with the general Dutch population, twice as many young adults who were born very preterm and/or with a very low birth weight were poorly educated, and 3 times as many were neither employed nor in school at age 19.

Very preterm mortality and morbidity differed between European regions, raising questions about variability in treatment provided to these infants. Comparative follow-up studies are necessary to evaluate the impact of these differences on rates of cerebral palsy and other disabilities associated with preterm birth.

Objective To study the impact of terminations of pregnancy (TOP) on very preterm mortality in Europe.Design European prospective population-based cohort study.Setting Ten regions from nine European countries participating in the MOSAIC (Models of OrganiSing Access to Intensive Care for very preterm babies) study. These regions had different policies on screening for congenital anomalies (CAs) and on pregnancy termination.Population or sample Births 22-31 weeks gestational age.Methods The analysis compares the proportion of TOP among very preterm births and assesses differences in mortality between the regions.Main outcome measures Pregnancy outcomes (termination, antepartum death, intrapartum death and live birth) and reasons for termination, presence of CAs and causes of death for stillbirths and live births in 2003.Results Pregnancy terminations constituted between 1 and 21.5% of all very preterm births and between 4 and 53% of stillbirths. Most terminations were for CAs, although some were for obstetric indications (severe pre-eclampsia, growth restriction, premature rupture of membranes). TOP contributed substantially to overall fetal mortality rates in the two regions with late second-trimester screening. There was no clear association between policies governing screening and pregnancy termination and the proportion of CAs among stillbirths and live births, except in Poland, where neonatal deaths associated with CAs were more frequent, reflecting restrictive pregnancy termination policies.Conclusion Proportions of TOP among very preterm births varied widely between European regions. Information on terminations should be reported when very preterm live births and stillbirths are compared internationally since national policies related to screening for CAs and the legality and timing of medical terminations differ.

A randomised clinical trial was conducted to establish the effects of oral and intramuscular administration of vitamin K at birth on plasma concentrations ofvitamin K1, proteins induced by vitamin K absence (PIVKA-II), and clotting factors. Two groups of about 165 healthy breast fed infants who received at random 1 mg vitamin K1 orally or intramuscularly after birth were studied at 2 weeks and 1 and 3 months of age. Although vitamin K1 concentrations were statistically significantly higher in the intramuscular group, blood coagulability, activities of factors VII and X and PIVKA-II concentrations did not reveal any difference between the two groups. At 2 weeks of age vitamin K, concentrations were raised compared with reported unsupplemented concentrations and no PIVKA-II was detectable. At 3 months vitamin K1 concentrations were back at unsupplemented values and PIVKA-II was detectable in 11.5% of infants. Therefore, a repeated oral prophylaxis will be necessary to completely prevent (biochemical) vitamin K deficiency beyond the age of 1 month.

A prospective study of Acinetobacter isolates from a neonatal intensive care unit was performed for 24 months. Fifty-six isolates were obtained from 21 patients, and another eight were obtained from environmental specimens. Infection due to Acinetobacter organisms was established for 16 patients, 6 with septicemia, 9 with pneumonia, and 1 with a wound infection. Further investigations were performed with 38 representative isolates. Twenty-nine isolates were identified as unnamed DNA-DNA hybridization group (genomospecies) 3, three were identified as genomospecies 2 (Acinetobacter baumannii), one was identified as genomospecies 5 (Acinetobacter junii), three were identified as genomospecies 14, and two were unclassified. Eight distinguishable protein profiles, coded I through VIII, were found by cell envelope protein electrophoresis. Profile V, a common profile, was observed for 17 isolates that had been recovered from 11 patients and 1 dust specimen. These isolates, all of which belonged to genomospecies 3, had similar antibiograms and biotypes. This study has revealed that genomospecies 3 can be associated with infection and be spread in hospitals.

Changes in reported policies for management of extremely preterm births were related to mortality declines.

Hepatocyte nuclear factors 3 (HNF-3α, -3β and -3γ) belong to an evolutionarily conserved family of transcription factors that are critical for diverse biological processes such as development, differentiation and metabolism. Gene expression studies have shown that HNF3 proteins are critical regulators of the early-onset type 2 diabetes genes HNF-1α, HNF-4α and IPF-1/PDX-1 (MODY3, 1 and 4, respectively) and of glucagon transcription and pancreatic α-cell function. In this study, we investigated whether genetic variation in the genes encoding HNF-3α, HNF-3β and HNF-3γ predisposes humans to hyperglycemic or hypoglycemic syndromes. In addition, we report the cloning and partial nucleotide sequence of the human HNF-3α, -3β and -3γ genes. Mutation screening included 96 subjects with type 2 diabetes mellitus, as well as one family with persistent neonatal hypoglycemia. No functional mutations were detected in the coding sequences of the three HNF-3 genes. Our results suggest that mutations in HNF-3 genes are not a common cause of type 2 diabetes mellitus. The data provided will facilitate genetic studies in other populations and will advance our understanding of the role HNF-3 plays in the development of diabetes mellitus and other metabolic disorders of glucose homeostasis.