Preterm infants' early developmental status is associated with later developmental outcome.

AIM: To assess the development of preterm infants from 40 weeks gestational age to 18 months corrected age to identify early predictors of later development. METHODS: Fifty-one infants were involved. Infant development was assessed at 40 and 44 weeks gestational age with the Brazelton neonatal behavioral assessment scale and a self-regulation scale and at 3, 6, 10, 18 months corrected age with the Bayley Scales of Infant Development. The quality of general movements was assessed at 1 and 3 months corrected age and maternal attachment style at infant's age of 6 months corrected age with the Relation Scale Questionnaire. RESULTS: At term age and 1-month corrected age, preterm infants were less mature and had lower levels of self-regulation than full-term infants. At 3 months corrected age, a higher proportion of preterm infants (43%) had mildly abnormal motor quality compared to the general population (25%). At all follow-ups, preterm infants had delayed mental, motor and behavioural development, which was associated with the level of self-regulation, motor quality and maternal attachment style. Maternal education level was the most predominant background factor related to infant development. CONCLUSION: Preterm infants show early-in-life deviations in self-regulation, motor quality and development. These deviations are risk factors for later optimal functioning.

Fatty acid patterns early after premature birth, simultaneously analysed in mothers' food, breast milk and serum phospholipids of mothers and infants.

BACKGROUND: The supply of long-chain polyunsaturated fatty acids via the placenta is interrupted in premature infants, making them exclusively dependent on breast milk, which varies in fatty acid (FA) concentrations depending on the mother's diet. OBJECTIVE: To in a longitudinal study explore the relation between FA status in mothers and infants from an unselected cohort of prematures, not requiring intensive care. DESIGN: Breast milk and mothers' and infants' plasma phospholipid FA concentrations from birth to 44 weeks of gestational age were analysed and compared with mothers' food intake, assessed using a 3-day diary. Fatty acids were analysed by capillary gas-liquid chromatography. RESULTS: The energy intake was low in 75% of mothers, and 90% had low intake of essential FAs (EFAs). Dietary linoleic acid (LA, 18:2w6), but not w3 FAs, correlated to concentrations in breast milk. Infants' plasma and breast milk correlated for arachidonic (AA, 20:4w6), eicosapentaenoic (EPA, 20:5w3) and docosahexaenoic (DHA, 22:6w3) acids. A high concentration of mead acid (20:3w9) in the infants at birth correlated negatively to the concentrations of LA, AA and w3 FAs. Infants of mothers who stopped breastfeeding during the study period showed decreased DHA concentrations and increased w6/w3 ratios, with the opposite FA pattern seen in the mothers' plasma. CONCLUSION: Although dietary w3 FAs were insufficient in an unselected cohort of mothers of premature infants, breastfeeding resulted in increased levels of DHA in the premature infants at the expense of the mothers, suggesting a general need to increase dietary w3 FAs during pregnancy and lactation.

A generally applicable translational strategy identifies S100A4 as a candidate gene in allergy.

The identification of diagnostic markers and therapeutic candidate genes in common diseases is complicated by the involvement of thousands of genes. We hypothesized that genes co-regulated with a key gene in allergy, IL13, would form a module that could help to identify candidate genes. We identified a T helper 2 (TH2) cell module by small interfering RNA-mediated knockdown of 25 putative IL13-regulating transcription factors followed by expression profiling. The module contained candidate genes whose diagnostic potential was supported by clinical studies. Functional studies of human TH2 cells as well as mouse models of allergy showed that deletion of one of the genes, S100A4, resulted in decreased signs of allergy including TH2 cell activation, humoral immunity, and infiltration of effector cells. Specifically, dendritic cells required S100A4 for activating T cells. Treatment with an anti-S100A4 antibody resulted in decreased signs of allergy in the mouse model as well as in allergen-challenged T cells from allergic patients. This strategy, which may be generally applicable to complex diseases, identified and validated an important diagnostic and therapeutic candidate gene in allergy.