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Several randomized controlled trials (RCTs) have investigated the prophylactic use of probiotics in preterm infants aimed at reducing the rate of necrotising enterocolitis (NEC). There are 4 meta-analyses on this subject. 2 more RCTs have been published since these meta-analyses were completed. Each meta-analysis, as well as the 2 recent RCTs, document reduced rates of NEC and mortality with the use of prophylactic probiotics. We calculated meta-analyses based on 3 approaches: A - RCTs common to all meta-analyses, B - RCTs ever accounted for in a meta-analysis but not common to all, and C - the 2 recent RCTs. The 3 subgroups yield similar results, with an overall reduction in the relative risk (RR) of NEC (Bell > or =2) to 0.35 (95% CI 0.23-0.55) and of mortality to 0.41 (0.28-0.60). NEC rates and mortalities in the dominant RCTs are in the range reported from North American and European networks. Best results appear to be achieved with probiotics based on 2 or more probiotic species and/or with a combination of Bifidusbacterium spp. and Lactobacillus acidophilus. No unwanted side effects have been reported among 1 117 infants randomized to receive probiotics. We conclude that probiotics are safe and beneficial in preterm infants at risk for NEC.

Introduction Maternal body mass index has an impact on maternal and fetal pregnancy outcome. An increased maternal BMI is known to be associated with admission of the newborn to a neonatal care unit. The reasons and impact of this admission on fetal outcome, however, are unknown so far. Objective The aim of our study was to investigate the impact of maternal BMI on maternal and fetal pregnancy outcome with special focus on the children admitted to a neonatal care unit. Methods A cohort of 2049 non-diabetic mothers giving birth in the Charite university hospital was prospectively studied. The impact of maternal BMI on maternal and fetal outcome parameters was tested using multivariate regression analysis. Outcome of children admitted to a neonatal ward (n = 505) was analysed. Results Increased maternal BMI was associated with an increased risk for hypertensive complications, peripheral edema, caesarean section, fetal macrosomia and admission of the newborn to a neonatal care unit, whereas decreased BMI was associated with preterm birth and lower birthweight. In the neonatal ward children from obese mothers are characterized by hypoglycaemia. They need less oxygen, and exhibit a shorter stay on the neonatal ward compared to children from normal weight mothers, whereas children from underweight mothers are characterized by lower umbilical blood pH and increased incidence of death corresponding to increased prevalence of preterm birth. Conclusion Pregnancy outcome is worst in babies from mothers with low body mass index as compared to healthy weight mothers with respect to increased incidence of preterm birth, lower birth weight and increased neonate mortality on the neonatal ward. We demonstrate that the increased risk for neonatal admission in children from obese mothers does not necessarily indicate severe fetal impairment.

Background: The mechanisms during the initial phase of oxygen toxicity leading to pulmonary tissue damage are incompletely known. Increase of tumour necrosis factor alpha (TNFalpha) represents one of the first pulmonary responses to hyperoxia. We hypothesised that, in the initial phase of hyperoxia, TNFalpha activates the caspase cascade in type II pneumocytes (TIIcells).

alpha-Tocopherol transfer protein (alpha-TTP) supplements nascent very-low-density lipoprotein (VLDL) preferentially with alpha-tocopherol by selecting the alpha-isomers against other stereoisomers of tocopherol. It is exclusively expressed in liver. We investigated whether the expression of the hepatic alpha-TTP can be induced by dietary tocopherols. Vitamin E-depleted rats were fed with a diet containing alpha- and delta-tocopherol (ratio 1:3). The expression of alpha-TTP mRNA was measured in liver tissue. The ratio of tocopherol stereoisomers was determined in plasma, plasma lipoproteins and tissues to measure the metabolic action of alpha-TTP. Refeeding a diet containing either alpha- or delta-tocopherol, or both, caused a steady increase of the expression of alpha-TTP mRNA. In parallel the alpha/delta-tocopherol ratio increased in plasma, VLDL, high-density lipoprotein and low-density lipoprotein as well as in liver tissue, when the diet was fed containing both isomers. The alpha-tocopherol/delta-tocopherol ratio of heart, kidney, lung, lamellar bodies of lung and in lung lavage showed no or a comparatively low increase. The data show that both tocopherol isomers were able to induce alpha-TTP mRNA in rat liver and, thus, the ability of liver to select for the alpha-isomer. On the other hand, tocopherol depletion did not change the expression of hepatic alpha-TTP mRNA in the rat.

Members of the fatty-acid-binding protein (FABP) family are thought to play an important role in fatty acid transport within the cytosol and thus to be involved in lipid metabolism. As previous data on the occurrence of distinct FABP types in total lung are contradictory, we determined the expression of FABP types in three isolated cell types of rat lung, which are characterised by active lipid metabolism. Alveolar type-II cells synthesise, store and secrete pulmonary surfactant, a phospholipid-rich surfacetension-lowering agent, whereas lung fibroblasts, localised adjacent to the alveolar type-II cells, are assumed to provide neutral lipid substrate to alveolar type-II cells around birth, and alveolar macrophages are known to degrade complex lipids. Initial screening by reverse transcriptase PCR revealed the occurrence of heart (H-), epidermal (E-) and liver FABP in rat lung, the latter being not detectable in the three cell types studied. Cells were analysed by northern and western blotting, then quantitatively by sandwich ELISA, for which recombinant rat E-FABP was prepared. E-FABP mRNA was found in all three cell types, and E-FABP was detected in the following amounts: 240.9Ϯ19.0 ng/mg cytosolic protein in alveolar type-II cells; 172.3Ϯ0.7 ng/mg protein for lung fibroblasts ; and 36.9 Ϯ3.5 ng/mg protein for alveolar macrophages. This indicates a basic function of E-FABP in cellular lipid metabolism. In contrast, H-FABP probably is involved in the metabolism of neutral lipids because H-FABP mRNA was found only in lung fibroblasts with a corresponding protein level of 315.5Ϯ6.9 ng/mg. Small amounts of H-FABP protein were present in alveolar type-II cells and alveolar macrophages.Keywords : fatty-acid-binding protein; alveolar type-II cell; lung fibroblast ; alveolar macrophage; ELISA.In rat lung, alveolar type-II cells synthesise, store and secrete thought to be involved in a facilitated on-demand supply of surfactant substrate [9]. pulmonary surfactant, a phospholipid · protein complex that preParticipation of alveolar macrophages in surfactant metabovents the collapse of the alveoli by reducing surface tension at lism was suggested from in vivo and in vitro experiments [10Ϫ the air-liquid interface. This surfactant is highly enriched in 12]. Theoretically, alveolar macrophages could account for the phospholipids, particularly dipalmitoyl phosphatidylcholine.entire catabolism of alveolar surfactant in rat lung [11]. Fatty Fatty acids required for the biosynthesis of phospholipids are acids derived from phosphatidylcholine degradation are reused either synthesised de novo within this type-II cell [1Ϫ3] or taken for triacylglycerol synthesis [13]. up from exogenous sources [4Ϫ6]. Uptake and intracellular It is obvious from the above that fatty acids are needed for transfer of fatty acids by these alveolar type-II cells are not well lung surfactant homeostasis, in which the three cell types menunderstood [7], but the high turnover of phospholipids requires tioned appear to be involved. As a consequence, fatty ac...

Both early diagnostic and prognostic assessment of the acute abdomen in preterm infants are hampered by the lack of a sensitive and specific parameter for intestinal injury. In this prospective clinical study we wanted to estimate the value of intestinal (I-) and liver (L-) fatty acid binding protein (FABP) in diagnosing necrotizing enterocolitis (NEC). Using highly sensitive and specific sandwich ELISAs which employ recombinant human I- and L-FABP as standard proteins (limit of detection 0.1 ng/ml plasma), the L-FABP concentration (median 7.6 ng/ml) was determined to be about 3 fold that of I-FABP (median 2.52 ng/ml) in plasma of healthy preterm infants. I- and L-FABP concentrations significantly increased with birth weight (1.6 and 5.0 ng/ ml per kg, respectively). At onset of symptoms, I-FABP concentration was significantly higher in infants who later developed severe NEC compared to healthy infants and those, whose illness remained confined to stage I or II. L-FABP was significantly elevated compared to the control group at onset of symptoms regardless of the further course of NEC. In conclusion, I-FABP appears to be a specific parameter for early detection of intestinal injury leading to severe NEC stage III. L-FABP, however, is a promising sensitive marker even for stage I of NEC.