Major contributors to hospital mortality in very-low-birth-weight infants: data of the birth year 2010 cohort of the German Neonatal Network.

The German Neonatal Network (GNN) is a prospective cohort study with the focus on long term development of very-low-birth-weight infants. It was the aim of this study to determine detailed information on causes of mortality in the GNN birth cohort 2010.Major contributors to hospital mortality were recorded by the attending neonatologists for the cohort of very-low-birth-weight (VLBW) infants born in centres of the German Neonatal Network (GNN) in 2010. The data quality was approved by on-site monitoring.2 221 VLBW infants were born in GNN centres in 2010, and death occurred in 221 infants. Male infants carried a higher risk than females (58.8% males among non-survivors vs. 51.7% among survivors, p=0.047). In 11 infants, the major contributor to death was not determined by the attending neonatologist. In 25 infants born at the limit of viability, comfort palliative care was primarily initiated and 14 infants had lethal malformations. The majority of non-survivors suffered from inflammatory diseases including sepsis- or necrotizing enterocolitis (NEC)-associated death (n=56). Respiratory pathology was a major contributor to death in 65 infants including 11 infants who died from pulmonary haemorrhage.Potentially preventable complications of preterm birth such as sepsis, NEC and pulmonary haemorrhage predominate the major contributors to mortality in the GNN 2010 cohort. In order to decrease the rate of these associated deaths, future trials should focus on prophylaxis and therapy optimization strategies for these outcomes.

A new coculture-system of bronchial epithelial and endothelial cells as a model for studying ozone effects on airway tissue.

In order to study the inflammatory potential of ozone on the airway tissue, we developed an in vitro model system in which human bronchial epithelial cells (BEAS 2B) and human umbilical vein endothelial cells (ECV304) were able to communicate with each other. The BEAS 2B cells were grown on filter supports which were inserted into six-well culture dishes. Endothelial cells were cultivated on the bottom of the basolateral compartment. The upper epithelial cells were exposed to 0.15 ppm ozone for 90 min. Supernatants were collected after 1, 4 and 24 h and were quantified for IL-6 and IL-8 secretion. At the same time points we measured the expression of ICAM-1 on the umbilical vein endothelial cells. Exposure of the coculture-system to air or ozone induced the production of IL-6 as well as IL-8 that exceeded the sum of the amounts produced by the two cell types when exposed separately. At 24 h after ozone exposure the IL-6 and IL-8 levels were significantly elevated compared with the air treated cells. Concerning the ICAM-1 expression on ECV304 cells we found elevated ICAM-1 levels on cells which had been cocultured with BEAS 2B cells compared with cells cultured alone. This might be a hint for the secretion of a soluble factor that acts as a mediator in amplifying the response of epithelial cells.