Fetal alcohol syndrome is a leading cause of mental retardation. The neuropathology found in patients with fetal alcohol syndrome overlaps with those with mutations in the gene for cell adhesion molecule (L1). We have previously shown that L1‐mediated neurite outgrowth and L1 activation of extracellular receptor kinases 1/2 are inhibited at low concentrations of ethanol. One possible mechanism for this effect is through disruption of a tyrosine‐based sorting signal, Y(1176)RSLE, on the cytoplasmic domain of L1. Our goal was to determine if ethanol inhibited the sorting signal or its phosphorylation state. Using cerebellar granule neurons and dorsal root ganglion neurons, we found that ethanol had no effect on L1 distribution to the growth cone or its ability to be expressed on the cell surface as determined by confocal microscopy. In cerebellar granule neurons, clustering of L1 resulted in increased dephosphorylation of Y(1176), increased L1 tyrosine phosphorylation, and an increase in the activation of pp60src as measured by immunoblot. All changes were inhibited by 25 mM ethanol. Using PP2 to inhibit pp60src activation resulted in inhibition of increases in L1 tyrosine and extracellular receptor kinases 1/2 phosphorylation, and Y(1176) dephosphorylation. We conclude that ethanol disrupts L1 trafficking/signaling following its expression on the surface of the growth cone, and prior to its activation of pp60src.

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Objectives: Pneumothorax (PTX) in newborns is a life-threatening condition associated with high morbidity and mortality especially in premature infants. The frequency of PTX in neonates at different gestational ages (GA) and its impact on neonatal mortality have not been quantified. We aimed to determine: (1) the prevalence of PTX in neonates at different GA from ≤24 to ≥37 weeks, (2) the impact of PTX on mortality per GA, and (3) the impact of PTX on the length of stay (LOS) per GA.Methods: The national Kids' Inpatient Database for the years of 2006-2012 were used. We included all infants admitted to the hospital with a documented GA and International Classification of Disease 9 code of PTX. Bivariate and multivariate analyses were conducted and odds ratios (OR) were calculated.Results: A total of 10,625,036 infants were included; of them 3665 infants (0.034%) had a diagnosis of PTX, with highest prevalence at ≤24 weeks GA (0.67%), and lowest at term (0.02%). The overall mortality rate of patients with PTX was 8.8%, and greater in preterm (16.3%) versus term infants (2.7%). The association of mortality with PTX was greatest at GA of 29-32 weeks (OR = 8.55; 95% confidence interval: 6.56-11.13). Infants who survived until discharge had a median of 2-12 days longer LOS depending on GA category.

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