No abstract

Pulmonary surfactant is essential to maintain alveolar patency, and invariably fatal neonatal lung disease has been recognized to involve mutations in the genes encoding surfactant protein-B or ATP-binding cassette transporter family member ABCA3. The lipid transporter ABCA3 targets surfactant phospholipids to lamellar bodies that are lysosomal-derived organelles of alveolar type II cells. ABCA3À/À mice have grossly reduced surfactant phosphatidyl glycerol levels and die of respiratory failure soon after birth. We studied lung biopsy samples of two siblings with a novel homozygous ABCA3 mutation at nucleotide position 578 (c.578C4G), leading to a Pro193Arg amino-acid exchange, who died at 55 and 105 days of age. Light microscopy revealed thickened alveolar septa with abundant myxoid interstitial matrix, marked hyperplasia of type II pneumocytes, desquamation of alveolar macrophages and focal alveolar proteinosis. Surfactant protein-B was detected by immunohistochemistry after antigen retrieval. Transmission electron microscopy showed rare cytoplasmic inclusions with concentric membranes and eccentrically placed electron-dense aggregates. These 'fried-egg'-appearing lamellar bodies differed both from normal lamellar bodies and the larger, poorly formed composite bodies with multiple vesicular inclusions observed in surfactant protein-B deficiency. In conclusion, our findings underscore that the implications of interstitial lung disease in infant lungs differ from those in adults. In infants with a desquamative interstitial pneumonitis pattern, surfactant or ABCA3 mutations should be evaluated. Importantly, these findings support the notion that electron microscopy is useful in distinguishing between surfactant protein-B and ABCA3 deficiency, and has an important role in evaluating biopsies or autopsies of term infants with unexplained severe respiratory failure and interstitial lung disease.

No abstract

This report provides estimates of the costs associated with bank resolution both in terms of the expected costs that might arise should a bank fail (i.e. as "ex-post" costs), as well as the cost associated with the likelihood that a solvent bank might fail (i.e. as "ex-ante" costs) over the next year. It finds that expected resolution costs (ex-post costs) have dropped recently due to higher average capital ratios and a lower level of bank liabilities as a percentage of GDP. The annualised value of these expected resolution costs (ex-ante costs), which increased sharply after 2008, has since subsided, but remains well above its 2008 level. Overall, the estimates produced in this report support the notion that recent financial sector reforms have had an impact on reducing the costs associated with bank failure, including the expected costs to taxpayers. However, estimates are in most cases yet to return to pre-crisis levels.

Psychophysical and electroretinographic observations in normal observers and achromats (who lack cone vision) suggest that rod signals have access to two retinal pathways: one, slow and sensitive; the other, fast and insensitive. The two are revealed by double-branched rod-detected flicker threshold vs intensity (ftvi) curves, and by a suprathreshold intensity region (below cone detection)—the perceptual null—within which the sensation of 15-Hz flicker is canceled. The cause of the null is believed to be destructive interference between signals conveyed by the two pathways. Here we report that the break in the 15-Hz ftvi curve and the perceptual null is not found, in either the normal or achromat observer when the flickering target is ≤2° in diameter. Phase measurements (relative to a cone standard) indicate that the faster rod pathway mediates flicker detection for targets of ≤2°, not because the signals from the slow pathway are severely diminished but because destructive interference between the slow and fast rod flicker signals keeps the slow signals from ever exceeding threshold. There is therefore no need to invoke differences in spatial integration between the two pathways to explain the large difference in the ftvi curves.