Melt onset over Arctic sea ice controlled by atmospheric moisture transport

The timing of melt onset affects the surface energy uptake throughout the melt season. Yet the processes triggering melt and causing its large interannual variability are not well understood. Here we show that melt onset over Arctic sea ice is initiated by positive anomalies of water vapor, clouds, and air temperatures that increase the downwelling longwave radiation (LWD) to the surface. The earlier melt onset occurs; the stronger are these anomalies. Downwelling shortwave radiation (SWD) is smaller than usual at melt onset, indicating that melt is not triggered by SWD. When melt occurs early, an anomalously opaque atmosphere with positive LWD anomalies preconditions the surface for weeks preceding melt. In contrast, when melt begins late, clearer than usual conditions are evident prior to melt. Hence, atmospheric processes are imperative for melt onset. It is also found that spring LWD increased during recent decades, consistent with trends toward an earlier melt onset. ©2016. American Geophysical Union. All Rights Reserved

Electrorefining beryllium : preliminary studies /

Includes bibliographic references.Mode of access: Internet

Polymorphism in the innate immune receptor SIRPα controls CD47 binding and autoimmunity in the nonobese diabetic mouse

The signal regulatory protein (SIRP) locus encodes a family of paired receptors that mediate both activating and inhibitory signals and is associated with type 1 diabetes (T1D) risk. The NOD mouse model recapitulates multiple features of human T1D and enables mechanistic analysis of the impact of genetic variations on disease. In this study, we identify Sirpa encoding an inhibitory receptor on myeloid cells as a gene in the insulin-dependent diabetes locus 13.2 (Idd13.2) that drives islet inflammation and T1D. Compared to T1D-resistant strains, the NOD variant of SIRPa displayed greater binding to its ligand CD47, as well as enhanced T cell proliferation and diabetogenic potency. Myeloid cell-restricted expression of a Sirpa transgene accelerated disease in a dosedependent manner and displayed genetic and functional interaction with the Idd5 locus to potentiate insulitis progression. Our study demonstrates that variations in both SIRPa sequence and expression level modulate T1D immunopathogenesis. Thus, we identify Sirpa as a T1D risk gene and provide insight into the complex mechanisms by which disease-associated variants act in concert to drive defined stages in disease progressio