Warm winds from the Pacific caused extensive Arctic sea-ice melt in summer 2007

During summer 2007 the Arctic sea-ice shrank to the lowest extent ever observed. The role of the atmospheric energy transport in this extreme melt event is explored using the state-of-the-art ERA-Interim reanalysis data. We find that in summer 2007 there was an anomalous atmospheric flow of warm and humid air into the region that suffered severe melt. This anomaly was larger than during any other year in the data (1989–2008). Convergence of the atmospheric energy transport over this area led to positive anomalies of the downward longwave radiation and turbulent fluxes. In the region that experienced unusual ice melt, the net anomaly of the surface fluxes provided enough extra energy to melt roughly one meter of ice during the melting season. When the ocean successively became ice-free, the surface-albedo decreased causing additional absorption of shortwave radiation, despite the fact that the downwelling solar radiation was smaller than average. We argue that the positive anomalies of net downward longwave radiation and turbulent fluxes played a key role in initiating the 2007 extreme ice melt, whereas the shortwave-radiation changes acted as an amplifying feedback mechanism in response to the melt

Characterization of Human Late Outgrowth Endothelial Progenitor-Derived Cells under Various Flow Conditions.

Background: Endothelial progenitor-derived cells (EPC) are a cell therapy tool in peripheral arterial disease and for re-endothelialization of bypasses and stents. Objective: To assess EPC behavior under flow conditions normally found in vivo. Results: EPC were isolated from human cord blood, cultured on compliant tubes and exposed in an in vitro flow system mimicking hemodynamic environments normally found in medium and large arteries. EPC exposed for 24 h to unidirectional (0.3 ± 0.1 or 6 ± 3 dynes/cm(2)) shear stress oriented along flow direction, while those exposed to bidirectional shear stress (0.3 ± 3 dynes/cm(2)) or static conditions had random orientation. Under bidirectional flow, tissue factor (TF) activity and mRNA expression were significantly increased (2.5- and 7.0-fold) compared to static conditions. Under low shear unidirectional flow TF mRNA increased 4.9 ± 0.5-fold. Similar flow-induced increases were observed for TF in mature umbilical vein-derived endothelial cells. Expression of tissue-type plasminogen activator (t-PA), urokinase (u-PA) and monocyte chemotactic protein 1 (MCP1) were reduced by 40-60% in late outgrowth endothelial progenitor-derived cells (LO-EPC) exposed to any flow environment, while MCP1, but not t-PA or u-PA, was decreased in HUVEC. Conclusions: Flow, in particular bidirectional, modifies the hemostatic balance in LO-EPC with increased TF and decreased plasminogen activator expression