Airborne investigation of quasi-specular Ku-band radar scattering for satellite altimetry over snow-covered Arctic sea ice

Surface-based Ku-band radar altimetry investigations indicate the radar signal is typically backscattered from well above the snow-sea ice interface. However, this would induce a bias in satellite altimeter sea ice thickness retrievals not reflected by buoy validation. Our study presents a mechanism to potentially explain this paradox: probabilistic quasi-specular radar scattering from the snow-ice interface. We introduce the theory for this mechanism before identifying it in airborne Ku-band radar observations collected over landfast first year Arctic sea ice near Eureka, Canada, in spring 2016. Based on SAR data, this study area likely represents level first year sea ice across the Arctic. Radar backscatter from the snow and ice interfaces were estimated by co-aligning laser scanner and radar observations with in situ measurements. On average, 4-5 times more radar power was scattered from the snow-ice than the air-snow interface over first-year ice. However, return power varied by up to 20 dB between consecutive radar echoes, particularly from the snow-ice interface, depending on local slope and roughness. Measured laser-radar snow depths were more accurate when radar returns were specular, but there was no systematic bias between airborne and in situ snow depths. The probability and strength of quasi-specular returns depend on the measuring height above and slope distribution of sea ice, so these findings have implications for satellite altimetry snow depth and freeboard estimates. This mechanism could explain the apparent differences in Ku-band radar penetration into snow on sea ice when observed from the range of a surface-, airborne- or satellite-based sensor

Kynurenine metabolites predict survival in pulmonary arterial hypertension: A role for IL-6/IL-6Rα

Activation of the kynurenine pathway (KP) has been reported in patients with pulmonary arterial hypertension (PAH) undergoing PAH therapy. We aimed to determine KP-metabolism in treatment-naïve PAH patients, investigate its prognostic values, evaluate the effect of PAH therapy on KP-metabolites and identify cytokines responsible for altered KP-metabolism. KP-metabolite levels were determined in plasma from PAH patients (median follow-up 42 months) and in rats with monocrotaline- and Sugen/hypoxia-induced PH. Blood sampling of PAH patients was performed at the time of diagnosis, six months and one year after PAH therapy. KP activation with lower tryptophan, higher kynurenine (Kyn), 3-hydroxykynurenine (3-HK), quinolinic acid (QA), kynurenic acid (KA), and anthranilic acid was observed in treatment-naïve PAH patients compared with controls. A similar KP-metabolite profile was observed in monocrotaline, but not Sugen/hypoxia-induced PAH. Human lung primary cells (microvascular endothelial cells, pulmonary artery smooth muscle cells, and fibroblasts) were exposed to different cytokines in vitro. Following exposure to interleukin-6 (IL-6)/IL-6 receptor α (IL-6Rα) complex, all cell types exhibit a similar KP-metabolite profile as observed in PAH patients. PAH therapy partially normalized this profile in survivors after one year. Increased KP-metabolites correlated with higher pulmonary vascular resistance, shorter six-minute walking distance, and worse functional class. High levels of Kyn, 3-HK, QA, and KA measured at the latest time-point were associated with worse long-term survival. KP-metabolism was activated in treatment-naïve PAH patients, likely mediated through IL-6/IL-6Rα signaling. KP-metabolites predict response to PAH therapy and survival of PAH patients