Niskamoon Corporation

Abstract A large under‐ice plume forms because of the regulated winter discharge from the La Grande River hydroelectric complex (NE James Bay, Canada), which is among the largest winter discharges in the circumpolar north. In 2016–2017, field campaigns were completed to characterize the under‐ice plume's structure, extent, and short‐term dynamics related to tides, weather, and discharge. Amid concerns of the freshwater's impact on eelgrass, the lateral spreading of the under‐ice plume into inshore areas was also assessed. When discharges averaged 4,800 m3 s−1 throughout the January–March periods, the freshwater influence of La Grande River extended more than 100 km north along the James Bay coast, with the brackish (salinity <25) under‐ice plume more than three times larger than for a natural winter discharge of ∼460 m3 s−1. The core area of the under‐ice plume, defined as the area with a highly stratified water column and surface layer of salinity <5, extended 30–35 km north and >20 km south. It was stable throughout the January–March 2016–2017 periods and, despite 30% higher winter discharge, was not significantly larger compared to survey periods in 1984–1987. This stability appears to be due to coastal geometry and width of the landfast ice cover, under which the plume can spread with limited mixing. Inshore salinity was about 5–10 units lower in winter versus the open‐water period. The seasonal duration of reduced salinity at eelgrass habitats will depend on landfast ice duration as well as river discharge magnitude.

Aicardi-Goutiéres syndrome (AGS) is an early onset, progressive encephalopathy characterised by calcification of the basal ganglia, white matter abnormalities, and a chronic cerebrospinal fluid (CSF) lymphocytosis. Cree encephalitis shows phenotypic overlap with AGS although the conditions have been considered distinct because of immunological abnormalities observed in Cree encephalitis. We report that levels of interferon alpha (IFN-α), a marker of AGS, are raised in Cree encephalitis. Moreover, linkage analysis indicates that the disorders are allelic and refines the AGS1 locus to a 3.47 cM critical interval. Our data show that a CSF lymphocytosis is not necessary for the diagnosis of AGS and strongly suggest that AGS and pseudo-TORCH syndrome are the same disorder. Recognition of immunological dysfunction as part of the AGS phenotype provides further evidence of a primary pathogenic role for abnormal IFN-α production in AGS.