Integrating snow science and wildlife ecology in Arctic-boreal North America

Snow covers Arctic and boreal regions (ABRs) for approximately 9 months of the year, thus snowscapes dominate the form and function of tundra and boreal ecosystems. In recent decades, Arctic warming has changed the snowcover\u27s spatial extent and distribution, as well as its seasonal timing and duration, while also altering the physical characteristics of the snowpack. Understanding the little studied effects of changing snowscapes on its wildlife communities is critical. The goal of this paper is to demonstrate the urgent need for, and suggest an approach for developing, an improved suite of temporally evolving, spatially distributed snow products to help understand how dynamics in snowscape properties impact wildlife, with a specific focus on Alaska and northwestern Canada. Via consideration of existing knowledge of wildlife-snow interactions, currently available snow products for focus region, and results of three case studies, we conclude that improving snow science in the ABR will be best achieved by focusing efforts on developing data-model fusion approaches to produce fit-for-purpose snow products that include, but are not limited to, wildlife ecology. The relative wealth of coordinated in situ measurements, airborne and satellite remote sensing data, and modeling tools being collected and developed as part of NASA\u27s Arctic Boreal Vulnerability Experiment and SnowEx campaigns, for example, provide a data rich environment for developing and testing new remote sensing algorithms and retrievals of snowscape properties

The chemokine receptor 5 Δ32 mutation is associated with increased renal survival in patients with IgA nephropathy

The chemokine receptor 5 Δ32 mutation is associated with increased renal survival in patients with IgA nephropathy.BackgroundChemokine receptor 5 (CCR5) plays an important role in the recruitment of monocytes and T cells in inflammation and experimental studies suggest that CCR5 might be involved in the pathogenesis of IgA nephropathy. A mutation in the CCR5 gene (CCR5 Δ32), leading to a nonfunctional receptor, was recently described. We therefore evaluated the potential role of this mutation on renal survival in patients with IgA nephropathy.MethodsThe distribution of the CCR5 Δ32 genotype was determined by polymerase chain reaction (PCR) analysis in 228 patients with biopsy-proven IgA nephropathy. In 190 patients with available demographic and clinical follow-up data, the effect of the mutation on the clinical outcome was analyzed using the Log-rank test and the Cox proportional hazard model. In vitro, the influence of the CCR5 Δ32 genotype on the chemotactic response of monocytes was assessed.ResultsOf the 190 patients, 158 (83.2%) had a CCR5 wild-type genotype, 29 (15.3%) were heterozygous, and three patients had a homozygous CCR5 Δ32 genotype (1.6%). Renal survival was significantly longer in patients with the CCR5 Δ32 genotype than in the wild-type group (Log-rank P < 0.001). Using the multivariate Cox proportional hazard model, the CCR5 Δ32 genotype was identified as an independent factor associated with a lower risk to develop end-stage renal disease (ESRD) [hazard ratio (HR) 0.23, 95% CI 0.09 to 0.57, P = 0.002]. In vitro analysis of monocytes from CCR5 Δ32 carriers showed a reduced chemotactic response to CCR5 ligands in vitro.ConclusionOur study demonstrates an independent role of the CCR5 Δ32 genotype for the clinical outcome in IgA nephropathy. In vitro experiments revealed a reduced chemotactic response of monocytes from CCR5 Δ32 carriers, thus pointing out a possible pathophysiologic explanation for the beneficial effect of the CCR5 Δ32 genotype