Combining food web and species distribution models for improved community projections

The ability to model biodiversity patterns is of prime importance in this era of severe environmental crisis. Species assemblage along environmental gradients is subject to the interplay of biotic interactions in complement to abiotic filtering and stochastic forces. Accounting for complex biotic interactions for a wide array of species remains so far challenging. Here, we propose using food web models that can infer the potential interaction links between species as a constraint in species distribution models. Using a plant–herbivore (butterfly) interaction dataset, we demonstrate that this combined approach is able to improve species distribution and community forecasts. The trophic interaction network between butterfly larvae and host plant was phylogenetically structured and driven by host plant nitrogen content allowing forecasting the food web model to unknown interactions links. This combined approach is very useful in rendering models of more generalist species that have multiple potential interaction links, where gap in the literature may occur. Our combined approach points toward a promising direction for modeling the spatial variation in entire species interaction networks.     

Alberta's Friends of Medicare seek acceptance in a sceptical province

Alberta has probably made the strongest efforts of any province to reduce its health care costs. Leading the opposition to the cuts is an organization called the Friends of Medicare, a motley mix of underfinanced public-interest groups that is fighting to stop the province from sliding toward a two-tier health care system. “Alberta is dragging the rest of the country down to a two-tier system,” says Dr. Hubert Kammerer, a family physician who serves as a spokesperson for the organization. He warns that many Albertans worry that their health care system is deteriorating.     

P2X7 Cell Death Receptor Activation and Mitochondrial Impairment in Oxaliplatin-Induced Apoptosis and Neuronal Injury: Cellular Mechanisms and In Vivo Approach

Limited information is available regarding the cellular mechanisms of oxaliplatin-induced painful neuropathy during exposure of patients to this drug. We therefore determined oxidative stress in cultured cells and evaluated its occurrence in C57BL/6 mice. Using both cultured neuroblastoma (SH-SY5Y) and macrophage (RAW 264.7) cell lines and also brain tissues of oxaliplatin-treated mice, we investigated whether oxaliplatin (OXA) induces oxidative stress and apoptosis. Cultured cells were treated with 2–200 µM OXA for 24 h. The effects of pharmacological inhibitors of oxidative stress or inflammation (N-acetyl cysteine, ibuprofen, acetaminophen) were also tested. Inhibitors were added 30 min before OXA treatment and then in combination with OXA for 24 h. In SH-SY5Y cells, OXA caused a significant dose-dependent decrease in viability, a large increase in ROS and NO production, lipid peroxidation and mitochondrial impairment as assessed by a drop in mitochondrial membrane potential, which are deleterious for the cell. An increase in levels of negatively charged phospholipids such as cardiolipin but also phosphatidylserine and phosphatidylinositol, was also observed. Additionally, OXA caused concentration-dependent P2X7 receptor activation, increased chromatin condensation and caspase-3 activation associated with TNF-α and IL-6 release. The majority of these toxic effects were equally observed in Raw 264.7 which also presented high levels of PGE2. Pretreatment of SH-SY5Y cells with pharmacological inhibitors significantly reduced or blocked all the neurotoxic OXA effects. In OXA-treated mice (28 mg/kg cumulated dose) significant cold hyperalgesia and oxidative stress in the tested brain areas were shown. Our study suggests that targeting P2X7 receptor activation and mitochondrial impairment might be a potential therapeutic strategy against OXA-induced neuropathic pain.     

Carbohydrate and Domain Architecture of an Immature Antibody Glycoform Exhibiting Enhanced Effector Functions

Antibodies contain a conserved glycosylation site that has emerged as a target for the modulation of antibody effector functions. The crystal structure of a biosynthetic intermediate of human IgG1, bearing immature oligomannose-type glycans and reported to display increased antibody-dependent cellular cytotoxicity, demonstrates that glycan engineering can bias the Fc to an open conformation primed for receptor binding.     

Seasonal human coronavirus antibodies are boosted upon SARS-CoV-2 infection but not associated with protection

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