The international co-operative movement has prioritised supportive legal frameworks as a key constituent of co-operative growth (ICA, 2013). Unfortunately, there is not a robust literature on co-operative policy to help meet this need. Supportive legal frameworks for co-operatives are a “deeply under-researched area” (Adeler, 2014: 50). We recently conducted a review of the existing research and found that despite its dearth, the literature points to six primary forms of policy support that have been successfully deployed internationally to support co-operative growth: co-operative recognition, financing, sectoral financing, preferential taxation, supportive infrastructure, and preferential procurement. The most developed examples of these policies are found in areas of dense co -operative concentration, or “co-op hot spots”: the Basque region of Spain, Emilia Romagna in Northern Italy, and Quebec, Canada. This article accounts for how these six policy forms appear in the co-operative dense regions. The aim of this analysis is to facilitate further research in the understudied area of co-operative policy, and to clarify policy successes for organisers in the co-operative movement interested in emulating them.

After the financial crisis in 2008 and amid growing concerns about climate change, interest in systemic alternatives to neoliberal capitalism is growing. This cultural shift helps explain the enthusiasm from political elites, media, and academics that greeted the launch of Evergreen Co-operative Corporation in 2009. Based in Cleveland Ohio, Evergreen is a network of worker-owned co-operatives with scalability and replicability woven into its design. But how warranted is the broad-based enthusiasm around Evergreen? Is this a model that can be replicated across North America as its founders suggest? Based on site visits and stakeholder interviews, we argue that there are important limits on desires to reproduce the “Cleveland Model.” However, its ambitions for scalability and replicability position it to contribute to the important project of movement building that can facilitate the policy change needed to scale up the co-operative alternative.

Oral infection of C57BL/6J mice with Toxoplasma gondii results in a marked bacterial dysbiosis and the development of severe pathology in the distal small intestine that is dependent on CD4+ T cells and interferon gamma (IFN-γ). This dysbiosis and bacterial translocation contribute to the development of ileal pathology, but the factors that support the bloom of bacterial pathobionts are unclear. The use of microbial community profiling and shotgun metagenomics revealed that Toxoplasma infection induces a dysbiosis dominated by Enterobacteriaceae and an increased potential for nitrate respiration. In vivo experiments using bacterial metabolic mutants revealed that during this infection, host-derived nitrate supports the expansion of Enterobacteriaceae in the ileum via nitrate respiration. Additional experiments with infected mice indicate that the IFN-γ/STAT1/iNOS axis, while essential for parasite control, also supplies a pool of nitrate that serves as a source for anaerobic respiration and supports overgrowth of Enterobacteriaceae Together, these data reveal a trade-off in intestinal immunity after oral infection of C57BL/6J mice with T. gondii, in which inducible nitric oxide synthase (iNOS) is required for parasite control, while this host enzyme is responsible for specific modification of the composition of the microbiome that contributes to pathology.IMPORTANCEToxoplasma gondii is a protozoan parasite and a leading cause of foodborne illness. Infection is initiated when the parasite invades the intestinal epithelium, and in many host species, this leads to intense inflammation and a dramatic disruption of the normal microbial ecosystem that resides in the healthy gut (the so-called microbiome). One characteristic change in the microbiome during infection with Toxoplasma-as well as numerous other pathogens-is the overgrowth of Escherichia coli or similar bacteria and a breakdown of commensal containment leading to seeding of peripheral organs with gut bacteria and subsequent sepsis. Our findings provide one clear explanation for how this process is regulated, thereby improving our understanding of the relationship between parasite infection, inflammation, and disease. Furthermore, our results could serve as the basis for the development of novel therapeutics to reduce the potential for harmful bacteria to bloom in the gut during infection.