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BSDB Spring meeting 2020Jointly with Genetics Societydate: 15-18 March 2020location: Warwickorganisers: Stefan Hoppler (GenSoc), Aziz Aboobaker (GenSoc), Tanya Whitfield (BSDB), Clare Baker (BSDB), Sally Lowell (BSDB)

This paper develops new perspectives of cross-disciplinary methods combining futures studies and urbanplanning to help imagine healthier futures for compact urban cores. Our empirical basis lies in research-based collaboration between 2016 and 2019 with the City of Turku, the former capital of Finland. The goal was the creation of an ambitious but realistic vision and strategic plan focused on liveability and wellbeing and addressing challenges posed by spatial fragmentation and lack of cohesion. Through the process, it was concluded that to create a positive transition, planning requires the adoption of a ‘greensight’ perspective as a point of departure. The basic argument was that in order to reach a new level of human-centredness andinterconnectedness, urban cores need to act as the strong support system for the healthier urban societies of the future. In this paper, we explain the lessons learned and provide an analysis of green areas in the context of Turku. We share wisdom on two key aspects: 1) the growing importance of human health for a more future-oriented approach to the planning of green areas and 2) the rising levels of urban complexity that make adequate distribution of green areas hard to achieve., SHAPING URBAN CHANGE – Livable City Regions for the 21st Century. Proceedings of REAL CORP 2020, 25th International Conference on Urban Development and Regional Planning in the Information Society, 1239-1249

Necrosis of infected macrophages constitutes a critical pathogenetic event in tuberculosis by releasing mycobacteria into the growth-permissive extracellular environment. In zebrafish infected with Mycobacterium marinum or Mycobacterium tuberculosis, excess tumor necrosis factor triggers programmed necrosis of infected macrophages through the production of mitochondrial reactive oxygen species (ROS) and the participation of cyclophilin D, a component of the mitochondrial permeability transition pore. Here, we show that this necrosis pathway is not mitochondrion-intrinsic but results from an inter-organellar circuit initiating and culminating in the mitochondrion. Mitochondrial ROS induce production of lysosomal ceramide that ultimately activates the cytosolic protein BAX. BAX promotes calcium flow from the endoplasmic reticulum into the mitochondrion through ryanodine receptors, and the resultant mitochondrial calcium overload triggers cyclophilin-D-mediated necrosis. We identify ryanodine receptors and plasma membrane L-type calcium channels as druggable targets to intercept mitochondrial calcium overload and necrosis of mycobacterium-infected zebrafish and human macrophages.