4 research outputs found

    Flood risk mapping worldwide : a flexible methodology and toolbox

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    Flood risk assessments predict the potential consequences of flooding, leading to more effective risk management and strengthening resilience. However, adequate assessments rely on large quantities of high-quality input data. Developing regions lack reliable data or funds to acquire them. Therefore, this research has developed a flexible, low-cost methodology for mapping flood hazard, vulnerability and risk. A generic methodology was developed and customized for freely available data with global coverage, enabling risk assessment worldwide. The default workflow can be enriched with region-specific information when available. The practical application is assured by a modular toolbox developed on GDAL and PCRASTER. This toolbox was tested for the catchment of the river Moustiques, Haiti, for which several flood hazard maps were developed. Then, the toolbox was used to create social, economic and physical vulnerability maps. These were combined with the hazard maps to create the three corresponding flood risk maps. After creating these with the default data, more detailed information, gathered during field work, was added to verify the results of the basic workflow. These first tests of the developed toolbox show promising results. The toolbox allows policy makers in developing countries to perform reliable flood risk assessments and generate the necessary maps

    Survival of single positive thymocytes depends upon developmental control of RIPK1 kinase signaling by the IKK complex independent of NF-κB

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    NF-kappa B(nuclear factor kappa B) signaling is considered critical for single positive (SP) thymocyte development because loss of upstream activators of NF-kappa B, such as the IKK complex, arrests their development. We found that the compound ablation of RelA, cRel, and p50, required for canonical NF-kappa B transcription, had no impact upon thymocyte development. While IKK-deficient thymocytes were acutely sensitive to tumor necrosis factor (TNF)-induced cell death, Rel-deficient cells remained resistant, calling into question the importance of NF-kappa B as the IKK target required for thymocyte survival. Instead, we found that IKK controlled thymocyte survival by repressing cell-death-inducing activity of the serine/threonine kinase RIPK1. We observed that RIPK1 expression was induced during development of SP thymocytes and that IKK was required to prevent RIPK1-kinase-dependent death of SPs in vivo. Finally, we showed that IKK was required to protect Rel-deficient thymocytes from RIPK1-dependent cell death, underscoring the NF-kappa B-independent function of IKK during thymic development