27 research outputs found

    A conceptual governance framework for climate change adaptation and disaster risk reduction integration

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    Climate change adaptation (CCA) and disaster risk reduction (DRR) have similar targets and goals in relation to climate change and related risks. The integration of CCA in core DRR operations is crucial to provide simultaneous benefits for social systems coping with challenges posed by climate extremes and climate change. Although state actors are generally responsible for governing a public issue such as CCA and DRR integration, the reform of top-down governing modes in neoliberal societies has enlarged the range of potential actors to include non state actors from economic and social communities. These new intervening actors require in-depth investigation. To achieve this goal, the article investigates the set of actors and their bridging arrangements that create and shape governance in CCA and DRR integration. The article conducts a comprehensive literature review in order to retrieve main actors and arrangements. The article summarizes actors and arrangements into a conceptual governance framework that can be used as a backdrop for future research on the topic. However, this framework has an explorative form, which must be refined according to site- and context-specific variables, norms, or networks. Accordingly, this article promotes an initial application of the framework to different contexts. Scholars may adopt the framework as a roadmap with which to corroborate the existence of a theoretical and empirical body of knowledge on governance of CCA and DRR integration

    Interleukin-2 gene variation impairs regulatory T cell function and causes autoimmunity.

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    Autoimmune diseases are thought to result from imbalances in normal immune physiology and regulation. Here, we show that autoimmune disease susceptibility and resistance alleles on mouse chromosome 3 (Idd3) correlate with differential expression of the key immunoregulatory cytokine interleukin-2 (IL-2). In order to test directly that an approximately twofold reduction in IL-2 underpins the Idd3-linked destabilization of immune homeostasis, we show that engineered haplodeficiency of Il2 gene expression not only reduces T cell IL-2 production by twofold but also mimics the autoimmune dysregulatory effects of the naturally occurring susceptibility alleles of Il2. Reduced IL-2 production achieved by either genetic mechanism correlates with reduced function of CD4(+) CD25(+) regulatory T cells, which are critical for maintaining immune homeostasis
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