Reduced emissions from deforestation and forest degradation (REDD): a climate change mitigation strategy on a critical track

<p>Abstract</p> <p>Background</p> <p>Following recent discussions, there is hope that a mechanism for reduction of emissions from deforestation and forest degradation (REDD) will be agreed by the Parties of the UNFCCC at their 15th meeting in Copenhagen in 2009 as an eligible action to prevent climate changes and global warming in post-2012 commitment periods. Countries introducing a REDD-regime in order to generate benefits need to implement sound monitoring and reporting systems and specify the associated uncertainties. The principle of conservativeness addresses the problem of estimation errors and requests the reporting of reliable minimum estimates (RME). Here the potential to generate benefits from applying a REDD-regime is proposed with reference to sampling and non-sampling errors that influence the reliability of estimated activity data and emission factors.</p> <p>Results</p> <p>A framework for calculating carbon benefits by including assessment errors is developed. Theoretical, sample based considerations as well as a simulation study for five selected countries with low to high deforestation and degradation rates show that even small assessment errors (5% and less) may outweigh successful efforts to reduce deforestation and degradation.</p> <p>Conclusion</p> <p>The generation of benefits from REDD is possible only in situations where assessment errors are carefully controlled.</p

Recarbonization of the Humid Tropics

To curb the effects of anthropogenic carbon (C) emissions, it is essential to explore the capacity of natural ecosystems to store and sequester atmospheric C. Tropical humid forests store most of their carbon in their above ground biomass which can be rapidly depleted by extractive industries or rapidly replenished through natural regeneration or reforestation. This rapid exchange of carbon dioxide between the forest and the atmosphere make humid tropical forests one of the most dynamic C pools on Earth. Tropical humid forests act as a store and sink for C, but are also the source of almost all anthropogenic C emissions from the land-use and land-use change. The influence of tropical humid forests also extends far beyond the edges of their canopies, affecting global C cycles, biodiversity, hydrological cycles, and the livelihoods of millions of rural people. These interlinked factors are what make tropical humid forests one of the most compelling actors in the recarbonization of the biosphere. This report presents the current state of knowledge on C stocks and fluxes in humid tropical forests, and investigate management interventions for the recarbonization the humid tropics. The C sequestration potential of seven recarbonization options is explored as well as co- benefits, risks and costs. Finally, relevant policies that could be harnessed to encourage recarbonization in humid tropics are reviewed

Hyperinflammation in chronic granulomatous disease and anti-inflammatory role of the phagocyte NADPH oxidase

Chronic granulomatous disease (CGD) is an immunodeficiency caused by the lack of the superoxide-producing phagocyte nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. However, CGD patients not only suffer from recurrent infections, but also present with inflammatory, non-infectious conditions. Among the latter, granulomas figure prominently, which gave the name to the disease, and colitis, which is frequent and leads to a substantial morbidity. In this paper, we systematically review the inflammatory lesions in different organs of CGD patients and compare them to observations in CGD mouse models. In addition to the more classical inflammatory lesions, CGD patients and their relatives have increased frequency of autoimmune diseases, and CGD mice are arthritis-prone. Possible mechanisms involved in CGD hyperinflammation include decreased degradation of phagocytosed material, redox-dependent termination of proinflammatory mediators and/or signaling, as well as redox-dependent cross-talk between phagocytes and lymphocytes (e.g. defective tryptophan catabolism). As a conclusion from this review, we propose the existence of ROS high and ROS low inflammatory responses, which are triggered as a function of the level of reactive oxygen species and have specific characteristics in terms of physiology and pathophysiology