Aboveground forest biomass varies across continents, ecological zones and successional stages: refined IPCC default values for tropical and subtropical forests

For monitoring and reporting forest carbon stocks and fluxes, many countries in the tropics and subtropics rely on default values of forest aboveground biomass (AGB) from the Intergovernmental Panel on Climate Change (IPCC) guidelines for National Greenhouse Gas (GHG) Inventories. Default IPCC forest AGB values originated from 2006, and are relatively crude estimates of average values per continent and ecological zone. The 2006 default values were based on limited plot data available at the time, methods for their derivation were not fully clear, and no distinction between successional stages was made. As part of the 2019 Refinement to the 2006 IPCC Guidelines for GHG Inventories, we updated the default AGB values for tropical and subtropical forests based on AGB data from >25 000 plots in natural forests and a global AGB map where no plot data were available. We calculated refined AGB default values per continent, ecological zone, and successional stage, and provided a measure of uncertainty. AGB in tropical and subtropical forests varies by an order of magnitude across continents, ecological zones, and successional stage. Our refined default values generally reflect the climatic gradients in the tropics, with more AGB in wetter areas. AGB is generally higher in old-growth than in secondary forests, and higher in older secondary (regrowth >20 years old and degraded/logged forests) than in young secondary forests (⩽20 years old). While refined default values for tropical old-growth forest are largely similar to the previous 2006 default values, the new default values are 4.0–7.7-fold lower for young secondary forests. Thus, the refined values will strongly alter estimated carbon stocks and fluxes, and emphasize the critical importance of old-growth forest conservation. We provide a reproducible approach to facilitate future refinements and encourage targeted efforts to establish permanent plots in areas with data gaps

Huntingtin inhibits caspase-3 activation

Huntington's disease results from a mutation in the HD gene encoding for the protein huntingtin. The function of huntingtin, although beginning to be elucidated, remains largely unclear. To probe the prosurvival function of huntingtin, we modulate levels of wild-type huntingtin in a number of cellular and in vivo models. Huntingtin depletion resulted in caspase-3 activation, and overexpression of huntingtin resulted in caspase-3 inhibition. Additionally, we demonstrate that huntingtin physically interacts with active caspase-3. Interestingly, mutant huntingtin binds active caspase-3 with a lower affinity and lower inhibitory effect on active caspase-3 than does wild-type huntingtin. Although reduction of huntingtin levels resulted in caspase-3 activation in all conditions examined, the cellular response was cell-type specific. Depletion of huntingtin resulted in either overt cell death, or in increased vulnerability to cell death. These data demonstrate that huntingtin inhibits caspase-3 activity, suggesting a mechanism whereby caspase-mediated huntingtin depletion results in a detrimental amplification cascade leading to further caspase-3 activation, resulting in cell dysfunction and cell death

Granulomatose de Wegener Wegener's granulomatosis

A granulomatose de Wegener caracteriza-se por vasculite necrosante granulomatosa que acomete preferencialmente vias aéreas superiores, inferiores e rins. Seu diagnóstico é feito associando-se as manifestações clínicas, radiológicas (multiplos nódulos escavados) e os achados anatomopatológicos e o anticorpo anticitoplasma de neutrófilos positivo. O tratamento com corticosteróides e ciclofosfamida leva a 90% de remissão da doença em 1 ano.<br>Wegener's granulomatosis is characterized by granulomatous necrotizing vasculitis that primarily affects the airways (upper and lower) and the kidneys. The diagnosis is made by analyzing the clinical and radiological manifestations (multiple pulmonary cavitations), together with the pathological findings and results of the test for cytoplasmic-pattern antineutrophil cytoplasmic antibodies. Treatment consists of corticosteroids and cyclophosphamide and leads to remission of the disease within one year in 90% of cases