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Aging and psychosocial stress are associated with increased inflammation and disease risk, but the underlying molecular mechanisms are unclear. Because both aging and stress are also associated with lasting epigenetic changes, a plausible hypothesis is that stress along the lifespan could confer disease risk through epigenetic effects on molecules involved in inflammatory processes. Here, by combining large-scale analyses in human cohorts with experiments in cells, we report that FKBP5, a protein implicated in stress physiology, contributes to these relations. Across independent human cohorts (total n > 3,000), aging synergized with stress-related phenotypes, measured with childhood trauma and major depression questionnaires, to epigenetically up-regulate FKBP5 expression. These age/stress-related epigenetic effects were recapitulated in a cellular model of replicative senescence, whereby we exposed replicating human fibroblasts to stress (glucocorticoid) hormones. Unbiased genome-wide analyses in human blood linked higher FKBP5 mRNA with a proinflammatory profile and altered NF-κB–related gene networks. Accordingly, experiments in immune cells showed that higher FKBP5 promotes inflammation by strengthening the interactions of NF-κB regulatory kinases, whereas opposing FKBP5 either by genetic deletion (CRISPR/Cas9-mediated) or selective pharmacological inhibition prevented the effects on NF-κB. Further, the age/stress-related epigenetic signature enhanced FKBP5 response to NF-κB through a positive feedback loop and was present in individuals with a history of acute myocardial infarction, a disease state linked to peripheral inflammation. These findings suggest that aging/stress-driven FKBP5–NF-κB signaling mediates inflammation, potentially contributing to cardiovascular risk, and may thus point to novel biomarker and treatment possibilities.

Aging and psychosocial stress are associated with increased inflammation and disease risk, but the underlying molecular mechanisms are poorly understood. Because both aging and stress are also associated with lasting epigenetic changes, a plausible hypothesis is that stress exposure along the lifespan could confer disease risk by epigenetically deregulating molecules involved in inflammatory processes. Here, by combining large-scale analyses in human cohorts with mechanistic in vitro investigations, we found that FKBP5, a protein implicated in stress physiology, contributes to these relations. Across independent human cohorts (total n=3,131), aging and stress-related phenotypes were synergistically associated with epigenetic derepression of FKBP5. These age/stress-related epigenetic effects were recapitulated in an in vitro model of replicative senescence, whereby we exposed replicating human fibroblasts to stress (glucocorticoid) hormones. Unbiased genome-wide analyses in human blood linked higher FKBP5 mRNA with a proinflammatory profile and altered NF-kB-related gene networks. Accordingly, experiments in immune cells showed that FKBP5 overexpression promotes inflammation by strengthening the interactions of NF-kB regulatory kinases, whereas opposing FKBP5 either by genetic deletion (CRISPR/Cas9-mediated) or selective pharmacological inhibition prevented the effects on NF-kB. Further, the age/stress-related epigenetic signature enhanced FKBP5 responsivity to NF-kB through a positive feedback loop and was present in individuals with a history of acute myocardial infarction, a disease state linked to peripheral inflammation. These findings suggest that FKBP5-NF-kB signaling mediates inflammation associated with aging and stress, potentially contributing to cardiovascular risk, and may thus point to novel biomarker and treatment possibilities.

Aging and psychosocial stress are associated with increased inflammation and disease risk, but the underlying molecular mechanisms are poorly understood. Because both aging and stress are also associated with lasting epigenetic changes, a plausible hypothesis is that stress exposure along the lifespan could confer disease risk by epigenetically deregulating molecules involved in inflammatory processes. Here, by combining large-scale analyses in human cohorts with mechanistic in vitro investigations, we found that FKBP5, a protein implicated in stress physiology, contributes to these relations. Across independent human cohorts (total n=3,131), aging and stress-related phenotypes were synergistically associated with epigenetic derepression of FKBP5. These age/stress-related epigenetic effects were recapitulated in an in vitro model of replicative senescence, whereby we exposed replicating human fibroblasts to stress (glucocorticoid) hormones. Unbiased genome-wide analyses in human blood linked higher FKBP5 mRNA with a proinflammatory profile and altered NF-κB-related gene networks. Accordingly, experiments in immune cells showed that FKBP5 overexpression promotes inflammation by strengthening the interactions of NF-κB regulatory kinases, whereas opposing FKBP5 either by genetic deletion (CRISPR/Cas9-mediated) or selective pharmacological inhibition prevented the effects on NF-κB. Further, the age/stress-related epigenetic signature enhanced FKBP5 responsivity to NF-κB through a positive feedback loop and was present in individuals with a history of acute myocardial infarction, a disease state linked to peripheral inflammation. These findings suggest that FKBP5-NF-κB signaling mediates inflammation associated with aging and stress, potentially contributing to cardiovascular risk, and may thus point to novel biomarker and treatment possibilities. Diseases of the aging are the leading cause of morbidity and mortality. Elucidating the molecular mechanisms through which modifiable factors, such as psychosocial stress, confer risk for aging-related disease can have profound implications. Here, by combining studies in humans with experiments in cells, we find that aging and stress synergize to epigenetically derepress FKBP5, a protein implicated in stress physiology. Higher FKBP5 promotes inflammation by activating the master immune regulator NF-κB, whereas opposing FKBP5 – either genetically or pharmacologically– prevents the effects on NF-κB. Further, the age/stress-related epigenetic signature of FKBP5 is associated with history of myocardial infarction, a disease state linked to inflammation. These findings provide molecular insights into stress-related disease and may point to novel biomarker and treatment possibilities.

Cerrado is the second largest biome in South America and accounted for the second largest contribution to carbon emissions in Brazil for the last 10 years, mainly due to land-use changes. It comprises approximately 2 million km2 and is divided into 22 ecoregions, based on environmental conditions and vegetation. The most dominant vegetation type is cerrado sensu stricto (cerrado ss), a savanna woodland. Quantifying variation of biomass density of this vegetation is crucial for climate change mitigation policies. Integrating remote sensing data with adequate allometric equations and field-based data sets can provide large-scale estimates of biomass. We developed individual-tree aboveground biomass (AGB) allometric models to compare different regression techniques and explanatory variables. We applied the model with the strongest fit to a comprehensive ground-based data set (77 sites, 893 plots, and 95,484 trees) to describe AGB density variation of cerrado ss. We also investigated the influence of physiographic and climatological variables on AGB density; this analysis was restricted to 68 sites because eight sites could not be classified into a specific ecoregion, and one site had no soil texture data. In addition, we developed two models to estimate plot AGB density based on plot basal area. Our data show that for individual-tree AGB models a) log-log linear models provided better estimates than nonlinear power models; b) including species as a random effect improved model fit; c) diameter at 30 cm above ground was a reliable predictor for individual-tree AGB, and although height significantly improved model fit, species wood density did not. Mean tree AGB density in cerrado ss was 22.9 tons ha-1 (95% confidence interval = ± 2.2) and varied widely between ecoregions (8.8 to 42.2 tons ha-1), within ecoregions (e.g. 4.8 to 39.5 tons ha-1), and even within sites (24.3 to 69.9 tons ha-1). Biomass density tended to be higher in sites close to the Amazon. Ecoregion explained 42% of biomass variation between the 68 sites (P < 0.01) and shows strong potential as a parameter for classifying regional biomass variation in the Cerrado.

The tropical savanna in Brazil known as the Cerrado covers circa 23% of the Brazilian territory, but only 3% of this area is protected. High rates of deforestation and degradation in the woodland and forest areas have made the Cerrado the second-largest source of carbon emissions in Brazil. However, data on these emissions are highly uncertain because of the spatial and temporal variability of the aboveground biomass (AGB) in this biome. Remote-sensing data combined with local vegetation inventories provide the means to quantify the AGB at large scales. Here, we quantify the spatial distribution of woody AGB in the Rio Vermelho watershed, located in the centre of the Cerrado, at a high spatial resolution of 30 metres, with a random forest (RF) machine-learning approach. We produced the first high-resolution map of the AGB for a region in the Brazilian Cerrado using a combination of vegetation inventory plots, airborne light detection and ranging (LiDAR) data, and multispectral and radar satellite images (Landsat 8 and ALOS-2/PALSAR-2). A combination of random forest (RF) models and jackknife analyses enabled us to select the best remote-sensing variables to quantify the AGB on a large scale. Overall, the relationship between the ground data from vegetation inventories and remote-sensing variables was strong (R2 = 0.89), with a root-mean-square error (RMSE) of 7.58 Mg ha−1 and a bias of 0.43 Mg ha−1.

Deforestation of riparian areas is a major driver of biodiversity loss in aquatic ecosystems. Thus, we investigated the influence of forest cover and physical and chemical characteristics of streams on zooplankton communities in the southeastern Amazon. We addressed the following questions: (1) Are environmental factors (water physical and chemical characteristics and landscape variables) and dispersive processes (reflected in the spatial structure among sampling sites) efficient predictors of zooplankton communities in different hydrologic seasons? (2) Can zooplankton species be indicators of watersheds’ forest-cover levels? We sampled 15 streams located in nine rural settlements in northern Mato Grosso, Brazil, in the dry (August) and rainy (March) seasons of 2017. The forest-cover level had a significant effect on the physical and chemical characteristics (conductivity, dissolved oxygen, and temperature) of streams and also on the structure and composition of zooplankton communities, mainly of rotifers and testate amoebae. Areas with low vegetation cover had seasonal changes in species richness, individuals density, and zooplankton community structure. Environmental and spatial variables had no significant effect on the structure of zooplankton communities, which may indicate the strong influence of stochastic factors. Species from three zooplankton groups (rotifers, microcrustaceans, and testate amoebae) were indicators of forest-cover classes. This study provided valuable contributions to the conservation of riparian ecosystems and the use of biological indicators in environmental monitoring programs.

Decisions at the end of life pose a serious challenge to criminal law, which supposes the exercise of punitive power by the state in defense of legal rights whose violation is of such magnitude that only a criminal sanction can appropriately address it. Such challenges also exist in light of civil law in considering the autonomy of a patient who is a minor, and the role of parents and/or legal representatives in decision making. Decisions made in relation to the withdrawal or withholding of life-sustaining treatment in pediatrics can be some of the most controversial and morally challenging. These challenges are compounded by fears related to the status of decisions that are considered to be ethically optimal, even though legally questionable.

Romulea rosea (Iridaceae: Crocoideae), a species original of South Africa, is cited for the first time for Chile. The species is described, and therefore Calydorea chilensis M.Muñoz published recently, is reduced to nomenclatural synonym.