Looking beyond forest cover: an analysis of landscape-scale predictors of forest degradation in the Brazilian Amazon.

While forest degradation rates and extent exceed deforestation in the Brazilian Amazon, less attention is given to the factors controlling its spatial distribution. No quantified correlation exists between changes of forest structure due to anthropogenic disturbances and dynamics of land use and cover change occurring at broader spatial levels. This study examines the influence of multi-scale landscape structure factors (i.e. spatial composition, configuration and dynamic of land use/cover) on primary forest's aboveground biomass (AGB), spanning from low to highly degraded, in Paragominas municipality (Pará state). We used random forest models to identify the most important landscape predictors of degradation and clustering methods to analyze their distribution and interactions. We found that 58% of the variance of AGB could be explained by metrics reflecting land use practices and agricultural dynamics around primary forest patches and that their spatial patterns were not randomly distributed. Forest degradation is mainly driven by fragmentation effects resulting from old deforestation and colonization events linked with cropland expansion (e.g. soybean and maize) coupled with high accessibility to market. To a lesser extent, degradation is driven by recent and ongoing (1985?2015) deforestation and fragmentation in slash-and-burn agricultural areas, characterized by heterogeneous mosaics of pastures and fallow lands combined with high use of fire. Our findings highlight the potential of landscape-level framework and remotely sensed land cover data for a thorough understanding of the distribution of forest degradation across human-modified landscapes. Addressing these spatial determinants by looking at agricultural dynamics beyond forest cover is necessary to improve forest management which has major implications for biodiversity, carbon and other ecosystem services

The need for eco-efficient landscapes to prevent irreversible degradation of agroecosystems in deforested Amazonia.

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UAV-based canopy textures assess changes in forest structure from long-term degradation

Degraded tropical forests dominate agricultural frontiers and their management is becoming an urgent priority. This calls for a better understanding of the different forest cover states and cost-efficient techniques to quantify the impact of degradation on forest structure. Canopy texture analyses based on Very High Spatial Resolution (VHSR) optical imagery provide proxies to assess forest structures but the mechanisms linking them with degradation have rarely been investigated. To address this gap, we used a lightweight Unmanned Aerial Vehicle (UAV) to map 739 ha of degraded forests and acquire both canopy VHSR images and height model. Thirty-three years of degradation history from Landsat archives allowed us to sample 40 plots in undisturbed, logged, over-logged and burned and regrowth forests in tropical forested landscapes (Paragominas, Para, Brazil). Fourier (FOTO) and lacunarity textures were used to assess forest canopy structure and to build a typology linking degradation history and current states. Texture metrics capture canopy grain, heterogeneity and openness gradients and correlate with forest structure variability (R2 = 0.58). Similar structures share common degradation history and can be discriminated on the basis of canopy texture alone (accuracy = 55%). Over-logging causes a lowering in forest height, which brings homogeneous textures and of finer grain. We identified the major changes in structures due to fire following logging which changes heterogeneous and intermediate grain into coarse textures. Our findings highlight the potential of canopy texture metrics to characterize degraded forests and thus be used as indicators for forest management and degradation mitigation. Inexpensive and agile UAV open promising perspectives at the interface between field inventory and satellite characterization of forest structure using texture metrics

Impact of different land management on soil spiders (Arachnida : Araneae) in two Amazonian areas of Brazil and Colombia

The global demand for different land-use practice commodities in the Amazonia is growing, and this region is increasingly affected by the impacts of land management. The aim of this study was to evaluate the influence of land-use intensification on soil spider assemblages from six different land-use systems in Colombia and Brazil. The systems were fallows after crops and pastures, forest, crops, pastures and plantations. Spider species richness and density decreased with increasing farming management intensity. A principal component analysis (PCA) showed forests and fallows were separated from systems with stronger anthropogenic soil disturbance. The relationships of ten spider guilds differed significantly between land-uses, suggesting that they can be a reliable parameter for studies of ecological indicators

Tenascin-C increases lung metastasis by impacting blood vessel invasions

Metastasis is a major cause of death in cancer patients. The extracellular matrix molecule tenascin-C is a known promoter of metastasis, however the underlying mechanisms are not well understood. To further analyze the impact of tenascin-C on cancer progression we generated MMTV-NeuNT mice that develop spontaneous mammary tumors, on a tenascin-C knockout background. We also developed a syngeneic orthotopic model in which tumor cells derived from a MMTV-NeuNT tumor. Tumor cells were transfected with control shRNA or with shRNA to knockdown tenascin-C expression and, were grafted into the mammary gland of immune competent, wildtype or tenascin-C knockout mice. We show that stromal-derived tenascin-C increases metastasis by reducing apoptosis and inducing the cellular plasticity of cancer cells located in pulmonary blood vessels invasions (BVI), before extravasation. We characterized BVI as organized structures of tightly packed aggregates of proliferating tumor cells with epithelial characteristics, surrounded by Fsp1+ cells, internally located platelets and, a luminal monolayer of endothelial cells. We found extracellular matrix, in particular, tenascin-C, between the stromal cells and the tumor cell cluster. In mice lacking stromal-derived tenascin-C, the organization of pulmonary BVI was significantly affected, revealing novel functions of host-derived tenascin-C in supporting the integrity of the endothelial cell coat, increasing platelet abundance, tumor cell survival, epithelial plasticity, thereby promoting overall lung metastasis. Many effects of tenascin-C observed in BVI including enhancement of cellular plasticity, survival and migration, could be explained by activation of TGF-β signaling. Finally, in several human cancers, we also observed BVI to be surrounded by an endothelial monolayer and to express tenascin-C. Expression of tenascin-C is specific to BVI and is not observed in lymphatic vascular invasions frequent in breast cancer, which lack an endothelial lining. Given that BVI have prognostic significance for many tumor types, such as shorter cancer patient survival, increased metastasis, vessel occlusion, and organ failure, our data revealing a novel mechanism by which stromal tenascin-C promotes metastasis in human cancer, may have potential for diagnosis and therapy

Tenascin-C increases lung metastasis by impacting blood vessel invasions

Metastasis is a major cause of death in cancer patients. The extracellular matrix molecule tenascin-C is a known promoter of metastasis, however the underlying mechanisms are not well understood. To further analyze the impact of tenascin-C on cancer progression we generated MMTV-NeuNT mice that develop spontaneous mammary tumors, on a tenascin-C knockout background. We also developed a syngeneic orthotopic model in which tumor cells derived from a MMTV-NeuNT tumor. Tumor cells were transfected with control shRNA or with shRNA to knockdown tenascin-C expression and, were grafted into the mammary gland of immune competent, wildtype or tenascin-C knockout mice. We show that stromal-derived tenascin-C increases metastasis by reducing apoptosis and inducing the cellular plasticity of cancer cells located in pulmonary blood vessels invasions (BVI), before extravasation. We characterized BVI as organized structures of tightly packed aggregates of proliferating tumor cells with epithelial characteristics, surrounded by Fsp1+ cells, internally located platelets and, a luminal monolayer of endothelial cells. We found extracellular matrix, in particular, tenascin-C, between the stromal cells and the tumor cell cluster. In mice lacking stromal-derived tenascin-C, the organization of pulmonary BVI was significantly affected, revealing novel functions of host-derived tenascin-C in supporting the integrity of the endothelial cell coat, increasing platelet abundance, tumor cell survival, epithelial plasticity, thereby promoting overall lung metastasis. Many effects of tenascin-C observed in BVI including enhancement of cellular plasticity, survival and migration, could be explained by activation of TGF-β signaling. Finally, in several human cancers, we also observed BVI to be surrounded by an endothelial monolayer and to express tenascin-C. Expression of tenascin-C is specific to BVI and is not observed in lymphatic vascular invasions frequent in breast cancer, which lack an endothelial lining. Given that BVI have prognostic significance for many tumor types, such as shorter cancer patient survival, increased metastasis, vessel occlusion, and organ failure, our data revealing a novel mechanism by which stromal tenascin-C promotes metastasis in human cancer, may have potential for diagnosis and therapy