A geospatial GIS-linked spreadsheet model (Nutrient Budget Model—Nova Scotia: NBM-NS) was developed for Nova Scotia to assess the long-term sustainability of forest harvest scenarios as constrained by primary nutrien...
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A geospatial GIS-linked spreadsheet model (Nutrient Budget Model—Nova Scotia: NBM-NS) was developed for Nova Scotia to assess the long-term sustainability of forest harvest scenarios as constrained by primary nutrient inputs and outputs due to atmospheric deposition, soil weathering, and leaching. Harvest scenarios refer to user-defined stand-specific removal rates of bole wood, bark, branches, and foliage, based on current or projected forest inventories. These scenarios are evaluated within the context of existing data layers for current climate (mean annual precipitation and air temperatures), atmospheric deposition (N, S, Ca, Mg, K), and soil/substrate types, supplemented by species-specific look-up tables containing expected biomass fractions and nutrient concentrations. This article introduces this model to assess relative site quality and limiting nutrients for red spruce and sugar maple across Nova Scotia. This is followed by an output comparison involving 25 spruce plantations whereby NBM-NS determinations derived using “default” soil survey data are compared with those derived using plantation-specific soil data. Model output shows that (i) Ca and N are the main growth-limiting nutrients across Nova Scotia, (ii) currently projected plantation yields are generally not sustainable on sites underlain by slowly weathering soils, (iii) current soil base cation contents are generally lower than what is reported in historic soil survey reports, and (iv) model results are expected to vary within the context of changing climate, acid deposition levels, and data accuracy.
His-tRNA synthetase (HARS) is targeted by autoantibodies in chronic and acute inflammatory anti-Jo-1-positive antisynthetase syndrome. The extensive activation and migration of immune cells into lung and muscle are as...
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His-tRNA synthetase (HARS) is targeted by autoantibodies in chronic and acute inflammatory anti-Jo-1-positive antisynthetase syndrome. The extensive activation and migration of immune cells into lung and muscle are associated with interstitial lung disease, myositis, and morbidity. It is unknown whether the sequestration of HARS is an epiphenomenon or plays a causal role in the disease. Here, we show that HARS circulates in healthy individuals, but it is largely undetectable in the serum of anti-Jo-1-positive antisynthetase syndrome patients. In cultured primary human skeletal muscle myoblasts (HSkMC), HARS is released in increasing amounts during their differentiation into myotubes. We further show that HARS regulates immune cell engagement and inhibits CD4+ and CD8+ T-cell activation. In mouse and rodent models of acute inflammatory diseases, HARS administration downregulates immune activation. In contrast, neutralization of extracellular HARS by high-titer antibody responses during tissue injury increases susceptibility to immune attack, similar to what is seen in humans with anti-Jo-1-positive disease. Collectively, these data suggest that extracellular HARS is homeostatic in normal subjects, and its sequestration contributes to the morbidity of the anti-Jo-1-positive antisynthetase syndrome.
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