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Arctic tundra landscapes are composed of a complex mosaic of patterned ground features, varying in soil moisture, vegetation composition, and surface hydrology over small spatial scales (10-100 m). The importance of microtopography and associated geomorphic landforms in influencing ecosystem structure and function is well founded, however, spatial data products describing local to regional scale distribution of patterned ground or polygonal tundra geomorphology are largely unavailable. Thus, our understanding of local impacts on regional scale processes (e.g., carbon dynamics) may be limited. We produced two key spatiotemporal datasets spanning the Arctic Coastal Plain of northern Alaska (similar to 60,000 km(2)) to evaluate climate-geomorphological controls on arctic tundra productivity change, using (1) a novel 30m classification of polygonal tundra geomorphology and (2) decadal-trends in surface greenness using the Landsat archive (1999-2014). These datasets can be easily integrated and adapted in an array of local to regional applications such as (1) upscaling plot-level measurements (e.g., carbon/energy fluxes), (2) mapping of soils, vegetation, or permafrost, and/or (3) initializing ecosystem biogeochemistry, hydrology, and/or habitat modeling.
In a subset of patients, non-alcoholic fatty liver disease (NAFLD) is complicated by cell death and inflammation resulting in non-alcoholic steatohepatitis (NASH), which may progress to fibrosis and subsequent organ failure. Apart from cytokines, prostaglandins, in particular prostaglandin E-2 (PGE(2)), play a pivotal role during inflammatory processes. Expression of the key enzymes of PGE(2) synthesis, cyclooxygenase 2 and microsomal PGE synthase 1 (mPGES-1), was increased in human NASH livers in comparison to controls and correlated with the NASH activity score. Both enzymes were also induced in NASH-diet-fed wild-type mice, resulting in an increase in hepatic PGE(2) concentration that was completely abrogated in mPGES-1-deficient mice. PGE(2) is known to inhibit TNF-alpha synthesis in macrophages. A strong infiltration of monocyte-derived macrophages was observed in NASH-diet-fed mice, which was accompanied with an increase in hepatic TNF-alpha expression. Due to the impaired PGE(2) production, TNF-alpha expression increased much more in livers of mPGES-1-deficient mice or in the peritoneal macrophages of these mice. The increased levels of TNF-alpha resulted in an enhanced IL-1 beta production, primarily in hepatocytes, and augmented hepatocyte apoptosis. In conclusion, attenuation of PGE(2) production by mPGES-1 ablation enhanced the TNF-alpha-triggered inflammatory response and hepatocyte apoptosis in diet-induced NASH.