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Khanna, Jaya; Medvigy, David; Fueglistaler, Stephan; Walko, Robert
Abstract:
More than 20% Amazon rainforest has been cleared in the past three decades triggering important hydroclimatic changes. Small-scale (~few kilometers) deforestation in the 1980s has caused thermally-triggered atmospheric circulations that increase regional cloudiness and precipitation frequency. However, these circulations are predicted to diminish as deforestation increases. Here we use multi-decadal satellite records and numerical model simulations to show a regime shift in the regional hydroclimate accompanying increasing deforestation in Rondônia, Brazil. Compared to the 1980s, present-day deforested areas in downwind western Rondônia are found to be wetter than upwind eastern deforested areas during the local dry season. The resultant precipitation change in the two regions is approximately ±25% of the deforested area mean. Meso-resolution simulations robustly reproduce this transition when forced with increasing deforestation alone, showing a negligible role of large-scale climate variability. Furthermore, deforestation-induced surface roughness reduction is found to play an essential role in the present-day dry season hydroclimate. Our study illustrates the strong scale-sensitivity of the climatic response to Amazonian deforestation and suggests that deforestation is sufficiently advanced to have caused a shift from a thermally- to a dynamically-driven hydroclimatic regime.
The dataset contains the model file for the Global Adjoint Tomography Model 25 (GLAD-M25). The model file contains parameters defined on the spectral-element mesh and is recommend to be used in SPECFEM3D GLOBE for seismic wave simulation at the global scale.
Kim, Donghoon; Duffy, Thomas S.; Smith, Raymond F.; Ocampo, Ian K.; Coppari, Federica; Marshall, Michelle C.; Ginnane, Mary Kate; Wicks, June; Tracy, Sally J.; Millot, Marius; Lazicki, Amy; Rygg, Jame R.; Eggert, Jon H.
Chronic hepatitis B (CHB), caused by hepatitis B virus (HBV), remains a major medical problem. HBV has a high propensity for progressing to chronicity and can result in severe liver disease, including fibrosis, cirrhosis and hepatocellular carcinoma. CHB patients frequently present with viral coinfection, including HIV and hepatitis delta virus. About 10% of chronic HIV carriers are also persistently infected with HBV which can result in more exacerbated liver disease. Mechanistic studies of HBV-induced immune responses and pathogenesis, which could be significantly influenced by HIV infection, have been hampered by the scarcity of immunocompetent animal models. Here, we demonstrate that humanized mice dually engrafted with components of a human immune system and a human liver supported HBV infection, which was partially controlled by human immune cells, as evidenced by lower levels of serum viremia and HBV replication intermediates in the liver. HBV infection resulted in priming and expansion of human HLA-restricted CD8+ T cells, which acquired an activated phenotype. Notably, our dually humanized mice support persistent coinfections with HBV and HIV which opens opportunities for analyzing immune dysregulation during HBV and HIV coinfection and preclinical testing of novel immunotherapeutics.
