This study provides a detailed description of the sources, transport, dispersion, and deposition of two major dust events originating from the high‐altitude subtropical Puna‐Altiplano Plateau (15–26°S; 65–69°W) in South America. A long and severe drought provided the right conditions for the onset of both events in July 2009 and 2010. Dust was transported SE and deposited over the Pampas region and was observed to continue to the Atlantic Ocean. Dust monitoring stations located downwind recorded both events, and samples were characterized through chemical and textural analysis. Through a combination of meteorological data and satellite observations (CALIPSO and MODIS detectors), we estimate the emission flux for the 2010 event. This estimate was used to constrain the Hybrid Single Particle Lagrangian Integrated Trajectory (HYSPLIT) transport model and simulate the dust event. Both satellite imagery and model results agree in the location and extension of the dust cloud. CALIPSO detected dust between ~6000 and ~8500 m a.s.l., which remained at this height during most of its trajectory. The dust cloud mixed with a strong convective system in the region, and the associated precipitation brought down significant amounts of dust to the ground. Dust particle size analysis for both events indicates that near the sources dust samples show median modes of 12.4–14.1 µm, similar to modes observed 1300 km away. Chemical composition of sediments from potential dust sources shows distinct signatures within the Puna‐Altiplano Plateau, the Puna sector being clearly different from the Altiplano area. In addition, both sources are markedly different from the Patagonian chemical fingerprint. These results have important implications to improve the interpretation of paleo‐environmental archives preserved on the Argentine loess, Antarctic ice cores, and Southern Ocean marine sediments.
Although an eruption of information on the role of Toll-like receptor 4 (TLR4), the main receptor for bacterial lipopolysaccharide, in activating macrophages and dendritic cells has emerged, very little is known about the role of TLR4 present on epithelial cells from sterile environments like tumors. The main goal of this work was to investigate the consequences of TLR4 activation present on tumor cells in two different animal models of cancer: the Dunning rat prostate cancer and the B16 murine melanoma models. We show that (a) activating TLR4 signaling in two different tumor cell lines in vitro modifies the tumor outgrowth in vivo; (b) this effect is not due to a direct consequence of TLR4 signaling on the proliferation/apoptosis balance of the tumor cells; (c) the T-cell compartment is somehow involved in the described phenomenon because the inhibitory effect observed is not seen in athymic nude mice; and (d) tumor-infiltrating lymphocytes purified from tumors induced by TLR4-activated cells show strong induction of IFN; transcript in detriment of interleukin-10 transcript, suggesting a change in their functionality. We hypothesize that TLR4 signaling in tumor cells in vitro induces the expression of proinflammatory mediators, which could dramatically alter the maturation state of dendritic cells present at the site of inoculation, switching the type of immune response elicited against the tumor. These results open up new avenues for understanding the role of TLR4 in tumor cells and for identifying potential new therapy strategies for cancer.
Lead (Pb) is a developmental neurotoxicant found in industrial activities, many of them already prohibited worldwide. This study aimed to evaluate current blood Pb (PbB) levels in children in Cordoba, Argentina, and to compare these with similar studies performed before Pb was banned in gasoline in 1996. We also sought to identify mechanistically relevant biomarkers by measuring δ-aminolevulinic acid dehydratase (δ-ALAD), superoxide dismutase (SOD), and catalase (CAT) activities. We finally aimed to determine whether sociodemographic characteristics are associated with Pb toxicity. Blood samples collected from 161 healthy children between September 2009 and February 2010 revealed mean PbB levels of 2.58 ± 0.30 µg/dl. Enzymatic δ-ALAD, CAT, and SOD activities showed no significant variations when plotted against PbB levels. Finally, children living in the suburbs have higher PbB levels than their city counterparts, while low socioeconomic status increased δ-ALAD inhibition compared with that of middle-income children. Overall, these results evidenced a substantial reduction in exposure to Pb in this pediatric population over a decade after Pb was restricted in gasoline and reveal the importance of pursuing novel biomarkers of toxicity along with the sociodemographic profile to complement Pb diagnosis.
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