18 research outputs found

    Methylmercury Production in Denitrifying Woodchip Bioreactors

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    Several operational woodchip bioreactors were installed at the outlets of agricultural drainage systems located in east central Illinois. The potential for monomethylmercury (MMHg) production and export in these bioreactors was investigated from summer 2008 to summer 2010. The basic approach was to compare the chemistry of simultaneously-collected bioreactor inlet and outlet water samples in order to assess the extent of nitrate depletion, consumption of sulfate, and production of MMHg, plus other low-charge mercury species (LCHg). In making such a comparison, we implicitly assume that the reactor is near steady state, which is a reasonable approximation given hydraulic residence times on the order of hours. All mercury (Hg) speciation measurements were made using a first-generation mercury thiourea complex ion chromatography system for Hg speciation analysis, which reliably separates MMHg and HgII (mercuric mercury), but combines MMHg and a newly-discovered, unidentified Hg species of low charge (LCHg). Due to this analytical artifact, the results reported here constitute an upper bound on true Hg methylation. In no season was MMHg ever detected in inlet samples at concentrations at much above the detection limit of ~0.1 ng/L. However, levels of MMHg+LCHg over 2 ng/L were observed in the outlets during warm seasons when nitrate had become depleted within the bioreactor. Sulfate depletion was also observed in most samples with elevated [MMHg+LCHg]. The combination of sulfate depletion and MMHg production is consistent with nitrate inhibition of iron and sulfate reduction and with MMHg concentrations observed in other highly anaerobic environments, e.g., lake hypolimnia and wetland porewaters. The maximum [MMHg+LCHg] observed in any given bioreactor followed an inverse function of the bioreactor loading density, i.e., the ratio of the area drained to the area of the bioreactor pit. The function has a form similar to that observed for bioreactor denitrification efficacy and suggests that optimal bioreactor designs that permit substantial denitrification while minimizing Hg methylation are feasible. Finally, extremely high MMHg+LCHg levels were observed when stagnant water conditions occurred within the bioreactors. Thus, it is recommended that bioreactors not be built with bottom depresssional areas where stagnant water can reside, in order to avoid developing anoxic conditions where methylation occurs. For the same reasons, bioreactors should not be used simultaneously with controlled drainage (water table management) if restricting the drainage results in keeping the bioreactors flooded for long periods of time.Illinois Sustainable Technology Center (Grant No. HWR09215)Ope

    Comparison of NEXRAD-Based and Observed Rainfall Data and TOPMODEL Simulations, McTier Creek Watershed, South Carolina

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    2012 S.C. Water Resources Conference - Exploring Opportunities for Collaborative Water Research, Policy and Managemen

    5-Lipoxygenase Metabolic Contributions to NSAID-Induced Organ Toxicity

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    Discovery and functional prioritization of Parkinson's disease candidate genes from large-scale whole exome sequencing.

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    BACKGROUND: Whole-exome sequencing (WES) has been successful in identifying genes that cause familial Parkinson's disease (PD). However, until now this approach has not been deployed to study large cohorts of unrelated participants. To discover rare PD susceptibility variants, we performed WES in 1148 unrelated cases and 503 control participants. Candidate genes were subsequently validated for functions relevant to PD based on parallel RNA-interference (RNAi) screens in human cell culture and Drosophila and C. elegans models. RESULTS: Assuming autosomal recessive inheritance, we identify 27 genes that have homozygous or compound heterozygous loss-of-function variants in PD cases. Definitive replication and confirmation of these findings were hindered by potential heterogeneity and by the rarity of the implicated alleles. We therefore looked for potential genetic interactions with established PD mechanisms. Following RNAi-mediated knockdown, 15 of the genes modulated mitochondrial dynamics in human neuronal cultures and four candidates enhanced α-synuclein-induced neurodegeneration in Drosophila. Based on complementary analyses in independent human datasets, five functionally validated genes-GPATCH2L, UHRF1BP1L, PTPRH, ARSB, and VPS13C-also showed evidence consistent with genetic replication. CONCLUSIONS: By integrating human genetic and functional evidence, we identify several PD susceptibility gene candidates for further investigation. Our approach highlights a powerful experimental strategy with broad applicability for future studies of disorders with complex genetic etiologies
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