Sludge-derived iron-carbon material enhancing the removal of refractory organics in landfill leachate: Characteristics optimization, removal mechanism, and molecular-level investigation.

Mature landfill leachate is a refractory organic wastewater, and needs physical and chemical pretreatments contemporaneously, e.g. iron-carbon micro-electrolysis (IC-ME). In this study, a novel iron-carbon (Fe-C) material was synthesized from waste activated sludge to be utilized in IC-ME for landfill leachate treatment. The pyrolysis temperature, mass ratio of iron to carbon, and solid-liquid ratio in leachate treatment were optimized as 900 °C with 1.59 and 34.7 g/L. Under these optimal conditions, the chemical oxygen demand (COD) removal efficiency reached 79.44 %, which was 2.6 times higher than that of commercial Fe-C material (30.1%). This excellent COD removal performance was indicated to a better mesoporous structure, and uniform distribution of zero-valent iron in novel Fe-C material derived from sludge. The contribution order of COD removal in IC-ME treatment for landfill leachate was proven as coagulation, adsorption, and redox effects by a contrast experiment. The removal of COD includes synthetic organic compounds, e.g. carcinogens, pharmaceuticals and personal care products. The contents of CHO, CHON, and CHOS compounds of dissolved organic matter (DOM) in the leachate were decreased, and both the molecular weight and unsaturation of lipids, lignin, and tannic acids concentration were also reduced. Some newly generated small molecular DOM in the treated leachate further confirmed the existence of the redox effect to degrade DOM in leachate. The total cost of sludge-derived Fe-C material was only USD$ 152.8/t, which could save 76% of total compared with that of commercial Fe-C materials. This study expands the prominent source of Fe-C materials with excellent performance, and deepens the understanding of its application for leachate treatment.

Hyperactivation of the NLRP3 Inflammasome in Myeloid Cells Leads to Severe Organ Damage in Experimental Lupus.

Systemic lupus erythematosus (SLE) is an autoimmune syndrome associated with severe organ damage resulting from the activation of immune cells. Recently, a role for caspase-1 in murine lupus was described, indicating an involvement of inflammasomes in the development of SLE. Among multiple inflammasomes identified, the NLRP3 inflammasome was connected to diverse diseases, including autoimmune encephalomyelitis. However, the function of NLRP3 in SLE development remains elusive. In this study, we explored the role of NLRP3 in the development of SLE using the pristane-induced experimental lupus model. It was discovered that more severe lupus-like syndrome developed in Nlrp3-R258W mice carrying the gain-of-function mutation. Nlrp3-R258W mutant mice exhibited significantly higher mortality upon pristane challenge. Moreover, prominent hypercellularity and interstitial nephritis were evident in the glomeruli of Nlrp3-R258W mice. In addition, hyperactivation of the NLRP3 inflammasome in this mouse line resulted in proteinuria and mesangial destruction. Importantly, all of these phenotypes were largely attributed to the Nlrp3-R258W mutation expressed in myeloid cells, because Cre recombinase-mediated depletion of this mutant from such cells rescued mice from experimental lupus. Taken together, our study demonstrates a critical role for NLRP3 in the development of SLE and suggests that modulating the inflammasome signal may help to control the inflammatory damage in autoimmune diseases, including lupus.