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The present research article investigates the extraction of aluminum (Al) from an engineered CaO-Al2O3-SiO2 slag by leaching with aqueous HCl under atmospheric pressure conditions. The slag is the by-product of an aluminothermic reduction process to produce metallurgical-grade silicon (Si) in a more sustainable way compared to conventional carbothermic reduction. One major challenge in the acidic leaching of aluminosilicate materials, like the slag treated in this study, is the possibility of SiO2 gel formation during the leaching process. Extensive SiO2 gel formation can make the separation of pregnant leach solution (PLS) from the leached residue impossible. Consequently, any acid leaching of aluminosilicate materials must be optimized for avoidance of these gelation phenomena. The present study first explores the leaching behavior of the calcium aluminosilicate slag in relation to the S/L ratio, with all other hydrometallurgical factors remaining stable (20.2% wt. HCl solution, 80 °C, optimized stirring rate), to determine at which value of this parameter SiO2 gelation occurs. After determining the optimum S/L ratio for this system, an analysis of the behavior of Si in the PLS is presented, and the mechanism of SiO2 gelation is explained based on critical assessment of these results against data provided from the scientific literature. It was found that the value of the pH of the PLS and the concentration of dissolved CaCl2 and AlCl3 are critical factors for the formation of filterable amorphous SiO2. Under the optimum leaching conditions, PLS containing 37 g/L Al was obtained with concurrent avoidance of gelation phenomena. [ABSTRACT FROM AUTHOR]

In this study, microwave-assisted heating is presented as a suitable method to transform the hematite and goethite contained in bauxite residue into magnetite, wüstite, and metallic iron, with a short processing time. The final target was the production of a sinter with strong magnetic properties, allowing the magnetic separation of Fe from the residue. The influence of microwave energy on the sample, the effect of irradiation time, and the carbon/bauxite residue mass ratio (C/BR) were the parameters that have been analyzed to optimize the process. Their optimized combination allowed transforming 79% of the iron present in the sinter into metallic iron. However, hercynite was also formed, and the presence of this mineralogical phase could be considered a possible drawback for its magnetic properties.

Scandium, a valuable element with restricted production sources mainly situated in China and Russia, is typically obtained as a by-product during the production of various materials. As the demand for scandium grows in the expanding aluminum and fuel cell industries, and with significant investments in rare earth mining in the USA and Australia, there is a need to explore alternative recovery sources. This research investigates the recovery of scandium from an acid pregnant leaching solution using ion exchange resins. The pregnant leaching solution was obtained after the leaching of bauxite residue with sulfuric acid. Commercial resins with different functional groups were tested for their performance in scandium extraction. In addition, the co-adsorption of impurities, such as iron and titanium, was studied. The feed solution consisted of 12.7 mg/L Sc and main impurities of 272 mg/L Fe and 33.6 mg/L Ti and was pretreated before the ion exchange process by acidification with sulfuric acid and iron powder addition to suppress silica gel formation and minimize the Fe(III) content in the solution accordingly. Among the tested resins, a D2EHPA-impregnated resin had high selectivity for Sc towards Ti, while a monophosphonic resin was also a promising option since it had a higher capacity for Sc but co-extracted Ti. These findings offer promising opportunities for the recovery of scandium from acid leaching solutions and could contribute to addressing the growing demand for this valuable element. [ABSTRACT FROM AUTHOR]

M1 and M2 macrophage phenotypes, which mediate proinflammatory and antiinflammatory functions, respectively, represent the extremes of immunoregulatory plasticity in the macrophage population. This plasticity can also result in intermediate macrophage states that support a balance between these opposing functions. In sepsis, M1 macrophages can compensate for hyperinflammation by acquiring an M2-like immunosuppressed status that increases the risk of secondary infection and death. The M1 to M2 macrophage reprogramming that develops during LPS tolerance resembles the pathological antiinflammatory response to sepsis. Here, we determined that p21 regulates macrophage reprogramming by shifting the balance between active p65-p50 and inhibitory p50-p50 NF-κB pathways. p21 deficiency reduced the DNA-binding affinity of the p50-p50 homodimer in LPS-primed and -rechallenged macrophages, impairing their ability to attenuate IFN-β production and acquire an M2-like hyporesponsive status. High p21 levels in sepsis patients correlated with low IFN-β expression, and p21 knockdown in human monocytes corroborated its role in IFN-β regulation. The data demonstrate that p21 adjusts the equilibrium between p65-p50 and p50-p50 NF-κB pathways to mediate macrophage plasticity in LPS tolerance. Identifying p21-related pathways involved in monocyte reprogramming may lead to potential targets for sepsis treatment., Introduction Monocytes and macrophages play key functions in defense against pathogens and activation of adaptive immunity, as well as in initiation and resolution of inflammation (1, 2). One extraordinary property [...]

Sepsis is a complex biphasic syndrome characterized by both pro- and anti-inflammatory immune states. Whereas early sepsis mortality is caused by an acute, deleterious pro-inflammatory response, the second sepsis phase is governed by acute immunosuppression, which predisposes patients to long-term risk for life-threatening secondary infections. Despite extensive basic research and clinical trials, there is to date no specific therapy for sepsis, and mortality rates are on the rise. Although IFN-β is one of the most-studied cytokines, its diverse effects are not fully understood. Depending on the disease or type of infection, it can have beneficial or detrimental effects. As IFN-β has been used successfully to treat diverse diseases, emphasis has been placed on understanding the role of IFN-β in sepsis. Analyses of mouse models of septic shock attribute a pro-inflammatory role to IFN-β in sepsis development. As anti-inflammatory treatments in humans with antibodies to TNF-α or IL1-β resulted disappointing, cytokine modulation approaches were discouraged and neutralization of IFN-β has not been pursued for sepsis treatment. In the case of patients with delayed sepsis and immunosuppression, there is a debate as to whether the use of specific cytokines would restore the deactivated immune response. Recent reports show an association of low IFN-β levels with the hyporesponsive state of monocytes from sepsis patients and after endotoxin tolerance induction. These data, discussed here, project a role for IFN-β in restoring monocyte function and reversing immunosuppression, and suggest IFN-β-based additive immunomodulatory therapy. The dichotomy in putative therapeutic approaches, involving reduction or an increase in IFN-β levels, mirrors the contrasting nature of the early hyperinflammatory state and the delayed immunosuppression phase.

During budding, lentiviral particles (LVP) incorporate cell membrane proteins in the viral envelope. We explored the possibility of harnessing this process to generate LVP-expressing membrane proteins of therapeutic interest and studied the potential of these tools to treat different pathologies. Fas-mediated apoptosis is central to the maintenance of T cell homeostasis and prevention of autoimmune processes. We prepared LVP that express murine FasL on their surface. Our data indicate that mFasL-bearing LVP induce caspase 3 and 9 processing, cytochrome C release, and significantly more cell death than control LVP in vitro. This cytotoxicity is blocked by the caspase inhibitor Z-VAD. Analysis of the application of these reagents for the treatment of inflammatory arthritis in vivo suggests that FasL-expressing LVP could be useful for therapy in autoimmune diseases such as rheumatoid arthritis, where there is an excess of Fas-expressing activated T cells in the joint. LVP could be a vehicle not only for mFasL but also for other membrane-bound proteins that maintain their native conformation and might mediate biological activities.