21 research outputs found

    Low-temperature methanation of fermentation gas with Ni-based catalysts in a multicomponent system

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    Abstract A large amount of greenhouse gases, such as carbon dioxide and methane, are released during the production process of bioethanol and biogas. Converting CO2 into methane is a promising way of capturing CO2 and generating high-value gas. At present, CO2 methanation technology is still in the early stage. It requires high temperature (300ā€“400Ā ā„ƒ) and pressure (>ā€‰1Ā MPa), leading to high cost and energy consumption. In this study, a new catalyst, Niā€“Fe/Alā€“Ti, was developed. Compared with the activity of the common Ni/Al2O3 catalyst, that of the new catalyst was increased by 1/3, and its activation temperature was reduced by 100ā„ƒ. The selectivity of methane was increased to 99%. In the experiment using simulated fermentation gas, the catalyst showed good catalytic activity and durability at a low temperature and atmospheric pressure. Based on the characterization of catalysts and the study of reaction mechanisms, this article innovatively proposed a Niā€“Fe/Alā€“Ti quaternary catalytic system. Catalytic process was realized through the synergism of Alā€“Ti composite support and Niā€“Fe promotion. The oxygen vacancies on the surface of the composite carrier and the higher activity metals and alloys promoted by Fe accelerate the capture and reduction of CO2. Compared with the existing catalysts, the new Niā€“Fe/Alā€“Ti catalyst can significantly improve the methanation efficiency and has great practical application potential

    IL-30 protects against sepsis-induced myocardial dysfunction by inhibiting pro-inflammatory macrophage polarization and pyroptosis

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    Summary: Cardiac dysfunction is a well-recognized complication of sepsis and seriously affects the prognosis of sepsis patients. IL-30 has been reported to exert anti-inflammatory effects in various diseases. However, the role of IL-30 in sepsis-induced myocardial dysfunction (SIMD) remains unclear. Here, we explored the protective role of IL-30 in cecum ligation and puncture (CLP)-induced SIMD mice. IL-30 expression increased in the cardiac tissues of septic mice and was mainly derived from macrophages. IL-30 deletion or neutralization aggravated sepsis-induced cardiac dysfunction and injury, whereas recombinant IL-30 treatment significantly ameliorated it. Mechanistically, IL-30 deficiency exerts pro-inflammatory effects by promoting Ly6Chigh macrophage polarization and pyroptosis. Inhibiting NLRP3 with MCC950 significantly reversed cardiac dysfunction, macrophage polarization and pyroptosis aggravated by IL-30 deficiency. Recombinant IL-30 inhibited pro-inflammatory macrophage polarization and pyroptosis inĀ vivo and vitro. Taken together, these results suggest that IL-30 protects against SIMD by inhibiting pro-inflammatory macrophage polarization and pyroptosis
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