The catalytic oxidation of toluene to CO2 and H2O over nanoflower spinel CoMn2O4 synthesized by the oxalic acid sol–gel method has been investigated, and it demonstrates lower activation energy (35.5 kJ/mol) for toluene oxidation compared with that using the metal oxides (Co3O4, MnO x , and Co3O4/MnO x ), which shows nearly 100% conversion of toluene at 220 °C in the presence or absence of water vapor (2.0 vol %). Compared with the metal oxides (Co3O4/MnO x , MnO x , and Co3O4), the obtained spinel CoMn2O4 has a larger surface area, rich cationic vacancy, and high mobility of oxygen species, which are the reasons for its high activity for toluene oxidation. The different oxygen species shows the different role in VOCs oxidation, and the in situ designed-TP techniques are conducted to investigate the involvement of surface lattice oxygen, bulk lattice oxygen, and gaseous oxygen in catalytic oxidation of toluene over the spinel CoMn2O4 and Co3O4/MnO x catalysts. For spinel CoMn2O4, the surface lattice oxygen is the reactive oxygen species, which first induces the catalytic reaction. Furthermore, the gaseous oxygen moves to the bulk phase lattice and then migrates to the surface to form the surface lattice oxygen, which is different from the mixed-metal oxides Co3O4/MnO x that dissociates and activates gaseous oxygen only on the surface of the catalyst and requires a higher temperature. In addition, it is found that the toluene oxidation occurs via the benzyl alcohol–benzoate–anhydride–acetate reaction pathway over spinel CoMn2O4, and the conversion of the surface anhydride is the rate-controlling step, especially at 200–210 °C, which is also different from the mixed-metal oxides Co3O4/MnO x . These results could provide a considerable experimental basis for understanding the mechanism by which oxygen species participate in toluene oxidation.

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BackgroundLipocalin-2 (LCN2) is an indicator of the severity of lupus nephritis (LN) and plays a pivotal role in immune responses, but it is not known if its effect on LN pathogenesis derives from regulating the immune imbalance of T lymphocyte subsets.MethodsThe expression of LCN2 in T cells and kidneys was assessed in renal biopsies from patients with LN. We investigated the relationship between LCN2 levels and development of LN and systemic illness by injecting anti-LCN2 antibodies into MRL/lpr mice and analyzing pristane-treated LCN2−/− mice.ResultsLCN2 is highly expressed in CD4+ T cells and in renal tissues, and is associated with severe renal damage in patients with LN and in mice with experimental lupus. LCN2 promotes IFN-γ overexpression in CD4+ T cells through the IL-12/STAT4 pathway in an autocrine or paracrine manner. Both neutralization of LCN2 in MRL/lpr mice and genetic depletion of LCN2 in pristane-induced lupus mice greatly ameliorate nephritis. The frequency and number of splenic and renal Th1 cells decrease in proportion to LN disease activity. Conversely, administration of LCN2 exacerbates the disease with significantly higher renal activity scores and increased numbers of Th1 cells.ConclusionsLCN2 plays a crucial role in Th1 cell differentiation, and may present a potential therapeutic target for LN.

To gain a deep understanding of yeast-cell response to heat stress, multiple laboratory strains have been intensively studied via genome-wide expression analysis for the mechanistic dissection of classical heat-shock response (HSR). However, robust industrial strains of Saccharomyces cerevisiae have hardly been explored in global analysis for elucidation of the mechanism of thermotolerant response (TR) during fermentation. Herein, we employed data-independent acquisition and sequential window acquisition of all theoretical mass spectra based proteomic workflows to characterize proteome remodeling of an industrial strain, ScY01, responding to prolonged thermal stress or transient heat shock. By comparing the proteomic signatures of ScY01 in TR versus HSR as well as the HSR of the industrial strain versus a laboratory strain, our study revealed disparate response mechanisms of ScY01 during thermotolerant growth or under heat shock. In addition, through proteomics data-mining for decoding transcription factor interaction networks followed by validation experiments, we uncovered the functions of two novel transcription factors, Mig1 and Srb2, in enhancing the thermotolerance of the industrial strain. This study has demonstrated that accurate and high-throughput quantitative proteomics not only provides new insights into the molecular basis for complex microbial phenotypes but also pinpoints upstream regulators that can be targeted for improving the desired traits of industrial microorganisms.