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Challenges associated with lithium dendrite growth and the formation of dead lithium significantly limit the achievable energy density of lithium metal batteries (LMBs), particularly under high operating current densities. Our innovative design employs a state-of-the-art 2500 separator featuring a meticulously engineered cellulose acetate (CA) coating (CA@2500) to suppress dendrite nucleation and propagation. The CO functional groups in CA enhances charge transfer kinetics and triggering the decomposition of lithium bis(trifluoromethanesulfonyl)imide (LiTFSI), which leads to the formation of a more robust solid electrolyte interphase (SEI) composed primarily of LiF. Moreover, the introduction of polar functional groups in the CA enhances the separator's hydrophilic properties, facilitating the uniform Li⁺ flux and creating a conductive pathway for efficient lithium migration. As a result, the CA@2500 separator exhibits a high lithium-ion transfer number (0.88) and conductivity. The lithium symmetric cell assembles with the CA@2500 separator displays a stable cycling performance over 5500 h at a current density and capacity of 10 mA cm^-2 and 10 mAh cm^-2, respectively. Additionally, LPF battery with CA@2500 separator shows an excellent capacity retention at 0.2 C with an average decay of 0.055 % per cycle. Moreover, a high capacity of 105 mAh g^-1 is maintained after 500 cycles at 5 C with an average decay of only 0.027 % per cycle. This work achieved high stability of LMBs through simplified engineering.

Designing inexpensive, high-efficiency and durable bifunctional catalysts for urea oxidation reaction (UOR) and hydrogen evolution reaction (HER) is an encouraging tactic to produce hydrogen with reduced energy expenditure. Herein, oxygen vacancy-rich cobalt hydroxide/aluminum oxyhydroxide heterostructure on nickel foam (denoted as Co(OH)₂/AlOOH/NF-100) has been fabricated using one step hydrothermal process. Theoretical calculation and experimental results indicate the electrons transfer from Co(OH)₂ to highly active AlOOH results in the interfacial charge redistribution and optimization of electronic structure. Abundant oxygen vacancies in the heterostructure could improve the conductivity and simultaneously serve as the active sites for catalytic reaction. Consequently, the optimal Co(OH)₂/AlOOH/NF-100 demonstrates excellent electrocatalytic performance for HER (62.9 mV@10 mA cm^-2) and UOR (1.36 V@10 mA cm^-2) due to the synergy between heterointerface and oxygen vacancies. Additionally, the in situ electrochemical impedance spectrum (EIS) for UOR suggests that the heterostructured catalyst exhibits rapid reaction kinetics, mass transfer and current response. Importantly, the urea-assisted electrolysis composed of the Co(OH)₂/AlOOH/NF-100 manifests a low cell voltage (1.48 V @ 10 mA cm^-2) in 1 M KOH containing 0.5 M urea. This work presents a promising avenue to the development of HER/UOR bifunctional electrocatalysts.

Lipids are vital precursors to beef aroma compounds, but the exact lipid molecules influencing aroma generation remain unconfirmed. This study employs gas chromatography-olfactometry-mass spectrometry and absolute quantitative lipidomics to identify beef's aroma and lipid profiles and to examine lipid alterations post-thermal processing. The aim is to understand the role of lipids in aroma generation during beef's raw-to-cooked transition. Eighteen key aroma compounds were identified as significant contributors to the aroma of beef. 265 lipid molecules were quantified accurately, and we found that triglycerides containing C18:1 or C18:2 chains, such as TG(16:0_18:1_18:1), TG(16:0_18:1_18:2), TG(16:0_16:1_18:1), as well as phosphatidylcholine and phosphatidylethanolamine containing PC(16:1e_20:4), PC(16:0e_20:4), PC(18:2e_18:2), and PE(16:1e_20:4), played important roles in the generation of key aroma compounds in beef. C18:1, C18:2, C18:3, and C20:4 were key substrates for the formation of aroma compounds. In addition, lysophosphatidylcholine and lysophosphatidylethanolamine containing unsaturated fatty acid chains may serve as important aroma retainers.

The inhibitory properties and underlying mechanism of chlorine dioxide (ClO₂) fumigation on the pathogen Ceratocystis fimbriata (C. fimbriata) and resultant sweetpotato black rot were investigated in vitro and in vivo. Results revealed that the ClO₂ fumigation effectively inhibited fungal growth and induced obvious morphological variation of C. fimbriata mycelia. Furthermore, the mycelial membrane suffered damage, as evidenced by a significant increase in malondialdehyde content and the leakage of protein and nucleic acid from mycelia cells, accompanied by a marked decrease in ergosterol content. Additionally, ClO₂ fumigation caused spores cell membrane damage, a notable decrease in spore viability, and induced cell apoptosis as indicated by reductions in spore germination rate, two fluorescence staining observations, and flow cytometry analysis. Moreover, the decay diameter of sweetpotato black rot lesions decreased significantly after ClO₂ fumigation, and the growth of C. fimbriata was also inhibited. These findings present a novel and effective technology for inhibiting the progression of sweetpotato black rot.

The accumulation of small doses of hydrogen peroxide (H₂O₂) into food can cause many diseases in the human body, and it is urgent to develop efficient detection methods of H₂O₂. Herein, the hierarchical structure composite of NiCo-LDH nanosheets crosslinked NiMoO₄ nanorods was grown in situ on carbon cloth (NiMoO₄ NRs@NiCo-LDH NSs/CC) by micro-plasma assisted hydrothermal method. Thanks to the synergistic effect of three metals and (NiMoO₄ NRs@NiCo-LDH NSs/CC) provided by nanorods/nanosheets hierarchical structure, NiMoO₄ NRs@NiCo-LDH NSs/CC exposes more active sites and achieves rapid electron transfer. The H₂O₂ electrochemical sensor was constructed as the working electrode with a linear range of 1 μmol L^-1 to 9.0 mmol L^-1 and detection limit of 112 nmol L^-1. In addition, the sensor has been successfully applied to the detection of H₂O₂ in food samples, the recovery rate is 95.2%-106.62%, RSD < 4.89%.

Fermentation enhances the nutritional profile of foods and beverages like beer, wine, and fermented teas. Ginkgo biloba, long utilized for its health-enhancing properties, contains bioactive compounds like terpene trilactones and flavonoids, known for their antioxidant and neuroprotective effects. This study explores the feasibility of using dried Ginkgo biloba leaves in SCOBY-mediated fermentation to produce novel health-promoting beverages similar to kombucha. Infusions of dried Ginkgo biloba leaves with varying sugar concentrations are fermented over 21 days. Results showed that these beverages exhibited potent antioxidant properties, notably higher than tea-kombucha, attributed to increased polyphenol content. HPLC analysis identified significant levels of bioactive compounds such as catechin and apigenin. Sensory evaluation highlighted optimal acceptance of the seven-day fermented product. This research underscores the potential of Ginkgo biloba as a functional ingredient in fermented beverages, offering a healthier alternative to conventional soft drinks.

In this study, the oxidation of egg yolk lipids (EYL) by salt-induced heat and non-heat treatments was investigated for quality and flavor. The correlation between physicochemical properties, lipid oxidation and antioxidant activity was modeled using partial least squares discriminant analysis (PLS-DA). The results indicated that the prolonged salt-induced synergistic heat treatment produced the highest level of lipid oxidation, antioxidant activity and oil exudation, along with the lowest level of polyunsaturated fatty acid content. In addition, higher contents of pyrazines and fewer acid species were detected, which was not the case with the salt-free heat treatment. In total, 14 identical volatile organic compounds (VOCs) were produced, yet their overall flavor profiles determined by the electronic nose would remain dramatically distinguished. Therefore, heat treatment was particularly critical for lipid oxidation and the generation of aromatic compounds, implying that heat-treated EYL induced by salt is a flavor component with good antioxidant potential.

Backgroud: Exercise training is the main strategy for stroke rehabilitation, and it has shown that shifting microglia toward M2 phenotype is beneficial for the recovery of neurological function after stroke. The mechanisms governing exercise training and inflammatory response after cerebral ischemia remain largely unexplored. Herein, the aim of this study was to investigate the role of exercise training in immune response after cerebral ischemia.

Methods: The transient middle cerebral artery occlusion (MCAO) rat model and primary microglia under oxygen-glucose deprivation/reoxygenation (OGD/R) conditions were used to mimic the ischemic stroke in vivo and in vitro respectively. Treadmill exercise with gradually increased intensity was initiated the second day after MCAO for a maximum of 14 days. The beam balance test, forelimb placement test, cornering test, modified adhesive removal test were used to assess the behavioral recovery. The right peri-infarct cortex was taken from 3 rats per group for RNA sequencing (RNA-seq) analysis. Real-time PCR, western blot, immunofluorescence, and phagocytosis assay was performed after MCAO and/or OGD/R.

Results: Treadmill exercise could significantly improve behavioral outcomes and reduce the infarct volumes. In addition, treadmill exercise switched microglia polarization toward M2 phenotype (Iba⁺/CD206⁺) in the peri-infarct cortex, and significantly increased the levels of anti-inflammatory factors (TGF-β, IL10, Arg-1, CD206) and decreased a pool of pro-inflammatory factors (IL-1β, IL-6, TNF-α, iNOS, CD68) in the peri-infarct areas. RNA-seq analysis and further studies demonstrated that exercise training could significantly reduce the expression of MMP12. Through further immunofluorescence co-labeling analysis, we found that treadmill exercise predominantly reduced the expression of MMP-12 in microglia but not in neuron after MCAO. In primary microglia after OGD/R, MMP12 inhibition switched microglia polarization toward to M2 phenotype, increased the expression of M2 markers, and enhanced its phagocytic capacities.

Conclusions: Our data demonstrate that treadmill exercise could improve the inflammatory microenvironment in the brain after ischemic stroke, which may be caused by inhibition of MMP12 expression. MMP12 suppression in primary microglia could remodel microglia immune functions. In summary, this study may provide novel insights into the immune mechanism of exercise training for stroke and suggests potential targets for therapeutic approaches.