RESUMEN
Contact Electro-Catalysis (CEC) using commercial dielectric materials in contact-separation cycles with water triggers interfacial electron transfer, generating reactive oxygen species (ROS). However, the hydrophobicity of these materials limits reaction sites, and the generated ROS often combine to form hydrogen peroxide (H2O2), which does not decompose further, leading to suboptimal rates. Addressing H2O2 generation and activation is crucial for advancing CEC. Here, we synthesized a catalyst by loading polytetrafluoroethylene (PTFE) onto ZSM-5 (PZ), achieving uniform dispersion in water. Introducing an FeIII-initiated self-cycling Fenton system (SF-CEC), with synergistic O2 activation and FeIII-activated H2O2, enhanced ROS generation. This system enabled nearly 99% degradation of azo dyes within 10 minutes, a sixfold improvement over traditional CEC. It represents the fastest ultrasound-induced degradation rate of methyl orange dye to date. Without extra oxidants, it also achieved stable dissolution of precious metals in weakly acidic solutions at room temperature, with 80% gold dissolution within 2 hours-2.5 times faster than similar systems. This study corrects the perception of CEC under acidic conditions, offering new insights for dye degradation and precious metal recovery.
RESUMEN
The prevalence of insomnia has increased in recent years, significantly affecting the lives of many individuals. Coronavirus disease 2019 (COVID-19) infection has been found to have a substantial impact on the human gut microbiota (GM). Clinical studies have shown that the high prevalence, prolonged duration, and refractory treatment of insomnia symptoms following the COVID-19 pandemic may be related to the effect of COVID-19 infection on the GM. Therefore, the GM may be a potential target for the treatment of insomnia following COVID-19 infection. However, relevant studies have not been well-documented, and the GM has not been sufficiently analyzed in the context of insomnia treatment. Herein, we review the interaction between sleep and the GM, summarize the characteristics of COVID-19-induced abnormal changes in the GM and metabolites in patients with insomnia, and discuss potential mechanisms, including metabolic, immune, and neural pathways, by which these abnormal changes in the GM cause insomnia as well as the factors affecting the GM. Finally, we discuss the prospect of modulating the host GM community for the effective treatment of insomnia after COVID-19 infection and the need for further clinical studies.