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Designing a bifunctional catalyst for hydrogen oxidation reaction (HOR) and hydrogen evolution reaction (HER) is significant toward developing sustainable hydrogen-electric conversion systems. Herein, a cost-effective bifunctional catalyst, Ru/N-doped Carbon@WO 3 -W 2 C (Ru/NC@WOC), was developed via co-precipitation and polyol reduction. Ru/NC@WOC showed superior HOR/HER activity in alkaline solution in comparison with commercial Pt/C. HOR electrochemical tests showed that the mass activity at 0.05 V (1.96 mA mg À 1 Ru ) and exchange-current density were 7.5 and 1.2 times that of Pt/C. Additionality, Ru/NC@WOC exhibited up 30-fold HOR activity in mass activity compared with benchmark Ru/C. Moreover, it also displayed exceptional electrocatalytic HER with overpotentials of 31 mV at 10 mA cm À 2 and 119 mV at 100 mA cm À 2 , surpassing Pt/C, benchmark Ru/C, and most of the previously reported electrocatalysts. The outstanding catalytic activity of Ru/ NC@WOC probably arises from the synergy between Ru and NC@WOC matrix, suitable hydrogen binding energy, and highly conductive substrate. Thus, this work may pave a new avenue to fabricate low-cost bifunctional HOR/HER catalysts for alkaline fuel cells and water electrolyzer.

Diet can not only provide nutrition for intestinal microbiota, it can also remodel them. However, is unclear whether and how diet affects the spread of antibiotic resistance genes (ARGs) in the intestinal microbiota. Therefore, we employed selected high-sugar, high-fat, high-protein, and normal diets to explore the effect. The results showed that high-sugar, high-fat, and high-protein diets promoted the amplification and transfer of exogenous ARGs among intestinal microbiota, and up-regulated the expression of trfAp and trbBp while significantly altered the intestinal microbiota and its metabolites. Inflammation-related products were strongly correlated with the spread of ARGs, suggesting the intestinal microenvironment after diet remodeling might be conducive to the spreading of ARGs. This may be attributed to changes in bacterial membrane permeability, the SOS response, and bacterial composition and diversity caused by diet-induced inflammation. In addition, acceptor bacteria (zygotes) screened by flow cytometry were mostly Proteobacteria, Firmicutes and Actinobacteria , and most were derived from dominant intestinal bacteria remodeled by diet, indicating that the transfer of ARGs was closely linked to diet, and had some selectivity. Metagenomic results showed that the gut resistance genome could be affected not only by diet, but by exogenous antibiotic resistant bacteria (ARB). Many ARG markers coincided with bacterial markers in diet groups. Therefore, dominant bacteria in different diets are important hosts of ARGs in specific dietary environments, but the many pathogenic bacteria present may cause serious harm to human health.

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The gut microbiota represents an important reservoir of antibiotic-resistant bacteria (ARB), which poses a significant threat to public health. However, little is known about the emergence of ARB in the gut after the combined exposure to antibiotics and non-antibiotic pharmaceutics. Here, Escherichia coli , a common opportunistic pathogen in the gut microbiota, was exposed to the antidepressant duloxetine (2.5 µg/L–25 mg/L) and/or chloramphenicol (6 µg/L–4 mg/L). The resistant strains were isolated to determine the minimum inhibition concentration (MIC) of 29 antibiotics. Then, genome-wide DNA sequencing, global transcriptomic sequencing, and real-time quantitative polymerase chain reaction were performed to quantify the synergy between duloxetine and chloramphenicol. Combined exposure synergistically increased the mutation frequency of chloramphenicol resistance by 2.45–9.01 fold compared with the independent exposure. A combination index reaching 187.7 indicated strong duloxetine and chloramphenicol synergy. The resultant mutants presented heritable enhanced resistance to 12 antibiotics and became ARB to eight antibiotics. Furthermore, combined exposure significantly increased the transcriptomic expression of acrA, acrB , and marA in E. coli , and generated a more robust oxidative stress response. Together with the occurrence of DNA mutations in marR in the mutants, stronger triggers to the AcrAB-TolC transport system and the MlaFEDB ABC transporter via reactive oxygen species (ROS)-induced mutagenesis, verified by gene knockout, contributed to the synergistic enhancement of antibiotic resistance in the combined exposure group. Regardless of whether their formation was induced by duloxetine, chloramphenicol, or their combination, the E. coli mutants showed 1.1–1.7-fold increases in the expression levels of acrA, acrB, acrZ, mdtE , and mdtF . This pattern indicated that the mutants shared the same resistance mechanisms against chloramphenicol, involving the improved efflux pumps AcrAB-TolC and mdtEF . Our findings demonstrated that antibiotics and non-antibiotic pharmaceutics synergistically accelerate the evolution of ARB and may enhance their spread.