RESUMEN
The direct hydrogenation of greenhouse gas CO2 to higher alcohols (C2+OH) provides a new route for the production of high-value chemicals. Due to the difficulty of C-C coupling, the formation of higher alcohols is more difficult compared to that of other compounds. In this review, we summarize recent advances in the development of multifunctional catalysts, including noble metal catalysts, Co-based catalysts, Cu-based catalysts, Fe-based catalysts, and tandem catalysts for the direct hydrogenation of CO2 to higher alcohols. Possible reaction mechanisms are discussed based on the structure-activity relationship of the catalysts. The reaction-coupling strategy holds great potential to regulate the reaction network. The effects of the reaction conditions on CO2 hydrogenation are also analyzed. Finally, we discuss the challenges and potential opportunities for the further development of direct CO2 hydrogenation to higher alcohols.
RESUMEN
Viral myocarditis (VMC), commonly caused by coxsackievirus B3 (CVB3) infection, lacks specific treatments and leads to serious heart conditions. Current treatments, such as IFNα and ribavirin, show limited effectiveness. Herein, rather than inhibiting virus replication, this study introduces a novel cardiomyocyte sponge, intracellular gelated cardiomyocytes (GCs), to trap and neutralize CVB3 via a receptor-ligand interaction, such as CAR and CD55. By maintaining cellular morphology, GCs serve as sponges for CVB3, inhibiting infection. In vitro results revealed that GCs could inhibit CVB3 infection on HeLa cells. In vivo, GCs exhibited a strong immune escape ability and effectively inhibited CVB3-induced viral myocarditis with a high safety profile. The most significant implication of this study is to develop a universal antivirus infection strategy via intracellular gelation of the host cell, which can be employed not only for treating defined pathogenic viruses but also for a rapid response to infection outbreaks caused by mutable and unknown viruses.
RESUMEN
Diabetic foot infection (DFI) is a common complication in diabetes patients, with foot infections being the leading cause of amputations. Staphylococcus aureus is frequently found in diabetic foot infections, of which methicillin-resistant Staphylococcus aureus (MRSA) has become a major clinical and epidemiological challenge. Since MRSA strains are resistant to most ß-lactam antibiotics, and also partially resistant to other antibiotics, treatment is difficult and costly. The emergence of drug-resistant bacteria often arises from overuse or misuse of antibiotics. Clinically, canagliflozin is commonly used for the treatment of type 2 diabetes. On this basis, we investigated the antibacterial activity and mechanism of canagliflozin against MRSA, with the aim to discover novel functions of canagliflozin and provide new insights for the treatment of MRSA. Using the microbroth dilution method to determine the half maximal inhibitory concentration of drugs, we found that canagliflozin not only can inhibit the growth of methicillin-sensitive Staphylococcus aureus (MSSA) but also exhibits antibacterial activity against MRSA. The IC50 values, at approximately 56.01 µM and 57.60 µM, were almost the same. At 12 h, canagliflozin showed a significant antibacterial effect against MRSA at and above 30 µM. In addition, its combined use with penicillin achieved better antibacterial effects, which were increased by about three times. Additive antibacterial activity (FICI = 0.69) was found between penicillin and canagliflozin, which was better than that of doxycycline and canagliflozin (FICI = 0.95). Canagliflozin also affected bacterial metabolic markers, such as glucose, ATP, and lactic acid. The results of crystal violet staining indicate that canagliflozin disrupted the formation of bacterial biofilm. Our electron microscopy results showed that canagliflozin distorted the bacterial cell wall. The results of RT-PCR suggest that canagliflozin down-regulated the expressions of biofilm-related gene (clfA, cna, agrC, mgrA, hld) and methicillin-resistance gene (mecA), which was related to MRSA. Molecular docking also indicated that canagliflozin affected some interesting targets of MRSA, such as the sarA, crtM and fnbA proteins. In conclusion, canagliflozin exhibits antibacterial activity against MRSA by affecting bacterial metabolism, inhibiting its biofilm formation, distorting the bacterial cell wall, and altering the gene expression of biofilm formation and its virulence. Our study reveals the antibacterial activity of canagliflozin against MRSA, providing a new reference for treating diabetic foot infections.