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The traditional co‐polarised metasurface achieves 360° phase coverage only at the resonant frequency but not full phase coverage across a wide bandwidth. This paper proposes a multilayer structure metasurface, which composes of five layers of metal patch and four layers of medium, forming the Fabry–Perry resonator, using the principle of the cancellation of two polarisation conversion, which can achieve a wideband efficient co‐polarisation transmission. Based on the metasurface transmission phase principle, 360° phase coverage has been achieved by changing the geometric parameters of the intermediate metal patches. Through phase compensation arrangement, a metalens is designed using the proposed metasurface unit cell. At the same time, horn antenna is used as a feed to feed the metalens, which can significantly improve the gain of the antenna within a wideband. Simulated and measured results show that the proposed metalens antenna operates at 22–26 GHz, and the maximum measured gain of the metalens antenna reaches 24.16 dBi at 25 GHz, which is 10.85 dB higher than the horn antenna without metasurface compensation, showing good focusing performance. The proposed multilayer metasurface breaks the narrow band limit of the traditional stacked metasurface in principle, opening a way in the broadband metasurface design. [ABSTRACT FROM AUTHOR]

The rise of antibiotic tolerance in bacteria harboring genetic elements conferring resistance to antibiotics poses an increasing threat to public health. However, the primary factors responsible for the emergence of antibiotic tolerance and the fundamental molecular mechanisms involved remain poorly comprehended. Here, we demonstrate that the commonly utilized food additive Benzaldehyde (BZH) possesses the capacity to induce a significant level of fluoroquinolone tolerance in vitro among resistant Escherichia coli. Our findings from animal models reveal that the pre-administration of BZH results in an ineffective eradication of bacteria through ciprofloxacin treatment, leading to similar survival rates and bacterial loads as observed in the control group. These results strongly indicate that BZH elicits in vivo tolerance. Mechanistic investigations reveal several key factors: BZH inhibits the formation of bacterial flagella and releases proton motive force (PMF), which aids in expelling antibiotics from within cells to reducing their accumulation inside. In addition, BZH suppresses bacterial respiration and inhibits the production of reactive oxygen species (ROS). Moreover, exogenous pyruvate successfully reverses BZH-induced tolerance and restores the effectiveness of antibiotics, highlighting how crucial the pyruvate cycle is in combating antibiotic tolerance. The present findings elucidate the underlying mechanisms of BZH-induced tolerance and highlight potential hazards associated with the utilization of BZH. [ABSTRACT FROM AUTHOR]

Tigecycline (TIG) is one of the last effective options against multidrug resistance bacteria. Recently, the RND (resistance–nodulation–division) efflux pump gene cluster, tmexCD1-toprJ1, and the tetracycline-efflux pump tet(A) mutation were reported to mediate high level resistance to TIG in clinically important pathogens, weakening the efficacy of TIG. In this study, we report the potent synergistic effect of the antidiabetic drug metformin in combination with TIG against tet(A) mutant and tmexCD1-toprJ1 positive K. pneumoniae. The fractional inhibitory concentration index (FICI) of TIG and metformin were less than 0.05 for all the tested isolates. The time–kill curve assay showed that the combination of TIG and metformin exhibited much better antimicrobial effect than TIG alone. The synergistic effect was also confirmed in vivo using a well-studied Galleria mellonella larvae model. Mechanistic studies demonstrated that metformin disrupted the important component of proton motive force, the electric potential (Δψ) and the function of efflux pump, thereby increasing the intracellular concentration of TIG. This finding revealed that metformin might be a possible adjuvant of TIG for combating with superbugs carrying the tet(A) mutant and tmexCD1-toprJ1 genes. [ABSTRACT FROM AUTHOR]

The rising prevalence of multidrug-resistant (MDR) Gram-positive bacteria threatens the effectiveness of current antibiotic therapies. However, the development of new antibiotics has stagnated in recent years, highlighted the critical need for the discovery of innovative antimicrobial agents. This study aims to evaluate the antibacterial activity of naphthoquinones derived from Arnebia euchroma (Royle) Johnst (ADNs) and elucidate their underlying mechanisms. The antibacterial efficacy of ADNs was assessed using the microbroth dilution method. The antibacterial mechanism of acetylshikonin (ASK) was further explored through scanning electron microscopy, RNA-Seq and transcriptomic analysis, fluorescent probes, high-performance liquid chromatography, qRT-PCR and molecular docking. The results demonstrated that all the ADNs exhibit potent antibacterial activity against MDR Gram-positive pathogens, including methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant Enterococcus, and linezolid-resistant Enterococcus. Notably, ASK showed minimum inhibitory concentration of 1-2 μg/mL against MRSA. Mechanistic investigations revealed that ASK operates through a multifaceted antibacterial mechanism. First, ASK disrupts bacterial membrane integrity and dissipates proton motive force by targeting membrane phospholipids. Further analysis demonstrated a significant reduction in oxygen consumption and ATP production, indicative of respiratory chain inhibition. Additionally, ASK interferes with bacterial cell wall synthesis, as evidenced by reduction of peptidoglycan precursors and downregulated expression of genes involved in peptidoglycan synthesis. In conclusion, ASK represents a promising antimicrobial agent with potential efficacy against infections caused by MDR Gram-positive bacteria and offers valuable insights for the development of novel therapeutic strategies., (© 2024 John Wiley & Sons Ltd.)