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Sulfamethoxazole (SMX) and its antibiotic resistance genes (ARGs) are potential threats to public health. Microwave catalytic technology is an efficient environmental remediation technology, and a reasonable design of the catalyst enables the system to achieve an ideal remediation effect under low microwave power. In this study, a microwave catalyst (FeCO-2) that activates molecular oxygen (O 2 ) was designed on the basis of rational theoretical organization. Density functional theory (DFT) calculations were used to predict the catalytic performance of FeCO-2 in the microwave field. The mechanism of active substance generation and successful construction of the MW/FeCO-2 catalytic system were verified by experimental studies. The abundance of Fe-O bonds alters the electronic structure of the iron carbide material (Fe@C), adjusts the conduction band potential of the material, reduces the reaction energy barrier, facilitates exciton dissociation under microwave, and facilitate O 2 activation. The application of the MW/FeCO-2 system was verified with secondary effluent from a farm wastewater treatment process: 90.62 % SMX and over 86.77 % of ARGs were removed within 15 min. This study provides a new technique to efficiently simultaneously eliminate antibiotics and their resistance genes. In addition, this study provides ideas for the construction of a microwave catalytic system and explains the mechanism of the microwave catalytic process., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

The widespread occurrence and accumulation of N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine (6PPD) and its quinone metabolite, 6PPD quinone (6PPD-Q), have been globally recognized as a critical environmental issue. However, knowledge on the adverse effects of 6PPD and 6PPD-Q on freshwater invertebrates is limited. This study investigated the effects of 6PPD and its oxidative byproduct, 6PPD-Q, on the growth and reproduction of Daphnia pulex. Through 21-day exposure experiments, we measured the uptake of 0.1, 1, and 10 μg/L 6PPD and 6PPD-Q by D. pulex and assessed the effects on growth and fecundity of D. pulex. While 6PPD and 6PPD-Q did not affect the mortality rate of D. pulex, 6PPD-Q exposure inhibited the growth of D. pulex, indicating potential ecological risks. In particular, the reproductive capacity of D. pulex remained unaffected across the tested concentrations of 6PPD and 6PPD-Q, suggesting specific toxicological pathways that warrant further investigation. This study underscored the importance of evaluating the sublethal effects of emerging contaminants such as 6PPD and 6PPD-Q on aquatic invertebrates, and highlighted the need for comprehensive risk assessments to better understand their environmental impacts., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interest or personal relationship that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Chronic pancreatitis (CP) is a chronic wasting disease with an increasing incidence. As an important factor in the pathogenesis of CP, macrophages play a considerable role in the most typical pathological agents throughout the early to late stages of CP. Macrophage-associated cytokines are biomarkers that bring new possibilities for the early diagnosis of CP and differential diagnosis with pancreatic cancer and pancreatic diseases. In addition, in established CP, macrophage interactions with T lymphocytes leads to immune dysregulation, and macrophage secretion of proinflammatory cytokines is considered a potent driver of acinar-to-ductal metaplasia (ADM). In advanced CP, macrophages interact with pancreatic stellate cells (PSCs) and islet cells in an autocrine or paracrine manner to promote the development of pancreatic fibrosis and islet dysfunction. Here, we review the crosstalk of macrophages with pancreatic acinar cells, PSCs, other immune cells and islet cells at different stages of CP progression, as well as current CP immunotherapies targeting macrophages, which will help explain the decisive role of macrophages in CP and their potential as targets of CP immunotherapy. Furthermore, macrophage-targeted immunotherapy can be advanced, not only in terms of physiology and pathology but also in terms of further optimization of dose, forms and delivery. All these efforts are beneficial to enhancing the targeting of macrophages in the treatment of CP., Competing Interests: Declaration of Competing Interest The authors declare that this research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Astaxanthine (AST) has important biological activities including antioxidant and anti-inflammatory effects that could alleviate neurological and heart diseases, but its role in the prevention of cisplatin-induced hearing loss (CIHL) is not yet well understood. In our study, a steady interaction between AST and the E3 ligase adapter Kelch-like ECH-associated protein 1, a predominant repressor of nuclear factor erythroid 2-related factor 2 (NRF2), was performed and tested via computer molecular docking and dynamics. AST protected against cisplatin-induced ototoxicity via NRF2 mediated pathway using quantitative PCR and Western blotting. The levels of reactive oxygen species (ROS) and mitochondrial membrane potential revealed that AST reduced ROS overexpression and mitochondrial dysfunction. Moreover, AST exerted anti-apoptosis effects in mouse cochlear explants using immunofluorescence staining and HEI-OC1 cell lines using quantitative PCR and Western blotting. Finally, AST combined with poloxamer was injected into the middle ear through the tympanum, and the protection against CIHL was evaluated using the acoustic brain stem test and immunofluorescent staining in adult mice. Our results suggest that AST reduced ROS overexpression, mitochondrial dysfunction, and apoptosis via NRF2-mediated pathway in cisplatin-exposed HEI-OC1 cell lines and mouse cochlear explants, finally promoting cell survival. Our study demonstrates that AST is a candidate therapeutic agent for CIHL., (© 2022 Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. Production and hosting by Elsevier B.V.)