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Efficient removal of endocrine disruptors using nano zero-valent iron loaded organo-attapulgite: Mechanism and factors

Endocrine-disrupting pollutants have become a major problem in aquatic environments. Advanced oxidation processes are recognized as promising technologies for treating endocrine disruptor-contaminated water. Herein, a novel nanoscale zero-valent iron loaded organo-attapulgite (NZVI@OATP) was employed as a catalyst to activate persulfate (PDS) for phenanthrene (PHE) and dibutyl phthalate (DBP) degradation. NZVI@OATP with a NZVI:OATP mole ratio of 1:1 (CTAB:ATP = 1:200) exhibited 100 % PHE and 84 % DBP degradation within 30 min, and chloride was found to have a positive effect on their degradation. Radical scavenger and electron paramagnetic resonance studies revealed that the contribution of the active species follows the order of O2- ≈ 1O2>SO4- ≫ OH. The optimal degradation pathways were proposed based on the liquid chromatography-mass spectrometry and density functional theory and the possible degradation paths of PHE and DBP, including the 9,10-phenanthraquinone and phthalic acid pathways, respectively, were proposed. The toxicity estimation software tool showed that the toxicities of PHE and DBP were reduced after degradation. Moreover, 50 % PHE degradation could be achieved after five cycles, demonstrating that NZVI@OATP is a promising catalyst for endocrine disruptor treatment with PDS.

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Fe@Fe2O3/etched carbon felt as a cathode for efficient bisphenol a removal in a flow-through electro-Fenton system: Electron transfer pathway and underlying mechanism

The advanced oxidation processes based on the electro-Fenton reactions show great potentials as a wastewater treatment approach for removing emerging contaminants. In the electro-Fenton system, some factors still exist affecting the treatment efficiency, e.g., the formation of iron sludge, a narrow pH working range, and slow conversion rates between Fe2+ and Fe3+. In this research, a novel heterogeneous flow-through electro-Fenton system was constructed, and carbon felt was used as the template material for the preparation of an etched carbon felt cathode loaded with zero-valent iron and iron oxide (Fe@Fe2O3/ECF) for the degradation of bisphenol A, which addressed the aforementioned issues. The Fe@Fe2O3/ECF electrode showed excellent performance across a pH range between 3 and 11, with exceptional stability and resistance to other substances in water. For the three pollutants, bisphenol A, tetracycline and ciprofloxacin, the highest degradation efficiency can reach 99.3 %. Compared to traditional electro-Fenton systems, the novel process exhibited superior performances due to synergistic effects from feasible flow design, enhanced electrochemical reactivity and greater exposure of active sites. Through electron spin resonance and free-radical quenching experiments, it was determined that the primary species participating in the heterogeneous electro-Fenton process were the hydroxyl radical and superoxide anion. Specifically, the hydroxyl radical was identified as playing a pivotal role in the degradation of bisphenol A. After a continuous operation of 240 min, the electrode showed low metal ion leaching rate and good stability, with the concentrations of leached Fe and Co ions to be only 17 and 7 μg/L, respectively. Meanwhile, the removal efficiency was only decreased by 5.7 % during the process. Through density functional theory calculation and intermediate product analysis, three potential degradation pathways were proposed, with the cleavage of carbon bonds serving as the main degradation approach. The toxicity analysis demonstrated that the intermediates were generally less toxic than BPA during treatments. This research provides a fresh means for promoting a valence state cycling of ferric species in electro-Fenton system, which has potential applications in wastewater treatment containing emerging contaminants.

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Temporal dynamics of the microbial heterogeneity-diversity relationship in microcosmic systems.

Spatial heterogeneity significantly enhances biodiversity, representing one of the ecology's most enduring paradigms. However, many studies have found decreasing, humped, and neutral correlations between spatial heterogeneity and biodiversity (heterogeneity-diversity relationships, HDR). These findings have pushed this widely accepted theory back into controversy. Microbial HDR research has lagged compared to that of plants and animals. Nevertheless, microbes have features that add a temporal-scale perspective to HDR research that is critical to understanding patterns of HDR. In this study, 157 microcosms with different types spatial heterogeneity were set up to map the HDR of microorganisms and their temporal dynamics using high-throughput sequencing techniques. The results show that the following: 1. Spatial heterogeneity can significantly alter microbial diversity in microcosmic systems. Changes in microbial diversity, in turn, lead to changes in environmental conditions. These changes caused microorganisms to exhibit increasing, decreasing, humped, U-shaped, and neutral HDR patterns. 2. The emergence of HDR patterns is characterized by temporal dynamics. Additionally, the HDR patterns generated by spatial structural and compositional heterogeneity exhibit inconsistent emergence times. These results suggest that the temporal dynamics of HDR may be one of the reasons for the coexistence of multiple patterns in previous studies. The feedback regulation between spatial heterogeneity-biodiversity-environmental conditions is an essential reason for the temporally dynamics of HDR patterns. All future ecological studies should pay attention to the temporal dynamic patterns of ecological factors.

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Identification and Characterization of the Stimulator of Interferon Genes (STING) in Chinese Giant Salamander Andrias davidianus

The stimulator of interferon genes (STING) is a central and multifaceted mediator in innate immunity, and plays vital roles in defending against pathogen infection. In this study, we identified and functionally characterized the STING homolog from the Chinese giant salamander Andrias davidianus (AdSTING) for the first time. The open reading frame of AdSTING encodes a 362 amino acid protein with a predicted molecular mass of 41.6 kDa, which shares 31.1–46.7% of its sequence identity with STING homologs in other vertebrates. Structural analysis revealed that AdSTING possesses four predicted transmembrane domains (TMs) at the N-terminal, and a C-terminal domain (CTD) featuring a dimerization domain (DD), a c-di-GMP-binding domain (CBD), and a short C-terminal tail (CTT). Tissue distribution analysis showed that AdSTING mRNA was ubiquitously expressed in all examined tissues, with abundant expression in muscles, intestine, and thymus. During Andrias davidianus ranavirus (ADRV) infection, significant up-regulation of AdSTING expression was observed in the thymus, spleen, and kidney. Upon different stimuli in vitro, the expression of AdSTING was significantly induced by ADRV infection or polyinosin-polycytidylic acid (poly I:C) stimulation, but no obvious changes were observed during lipopolysaccharide (LPS) stimulation. Subcellular localization analysis revealed that AdSTING mainly localized in the cytoplasm in the Chinese giant salamander thymus cell line (GSTC) and co-localized with the endoplasmic reticulum (ER). Luciferase reporter assays confirmed the ability of AdSTING to activate the interferon-stimulated response element (ISRE) and interferon (IFN) promoter. Furthermore, overexpression of AdSTING effectively decreased ADRV infection, as evidenced by the reduction of virus titers and viral gene expression. Collectively, our findings underscore the pivotal role of AdSTING in the antiviral innate immunity of the Chinese giant salamander, offering insights into the functional evolution of STING in amphibians.

Open Access
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Tigecycline-resistance mechanisms and biological characteristics of drug-resistant Salmonella Typhimurium strains in vitro

Increased drug resistance of Gram-negative bacteria to tetracycline caused by the unreasonable overuse of tigecycline has attracted extensive attention to reveal potential mechanisms. Here, we identified a tigecycline-resistant strain called TR16, derived from Salmonella Typhimurium ATCC13311 (AT), and examined its biological characteristics. Compared with AT, the TR16 strain showed significantly higher resistance to amoxicillin but lower resistance to gentamicin. Although the growth curves of TR16 and AT were similar, TR16 showed a significantly increased capacity for biofilm formation and a notably decreased motility compared to AT. Furthermore, transcriptome sequencing and reverse transcription–quantitative PCR (RT-qPCR) were implemented to evaluate the genetic difference between AT and TR16. Whole genome sequencing (WGS) analysis was also conducted to identify single nucleotide polymorphism (SNPs) and screened out two genetic mutations (lptD and rpsJ). The acrB gene of TR16 was knocked out through CRISPR/Cas9 system to further elucidate underlying mechanisms of tigecycline resistance in Salmonella Typhimurium. The up-regulation of acrB in TR16 was verified by RNA-seq and RT-qPCR, and the lack of acrB resulted in a 16-fold reduction in tigecycline resistance in TR16. Collectively, these results implied that AcrB efflux pump plays a key role in the tigecycline resistance of Salmonella, shedding light on the potential of AcrB efflux pump as a novel target for the discovery and development of new antibiotics.

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Chlorogenic Acid Alleviated AFB1-Induced Hepatotoxicity by Regulating Mitochondrial Function, Activating Nrf2/HO-1, and Inhibiting Noncanonical NF-κB Signaling Pathway.

Aflatoxin B1 (AFB1), a kind of mycotoxin, imposes acute or chronic toxicity on humans and causes great public health concerns. Chlorogenic acid (CGA), a natural phenolic substance, shows a powerful antioxidant and anti-inflammatory effect. This study was conducted to investigate the effect and mechanism of CGA on alleviating cytotoxicity induced by AFB1 in L-02 cells. The results showed that CGA (160 μM) significantly recovered cell viability and cell membrane integrity in AFB1-treated (8 μM) cells. Furthermore, it was found that CGA reduced AFB1-induced oxidative injury by neutralizing reactive oxygen species (ROS) and activating the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. In addition, CGA showed anti-inflammatory effects as it suppressed the expression of inflammation-related genes (IL-6, IL-8, and TNF-α) and AFB1-induced noncanonical nuclear factor kappa-B (NF-κB) activation. Moreover, CGA mitigated AFB1-induced apoptosis by maintaining the mitochondrial membrane potential (MMP) and inhibiting mRNA expressions of Caspase-3, Caspase-8, Bax, and Bax/Bcl-2. These findings revealed a possible mechanism: CGA prevents AFB1-induced cytotoxicity by maintaining mitochondrial membrane potential, activating Nrf2/HO-1, and inhibiting the noncanonical NF-κB signaling pathway, which may provide a new direction for the application of CGA.

Open Access
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