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Array sensing employs cross-identification among analytes and various sensing units to identify substances or complex systems. This manuscript presents a fluorescence ratio sensing array based on lectin responses for the accurate identification of different bacteria. This strategy uses a saccharide-sensitive polymer as the sensing unit within the sensor. By incorporating various saccharides, it regulates the properties of the single sensing unit at the molecular level, altering its interaction with the analyte. This modulation leads to the generation of multiple distinct detection signals for the target, effectively facilitating the goal of array sensing. This approach streamlines the design and construction of the array sensor, while simultaneously enhancing detection efficiency. Not only does this sensing strategy achieve the differentiation and quantification of various types of lectins, but it also enables the identification of different bacterial species based on their unique lectin response profiles. This research introduces a novel approach that simplifies the construction of array sensors and simultaneously furnishes a potent tool for diagnosing and assessing bacterial infections within clinical settings.

Aqueous Zn-ion batteries (AZIBs) have attracted widespread attention owing to the feature of low cost, inherent safety and eco-friendliness. However, the poor reversibility of Zn anode severely hinders the practical applicability of AZIBs. Separator modification is an effective way to functionalize the electrode/electrolyte interface and improve the cycling performance. Here, we propose a modified glass fiber separator with Au coating (Au@GF), which could realize uniform Zn²⁺ distribution at the electrode/electrolyte interface and regulate the plating/stripping behaviors, achieving a dense and homogenous deposition. Zn||Zn symmetric cells assembled with Au@GF separator demonstrate evidently prolonged cycle life over 1600 h at the current density of 5 mA cm^-2 and the capacity of 1 mAh cm^-2, while symmetric cells with GF fail in less than 40 h. Even at the condition of 15 mA cm^-2/3 mAh cm^-2, lifespan of Zn||Zn cells with Au@GF is extended to 750 h, which is more than 3 times compared with that of GF. The modified separator with highly conductive coating is capable of a longtime stable Zn plating/stripping. Moreover, an enhanced cycling performance is also detected in a series of full cells with different cathode materials. This work provides an easy and efficient approach to homogenize Zn²⁺ deposition.

The aim of this study was to investigate the inhibitory effect of glutamate molecular structure and protein on breast cancer cell metastasis and the potential inhibitory mechanism of cell-derived exosomes via MAPK signaling pathway. Breast cancer cell lines with high metastatic potential were selected by in vitro cell culture technique. The effects of specific inhibitors of glutamic acid on the proliferation and metastasis of breast cancer cells were studied. Changes in protein expression profiles were analyzed by proteomics techniques to identify key proteins associated with breast cancer metastasis. Breast cancer cells were treated with inhibitors of the MAPK signaling pathway to evaluate their effect on cell metastasis and compare with exosome treatment. The results showed that the specific inhibitors of glutamate molecular structure could significantly inhibit the proliferation and metastasis of breast cancer cells. Proteomic analysis revealed several down-regulated proteins that are closely related to breast cancer metastasis.

As one of the most commonly used chemotherapeutic agents in clinical practice, cisplatin is unable to selectively accumulate in tumor tissue due to its lack of targeting ability, leading to increased systemic toxicities. Additionally, the effectiveness of monotherapy is greatly limited. Therefore, the development of new cisplatin-based drug delivery systems is essential to improve the effectiveness of tumor treatment. In this study, an iron-based metal-organic framework (MOF) was synthesized to encapsulate cisplatin, and then coated with hyaluronic acid (HA) to create a MOF-based nanoplatform called MPt@HA NPs. This novel nanoplatform achieved the combination of chemodynamic therapy (CDT) with targeted chemotherapy for the treatment of lung cancer. The results showed that MPt@HA NPs have stronger cytotoxicity compared to conventional doses of cisplatin due to the generation of reactive oxygen species (ROS) through the Fenton reaction and DNA damage caused by cisplatin. Therefore, MPt@HA NPs effectively inhibit the tumor growth and prolong the median survival of tumor-bearing mice. Therefore, the MOF-based nanoplatform MPt@HA NPs may present a new option for multi-modal therapy of solid tumors.

Crown rot caused by Fusarium proliferatum is a severe postharvest disease of banana fruit. The N⁶-methyladenosine (m⁶A) modification is the most common type of RNA modification and regulates gene expression in eukaryotes. Here, we analyzed transcriptome-wide changes in m⁶A methylation to investigate post-transcriptional regulation mechanisms of growth and fumonisin biosynthesis of F. proliferatum after fluopyram (Flu) treatment. The results demonstrated that Flu treatment inhibited F. proliferatum growth but induced fumonisins (FB1 and FB2) production both in vitro and in vivo. A transcriptome-wide m⁶A methylation profile showed that m⁶A hypomethylation was induced by Flu and enriched in start codons and the 3' untranslated region. FpAlkbh8 and FpYthdc1 may contribute to the decrease in m⁶A modifications after Flu treatment. The expression levels of m⁶A-containing mRNAs were higher than those of non-m⁶A-containing mRNAs. Furthermore, Flu decreased the acetyl-CoA content and regulated glycolysis and tricarboxylic acid cycle through m⁶A modifications, diverting the acetyl-CoA flux into fumonisin biosynthesis. Importantly, Flu-mediated regulation of energy and reactive oxygen species metabolism, cell wall and membrane, and transcription factors was associated with m⁶A modifications. Collectively, this study provides potential novel targets for improving fungicide efficiency to control fungal disease and highlights the potential of environmental risks of fungicides.

In esophageal squamous cell carcinoma (ESCC), the tumor microenvironment (TME) is characterized by a significant accumulation of cancer-associated fibroblasts (CAFs), which play a pivotal role in the host response against tumor cells. While fibroblasts are known to be crucial in the metabolic reprogramming of the TME, the specific metabolic alterations induced by these cells remain largely undefined. Utilizing single-cell RNA sequencing, we have identified a distinct subpopulation of antigen-presenting CAF (apCAF) within ESCC tumors. Our findings reveal that apCAF contribute to adverse patient outcomes by remodeling the tumor metabolic environment. Notably, apCAF modulate the glycosaminoglycan biosynthesis-heparan sulfate/heparin metabolism pathway in T cells, B cells, and macrophages. Disruption of this pathway may facilitate immune evasion by the tumor. These insights underscore the critical role of CAFs in shaping the metabolic landscape of the TME and lay the groundwork for developing therapeutic strategies aimed at enhancing anti-tumor immunity.

Background: The role of inflammation in the development of type 2 diabetes mellitus (T2DM) related skin complications necessitates further investigation. This study aims to explore the correlation between inflammation and cutaneous alterations in T2DM, enhancing comprehension of underlying mechanism involved.

Methods: Utilizing bioinformatics, the GSE38396 and GSE92724 datasets were employed to identify differentially expressed genes (DEGs) and potential hub genes in T2DM-related skin inflammation. Subsequently, gene functional enrichment analysis was employed for functional annotation. Finally, we validated the regulatory impact of hub gene on inflammation during high glucose incubation using the in vitro model.

Results: A comprehensive analysis identified 742 DEGs, including 9 hub genes and 4 potential biomarkers. Compared to the CON group, the expression of M2 macrophages was significantly upregulated in the T2DM group, while resting dendritic cells and eosinophils showed notable decreases, indicating a significant correlation with CEBPA. Furthermore, functional enrichment analysis revealed significant enrichment of DEGs in pathways linked to immunity and diabetes pathogenesis. Interestingly, overexpression of CEBPA demonstrated anti-inflammatory effects under hyperglycemic conditions, while silencing CEBPA expression appeared to worsen inflammation.

Conclusion: CEBPA emerges as a potential hub gene for skin inflammation in T2DM, shedding light on the underlying mechanisms of this condition.

Obesity and metabolic disorders are rising global health concerns, emphasizing the need for effective dietary interventions. High-viscosity dietary fibers such as bacterial cellulose (BC) and guar gum (GG) have unique properties that may complement each other in modulating gut microbiota and metabolic health. This study investigates their effects in high-fat diet-fed mice. BC and GG increase Bacteroides, which degrade polysaccharides and produce short-chain fatty acids (SCFAs), supporting metabolic health. BC enhances bile acid excretion and enriches Faecalibaculum, Duncaniella, and Paramuribaculum, promoting gut barrier integrity and reducing inflammation, potentially improving bile acid turnover and lipid metabolism. GG more effectively increases butyrate production by enhancing butyrate-producing bacteria, such as Clostridium XIVa and Kineothrix, and promotes Bifidobacterium, strengthening anti-inflammatory effects and gut barrier function. Both fibers upregulate bile acid biosynthesis, but BC's non-fermentable nature leads to higher bile acid excretion, while GG's fermentation causes lower excretion and broader liver metabolic changes. Both fibers reduce body weight, fat accumulation, and cholesterol levels, highlighting their potential in managing obesity and metabolic disorders. The complementary effects of BC and GG underscore the importance of fiber diversity for targeted dietary strategies to improve metabolic health.

Butylcholinesterase (BChE) is a key enzyme in living system, closely related to liver and neurological diseases. It is very challenge to develop near-infrared (NIR) fluorescence probe methods for highly selective and sensitive detection of BChE in vivo. Based on the differences in active sites and spatial pockets between acetylcholinesterase (AChE) and BChE, a new NIR BChE-responsive fluorescence probe Probe-BChE (λ_ex/λ_em = 600 nm/676 nm) was designed and synthesized by introducing dimethyl carbamate group as recognizing moiety to a NIR fluorophore hemicyanine skeleton. It was found that Probe-BChE specifically binds with BChE, rather than AChE, since BChE has a big cavity and strong intermolecular forces with Probe-BChE, which was supported by the molecular docking scores. The fluorescence method for the determination of BChE was developed with a detection limit of 0.14 U/mL BChE and high selectivity as well as short reaction time (∼3 s). The fluorescence imaging method using Probe-BChE efficiently image the levels of endogenous BChE in brains and main organs (heart, liver, spleen, lung and kidney) of Alzheimer's disease (AD) mice. The results reveal that the levels of endogenous BChE in old AD mice is higher than that in young AD mice, and endogenous BChE is enriched in the liver of AD mice. This work demonstrates that Probe-BChE is a promising fluorescence probe for imaging of endogenous BChE in AD mice. The design of NIR fluorescence probes for endogenous BChE in this work will promote to design NIR fluorescence probes for endogenous cholinesterase.