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Tungstate inhibits molybdenum-cofactor-dependent microbial respiratory pathways and shows potential as a selective treatment for microbial imbalances that occur during inflammation of the gastrointestinal tract. Countering colon inflammation Expansion of facultative anaerobic bacteria of the Enterobacteriaceae family in the gut is associated with dysbiosis—an imbalance in the microbiota—and inflammatory bowel disease. Sebastian Winter and colleagues show that tungstate treatment, which selectively inhibits molybdenum-cofactor-dependent microbial respiratory pathways that operate only during episodes of inflammation, mitigates inflammation in mouse models of colitis without causing any compositional alterations to the gut microbiota. This is a promising strategy for precision therapy of the microbiota in response to inflammatory disorders, but future work is needed to determine whether similar approaches could be relevant in humans. Inflammatory diseases of the gastrointestinal tract are frequently associated with dysbiosis 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , characterized by changes in gut microbial communities that include an expansion of facultative anaerobic bacteria of the Enterobacteriaceae family (phylum Proteobacteria). Here we show that a dysbiotic expansion of Enterobacteriaceae during gut inflammation could be prevented by tungstate treatment, which selectively inhibited molybdenum-cofactor-dependent microbial respiratory pathways that are operational only during episodes of inflammation. By contrast, we found that tungstate treatment caused minimal changes in the microbiota composition under homeostatic conditions. Notably, tungstate-mediated microbiota editing reduced the severity of intestinal inflammation in mouse models of colitis. We conclude that precision editing of the microbiota composition by tungstate treatment ameliorates the adverse effects of dysbiosis in the inflamed gut.

Polyoxometalates (POMs) exhibit significant potential for application in Alzheimer’s disease (AD) therapeutics owing to their inherent chemical and physical properties and structural tunability. Through transition metal substitution, functional modification, and the construction of POMs-based nanocomposites, POMs can precisely recognize and effectively modulate various key pathogenic proteins involved in Alzheimer’s disease. They can also intervene in disease progression through multiple mechanisms, including inhibition of Aβ aggregation, disaggregation of amyloid-β (Aβ), scavenging of reactive oxygen species (ROS), hydrolytic activity, and modulation of enzyme function. In addition, due to their outstanding physicochemical properties, the application of POMs in phototherapy has emerged as a significant direction in AD treatment research. This review systematically summarizes recent advances from 2011 to 2025 in POMs targeting key pathogenic proteins in AD, comprehensively analyzes their specific mechanisms of action across different therapeutic contexts, highlights their significant advantages and broad potential in AD treatment, and provides new insights for the future structural design, functional optimization, and clinical translation of POMs.

In contrast to AI hardware, neuromorphic hardware is based on neuroscience, wherein constructing both spiking neurons and their dense and complex networks is essential to obtain intelligent abilities. However, the integration density of present neuromorphic devices is much less than that of human brains. In this report, we present molecular neuromorphic devices, composed of a dynamic and extremely dense network of single-walled carbon nanotubes (SWNTs) complexed with polyoxometalate (POM). We show experimentally that the SWNT/POM network generates spontaneous spikes and noise. We propose electron-cascading models of the network consisting of heterogeneous molecular junctions that yields results in good agreement with the experimental results. Rudimentary learning ability of the network is illustrated by introducing reservoir computing, which utilises spiking dynamics and a certain degree of network complexity. These results indicate the possibility that complex functional networks can be constructed using molecular devices, and contribute to the development of neuromorphic devices. Neuromorphic hardware is based on principles of neuroscience, and has the potential to provide higher-level brain functions. Here, the authors develop a neuromorphic network device, constructed from single-walled carbon nanotubes and polyoxometalate, that mimics nerve impulse generation.

The ongoing progression of acetaminophen (APAP)-induced liver injury (AILI) resulting from excessive APAP intake can lead to acute liver failure (ALF). This process involves an imbalanced antioxidant system, upregulated inflammatory responses, and excessive accumulation of reactive oxygen and nitrogen species (RONS), which ultimately trigger apoptosis. In the present study, tannic acid-capped tungsten disulfide nanosheets (WS 2 @TA NSs), which are atomic crystals with a 2D structure, a high specific surface area, and abundant phenolic groups, were synthesized using a liquid-phase exfoliation method. WS 2 @TA NSs were investigated as highly effective anti-inflammatory nanomedicines for targeted enrichment therapy of AILI lesions. Enriched WS 2 @TA NSs in the liver were able to scavenge excess RONS, exhibiting potent antioxidant properties. Importantly, in addition of oxidative stress levels reducing, bioactive WS 2 @TA NSs, which are rich in variable valence states, were able to modulate multiple biosignaling pathways including Nrf2-Keap1, NF-κB, and apoptosis in advanced-stage AILI mice model, thereby enhancing liver tolerance to AILI. The present study reveals the clinical potential of WS 2 @TA NSs atomic crystals in targeted enrichment therapy for late-stage AILI lesions. Graphical abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by brain aggregates of amyloid-β (Aβ) plaques and Tau tangles. Despite extensive research, effective therapy for AD remains elusive. Polyoxometalates (POMs), a class of inorganic compounds with diverse chemical structures and properties, are emerging as potential candidates for AD treatment due to their ability to target key molecular players implicated in disease pathogenesis, such as Aβ, acetylcholinesterase (AChE) and butyryl acetylcholinesterase (BChE). Here, we use molecular docking to predict the binding pose and affinities of POMs to 10 top targets associated with AD. First, we validate our method by replicating experimentally known binding of POMs to Aβ (Δ G  = – 9.67 kcal/mol), AChE (Δ G  = – 9.39 kcal/mol) and BChE (Δ G  = – 10.86 kcal/mol). Then, using this method, we show that POM can also bind β-secretase 1 (BACE1, Δ G  = – 10.14 kcal/mol), presenilin 1 (PSEN1, Δ G  = – 10.65 kcal/mol), presenilin 2 (PSEN2, Δ G  = – 7.94 kcal/mol), Amyloid Precursor Protein (APP, Δ G  = – 7.26 kcal/mol), Apolipoprotein E (APOE4, Δ G  = – 10.05 kcal/mol), Microtubule-Associated Protein Tau (MAPT, Δ G  = – 5.28 kcal/mol) depending on phosphorylation, and α-synuclein (SNCA, Δ G  = – 7.64 kcal/mol). Through such binding, POMs offer the potential to mitigate APP cleavage, Aβ oligomer neurotoxicity, Aβ aggregation, thereby attenuating disease progression. Overall, our molecular docking study represents a powerful tool in the discovery of POM-based therapeutics for AD, facilitating the development of novel treatments for AD. Graphical abstract

Inhibitions of amyloid β (Aβ) aggregation and Aβ-haem peroxidase-like activity have received much attention because these two symptoms can be the primary targets of therapeutic strategies for Alzheimer’s disease (AD). Recently, our group found that polyoxometalate (POM) with a Wells–Dawson structure can efficiently inhibit Aβ aggregation. However, the interaction between POMs and Aβ is robust, but still needs to improve Aβ binding affinity. More importantly, it is unclear whether POMs can cross the blood–brain barrier and decrease Aβ-haem peroxidase-like activity. Here we show that our designed series of transition metal-functionalized POM derivatives with a defined histidine-chelated binding site have much better Aβ inhibition and peroxidase-like activity inhibition effects than the parent POM. More intriguingly, we show that these compounds can cross the blood–brain barrier and are metabolized after 48 h. Our work provides insights into the design, synthesis and screening of inorganic metal compounds as multifunctional therapeutic agents against AD. Beta amyloid aggregation, a process implicated in Alzheimer’s disease pathology, is inhibted by polyoxometalate with a Wells–Dawson structure. Gao et al. show that transition metal-functionalized derivatives are more effective at inhibiting beta amyloid aggregation than non-functionalized derivatives.

Dry reforming of hydrocarbons (DRH) is a pro-environmental method for syngas production. It owes its pro-environmental character to the use of carbon dioxide, which is one of the main greenhouse gases. Currently used nickel catalysts on oxide supports suffer from rapid deactivation due to sintering of active metal particles or the deposition of carbon deposits blocking the flow of gases through the reaction tube. In this view, new alternative catalysts are highly sought after. Transition metal carbides (TMCs) can potentially replace traditional nickel catalysts due to their stability and activity in DR processes. The catalytic activity of carbides results from the synthesis-dependent structural properties of carbides. In this respect, this review presents the most important methods of titanium, molybdenum, and tungsten carbide synthesis and the influence of their properties on activity in catalyzing the reaction of methane with carbon dioxide.

A sensitive electrochemical (voltammetric; DPV) sensor has been developed for the determination of coccidiostat drug (roxarsone) based on the use of an SPCE (screen-printed carbon electrode) modified with tungsten disulfide nanosheets (WS 2 NSs). The electrochemical detection of roxarsone on the WS 2 -modified SPCE was examined by electrochemical strategies. XPS, XRD, Raman, SEM, TEM, EDS and EIS were used to characterize the nanosheets. The effects of scan rate, pH values (phosphate buffer) and buffer concentration were optimized. A selective roxarsone sensor was developed that works best at -0.64 V (vs. Ag/AgCl) and performs much better than the bare SPCE. Features include (a) a wider linear range (0.05 to 490 μM), (b) a nanomolar detection limit (0.03 μM) and (c) high sensitivity (29 μA·μM -1 ·cm -2 ). The modified SPCEs have been successfully applied to the determination of roxarsone in spiked meat samples where they gave high accuracy and good recoveries. Graphical abstract Synthesis of WS 2 nanosheets and electrochemical detection of roxarsone.

Background In diabetic wounds, hyperglycemia-induced cytotoxicity and impaired immune microenvironment plasticity directly hinder the wound healing process. Regulation of the hyperglycemic microenvironment and remodeling of the immune microenvironment are crucial. Results Here, we developed a nanozymatic functionalized regenerative microenvironmental regulator (AHAMA/CS-GOx@Zn-POM) for the effective repair of diabetic wounds. This novel construct integrated an aldehyde and methacrylic anhydride-modified hyaluronic acid hydrogel (AHAMA) and chitosan nanoparticles (CS NPs) encapsulating zinc-based polymetallic oxonate nanozyme (Zn-POM) and glucose oxidase (GOx), facilitating a sustained release of release of both enzymes. The GOx catalyzed glucose to gluconic acid and (H₂O₂), thereby alleviating the effects of the hyperglycemic microenvironment on wound healing. Zn-POM exhibited catalase and superoxide dismutase activities to scavenge reactive oxygen species and H₂O₂, a by-product of glucose degradation. Additionally, Zn-POM induced M1 macrophage reprogramming to the M2 phenotype by inhibiting the MAPK/IL-17 signaling diminishing pro-inflammatory cytokines, and upregulating the expression of anti-inflammatory mediators, thus remodeling the immune microenvironment and enhancing angiogenesis and collagen regeneration within wounds. In a rat diabetic wound model, the application of AHAMA/CS-GOx@Zn-POM enhanced neovascularization and collagen deposition, accelerating the wound healing process. Conclusions Therefore, the regenerative microenvironment regulator AHAMA/CS-GOx@Zn-POM can achieve the effective conversion of a pathological microenvironment to regenerative microenvironment through integrated control of the hyperglycemic-immune microenvironment, offering a novel strategy for the treatment of diabetic wounds.

A nanohybrid mediated SERS substrate was prepared by in-situ synthesis and assembly of gold nanoparticles (AuNPs) on exfoliated nanosheets of tungsten disulfide (WS 2 ) to form plasmonic hotspots. The nanohybrid surface was functionalized with specific aptamers which imparted high selectivity for the cardiac marker myoglobin (Mb). The fabricated aptasensor was read by SERS using a 532 nm laser and demonstrated significant signal enhancement, and this allowed Mb to be determined in the 10 f. mL −1 to 0.1 μg mL −1 concentration range. The study presents an approach to synergistically exploit the unique chemical and electromagnetic properties of both WS 2 and AuNPs for many-fold enhancement of SERS signals. Graphical abstract Schematic presentation of a nanohybrid-mediated SERS substrate prepared by in-situ assembly of gold nanoparticles (AuNPs) reduced on exfoliated nanosheets of tungsten disulfide (WS 2 ) to form plasmonic hot spots. Specific aptamers immobilized on the SERS surface impart high sensitivity and selectivity for the cardiac marker myoglobin (Mb).