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The growing interest in single-atom catalysts (SACs) can be attributed to the continuous updates and iterations in their synthesis process. SACs exhibit remarkable advantages, including exceptional catalytic activity, excellent selectivity, and tunable reactivity to meet the specific requirements of diverse reactions. Consequently, SACs have emerged as pivotal players in numerous scientific domains. The hydrogen evolution reaction (HER) and oxygen evolution reaction (OER), as pivotal fundamental reactions, hold significant research value. In this work, a novel kind of SAC based on an electride/monolayer MoS2 heterostructure is predicted by using first-principles calculations. The anionic electron layer formed between the electride and MoS2 can effectively modulate the charge distribution on the surface of MoS2, thereby enabling indirect manipulation of the performance of the SACs. There exists a robust linear correlation between the adsorption energy and charge variation, which serves as a pivotal descriptor of catalyst performance. The energy difference between the O* process structure and slab structure exhibits a strong linear correlation with the overpotential in the OER, making it a valuable criterion for efficient screening of electride-based heterogeneous catalysts which streamlines the screening process for OER catalysts. The present study offers a novel strategy for enhancing the catalytic performance of SACs. [ABSTRACT FROM AUTHOR]

This article centers around the privacy‐preserving‐based secure H∞$$ {H}_{\infty } $$ filtering issue for interval type‐2 (IT‐2) fuzzy networked systems with false data injection (FDI) attacks. In order to achieve the goal of privacy preserving and significantly enhancing system security against potential eavesdropping threats, a novel encryption‐decryption mechanism (EDM) is adopted to safeguard the safety of signals across the network. The mechanism encrypts the transmitted signal by introducing artificial noise, secret key, and utilizing randomly selected nodes. This ensures that the actual transmitted data remains invisible to eavesdroppers while minimally the impact on the estimated performance of the proposed EDM. Given the network communication resources are becoming constrained due to the ever‐increasing network traffic, an adaptive event‐triggered mechanism (AETM) is employed to ease network congestion by an adaptively adjustable threshold. Then, various sufficient conditions have been outlined to ensure that the filtering error system meets the prescribed disturbance attenuation level. In the end, a numerical example is presented to evaluate both the precision and effectiveness of the developed algorithms. [ABSTRACT FROM AUTHOR]

Given the widespread application of glucocorticoids in ophthalmology, the associated elevation of intraocular pressure (IOP) has long been a vexing concern for clinicians, yet the underlying mechanisms remain inconclusive. Much of the discussion focuses on the extracellular matrix (ECM) of trabecular meshwork (TM). It is widely agreed that glucocorticoids impact the expression of matrix metalloproteinases (MMPs), leading to ECM deposition. Since Zn2+ is vital for MMPs, we explored its role in ECM alterations induced by dexamethasone (DEX). Our study revealed that in human TM cells treated with DEX, the level of intracellular Zn2+ significantly decreased, accompanied by impaired extracellular Zn2+ uptake. This correlated with changes in several Zrt-, Irt-related proteins (ZIPs) and metallothionein. ZIP8 knockdown impaired extracellular Zn2+ uptake, but Zn2+ chelation did not affect ZIP8 expression. Resembling DEX's effects, chelation of Zn2+ decreased MMP2 expression, increased the deposition of ECM proteins, and induced structural disarray of ECM. Conversely, supplementation of exogenous Zn2+ in DEX-treated cells ameliorated these outcomes. Notably, dietary zinc supplementation in mice significantly reduced DEX-induced IOP elevation and collagen content in TM, thereby rescuing the visual function of the mice. These findings underscore zinc's pivotal role in ECM regulation, providing a novel perspective on the pathogenesis of glaucoma. NEW & NOTEWORTHY: Our study explores zinc's pivotal role in mitigating extracellular matrix dysregulation in the trabecular meshwork and glucocorticoid-induced ocular hypertension. We found that in human trabecular meshwork cells treated with dexamethasone, intracellular Zn2+ significantly decreased, accompanied by impaired extracellular Zn2+ uptake. Zinc supplementation rescues visual function by modulating extracellular matrix proteins and lowering intraocular pressure, offering a direction for further exploration in glaucoma management. [ABSTRACT FROM AUTHOR]

The development of a high-efficiency, low-cost, and environmentally friendly catalyst for formaldehyde degradation is crucial for addressing the issue of indoor formaldehyde pollution. Given that modern individuals spend over 90% of their time indoors, effectively tackling indoor formaldehyde pollution holds significant importance. Therefore, this paper proposes an efficient catalyst for formaldehyde degradation: surface modification of MoS2 by single-atom Ni, which can convert formaldehyde into harmless H2O and CO2. The DFT method is employed to systematically investigate the oxidative degradation pathways of formaldehyde on the surface of Ni-doped MoS2. The research focuses on two common oxidative degradation pathways in both the L–H mechanism and E–R mechanism. Our findings demonstrate that these four reaction paths occur spontaneously within the temperature range of 300–800 K with a reaction equilibrium constant greater than 105. Moreover, even under extreme temperature conditions (100 K), the reaction rate remains favorable. Furthermore, our findings indicate that the minimum activation energy is merely 0.91 eV and H2O and CO2 only need to overcome an energy barrier of 0.71 eV for desorption from the catalyst surface. This substantiates its potential application both in indoor environments and under extreme temperature conditions. This theoretical research provides innovative ideas and strategies for effectively oxidizing formaldehyde. [ABSTRACT FROM AUTHOR]

Schematic representation of proposed mechanisms. In PD, active–MMP–9 is released infiltrates sites of the perivascular region, and cleaves the extracellular domain of β–DG, resulting in structural instability of the BM–astrocyte endfeet and AQP4 depolarization and glymphatic system dysfunction. The inhibition of MMP–9 prevents AQP4 depolarization–mediated glymphatic dysfunction and partially alleviates metabolic perturbations and DAergic neuron degeneration. [Display omitted] • AQP4 depolarization is a key factor responsible for glymphatic dysfunction in PD. • Abnormal MMP-9 activation triggers β-DG cleavage in PD. • This cleavage regulates glymphatic function via AQP4 polarization. • MMP-9 inhibition restored AQP4 polarization and basement membrane-astrocyte endfeet contact. • MMP-9 inhibition may serve as a potential target for enhancing glymphatic in PD. The glymphatic system offers a perivascular pathway for the clearance of pathological proteins and metabolites to optimize neurological functions. Glymphatic dysfunction plays a pathogenic role in Parkinson's disease (PD); however, the molecular mechanism of glymphatic dysfunction in PD remains elusive. To explore whether matrix metalloproteinase-9 (MMP-9)-mediated β-dystroglycan (β-DG) cleavage is involved in the regulation of aquaporin-4 (AQP4) polarity-mediated glymphatic system in PD. 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD and A53T mice were used in this study. The glymphatic function was evaluated using ex vivo imaging. TGN-020, an AQP4 antagonist, was administered to investigate the role of AQP4 in glymphatic dysfunction in PD. GM6001, an MMP-9 antagonist, was administered to investigate the role of the MMP-9/β-DG pathway in regulating AQP4. The expression and distribution of AQP4, MMP-9, and β-DG were assessed using western blotting, immunofluorescence, and co-immunoprecipitation. The ultrastructure of basement membrane (BM)-astrocyte endfeet was detected using transmission electron microscopy. Rotarod and open-field tests were performed to evaluate motor behavior. Perivascular influx and efflux of cerebral spinal fluid tracers were reduced in MPTP-induced PD mice with impaired AQP4 polarization. AQP4 inhibition aggravated reactive astrogliosis, glymphatic drainage restriction, and dopaminergic neuronal loss in MPTP-induced PD mice. MMP-9 and cleaved β-DG were upregulated in both MPTP-induced PD and A53T mice, with reduced polarized localization of β-DG and AQP4 to astrocyte endfeet. MMP-9 inhibition restored BM-astrocyte endfeet-AQP4 integrity and attenuated MPTP-induced metabolic perturbations and dopaminergic neuronal loss. AQP4 depolarization contributes to glymphatic dysfunction and aggravates PD pathologies, and MMP-9-mediated β-DG cleavage regulates glymphatic function through AQP4 polarization in PD, which may provide novel insights into the pathogenesis of PD. [ABSTRACT FROM AUTHOR]