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Abstract Background Schistosoma japonicum infection causes hepatic fibrosis, a primary cause of morbidity and mortality associated with the disease, and effective treatments are still lacking. Long non-coding RNAs (lncRNAs) have been implicated in the pathogenic process of various tissue fibroses. However, the role of lncRNAs in schistosomiasis hepatic fibrosis (HF) is poorly understood. Understanding the role of lncRNAs in schistosomiasis HF will enhance knowledge of disease processes and aid in the discovery of therapeutic targets and diagnostic biomarkers. Methods Differentially expressed lncRNA profiles in primary hepatic stellate cells (HSCs) of mice infected with S. japonicum were identified using high-throughput lncRNA sequencing. Primary HSCs were isolated from infected mice using collagenase digestion and density-gradient centrifugation, cultured in DMEM with 10% fetal bovine serum. Dual-luciferase reporter assays, nuclear cytoplasm fractionation and RIP assays were employed to assess the relationship between Malat1 and miRNA-96. Malat1 lentivirus and ASO-Malat1 were constructed for forced expression and downregulated expression of Malat1. The Malat1-KO mouse was constructed by CRISPR/Cas9 technology. Pathological features of the liver were evaluated by hematoxylin-eosin (HE), Masson’s trichrome staining and immunohistochemistry (IHC). The expression levels of fibrosis-related genes were determined by quantitative real-time PCR (qRT-PCR) and Western blot. Results A total of 1561 differentially expressed lncRNAs were identified between infected and uninfected primary HSCs. Among the top altered lncRNAs, the downregulated Malat1 was observed in infected HSCs and verified by qPCR. Treatment of infected mice with praziquantel (PZQ) significantly increased the Malat1 expression. Elevated Malat1 expression in infected primary HSC reduced the expressions of profibrogenic genes, whereas Malat1 knockdown had the opposite effect. Moreover, Malat1 was found to interact with miR-96, a profibrotic miRNA, by targeting Smad7. Forced Malat1 expression reduced miR-96 levels in infected primary HSCs, attenuating fibrogenesis and showing negative correlation between Malat1 expression and the expression levels of miR-96 and profibrogenic genes α-SMA and Col1α1. Notably, in Malat1-KO mice, knockout of Malat1 aggravates schistosomiasis HF, while restored Malat1 expression in the infected HSCs reduced the expression of profibrogenic genes. Conclusions We demonstrate that lncRNA is involved in regulation of schistosomiasis HF. Elevated lncRNA Malat1 expression in infected HSCs reduces fibrosis via the Malat1/miR-96/Smad7 pathway, thus providing a novel therapeutic target for schistosomiasis HF. Furthermore, Malat1 expression is sensitive to PZQ treatment, thus offering a potential biomarker for assessing the response to chemotherapy. Graphical abstract

N‐coordinated Ni sites (NiNx) are effective catalysts for the electrochemical reduction of CO2 to CO. In most researches, modulating the coordination environment of Ni atoms is focused on to improve electrochemical CO2 reduction (ECR) performance. However, the influence of the carbon substrate's structure on the intrinsic activity of NiNx is seldom investigated. The highly curved surface of carbon nanotubes (CNT) may provide a unique curvature effect on NiNx. It is found that the Ni residues in CNT can be atomized to form NiNx sites on the surface of CNT (Ni‐N/CNT@covalent triazine framework [CTF]) through high‐temperature pyrolysis, using a soluble CTF nanosheet as N precursor. The π‐conjugated and ultrathin 2D structure of CTF enables closer interfacial contact between CTF and CNT, which avoids the formation of a thick carbon layer to maximize the curvature effect. Theoretical data reveal that the NiN3 configuration may act as a highly active ECR site, and the curvature effect from CNT can further tune the electronic structure of NiN3, thus improving the ECR kinetics. The Ni‐N/CNT@CTF‐based flow‐cell electrolyzer exhibits a jCO of 201 mA cm−2 at −0.9 V with a high FECO of 98%.

Circular RNAs (circRNAs), a novel type of single-stranded noncoding RNAs with a covalently closed loop structure, are generated in a circular conformation via non-canonical splicing or back-splicing events. Functionally, circRNAs have been elucidated to soak up microRNAs (miRNAs) and RNA binding proteins (RBPs), serve as protein scaffolds, maintain mRNA stability, and regulate gene transcription and translation. Notably, circRNAs are strongly implicated in the regulation of β-cell functions, insulin resistance, adipocyte functions, inflammation as well as oxidative stress via acting as miRNA sponges and RBP sponges. Basic and clinical studies have demonstrated that aberrant alterations of circRNAs expressions are strongly associated with the initiation and progression of diabetes mellitus (DM) and its complications. Here in this review, we present a summary of the biogenesis, transportation, degradation and functions of circRNAs, and highlight the recent findings on circRNAs and their action mechanisms in DM and its complications. Overall, this review should contribute greatly to our understanding of circRNAs in DM pathogenesis, offering insights into the further perspectives of circRNAs for DM diagnosis and therapy.

Atomically dispersed metal sites (ADMSs) play key roles in electrochemical energy conversion. The covalent organic frameworks (COFs) enable the precise control of the chemical compositions and structures at the molecular level, making them ideal substrates for supporting ADMSs. In this review, we systematically summarize the recent progress on the design and synthesis of ADMSs in COFs, including embedding molecular catalysts into COFs, immobilizing ADMSs on heteroatom-containing COFs, and preparing COF-derived carbon materials through pyrolysis. The electrocatalytic performance of the resulting catalysts is presented for various electrochemical reactions, involving oxygen reduction reaction (ORR), carbon dioxide reduction reaction (CO2RR), oxygen evolution reaction (OER), hydrogen evolution reaction (HER), and nitrogen reduction reaction (NRR). The modulation strategies of AMDSs in COFs for enhanced activity, selectivity, and stability are highlighted, together with a perspective of the current challenges and the future opportunities in this field.

Vascular endothelial cells (ECs) senescence plays a crucial role in vascular aging that promotes the initiation and progression of cardiovascular disease. The mutation of Grb10-interacting GYF protein 2 (GIGYF2) is strongly associated with the pathogenesis of aging-related diseases, whereas its role in regulating ECs senescence and dysfunction still remains elusive. In this study, we found aberrant hyperexpression of GIGYF2 in senescent human ECs and aortas of old mice. Silencing GIGYF2 in senescent ECs suppressed eNOS-uncoupling, senescence, and endothelial dysfunction. Conversely, in nonsenescent cells, overexpressing GIGYF2 promoted eNOS-uncoupling, cellular senescence, endothelial dysfunction, and activation of the mTORC1-SK61 pathway, which were ablated by rapamycin or antioxidant N-Acetyl-l-cysteine (NAC). Transcriptome analysis revealed that staufen double-stranded RNA binding protein 1 (STAU1) is remarkably downregulated in the GIGYF2-depleted ECs. STAU1 depletion significantly attenuated GIGYF2-induced cellular senescence, dysfunction, and inflammation in young ECs. Furthermore, we disclosed that GIGYF2 acting as an RNA binding protein (RBP) enhances STAU1 mRNA stability, and that the intron region of the late endosomal/lysosomal adaptor MAPK and mTOR activator 4 (LAMTOR4) could bind to STAU1 protein to upregulate LAMTOR4 expression. Immunofluorescence staining showed that GIGYF2 overexpression promoted the translocation of mTORC1 to lysosome. In the mice model, GIGYF2flox/flox Cdh-Cre+ mice protected aged mice from aging-associated vascular endothelium-dependent relaxation and arterial stiffness. Our work discloses that GIGYF2 serving as an RBP enhances the mRNA stability of STAU1 that upregulates LAMTOR4 expression through binding with its intron region, which activates the mTORC1-S6K1 signaling via recruitment of mTORC1 to the lysosomal membrane, ultimately leading to ECs senescence, dysfunction, and vascular aging. Disrupting the GIGYF2-STAU1-mTORC1 signaling cascade may represent a promising therapeutic approach against vascular aging and aging-related cardiovascular diseases.

High-energy-density lithium-sulfur batteries has attracted substantial attention as competitive candidates for large-scale energy storage technologies. Still, the adverse “shuttle effect” and sluggish sulfur conversion reaction kinetics immensely obstruct their commercial viability. Herein, a two-dimensional metallic 1T phase WS2 (1T-WS2) nanosheets modified functional separator is developed to improve the electrochemical performance. Meanwhile, the semiconducting bulk-WS2 crystals, and 2H phase WS2 (2H-WS2) nanosheets with more basal-plane S-vacancy defects are also prepared to probe the contributions of the crystal structure (phase), S-vacancy defects, and edges to the Li–S batteries performance experimentally and theoretically. In merits of the synergistic effect of high ion and electron conductivity, enhanced binding ability to lithium polysulfides (LiPSs), and sufficient electrocatalytic active sites, the 1T-WS2 shows highly efficient electrocatalysis of LiPSs conversion and further improves Li–S battery performance. As expected, thus-fabricated cells with 1T-WS2 nanosheets present superior cycle stability that maintain capacity decline of 0.039% per cycle after 1000 cycles at 1.0 C. The strategy presented here offers a viable approach to reveal the critical factors for LiPSs catalytic conversion, which is beneficial to developing advanced Li–S batteries with enhanced properties.

As one of the most common cathode materials for aqueous zinc-ion batteries (AZIBs), manganese oxides have the advantages of abundant reserves, low cost, and low toxicity. However, the electrochemical mechanism at the cathode of aqueous zinc–manganese batteries (AZMBs) is complicated due to different electrode materials, electrolytes and working conditions. These complicated mechanisms severely limit the research progress of AZMBs system and the design of cells with better performance. Hence, the mechanism of AZMBs currently recognized by most researchers according to the classification of the main ions involved in the faradaic reaction is introduced in the review. Then a series of reasons that affect the electrochemical behavior of the battery are summarized. Finally, the failure mechanisms of AZMBs over prolonged cycling are discussed, and the current insufficient research areas of the system are explained, along with the direction of further research being prospected.

Rapid industrial development has led to excessive levels of various contaminants in natural water, which poses a challenge to the innovation of environmental remediation technology. In recent years, iron sulfide and its modified materials have attracted extensive attention in environmental remediation due to their high activity in advanced oxidation processes and widespread existence in anoxic environment. This paper reviewed the latest advances of the synthesis methods for iron sulfide and modified FeS. In addition, the application of persulfate activation by iron sulfide materials (FeS, FeSx, S−ZVI, FeS@Carbon materials and MFexSy) for contaminants remediation is also reviewed, and the enhancement of this system by photo irradiation, ultrasound, and microwave have also been concluded. Additionally, the interaction mechanism of iron sulfide and persulfate with contaminants was reviewed. Based on the above contents, we concluded that the long−term stability of iron sulfide, the toxicity to organisms of iron sulfide materials in the treated water, and the combination of FeS/PS with other assisted technologies should be focused in future.

The cultivation of strawberries in controlled environments presents challenges related to environmental stressors, especially insufficient light. Melatonin, as a widely investigated plant growth regulator, was considered as a potential candidate to mitigate damage, and enhance photosynthesis stability. However, whether melatonin can improve photosynthesis under light deficiency in woodland strawberry (Fragaria vesca) remains elusive. In this study, we evaluated gas exchange parameters, Chlorophyll fluorescence parameters, photochemical efficiency, and the related genes’ expression levels to decipher the multifaceted impact of melatonin on photosynthesis. We found concentration-dependent effects of melatonin on photosynthetic parameters, with potential benefits at lower concentration and inhibitory effects at higher concentration. Notably, melatonin increased non-photochemical quenching (NPQ), a mechanism for dissipating excess light energy, while leaving photochemical quenching (qP) relatively stable. Further analysis showed that melatonin up-regulated key xanthophyll cycle-related genes (DHAR, VDE, and PsbS), indicating its involvement in energy dissipation processes. In conclusion, our study uncovered the dual and complex role of melatonin in the short-term response of photosynthesis in woodland strawberries under low-light conditions.

Researchers studying heterogeneous catalysis are intrigued by single-atom catalysts (SACs) due to their ultrahigh atomic utilization. However, only a few reports on SAC-catalyzed classical organic transformations are available. In this work, atomically dispersed Pd sites are confined to a ZrO2 hybridized N-doped carbon skeleton with a smart design. UiO-66-NH2 is used to anchor Pd atoms by the coordination of the donor atoms including lone pairs of electrons and metal atoms. Subsequently, the in situ introduction of ZrO2 doping is achieved using pyrolysis, which helps improve the catalytic performance by modulating the electronic state. The Pd@ZrO2/N–C catalyst obtained from the unique design exhibits a high yield (99%) in eco-friendly media with an extremely low noble metal dosage (0.03 mol% Pd) for the Suzuki reaction. Moreover, Pd@ZrO2/N–C remains highly active after being reused several times and possesses versatility in a variety of substrates. This strategy offers a feasible alternative to designing SACs with atomically dispersed noble metals for heterogeneous reactions.

Abstract Fenton‐like reactions with persulfates as the oxidants have attracted increasing attentions for the remediation of emerging antibiotic pollutions. However, developing effective activators with outstanding activities and long‐term stabilities remains a great challenge in these reactions. Herein, a novel activator is successfully synthesized with single iron atoms anchored on porous N‐doped carbon (Fe‐N‐PC) by a facile chemical vapor deposition (CVD) method. The single Fe atoms are coordinated with four N atoms according to the XANES, and the Fe‐N4‐PC shows enhanced activity for the activation of peroxymonosulfate (PMS) to degrade sulfamethoxazole (SMX). The experiments and density functional theory (DFT) calculations reveal that the introduction of single Fe atoms will regulate the main active sites from graphite N into Fe‐N4, thus could enhance the stability and tune the PMS activation pathway from non‐radical into radical dominated process. In addition, the N atoms connected with single Fe atoms in the Fe‐N4‐C structure can be used to enhance the adsorption of organic molecules on these materials. Therefore, the Fe‐N4‐C here has dual roles for antibiotics adsorption and PMS activation. The CVD synthesized Fe‐N4‐C shows enhanced performance in persulfates based Fenton‐like reactions, thus has great potential in the environmental remediation field.

In-wheel motor electric vehicles have the advantages of independently controllable four-wheel torque, high energy utilization rate, and fast motor response speed, which greatly reduces the curb weight of the vehicle and simplifies the structure of the vehicle, making it an expert at home and abroad research hotspots. However, the in-wheel motor independently drives the electric vehicle. The in-wheel motor directly drives the vehicle, and the motion states of each wheel are independent of each other; that is, each wheel can be independently driven by wire control, which puts forward higher requirements for the torque distribution control of the entire vehicle. Starting from the driving form of the car, this paper focuses on the design of the torque distribution scheme of the in-wheel motor by experts and scholars in the past, such as the use of genetic algorithm, BP neural network, particle swarm algorithm, and fuzzy control algorithm to distribute the torque of the in-wheel motor, and the research on vehicle economy and stability under torque distribution optimization is reviewed. The future development direction of in-wheel motor torque distribution is prospected.

Perovskite-based electrocatalysts with compositional flexibility and tunable electronic structures have emerged as one of the promising non-noble metal candidates for oxygen evolution reaction (OER). Here, we propose a heterostructure comprising perovskite oxide (LaNiO3) nanorods and iron oxide hydroxide (FeOOH) nanosheets as an effective electrochemical catalyst for OER. The optimized 0.25Fe-LNO catalyst with an interesting 1D-2D hierarchical structure shows a low overpotential of 284 mV at 10 mA cm−2 and a small Tafel slope of 69 mV dec−1. The enhanced performance can be explained by the synergistic effect between LaNiO3 and FeOOH, resulting in an improved electrochemically active surface area, facilitated charge transfer and the optimized adsorption of OH intermediates.

Schistosomiasis remains a serious parasitic disease, which is characterized by granulomatous inflammation and hepatic fibrosis. MicroRNAs derived from parasites can regulate host genes and cell phenotype. Here, we showed that a miRNA derived from S. japonicum (Sja-miR-1) exists in the hepatic stellate cells (HSCs) of mice infected with the parasite and up-regulates the expression of collagens and α-SMA by targeting secreted frizzled-related protein 1 (SFRP1). A vector-mediated delivery of Sja-miR-1 into naive mice led to hepatic fibrogenesis in the mice. Accordingly, inhibition of Sja-miR-1 in the infected mice led to reduction of the parasite-induced hepatic fibrosis. The mechanism behind the Sja-miR-1-mediated activation of HSC could be through targeting SFRP1 to regulate the Wnt/β-catenin pathway. These findings reveal that parasite-derived small non-coding RNAs are implicated in cross-species regulation of host pathological process and persistent inhibition of Sja-miR-1 may provide a therapeutic potential for the parasite diseases.