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Water electrolysis via alkaline hydrogen evolution reaction (HER) is a promising approach for large-scale production of high-purity hydrogen at a low cost, utilizing renewable and clean energy. However, the sluggish kinetics derived from the high energy barrier of water dissociation impedes seriously its practical application. Herein, a series of hybrid Pt nanoclusters/Ru nanowires (Pt/Ru NWs) catalysts are demonstrated to accelerate alkaline HER. And the optimized Pt/Ru NWs (10 ​% wt Pt) exhibits exceptional performance with an ultralow overpotential (24 ​mV at 10 ​mA ​cm−2), a small Tafel slope (26.3 ​mV dec−1), and long-term stability, outperforming the benchmark commercial Pt/C-JM-20 ​% wt catalyst. This amazing performance also occurred in the alkaline anion-exchange membrane water electrolysis devices, where it delivered a cell voltage of about 1.9 ​V at 1 ​A ​cm−2 and an outstanding stability (more than 100 ​h). The calculations have revealed such a superior performance exhibited by Pt/Ru NWs stems from the formed heterointerfaces, which significantly reduce the energy barrier of the decisive rate step of water dissociation via cooperative-action between Pt cluster and Ru substance. This work provides valuable perspectives for designing advanced materials toward alkaline HER and beyond.

IntroductionAutonomous Underwater Vehicles (AUVs) are capable of independently performing underwater navigation tasks, with side-scan sonar being a primary tool for underwater detection. The integration of these two technologies enables autonomous monitoring of the marine environment.MethodsTo address the limitations of existing seabed detection methods, such as insufficient robustness and high complexity, this study proposes a comprehensive seabed detection method based on a sliding window technique. Additionally, this study introduces a sonar image stitching method that accounts for variations in image intensity and addresses challenges arising from multi-frame overlaps and gaps. Furthermore, an autonomous target perception framework based on shadow region segmentation is proposed, which not only identifies targets in side-scan sonar images but also provides target height measurements.ResultsComprehensive seabed detection method improves accuracy by 31.2% compared to the peak detection method. In experiments, the height measurement error for this method was found to be 9%.DiscussionTo validate the effectiveness of the proposed seabed detection method, sonar image stitching method, and target perception framework, comprehensive experiments were conducted in the Qingjiang area of Hubei Province. The results obtained from the lake environment demonstrated the effectiveness of the proposed methods.

The Autonomous Underwater Vehicle (AUV) is capable of autonomously conducting underwater cruising tasks. When combined with docking operations, the AUV can replenish its electric power after long-distance travel, enabling it to achieve long-range autonomous monitoring. This paper proposes a positioning method for the cruising and docking stages of AUVs. Firstly, a vision guidance algorithm based on monocular vision and threshold segmentation is studied to address the issue of regional noise that commonly occurs during underwater docking. A solution for regional noise based on threshold segmentation and proportional circle selection is proposed. Secondly, in order to enhance the positioning accuracy during the cruising stage, a fusion positioning algorithm based on particle filtering is presented, incorporating the Doppler Velocity Log (DVL) and GPS carried by the AUV. In simulation, this algorithm improves positioning accuracy by over 56.0% compared to using individual sensors alone. Finally, experiments for cruising and docking were conducted in Qingjiang, Hubei, China. The effectiveness of both methods is demonstrated, with successful docking achieved in four out of five attempts.

Background and objectives: The heterogeneity of pulmonary fibroblasts, a critical aspect of both murine and human models under physiological and pathological conditions, is well-documented. Yet, consensus remains elusive on the subtypes, lineage, biological attributes, signal transduction pathways, and plasticity of these fibroblasts. This ambiguity significantly impedes our understanding of the fibrotic processes that transpire in lung tissue during aging. This study aims to elucidate the transcriptional profiles, differentiation pathways, and potential roles of fibroblasts within aging pulmonary tissue.Methods: We employed single-cell transcriptomic sequencing via the 10x Genomics platform. The downstream data were processed and analyzed using R packages, including Seurat. Trajectory and stemness of differentiation analyses were conducted using the Monocle2 and CytoTRACE R packages, respectively. Cell interactions were deciphered using the CellChat R package, and the formation of collagen and muscle fibers was identified through Masson and Van Geison staining techniques.Results: Our analysis captured a total of 22,826 cells, leading to the identification of fibroblasts and various immune cells. We observed a shift in fibroblasts from lipogenic and immune-competent to fibrotic and myofibroblast-like phenotype during the aging process. In the aged stage, fibroblasts exhibited a diminished capacity to express chemokines for immune cells. Experimental validation confirmed an increase of collagen and muscle fiber in the aged compared to young lung tissues. Furthermore, we showed that TGFβ treatment induced a fibrotic, immunodeficient and lipodystrophic transcriptional phenotype in young pulmonary fibroblasts.Conclusion: We present a comprehensive single-cell transcriptomic landscape of lung tissue from aging mice at various stages, revealing the differentiation trajectory of fibroblasts during aging. Our findings underscore the pivotal role of fibroblasts in the regulation of immune cells, and provide insights into why age increases the risk of pulmonary fibrosis.

In almost all cellular phenomena and life activities, transmembrane exchange of signals and metabolites is indispensable, and heavily dependent on high selectivity of membrane pores and channels. The involved principles of natural selectivity are widely inspired and adopted for future membrane design, but often limited by the geometry of those artificial channels. Herein, a smectic liquid crystal polymeric (SmP) membrane embedded with tubular cut‐through pillar[5]arene dimers (P5Ds) by self‐assembly is first constructed. The physical confinement effect of inner subnanosized P5D cavity enables SmP membrane to behave with 1D continuous hydrogen sulfide ion (HS−) flow and ultrahigh physical selectivity for HS−. The simulated calculations and corresponding energy analyses show that it is essentially attributed to the size of ion–water cluster, not its own size. It is anticipated to provide a highly precise platform for separation and detection of human endogenous hydrogen sulfide as representative biomarker.

Summary: Dermal adipocyte lineage cells are highly plastic and can undergo reversible differentiation and dedifferentiation in response to various stimuli. Using single-cell RNA sequencing of developing or wounded mouse skin, we classify dermal fibroblasts (dFBs) into distinct non-adipogenic and adipogenic cell states. Cell differentiation trajectory analyses identify IL-1-NF-κB and WNT-β-catenin as top signaling pathways that positively and negatively associate with adipogenesis, respectively. Upon wounding, activation of adipocyte progenitors and wound-induced adipogenesis are mediated in part by neutrophils through the IL-1R-NF-κB-CREB signaling axis. In contrast, WNT activation, by WNT ligand and/or ablation of Gsk3, inhibits the adipogenic potential of dFBs but promotes lipolysis and dedifferentiation of mature adipocytes, contributing to myofibroblast formation. Finally, sustained WNT activation and inhibition of adipogenesis is seen in human keloids. These data reveal molecular mechanisms underlying the plasticity of dermal adipocyte lineage cells, defining potential therapeutic targets for defective wound healing and scar formation.

This paper proposes a consensus–coordinated control strategy to improve the stability and reliability of interconnected direct current (DC) microgrid cluster systems based on isolated bidirectional DC–DC converters. Compared with the traditional communication-based control strategy, the proposed method does not require an additional communication system. The proposed method is only based on local measurement information, making the whole cluster form an organic unit. No matter where the power disturbance occurs in the continuous-flow microgrid, all the balance units in the system can be linked to provide emergency power support for the disturbed microgrid, improve the dynamic characteristics of the DC voltage of the disturbed microgrid, and reduce the steady-state deviation of the DC voltage of the disturbed grid. The disturbance power is reasonably borne by the balance unit of the whole system according to its equivalent power distribution coefficient ratio. Finally, the effectiveness of the proposed control strategy is verified through the PSCAD/EMTDC simulation.

Anthracyclines, such as doxorubicin, represent one group of chemotherapy drugs with the most cardiotoxicity. Despite that anthracyclines are capable of treating assorted solid tumors and hematological malignancies, the side effect of inducing cardiac dysfunction has hampered their clinical use. Currently, the mechanism underlying anthracycline cardiotoxicity remains obscure. Increasing evidence points to mitochondria, the energy factory of cardiomyocytes, as a major target of anthracyclines. In this review, we will summarize recent findings about mitochondrial mechanism during anthracycline cardiotoxicity. In particular, we will focus on the following aspects: 1) the traditional view about anthracycline-induced reactive oxygen species (ROS), which is produced by mitochondria, but in turn causes mitochondrial injury. 2) Mitochondrial iron-overload and ferroptosis during anthracycline cardiotoxicity. 3) Autophagy, mitophagy and mitochondrial dynamics during anthracycline cardiotoxicity. 4) Anthracycline-induced disruption of cardiac metabolism.