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The redox reactions occurring in the Li-S battery positive electrode conceal various and critical electrocatalytic processes, which strongly influence the performances of this electrochemical energy storage system. Here, we report the development of a single-dispersed molecular cluster catalyst composite comprising of a polyoxometalate framework ([Co 4 (PW 9 O 34 ) 2 ] 10− ) and multilayer reduced graphene oxide. Due to the interfacial charge transfer and exposure of unsaturated cobalt sites, the composite demonstrates efficient polysulfides adsorption and reduced activation energy for polysulfides conversion, thus serving as a bifunctional electrocatalyst. When tested in full Li-S coin cell configuration, the composite allows for a long-term Li-S battery cycling with a capacity fading of 0.015% per cycle after 1000 cycles at 2 C (i.e., 3.36 A g −1 ). An areal capacity of 4.55 mAh cm −2 is also achieved with a sulfur loading of 5.6 mg cm − 2 and E/S ratio of 4.5 μL mg −1 . Moreover, Li-S single-electrode pouch cells tested with the bifunctional electrocatalyst demonstrate a specific capacity of about 800 mAh g −1 at a sulfur loading of 3.6 mg cm −2 for 100 cycles at 0.2 C (i.e., 336 mA g −1 ) with E/S ratio of 5 μL mg −1 . Efficient electrochemical energy storage in Li-S batteries is hindered by sluggish sulfur redox reactions. Here, the authors propose a polyoxometalate/multilayer graphene composite as a bifunctional electrocatalyst for battery performance improvement.

Dendrite growth of alkali metal anodes limited their lifetime for charge/discharge cycling. Here, we report near-perfect anodes of lithium, sodium, and potassium metals achieved by electrochemical polishing, which removes microscopic defects and creates ultra-smooth ultra-thin solid-electrolyte interphase layers at metal surfaces for providing a homogeneous environment. Precise characterizations by AFM force probing with corroborative in-depth XPS profile analysis reveal that the ultra-smooth ultra-thin solid-electrolyte interphase can be designed to have alternating inorganic-rich and organic-rich/mixed multi-layered structure, which offers mechanical property of coupled rigidity and elasticity. The polished metal anodes exhibit significantly enhanced cycling stability, specifically the lithium anodes can cycle for over 200 times at a real current density of 2 mA cm –2 with 100% depth of discharge. Our work illustrates that an ultra-smooth ultra-thin solid-electrolyte interphase may be robust enough to suppress dendrite growth and thus serve as an initial layer for further improved protection of alkali metal anodes. The dendrite growth of alkali metal anodes leads to charge/discharge cycling instability. Here, the authors show that electrochemical polishing can yield near-perfect anodes of three alkali metals by constructing smooth and thin solid-electrolyte interphase layers.

Background Keloids and hypertrophic scars frustrate patients by the deformity of appearance and organ dysfunction. Many modalities had been tried in clinic practice, but the results are unsatisfied. Objective We retrospectively analysed the combined application of bleomycin and triamcinolone for the treatment of keloids and hypertrophic scars. Methods The combination of bleomycin and triamcin acetonide was applied to the treatment of keloids and hypertrophic scars, 86 cases accepted the treatment. Follow‐up 2–5 years after treatment. Results (1) The pain of scars and itching symptoms have basically subsided through treatment. (2) After drug injection treatment, the keloid began to shrink, some of the keloids disappeared. (3) Small keloids did not recur after treatment. Large keloids had local recurrence after treatment. When further treatment was given, the recurrence disappeared. Conclusion The combined application of bleomycin and triamcin acetonide can effectively cure keloids and hypertrophic scars.

Sodium metal anodes combine low redox potential (−2.71 V versus SHE) and high theoretical capacity (1165 mAh g−1), becoming a promising anode material for sodium‐ion batteries. Due to the infinite volume change, unstable SEI films, and Na dendrite growth, it is arduous to achieve a long lifespan. Herein, an oxygen‐doped carbon foam (OCF) derived from starch is reported. Heteroatom doping can significantly reduce the nucleation resistance of sodium metal; combined with its rich pore structure and large specific surface area, OCF provides abundant nucleation sites to effectively guide the nucleation and subsequent growth of sodium metal, and the nature of this foam can accommodate the deposited sodium. Furthermore, a more uniform, robust, and stable SEI layer is observed on the surface of OCF electrode, so it can maintain ultra‐high reversibility and excellent integrity for a long time without dendritic growth. As a result, when the current density is 10 mA cm−2, the electrode can maintain stable 2000 cycles and the coulombic efficiency can reach to 99.83%. Na@OCF||Na3V2(PO4)3 full cell also has extremely high capacity retention of about 97.53% over 150 cycles. These results provide a simple but effective method for achieving the safety and commercialization of sodium metal anode. An O‐doped carbon foam with a sodiophilic surface is constructed and applied to the sodium metal anode. The excellent sodiophilic property, abundant porous structure, and large specific surface make the material stable during multiple plating/stripping processes, and no sodium dendrites are formed. Consequently, the sodium metal battery exhibits excellent electrochemical performance.

Key Points Recent studies provide strong evidence that glycogen synthase kinase 3 (GSK3) signalling has important roles in many neurodevelopmental processes, such as neurogenesis, neuronal polarization and axon outgrowth. Results from GSK3α-Ser21Ala/GSK3β-Ser9Ala double knock-in mice suggest that phosphorylation of GSK3s at their amino-terminal serine residues is not the major regulatory mechanism to control GSK3 activity in the nervous system. Other factors — such as disrupted in schizophrenia 1 (DISC1), partitionary defective 3 (PAR3) and low-density lipoprotein receptor-related protein 6 (LRP6) — may have more important roles in the regulation of GSK3 activity. Evidence suggests that during neurogenesis, GSK3 inactivation promotes neural progenitor proliferation, whereas GSK3 activation promotes neuronal differentiation. The role of GSK3 in neurogenesis might be achieved through regulation of protein stability and microtubule assembly. Several lines of evidence suggest that GSK3 signalling controls neuronal polarization by regulating microtubule stability through several microtubule-binding proteins. GSK3 signalling seems to be the converging point of many pathways that regulate neuronal polarity, such as the phosphatidylinositol 3-kinase (PI3K)–Akt pathway, the PAR3–PAR6–atypical protein kinase C (aPKC) pathway, the LKB1–SAD pathway, and the tuberous sclerosis (TSC) complex–mammalian target of rapamycin (mTOR) pathway. GSK3 as pleiotropic roles in controlling axon outgrowth depending on the substrates involved. Local inactivation of GSK3 towards primed substrates at distal axons is necessary for efficient axon outgrowth, whereas strong suppression of GSK3 activity prevents axon outgrowth, probably through regulation of unprimed substrates. GSK3 signalling can also regulate axon outgrowth by controlling transcriptional factors in the cell soma. The important role of GSK3 signalling in neural development is consistent with its involvement in neurodevelopmental disorders, such as schizophrenia and autism. Further studies may point to novel therapeutic treatments that target GSK3 signalling. Glycogen synthase kinase 3 (GSK3) proteins and their upstream and downstream regulators have key roles in neurodevelopmental processes. Hur and Zhou review the mechanisms that regulate GSK3 activity and discuss how GSK3 controls neurogenesis, neuronal polarization and axon growth. Recent evidence suggests that glycogen synthase kinase 3 (GSK3) proteins and their upstream and downstream regulators have key roles in many fundamental processes during neurodevelopment. Disruption of GSK3 signalling adversely affects brain development and is associated with several neurodevelopmental disorders. Here, we discuss the mechanisms by which GSK3 activity is regulated in the nervous system and provide an overview of the recent advances in the understanding of how GSK3 signalling controls neurogenesis, neuronal polarization and axon growth during brain development. These recent advances suggest that GSK3 is a crucial node that mediates various cellular processes that are controlled by multiple signalling molecules — for example, disrupted in schizophrenia 1 (DISC1), partitioning defective homologue 3 (PAR3), PAR6 and Wnt proteins — that regulate neurodevelopment.

Hyperspectral imaging acquired from unmanned aerial vehicles (UAVs) offers detailed spectral and spatial data that holds transformative potential for precision agriculture applications, such as crop classification, health monitoring, and yield estimation. However, traditional methods struggle to effectively capture both local and global features, particularly in complex agricultural environments with diverse crop types, varying growth stages, and imbalanced data distributions. To address these challenges, we propose CMTNet, an innovative deep learning framework that integrates convolutional neural networks (CNNs) and Transformers for hyperspectral crop classification. The model combines a spectral-spatial feature extraction module to capture shallow features, a dual-branch architecture that extracts both local and global features simultaneously, and a multi-output constraint module to enhance classification accuracy through cross-constraints among multiple feature levels. Extensive experiments were conducted on three UAV-acquired datasets: WHU-Hi-LongKou, WHU-Hi-HanChuan, and WHU-Hi-HongHu. The experimental results demonstrate that CMTNet achieved overall accuracy (OA) values of 99.58%, 97.29%, and 98.31% on these three datasets, surpassing the current state-of-the-art method (CTMixer) by 0.19% (LongKou), 1.75% (HanChuan), and 2.52% (HongHu) in OA values, respectively. These findings indicate its superior potential for UAV-based agricultural monitoring in complex environments. These results advance the precision and reliability of hyperspectral crop classification, offering a valuable solution for precision agriculture challenges.

Mesenchymal stem/progenitor cells (MSPCs) undergo rapid self-renewal and differentiation, contributing to fast skeletal growth during childhood and puberty. It remains unclear whether these cells change their properties during late puberty to young adulthood, when bone growth and accrual decelerate. Here we show that MSPCs in primary spongiosa of long bone in mice at late puberty undergo normal programmed senescence, characterized by loss of nestin expression. MSPC senescence is epigenetically controlled by the polycomb histone methyltransferase enhancer of zeste homolog 2 (Ezh2) and its trimethylation of histone H3 on Lysine 27 (H3K27me3) mark. Ezh2 maintains the repression of key cell senescence inducer genes through H3K27me3, and deletion of Ezh2 in early pubertal mice results in premature cellular senescence, depleted MSPCs pool, and impaired osteogenesis as well as osteoporosis in later life. Our data reveals a programmed cell fate change in postnatal skeleton and unravels a regulatory mechanism underlying this phenomenon. Mesenchymal stem cells are essential for bone development, but it is unclear if their activity is maintained after late puberty, when bone growth decelerates. The authors show that during late puberty in mice, these cells undergo senescence under the epigenetic control of Ezh2.

Microglia mediate multiple facets of neuroinflammation. They can be phenotypically divided into a classical phenotype (pro-inflammatory, M1) or an alternative phenotype (anti-inflammatory, M2) with different physiological characteristics and biological functions in the inflammatory process. Betaine has been shown to exert anti-inflammatory effects. In this study, we aimed to verify the anti-inflammatory effects of betaine and elucidate its possible molecular mechanisms of action in vitro. Lipopolysaccharide (LPS)-activated microglial cells were used as an inflammatory model to study the anti-inflammatory efficacy of betaine and explore its mechanism of regulating microglial polarisation by investigating the morphological changes and associated inflammatory changes. Cytokine and inflammatory mediator expression was also measured by ELISA, flow cytometry, immunofluorescence, and western blot analysis. Toll-like receptor (TLR)-myeloid differentiation factor 88 (Myd88)-nuclear factor-kappa B (NF-κB) p65, p-NF-κB p65, IκB, p-IκB, IκB kinase (IKK), and p-IKK expression was determined by western blot analysis. Betaine significantly mitigated the production of pro-inflammatory cytokines and increased the release of anti-inflammatory cytokines. It promoted the conversion of the microglia from M1 to M2 phenotype by decreasing the expression of inducible nitric oxide synthase and CD16/32 and by increasing that of CD206 and arginase-1. Betaine treatment inhibited the TLR4/NF-κB pathways by attenuating the expression of TLR4-Myd88 and blocking the phosphorylation of IκB and IKK. In conclusion, betaine could significantly alleviate LPS-induced inflammation by regulating the polarisation of microglial phenotype; thus, it might be an effective therapeutic agent for neurological disorders.

Joint pain is the defining symptom of osteoarthritis (OA) but its origin and mechanisms remain unclear. Here, we investigated an unprecedented role of osteoclast-initiated subchondral bone remodeling in sensory innervation for OA pain. We show that osteoclasts secrete netrin-1 to induce sensory nerve axonal growth in subchondral bone. Reduction of osteoclast formation by knockout of receptor activator of nuclear factor kappa-B ligand (Rankl) in osteocytes inhibited the growth of sensory nerves into subchondral bone, dorsal root ganglion neuron hyperexcitability, and behavioral measures of pain hypersensitivity in OA mice. Moreover, we demonstrated a possible role for netrin-1 secreted by osteoclasts during aberrant subchondral bone remodeling in inducing sensory innervation and OA pain through its receptor DCC (deleted in colorectal cancer). Importantly, knockout of Netrin1 in tartrate-resistant acid phosphatase-positive (TRAP-positive) osteoclasts or knockdown of Dcc reduces OA pain behavior. In particular, inhibition of osteoclast activity by alendronate modifies aberrant subchondral bone remodeling and reduces innervation and pain behavior at the early stage of OA. These results suggest that intervention of the axonal guidance molecules (e.g., netrin-1) derived from aberrant subchondral bone remodeling may have therapeutic potential for OA pain.

A bstract We investigate a novel gravitational wave (GW) production mechanism from gravitons generated during the pre-thermal phase of cosmic reheating, where the energy density is dominated by non-thermalized inflaton decay products, dubbed reheatons . We consider multiple production channels, including: i ) pure inflaton-inflaton annihilation, ii ) graviton Bremsstrahlung from inflaton decay, iii ) scatterings between an inflaton and a reheaton, and iv ) scatterings among reheatons. To determine the resulting GW spectrum, we solve the Boltzmann equation to obtain the graviton phase-space distribution for each channel. We find that the third channel, iii ), dominates due to the large occupation number of reheatons at highly-energetic states during the pre-thermalization phase. Notably, in scenarios with a low inflaton mass, the GW spectrum could fall within the sensitivity range of future experiments such as the Einstein Telescope, the Cosmic Explorer, the Big Bang Observer, and ultimate DECIGO.