Physics

Metal arene-based reducing agents, particularly sodium naphthalenide (Na–Naph) and lithium naphthalenide (Li–Naph), are highly capable of forming variety of nanoparticles (NPs) and quantum dots (QDs) of highly electropositive elements belonging from post-transition metal and semimetal and impurity-free intermetallic phases that can be used in technological fields. Nevertheless, this method is not much recognized. It offers many advantages over conventional hydride- and polyol-based routes. Their exceptional reducing strength and radical-driven mechanism enable the simultaneous coreduction of different metal ions, thereby effectively eliminating long-standing obstacles during the synthesis of ordered intermetallic phases. This review aims to give a comprehensive account of metal–arene-driven synthesis to prepare unary, binary, and ternary intermetallic compound (IMC) NPs. This review also explores the structure–property correlations, highlights emerging applications across diverse domains, and outlines sustainable pathways for green, scalable synthesis. Ultimately, the real potential of metal–arene-driven synthesis lies in using it as a strategic tool for designing the next generation of IMC NPs with a diversity of composition and architectures having tunable electronic and functional properties.

High-entropy alloys (HEAs) have emerged as a promising class of bifunctional electrocatalysts capable of simultaneously driving the hydrogen evolution reaction (HER) and the oxygen reduction reaction (ORR) with high activity and durability. Their near-equiatomic multicomponent compositions give rise to unique physicochemical characteristics, including lattice distortion, sluggish diffusion, high-entropy stabilization, and pronounced electronic heterogeneity, that collectively generate diverse and synergistic active sites inaccessible in conventional alloys. This review summarizes recent progress in HEA-based bifunctional electrocatalysis, with a focus on the fundamental mechanisms governing HER and ORR activity, stability, and selectivity. We discuss advances in synthesis strategies, ranging from confined growth and step-alloying to scalable continuous-flow methods, that enable precise control over composition, size, and surface structure. Complementary computational and data-driven approaches, including density functional theory, machine-learning-assisted screening, and descriptor development, are highlighted as essential tools for navigating the vast HEA design space and establishing structure–property relationships. Particular attention is paid to adsorption-energy distributions, multisite cooperativity, and environmental effects under realistic electrochemical conditions. Finally, we outline current challenges and future opportunities for integrating mechanistic understanding with AI-guided, closed-loop design frameworks to accelerate the discovery of next-generation HEA bifunctional electrocatalysts for sustainable energy conversion.

Cu@Sn core–shell nanoparticles have emerged as promising candidates for high-density electronic packaging owing to their excellent mechanical strength, electrical conductivity, and thermal stability. However, the intrinsic mismatch in the interdiffusion rates of Cu and Sn inevitably leads to the formation of severe Kirkendall voids, compromising the microstructural integrity and overall device reliability. In this work, a solid Cu@Sn core–shell nanostructure was constructed by introducing trace amounts of P during the Cu–Sn chemical displacement process, which shows an optimized Sn-to-Cu thickness ratio of ∼10%, with a Cu core of 2.65 ± 0.06 μm and an Sn shell of ∼0.29 μm. At the Sn/Cu interface, P selectively enriches on the Cu surface to form an adsorbed layer, suppressing the inward diffusion of Sn, where P promotes the in situ formation of ultrafine Cu3P nanocrystals and exerts a significant interfacial pinning effect on outward Cu diffusion and increases the vacancy formation energy. Notably, thermogravimetric analysis confirms the substantially enhanced oxidation resistance of the solid Cu@Sn nanoparticles (residual mass at 600 °C: 109.66% for Cu@Sn vs 123.54% for bare Cu). When used as soldering precursors, the P-mediated Cu@Sn solid nanoparticles form dense Cu3Sn intermetallic compound (IMC) frameworks after reflow at 300 °C, yielding void-free joints with remelting temperatures above 425 °C. This work not only elucidates the mechanism by which P-mediated interfacial engineering suppresses Kirkendall void formation but also highlights the significant potential of Cu@Sn nanoparticles for high-reliability electronic packaging, offering a promising pathway toward enhanced power density and device reliability.

In hypertrophic and failing hearts, fuel metabolism is reprogrammed toward enhanced glycolysis. Here, we identify asprosin, an adipokine, as a critical regulator of this process in pathological cardiac hypertrophy. In patients, circulating asprosin levels correlate with NT-proBNP and EF. Cardiomyocyte-specific asprosin overexpression aggravates hypertrophy, abnormal glycolysis, and impairs mitochondrial ATP production in male mice, whereas its deficiency confers protection against TAC- or Ang II-induced remodeling in male/female mice. Mechanistically, asprosin binds PFKP and inhibits the K48-linked ubiquitination by DTX3L, thereby stabilizing PFKP and driving aberrant glycolysis, PDK4 induction, PDH inhibition, and impaired respiration. Genetic knockdown of PFKP mitigates hypertrophy and fibrosis in male mice, whereas PFKP overexpression abolishes the protective effects conferred by FBN1 knockdown. Moreover, YY1 is identified as a transcriptional activator of asprosin in the hypertrophic hearts of male mice. Here we show that the YY1-asprosin-PFKP-PDK4-PDH axis underlies metabolic remodeling, and we highlight plasma asprosin as a potential early biomarker and therapeutic target for cardiac dysfunction.

Excessive avoidance is a core symptom of post-traumatic stress disorder (PTSD), yet its underlying circuit mechanisms remain poorly understood. Here, using a mouse model of PTSD induced by inescapable footshock, we observed a delayed and prolonged increase in avoidance behavior associated with selective activation of basolateral amygdala (BLA) projection neurons (PNs) targeting ventral hippocampus (BLA→vHPC PNs), but not nucleus accumbens, in both sexes. This projection-specific activation results from enhanced neuronal excitability and excitatory transmission driven by glucocorticoid receptor (GR) signaling. Among the cascade of GR signaling molecules, we identified serum- and glucocorticoid-regulated kinase 1 (Sgk1) as a key downstream mediator linking stress exposure to the hyperactivation of BLA→vHPC PNs and PTSD-like avoidance behavior. Manipulating Sgk1 expression bidirectionally regulates neuronal activity and susceptibility to stress-induced avoidance. These findings underscore the critical role of projection-specific upregulation of Sgk1 in BLA PNs in the pathogenesis of PTSD-like avoidance behavior.

Soil organic carbon (SOC) comprises particulate (POC) and mineral-associated organic carbon (MAOC), which differ in formation, stabilization, and loss mechanisms. While the current global distribution of POC and MAOC is characterized, their vulnerability under future climate scenarios remains unclear. Using 3284 topsoil (0-30 cm) observations from six continents, we identify high-latitude soils as global hotspots of SOC vulnerability under shared socioeconomic pathway scenarios (SSP126, SSP245, and SSP585). Under a high-emission scenario (SSP585), high-latitude soils are projected to lose substantial POC by 2100, accounting for about 81 ± 10% of total SOC losses. These declines are driven by the high proportion of SOC stored as POC (f_POC) and its high temperature sensitivity. We show that f_POC is a robust indicator of SOC vulnerability to climate change. Globally, the projected POC decline corresponds to a cumulative carbon dioxide (CO₂) release of 81.34 Pg CO₂-equivalent by 2100, highlighting the importance of preserving POC to mitigate climate feedbacks.

Atomically dispersed catalysts based on 3d metals have been extensively explored in the catalytic field, but stabilizing 4d and 5d metals like Ru, Pd, and Pt as single atoms remains a challenge due to their high cohesive energies. Herein, we develop a hydrogen-embrittlement-inspired strategy that leverages H₂ permeation to weaken metal-metal cohesion in 4d/5d metal clusters during high-temperature synthesis. Hydrogen diffuses into the clusters, driving their dissociation into individual atoms, which are subsequently stabilized by nitrogen dopants in carbon supports, resulting in the formation of stable M-N₄ single-atom sites. Taking Ru as a model system, ex-situ microscopy and spectroscopy offer definitive evidence that hydrogen permeation disrupts Ru-Ru bonding interactions, facilitating the conversion of Ru clusters into isolated RuN₄ sites during the H₂-assisted thermal activation process. Consequently, the prepared NC-Ru-950 catalyst achieves satisfactory activity and stability for acidic oxygen reduction and proton exchange membrane fuel cells. This work introduces a robust and universal strategy for stabilizing 4d and 5d transition metals as single-atom catalysts, offering a promising route to develop high-performance electrocatalysts.

Transcription factor EB (TFEB) is a master regulator of lysosomal biogenesis and cellular clearance pathways. TFEB activity is tightly controlled by multiple post-translational mechanisms, but the exact molecular mechanism controlling its stability has remained elusive. Here, we identify the IκB kinase (IKK) complex as a key regulator of TFEB protein stability through a phosphorylation-ubiquitination cascade. A high-content kinase inhibitor screen reveals that IKK inhibition increases TFEB protein levels, and genetic ablation of IKK components increases TFEB stability, upregulates lysosomal genes, and enhances lysosomal biogenesis and degradative capacity. Mechanistically, we show that IKK phosphorylates TFEB on a cluster of serine residues (⁴²³SPFPSLS⁴²⁹), generating a phosphodegron recognized by the E3 ligase β-TrCP2, which in turn targets TFEB for proteasomal degradation via ubiquitination of adjacent lysine residues (K430 and K431). Mutation of either the phosphosites or the ubiquitination sites stabilizes TFEB without impairing its ability to translocate to the nucleus, activate target gene expression, or promote tau clearance in a cell model of tauopathy. These findings establish IKK-β-TrCP2 as a core regulatory axis controlling TFEB protein turnover and levels and reveal a mechanistically distinct layer of TFEB regulation that may be leveraged to enhance lysosomal function in disease contexts.

Bacteria span Earth's ecosystems, coupling ecological versatility with genome-architectural reconfiguration across shifting physicochemical conditions. Yet the genomic routes by which free-living lineages cross ecosystem boundaries, and the consequences for genome architecture, remain poorly understood. Here, we use comparative and evolutionary genomics to investigate a soil-to-sediment-to-freshwater transition in Limnocylindria, an abundant clade within the Chloroflexota phylum. Two sister families show contrasting strategies. CSP1-4 expands genomes through niche-specific gene acquisition, whereas Limnocylindraceae undergoes genome reduction and metabolic simplification-revealing alternative evolutionary routes to similar ecological outcomes. In Limnocylindraceae, the loss of key DNA glycosylases coincides with degradation of base excision repair and is consistent with a hypermutator state that may have accelerated genomic erosion during freshwater specialization, potentially facilitating ecological expansion. This reductive genome trajectory is associated with a freshwater-adapted lineage with unexpectedly high GC content, challenging canonical links between base composition and genome size. While mutational processes appear to dominate genome restructuring, proteome-level patterns suggest selection favoring carbon- and nitrogen-efficient amino acid usage, implying that adaptive refinement can emerge alongside primarily non-adaptive dynamics. Overall, our findings are consistent with mutation-driven genome reduction and proteome optimization acting in concert to support cross-ecosystem boundary crossing and freshwater specialization in a free-living Chloroflexota lineage.

Long-range dispersals of marine bacteria in the oceans have remained largely indecipherable, which is particularly relevant for Vibrio, responsible for global epidemics in humans and animals. Here, we combine the analysis of 40 terabases of metagenomic data and satellite-tracked surface drifter data, from across the globe revealing that Vibrio are abundant members of the ocean surface and show a strong association with microplankton, which appears to govern their distribution and connectivity at a global scale. We identify long-distance biological corridors connecting Vibrio communities, including potentially pathogenic Vibrio. These corridors allow movement over thousands of kilometres in a fairly short time, with estimates of less than 1.5 years to cross an ocean basin. These findings have deep implications for the demography and community dynamics of Vibrio species and the epidemiology of associated diseases.

Although biomimetic nanostructured surfaces can impart exceptional properties, their inherent fragility makes them prone to failure under mechanical wear. This study presents a method for friction-induced atomic-scale surface reconstruction of sapphire, resulting in durable, scale-like nanostructures that retain the hardness of bulk the sapphire (27.2 GPa). Friction experiments and reactive force field molecular dynamics simulation reveal that surface reconstruction is driven by the selective removal of atoms from less chemically inert crystal planes of sapphire via interfacial bridge bonds during friction with SiO₂. Subsurface characterizations demonstrate that the nanostructures maintain a consistent single-crystal structure with the original sapphire, thereby ensuring their exceptional mechanical properties. To evaluate its triboelectric performance and wear resistance, nanostructured sapphire is integrated into triboelectric nanogenerators (TENGs) with a diamond-like carbon (DLC) friction layer. Triboelectric tests indicate that after 100k cycles of friction, the discharge performance of TENGs exhibits no significant decline, and the nanostructures show negligible wear, demonstrating their extraordinary durability. This study introduces an atomic-scale strategy for nanostructure fabrication, providing an approach to surface reconstruction of sapphire and insights into the development of wear-resistant nanostructures.

Controlled generation of topological spin textures, such as merons and their bound state, the bimerons, is essential for advancing spintronic technologies and elucidating soliton physics in condensed matter. Using in situ Lorentz transmission electron microscopy coupled with femtosecond laser pulse, we demonstrate the creation of two distinct Bloch-type bimeron states in chiral magnet Co₈Zn₈Mn₄ thin plates at room temperature. Magnetic imaging and micromagnetic simulations reveal that bimeron density varies with applied magnetic field strength, enabling dynamic topological control. We further establish that the topological classification of laser-generated bimerons is invariant with specimen thickness. Field-driven reversible transformations between elongated and circular bimeron morphologies are observed, governed by the competition of Zeeman energy and magnetic shape anisotropy. Micromagnetic simulations quantitatively reproduce these metastable states, validating a unified meron-skyrmion topological framework. This work establishes a single-pulse protocol for optical manipulation of topological spin textures.

Genome annotation currently requires performing dozens of molecular assays in hundreds of cell and tissue samples, an expensive endeavor which is impractical to replicate across all species and conditions of interest. Here, we introduce BioSeq2Seq, a deep learning framework that infers cell-line-specific molecular assays widely used for genome annotation by leveraging a tri-modal input: evolutionarily conserved DNA sequence features, together with cell-line-specific transcriptional activity and directionality captured by a single run-on sequencing assay. BioSeq2Seq enables flexible genome annotation tasks through parameterized configurations of input features and output targets, combined with gradient-guided architectural refinement for specific biological objectives. Our model demonstrates high accuracy across four downstream tasks, showing improvements of 14.27% in histone modification prediction, 2.50% in functional element identification, and 2.90% in gene expression prediction compared to state-of-the-art methods. In transcription factor binding site (TFBS) prediction, it maintains performance comparable to that of leading existing approaches. By achieving competitive performance across tasks with single-cell-line input data, BioSeq2Seq provides an efficient and low-cost alternative for genome annotation.

Gain-of-function mutations in the human follicle-stimulating hormone receptor (FSHR) cause spontaneous ovarian hyperstimulation syndrome (OHSS), a serious reproductive disorder. However, the molecular physiology and treatment options for OHSS remain elusive. Notably, estrildid finches naturally carry an FSHR variant (Thr449Ala) analogous to the pathogenic mutation in humans yet are resistant to OHSS. Here we show that this resistance stems from significantly reduced luteinizing hormone receptor expression in estrildid ovarian granulosa cells. Furthermore, treatment with the luteinizing hormone receptor antagonist alleviates OHSS symptoms in mouse models. Single-cell RNA transcriptomic reveals functional compensation of the two receptors to regulate estrogen production and vascular permeability, resembling the adaptive mechanisms observed in estrildid finches. Our study unravels the molecular mechanism underlying the physiological adaptation of estrildid ovaries to high FSHR constitutive activity and is a example of how the concept of Darwinian Medicine could be exploited to identify novel drug targets for ovarian hyperstimulation syndrome treatment.

The development of high-performance solid-state electrolytes (SSEs) has entered a critical stage, where entropy-driven strategies offer transformative potential for enhancing electrochemical properties. By engineering local environments for conductive ions alongside introducing disorder, these approaches can significantly improve conductivity. However, embracing high-entropy designs does not always guarantee improved performance. Current entropy descriptions oversimplify disorder by accounting solely for host framework configurations, neglecting conductive ion-induced disorder, rendering such descriptions incomplete. Herein, we propose path entropy (S_p) as a descriptor that quantifies diffusion pathway diversity, directly capturing diffusional disorder. Combining Markov state model with transition path theory, we reveal the interplay between diffusion pathway diversity of lithium and microscopic local environments in inorganic thiophosphates. Generalizing this path-informative S_p for high-throughput screening, we demonstrate its broad applicability in identifying and designing high-performance SSEs. Our work establishes a critical link between entropy evolution underlying ion conduction and practical entropy-driven design principles.

Recently, topological deep learning (TDL), which integrates algebraic topology with deep neural networks, has achieved significant success in processing point-cloud data and has emerged as a promising paradigm in data science. However, TDL has not been extended to differentiable-manifold data, including images, due to the challenges introduced by differential topology. We address this challenge by introducing a manifold topological deep learning (MTDL) framework. To apply Hodge theory, we integrate it into a streamlined convolutional neural network within the MTDL framework. In this framework, original images are represented as smooth manifolds with vector fields that are decomposed into three orthogonal components based on Hodge theory. These components are then concatenated to form an input image for the convolutional neural network architecture. The performance of MTDL is evaluated using the MedMNIST v2 benchmark database, which comprises 717,287 biomedical images from eleven 2D and six 3D datasets. MTDL significantly outperforms other competing methods, extending TDL to a wide range of data on smooth manifolds.

Allergic asthma is promoted by type 2 inflammation involving cytokines such as IL-4, IL-5, and IL-13, with group 2 innate lymphoid cells (ILC2s) playing a key pathogenic role. Here, we identify T cell immunoglobulin and mucin domain-containing protein 3 (Tim-3) as a negative regulator of ILC2 function. Tim-3 expression is upregulated in activated pulmonary ILC2s, and engagement with Tim-3 agonists inhibits ILC2 activation, proliferation, and type 2 cytokine production via the Nemo Like Kinase (NLK) signaling pathway and suppression of mitochondrial metabolism. In vivo, Tim-3 agonists alleviate airway hyperreactivity (AHR) and inflammation in both IL-33- and Alternaria alternata-induced AHR models, while ILC2-specific Tim-3 deletion exacerbates AHR. These results are confirmed in human ILC2s and humanized mice, supporting the translational relevance. Our findings establish Tim-3 as an inhibitory checkpoint for ILC2s and suggest its potential as a therapeutic target in allergic asthma and other ILC2-mediated diseases.

Nanoscale chromatin domains have emerged as fundamental units of mammalian genome organization during interphase and mitosis. Single-molecule localization microscopy now enables their direct visualization, revealing conserved features including characteristic packing, enrichment of linker histones, and radial stratification of histone marks. These domains act as dynamic regulators of gene activity, remodel in response to developmental and environmental cues, and become disrupted in disease. Experimental findings and biophysical modelling point to internucleosomal interactions and epigenetic reactions as key drivers of their organization. By situating them alongside lamin- and nucleolus-associated domains, we propose a unified biophysical framework for genome organization across scales. Their recurrent disruption in aging and disease makes them compelling targets for diagnosis and intervention.

Metal halide perovskite light-emitting diodes have exhibited great potential for the next-generation displays. However, the realization of highly efficient and bright pure-blue devices with narrow emission bandwidth remains a significant challenge. Herein, we propose a controllable crystal facet growth to diminish random crystal facet-correlated defects and reveal the underlying mechanism of energy-driven facet-selective crystal growth. This strategy enables high-quality pure-blue emitters with high crystallinity, low defects, and large exciton binding energy. Consequently, we achieve highly performing pure-blue devices with a narrow emission bandwidth of 14 nm, an external quantum efficiency of 14.0% at 1699 cd m^-2, and an impressive peak brightness of 8334 cd m^-2 at an emission of 473 nm. We verify a good applicability of the strategy in achieving high-performance sky-blue devices with a narrow emission of 15 nm, a high efficiency of 23.8%, and a large luminance of 13,230 cd m^-2 at 488 nm.

Photocatalysis involves photogenerated charge carriers transferring to reactants via active sites. While carrier-reactant interactions are widely studied, carrier-site interactions remain overlooked. Here, we report a wavelength-gated in situ site regeneration strategy to improve catalyst stability. In photocatalytic CO₂ reduction, the Au/Ce_0.95Cu_0.05O_2-x solid-solution catalyst exhibited a high stability exceeding 48 h and a C₂H₆ production rate of 63.8 μmol g^-1 h^-¹. Notably, the catalyst initially deactivates rapidly under 375 nm light but can be reactivated under 535 nm light. In situ spectroscopy and theoretical simulation attributed this to an in situ redox process involving the active sites and reactants. Under 375 nm light, the Cu⁺-O₃-Ce site binds with dissociated O atoms from CO₂, transforming to an inactive Cu²⁺-O₄-Ce structure, which is subsequently reactivated by localized surface plasmon resonance hot electrons generated under 535 nm light. This work presents a universal strategy for designing catalysts with long-term stability.

Ischemic heart failure remains a major clinical challenge, underscoring the need to better understand post-infarction immune mechanisms and identify new therapeutic targets. Both innate and adaptive immunity contribute to adverse cardiac remodeling following myocardial infarction (MI), yet the role of cytotoxic cells such as natural killer (NK) cells remains poorly defined. Here, we show that after acute MI in mice, NK cells are recruited to the ischemic myocardium in a CCR2-dependent manner and become activated. Activated NK cells locally release granzyme B, promoting cardiomyocyte apoptosis, adverse ventricular remodeling, and impaired cardiac function. Genetic deletion or pharmacological depletion of NK cells reduces cardiomyocyte death, attenuates inflammation, limits myocardial injury, and improves cardiac function. In contrast, NK cell activation using an anti-NKG2A monoclonal antibody exacerbates ischemic heart failure. We further demonstrate that NK cells regulate bone marrow myelopoiesis through local GM-CSF production. Finally, we identify a distinct NK cellular and transcriptomic signature in human ischemic heart tissue at early stages. Together, these findings reveal a detrimental role for NK cells following acute MI and highlight NK cells as potential therapeutic targets to limit adverse cardiac remodeling.