Browse Articles

Local lateral connectivity is sufficient for replicating cortex-like topographical organization in deep neural networks

Moiré collapse and Luttinger liquids in twisted anisotropic homobilayers

We introduce twisted anisotropic homobilayers as a distinct class of moiré systems, characterized by a distinctive “magic angle,” θ M , where the moiré unit cell collapses. Unlike conventional studies of moiré materials, which primarily focus on small lattice misalignments, we demonstrate that this moiré collapse occurs at large twist angles in generic twisted anisotropic homobilayers. The collapse angle, θ M , is likely to give rise quasi-crystal behavior as well as to the formation of strongly correlated states, that arise not from flat bands, but from the presence of ultra-anisotropic electronic states, where non-Fermi liquid phases can be stabilized. In this work, we develop a continuum model for electrons based on extensive ab initio calculations for twisted bilayer black phosphorus, enabling a detailed study of the emerging moiré collapse features in this prototypical system. We show that the (temperature) stability criterion for the emergence of (sliding) Luttinger liquids is generally met as the twist angle approaches θ M . Furthermore, we explicitly formulate the collapsed single-particle one-dimensional (1D) continuum Hamiltonian and provide the fully interacting, Hamiltonian applicable at low doping levels. Our analysis reveals a rich landscape of multichannel Luttinger liquids, potentially enhanced by valley degrees of freedom at large twist angles.

Calcium-enriched mesoporous silica/PLGA scaffolds enhance bone repair in a rabbit femoral condylar defect model

Programmable ferroelectric rectifier for reliable and efficient neuromorphic crossbar array

Modulation of electronic structure via dual moiré patterns in twisted 1 <i>T</i> -TaSe ₂

We investigate a twisted bilayer of 1 T -TaSe 2 (twist angle &lt; 4 ° ) using scanning tunneling microscopy and spectroscopy, revealing that the coexisting twisted atomic lattice and charge density wave (CDW) superlattice generate a dual moiré structure with distinct electronic modulation effects: The topographic moiré pattern stems from atomic lattice twisting modulating CDW intensity, while the twisted CDW superlattice drives a continuous insulator-to-metal transition, as evidenced by electronic gap evolution from large to metallic states. Density functional theory calculations show this transition arises from twist-induced changes in star of David motif stacking. Using the moiré-period gap map as the interlayer potential V ( r ) , we construct a continuum model via its Fourier components V G , finding that V G mediates multiple interlayer scattering processes that produce numerous superposition states manifesting as split flat-band pairs with distinct energy gaps. This work elucidates a CDW-twist-based mechanism for electronic control in 1 T -TaSe 2 and provides insights into Mott physics and complex electronic phases in related materials.

Knowledge, attitudes, and practices regarding transfusion-related acute lung injury among healthcare providers in Jiangsu: a multicenter cross-sectional study

Structures of respiratory supercomplexes and ATP synthase oligomers in mammalian mitochondrial inner membrane

Bridging developmental and statistical approaches to variation and evolution

Phenotypic variation is the raw material for evolutionary diversification and adaptation. However, a critical gap remains in evolutionary theory between developmental and statistical representations of phenotypic variation, limiting our ability to understand and predict evolutionary change. In this paper, we close this gap by establishing a formal bridge between developmental and statistical accounts of phenotypic variation. Representing development as a dynamical system, we derive explicit relationships between perturbations to developmental systems and quantitative-genetic parameters. Through this framework, we obtain two important results. First, we show that the full developmental trajectory contains information that can improve the estimation of statistical parameters relevant to evolution. Second, we explain how different sources of variation—genetic, environmental, and stochastic—shape the distribution of phenotypic variation. This reveals conditions under which covariance matrices are expected to align, offering a developmental explanation for statistical patterns of phenotypic variation at both micro- and macroevolutionary scales. These findings advance our understanding of how developmental processes structure phenotypic variation, shape evolutionary dynamics, and influence evolvability.

Correction: Endometrial biopsy performed before the first in vitro fertilization does not impact the early pregnancy rate

A blueprint for local and distal invasion programs in glioblastoma

Ubiquitin-specific peptidase-19 links TDP-43 aggregation to ER stress

Aggregation and deposition of TAR DNA-binding protein 43 (TDP-43) is a salient pathological signature of amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration-TDP (FTLD-TDP). TDP-43 proteostasis and aggregation are controlled by several posttranslational modifications, including ubiquitination. While multiple E3 ubiquitin ligases are known to facilitate TDP-43 clearance, little is known about the role of deubiquitinases (DUBs) in controlling TDP-43 proteostasis. Through an unbiased discovery screen of DUBs, here we identify and demonstrate using in vitro and in vivo models, as well as human brain tissue, that ubiquitin-specific peptidase-19 (USP19) acts as a TDP-43-directed DUB that removes K48- and K63-linked ubiquitin conjugates from TDP-43 and preferentially promotes cytoplasmic aggregation of TDP-43 C-terminal fragments (TDP-CTFs) through its catalytic activity. Specifically, the endoplasmic reticulum (ER)-anchored USP19 isoform (USP19-ER) exhibits superior activity in deubiquitinating TDP-CTFs, enhancing its phase separation and aggregation, compared to its cytosolic isoform (USP19-Cyto). Furthermore, as TDP-CTFs are generated at the ER, USP19 acts to couple the aggregation of TDP-CTFs to ER stress (ATF6, ATF4, IRE1, &amp; CHOP). In humans, USP19 protein levels increase in FTLD-TDP brains, which extensively colocalize with cytoplasmic phospho-TDP-43 (pTDP-43) pathology. Importantly, we demonstrate in vivo that genetic reduction of usp19 mitigates pTDP-43 pathology, astrogliosis, and ER stress while reversing long-term potentiation (LTP) and motor deficits in a mouse model of TDP-43 pathogenesis (TAR4 mice). These findings establish a critical role of USP19 at the nexus of TDP-43 proteostasis and ER stress, implicating its pathogenic role in FTLD-TDP and ALS.

Tribolium castaneum with longer duration of tonic immobility have more variations corresponding to the human Parkinson’s disease genomic region

Structural evolution of carbon frameworks realizes in vitro interfacial transport in metabolically reprogrammed senescent cells for senolysis

Histone modification clocks for robust cross-species biological age prediction and elucidating senescence regulation

Histone modifications represent an untapped resource for biological age prediction that overcomes limitations of traditional DNA methylation-based epigenetic clocks. Here, we developed and validated histone modification-based epigenetic clocks by systematically analyzing publicly available ChIP-seq datasets spanning six tissue types and six histone marks. We identified age-associated loci and constructed 36 tissue-specific epigenetic clocks that demonstrated strong resilience to technical and biological noise, with performance comparable to established DNA methylation clocks. Our models successfully detected biological age acceleration in leukemia samples and captured age reversal following therapeutic interventions. Importantly, we found that many aging-associated loci follow nonlinear trajectories with peak modification levels at midlife, revealing previously unrecognized dynamics in epigenetic aging. We observed age-related fragmentation of super enhancer regions, suggesting progressive chromatin disorganization during aging. Functional validation of a model-selected H3K27ac peak near IGF2BP3 confirmed its causal role in cellular senescence through regulation of TRA2A expression. Extending beyond mammals, we demonstrated the applicability of histone-based clocks in Drosophila melanogaster , a species lacking DNA methylation, highlighting the evolutionary conservation and broader utility of histone modifications as aging biomarkers. Our findings establish histone modifications as accurate, biologically meaningful, and robust indicators of biological age with potential applications in aging research, disease monitoring, and therapeutic development across diverse species.

Innovative generating-information function for consecutive lifetime systems in health research

Vertical substitution strategy to enable cooperation between spin–orbit coupling and transition dipoles for organic phosphorescence

Abstract The emission from organic molecules can be broadly classified as fluorescence or phosphorescence, and it is used in a wide range of applications from optoelectronics to bioimaging. The common method to enhance the fluorescence from organic chromophores is to introduce horizontal substituents into long conjugated structures. However, this concept does not allow the phosphorescence efficiency in the visible range to be increased to the fluorescence efficiency. Here we introduce a molecular design of conjugated molecules that effectively cooperate spin-orbit and transition dipoles. Increasing the through-space substitution of main-group elements perpendicular to the conjugated plane produces a cooperative effect of the spin–orbit and large transition dipoles of the conjugated plane to enhance the organic phosphorescence. This molecular design, which is different from the fluorescence, will increase the efficiency of the organic phosphorescence to the same level as the fluorescence at all visible wavelengths.

Collective bacterial condensation is fundamentally constrained by the emergence of active turbulence

Collective bacterial condensation arises from positive feedback between the ability of bacteria to generate chemical gradients in their environment and their chemotactic ability to follow those gradients. This feedback drives the spontaneous formation of local cell accumulations, characterized by sharp cell-density gradients, even in the absence of physical boundaries. By following the dynamics of bacterial condensation in uniform acidic environments, we show that condensation is critically constrained by the spontaneous emergence of correlated bacterial swimming and the associated active turbulence. These collective behaviors generate vortex-like cell motion with a pronounced radial component directed down the cell-density gradient. This, in turn, induces local fluid motion that broadens the condensate and expels nonchemotactic bacteria. When condensates are strongly confined in thin layers, the radial component of fluid motion diminishes and condensation is enhanced. Moreover, in porous environments, correlated bacterial motion is strongly suppressed, allowing spontaneous condensation to progress even further until it reaches the limits imposed by the nonlocal nature of bacterial chemotaxis. Overall, these findings highlight the fundamental interplay between self-generated bacterial condensation and correlated swimming.

Explainable VGG16 transfer learning with SHAP and grad-CAM for wax moth pest and infestation detection in honeybee apiaries using imaging data

A cyanide-free route towards the electrosynthesis of nitriles

Sleep deprivation exhibits an age-dependent effect on infraslow global brain activity

Infraslow (&lt;0.1 Hz) global brain activity, quantified by the global mean blood-oxygenation-level-dependent (gBOLD) signal in resting-state functional magnetic resonance imaging (fMRI), is elevated during sleep and coupled to cerebrospinal fluid (CSF) dynamics, a key pathway for the brain waste clearance implicated in neurodegenerative disorders such as Alzheimer’s disease. However, the effect of sleep deprivation on gBOLD activity and its interaction with aging remain poorly understood. Using a rigorously controlled in-laboratory total sleep deprivation (TSD) protocol, we demonstrate that TSD significantly increases both the gBOLD signal amplitude and its coupling with CSF flow, suggesting a compensatory mechanism that may enhance glymphatic clearance following acute sleep loss. Notably, these TSD-induced enhancements exhibit robust age dependency, with markedly attenuated responses in midlife adults (40 to 50 y). The absence of this compensatory mechanism in midlife may exacerbate age-related impairments in neurotoxic clearance and increase dementia susceptibility, thereby offering mechanistic insights into the nexus between sleep disruption, aging, and neurodegeneration.