Browse Articles

Warming-driven shifts in global building energy use reshape climate mitigation planning

Coupled Hg isotope dynamics reveal eruption pulses across the Permian–Triassic mass extinction

Natural killer cell-mediated immunosurveillance modulates liver cancer evolution through cancer stemness enhancement and lipid metabolism reprogramming

Low-hygroscopic solvents enable ambient blade coating of efficient perovskite solar cells

Layer-by-layer shear densification for multiscale hierarchical alignment in bulk hydrogels

Current-induced creation and dynamics of embedded magnetic skyrmion bags

Abstract Magnetic skyrmion bags—vortex-like structures hosting multiple skyrmions with tunable topological charge ( Q )—hold significant promise for next-generation spintronic computing. However, while their creation using magnetic fields has been demonstrated, their direct electrical generation remains an outstanding challenge. Here, we report the direct current-induced formation and manipulation of embedded skyrmion bags in a FeGe nanoplate under zero magnetic field. Using in-situ Lorentz transmission electron microscopy, we capture the transformation of a distorted helical ground state into embedded skyrmion bags with diverse configurations, driven by nanosecond current pulses. Theoretical analysis indicates that this process is driven by the spin-transfer-torque-induced fracture of the helical state. Furthermore, we demonstrate electrically-induced transitions between skyrmion bags of different Q , leading to the stabilization of complex three-dimensional topological structures, including experimental signatures of magnetic monopoles and bobbers. Our work establishes a foundation for all-electrical control of high- Q topological spin textures and topological defects, paving the way for their application in functional spintronic devices.

Bone-derived Osterix+ osteolineage cells are a source of tumor-promoting myofibroblastic cancer-associated fibroblasts in breast cancer

Abstract Cancer-associated fibroblasts (CAFs) are major regulators of breast cancer (BC) progression and therapeutic resistance, yet the extent to which CAF heterogeneity is dictated by distinct cellular origins remains unresolved. Here, we identify bone-derived Osterix + (Osx) osteolineage cells as a source of CAFs in BC. Using BC models in female mice and biopsies from women with BC, we show that bone-resident Osx + cells are recruited to primary tumors. These cells preferentially differentiate into a myofibroblastic CAF subset with unique osteolineage identity (OsteoLin-myCAFs). OsteoLin-myCAFs are transcriptionally and functionally distinct from other subsets, exhibit enhanced extracellular matrix remodeling and pronounced pro-tumorigenic activity. Mechanistically, Osx drives expression of matrix-remodeling programs, including MMP13, which supports tumor growth. Cross-species analyses show a conserved 54-gene osteolineage signature in myCAFs from human BC samples, strongly associated with poor survival. Together, these findings identify a distinct bone-derived osteolineage cell that gives rise to OsteoLin-myCAFs and is linked to adverse clinical outcomes.

Babies’ birth weight improves with help of payments to parents

Tumor-resident T cells and dendritic cells form an in situ archetype during immunotherapy response in melanoma

Device could sniff out fusion reactors secretly making material for a nuclear bomb

Spatiotemporal organisation of residual disease in mouse and human BRCA1-deficient mammary tumours and breast cancer

Abstract Breast cancer remains a leading cause of death worldwide. Although chemotherapy reduces primary and metastatic tumour burden, persisting drug-tolerant tumour cell populations, known as minimal residual disease (MRD), pose a significant risk of recurrence and therapy resistance. In this study, we describe the spatiotemporal organisation of therapy response and MRD in BRCA1;p53-deficient mouse mammary tumours and human clinical samples. By integrating single-cell RNA sequencing, spatial transcriptomics, and imaging mass cytometry across multiple treatment timepoints, we characterise dynamic interactions between tumour cell subpopulations and their surrounding microenvironment. Our multiomic analysis uncovers a distinct, chemotherapy-tolerant epithelial-mesenchymal transition (EMT) cancer cell population that displays a conserved expression programme in human BRCA1-deficient tumours, significantly correlates with adverse clinical outcomes, and can be pharmacologically targeted in preclinical models. We reveal the spatial distribution of residual EMT-like tumour cells within discrete anatomical niches, providing a framework for understanding the persistence of MRD and potential therapeutic vulnerabilities.

Genome-wide association study of cocaine self-administration behavior in Heterogeneous Stock rats

Abstract Cocaine use disorder (CUD) is a major public health crisis. The specific genes mediating CUD remain largely unknown. We conducted a genome-wide association study (GWAS) using outbred N/NIH Heterogeneous Stock (HS; n  = 836, female = 415, male = 421) rats. We examined CUD-related phenotypes including acquisition of self-administration, escalation of intake, and compulsive-like responding. These traits were phenotypically correlated and exhibited modest SNP heritability (h 2  = 0.07 – 0.16). We identified six genome-wide significant associations (>-log 10 (p)=5.58; α = 0.05 by permutation). One locus on chromosome 19 was associated with variable time between cocaine infusions (post infusion interval) and contains several carboxylesterase genes that are orthologous to the human CES1 gene. Notably, carboxylesterases metabolize cocaine. Three non-synonymous coding variants in Ces1c and Ces1d were in perfect linkage disequilibrium with this locus. The other five loci contained promising coding and expression variants, including Trak2 , a gene previously associated with CUD in human GWAS and Slc10a7 , Plcl1 , and Satb2 which have been associated with alcohol and tobacco use disorder. This is the largest genetic study of cocaine self-administration ever conducted in rats. Our results replicate previous loci associated with CUD in humans and provide several novel biological insights including the potential of pharmacological strategies targeting carboxylesterases.

Isolation of genome-predicted Caldatribacterium (Atribacterota) reveals pervasive microbial cultivation problem due to folate precipitation

Investigating and inhibiting cathode-side gas generation for practical low-temperature and fast Li-ion batteries

Thermal-decoupled selenization enables kesterite solar cells with 15.3% certified efficiency

Targeting SMC3 deacetylation synergizes with XPO1 inhibition to reprogram the epigenetic landscape and suppress NPM1-mutated acute myeloid leukemia

Saturation editing of RNU4-2 reveals distinct dominant and recessive disorders

Abstract Recently, de novo variants in an 18-nucleotide region in the centre of RNU4-2 were shown to cause ReNU syndrome, a syndromic neurodevelopmental disorder that is predicted to affect tens of thousands of individuals worldwide 1,2 . RNU4-2 is a non-protein-coding gene that is transcribed into the U4 small nuclear RNA component of the major spliceosome 3 . ReNU syndrome variants disrupt spliceosome function and alter 5′ splice site selection 1,4 . Here we performed saturation genome editing (SGE) of RNU4-2 to identify the functional and clinical impact of variants across the entire gene. The resulting SGE function scores, derived from variants’ effects on cell fitness, discriminate ReNU syndrome variants from those observed in the population and markedly outperform in silico variant effect prediction. Using these data, we redefine the ReNU syndrome critical region at single-nucleotide resolution, resolve variant pathogenicity for variants of uncertain significance and show that SGE function scores delineate variants by phenotypic severity and the extent of observed splicing disruption. Furthermore, we identify variants affecting function in regions of RNU4-2 that are critical for interactions with other spliceosome components. We show that these variants cause a new recessive neurodevelopmental disorder that is distinct from ReNU syndrome. Together, this work defines the landscape of variant function across RNU4-2 , providing critical insights for both diagnosis and therapeutic development.

Light-triggered oxygen redox activity at the edge of cobalt oxyhydroxide for superior water oxidation

Abstract Introducing oxygen redox chemistry into cobalt oxyhydroxide effectively enhances catalytic activity by enabling direct O-O coupling, thereby bypassing the rate-limiting * OOH step in the conventional adsorbate evolution mechanism. However, the key challenge is to preserve the accessibility of non-bonding oxygen states while maintaining cobalt-oxygen covalency. Here we show that light irradiation triggers ligand-to-metal charge transfer in sulfur-treated cobalt oxyhydroxide (S-CoOOH), generating non-bonding oxygen states. These states then couple with adjacent ones to form direct O-O bonds. Through this way, the sulfur-treated sample performs enhanced OER activity under light, achieving an overpotential of 194 ± 3 mV at 10 mA cm −2 , which is 41 mV lower than in the dark. Further analysis reveals that light-induced oxygen redox activity is confined to the edge of catalyst. This activity originates from electron transitions from (M-O) to non-overlapping regions of Co 3  d and 4 p orbitals, driven by high-spin Co 3+ at the edge. This work highlights the critical role of light in inducing non-bonding oxygen states in transition metal-based catalysts and guides the development of oxygen-redox electrocatalysts.

TRNAU1AP and PRPF39 establish integrated control over processing of most abundant human non-coding RNAs

From breakthroughs to blueprints: evolving evidence and future directions in relapsed and refractory large B-cell lymphoma

Abstract The therapeutic landscape for relapsed or refractory large B-cell lymphoma (R/R LBCL) has undergone rapid and profound change, driven by cellular therapies, bispecific antibodies, and next-generation antibody-drug conjugates (ADCs). These advances have redefined historical standards while exposing persistent gaps in trial design, biological insight, and therapeutic sequencing. Recent randomized studies show that ADC- and bispecific-anchored regimens can outperform legacy chemotherapy comparators, yet interpretation is hindered by geographic heterogeneity, selective enrollment, and a proliferation of trials lacking contemporary control arms. Next-generation approaches, including bispecific-ADC combinations, dual-target chimeric antigen receptor T-cell therapy (CAR-T) constructs, and strategies explicitly designed to circumvent antigen escape, are poised to challenge long-standing therapeutic hierarchies and may broaden curative potential to patients who are ineligible for, or relapse after, CAR-T. The field now stands at an inflection point at which therapeutic innovation is advancing faster than the evidence infrastructure required to guide practice. Delivering durable, equitable benefit will require control arms aligned with current CAR-T standards, harmonized eligibility criteria, prospective molecular profiling, and adaptive trial platforms capable of evolving with the standard of care. As ADCs and bispecifics move earlier in treatment and diffuse into community practice, the central challenge is no longer the development of active therapies alone, but the creation of biologically rational, accessible, and interpretable pathways that make tolerable, curative treatments a realistic and universal goal for all patients with R/R LBCL.