All-solid-state batteries require advanced cathode designs to realize their potential for high energy density and economic viability1-3. Integrated all-in-one cathodes, which eliminate inactive conductive additives and heterogeneous interfaces, hold promise for substantial energy and stability gains but are hindered by materials lacking sufficient Li+/e- conductivity, mechanical robustness and structural stability4-14. Here we present Li1.3Fe1.2Cl4, a cost-effective halide material that overcomes these challenges. Leveraging reversible Fe2+/Fe3+ redox and rapid Li+/e- transport within its framework, Li1.3Fe1.2Cl4 achieves an electrode energy density of 529.3 Wh kg-1 versus Li+/Li. Critically, Li1.3Fe1.2Cl4 shows unique dynamic properties during cycling, including reversible local Fe migration and a brittle-to-ductile transition that confers self-healing behaviour. This enables exceptional cycling stability, maintaining 90% capacity retention for 3,000 cycles at a rate of 5 C. Integration of Li1.3Fe1.2Cl4 with a nickel-rich layered oxide further increases the energy density to 725.6 Wh kg-1. By harnessing the advantageous dynamic mechanical and diffusion properties of all-in-one halides, this work establishes all-in-one halides as an avenue for energy-dense, durable cathodes in next-generation all-solid-state batteries.

The global crisis of plastic waste accumulation threatens wildlife and ecosystems1. Catalytic processes that convert plastic waste into valuable chemicals and fuels offer promising solutions2. Recycling or upcycling of real-life plastic mixtures is challenging owing to their diverse composition and structure3. Here we propose a product-oriented strategy leveraging the orthogonality in reactivities of different functional groups in plastic mixtures to yield valuable products. This approach involves identifying functional groups followed by converting a selective component in the mixture to valuable products. We use mixtures of polystyrene, polylactic acid, polyurethane, polycarbonate, polyvinyl chloride, polyethylene terephthalate, polyethylene and polypropylene, as well as real-life plastics, to demonstrate the feasibility and effectiveness of the proposed strategy. The diverse physical and chemical properties of these components, which typically hinder direct recovery, offer opportunities for extraction and transformation with the proposed strategy. From a 20-g mixture of real-life plastics, including polystyrene foam, a polylactic acid straw, a polyurethane tube, a polycarbonate mask, a polyvinyl chloride bag, a polyethylene terephthalate bottle, a polyethylene dropper and a polypropylene bottle, we obtained more than 8 separate chemicals: 1.3 g of benzoic acid, 0.5 g of plasticizer, 0.7 g of alanine, 0.7 g of lactic acid, 1.4 g of aromatic amine salt, 2.1 g of bisphenol A, 2.0 g of terephthalic acid and 3.5 g of C3-C6 alkanes. This study reveals the potential for designing transformation strategies for complex plastic waste based on their chemical nature and opens paths for managing end-of-life plastic mixtures.

The nervous system has a pivotal role in cancer biology, and pathological investigations have linked intratumoural nerve density to metastasis1. However, the precise impact of cancer-associated neurons and the communication channels at the nerve-cancer interface remain poorly understood. Previous cancer denervation models in rodents and humans have highlighted robust cancer dependency on nerves, but the underlying mechanisms that drive nerve-mediated cancer aggressivity remain unknown2,3. Here we show that cancer-associated neurons enhance cancer metabolic plasticity by transferring mitochondria to cancer cells. Breast cancer denervation and nerve-cancer coculture models confirmed that neurons significantly improve tumour energetics. Neurons cocultured with cancer cells undergo metabolic reprogramming, resulting in increased mitochondrial mass and subsequent transfer of mitochondria to adjacent cancer cells. To precisely track the fate of recipient cells, we developed MitoTRACER, a reporter of cell-to-cell mitochondrial transfer that permanently labels recipient cancer cells and their progeny. Lineage tracing and fate mapping of cancer cells acquiring neuronal mitochondria in primary tumours revealed their selective enrichment at metastatic sites following dissemination. Collectively, our data highlight the enhanced metastatic capabilities of cancer cells that receive mitochondria from neurons in primary tumours, shedding new light on how the nervous system supports cancer metabolism and metastatic dissemination.

An increasing number of scholars, policymakers and grassroots communities argue that artificial intelligence (AI) research-and computer-vision research in particular-has become the primary source for developing and powering mass surveillance1-7. Yet, the pathways from computer vision to surveillance continue to be contentious. Here we present an empirical account of the nature and extent of the surveillance AI pipeline, showing extensive evidence of the close relationship between the field of computer vision and surveillance. Through an analysis of computer-vision research papers and citing patents, we found that most of these documents enable the targeting of human bodies and body parts. Comparing the 1990s to the 2010s, we observed a fivefold increase in the number of these computer-vision papers linked to downstream surveillance-enabling patents. Additionally, our findings challenge the notion that only a few rogue entities enable surveillance. Rather, we found that the normalization of targeting humans permeates the field. This normalization is especially striking given patterns of obfuscation. We reveal obfuscating language that allows documents to avoid direct mention of targeting humans, for example, by normalizing the referring to of humans as 'objects' to be studied without special consideration. Our results indicate the extensive ties between computer-vision research and surveillance.

The brain represents sensory variables in the coordinated activity of neural populations, in which tuning curves of single neurons define the geometry of the population code1,2. Whether the same coding principle holds for dynamic cognitive variables remains unknown because internal cognitive processes unfold with a unique time course on single trials observed only in the irregular spiking of heterogeneous neural populations3-8. Here we show the existence of such a population code for the dynamics of choice formation in the primate premotor cortex. We developed an approach to simultaneously infer population dynamics and tuning functions of single neurons to the population state. Applied to spike data recorded during decision-making, our model revealed that populations of neurons encoded the same dynamic variable predicting choices, and heterogeneous firing rates resulted from the diverse tuning of single neurons to this decision variable. The inferred dynamics indicated an attractor mechanism for decision computation. Our results reveal a unifying geometric principle for neural encoding of sensory and dynamic cognitive variables.

Glioblastoma (GBM) is the most lethal primary brain malignancy1. Immunosuppression in the GBM tumour microenvironment (TME) is an important barrier to immune-targeted therapies, but our understanding of the mechanisms of immune regulation in the GBM TME is limited2. Here we describe a viral barcode interaction-tracing approach3 to analyse TME cell-cell communication in GBM clinical samples and preclinical models at single-cell resolution. We combine it with single-cell and bulk RNA-sequencing analyses, human organotypic GBM cultures, in vivo cell-specific CRISPR-Cas9-driven genetic perturbations as well as human and mouse experimental systems to identify an annexin A1-formyl peptide receptor 1 (ANXA1-FPR1) bidirectional astrocyte-GBM communication pathway that limits tumour-specific immunity. FPR1 inhibits immunogenic necroptosis in tumour cells, and ANXA1 suppresses NF-κB and inflammasome activation in astrocytes. ANXA1 expression in astrocytes and FPR1 expression in cancer cells are associated with poor outcomes in individuals with GBM. The inactivation of astrocyte-glioma ANXA1-FPR1 signalling enhanced dendritic cell, T cell and macrophage responses, increasing infiltration by tumour-specific CD8+ T cells and limiting T cell exhaustion. In summary, we have developed a method to analyse TME cell-cell interactions at single-cell resolution in clinical samples and preclinical models, and used it to identify bidirectional astrocyte-GBM communication through ANXA1-FPR1 as a driver of immune evasion and tumour progression.

Mitotic onset is a critical transition for eukaryotic cell proliferation. The commonly held view of mitotic control is that the master regulator, cyclin-dependent kinase (CDK), is first activated in the cytoplasm, at the centrosome, initiating mitosis1-3. Bistability in CDK activation ensures that the transition is irreversible, but how this unfolds in a spatially compartmentalized cell is unknown4-8. Here, using fission yeast, we show that CDK is first activated in the nucleus, and that the bistable responses differ markedly between the nucleus and the cytoplasm, with a stronger response in the nucleus driving mitotic signal propagation from there to the cytoplasm. Abolishing cyclin-CDK localization to the centrosome led to activation occurring only in the nucleus, spatially uncoupling the nucleus and cytoplasm mitotically, suggesting that centrosomal cyclin-CDK acts as a 'signal relayer'. We propose that the key mitotic regulatory system operates in the nucleus in proximity to DNA, which enables incomplete DNA replication and DNA damage to be effectively monitored to preserve genome integrity and to integrate ploidy within the CDK control network. This spatiotemporal regulatory framework establishes core principles for control of the onset of mitosis and highlights that the CDK control system operates within distinct regulatory domains in the nucleus and cytoplasm.

The Tweety homologues (TTYHs) constitute a family of eukaryotic membrane proteins that, on the basis of structural features, were recently proposed to contribute to lipid transfer between soluble carriers and cellular membranes1. However, in the absence of supporting data, this function was hypothetical. Here through pull-down of endogenous proteins, we identify APOE as the interaction partner of human TTYH2. Subcellular fractionation and immunocytochemistry assays showed that both proteins colocalize in endosomal compartments. Characterization of the specific interaction between APOE and TTYH2 through binding assays and structural studies enabled us to identify an epitope in an extended domain of TTYH2 that faces the endosomal lumen. Structures of complexes with APOE-containing lipoprotein particles revealed a binding mode that places lipids in a suitable position to facilitate their diffusion into the membrane. Moreover, in vitro studies revealed that lipid transfer is accelerated by TTYH2. Collectively, our findings indicate that TTYH2 has a role in the unloading of APOE-containing lipoproteins after they are endocytosed. These results define a new protein class that facilitates the extraction of lipids from and their insertion into cellular membranes. Although ubiquitous, this process could be of particular relevance in the brain, where APOE is involved in the transfer of lipids between astrocytes and neurons.

Gastrointestinal (GI) motility disorders represent a major medical challenge, with few effective therapies available. These disorders often result from dysfunction of inhibitory nitric oxide (NO)-producing motor neurons in the enteric nervous system, which are essential for regulating gut motility. Loss or dysfunction of NO neurons is linked to severe conditions, including achalasia, gastroparesis, intestinal pseudo-obstruction and chronic constipation1,2. Here we introduce a platform based on human pluripotent stem cells (hPSCs) for therapeutic development targeting GI motility disorders. Using an unbiased screen, we identified drug candidates that modulate NO neuron activity and enhance motility in mouse colonic tissue ex vivo. We established a high-throughput strategy to define developmental programs driving the specification of NO neurons and found that inhibition of platelet-derived growth factor receptors (PDGFRs) promotes their differentiation from precursors of the enteric nervous system. Transplantation of these neurons into NO-neuron-deficient mice led to robust engraftment and improved GI motility, offering a promising cell-based therapy for neurodegenerative GI disorders. These studies provide a new framework for understanding and treating enteric neuropathies.

Mirroring the complex structures and diverse functions of natural organisms is a long-standing challenge in robotics1-4. Modern fabrication techniques have greatly expanded the feasible hardware5-8, but using these systems requires control software to translate the desired motions into actuator commands. Conventional robots can easily be modelled as rigid links connected by joints, but it remains an open challenge to model and control biologically inspired robots that are often soft or made of several materials, lack sensing capabilities and may change their material properties with use9-12. Here, we introduce a method that uses deep neural networks to map a video stream of a robot to its visuomotor Jacobian field (the sensitivity of all 3D points to the robot's actuators). Our method enables the control of robots from only a single camera, makes no assumptions about the robots' materials, actuation or sensing, and is trained without expert intervention by observing the execution of random commands. We demonstrate our method on a diverse set of robot manipulators that vary in actuation, materials, fabrication and cost. Our approach achieves accurate closed-loop control and recovers the causal dynamic structure of each robot. Because it enables robot control using a generic camera as the only sensor, we anticipate that our work will broaden the design space of robotic systems and serve as a starting point for lowering the barrier to robotic automation.

Tailoring magnetic ordering in solid-state materials is essential for emerging spintronics1,2. However, substitutional lattice doping in magnetic semiconductors is often constrained by the low solubility of magnetic elements3-5, limiting the maximum achievable doping concentration (for example, less than 5%) and ferromagnetic ordering temperature6. The intercalation of magnetic elements in layered two-dimensional atomic crystals (2DACs) without breaking in-plane covalent bonds offers an alternative approach to incorporate a much higher concentration of magnetic atoms (for example, up to 50%) beyond the typical solubility limit. However, commonly used chemical and electrochemical intercalation methods are largely confined to a few isolated examples so far. Here we report a general two-step intercalation and cation-exchange strategy to produce a library of highly ordered magnetic intercalation superlattices (MISLs) with tunable magnetic ordering. Monovalent transition-metal cations Cu+ and Ag+, divalent magnetic cations Mn2+, Fe2+, Co2+ and Ni2+, and trivalent rare-earth cations Eu3+ and Gd3+ have been successfully incorporated into group-VIB 2DACs, including MoS2, MoSe2, MoTe2, WS2, WSe2 and WTe2, and group-IVB, -VB, -IIIA, -IVA and -VA 2DACs, including TiS2, NbS2, NbSe2, TaS2, In2Se3, SnSe2, Bi2Se3 and Bi2Te3. We show that these MISLs can be prepared with tunable concentrations of magnetic intercalants, enabling tailored magnetic ordering across a diverse array of functional 2DACs, including semiconductors, topological insulators, and superconductors. This work establishes a versatile material platform for both fundamental investigations and spintronics applications.

The broad bandgap tunability of both perovskites and organic semiconductors enables the development of perovskite-organic tandem solar cells with promising theoretical efficiency. However, the certified efficiencies of reported perovskite-organic tandem solar cells remain lower than those of single-junction perovskite solar cells, primarily because of insufficient near-infrared photocurrent in narrow-bandgap organic subcells1-3. Here we design and synthesize an asymmetric non-fullerene acceptor (NFA), P2EH-1V, featuring a unilateral conjugated π-bridge to reduce the optical bandgap to 1.27 eV while maintaining ideal exciton dissociation and nanomorphology. Transient absorption spectroscopy confirms efficient hole transfer from P2EH-1V to the donor PM6. Devices based on P2EH-1V exhibit reduced non-radiative voltage losses of 0.20 eV without compromising charge-generation efficiency. We achieve a 17.9% efficiency for the organic bottom cell, with a high short-circuit current density (Jsc) of 28.60 mA cm-2. Furthermore, we minimize interface recombination losses, enabling the perovskite top cell to achieve an impressive open-circuit voltage (Voc) of 1.37 V and a fill factor (FF) of 85.5%. These advancements result in perovskite-organic tandem solar cells achieving a record efficiency of 26.7% (certified at 26.4%) over an aperture area greater than 1 cm2.

Postmitotic neurons have high levels of methylated cytosine and its oxidized intermediates such as 5-hydroxymethylcytosine1. However, the functional relevance of these epigenetic modifications of DNA are poorly understood. Here we show that some cytidine analogues, such as cytarabine, cause DNA double-strand breaks during TET-mediated active 5-methylcytosine demethylation by interrupting TDG-dependent base excision repair. These double-strand breaks are frequently converted into deletions and translocations by DNA ligase 4. In vivo, Purkinje and Golgi cells in the cerebellum are the only neuronal populations that exhibit high levels of DNA damage due to cytarabine. In Purkinje cells, TET targets highly expressed gene bodies marked by enhancer-associated histone modifications. Many of these genes control movement coordination, which explains the long-recognized cerebellar neurotoxicity of cytarabine2. We show that other cytidine analogues, such as gemcitabine, cause only single-strand breaks in neurons, which are repaired by DNA ligase 3 with minimal toxicity. Our findings uncover a mechanistic link between TET-mediated DNA demethylation, base excision repair and gene expression in neurons. The results also provide a rational explanation for the different neurotoxicity profiles of an important class of antineoplastic agents.

Aggregation pheromone, 4-vinylanisole (4VA), is specifically released by gregarious migratory locusts, and is crucial in forming locust swarms that cause destructive plagues1. Control of locust plagues relies heavily on the extensive application of chemical pesticides, which has led to severe environmental and health issues2. As pheromones are primary mediators of insect communication and behaviour3, exploring their biosynthesis can provide important cues to develop innovative behavioural regulators, potentially reducing the reliance on chemical pesticides. Here we resolve the biosynthesis of 4VA and behavioural responses of locusts when enzymes in the 4VA biosynthetic pathway are manipulated. The process initiates with phenylalanine derived from food plants and proceeds through three precursors: cinnamic acid, p-hydroxycinnamic acid and 4-vinylphenol (4VP). Notably, the conversion from 4VP to 4VA through methylation is unique to gregarious locusts. This step is catalysed by two crucial methyltransferases, 4VPMT1 and 4VPMT2. Guided by the X-ray co-crystal structure of 4VPMT2 bound with 4VP and S-adenosyl-L-methionine, we developed 4-nitrophenol as a substrate surrogate. We identified several chemicals that can block 4VA production by inhibiting the enzymatic activities of 4VPMT proteins, thereby suppressing locust aggregative behaviour. The findings uncover the chemical logic behind 4VA biosynthesis and pinpoint two crucial enzymes as novel targets for locust swarm management.