Quantum computers promise to tackle quantum simulation problems that are classically intractable1. Although a lot of quantum algorithms2-4 have been developed for simulating quantum dynamics, a general-purpose method for simulating low-temperature quantum phenomena remains unknown. In classical settings, the analogous task of sampling from thermal distributions has been largely addressed by Markov Chain Monte Carlo (MCMC) methods5,6. Here we propose an efficient quantum algorithm for thermal simulation that-akin to MCMC methods-exhibits detailed balance, respects locality and serves as a toy model for thermalization in open quantum systems. The enduring impact of MCMC methods suggests that our new construction may play an equally important part in quantum computing and applications in the physical sciences and beyond.

Spectroscopy is a pivotal tool for determining the physical structures and chemical compositions of materials and environments, and it is commonly used across diverse scientific fields1-16. Conventionally, spectroscopic techniques rely on narrow slits or gratings, which impose a trade-off between spectral resolution and optical transmittance17-22, thus precluding measurements with simultaneous high sensitivity and high efficiency. Here we introduce RAFAEL, a sub-ångström ultra-high-transmittance snapshot spectroscopic technique, which targets this trade-off with integrated and reconfigurable photonics based on lithium niobate. Its design comprises bulk lithium niobate as an interference mask with a pixel-wise electrically tunable spectral response and delivers picometre-scale modulation with a high optical transmittance. Our approach achieves 88-Hz snapshot spectroscopy with a spectral resolution of approximately 0.5 Å at 400-1,000 nm (R = 12,000), spatial resolution of 2,048 × 2,048 and 73.2% total optical transmittance. Compared with state-of-the-art spectroscopic imagers23-34, RAFAEL offers double the total transmittance and a nearly two orders of magnitude improvement in spectral resolving power, as verified by extensive experiments. In particular, RAFAEL captured sub-ångström spectra, including all atomic absorption peaks, of up to 5,600 stars in a single snapshot, indicating ×100-10,000 improvement in observational efficiency compared with world-class astronomical spectrometers17-21. This high-performing yet easily integrated snapshot spectroscopic method could drive advances in fields ranging from material science to astrophysics.

Stencilling, in which patterns are created by painting over masks, has ubiquitous applications in art, architecture and manufacturing. Modern, top-down microfabrication methods have succeeded in reducing mask sizes to under 10 nm (refs. 1,2), enabling ever smaller microdevices as today's fastest computer chips. Meanwhile, bottom-up masking using chemical bonds or physical interactions has remained largely unexplored, despite its advantages of low cost, solution-processability, scalability and high compatibility with complex, curved and three-dimensional (3D) surfaces3,4. Here we report atomic stencilling to make patchy nanoparticles (NPs), using surface-adsorbed iodide submonolayers to create the mask and ligand-mediated grafted polymers onto unmasked regions as 'paint'. We use this approach to synthesize more than 20 different types of NP coated with polymer patches in high yield. Polymer scaling theory and molecular dynamics (MD) simulation show that stencilling, along with the interplay of enthalpic and entropic effects of polymers, generates patchy particle morphologies not reported previously. These polymer-patched NPs self-assemble into extended crystals owing to highly uniform patches, including different non-closely packed superlattices. We propose that atomic stencilling opens new avenues in patterning NPs and other substrates at the nanometre length scale, leading to precise control of their chemistry, reactivity and interactions for a wide range of applications, such as targeted delivery, catalysis, microelectronics, integrated metamaterials and tissue engineering5-11.

Water is essential for almost every aspect of life on our planet and, unsurprisingly, its properties have been studied in great detail1. However, disproportionately little remains known about the electrical properties of interfacial and strongly confined water2,3, in which the structure deviates from that of bulk water, becoming distinctly layered4,5. The structural change is expected to affect the conductivity of water and particularly its polarizability, which in turn modifies intermolecular forces that play a crucial role in many physical and chemical processes6-9. Here we use scanning dielectric microscopy (SDM)10 to probe the in-plane electrical properties of water confined between atomically flat surfaces separated by distances down to 1 nm. For confinement exceeding several nanometres, water exhibits an in-plane dielectric constant close to that of bulk water and its proton conductivity is notably enhanced, gradually increasing with decreasing water thickness. This trend abruptly changes when the confined water becomes only a few molecules thick. Its in-plane dielectric constant reaches large, ferroelectric-like values of about 1,000, whereas the conductivity peaks at several S m-1, close to values characteristic of superionic liquids. We attribute the enhancement to strongly disordered hydrogen bonding induced by the few-layer confinement, which facilitates both easier in-plane polarization of molecular dipoles and faster proton exchange. This insight into the electrical properties of nanoconfined water is important for understanding many phenomena that occur at aqueous interfaces and in nanoscale pores.

Tropical forests act as important global carbon sinks1, and Earth System Models predict increasing near-term carbon sink capacity for these forests, with elevated atmospheric carbon dioxide concentration thought to stimulate tree growth2,3. However, current forest inventory data analyses suggest that the carbon sink capacity of intact tropical forests may be in decline, portending a possible future switch from carbon sinks to carbon sources3-7. Here we use long-term forest inventory data (1971-2019) from Australian moist tropical forests and a causal inference framework8-10 to assess the carbon balance of woody aboveground standing biomass over time, the demographic processes accounting for it, and its climatic drivers, including cyclones. We find that a transition from sink (0.62 ± 0.04 Mg C ha-1 yr-1: 1971-2000) to source (-0.93 ± 0.11 Mg C ha-1 yr-1: 2010-2019) has occurred for the aboveground woody biomass of these forests, with sink capacity declining at a rate of 0.041 ± 0.032 Mg C ha-1 yr-1. The transition was driven by increasingly extreme temperature and other climate anomalies, which have increased tree mortality and associated biomass losses4, with no evidence of the carbon fertilization (stimulation) of woody tree growth. Forest dynamics underlying carbon sink capacity were also punctuated by cyclones, with impacts of a similar magnitude to long-term climate-induced changes. Our findings suggest the potential for a similar response to climate change by woody aboveground biomass in moist tropical forests globally, which could culminate in a long-term switch from carbon sinks to carbon sources.

Recalled memories become transiently labile and require stabilization1-3. The mechanism for stabilizing memories of survival-critical experiences, which are often emotionally salient and repeated, remains unclear4. Here we identify an astrocytic ensemble that is transcriptionally primed by emotional experience and functionally triggered by repeated experience to stabilize labile memory. Using a novel brain-wide Fos tagging and imaging method, we found that astrocytic Fos ensembles were preferentially recruited in regions with neuronal engrams5 and were more widespread during fear recall than during conditioning. We established the induction mechanism of the astrocytic ensemble, which involves two steps: (1) an initial fear experience that induces day-long, slow astrocytic state changes with noradrenaline receptor upregulation; and (2) enhanced noradrenaline responses during recall, a repeated experience, enabling astrocytes to integrate coincident signals from local engrams and long-range noradrenergic projections, which induce secondary astrocytic state changes, including the upregulation of Fos and the neuromodulatory molecule IGFBP2. Pharmacological and genetic perturbation of the astrocytic ensemble signalling modulate engrams, and memory stability and precision. The astrocytic ensemble thus acts as a multiday trace in a subset of astrocytes after experience-dependent neural activity, which are eligible to capture future repeated experiences for stabilizing memories.

Compartmentalization of eukaryotic genome into euchromatin and heterochromatin is of critical biological significance1-3. Previous studies have suggested a self-templating pathway involving the reading and writing of histone H3 lysine 9 methylation by SUV39H as the core mechanism for heterochromatin reassembly during cell division1,3. In fission yeast, the mammalian SUV39H homologue Clr4 forms a complex containing ubiquitin ligase Cul4, which catalyses H3K14 mono-ubiquitination (H3K14ub) to promote heterochromatin formation. However, whether heterochromatin reassembly in dividing mammalian cells involves a similar pathway is unknown. Here we identified G2E3 as an H3K14ub-specific, pericentromeric heterochromatin-localized E3 ligase. G2E3-catalysed H3K14ub potentiates histone H3 lysine 9 trimethylation (H3K9me3) by SUV39H and is specifically required for SUV39H compartmentalization and H3K9me3 in pericentromeric heterochromatin. Mechanistically, we found that G2E3 is highly expressed in G2/M phase and associates with mitotic chromosomes in an RNA-dependent manner to catalyse H3K14ub, which is essential for the subsequent sequential recruitment of SUV39H and HP1. The SUV39H chromodomain is a reader of dual H3K9me3 and H3K14ub modifications and SUV39H associates with pericentromeric heterochromatin primarily through its H3K14ub-binding activity. Notably, loss of G2E3 severely impairs pericentromeric heterochromatin organization and results in the aberrant accumulation of SUV39H and H3K9me3 in numerous euchromatin regions and widespread transcriptional repression. Thus, our findings revealed the H3K14ub-dependent SUV39H compartmentalization as a unified mechanism of pericentromeric heterochromatin formation, which is essential for proper euchromatin compartmentalization and transcriptional regulation.

During the Late Triassic epoch (237-201 million years ago), the terrestrial ecosystems of Pangaea underwent drastic changes1,2 that led to the rise and diversification of mammaliaforms3, crocodylomorphs4 and dinosaurs5. Although the Carnian sedimentary rocks of South America provided much of the available evidence for understanding the early evolution of these clades, key discoveries have remained restricted to the Ischigualasto-Villa Unión6,7 and Paraná basins8 in Argentina and Brazil, respectively. Here we report a Carnian tetrapod assemblage from the previously unrecognized Northern Precordillera Basin in northwestern Argentina. Discoveries at this basin, in the Quebrada Santo Domingo site, include a nearly complete skeleton of the early sauropodomorph Huayracursor jaguensis gen. et sp. nov., and typical components of Late Carnian faunas, such as hyperodapedontine rhynchosaurs, gomphodontosuchine traversodontid cynodonts, and aetosaurs. Compared to its generally small and short-necked Carnian counterparts9,10, Huayracursor is larger and exhibits an incipient elongation of its cervical vertebrae, representing an intermediate condition for size and cervical elongation between known Carnian and Norian sauropodomorphs11. This discovery provides one of the oldest pieces of evidence of increased body mass and neck elongation in early Sauropodomorpha.

The properties of mammalian cells depend on their location within organs. Gene expression in the liver varies between periportal and pericentral hepatocytes1-3, and in the intestine from crypts to villus tips4,5. A key element of tissue spatial organization is probably metabolic, but direct assessments of spatial metabolism remain limited. Here we map spatial metabolic gradients in the mouse liver and intestine. We develop an integrated experimental-computational workflow using matrix-assisted laser desorption/ionization (MALDI) imaging mass spectrometry (IMS), isotope tracing and deep-learning artificial intelligence. Most measured metabolites (>90%) showed significant spatial concentration gradients in the liver lobules and intestinal villi. In the liver, tricarboxylic acid (TCA)-cycle metabolites and their isotope labelling from both glutamine and lactate localized periportally. Energy-stress metabolites, including adenosine monophosphate (AMP), also localized periportally, consistent with a high periportal energy demand. In the intestine, the TCA intermediates malate (tip) and citrate (crypt) showed opposite spatial patterns, aligning with higher glutamine catabolism in tips and lactate oxidation in crypts based on isotope tracing. Finally, we mapped the fate of the obesogenic dietary sugar fructose. In the intestine, oral fructose was catabolized faster in the villus bottom than in the tips. In the liver, fructose-derived carbon accumulated pericentrally as fructose-1-phosphate and triggered pericentral adenosine triphosphate (ATP) depletion. Thus, we both provide foundational knowledge regarding intestine and liver metabolic organization and identify fructose-induced focal derangements in liver metabolism.

Unravelling the genetic basis of the remarkable phenotypic diversity observed in natural populations remains a central challenge in biology1-4. Despite major advances5-19, no species has yet been characterized with a truly comprehensive atlas of genetic variation. Here we present an extensive genomic and phenotypic resource for the yeast Saccharomyces cerevisiae based on near telomere-to-telomere assemblies of 1,086 natural isolates. Leveraging these high-contiguity assemblies, we generated a highly complete species-wide structural variant atlas, gene-based pangenome and graph pangenome. By incorporating the full spectrum of genetic variation captured across the species, we conducted genome-wide association studies across 8,391 molecular and organismal traits19-22. The inclusion of structural variants and small insertion-deletion mutations improved heritability estimates by an average of 14.3% compared with analyses based only on single-nucleotide polymorphisms. Structural variants were more frequently associated with traits and exhibited greater pleiotropy than other variant types. Notably, the genetic architecture of molecular and organismal traits differed markedly. Together, this work provides a unique dataset that illuminates how diverse forms of genetic variation shape phenotypic diversity and lays the groundwork for integrative, genome-scale studies in other eukaryotic systems.

All mammalian organs depend on resident macrophage populations to coordinate repair and facilitate tissue-specific functions1-3. Functionally distinct macrophage populations reside in discrete tissue niches and are replenished through a combination of local proliferation and monocyte recruitment4,5. Declines in macrophage abundance and function have been linked to age-associated pathologies, including atherosclerosis, cancer and neurodegeneration6-8. However, the mechanisms that coordinate macrophage organization and replenishment within ageing tissues remain largely unclear. Here we show that capillary-associated macrophages (CAMs) are selectively lost over time, contributing to impaired vascular repair and reduced tissue perfusion in older mice. To investigate resident macrophage behaviour in vivo, we used intravital two-photon microscopy in live mice to non-invasively image the skin capillary plexus, a spatially well-defined vascular niche that undergoes rarefication and functional decline with age. We find that CAMs are lost at a rate exceeding capillary loss, resulting in macrophage-deficient vascular niches in both mice and humans. CAM phagocytic activity was locally required to repair obstructed capillary blood flow, leaving macrophage-deficient niches selectively vulnerable under homeostatic and injury conditions. Our study demonstrates that homeostatic renewal of resident macrophages is less precisely regulated than previously suggested9-11. Specifically, neighbouring macrophages do not proliferate or reorganize to compensate for macrophage loss without injury or increased growth factors, such as colony-stimulating factor 1 (CSF1). These limitations in macrophage renewal may represent early and targetable contributors to tissue ageing.

Highly pathogenic avian influenza A(H5) viruses globally impact wild and domestic birds, and have caused severe infections in mammals, including humans, underscoring their pandemic potential1-5. The antigenic evolution of the A(H5) haemagglutinin (HA) poses challenges for pandemic preparedness and vaccine design6. Here the global antigenic evolution of the A(H5) HA was captured in a high-resolution antigenic map. The map was used to design immunogenic and antigenically central vaccine HA antigens, eliciting antibody responses that broadly cover the A(H5) antigenic space. In ferrets, a central antigen protected as well as homologous vaccines against heterologous infection with two antigenically distinct viruses. This work showcases the rational design of subtype-wide influenza A(H5) pre-pandemic vaccines and demonstrates the value of antigenic maps for the evaluation of vaccine-induced immune responses through antibody profiles.