Nature最新文献

Under high electrical current, some materials can emit electromagnetic radiation beyond incandescence. This phenomenon, referred to as electroluminescence, leads to the efficient emission of visible photons and is the basis of domestic lighting devices (for example, light-emitting diodes)^1,2. In principle, electroluminescence can lead to mid-infrared emission of confined light–matter excitations called phonon polaritons^3,4, resulting from the coupling of photons with crystal lattice vibrations (optical phonons). In particular, phonon polaritons arising in the van der Waals crystal hexagonal boron nitride (hBN) present hyperbolic dispersion, which enhances light–matter coupling^5,6. For this reason, electroluminescence of hyperbolic phonon polaritons (HPhPs) has been proposed as an explanation for the peculiar radiative energy transfer within hBN-encapsulated graphene transistors^7,8. However, as HPhPs are locally confined, they are inaccessible in the far field, and as such, any hint of electroluminescence has been based on indirect electronic signatures and has yet to be confirmed by direct observation. Here we demonstrate far-field mid-infrared (wavelength approximately 6.5 μm) electroluminescence of HPhPs excited by strongly biased high-mobility graphene within a van der Waals heterostructure, and we quantify the associated radiative energy transfer through the material. The presence of HPhPs is revealed by far-field mid-infrared spectroscopy owing to their elastic scattering at discontinuities in the heterostructure. The resulting radiative flux is quantified by mid-infrared pyrometry of the substrate receiving the energy. This radiative energy transfer is also shown to be reduced in hBN with nanoscale inhomogeneities, demonstrating the central role of the electromagnetic environment in this process.

Depicting spatial distributions of disease-relevant cells is crucial for understanding disease pathology^1,2. Here we present genetically informed spatial mapping of cells for complex traits (gsMap), a method that integrates spatial transcriptomics data with summary statistics from genome-wide association studies to map cells to human complex traits, including diseases, in a spatially resolved manner. Using embryonic spatial transcriptomics datasets covering 25 organs, we benchmarked gsMap through simulation and by corroborating known trait-associated cells or regions in various organs. Applying gsMap to brain spatial transcriptomics data, we reveal that the spatial distribution of glutamatergic neurons associated with schizophrenia more closely resembles that for cognitive traits than that for mood traits such as depression. The schizophrenia-associated glutamatergic neurons were distributed near the dorsal hippocampus, with upregulated expression of calcium signalling and regulation genes, whereas depression-associated glutamatergic neurons were distributed near the deep medial prefrontal cortex, with upregulated expression of neuroplasticity and psychiatric drug target genes. Our study provides a method for spatially resolved mapping of trait-associated cells and demonstrates the gain of biological insights (such as the spatial distribution of trait-relevant cells and related signature genes) through these maps.

Modern birds have diversified into a striking array of forms, behaviours and ecological roles. Analyses of molecular evolutionary rates can reveal the links between genomic and phenotypic change^1,2,3,4, but disentangling the drivers of rate variation at the whole-genome scale has been difficult. Using comprehensive estimates of traits and evolutionary rates across a family-level phylogeny of birds^5,6, we find that genome-wide mutation rates across lineages are predominantly explained by clutch size and generation length, whereas rate variation across genes is driven by the content of guanine and cytosine. Here, to find the subsets of genes and lineages that dominate evolutionary rate variation in birds, we estimated the influence of individual lineages on decomposed axes of gene-specific evolutionary rates. We find that most of the rate variation occurs along recent branches of the tree, associated with present-day families of birds. Additional tests on axes of rate variation show rapid changes in microchromosomes immediately after the Cretaceous–Palaeogene transition. These apparent pulses of evolution are consistent with major changes in the genetic machineries for meiosis, heart performance, and RNA splicing, surveillance and translation, and correlate with the ecological diversity reflected in increased tarsus length. Collectively, our analyses paint a nuanced picture of avian evolution, revealing that the ancestors of the most diverse lineages of birds underwent major genomic changes related to mutation, gene usage and niche expansion in the early Palaeogene period.

Entangled photon pairs from spontaneous parametric down-conversion (SPDC)¹ are central to many quantum applications^2,3,4,5,6. SPDC is typically performed in non-centrosymmetric systems⁷ with an inherent second-order nonlinearity (χ⁽²⁾)^8,9,10. We demonstrate strong narrowband SPDC with an on-chip rate of 0.8 million pairs per second in Si₃N₄. Si₃N₄ is the pre-eminent material for photonic integration and also exhibits the lowest waveguide loss (which is essential for integrated quantum circuits). However, being amorphous, silicon nitride lacks an intrinsic χ⁽²⁾, which limits its role in photonic quantum devices. We enabled SPDC in Si₃N₄ by combining strong light-field enhancement inside a high optical Q-factor microcavity with an optically induced space-charge field. We present narrowband photon pairs with a high spectral brightness. The quantum nature of the down-converted photon pairs is verified through coincidence measurements. This light source, based on Si₃N₄ integrated photonics technology, unlocks new avenues for quantum systems on a chip.

Voltage-gated potassium (K_V) channels contain cytoplasmically exposed β-subunits^1,2,3,4,5 whose aldo-keto reductase activity^6,7,8 is required for the homeostatic regulation of sleep⁹. Here we show that Hyperkinetic, the β-subunit of the K_V1 channel Shaker in Drosophila⁷, forms a dynamic lipid peroxidation memory. Information is stored in the oxidation state of Hyperkinetic’s nicotinamide adenine dinucleotide phosphate (NADPH) cofactor, which changes when lipid-derived carbonyls^10,11,12,13, such as 4-oxo-2-nonenal or an endogenous analogue generated by illuminating a membrane-bound photosensitizer^9,14, abstract an electron pair. NADP⁺ remains locked in the active site of K_Vβ until membrane depolarization permits its release and replacement with NADPH. Sleep-inducing neurons^15,16,17 use this voltage-gated oxidoreductase cycle to encode their recent lipid peroxidation history in the collective binary states of their K_Vβ subunits; this biochemical memory influences—and is erased by—spike discharges driving sleep. The presence of a lipid peroxidation sensor at the core of homeostatic sleep control^16,17 suggests that sleep protects neuronal membranes against oxidative damage. Indeed, brain phospholipids are depleted of vulnerable polyunsaturated fatty acyl chains after enforced waking, and slowing the removal of their carbonylic breakdown products increases the demand for sleep.