The electronic quality of two-dimensional systems is crucial when exploring quantum transport phenomena. In semiconductor heterostructures, decades of optimization have yielded record-quality two-dimensional gases with transport and quantum mobilities reaching close to 108 and 106 cm2 V-1 s-1, respectively1-10. Although the quality of graphene devices has also been improving, it remains comparatively lower11-17. Here we report a transformative improvement in the electronic quality of graphene by employing graphite gates placed in its immediate proximity, at 1 nm separation. The resulting screening reduces charge inhomogeneity by two orders of magnitude, bringing it down to a few 107 cm-2 and limiting potential fluctuations to less than 1 meV. Quantum mobilities reach 107 cm2 V-1 s-1, surpassing those in the highest-quality semiconductor heterostructures by an order of magnitude, and the transport mobilities match their record9,10. This quality enables Shubnikov-de Haas oscillations in fields as low as 1 mT and quantum Hall plateaux below 5 mT. Although proximity screening predictably suppresses electron-electron interactions, fractional quantum Hall states remain observable with their energy gaps reduced only by a factor of 3-5 compared with unscreened devices, demonstrating that many-body phenomena at spatial scales shorter than 10 nm remain robust. Our results offer a reliable route to improving electronic quality in graphene and other two-dimensional systems, which should facilitate the exploration of new physics previously obscured by disorder.

Nuclear fusion research for energy applications aims to create conditions that release more energy than required to initiate the fusion process1. To generate meaningful amounts of energy, fuels such as deuterium need to be spatially confined to increase the collision probability of particles2-4. We therefore set out to investigate whether electrochemically loading a metal lattice with deuterium fuel could increase the probability of nuclear fusion events. Here we report a benchtop fusion reactor that enabled us to bombard a palladium metal target with deuterium ions. These deuterium ions undergo deuterium-deuterium fusion reactions within the palladium metal. We showed that the in situ electrochemical loading of deuterium into the palladium target resulted in a 15(2)% increase in deuterium-deuterium fusion rates. This experiment shows how the electrochemical loading of a metal target at the electronvolt energy scale can affect nuclear reactions at the megaelectronvolt energy scale.

Prenatal cannabis exposure (PCE) is associated with mental health problems in early adolescence, but the possible neurobiological mechanisms remain unknown. In a large longitudinal sample of adolescents (ages 9-12, n=9,322-10,186), we find that PCE is associated with localized differences in gray and white matter of the frontal and parietal cortices, their associated white matter tracts, and with striatal resting state connectivity, even after accounting for potential pregnancy, familial, and child confounds. Variability in forceps minor and pars triangularis diffusion metrics partially longitudinally mediate PCE-ADHD associations. PCE-related differences in brain development may confer vulnerability to worse mental health in early adolescence.

Human-caused climate change worsens with every increment of additional warming, although some impacts can develop abruptly. The potential for abrupt changes is far less understood in the Antarctic compared with the Arctic, but evidence is emerging for rapid, interacting and sometimes self-perpetuating changes in the Antarctic environment. A regime shift has reduced Antarctic sea-ice extent far below its natural variability of past centuries, and in some respects is more abrupt, non-linear and potentially irreversible than Arctic sea-ice loss. A marked slowdown in Antarctic Overturning Circulation is expected to intensify this century and may be faster than the anticipated Atlantic Meridional Overturning Circulation slowdown. The tipping point for unstoppable ice loss from the West Antarctic Ice Sheet could be exceeded even under best-case CO2 emission reduction pathways, potentially initiating global tipping cascades. Regime shifts are occurring in Antarctic and Southern Ocean biological systems through habitat transformation or exceedance of physiological thresholds, and compounding breeding failures are increasing extinction risk. Amplifying feedbacks are common between these abrupt changes in the Antarctic environment, and stabilizing Earth's climate with minimal overshoot of 1.5 °C will be imperative alongside global adaptation measures to minimise and prepare for the far-reaching impacts of Antarctic and Southern Ocean abrupt changes.

Laser-based displays are highly sought after for their superior brightness and colour performance1, especially in advanced applications such as augmented reality (AR)2. However, their broader use has been hindered by bulky projector designs and complex optical module assemblies3. Here we introduce a laser display architecture enabled by large-scale visible photonic integrated circuits (PICs)4-7 to address these challenges. Unlike previous projector-style laser displays, this architecture features an ultra-thin, flat-panel form factor, replacing bulky free-space illumination modules with a single, high-performance photonic chip. Centimetre-scale PIC devices, which integrate thousands of distinct optical components on-chip, are carefully tailored to achieve high display uniformity, contrast and efficiency. We demonstrate a 2-mm-thick flat-panel laser display combining the PIC with a liquid-crystal-on-silicon (LCoS) panel8,9, achieving 211% of the colour gamut and more than 80% volume reduction compared with traditional LCoS displays. We further showcase its application in a see-through AR system. Our work represents an advancement in the integration of nanophotonics with display technologies, enabling a range of new display concepts, from high-performance immersive displays to slim-panel 3D holography.

Stars are initially powered by the fusion of hydrogen to helium. These ashes serve as fuel in a series of stages1-3, transforming massive stars into a structure of shells. These are composed of natal hydrogen on the outside and consecutively heavier compositions inside, predicted to be dominated by He, C/O, O/Ne/Mg and O/Si/S (refs. 4,5). Silicon and sulfur are fused into iron, leading to the collapse of the core and either a supernova explosion or the formation of a black hole6-9. Stripped stars, in which the outer hydrogen layer has been removed and the internal He-rich or even the C/O layer below it is exposed10, provide evidence for this shell structure and the cosmic element production mechanism it reflects. The supernova types that arise from stripped stars embedded in shells of circumstellar material (CSM) confirm this scenario11-15. However, direct evidence for the most interior shells, which are responsible for producing elements heavier than oxygen, is lacking. Here we report the discovery of the supernova (SN) 2021yfj resulting from a star stripped to its O/Si/S-rich layer. We directly observe a thick, massive Si/S-rich shell, expelled by the progenitor shortly before the supernova explosion. Exposing such an inner stellar layer is theoretically challenging and probably requires a rarely observed mass-loss mechanism. This rare supernova event reveals advanced stages of stellar evolution, forming heavier elements, including silicon, sulfur and argon, than those detected on the surface of any known class of massive stars.

Alcohol-use disorder and alcohol-associated liver disease (ALD) are major causes of death and liver transplantation1. The gut-liver axis has a crucial yet poorly understood role in ALD pathogenesis, which depends on microbial translocation. Intestinal goblet cells (GCs) educate the immune system by forming GC-associated antigen passages (GAPs) on activation of muscarinic acetylcholine receptor M4 (mAChR4, also known as M4), enabling sampling of luminal antigens by lamina propria antigen-presenting cells. Here we show that chronic alcohol use in humans and mice downregulates small intestinal mAChR4 and reduces GAP formation, disrupting antimicrobial immunity. This is reversed on activation of intestinal IL-6 signal transducer (IL6ST, also known as glycoprotein 130; gp130), which restores mAChR4 expression and GAP formation, enabling induction of downstream type-3 innate lymphoid cell-derived IL-22 and antimicrobial REG3 proteins. This blunts translocation of enteric bacteria to the liver, thereby conferring ALD resistance. GAP induction by GC-specific mAChR4 activation was essential and sufficient for prevention of ethanol-induced steatohepatitis. These results lay the foundation for a therapeutic approach using mAChR4 or IL6ST agonists to promote GAP formation and prevent ALD by inhibiting microbial translocation.

B-1 cells are innate-like immune cells abundant in serosal cavities with antibodies enriched in bacterial recognition, yet their existence in humans has been controversial1-3. The CD5+ B-1a subset expresses anti-inflammatory molecules including IL-10, PDL1 and CTLA4 and can be immunoregulatory4-6. Unlike conventional B cells that are continuously replenished, B-1a cells are produced early in life and maintained through self-renewal7. Here we show that the transcription factors TCF1 and LEF1 are critical regulators of B-1a cells. LEF1 expression is highest in fetal and bone marrow B-1 progenitors, whereas the levels of TCF1 are higher in splenic and peritoneal B-1 cells than in B-1 progenitors. TCF1-LEF1 double deficient mice have reduced B-1a cells and defective B-1a cell maintenance. These transcription factors promote MYC-dependent metabolic pathways and induce a stem-like population upon activation, partly via IL-10 production. In the absence of TCF1 and LEF1, B-1 cells proliferate excessively and acquire an exhausted phenotype with reduced IL-10 and PDL1 expression. Furthermore, adoptive transfer of B-1 cells lacking TCF1 and LEF1 fails to suppress brain inflammation. These transcription factors are also expressed in human chronic lymphocytic leukaemia B cells and in a B-1-like population that is abundant in pleural fluid and circulation of some patients with pleural infection. Our findings define a TCF1-LEF1-driven transcriptional program that integrates stemness and regulatory function in B-1a cells.