Quantum simulations of electronic structure and strongly correlated quantum phases are among the most promising applications of quantum computing. These computations benefit from native fermionic encodings1,2, enforcing fermionic statistics and conservation laws such as particle number and magnetization3 independent of gate errors. While ultracold atoms in optical lattices have become established as powerful analogue simulators of strongly correlated fermionic matter4-7, neutral-atom platforms have concurrently emerged as versatile, scalable architectures for spin-based digital quantum computation8. Unifying these capabilities requires high-fidelity motionally coherent gates for fermionic atoms9-11, similar to collisional gates in bosonic systems12,13, paving the way for programmable fermionic quantum processors. Here we demonstrate collisional entangling gates with fidelities up to 99.75(6)% and Bell-state lifetimes exceeding 10 s, realized by means of controlled interactions of fermionic atoms in an optical superlattice. Using quantum gas microscopy14, we microscopically characterize spin-exchange and pair-tunnelling gates and realize a robust composite pair-exchange gate, a key building block for quantum chemistry simulations3,15. Our results establish controlled collisions in optical lattices as a competitive and complementary route to high entangling gate fidelities in neutral-atom quantum computers. Operating intrinsically with fermions, this capability naturally extends to many-qubit architectures, in which fermionic statistics become relevant, enabling complex state preparation and advanced readout16-19 in scalable analogue-digital hybrid quantum simulators. Combined with local addressing20,21, these gates mark a crucial step towards a fully digital fermionic quantum computer based on controlled motion and entanglement of neutral atoms.

Ruddlesden-Popper nickelates have emerged as a crucial platform for exploring the mechanisms of high-temperature superconductivity1-7. However, the Fermi surface topology required for superconductivity remains unknown. Here, beyond the superconducting pure bilayer (2222) phase, we report the thin film growth and ambient-pressure superconductivity of monolayer-bilayer (1212) and bilayer-trilayer (2323) superstructures, together with the absence of superconductivity in monolayer-trilayer (1313) superstructure, under identical compressive epitaxial strain. The onset superconducting transition temperatures range from 46 K to 50 K, exceeding the McMillan limit. Angle-resolved photoemission spectroscopy shows key Fermi surface differences in these atomically engineered structures. In superconducting 1212 and 2222 films, a dispersive hole-like band (γΙΙ) forms an underlying Fermi pocket, surrounding the Brillouin zone corner. By contrast, the top of the flat band (γΙΙΙ) is observed at about 70 meV below EF in the non-superconducting 1313 films. Particularly, the superconducting 2323 films host both γΙΙ and γΙΙΙ bands. The polarization dependence of the γ bands reveals their Ni dz2 origin. Our findings expand the family of ambient-pressure nickelate superconductors and establish a connection between structural configuration, electronic structure and the emergence of superconductivity in nickelates.

Cell-type-specific promoters are used in gene therapy to restrict expression of the therapeutic payload. However, these promoters often have suboptimal strength, selectivity and size. Here, leveraging recent insights into the function of enhancers, we developed synthetic super-enhancers (SSEs) by assembling functionally validated enhancer fragments into multipart arrays. Focusing on the core SOX2-driven and SOX9-driven transcriptional regulatory network in glioblastoma stem cells (GSCs)1, we engineered SSEs with robust activity and high selectivity. Single-cell profiling, biochemical analyses and genome-binding data indicated that SSEs integrate neurodevelopmental and signalling-state transcription factors to trigger the formation of large multimeric complexes of transcription factors. Moreover, GSC-selective expression of a combination of cytotoxic (HSV-TK and ganciclovir) and immunomodulatory (IL-12) payloads, delivered using adeno-associated virus vectors, as a single treatment led to curative outcomes in a mouse model of aggressive glioblastoma. Notably, IL-12 induced an immunological memory that prevented tumour recurrence. The activity and selectivity of the adeno-associated virus and SSE were validated using primary human glioblastoma tissue and normal cortex samples. In summary, SSEs harness the unique core transcriptional programs that define the GSC phenotype and enable precision immune activation. This approach may have broader applications in other contexts when precise control of transgene expression in specific cell states is necessary.

Quantum computing represents a central challenge in modern science. Neutral atoms in optical lattices have emerged as a leading computing platform, with collisional gates offering a stable mechanism for quantum logic1-10. However, previous experiments have treated ultracold collisions as a dynamically fine-tuned process11-22, which obscures the underlying quantum geometry and quantum statistics crucial for realizing intrinsically robust operations. Here we propose and experimentally demonstrate a purely geometric two-qubit SWAP gate by transiently populating qubit doublon states of fermionic atoms in a dynamical optical lattice. The presence of these doublon states, together with fermionic exchange anti-symmetry, enables a two-particle quantum holonomy-a geometric evolution in which dynamical phases are absent23. This yields a gate mechanism that is intrinsically protected against fluctuations and inhomogeneities of the confining potentials. The resilience of the gate is further reinforced by time-reversal and chiral symmetries of the Hamiltonian. We experimentally validate this exceptional protection, achieving a loss-corrected amplitude fidelity of 99.91(7)% measured across the entire system consisting of more than 17,000 atom pairs. When combined with recently developed topological pumping methods for atom transport16, our results pave the way for large-scale, highly connected quantum processors. This work introduces a new model for quantum logic that transforms fundamental symmetries, including quantum statistics, into a powerful resource for fault-tolerant computation.

Heart failure remains a leading cause of morbidity and mortality, yet no approved therapies effectively prevent or reverse pathological cardiac fibrosis and the associated decline in cardiac function1-4. Chronic inflammation is a central driver of pathological fibrosis after ischaemic or haemodynamic stress, but strategies that locally rebalance injurious and reparative immune responses without systemic immunosuppression are lacking5,6. Dendritic cells (DCs) are key regulators of immune activation and tolerance, providing an opportunity for therapeutic immune reprogramming in cardiac diseases7,8. Here we show that engineered immunosuppressive and fibrosis-targeted DCs (iCDCs) effectively protect against pathological cardiac remodelling. In mouse models of ischaemia-reperfusion injury, myocardial infarction and pressure overload, iCDC therapy reduced inflammatory cardiac fibrosis, improved cardiac perfusion and preserved contractility. Mechanistically, iCDCs conferred sustained cardioprotection directly by suppressing immune and stromal cell activation or indirectly through promoting clonal expansion of regulatory T cells. Importantly, in a non-human primate model of myocardial infarction, iCDC therapy also reduced cardiac fibrosis, improved cardiac perfusion and contractile function without inducing systemic toxicity. These findings establish lesion-targeted immune modulation as a feasible strategy to control cardiac fibrosis and identify engineered dendritic cells as a promising therapeutic platform for treating cardiac remodelling and heart failure.

Artificial selection has greatly shaped crop agronomic traits1-3; however, the mechanistic basis of how immunity is selected remains unclear. Here we identify the Oryza sativa nucleotide-binding site and leucine-rich repeat (NLR) receptor XA48 and downstream transcription factors OsVOZ1 and OsVOZ2 (OsVOZ1/2), which confer resistance to bacterial blight. XA48 perceives the ancient pathogen effector XopG, activating effector-triggered immunity by degrading the negative regulator OsVOZ1/2. The XA48-OsVOZ1 module has undergone subspecies-specific selection: Xa48 is retained only in Oryza sativa indica and was lost in Oryza sativa japonica. By contrast, OsVOZ1 has diverged into two haplotypes-O. s. indica retains both OsVOZ1A/S alleles compatible with Xa48, whereas O. s. japonica has only OsVOZ1A. Reintroducing Xa48 into O. s. japonica severely compromises yield owing to the XA48-OsVOZ1A-mediated immune incompatibility. Stacking XA48-mediated effector-triggered immunity with XA21-mediated pattern-triggered immunity reconstitutes the broad-spectrum resistance from wild rice. Our study therefore reveals how asymmetric selection of an NLR-transcription factor module shapes disease resistance and reproductive development, providing a strategy for breeding crops by harnessing the relative immunity of wild rice.

The human maternal-fetal interface is characterized by mosaic intermingling of maternal and fetal cells1. Yet the underlying cellular, molecular and spatial programmes remain incompletely defined. Here we generate a comprehensive atlas of the human maternal-fetal interface across normal pregnancies from early gestation to term by integrating large-scale paired single-nucleus transcriptomic and chromatin accessibility profiling with submicrometre-resolution spatial transcriptomics and CODEX multiplex protein imaging2, substantially boosting the spatiotemporal resolution of prior research3. This framework delineates common and transient cell types, states and spatial niches across the fetal and maternal compartments, reconstructs transcriptional programmes that guide cytotrophoblast and decidual stromal cell differentiation, and resolves recurrent architecture structural units that build this interface. We identify previously unrecognized arterial endothelial state transitions during cytotrophoblast-mediated spiral artery remodelling and develop a machine learning model that predicts cytotrophoblast invasiveness from transcriptomic signatures. We further discover a decidual stromal cell subtype that suppresses cytotrophoblast invasion via endocannabinoid signalling at the human maternal-fetal interface. By integrating the atlas with genome-wide association data, we pinpoint maternal and fetal cells that are most vulnerable to pre-eclampsia, preterm birth or miscarriage. This resource provides a comprehensive spatially resolved single-cell multiomic reference of the human placenta and decidua and offers a framework for decoding their normal and disordered development.