From Renaissance drapery to tissue morphogenesis, pattern formation exemplifies how geometry and constraints generate complex structures. In soft and architected matter, motifs such as creases, kinks, and domain walls function as order-parameter textures mediating structural transitions. Yet deterministic and reprogrammable control of such patterns remains a central challenge: conventional geometry-based strategies hardwire functionality into structure, leaving deformation modes defect-sensitive and difficult to reconfigure. Here we introduce a pseudo-dynamic mapping that interprets static deformation fields as trajectories of fictitious particles evolving in engineered energy landscapes. This paradigm provides a forward design strategy in which reshaping potential symmetry and bifurcation structure prescribes diverse reprogrammable solitonic domain-wall-lattices in a single, defect-free metamaterial solely under uniform loading. We demonstrate initiation, modulation, inversion, melting, and annihilation of these patterns, governed by a tunable bifurcation landscape. Predictions are validated through simulation and experiment, culminating in a mechanical display that encodes digital information via domain-wall-bits. This approach bridges nonlinear field theory with practical pattern reprogramming, offering a versatile route for programmable design in architected and adaptive materials.

The orbital Fulde-Ferrell-Larkin-Ovchinnikov (orb-FFLO) state has lately emerged as an exotic dissipationless state, but a thermodynamic demonstration, which is key for its establishment, has been lacking. Here, we reveal a first-order quantum phase transition in the tunneling spectroscopy under an in-plane magnetic field on multilayer 2H-NbSe2. The transition manifests itself as a sudden enhancement of the superconducting gap with prominent hysteresis by sweeping the in-plane magnetic field well below the upper critical field. Such a first-order transition quickly disappears once the magnetic field tilts away from the in-plane direction by about one degree, and it depends sensitively on disorder. Furthermore, we obtain a comprehensive phase diagram of the phase transition as a function of magnetic field, temperature, and the sample thickness. These observed behaviors can be reproduced by the theory that considers the energetics between a uniform Ising superconductor and the orb-FFLO state.

Strain resilient nanocomposite conductors with self-healing ability are vital for skin-mounted devices and system-level bioelectronics, especially for wireless systems that require extremely low surface resistance and high stability of electromagnetic wave transmission. However, nanocomposite conductors inherently suffer from a trade-off between conductivity and flexible deformability or self-healing ability. Herein, a strain resilient and self-healing conductor (with ultralow sheet resistance of 10.8 mΩ/sq) is fabricated based on a well-designed polymer binder. It not only maintains outstanding stretchability (a break at elongation over 700%) and electrical stability during repeated stretching (1000 cycles) but also exhibits self-healing performance. On this basis, a flexible antenna with outstanding electromagnetic performance (realized gain of 5.25 dBi, nearly equivalent to that of copper-based devices), excellent self-healing ability is realized for wireless e-skin which can support instant communication exceeding 70 m. This approach overcomes the trade-off between high conductivity and excellent mechanical property in nanocomposite conductor and paves the way for completely self-healing flexible antenna towards wireless e-skins.

Design of active but stable interfaces in supported metal catalysts represents an emerging research theme lately, given its critical importance for tailoring and enabling selectivity and efficiency of heterogeneous reactions. Herein, we report a generic sunlight-driven epitaxial growth strategy to engineer catalytically active interfacial perimeters defined by subnanometric Pt dispersed on TiO2 nanoparticle supports. Such interfacial perimeters are populated with a unique type of Pt4+-O-Ti3+ reactive sites, resulting in much more efficient and robust CO oxidation than most supported Pt catalysts reported so far. These subnanometric PtOx-TiO2 interfacial structures are found to dynamically evolve during CO oxidation, adaptively optimizing their adsorption behaviors toward reactants and SO2. Combined with the activated interfacial lattice oxygen species via the electronic metal-support interaction effect, the Mars-van Krevelen pathway is activated at low temperature to oxidize CO at high conversion efficiency. The sunlight-driven synthetic strategy is successfully extended to other metal catalysts supported by metal oxide and perovskite materials, offering a new paradigm for designing adaptive catalysts toward a variety of heterogeneous catalytic reactions.

Despite mitigation efforts, anthropogenic emissions are projected to cause a global mean sea level rise of approximately 0.44 m and sustained sea levels over human timescales (e.g., centuries). Even without glacial melting, sea level remains elevated for centuries due to the substantial thermal inertia of the ocean interior. However, mechanisms governing persistent sea level rise remain inadequately understood. Here, using a fully coupled climate model, we demonstrate that a distinct sea surface temperature pattern drives enhanced and prolonged sea level rise. This surface warming pattern enhances the absorption of shortwave radiation through climate feedbacks, such as low cloud and sea ice-albedo feedbacks, thereby sustaining ocean heat uptake, thermal expansion, and continued sea level rise. Atmosphere-only simulations confirm that the sea surface temperature pattern alone explains the increased shortwave radiation through the positive feedbacks. These findings underscore the importance of accurately representing surface warming patterns and associated cloud responses in future sea level rise projections.

Interferon regulatory factors (IRFs) are innate immune transcription factors responsible for inducing the expression of type I interferons (IFN-I), which combat pathogen invasions via initiating the downstream Janus kinase signal transducer and activator of transcription (JAK-STAT) pathway. Among them, IRF7 plays a central role by forming heterodimers with IRF3 to initiate IFN-I production and is therefore frequently targeted by viruses to evade immune detection. Contrary to this common paradigm, we show that IRF7 is activated and upregulated by the retrovirus human T-cell leukemia virus type 1 (HTLV-1), via its oncoprotein HBZ. Moreover, IRF7 is highly expressed in HTLV-1 induced CD4 T-cell malignancy named adult T-cell leukemia/lymphoma (ATLL), and promotes the proliferation of infected cells both in vitro and in vivo. Intriguingly, HBZ is able to interfere with the interaction of IRF7 and IRF3, suppressing IFN-I pathway activation. On the other hand, IRF7 was found to upregulate and activate STAT5B, a transcription factor of the JAK-STAT pathway frequently mutated in hematological malignancies. Together, these findings reveal a mechanism by which HTLV-1 hijacks a critical innate immune effector to sustain persistent infection and drive oncogenesis without activating antiviral IFN-I pathway.

The synthetic positive allosteric modulator (PAM) of cannabinoid receptor CB2, Ec21a, exhibits better subtype selectivity and receptor specificity over orthosteric ligands, which holds promise for treating neuropathic pain and seizure without causing psychotropic side effects mediated by CB1. The poor understanding of allosteric binding site and regulatory mechanism of Ec21a hinders further development of CB2 allosteric modulators. Here, we resolve the cryo-EM structure of CB2 in complex with PAM Ec21a and agonist CP55940, revealing a sandwich-like pattern of ECL2-Ec21a-CP55940, in which Ec21a binds above CP55940 acting as a "plug" and sterically hinders the dissociation of the CP55940. Through structural analysis and cell functional experiments, we find that Ec21a significantly enhances the activation efficiency of CP55940 via increasing and prolonging the interaction between CP55940 and CB2. Furthermore, by assessing the allosteric effects of Ec21a in combination with various agonists, we expand the potential range of ligand pairings and provide a structural framework for the design of bitopic ligands. Our findings address a gap in the understanding of the CB2 allosteric site and offer valuable guidance for the rational design of CB2 allosteric and bitopic ligands.

Pathogenesis, progression, and therapeutic response of numerous digestive system tumors are associated with reduced intestinal barrier integrity. Here, we find that oral delivery of enterocyte-mimicking butyrate-loaded nanoparticles (EMBNs) capable of repairing the gut barrier can inhibit the occurrence, growth, and metastasis of digestive system tumors. EMBNs are prepared via loading butyrate into electrostatically complexed and sodium triphosphate-stabilized chitosan/hyaluronic acid nanoparticles, which are further coated with cell membranes extracted from enterocytes. The presented membrane receptors adsorb lipopolysaccharide and zonulin, known promoters of intestinal barrier impairment, while the loaded butyrate strengthens the function of the intestinal barrier. Mechanistically, the inhibition of autophagy in enterocytes and the promotion of a healthy microbial composition contribute to the repair of the gut barrier. Oral ingestion of EMBNs suppresses the disturbance of the liver immune microenvironment via alleviating the disruption of the intestinal barrier, achieving potent inhibition against hepatocellular carcinoma and hepatic metastasis of colonic carcinoma in dextran sulfate sodium-induced model in male mice. The reinforcement of the gut barrier spotlights a strategy to prevent and treat digestive system tumors.