Active fluids churn, swirl, and never sit still. But what happens when such restless materials are placed next to a passive, placid liquid? Spera et al. show that the passive partner inherits the active chaos, but only in broad strokes, as short-wavelength fluctuations are filtered out where the interface acts as a low-pass filter for momentum.

Cardiac hypertrophy involves dynamic heart remodeling associated with mechanical and biochemical stimuli, while physiological and pathological cardiac hypertrophy can lead to distinct clinical outcomes. However, most previous models fail to distinguish these types, or properly account for cytoskeletal-extracellular matrix (ECM) remodeling effects. In this study, we develop a multiscale mechanobiological model by coupling cardiac mechanical behaviors with cardiomyocyte growth through mechanosensitive signaling pathways. This model considers tissue microstructures to characterize how cytoskeletal-ECM remodeling alters the mechanical forces sensed by cardiomyocytes. Our model can well predict experimental measurements of ventricular wall thickness and signaling activation in both physiological and pathological hypertrophy, enabling their clear differentiation. We demonstrate that exercise-induced hypertrophy attenuates pathological remodeling by alleviating myocardial mechanical stress to suppress mechanotransduction. We also elucidate the synergistic or antagonistic interaction mechanisms among factors such as hypertension, exercise, cardiomyocyte death and fibrosis in cardiomyocyte growth and pathological signaling. These results highlight the importance of myocardial microenvironment in cardiac remodeling. Furthermore, computational evaluation demonstrates that muscle LIM protein-targeted therapies have potential for treating pathological hypertrophy through mechanotransduction modulation, but excessive dosing may elevate arrhythmia risks. This study not only advances mechanistic understanding of physiological and pathological cardiac hypertrophy, but also provides a theoretical basis for developing mechanobiology-informed therapeutic techniques.

Cell migration through spatially confined microenvironments occurs in many biological processes such as embryonic development, immune surveillance, and cancer metastasis. A major bottleneck during such migration is the nucleus, which acts not only as a rigid mechanical obstacle but also as a crucial mechanosensor that modulates downstream signaling pathways. However, it remains poorly understood how nuclear deformation and mechanosensation together regulate cell migration through confined spaces. Here, we propose a three-dimensional (3D) mechanochemical model of confined nuclear translocation that integrates nuclear deformation with deformation-induced calcium signaling and subsequent regulation of cytoskeletal contractility. We show that cells undergo adaptive nuclear deformation, including nuclear envelope elongation and 3D buckling, to efficiently navigate confinements of varying sizes. There exists a biphasic relation between nuclear velocity and confinement size, arising from the interplay between nuclear deformability and mechanosensitive feedback. We demonstrate that local nuclear envelope rupture can occur under large deformation, enabling nuclear translocation through extreme confinements, as observed in prior experiments. Furthermore, we elucidate the critical roles of chromatin organization in nuclear translocation. This work reveals key mechanochemical mechanisms driving confined cell migration and provides a theoretical framework for studying nuclear dynamics across physiological and pathological contexts.

Collective cell migration governs a range of physiological and pathological processes, from tissue morphogenesis to cancer invasion, in which topological defects arise as an inevitable consequence of frequent cellular rearrangement and migration. Here, we employ an Active Vertex Model to investigate structural defects generated in the wake of transported cells. We find that while the drag coefficient of a cell in a perfect lattice is anisotropic, the threshold drag force required to mobilize the cell is isotropic. Remarkably, we find that dragging two neighboring cells along the direction of least-resistance minimizes lattice disruption. By comparing defect-healing behaviors across different physical models, we disentangle the contributions of cell adhesion and many-body interactions. Together, our findings provide new insights into the topological organization of confluent tissues during collective migration, advancing our physical understanding of cellular transport processes such as wound healing, tissue repair, and cancer metastasis.

Unidirectional guided resonances (UGRs)-topological polarization singularities in momentum space with intrinsic unidirectional radiation-have recently garnered widespread attention. However, previous studies have been largely limited to realizing only a few discrete UGRs. We demonstrate an unprecedented continuous ring of UGRs in a hexagonal bilayer cylinder array, whose formation is governed by isotropic interband coupling, ensuring robust and azimuthally continuous unidirectional emission. Furthermore, by leveraging an in-plane inversion symmetry-protected bound state in the continuum at the Gamma point, the continuous ring of UGRs acquires its topological properties from the enclosed bound state in the continuum, manifesting as a phase vortex with a nontrivial topological charge. This unique combination of continuous unidirectionality and a global topological charge provides a robust platform for developing novel devices, such as unidirectional vortex lasers.

Modeling viscoelastic behavior is crucial in engineering and biomechanics, where materials undergo time-dependent deformations, including stress relaxation, creep buckling and biological tissue development. Traditional numerical methods, like the finite element method, often require explicit meshing, artificial perturbations or embedding customised programs to capture these phenomena, adding computational complexity. In this study, we develop an energy-based physics-informed neural network (PINN) framework using an incremental approach to model viscoelastic creep, stress relaxation, buckling, and growth-induced morphogenesis. Physics consistency is ensured by training neural networks to minimize the systems potential energy functional, implicitly satisfying equilibrium and constitutive laws. We demonstrate that this framework can naturally capture creep buckling without pre-imposed imperfections, leveraging inherent training dynamics to trigger instabilities. Furthermore, we extend our framework to biological tissue growth and morphogenesis, predicting both uniform expansion and differential growth-induced buckling in cylindrical structures. Results show that the energy-based PINN effectively predicts viscoelastic instabilities, post-buckling evolution and tissue morphological evolution, offering a promising alternative to traditional methods. This study demonstrates that PINN can be a flexible robust tool for modeling complex, time-dependent material behavior, opening possible applications in structural engineering, soft materials, and tissue development.

Cell adhesion is a fundamental biological process that governs cell proliferation, differentiation, migration, and tissue development. Cells adhere to the extracellular matrix through specialized transmembrane proteins, whose structures and functions are well characterized. However, it remains unclear how mechanical, chemical, and biological factors interact to regulate these proteins and hence to shape cross-scale adhesion dynamics from molecular clustering to cellular migration. Here, we propose a multiscale mechanobiochemical coupling framework to investigate the dynamics of cell-substrate adhesions, integrating key molecular steps in the integrin life cycle, from activation and clustering to signal transduction and internalization. Our model elucidates the roles of caveolin-mediated trafficking and actin-generated traction in modulating integrin dynamics and focal adhesion (FA) morphology. It identifies an antagonistic interplay between integrin internalization and clustering that governs cross-scale adhesion dynamics. Furthermore, our model quantitatively demonstrates how the substrate stiffness regulates the integrin clustering size and internalization rate. These findings provide mechanistic insights into the adhesion-associated regulation of cell migration, particularly the experimentally observed transition between durotaxis and negative durotaxis, driven by intracellular and extracellular microenvironmental factors. Our model therefore offers an effective framework for understanding the cross-scale regulation of cell adhesion involved in physiological and pathological activities, such as stem cell differentiation and cancer metastasis.

Fracture typically signifies mechanical failure in engineering materials, whereas controlled cracking may actively sculpt tissues through precise biological regulation. Here, we establish a multiscale nonlinear peridynamic theory that accounts for cellular mechanosensing to decipher the spontaneous fracture of active tissues. We show that tissues cultured in a ring-shaped domain can undergo periodic fracture to generate multicellular aggregates with regular spacing, recapitulating prior morphogenetic experiments on avian dermal cell collectives. It is found that the number of cracks varies nonmonotonically with the substrate stiffness. We predict that a narrow tissue favors equally spaced radial cracking, while such ordered cracks deflect, branch, and randomize increasingly as the tissue broadens, attributable to the anisotropy-isotropy transition of tissue stresses induced by the interplay of active contraction and domain geometry. Backed by energetic arguments, we identify the factors that control the characteristic size of tissue fracture. Our Letter reveals a synergy of physics, geometry, and cellular mechanosensing in controlling active tissue fracture to achieve tissue-level organization.

The formation of cell-in-cell structures is a complex dynamic process that profoundly influences tissue development and cancer progression. Here, we decipher the physical principles governing three-dimensional (3D) cell-in-cell formation, including cannibalism and entosis, and their cooperation that are observed experimentally. We show that active engulfing cells behave like a material flow or deform as a solid, determined by the cytoskeleton arrangement, whereas the cytoskeleton in invading cells can spontaneously break the left-right symmetry, organizing into a 3D vortex-like topological defect to facilitate internalization. The microscopic stiffness mismatch between the interacting cells markedly affects the cell-in-cell formation and may even lead to escape of the internalized cells. Backed by prior experiments, we predict that the stress localization at the interacting interface may induce the formation of a contractile multimolecular ring structure, favoring cell penetration and cavity closure. Our findings provide a multiscale physical basis for understanding cell-in-cell dynamics in various physiological and pathological contexts.

During the immune response, lymph nodes (LNs) undergo significant coupled evolutions in their geometric structures, cellular compositions, and mechanical properties. The efficiency of the immune response (IR) is governed by the interplay between internal cellular activity and mechanical deformation throughout the inflammation-homeostasis process. While mechanical forces are known to play a crucial role in LN remodeling, the underlying mechanisms of mechanoimmunology synergy within LNs remain poorly understood. In this paper, we propose a mechanoimmunology theory that conceptualizes LNs as integrated, dynamically evolving structures during IR and establish a mechano-immunological landscape to quantify distinct LN states. This framework introduces a novel paradigm for evaluating IR efficiency based on metrics derived from mechano-chemo-biological mechanisms. We identify the range of mechanical properties that optimize IR efficiency and propose that immune exhaustion in tumor-draining LNs arises from mechanical damage, leading to an immune anergic state. Using the proposed mechanoimmunological methodology, we demonstrate that this anergic state can be mitigated by modulating collective immune cell migration to align with the optimal IR efficiency range, thereby offering potential therapeutic strategies to enhance IR efficiency.

Collective cell dynamics are fundamental to numerous physiological processes, including embryo development, tissue morphogenesis, immune response, and disease progression. Accurately modeling these dynamics across scales remains challenging, as traditional physics-based models usually rely on many unmeasurable parameters and unclear active physics, limiting their ability to capture both single-cell features and emergent multicellular behaviors. Here, we introduce a scale-adaptive hybrid machine learning (ML) framework, in which complementary physics-guided and physics-agnostic method each resolves an above key issue at single-cell and multicellular scales, respectively. The physics-guided ML method integrates physical models with experimental data to infer previously unmeasurable parameters, enabling more accurate characterization of single-cell shape and velocity features, but unknown active forces and inherent physical assumptions still constrain its ability to predict multicellular scale dynamics. In contrast, the physics-agnostic ML method bypasses explicit physical assumptions to directly model multicellular behaviors from historical state sequences. This method provides robust long-term predictions of coarse-grained density oscillations and waves observed experimentally, yet it suffers from high stochasticity when applied to single-cell scale modeling. By assigning each approach to the scale where it is most effective, our framework leverages their respective strengths while mitigating their limitations. This complementary strategy bridges the gap between theoretical modeling and experimental observations, offering a versatile computational paradigm for multiscale collective cell dynamics with broad potential in diverse physiological and pathological contexts.

ABSTRACT Existing realizations of Janus bound states in the continuum (BICs) rely primarily on manipulating polarization singularities derived from accidental BICs. Here, we introduce a distinct strategy to engineer high‐order Janus BICs by leveraging interband‐coupling‐induced unidirectional guided resonances (UGRs). By breaking the out‐of‐plane symmetry in a square‐lattice photonic crystal slab, we manipulate the momentum‐space evolution of UGRs, driving them to coalesce with an intrinsic symmetry‐protected BIC at the Brillouin zone center. This process gives rise to a high‐order Janus BIC exhibiting extreme radiative asymmetry: it yields an upward‐radiated vortex beam with a topological charge of −3, while maintaining a +1 charge downward. Our findings establish a novel paradigm for tailoring momentum‐space polarization singularities, unlocking new potential for generating vortex beams with direction‐dependent topological charges in advanced optical information processing.

Aneurysm is a life-threatening arterial disease. Its formation and development involve tissue growth, collagen fiber reorientation, matrix damage, and residual stretch remodeling, which are regulated by both mechanical stimuli and biochemical signals. In this paper, we propose a mechanobiological theory that integrates stress-modulated growth, remodeling, and damage to elucidate the mechanisms underlying the morphogenesis of aneurysms. Linear stability analysis elucidates the mechanobiological bifurcation leading to arterial bulging, while finite element simulations corroborate theoretical predictions and trace the postbuckling evolution from normal arteries to aneurysms. Our results reveal that the decreased circumferential homeostatic stress tends to stabilize the arteries, whereas the internal pressure exerts little influence due to compensatory artery wall thickening through long-term growth and remodeling. Oscillations emerge following the mechanobiological bulging bifurcation but diminish as the matrix damage accumulates. We also show that reduced mechanosensitivity in aged vascular smooth muscle cells can trigger mechanobiological instability, thereby initiating aneurysm formation. By introducing initial damage, we demonstrate that the self-healing response observed in previous experiments on the artificial rabbit abdominal aortic aneurysms may arise from the mechanobiological stability of the non-aneurysmal arteries. This work provides a mechanobiological framework for analyzing diverse tissue growth, damage, and remodeling processes in both physiological and pathological contexts.

Slender biological structures, which are widely observed in nature, exhibit exceptional properties and biological functions. A notable example is the Curculio rostrum that can drill into fruits for feeding and egg-laying without buckling. However, it remains unknown how the slender and curved Curculio rostrum resists buckling. In this article, we propose an elastic rod model for the rostrum that has multi-layered microstructures reinforced by helical chitin fibres. Its buckling behaviour is investigated through the combination of theoretical analysis and numerical simulations. The critical buckling load is derived and verified by experiments. It is found that despite the coupled twisting deformation induced by the helical microstructure, the originally curved rostrum exhibits a two-dimensional buckling mode. The critical buckling load for this two-dimensional buckling is much higher than for three-dimensional buckling, owing to the relatively large stiffness of the outermost layer. The macroscopic straight-curved shape helps the rostra to achieve similar buckling resistance capability among individuals, thereby enabling them to sustain the same feeding habits. Our results reveal that the macroscopic shape and helical microstructure synergistically contribute to the buckling resistance of Curculio rostra. This work could also inspire the bionic design of high-performance slender structures and soft robots.

Orbital angular momentum (OAM) multiplexing holography has emerged as a pivotal technology for high-capacity optical communication, encryption and display, but it requires multiple inputs for decoding and its security remain constrained due to the rotational symmetry of topological charge (TC) distribution in conventional OAM modes. Here, we introduce a general paradigm of OAM multiplexing holography that enables multi-channel holographic encoding using a single incident light. Our methodology leverages a discontinuous OAM with a spatially varying TC across the azimuth, which breaks the rotational symmetry and imposes angular selectivity for information retrieval. Notably, by rationally designing the TC distribution, the discontinuous OAM exhibits self-orthogonality at different rotation angles, laying the foundation for multiplexed holography. A modified weighted Gerchberg-Saxton algorithm is developed to calculate the holographic phase profile, which can then be encoded onto a pure geometry-phase metasurface. By further integrating different pairs of discontinuous OAMs, we successfully expand the channel capacity for holographic multiplexing, significantly advancing high-security and high-capacity optical information encryption. Our work establishes discontinuous OAM as a versatile platform for secure optical communications, high-density data storage, and dynamic holographic displays, bridging the gap between structured light manipulation and cryptographic robustness.

A wide variety of dynamic behaviors of cells are closely associated with the active contraction of the cytoskeleton and the cell-substrate adhesion. By inhibiting cell-substrate adhesion, here we experimentally show that an isolated cell exhibits diverse morphological geometries and dynamic behaviors on different adhesion-inhibiting substrates. A biochemomechanical tensegrity model of cytoskeletons is adopted to elucidate the biophysical mechanisms underlying the spontaneous dynamic behaviors of isolated cells. Theoretical analysis shows that the dynamic behaviors of cells depend on the intrinsic active contraction of cytoskeletons and the adherent condition. Combining living cell experiments and numerical simulations, we find that cells may transform from oscillation mode to protrusion mode and then to spreading mode due to the increase of the adhesion force threshold. Furthermore, for oscillating cells, two characteristic patterns, including global oscillation and traveling wave, are captured. These findings highlight the role of environmental adherent properties in mediating cellular spatiotemporal dynamics.

Cell adhesion is a fundamental biological process that governs cell proliferation, differentiation, migration, and tissue development. Cells adhere to the extracellular matrix through specialized transmembrane proteins, whose structures and functions are well studied. However, how mechanical, chemical, and biological factors interact to regulate these proteins and hence to shape cross-scale adhesion dynamics from molecular clustering to cellular migration remains unclear. Here, we propose a multiscale mechano-biochemical coupling framework to investigate the dynamics of cell–substrate adhesions, incorporating comprehensive molecular steps in the integrin life cycle, including activation, clustering, signal transduction and internalization. Our model elucidates the roles of caveolin transport and actin flow in modulating integrin dynamics and FA morphology. We identify the antagonistic interplay between integrin internalization and clustering that governs cross-scale adhesion dynamics. Furthermore, our model quantitatively demonstrates how the substrate stiffness regulates the integrin clustering size and internalization rate. These findings provide mechanistic insights into the regulation of cell migration, particularly the transition between durotaxis and negative durotaxis, driven by intracellular and extracellular microenvironmental factors. Our model offers an effective framework for understanding the cross-scale regulation process of cell adhesion involved in physiological and pathological activities, such as stem cell differentiation and cancer metastasis. ### Competing Interest Statement The authors have declared no competing interest. National Natural Science Foundation of China

The increasing complexity and diversity of aerospace missions have resulted in the need for deployable arms with high load-bearing capacity and structural stiffness. High stiffness ensures the stability and reliability of a structure in environments with extreme temperatures and microgravity while effectively mitigating vibration during missions. In this study, an approach to synthesize customizable-stiffness triangular-prism deployable arms (TPDAs) is proposed. The synthesis approach achieves high structural stiffness during the configuration synthesis phase. First, deployable unit graphs are generated from statically determinate truss structures on the basis of graph theory, leading to the development of a deployable unit configuration library for TPDAs. Second, a general equivalent stiffness model is formulated for deployable unit configurations on the basis of equivalent beam theory. This model ensures that the stiffness of all configurations in the library can be determined efficiently, and that the stiffness model and configuration synthesis methods can be combined for the design of customized stiffness. Last, a configuration is selected from the deployable unit configuration library as an example to construct a TPDA and conduct prototype experiments. The presented synthesis method is able to analyze the configuration stiffness in the configuration synthesis stage and meets the requirements for high stiffness in TPDAs.

Metal oxide and graphene composite material have been a promising material for developing electrochemical sensors. In this work, we prepared graphene (rGO) doped MoO2 hollow nanosphere composite (MoO2/rGO) using a simple one-step solvothermal without any template.The hollow nanosphere was constructed by nano- particles and uniformly anchored onto graphene sheets.The dopamine (DA) sensor was constructed by modifying the MoO2/rGO composite to the glass carbon electrode (GCE) surface with a simple drop coating (MoO2/rGO/ GCE), which shows high sensitivity(101.20 mu A center dot mu M-1 center dot cm-2), low detection limit (6.8 nM), high selectivity and good stability for DA. Meanwhile, the MoO2/rGO/GCE demonstrates very little interference with dopamine determination when both Uric acid (UA) and ascorbic acid (AA) are present. The exceptional efficacy of the sensor is attributed to the MoO2/rGO composite's unique attributes,which include a hollow structure, low charge transfer resistance, a large electrochemical active area, and an abundance of active sites. Furthermore, the MoO2/ rGO/GCE sensor demonstrates capabilities for the detection of minute dopamine levels in human serum, utilizing the standard addition method. This suggests its applicability in the realm of biomedical diagnostics.