Sungmin Nam

ABSTRACT Implant-associated infections are driven by bacterial biofilm formation and remain difficult to eradicate using conventional antibiotic-based strategies. Here, we present a dynamically actuated reconfigurable topographical surface (DARTS) that integrates intrinsically bactericidal nanoscale surface topography with programmable mechanical actuation to achieve durable, antibiotic-free infection control. Using a scalable bottom-up nanofabrication strategy, we generate tunable wrinkled MXene topographies that exhibit contact-mediated bactericidal activity against both Gram-positive and Gram-negative bacteria without chemical leaching. Integration with a soft robotic actuator enables reversible modulation of surface geometry, which synergistically enhances bacterial removal and killing, resulting in near-complete disruption of mature biofilms. Dynamic actuation further sensitizes released bacteria to antibiotic treatment. In a mouse subcutaneous implant infection model, DARTS with actuation achieves sustained suppression of bacterial burden and markedly improves host tissue outcomes. Remote, noninvasive actuation using near-infrared laser stimulation further highlights the translational potential of this platform for implantable antibacterial applications. Significance Statement Implant infections are difficult to treat because bacteria form biofilms that protect them from antibiotics and the immune system. Current materials often rely on chemical release, which can lose effectiveness over time. Here, we present a new surface that both kills bacteria and removes them. The surface uses nanoscale features to physically damage bacterial cells, while dynamic motion clears attached bacteria and biofilms. This allows continuous, chemical-free control of infection. In a mouse implant model, the system greatly reduced bacterial burden and improved tissue healing. This work introduces a new way to control bacteria using dynamic surface design and could be applied not only to medical implants but also to environmental, food, textile, and marine systems.

ABSTRACT Cell division within mechanically confining extracellular matrices (ECMs) is a key regulator of tissue morphogenesis and cancer progression. Although the intracellular force-generation mechanisms that drive volumetric growth and mitotic elongation are well characterized, how ECMs resist these forces remains poorly understood. Unlike linearly elastic materials, fibrillar ECMs exhibit nonlinear and viscoelastic behaviors that fundamentally alter how they oppose cell-generated stresses. Using a fiber-level computational model, we dissected the origins of ECM-mediated mechanical confinement during mitosis. We identified three distinct modes of resistance: compressive resistance at the cell poles, shear resistance from a pericellular shell, and tensile resistance at the cell equator. The relative contributions of these modes depended on fiber architecture and connectivity; however, shear resistance from the pericellular shell—pre-tensed by volumetric growth during G1—consistently dominated as the primary mechanical barrier to mitotic elongation. These findings suggest that the pericellular shell functions as a natural mechanical checkpoint on cell division within collagen-rich microenvironments. Notably, a finite element continuum model, despite being the most widely used framework for tissue mechanics, failed to reproduce these behaviors, underscoring the necessity of fiber-resolution approaches. We propose that overcoming this mechanical checkpoint is a critical step in cancer progression, enabling cells to divide within the dense stromal matrices characteristic of metastatic tumors.

Mechanical cues from the cellular microenvironment critically influence cell behavior, fate, and function through coordinated regulation of metabolism and gene expression. This review discusses how mechanical signals are sensed and transduced into biochemical responses that reshape metabolic pathways and the epigenetic landscape. We highlight emerging evidence linking mechanotransduction, metabolic reprogramming, and chromatin modifications, and propose directions for future research to unravel how mechanical forces orchestrate this dynamic and reciprocal interplay.

Tough hydrogels are promising for soft robotics, bioelectronics, and tissue adhesives due to their exceptional resilience and biocompatibility, yet precise spatiotemporal control of their mechanics remains challenging. Here, we present a hydrogel platform that enables spatiotemporal modulation of toughness through a latent ionic cross-linking mechanism. By embedding calcium carbonate (CaCO 3 ) microparticles in alginate/polyacrylamide double-network hydrogels, we create a system where localized calcium release and thus ionic cross-linking can be programmed in both space and time. Spatial control is achieved by direct ink writing of CaCO 3 , while temporal activation is triggered by glucono-δ-lactone, a biocompatible acidifier that releases calcium on demand. This strategy allows user-defined tuning of stiffness and toughness, enabling fabrication of three-dimensional (3D) hydrogels with tailored mechanical profiles. The resulting materials offer a versatile platform for anisotropic impact shielding, directional strain sensing, and 3D-printed tissue adhesives, representing a paradigm shift for adaptive, reconfigurable, and multifunctional soft materials.

Wounds often necessitate the use of instructive biomaterials to facilitate effective healing. Yet, consistently filling the wound and retaining the material in place presents notable challenges. Here, we develop a new class of injectable tissue adhesives by leveraging the dynamic crosslinking chemistry of Schiff base reactions. These adhesives demonstrate outstanding mechanical properties, especially in regard to stretchability and self-healing capacity, and biodegradability. Furthermore, they also form robust adhesion to biological tissues. Their therapeutic potential was evaluated in a rodent model of volumetric muscle loss (VML). Ultrasound imaging confirmed that the adhesives remained within the wound site, effectively filled the void, and degraded at a rate comparable to the healing process. Histological analysis indicated that the adhesives facilitated muscle fiber and blood vessel formation, and induced anti-inflammatory macrophages. Notably, the injured muscles of mice treated with the adhesives displayed increased weight and higher force generation than the control groups. This approach to adhesive design paves the way for the next generation of medical adhesives in tissue repair.