There is an unmet need in the glaucoma clinic to control changes in the intraocular pressure (IOP), i.e., patient‐specific hypotony and tissue fibrosis‐mediated ocular hypertension, owing to the fixed tube diameter of the glaucoma drainage device. As a potential solution, the tube diameter can be adjusted, depending on the IOP, by shape memory polymer (SMP) and clinical laser systems, which can control the energy level, focus, and frequency by minimizing untargeted influences. To develop a translatable device, a laser‐responsive SMP with two additional elements: i) a tube with an intimal gel coating to release 5‐fluorouracil as an anti‐fibrotic drug and ii) a safety lock ring to block late hypotony in special cases is employed. When the SMP tube is inserted into a silicone tube and wrapped externally by the ring, intimal gel degradation and argon laser‐triggered diameter increase enable a three‐step IOP control. Sustained drug release of the intimal gel suppresses tissue fibrosis, and the ring prevents late hypotony by externally squeezing the silicone tube. The advanced design and functions are validated using computational in vitro and rabbit glaucoma models by determining clinic‐friendly argon laser parameters.

The structural stability of medical devices is established by managing stress distribution in response to organ movement. Veins abruptly dilate upon arterial grafting due to the mismatched tissue property, resulting in flow disturbances and consequently stenosis. Vascular cast is designed to wrap the vein‐artery grafts, thereby adjusting the diameter and property mismatches by relying on the elastic fixity. Here, a small bridge connection in the cast structure serves as an essential element to prevent stress concentrations due to the improved elastic fixity. Consequently, the vein dilation is efficiently suppressed, healthy (laminar and helical) flow is induced effectively, and the heathy functions of vein grafting are promoted, as indicated by the flow directional alignment of endothelial cells with arterialization, muscle expansion, and improved contractility. Finally, collaborative effects of the bridge drastically suppress stenosis with patency improvement. As a key technical point, the advantages of the bridge addition are validated via the computational modeling of fluid–structure interaction, followed by a customized ex vivo set‐up and analyses. The calculated effects are verified using a series of cell, rat, and canine models towards translation. The bridge acted like “Little Dutch boy” who saved the big mass using one finger by supporting the cast function.

Clinical translation of nanoparticles is limited because of their short circulation time, which hampers targeting to prolong therapeutic effects. Angiogenesis is required to regenerate damaged sites under inflammation, and CD11b+ cells turn vasculogenic under hypoxia. As a turning‐point strategy to increase the circulation time, this study explores liposomal targeting of splenic CD11b+ cells, which are gathered in the spleen and move to inflamed sites inherently. Moreover, nano‐hypoxia is strategized as a therapeutic method by loading liposomes with a hypoxic‐mimetic agent (CoCl2) to induce in situ reprogramming of splenic CD11b+ cells upon venous injection. Consequently, the vasculogenic potential of reprogrammed cells accelerates regeneration through inflammation‐responsive homing. Hydrophilic coating of liposomes improves the selectivity of splenic targeting in contrast to fast targeting without coating. Hypoxia chambers and surgical induction of splenic hypoxia are compared to validate the reprogramming effect. The strategy is validated in mouse models of inflamed skin, ischemic hindlimbs, and 70% hepatectomy compared with a conventional approach using bone marrow cells. Intravital multiphoton microscopy, 19F 2D/3D MRI, and microchannel hydrogel chips for 3D tissue culture are used as advanced tools. Overall, nanocarrier change to CD11b+ cells prolong targeting by inducing in situ reprogramming for inflammation‐responsive vasculogenic therapy.

Continuous progress has been made in elucidating the relationship between material property, device design, and body function to develop surgical meshes. However, an unmet need still exists wherein the surgical mesh can handle the body motion and thereby promote the repair process. Here, the hernia mesh design and the advanced polymer properties are tailored to synchronize with the anisotropic abdominal motion through shape configuration. The thermomechanical property of shape configurable polymer enables molding of mesh shape to fit onto the abdominal structure upon temperature shift, followed by shape fixing with the release of the heat energy. The microstructural design of mesh is produced through finite element modeling to handle the abdominal motion efficiently through the anisotropic longitudinal and transverse directions. The design effects are validated through in vitro, ex vivo, and in vivo mechanical analyses using a self‐configurable, body motion responsive (BMR) mesh. The regenerative function of BMR mesh leads to effective repair in a rat hernioplasty model by effectively handling the anisotropic abdomen motion. Subsequently, the device‐tissue integration is promoted by promoting healthy collagen synthesis with fibroblast‐to‐myofibroblast differentiation. This study suggests a potential solution to promote hernia repair by fine‐tuning the relationship between material property and mesh design.

Clinical laser systems enable user-specified control of the energy level, focus, and frequency by minimizing untargeted influences, which has never been applied to implantable shape memory polymers (SMPs). The glaucoma clinic possesses multi-decade issues to control progressive fluctuations in intraocular pressure (IOP) with tissue fibrosis upon implantation of silicone drainage devices. As a translatable device, we applied a laser-responsive SMP to develop i) a tube with intimal gel coating to release anti-fibrotic drugs and ii) safety lock ring. When the SMP tube was inserted into a silicone tube with wrapping externally by the ring, intimal gel degradation and argon laser-triggered diameter increase enabled three-step IOP control. Sustained drug release of the intimal gel suppressed tissue fibrosis, and the ring prevented late hypotonic IOP by externally squeezing the silicone tube. The unprecedented design and functions were validated using computational, in vitro, and rabbit glaucoma models by determining clinic-friendly argon laser parameters.