ABSTRACT
Abstract Active control of the shape of soft robots is challenging. Despite having an infinite number of passive degrees of freedom (DOFs), soft robots typically only have a few actively controllable DOFs, limited by the number of degrees of actuation (DOAs). The complexity of actuators restricts the number of DOAs that can be incorporated into soft robots. Active shape control is further complicated by the buckling of soft robots under compressive forces; this is particularly challenging for compliant continuum robots due to their long aspect ratios. In this study, we show how variable stiffness enables shape control of soft robots by addressing these challenges. Dynamically changing the stiffness of sections along a compliant continuum robot selectively "activates" discrete joints. By changing which joints are activated, the output of a single actuator can be reconfigured to actively control many different joints, thus decoupling the number of controllable DOFs from the number of DOAs. We demonstrate embedded positive pressure layer jamming as a simple method for stiffness change in inflated beam robots, its compatibility with growing robots, and its use as an "activating" technology. We experimentally characterize the stiffness change in a growing inflated beam robot and present finite element models that serve as guides for robot design and fabrication. We fabricate a multisegment everting inflated beam robot and demonstrate how stiffness change is compatible with growth through tip eversion, enables an increase in workspace, and achieves new actuation patterns not possible without stiffening.
ABSTRACT
Most cancer patients die from metastasis. Recent studies have shown that gold nanoparticles (AuNPs) can slow down the migration/invasion speed of cancer cells and suppress metastasis. Since nuclear stiffness of the cell largely decreases cell migration, our hypothesis is that targeting AuNPs to the cell nucleus region could enhance nuclear stiffness, and therefore inhibit cell migration and invasion. Our results showed that upon nuclear targeting of AuNPs, the ovarian cancer cell motilities decrease significantly, compared with nontargeted AuNPs. Furthermore, using atomic force microscopy, we observed an enhanced cell nuclear stiffness. In order to understand the mechanism of cancer cell migration/invasion inhibition, the exact locations of the targeted AuNPs were clearly imaged using a high-resolution three-dimensional imaging microscope, which showed that the AuNPs were trapped at the nuclear membrane. In addition, we observed a greatly increased expression level of lamin A/C protein, which is located in the inner nuclear membrane and functions as a structural component of the nuclear lamina to enhance nuclear stiffness. We propose that the AuNPs that are trapped at the nuclear membrane both (1) add to the mechanical stiffness of the nucleus and (2) stimulate the overexpression of lamin A/C located around the nuclear membrane, thus increasing nuclear stiffness and slowing cancer cell migration and invasion.
