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Fluidic soft actuators are enlarging the robotics toolbox by providing flexible elements that can display highly complex deformations. Although these actuators are adaptable and inherently safe, their actuation speed is typically slow because the influx of fluid is limited by viscous forces. To overcome this limitation and realize soft actuators capable of rapid movements, we focused on spherical caps that exhibit isochoric snapping when pressurized under volume-controlled conditions. First, we noted that this snap-through instability leads to both a sudden release of energy and a fast cap displacement. Inspired by these findings, we investigated the response of actuators that comprise such spherical caps as building blocks and observed the same isochoric snapping mechanism upon inflation. Last, we demonstrated that this instability can be exploited to make these actuators jump even when inflated at a slow rate. Our study provides the foundation for the design of an emerging class of fluidic soft devices that can convert a slow input signal into a fast output deformation. 

Cancer cell migration through narrow constrictions generates compressive stresses on the nucleus that deform it and cause rupture of nuclear membranes. Nuclear membrane rupture allows uncontrolled exchange between nuclear and cytoplasmic contents. Local tensile stresses can also cause nuclear deformations, but whether such deformations are accompanied by nuclear membrane rupture is unknown. Here we used a direct force probe to locally deform the nucleus by applying a transient tensile stress to the nuclear membrane. We found that a transient (∼0.2 s) deformation (∼1% projected area strain) in normal mammary epithelial cells (MCF-10A cells) was sufficient to cause rupture of the nuclear membrane. Nuclear membrane rupture scaled with the magnitude of nuclear deformation and the magnitude of applied tensile stress. Comparison of diffusive fluxes of nuclear probes between wild-type and lamin-depleted MCF-10A cells revealed that lamin A/C, but not lamin B2, protects the nuclear membranes against rupture from tensile stress. Our results suggest that transient nuclear deformations typically caused by local tensile stresses are sufficient to cause nuclear membrane rupture.