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Shock waves are used clinically for breaking kidney stones and treating musculoskeletal indications. The mechanisms by which shock waves interact with tissue are still not well understood. Here, ultra-high-speed imaging was used to visualize the deformation of individual cells embedded in a tissue-mimicking phantom when subject to shock-wave exposure from a clinical source. Three kidney epithelial cell lines were considered to represent normal healthy (human renal epithelial), cancer (CAKI-2), and virus-transformed (HK-2) cells. The experimental results showed that during the compressive phase of the shock waves, there was a small ([Formula: see text] 2%) decrease in the projected cell area, but during the tensile phase, there was a relatively large (∼10%) increase in the projected cell area. The experimental observations were captured by a numerical model with a constitutive material framework consisting of an equation of state for the volumetric response and hyper-viscoelasticity for the deviatoric response. To model the volumetric cell response, it was necessary to change from a higher bulk modulus during the compression to a lower bulk modulus during the tensile shock loading. It was discovered that cancer cells showed a smaller deformation but faster response to the shock-wave tensile phase compared to their noncancerous counterparts. Cell viability experiments, however, showed that cancer cells suffered more damage than other cell types. These data suggest that the cell response to shock waves is specific to the type of cell and waveforms that could be tailored to an application. For example, the model predicts that a shock wave with a tensile stress of 4.59 MPa would increase cell membrane permeability for cancer cells with minimal impact on normal cells.

In traumatic brain injuries (TBIs) or spinal cord injuries (SCIs), neural tissue and thus axons are subjected to a range of damaging strains and strain rates. These injuring mechanical causes are translated into biochemical and biological alterations and/or responses. Despite extensive experimental campaigns, these mechanisms remain unclear. For instance, it is still not clear how injuring mechanical causes are transferred into electrophysiological alterations, affect action potential propagation, and ultimately change cell behaviour. Moreover the specific microscale mechanisms leading to brain or spinal cord injury are still unknown, and the role of the external loading conditions are yet to be identified. One major obstacle is that experimental campaigns on neurons remain highly challenging. Recent studies show that acute neurophysiological changes not only occur immediately after injury but can also be observable through secondary mechanisms up to a few days later. Therefore electrophysiological properties and mechanical deformations should be monitored simultaneously during and after injury at the cell level. To address these issues we have set up a multi-functional patch-clamp electrophysiology rig which not only enables measurement of electrophysiological properties in parallel with mechanical loading but also provides means for applying various, yet specific, loading conditions reliably and repeatedly. The proposed experimental approach will enhance our understanding of electrophysiological-mechanical coupling in neurons, and more direct damages such as in traumatic brain injuries. Such approach will promote the technology transfer from basic and pre-clinical findings into clinical applications and consequently, medical treatment or prevention.