Nerve regeneration is a key biological process in those recovering from neural trauma. From animal models it is known that the regenerative capacity of the peripheral nervous system (PNS) relies heavily on the remarkable ability of Schwann cells to undergo a phenotypic shift from a myelinating phenotype to one that is supportive of neural regeneration. In rodents, a great deal is known about the molecules that control this process, such as the transcription factors c-Jun and early growth response protein 2 (EGR2/KROX20), or mark the cells and cellular changes involved, including SOX10 and P75 neurotrophin receptor (p75NTR). However, ethical and practical challenges associated with studying human nerve injury have meant that little is known about human nerve regeneration. The present study addresses this issue, analysing 34 denervated and five healthy nerve samples from 27 patients retrieved during reconstructive nerve procedures. Using immunohistochemistry and Real-Time quantitative Polymerase Chain Reaction (RT-qPCR), the expression of SOX10, c-Jun, p75NTR and EGR2 was assessed in denervated samples and compared to healthy nerve. Nonparametric smoothing linear regression was implemented to better visualise trends in the expression of these markers across denervated samples. It was found, first, that two major genes associated with repair Schwann cells in rodents, c-Jun and p75NTR, are also up-regulated in acutely injured human nerves, while the myelin associated transcription factor EGR2 is downregulated, observations that encourage the view that rodent models are relevant for learning about human nerve injury. Second, as in rodents, the expression of c-Jun and p75NTR declines during long-term denervation. In rodents, diminishing c-Jun and p75NTR levels mark the general deterioration of repair cells during chronic denervation, a process thought to be a major obstacle to effective nerve repair. The down-regulation of c-Jun and p75NTR reported here provides the first molecular evidence that also in humans, repair cells deteriorate during chronic denervation.

To counter the many disadvantages of prolonged wheelchair use, patients with spinal cord injuries (SCI) are beginning to turn towards robotic exoskeletons. However, we are currently unaware of the magnitude and distribution of forces acting between the user and the exoskeleton. This is a critical issue, as SCI patients have an increased susceptibility to skin lesions and pressure ulcer development. Therefore, we developed a real-time force measuring apparatus, which was placed at the physical human-robot interface (pHRI) of a lower limb robotic exoskeleton. Experiments captured the dynamics of these interaction forces whilst the participants performed a range of typical stepping actions. Our results indicate that peak forces occurred at the anterior aspect of both the left and right legs, areas that are particularly prone to pressure ulcer development. A significant difference was also found between the average force experienced at the anterior and posterior sensors of the right thigh during the swing phase for different movement primitives. These results call for the integration of instrumented straps as standard in lower limb exoskeletons. They also highlight the potential of such straps to be used as an alternative/complementary interface for the high-level control of lower limb exoskeletons in some patient groups.