Lower Limb Knee Exoskeleton

This project is the primary phase to develop a prototype of a lower limb exoskeleton through the implementation of novel hardware and software techniques that will overcome specific issues those current exoskeletons suffer from, such as lack of robust controllability, bulkiness, and actuation performance. At this phase, a knee exoskeleton with a linear actuator has been constructed. It is controlled by using data received from electromyography (EMG) signals. Furthermore, 3D printed parts of the exoskeleton frame have been developed in order to reduce weight and for rapid prototyping. The device is to be designed as an assistive device for a non-handicapped person. The main requirement of the device is to aim more less 20% of the knee joint torque of the average human male (20-35 years) during walking. Furthermore, preliminary studies on electromechanical properties of soft robotic materials have been performed in order to explore their capabilities for this application

Tumor necrosis factor stimulates fibroblast growth factor 23 levels in chronic kidney disease and non-renal inflammation.

Fibroblast growth factor 23 (FGF23) regulates phosphate homeostasis, and its early rise in patients with chronic kidney disease is independently associated with all-cause mortality. Since inflammation is characteristic of chronic kidney disease and associates with increased plasma FGF23 we examined whether inflammation directly stimulates FGF23. In a population-based cohort, plasma tumor necrosis factor (TNF) was the only inflammatory cytokine that independently and positively correlated with plasma FGF23. Mouse models of chronic kidney disease showed signs of renal inflammation, renal FGF23 expression and elevated systemic FGF23 levels. Renal FGF23 expression coincided with expression of the orphan nuclear receptor Nurr1 regulating FGF23 in other organs. Antibody-mediated neutralization of TNF normalized plasma FGF23 and suppressed ectopic renal Fgf23 expression. Conversely, TNF administration to control mice increased plasma FGF23 without altering plasma phosphate. Moreover, in Il10-deficient mice with inflammatory bowel disease and normal kidney function, plasma FGF23 was elevated and normalized upon TNF neutralization. Thus, the inflammatory cytokine TNF contributes to elevated systemic FGF23 levels and also triggers ectopic renal Fgf23 expression in animal models of chronic kidney disease