Home-Based Rehabilitation: Enabling Frequent and Effective Training

Rehabilitation studies have recently demonstrated that the amount of time spent training is one of the most important factors in one’s ability to regain motor control. The methods employed need to be effective, but individuals need to spend significant amounts of time retraining. One of the most effective ways to enable more training time is for rehabilitation to occur in one’s home so individuals have adequate access to it and there is no cost associated with traveling to the clinic. There are several challenges that need to be overcome to make home rehabilitation more common; for example adapting the methods from the clinical setting to the home setting, ensuring safety, and providing motivation. This chapter outlines existing technologies for upper and lower limb rehabilitation and how they could be adapted for use in one’s home. Although many types of disabilities would benefit from home-based rehabilitation, this discussion will focus on traumatic brain injuries, specifically stroke related. Many of the methods that could be used at home for stroke would also have application for helping in other circumstances

Oxidative Stress Promotes Peroxiredoxin Hyperoxidation and Attenuates Pro-survival Signaling in Aging Chondrocytes

Oxidative stress-mediated post-translational modifications of redox-sensitive proteins are postulated as a key mechanism underlying age-related cellular dysfunction and disease progression. Peroxiredoxins (PRX) are critical intracellular antioxidants that also regulate redox signaling events. Age-related osteoarthritis is a common form of arthritis that has been associated with mitochondrial dysfunction and oxidative stress. The objective of this study was to determine the effect of aging and oxidative stress on chondrocyte intracellular signaling, with a specific focus on oxidation of cytosolic PRX2 and mitochondrial PRX3. Menadione was used as a model to induce cellular oxidative stress. Compared with chondrocytes isolated from young adult humans, chondrocytes from older adults exhibited higher levels of PRX1–3 hyperoxidation basally and under conditions of oxidative stress. Peroxiredoxin hyperoxidation was associated with inhibition of pro-survival Akt signaling and stimulation of pro-death p38 signaling. These changes were prevented in cultured human chondrocytes by adenoviral expression of catalase targeted to the mitochondria (MCAT) and in cartilage explants from MCAT transgenic mice. Peroxiredoxin hyperoxidation was observed in situ in human cartilage sections from older adults and in osteoarthritic cartilage. MCAT transgenic mice exhibited less age-related osteoarthritis. These findings demonstrate that age-related oxidative stress can disrupt normal physiological signaling and contribute to osteoarthritis and suggest peroxiredoxin hyperoxidation as a potential mechanism