In summary, all these results allow us to suggest that determination of cell viability and functionality of human TMJF cell kept in culture using highly-sensitive methods must be one of the key parameters that should be determined during the quality control of TMJF for clinical cell transplantation, and we propose that all cells to be used for clinical purposes be previously analyzed using the highly-sensitive methods used in this work. In general, our data imply that the highest cell viability levels correspond to TMJF passages 6 and 5 and the most functional passage is the passage 5. We therefore suggest that cell passages P5 and P6 should be preferentially used in cell therapy and tissue engineering protocols using this cell type. Skeletal Catharanthine sulfate muscle wasting is a common debilitating condition associated with human immobilization and aging resulting in a reduced muscle function. In animal models, loss of muscle mass with immobilization or unloading has been suggested primarily to occur through an accelerated degradation of myofibrillar proteins via the ubiquitin-proteasome pathway, although rapid decreases in protein synthesis also has been shown. Somewhat in contrast, studies in young human individuals have suggested that a 
decline in protein synthesis rather than accelerated protein breakdown is responsible for the muscle loss observed with disuse. With aging, muscle loss is suggested to be associated with increased inflammation, decreased anabolic signaling, increased apoptosis, impaired myogenic responsiveness as well as decreased mitochondrial function. Moreover, aging has been found to affect signaling pathways that regulate myogenic growth factors and myofibrillar protein turnover in skeletal muscle of rodents. However, the differential involvement and time course of such signaling pathways remains undescribed in elderly humans exposed to immobilization. We therefore set to investigate the modulation in cellular signaling pathways involved in the initiation and temporal development of human disuse muscle atrophy, and specifically examine if aging affects the molecular regulation of human disuse related muscle loss. Recent data from our group indicate that, although immobility induces muscle atrophy in both young and old individuals, the loss in muscle mass was more pronounced in young, as also demonstrated in rodent models. An agespecific regulation of the signaling pathways orchestrating the initiation and time-course of human disuse muscle atrophy was therefore hypothesized and a range of genes from signaling pathways previously demonstrated to play a central role in the regulation of skeletal muscle atrophy and hypertrophy in a variety of animal models was profiled. From the ubiquitin-dependent proteolytic system expression levels of Muscle-specific muscle Ring Finger 1 and 4-(Benzyloxy)phenol Atrogin-1 was assessed as they have been demonstrated to play a key role in the induction of muscle atrophy in multiple animal disuse models, although data from human in vivo studies have been less consistent. As aging and muscle loss is associated with a decrease in the activation and sensitivity of the IGF-1/Akt signaling pathway gene expression profiles of Insulin-like Growth Factor 1 Ea and Mechano growth factor were assessed, along with protein levels of total and phosphorylated Akt as well as total and phosphorylated ribosomal protein S6. Furthermore, since autophagy in parallel with proteolysis, has been demonstrated to be an important stimulator of muscle atrophy in animal models.