[History and Further Discussion about Sports for People with Mental Health Problems].

Our study mainly focused on summarizing the history and issues of the Sports for People with Mental Health Problems in Japan. Since it had been shifted from inpatients activity to a community based sport activity, it was the matter of great urgency for us to expand and rein- force its organizational foundation. The first competition of volleyball for people with mental health problems was held on 2001, and since 2008 the Sports for People with Mental Health Problems was officially admitted to participate in the National Sports Festival for People with an Impairment. The basic principal required protecting participants' privacy at the same level of other disabilities. We needed clearly define the qualification for participants, such as restricting participants only with disability certification issued by Japan Federation for Mental Health and Welfare. Furthermore, the first International Symposium/Meeting on Sport for People with Mental Health Problems was held in Tokyo in 2013, and the first international sports competi- tion for people with mental health problems was held in Japan, which was a milestone for the internationalization of World sport championship for people with mental health problems. For the upcoming the Japan Olympic and Paralympic in 2020, we recognize the public interests for sports for people with mental health problems. It is the great opportunity for us to trigger to popularize it. Since the activities with all three types of disability will grow not only in sports but also in other fields, it is very important to bring information together.

A mitochondrial thioredoxin-sensitive mechanism regulates TGF-ß-mediated gene expression associated with epithelial-mesenchymal transition.

Transforming growth factor (TGF)-ß is a pro-oncogenic cytokine that induces the epithelial-mesenchymal transition (EMT), a crucial event in tumor progression. During TGF-ß-mediated EMT in NMuMG mouse mammary epithelial cells, we observed sustained increases in reactive oxygen species (ROS) levels in the cytoplasm and mitochondria with a concomitant decrease in mitochondrial membrane potential and intracellular glutathione levels. In pseudo ρ0 cells, whose respiratory chain function was impaired, the increase in intracellular ROS levels was abrogated, suggesting an important role of mitochondrial activity as a trigger for TGF-ß-stimulated ROS generation. In line with this, TGF-ß-mediated expression of the EMT marker fibronectin was inhibited not only by chemicals that interfere with ROS signaling but also by exogenously expressed mitochondrial thioredoxin (TXN2) independent of Smad signaling. Of note, TGF-ß-mediated induction of HMGA2, a central mediator of EMT and metastatic progression, was similarly impaired by TXN2 expression, revealing a novel mechanism involving a thiol oxidation reaction in mitochondria, which regulates TGF-ß-mediated gene expression associated with EMT.