Miscibility or compatibilization via transreactions in blends of one of two copolyesters, poly(butylene adipate-co-butylene terephthalate) [P(BA-co-BT)] or poly(butylene succinate-co-butylene terephthalate) [P(BS-co-BT)], with poly(hydroxy ether of bisphenol A) (phenoxy) were investigated. The P(BA-co-BT)/phenoxy blend exhibited a homogeneous phase and a composition-dependent glass transition temperature (T g) without any heat annealing. The copolymer–polymer interaction parameter (χ12) for the P(BA-co-BT)/phenoxy blend was calculated from the melting-point-depression method to be −0.12. However, variation in the composition and structure of the copolyesters easily causes phase separation in copolyester/phenoxy blends. The P(BS-co-BT)/phenoxy blend had a phase morphology that could be homogenized only following annealing at high temperatures. As-blended P(BS-co-BT)/phenoxy (50/50 composition) exhibited immiscible phases with two distinct T gs, but the initially phase-separated blends finally merged to form a homogeneous phase with a single T g upon heating and annealing for 60 min at 280 °C. Chemical exchange reactions upon heat annealing of the P(BS-co-BT)/phenoxy blend caused phase homogenization.

It is well known that regular physical activity helps improve overall health and fitness and reduces the risk of many chronic diseases. However, excessive exercise might be harmful. Exercise addiction (EA) is a pattern of uncontrolled exercise that involves a craving for overwhelming exercise with addictive attributes. So far, little is known about this unique behavioral addiction. The aim of the current study is to introduce the diagnosis and assessment of EA, and to summarize several developing theoretical models. Eating disorders, body image disorder, low self-esteem, and high narcissism are related to high risk of EA. The paper also discusses the distinction between EA and highly involved physical activity.

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Aging causes a decline in skeletal muscle function, resulting in a progressive loss of muscle mass, quality, and strength. A weak regenerative capacity is one of the critical causes of dysfunctional skeletal muscle in elderly individuals. The extracellular matrix (ECM) maintains the tissue framework structure in skeletal muscle. As shown by previous reports and our data, the gene expression of ECM components decreases with age, but the accumulation of collagen substantially increases in skeletal muscle. We examined the structural changes in ECM in aged skeletal muscle and found restricted ECM degradation. In aged skeletal muscles, several genes that maintain ECM structure, such as transforming growth factor β (TGF-β), tissue inhibitors of metalloproteinases (TIMPs), matrix metalloproteinases (MMPs), and cathepsins, were downregulated. Muscle injury can induce muscle repair and regeneration in young and adult skeletal muscles. Surprisingly, muscle injury could not only efficiently induce regeneration in aged skeletal muscle, but it could also activate ECM remodeling and the clearance of ECM deposition. These results will help elucidate the mechanisms of muscle fibrosis with age and develop innovative antifibrotic therapies to decrease excessive collagen deposition in aged muscle.