SynopsisIn the previous paper a practical method has been applied for an analysis of nonisothermal crystallization in terms of data of isothermal crystallization. The fundamental equation was written on the assumption of the isokinetic conditions in the following form:where X(t) is the degree of phase transformation at time t, and 7t is the Avrami index determined in the isothermal experiments; K ( T) is connected with the crystallization rate constant of the isothermal crystallization, k(T), through the relation K ( T ) = k(T)"n. The equation is derived on the basis of the well-known theory of phase transformation. Experiments of nonisothermal crystallization of high-density polyethylene were carried out under various cooling conditions. The change in crystallinity during the process was followed by using the above equation in the course of the primary crystallization. A procedure of the analysis of the whole, including both the primary and secondary processes, is suggested as an eminently practical one on a more general assumption.

synopsisThe changes in temperature and crystallinity of polymer during nonisothermal crystallization were theoretically analyzed assuming a cooling condition under which heat transfer occurs at a rate proportional to the difference in temperature between polymer and the,environment. When a plateau appears in the temperature change during crystallization, crystallization temperature can be predicted by a simple method. This method gives nearly the same value as that obtained by successive calculations of temperature and crystallinity throughout the whole process. In addition, a graphic method is presented to predict crystallization temperature. By using the plateau temperature observed in melt-spinning experiments, the crystallization rate under molecular orientation is evaluated. Furthermore, a method applicable to estimating the ultimate crystallinity is proposed. A rough estimation of the increase in the rate of crystallization under molecular orientation was carried out for very high-speed spinning of poly(ethy1ene terephthalate ).

Duchenne muscular dystrophy (DMD) is an X-linked lethal muscle disorder caused by mutations in the Dmd gene encoding Dystrophin12. DMD model animals, such as mdx mice and canine X-linked muscular dystrophy dogs, have been widely utilized in the development of a treatment for DMD3. Here, we demonstrate the generation of Dmd-mutated rats using a clustered interspaced short palindromic repeats (CRISPR)/Cas system, an RNA-based genome engineering technique that is also adaptive to rats. We simultaneously targeted two exons in the rat Dmd gene, which resulted in the absence of Dystrophin expression in the F0 generation. Dmd-mutated rats exhibited a decline in muscle strength, and the emergence of degenerative/regenerative phenotypes in the skeletal muscle, heart, and diaphragm. These mutations were heritable by the next generation, and F1 male rats exhibited similar phenotypes in their skeletal muscles. These model rats should prove to be useful for developing therapeutic methods to treat DMD.

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Duchenne muscular dystrophy (DMD) is a progressive disease characterised by chronic muscle degeneration and inflammation. Our previously established DMD model rats (DMD rats) have a more severe disease phenotype than the broadly used mouse model. We aimed to investigate the role of senescence in DMD using DMD rats and patients. Senescence was induced in satellite cells and mesenchymal progenitor cells, owing to the increased expression of CDKN2A, p16- and p19-encoding gene. Genetic ablation of p16 in DMD rats dramatically restored body weight and muscle strength. Histological analysis showed a reduction of fibrotic and adipose tissues invading skeletal muscle, with increased muscle regeneration. Senolytic drug ABT263 prevented loss of body weight and muscle strength, and increased muscle regeneration in rats even at 8 months—the late stage of DMD. Moreover, senescence markers were highly expressed in the skeletal muscle of DMD patients. In situ hybridization of CDKN2A confirmed the expression of it in satellite cells and mesenchymal progenitor cells in patients with DMD. Collectively, these data provide new insights into the integral role of senescence in DMD progression.