Accumulative Roll Bonding (ARB) is a technique of grain refinement by severe plastic deformation, which involves multiple repetitions of surface treatment, stacking, rolling, and cutting. The rolling with 50% reduction in thickness bonds the sheets. After several cycles, ultrafine-grained (UFG) materials are produced. Since ARB enables the production of large amounts of UFG materials, its adoption into industrial practice is favoured. ARB has been successfully used for preparation of UFG sheets from different ingot cast aluminium alloys. Twin-roll casting (TRC) is a cost and energy effective method for manufacturing aluminium sheets. Fine particles and small grain size are intrinsic for TRC sheets making them good starting materials for ARB. The paper presents the results of a research aimed at investigating the feasibility of ARB processing of three TRC alloys, AA8006, AA8011 and AA5754, at ambient temperature. The microstructure and properties of the ARB were investigated by means of light and transmission electron microscopy and hardness measurements. AA8006 specimens were ARB processed without any problems. Sound sheets of AA8011 alloy were also obtained even after 8 cycles of ARB. The AA5754 alloy suffered from severe edge and notch cracking since the first cycle. The work hardening of AA8006 alloy saturated after the 3rd cycle, whereas the hardness of AA5754 alloy increased steadily up to the 5th cycle. Monotonous increase in strength up to 280 MPa was observed in the ARB processed AA8011 alloy.

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Familial Mediterranean Fever (FMF) is usually an autosomal recessive autoinflammatory disease characterized by recurrent attacks of fever and serositis. FMF develops before the age of 20 years in 90% of patients. It has intervals of 1 week to several years between attacks, which leads to renal dysfunction-amyloidosis. We report a case of atypical FMF that developed in a long-term hemodialysis patient. A 65-year-old Japanese female undergoing hemodialysis for 32 years was referred to our hospital with a fever of unknown origin (FUO) following cervical laminoplasty. The fever occurred as recurrent attacks accompanied by oligoarthralgia of the left hip and knee. We suspected FMF because of recurrent self-limited febrile attacks, although the patient showed atypical clinical features such as late-onset and highly frequent attacks. After receiving treatment, she achieved a complete response to colchicine. Therefore, a diagnosis of FMF was made based on the Tel-Hashomer criteria, which was confirmed by genetic testing. The case suggests that FMF may be of note in long-term hemodialysis patients developing FUO.

Background and Aims We previously reported that an increase of lymphocytes in peritoneal dialysis (PD) effluent was correlated with risk of encapsulating peritoneal sclerosis (EPS). In the present study, we analyzed subsets of lymphocytes in PD effluent by flow cytometry and evaluated their changes every six month to elucidate the etiological background of peritoneal dysfunction. Method We enrolled patients who started PD between 2006 and 2017, and of whom the data for PET and flow cytometric analysis was available at least for three consecutive times with an interval of six months. We excluded the patients who experienced PD peritonitis during the observation period. Consequently, the levels and changes of lymphocyte subset, such as CD4+/CD8+ naïve T cell (CCR7+/CD45RA+), CD4+/CD8+ central memory T cell (CCR7+/CD45RA-), CD4+/CD8+ effector memory T cell (CCR7-/CD45RA-), CD4+/CD8+ terminally differentiated effector memory T cell (CCR7-/CD45RA+), D/P creatinine ratio, FSC ratio of mesothelial cells and lymphocytes (a possible indicator for mesothelial cell size) were analysed in 23 patients over one year. Results We evaluated whether the observed variables on the first evaluation (six months after initiation of PD) affected the changes of D/P creatinine and FSC ratio over one year by a simple linear regression analysis. In the examined variables, only a fraction of CD8+ central memory T cell was significantly correlated with the change rate of D/P creatinine ratio (β=1.47, p=0.001, adjusted R2=0.379). We also evaluated whether the change rate of observed variables was correlated with the change rate of D/P creatinine and FSC ratio by a simple linear regression analysis. A fraction of CD8+ naïve T cell or CD8+ central memory cell was negatively correlated with the change rate of D/P creatinine ratio (naïve T cell; β=-0.058, p=0.022, adjusted R2=0.188, central memory T cell; β=-0.096, p=0.046, adjusted R2=0.137). The change rate of CD8+ effector memory T cell was not significantly correlated with the change rate of D/P creatinine ratio (β=0.172, p=0.096, adjusted R2=0.085). However, the change rate of D/P creatinine ratio tends to be higher in accordance with the increased change rate of CD8+ effector memory T cell by One way ANOVA, where the change rate was divided into three groups in descending order (p=0.0796) (Fig.1). Besides, the change rate of CD8+ effector memory T cell tends to be higher in accordance with the increased fraction of CD8+ central memory T cell at the first evaluation by Kruskall-Wallis test, where the change rate was divided into three groups in descending order (p=0.169) (Fig.2). Conclusion A decrease in the fraction of CD8+ naïve or central memory T cell was significantly correlated with the increase of D/P creatinine ratio. An Increase in the fraction of CD8+ effector memory T cell was also possibly correlated with the increase of D/P creatinine ratio, although it was not statistically significant (p=0.096). An initial fraction of CD8+ central memory T cell was significantly correlated with the change rate of D/P creatinine ratio. From these results, central memory T cells and naïve T cells at an initial stage may be transformed into effector memory T cells by repeated exposure to unknown antigens derived from PD solution and these effector memory T cells may damage the peritoneum to increase D/P creatinine ratio. An initial higher fraction of CD8+ central memory T cell suggested an acceleration in the transformation into CD8+ effector memory T cell.