The muscle strength of the knee extension and plantarflexion plays a crucial role in determining gait speed. Recent studies have shown that no-load angular velocity of the lower limb joints is essential for determining gait speed. However, no reports have compared the extent to which lower limb functions, such as knee extension strength, knee extension velocity, plantarflexion strength, and plantarflexion velocity, impact gait speed in a single study. Therefore, this study aimed to examine the relative importance of maximum strength and no-load angular velocity on gait speed. Overall, 164 community-dwelling older adults (72.9 ± 5.0 years) participated in this study. We measured the gait speed and lower limb function (the strength and velocity of knee extension and plantarflexion). Strength was measured with a hand-held dynamometer, and velocity with a gyroscope. A multiple regression analysis was performed with gait speed as the dependent variable and age, sex, and lower-limb function as independent variables. Plantarflexion velocity (β = 0.25) and plantarflexion strength (β = 0.21) were noted to be significant predictors of gait speed. These findings indicate that no-load plantarflexion velocity is more important than the strength of plantarflexion and knee extensions as a determinant of gait speed, suggesting that improvement in plantarflexion velocity may increase gait speed.

Total knee arthroplasty (TKA) is aimed mainly at reducing pain and restoring mobility. However, mobility deficits can persist even longer than 1 year. The trunk function and movement velocity of any region have been recently recognized to be critical for determining mobility in older people. Therefore, the main goal of this quasi-randomized trial is to clarify the effectiveness of a novel training method, the seated side tapping (SST) training, for improving mobility by focusing on movement velocity of trunk function in the short term after TKA. SST training consists of side trunk movements repeated as quickly as possible in a seated position. All participants after TKA were randomly assigned to the SST training group (n = 37) or control training group (n = 38). The participants in the SST group performed SST training plus the standard rehabilitation program 5 days per week for 3 weeks after TKA, while the control group performed only the standard rehabilitation programs. The primary outcome was the effect of SST training on mobility, indicated by gait speed and the timed up and go test (TUG) time. Measurements were performed before and 1, 2, and 3 weeks after surgery. At all-time points, the patients in the SST group showed significantly better mobility, despite that knee function, represented by muscle strength, range of motion, and degree of pain at the knee joint, was similar in both groups. The difference in gait speed between the groups was >0.1 m/s at all time points, which is clinically significant. SST training significantly improved patients’ mobility within 3 weeks after TKA, despite that no additional benefit was observed in knee function. The findings in this study indicate that SST training may be considered as a part of the rehabilitation program after TKA, although further evaluation of its long-term effectiveness is needed. University Hospital Medical Information Network Clinical Trials Registry (UMIN-CTR; UMIN000027909).

Apolipoprotein E (ApoE) is a major apolipoprotein in the central nervous system (CNS) that plays an important role in Alzheimer's disease. It may also be involved in other CNS disorders including ischemic injury. We investigated the changes of ApoE protein and mRNA expression in the brain with middle cerebral artery occlusion (MCAO) to clarify its origin after focal ischemia in rats. Increased ApoE immunoreactivity was recognized in astrocytes 3-14 days after MCAO in the affected side of cortex, and in neurons 4-14 days after MCAO in the same area. ApoE immunoreactivity was also detected in macrophages in the ischemic core 3-14 days after MCAO. In contrast, ApoE mRNA was expressed in astrocytes and macrophages, but not in neurons. These results suggested that neuronal ApoE was not synthesized in neurons, but derived from astrocytes.