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The advancement in depth-sensor technology increased the potential for the clinical use of markerless three-dimensional motion analysis (3DMA); however, the accurate quantification of depth-sensor-based 3DMA on gait characteristics deviating from normal patterns is unclear. This study investigated the concurrent validity of the measurements of compensatory movements measured by depth-sensor-based 3DMA compared to those measured by marker-based 3DMA. We induced swing-phase compensatory movements due to insufficient toe clearance by restricting unilateral ankle and knee joint movements in healthy individuals. Thirty-two healthy young adults (nineteen males, aged 20.4   ±   2.0 years, height 164.4   ±   9.8 cm, weight 60.0   ±   9.3 kg [average ± standard deviation]) walked the 6 m walkway in slow speed, very slow speed, and knee–ankle–foot orthosis (KAFO; participants wore KAFOs on the right leg) conditions. Gait kinematics were measured with marker-based and depth-sensor-based 3DMA systems. The intraclass correlation coefficient (ICC3,1) was used to measure the relative agreement between depth-sensor-based and marker-based 3DMA and demonstrated good or moderate validity for swing-phase compensatory movement measurement. Additionally, the ICC2,1 measured absolute agreement between the systems and showed lower validity than the ICC3,1. The measurement errors for contralateral vaulting, trunk lateral flexion, hip hiking, swing-side hip abduction, and circumduction between instruments were 0.01 m, 1.30°, 1.99°, 2.37°, and 1.53°, respectively. Depth-sensor-based 3DMA is useful for determining swing-phase compensatory movements, although the possibility of missing a slight measurement error of 1–2° must be considered. [ABSTRACT FROM AUTHOR]

Abstract: Nestin is an intermediate filament found in neurogenic progenitors and non-neuronal cells. Nestin-immunoreactivity (IR) in the brain often increases after brain damage. Here we show that amygdala kindling, which mimics the epileptic seizures, also induces nestin expression in the brain. Nestin-IR was greatly enhanced in the leptomeninges (pia and arachnoid maters) and neocortical parenchyma, but not much in the SVZ around the lateral ventricle, SGZ in the dentate gyrus, or the endothelial progenitor cells of blood vessels, fimbria, or choroid plexus after kindling. Electron microscopy revealed that nestin-IR in the leptomeninges was localized to granule cells, where it co-localized with GAD67-IR after electrical stimulation. The nestin-positive granule cells in the leptomeninges, especially around the emissary vein, were proliferative. However, nestin-IR in the neocortical parenchyma was expressed in NG2 glia and did not co-localize with GAD67-IR. Deletion of nestin-positive cells resulted in a high susceptibility to electrical stimulation. Consequently, almost all of the mice died or dropped out during kindling progression in 20 days, from naturally generated epileptic seizure or exhaustion. We speculate that the nestin-positive cells activated by amygdala kindling may involve in the protection of the brain from epilepsy. [Copyright &y& Elsevier]

[Purpose] The purpose of this study was to make clear the mobility of the distal tibiofibular syndesmosis (dTS) when the angle of the ankle joint changes, using ultrasonic diagnostic equipment. [Subjects] We investigated 28 bilateral limbs of 14 normal adults. [Methods] The subjects moved their ankle joints from the plantar flexion position to dorsiflexion. Sequential changes of the dissociation of dTS were recorded using ultrasonic diagnostic equipment, and measured by image analysis. [Results] The dissociation increased gradually in the early stages, and rapidly in the later stages, depending on the position of the ankle joint, from plantar flexion to dorsiflexion. [Conclusion] The results suggest that the separation of dTS was related to muscular activity as well as the amplitude of the trochlea of talus. [ABSTRACT FROM AUTHOR]

[Purpose] The purpose of this study was to clarify the relationship between physical therapy clinical educators' motivations and negative personal factors. [Participants and Methods] The authors sent a questionnaire on clinical education to 790 physical therapists working in hospitals across Japan, and received 345 valid responses. The study defined motivated and unmotivated clinical educators based on their answers to the "interests" and "enjoyment" aspects of clinical education. It also calculated the negative response rate out of 10 questions and odds ratio based on motivated clinical educators. [Results] The motivated group comprised 287 clinical educators (years of clinical experience: 8.1 ± 6.3) and the unmotivated group 58 (years of clinical experience: 7.0 ± 5.2). There was no statistically significant difference in years of clinical experience between the two groups. Two questions-"Is student guidance necessary for growth as a therapist (self-improvement)?" and "Do you want to learn about instructional methods?"-showed very high odds ratios. [Conclusion] This study reveals negative personal factors for the clinical educators who lack the will to educate students, such as preparation for clinical education, self-improvement, and cooperation with class instructors. Longitudinal research on motivated and unmotivated clinical educators will help identify these negative factors to improve their motivation., Competing Interests: The authors declare that they have no conflict of interest., (2020©by the Society of Physical Therapy Science. Published by IPEC Inc.)

Tissue factor pathway inhibitor-2 (TFPI-2) is a major inhibitor of extracellular matrix degradation. Decreases in TFPI-2 contribute to malignant tumor cell production, and TFPI-2 is a presumed tumor suppressor. TFPI-2 gene transcription is regulated by two epigenetic mechanisms: DNA methylation of the promoter and K4 methylation of histone 3 (H3). Lysine-specific demethylase 1 (LSD1) and LSD2 demethylate H3K4me2/1. LSD1 has been implicated in TFPI-2 regulation through both epigenetic mechanisms, but the involvement of LSD2 remains unknown. We prepared a monoclonal anti-LSD2 antibody that clearly distinguishes LSD2 from LSD1. Knockdown of LSD1 or LSD2 by siRNAs increased TFPI-2 protein and mRNA. Simultaneous knockdown of both LSD1 and LSD2 showed additive effects. Bisulfite sequencing revealed that CpG sites in the TFPI-2 promoter region were unmethylated. These results indicate that LSD2 also contributes to TFPI-2 regulation through histone modification, and that further studies of the involvement of LSD2 in tumor malignancy are warranted.