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The objectives of this study were to compare the effects of two in-season velocity loss training methods (VBT) on performance outcomes and to evaluate the effects of velocity-based training compared to traditional resistance training (TRT) on performance outcomes in young elite soccer players. VBT utilized the same relative load but varied in the extent of velocity loss during the set: 15% (VL15%) and 30% (VL30%). Thirty-four players were recruited and randomly distributed into three groups: the VL15% group (n = 12; age = 18.50 ± 0.67 years; stature = 183.41 ± 4.25 cm; body mass = 75.08 ± 5.57 kg), the VL30% group (n = 11; age = 17.91 ± 0.60 years; stature = 181.21 ± 6.56 cm, body mass = 73.58 ± 6.22 kg), and the traditional strength training group TRT (n = 11; age = 18.14 ± 0.74 years; stature = 182.17 ± 5.52 cm; body mass = 74.86 ± 6.68 kg). Alongside regular soccer sessions and matches, the groups underwent a four-week (2 sesions per week) resistance training intervention with back squats involved. Changes in leg strength (SQ1RM), 20 m sprint time (SPR 20 m), countermovement jump height (CMJ), reactive strength index (RSI), and change of direction (COD) from before and after were evaluated using a 3 × 2 ANOVA. While no significant interaction was found for SQ1RM and SPR20, all of the groups showed significant pre to post improvements. Significant interactions were observed for CMJ (F = 38.24, p = 0.000), RSI (F = 8.33; p = 0.001), and change of direction agility test (COD) (F = 3.64; p = 0.038), with a post hoc analysis showing differences between the VL15 (6.0%) and TRT (1.7%) groups (p = 0.034); VL15 (12.2%) and VL30 (3.2%) groups (p = 0.004); VL15 and TRT (0.4%) (p = 0.018); VL15 (2.4%) and VL30 (1.5%) (p = 0.049); and between the VL15 and TRT (0.4%) groups (p = 0.015). Four weeks of VL15% training during the season induced similar strength increases to VL30% and TRT, superior improvements in RSI and COD compared to VL30%, and superior improvements in CMJ, RSI, and COD tests compared to TRT. Thus, incorporating the VL15% training method may be recommended to improve power-related performance metrics in elite young soccer players.

Collaborative robotics is a major topic in current robotics research, posing new challenges, especially in human–robot interaction. The main aspect in this area of research focuses on understanding the behavior of robots when engaging with humans, where reinforcement learning is a key discipline that allows us to explore sophisticated emerging reactions. This review aims to delve into the relevance of different sensors and techniques, with special attention to EEG (electroencephalography data on brain activity) and its influence on the behavior of robots interacting with humans. In addition, mechanisms available to mitigate potential risks during the experimentation process such as virtual reality are also be addressed. In the final part of the paper, future lines of research combining the areas of collaborative robotics, reinforcement learning, virtual reality, and human factors are explored, as this last aspect is vital to ensuring safe and effective human–robot interactions.

Demyelinating Charcot–Marie–Tooth 4G (CMT4G) results from a recessive mutation in the 5′UTR region of the Hexokinase 1 (HK1) gene. HK participates in mitochondrial calcium homeostasis by binding to the Voltage-Dependent Anion Channel (VDAC), through its N-terminal porin-binding domain. Our hypothesis is that CMT4G mutation results in a broken interaction between mutant HK1 and VDAC, disturbing mitochondrial calcium homeostasis. We studied a cohort of 25 CMT4G patients recruited in the French gypsy population. The disease was characterized by a childhood onset, an intermediate demyelinating pattern, and a significant phenotype leading to becoming wheelchair-bound by the fifth decade of life. Co-IP and PLA studies indicated a strong decreased interaction between VDAC and HK1 in the patients' PBMCs and sural nerve. We observed that either wild-type HK1 expression or a peptide comprising the 15 aa of the N-terminal wild-type HK1 administration decreased mitochondrial calcium release in HEK293 cells. However, mutated CMT4G HK1 or the 15 aa of the mutated HK1 was unable to block mitochondrial calcium release. Taken together, these data show that the CMT4G-induced modification of the HK1 N-terminus disrupts HK1-VDAC interaction. This alters mitochondrial calcium buffering that has been shown to be critical for myelin sheath maintenance.

Boutary et al. describe siRNA based therapy conjugated with squalene nanoparticles as an efficient approach to normalize PMP22 protein levels, restore locomotor activity, electrophysiological parameters and function of myelin sheath in CMT1A mouse models. These findings could be useful to develop therapeutic strategies for inherited peripheral neuropathies.

Molecular defects in type 1 facioscapulohumeral muscular dystrophy (FSHD) are caused by a heterozygous contraction of the D4Z4 repeat array from 1 to 10 repeat units (RUs) on 4q35. This study compared (1) the phenotype and severity of FSHD1 between patients carrying 6−8 vs. 9−10 RUs, (2) the amount of methylation in different D4Z4 regions between patients with FSHD1 with different clinical severity scores (CSS). This cross-sectional multicenter study was conducted to measure functional scales and for genetic analysis. Patients were classified into two categories according to RUs: Group 1, 6−8; Group 2, 9−10. Methylation analysis was performed in 27 patients. A total of 99 carriers of a contracted D4Z4 array were examined. No significant correlations between RUs and CSS (r = 0.04, p = 0.73) and any of the clinical outcome scales were observed between the two groups. Hypomethylation was significantly more pronounced in patients with high CSS (>3.5) than those with low CSS (