Studies will need to address not only all vehicle features but also the entire travel journey.The fatigue-induced neuromuscular mechanism remains to be fully elucidated. So far, the macroscopic mechanism using global surface electromyogram (sEMG) has been widely investigated. However, the microscopic mechanism using high-level neural information based on motor unit (MU) spike train from the spinal cord lacks attention, especially for the conditions under dynamic contraction task. The synchronization of the MU spike train is generally assumed to be an excellent indicator to represent the activities of spinal nerves. Accordingly, this study employed synchronization of MU spike train decomposed from high-density sEMG (HD-sEMG) to investigate the fatigue condition in muscular contractions within the Biceps Brachii muscle under both isometric and dynamic contraction tasks, giving a complete picture of the microscopic fatigue mechanism. We compared the synchronization of MU in Delta (1-4 Hz), alpha (8-12 Hz), Beta (15-30 Hz), and Gamma (30-60 Hz) frequency bands during the fatigue condition induced by different contractions. Our results showed that MU synchronization increased significantly (p less then 0.05) in all frequency bands across the two contraction tasks. The results indicate that the microscopic fatigue mechanism of Biceps Brachii muscle does not vary due to different contraction tasks.Drug addiction is underscored by the transition from experimental use to dependent use of addictive drugs. Acute use of methamphetamine (METH) causes a range of clinical symptoms, including hyperlocomotion. Dopamine D1 receptor (D1R)-mediated negative regulation of phosphorylated calcium/calmodulin-dependent protein kinase IIα (p-CaMKIIα, threonine [Thr] 286) is involved in the acute effects induced by single METH administration. Protein phosphatase 2A (PP2A) is a potential bridge that links D1R and p-CaMKIIα (Thr 286) after acute METH administration. However, the mechanisms underlying hyperlocomotion induced by single METH administration remain unclear. In this study, SCH23390 (a D1R inhibitor) and LB100 (a PP2A inhibitor) were administered to examine the involvement of D1R and PP2A signaling in acute METH-induced hyperlocomotion in mice. check details The protein levels of methylated PP2A-C (m-PP2A-C, leucine [Leu] 309), phosphorylated PP2A-C (p-PP2A-C, tyrosine [Tyr] 307), PP2A-C, p-CaMKIIα (Thr 286), and CaMKIIα in the prefrontal cortex (PFc), nucleus accumbens (NAc), and caudate putamen (CPu) were measured. Administration of 0.5 mg/kg SCH23390 reversed the acute METH-induced increase in protein levels of m-PP2A-C (Leu 309) and the decrease in protein levels of p-PP2A-C (Tyr 307) in the CPu, but not in the PFC and NAc. Moreover, prior administration of 0.1 mg/kg LB100 attenuated hyperlocomotion induced by single METH administration and reversed the decrease in protein levels of p-CaMKII (Thr 286) in the PFC, NAc, and CPu. Collectively, these results indicate that the D1R/PP2A/p-CaMKIIα signaling cascade in the CPu may be involved in hyperlocomotion after a single administration of METH.Electrophysiological group studies in brain-damaged patients can be run to capture the EEG correlates of specific cognitive impairments. Nonetheless, this procedure is not adequate to characterize the inter-individual variability present in major neuropsychological syndromes. We tested the possibility of getting a reliable individual EEG characterization of deficits of endogenous orienting of spatial attention in right-brain damaged (RBD) patients with left spatial neglect (N+). We used a single-trial topographical analysis (STTA; [39] of individual scalp EEG topographies recorded during leftward and rightward orienting of attention with central cues in RBD patients with and without (N-) neglect and in healthy controls (HC). We found that the STTA successfully decoded EEG signals related to leftward and rightward orienting in five out of the six N+, five out of the six N- patients and in all the six HC. In agreement with findings from conventional average-group studies, successful classifications of EEG signals in N+ were observed during the 400-800 ms period post-cue-onset, which reflects preserved voluntary engagement of attention resources (ADAN component). These results suggest the possibility of acquiring reliable individual EEG profiles of neglect patients.Humans spontaneously alternate between walking and running with a change in locomotion speed, which is termed gait transition. It has been suggested that sensory information in the muscle is a factor that triggers the gait transition; however, direct evidence for this has not been presented. In addition, it has been suggested that upper limb movement during human gait facilitates leg muscle activity due to the neural coupling between the upper and lower limbs. We hypothesized that a disturbance of afferent inputs in the neural coupling between the upper and lower limbs suppressively act on the gait transition. Here, we aimed to deepen the understanding of contribution of the afferent inputs in neural coupling between the upper and lower limbs to the gait transition. Eight participants performed spontaneous walk-to-run and run-to-walk transitions under two different conditions Normal (arms swinging normally); and TIS (partial blocking of afferent inputs from the arms by inducing tourniquet ischemia). We compared the preferred gait transition speeds (PTS), joint angles, muscle activities, and muscle synergies between the two conditions. Control of coordinated muscle activities can be investigated by analyzing muscle synergies, which are groups of muscles that activate together. The PTS, joint angle profiles, muscle activity profiles, and muscle synergies were nearly identical between conditions (walk-to-run PTS at Normal and TIS 6.9 ± 0.4 and 6.9 ± 0.4 km/h; run-to-walk PTS at Normal and TIS 6.6 ± 0.4 and 6.5 ± 0.4 km/h; p = 0.869 and p = 0.402, respectively). Therefore, we conclude that the control of gait transition is little affected by disturbing the neural coupling between the upper and lower limbs by reducing afferent inputs from the forearms and distal upper arms. Our findings might reflect robustness of the neural coupling between the upper and lower limbs during locomotion against neural perturbations or disturbances.