In literature, it has been suggested that the CNS anticipates spontaneous change in body position during quiet stance and continuously modulates ankle extensor muscle activity to compensate for the change. The purpose of this study was to investigate whether velocity feedback contributes by modulating ankle extensor activities in an anticipatory fashion, facilitating effective control of quiet stance. Both theoretical analysis and experiments were carried out to investigate to what extent velocity feedback contributes to controlling quiet stance. The experiments were carried out with 16 healthy subjects who were asked to stand quietly with their eyes open or closed. During the experiments, the center of pressure (COP) displacement (COPdis), the center of mass (COM) displacement (COMdis), and COM velocity (COMvel) in the anteroposterior direction were measured. Rectified electromyograms (EMGs) were used to measure muscle activity in the right soleus muscle, the medial gastrocnemius muscle, and the lateral gastrocnemius muscle. The simulations were performed using an inverted pendulum model that described the anteroposterior kinematics and dynamics of quiet stance. In the simulations, an assumption was made that the COMdis of the body would be regulated using a proportional-derivative (PD) controller. Two different PD controllers were evaluated in these simulations: 1) a controller with the high-derivative/velocity gain (HDG) and 2) a controller with the low-derivative/velocity gain (LDG). Cross-correlation analysis was applied to investigate the relationships between time series obtained in experiments 1) COMdis and EMGs and 2) COMvel and EMGs. Identical cross-correlation analysis was applied to investigate the relationships between time series obtained in simulations 3) COMdis and ankle torque and 4) COMvel and ankle torque. The results of these analyses showed that the COMdis was positively correlated with all three EMGs and that the EMGs temporally preceded the COMdis. These findings agree with the previously published studies in which it was shown that the lateral gastrocnemius muscle is actively modulated in anticipation of the body's COM position change. The COMvel and all three EMGs were also correlated and the cross-correlation function (CCF) had two peaks: one that was positive and another that was negative. The positive peaks were statistically significant, unlike the negative ones; they were larger than the negative peaks; and their time shifts were much shorter compared with the time shifts of the negative peaks. When these results were compared with the CCF results obtained for simulated time series, it was discovered that the cross-correlation results for the HDG controller closely matched cross-correlation results for the experimental time series. On the other hand, the simulation result obtained for LDG controller did not match the experimental results. These findings suggest that the actual postural control system during quiet stance adopts a control strategy that relies notably on velocity inform...

A double-hyperfragment event has been found in a hybrid-emulsion experiment. It is identified uniquely as the sequential decay of ( 6)(LambdaLambda)He emitted from a Xi(-) hyperon nuclear capture at rest. The mass of ( 6)(LambdaLambda)He and the Lambda-Lambda interaction energy DeltaB(LambdaLambda) have been measured for the first time devoid of the ambiguities due to the possibilities of excited states. The value of DeltaB(LambdaLambda) is 1.01+/-0.20(+0.18)(-0.11) MeV. This demonstrates that the Lambda-Lambda interaction is weakly attractive.

Rehabilitative water-walking exercise could be designed to incorporate large-muscle activities, especially of the lower-limb extensor muscles, through full joint range of motion and minimization of joint moments.

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Myotonic dystrophy (DM) is caused by the expression of mutant RNAs containing expanded CUG repeats that sequester muscleblind-like (MBNL) proteins, leading to alternative splicing changes. Cardiac alterations, characterized by conduction delays and arrhythmia, are the second most common cause of death in DM. Using RNA sequencing, here we identify novel splicing alterations in DM heart samples, including a switch from adult exon 6B towards fetal exon 6A in the cardiac sodium channel, SCN5A. We find that MBNL1 regulates alternative splicing of SCN5A mRNA and that the splicing variant of SCN5A produced in DM presents a reduced excitability compared with the control adult isoform. Importantly, reproducing splicing alteration of Scn5a in mice is sufficient to promote heart arrhythmia and cardiac-conduction delay, two predominant features of myotonic dystrophy. In conclusion, misregulation of the alternative splicing of SCN5A may contribute to a subset of the cardiac dysfunctions observed in myotonic dystrophy.

Although recent vertebrate studies have revealed that different spinal networks are recruited in locomotor mode- and speed-dependent manners, it is unknown whether humans share similar neural mechanisms. Here, we tested whether speed- and mode-dependence in the recruitment of human locomotor networks exists or not by statistically extracting locomotor networks. From electromyographic activity during walking and running over a wide speed range, locomotor modules generating basic patterns of muscle activities were extracted using non-negative matrix factorization. The results showed that the number of modules changed depending on the modes and speeds. Different combinations of modules were extracted during walking and running, and at different speeds even during the same locomotor mode. These results strongly suggest that, in humans, different spinal locomotor networks are recruited while walking and running, and even in the same locomotor mode different networks are probably recruited at different speeds.

Rationale Electrogram-based catheter ablation, targeting complex fractionated atrial electrograms (CFAEs), is empirically known to be effective in halting persistent/permanent atrial fibrillation (AF). However, the mechanisms underlying CFAEs and electrogram-based ablation remain unclear. Objective Because atrial fibrosis is associated with persistent/permanent AF, we hypothesized that electrotonic interactions between atrial myocytes and fibroblasts play an important role in CFAE genesis and electrogram-based catheter ablation. Methods and Results We used a human atrial tissue model in heart failure and simulated propagation and spiral wave reentry with and without regionally proliferated fibroblasts. Coupling of fibroblasts to atrial myocytes resulted in shorter action potential duration, slower conduction velocity, and lower excitability. Consequently, heterogeneous fibroblast proliferation in the myocardial sheet resulted in frequent spiral wave breakups, and the bipolar electrograms recorded at the fibroblast proliferation area exhibited CFAEs. The simulations demonstrated that ablation targeting such fibroblast-derived CFAEs terminated AF, resulting from the ablation site transiently pinning the spiral wave and then pushing it out of the fibroblast proliferation area. CFAEs could not be attributed to collagen accumulation alone. Conclusions Fibroblast proliferation in atria might be responsible for the genesis of CFAEs during persistent/ permanent AF. Our findings could contribute to better understanding of the mechanisms underlying CFAE-targeted AF ablation.

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