Studies on the structural-functional connectomes of the human brain have demonstrated the existence of synchronous firings in a specific brain network motif. In particular, synchronization of high-frequency oscillations (HFOs) has been observed in the experimental data sets of temporal lobe epilepsy (TLE). In addition, both clinical and experimental evidences have accumulated to demonstrate the effect of electrical stimulation on TLE, which, however, remains largely unexplored. In this work, we first employ our previously proposed dentate gyrus (DG)-CA3 network model to investigate the influence of an external electrical stimulus on the HFO transitions. The results indicate that the reinforcing stimulus can induce the HFO transitions of the DG-CA3 system from the gamma band to the fast ripples band. Along with that, the consistent oscillations of neurons within DG-CA3 can also be enhanced with the increasing of stimulus. Then, we expand into a simple motif of three coupled DG-CA3 systems in both the feedforward inhibition and feedback inhibition connections, to investigate the synchronous evolutions of HFOs by regulating both the stimulation strength and inhibitory function. It is shown that the comprehensive effects, which lead to band transition, are independent of the motif configurations. The enhanced external electrical stimulus weakens the synchronism and correlation of connected motifs. In contrast, we demonstrate that the increased inhibitory coupling could facilitate correlation to some extent. Overall, our work highlights the possible origin of synchronous HFOs of hippocampal motifs governed by external inputs and inhibitory connection, which might contribute to a better understanding of the interplay between synchronization dynamics and epileptic structure in the human brain.
In this study, we explored the effect of vessel diameter of coronary artery where the stenosis is located on FFR at the same vascular level. This study is divided into two parts: clinical statistics and numerical simulation. In the clinical statistics section, we compared the blood vessel diameter where the stenosis is located of the ischemic group and the non-ischemic group. In the numerical simulation section, we further explored the effect of diameter on myocardial ischemia by using an ideal model. With the increase in stenosis rate and stenotic vessel flow, the FFR rate of the larger stenotic vessels was higher than that of smaller stenotic vessels. The larger blood vessels are more prone to ischemia when coronary artery stenosis occurs.
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