Centrosome cohesion, mostly regarded as a proteinaceous linker between parental centrioles, ensures the interphase centrosome(s) to function as a single microtubule-organizing center. Impairment of centrosome cohesion leads to the splitting of centrosomes. Although the list of cohesion proteins is growing, the precise composition and regulation of centrosome cohesion are still largely unknown. In this study, we identify that the novel centriolar protein, Centlein, localizes to the proximal ends of the centrioles and directly interacts with both C-Nap1 and Cep68. Moreover, Centlein complexes with C-Nap1 and Cep68 at the proximal ends of centrioles during interphase and functions as a molecular link between C-Nap1 and Cep68. Depletion of Centlein impairs recruitment of Cep68 to the centrosomes, in turn, results in centrosome splitting. Both Centlein and Cep68 are novel Nek2A substrates. Collectively, our data bring to light centrosome cohesion maintained by the novel complex of C-Nap1-Centlein-Cep68.
The purpose of this study was to investigate the effect of transcranial pulsed current stimulation (tPCS) on fatigue delay after medium-intensity training. Materials and Methods: Ninety healthy college athletes were randomly divided into an experimental group (n = 45) and control group (n = 45). The experimental group received medium-intensity training for a week. After each training, the experimental group received true stimulation of tPCS (continuous 15 min 1.5 mA current intensity stimulation). The control group received sham stimulation. The physiological and biochemical indicators of participants were tested before and after the experiment, and finally 30 participants in each group were included for data analysis. Results: In the experimental group, creatine kinase (CK), cortisol (C), time-domain heart rate variability indices root mean square of the successive differences (RMSSD), standard deviation of normal R-R intervals (SDNN), and frequency domain indicator low frequency (LF) all increased slowly after the intervention. Among these, CK, C, and SDNN values were significantly lower than those in the control group (p < 0.05). Testosterone (T), T/C, and heart rate variability frequency domain indicator high frequency (HF) in the experimental group decreased slowly after the intervention, and the HF value was significantly lower than that in the control group (p < 0.05). The changes in all of the indicators in the experimental group were smaller than those in the control group. Conclusion: The application of tPCS after medium-intensity training enhanced the adaptability to training and had a significant effect on the maintenance of physiological state. The application of tPCS can significantly promote the recovery of autonomic nervous system function, enhance the regulation of parasympathetic nerves, and delay the occurrence of fatigue.
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