Objective. As one of the commonly used control signals of brain-computer interface (BCI), steady-state visual evoked potential (SSVEP) exhibits advantages of stability, periodicity and minimal training requirements. However, SSVEP retains the non-linear, non-stationary and low signal-to-noise ratio (SNR) characteristics of EEG. The traditional SSVEP extraction methods regard noise as harmful information and highlight the useful signal by suppressing the noise. In the collected EEG, noise and SSVEP are usually coupled together, the useful signal is inevitably attenuated while the noise is suppressed. Also, an additional band-pass filter is needed to eliminate the multi-scale noise, which causes the edge effect. Approach. To address this issue, a novel method based on underdamped second-order stochastic resonance (USSR) is proposed in this paper for SSVEP extraction. Main results. A synergistic effect produced by noise, useful signal and the nonlinear system can force the energy of noise to be transferred into SSVEP, and hence amplifying the useful signal while suppressing multi-scale noise. The recognition performances of detection are compared with the widelyused canonical coefficient analysis (CCA) and multivariate synchronization index (MSI). Significance. The comparison results indicate that USSR exhibits increased accuracy and faster processing speed, which effectively improves the information transmission rate (ITR) of SSVEP-based BCI.

Aim: The purpose of the present study was to explore the function and mechanism of tensin 1 (TNS1) in non-small cell lung cancer (NSCLC) progression. Methods: The expression of TNS1 in NSCLC cells and tissues was assessed by RT-PCR and Western blot. Besides, Kaplan–Meier survival analysis was recruited to explore the association between TNS1 and NSCLC. Cell growth was analyzed by MTT and flow cytometry assay, while cell metastasis was determined by wound healing and transwell assays. The targeting relationship between TNS1 and miR-152 was assessed by luciferase activity assays. And Western blot was employed to determine the expression of related proteins of Akt/mTOR/RhoA pathway. Results: TNS1 level was boosted in NSCLC cells and tissues, related to the prognosis of NSCLC patients. Furthermore, it was proved that TNS1 promoted the growth and metastasis of NSCLC cells via Akt/mTOR/RhoA pathway. And miR-152 targeted TNS1 to affect the progression of NSCLC. Conclusion: miR-152/TNS1 axis inhibits the progression of NSCLC by Akt/mTOR/RhoA pathway.

No abstract

No abstract

N-methyl-D-aspartate receptors (NMDARs) are glutamate-gated calcium-permeable excitatory channels. They have attracted great interest as potential targets for the treatment of depression in recent years. NMDARs typically assemble as heterotetramers composed of two GluN1 and two alternative GluN2 (2A-2D) subunits, the latter of which endow various subtypes with diverse gating and pharmacological properties. To date, limited molecules with GluN2 specificity have been identified to show antidepressant effects. Here, we identify a compound termed YY-23 extracted from Rhizoma Anemarrhenae allosterically inhibited the channel activities of GluN2C- or GluN2D-incorporated NMDARs, an effect that was presumably influenced by the S2 segment in the ligand-binding domain of the GluN2 subunit. We found that prefrontal GluN2D-containing NMDARs were predominantly expressed at GABAergic interneurons rather than pyramidal neurons. Furthermore, we revealed that YY-23 suppressed the activity of GluN2D-containing NMDARs and GABAergic neurotransmission in the medial prefrontal cortex (mPFC). As a consequence, this GABAergic disinhibition facilitated the excitatory transmission. Behavioural experiments showed that YY-23 acted as a rapid antidepressant in both stress-naive and stressed animal models, which was abolished in Grin2d-knockout mice. Together, our findings suggest that GluN2D-incorporated NMDARs on GABAergic interneurons might be promising therapeutic targets for the treatment of depression.