Differences in brain activation during working memory tasks between badminton athletes and non-athletes: An fNIRS study.

BACKGROUND: Working memory refers to our ability to temporarily store and process information, and it is crucial for efficient cognition and motor control. In the context of badminton matches, athletes need to make quick decisions and reactions in rapidly changing situations. Athletes with strong working memory capacity can better process this information and translate it into actual motor performance. Although previous research has demonstrated that exercise can improve brain function and structure, it remains unclear how the brain functions of athletes engaged in long-term professional training are specifically involved in performing working memory tasks. METHOD: In this study, we assessed behavioral performance and cerebral oxygenation in the prefrontal lobe, using functional near-infrared spectroscopy, with 22 athletes and 30 non-athletes. Each participant was evaluated while performing 1-back, 2-back, and 3-back tasks. The area under the curve (AUC) of HbO (oxyhemoglobin) is used as an indicator of cortical brain oxygenation. RESULTS: The behavioral performance results indicated no difference between badminton athletes and non-athletes in the n-back task. We observed significantly different activation in channels of left FPA, right DLPFC, and left VLPFC when performing 3-back tasks. Brain activation indicated that long-term training in badminton caused a better performance in high-load working memory tasks. CONCLUSIONS: Long-term professional training in badminton primarily activates the left frontal-parietal attention network (left FPA), right dorsolateral prefrontal cortex (right DLPFC), and left ventrolateral prefrontal cortex (left VLPFC) during working memory tasks.

Paxillin mediates ATP-induced activation of P2X7 receptor and NLRP3 inflammasome.

BACKGROUND: Extracellular adenosine triphosphate (ATP), a key danger-associated molecular pattern (DAMP) molecule, is released to the extracellular medium during inflammation by injured parenchymal cells, dying leukocytes, and activated platelets. ATP directly activates the plasma membrane channel P2X7 receptor (P2X7R), leading to an intracellular influx of K+, a key trigger inducing NLRP3 inflammasome activation. However, the mechanism underlying P2X7R-mediated activation of NLRP3 inflammasome is poorly understood, and additional molecular mediators have not been identified. Here, we demonstrate that Paxillin is the molecule connecting the P2X7 receptor and NLRP3 inflammasome through protein interactions. RESULTS: We show a distinct mechanism by which Paxillin promotes ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome. Extracellular ATP induces Paxillin phosphorylation and then facilitates Paxillin-NLRP3 interaction. Interestingly, Paxillin enhances NLRP3 deubiquitination and activates NLRP3 inflammasome upon ATP treatment and K+ efflux. Moreover, we demonstrated that USP13 is a key enzyme for Paxillin-mediated NLRP3 deubiquitination upon ATP treatment. Notably, extracellular ATP promotes Paxillin and NLRP3 migration from the cytosol to the plasma membrane and facilitates P2X7R-Paxillin interaction and PaxillinNLRP3 association, resulting in the formation of the P2X7R-Paxillin-NLRP3 complex. Functionally, Paxillin is essential for ATP-induced NLRP3 inflammasome activation in mouse BMDMs and BMDCs as well as in human PBMCs and THP-1-differentiated macrophages. CONCLUSIONS: We have identified paxillin as a mediator of NLRP3 inflammasome activation. Paxillin plays key roles in ATP-induced activation of the P2X7 receptor and NLRP3 inflammasome by facilitating the formation of the P2X7R-Paxillin-NLRP3 complex.

Reduced left dorsolateral prefrontal activation in problematic smartphone users during the Stroop task: An fNIRS study.

Introduction: The widespread use of smartphones has triggered concern over problematic smartphone use (PSPU), as well as the need to elucidate its underlying mechanisms. However, the correlation between cortical activation and deficient inhibitory control in PSPU remains unclear. Methods: This study examined inhibitory control using the color-word matching Stroop task and its cortical-activation responses using functional near-infrared spectroscopy (fNIRS) in college students with PSPU (n = 56) compared with a control group (n = 54). Results: At the behavioral level, Stroop interference, coupled with reaction time, was significantly greater in the PSPU group than in the control group. Changes in oxygenated hemoglobin (Oxy-Hb) signals associated with Stroop interference were significantly increased in the left ventrolateral prefrontal cortex, left frontopolar area, and bilateral dorsolateral prefrontal cortex (DLPFC). Moreover, the PSPU group had lower Oxy-Hb signal changes associated with Stroop interference in the left-DLPFC, relative to controls. Discussion: These results provide first behavioral and neuroscientific evidence using event-related fNIRS method, to our knowledge, that college students with PSPU may have a deficit in inhibitory control associated with lower cortical activation in the left-DLPFC.

MYSM1 Suppresses Cellular Senescence and the Aging Process to Prolong Lifespan.

Aging is a universal feature of life that is a major focus of scientific research and a risk factor in many diseases. A comprehensive understanding of the cellular and molecular mechanisms of aging are critical to the prevention of diseases associated with the aging process. Here, it is shown that MYSM1 is a key suppressor of aging and aging-related pathologies. MYSM1 functionally represses cellular senescence and the aging process in human and mice primary cells and in mice organs. MYSM1 mechanistically attenuates the aging process by promoting DNA repair processes. Remarkably, MYSM1 deficiency facilitates the aging process and reduces lifespan, whereas MYSM1 over-expression attenuates the aging process and increases lifespan in mice. The functional role of MYSM1 is demonstrated in suppressing the aging process and prolonging lifespan. MYSM1 is a key suppressor of aging and may act as a potential agent for the prevention of aging and aging-associated diseases.

SOX2 Represses Hepatitis B Virus Replication by Binding to the Viral EnhII/Cp and Inhibiting the Promoter Activation.

Hepatitis B virus (HBV) replication is controlled by four promoters (preS1, preS2, Cp, and Xp) and two enhancers (EnhI and EnhII). EnhII stimulates Cp activity to regulate the transcriptions of precore, core, polymerase, and pregenomic RNAs, and therefore, EnhII/Cp is essential for the regulation of HBV replication. This study revealed a distinct mechanism underlying the suppression of EnhII/Cp activation and HBV replication. On the one hand, the sex determining region Y box2 (SOX2), a transcription factor, is induced by HBV. On the other hand, SOX2, in turn, represses the expression levels of HBV RNAs, HBV core-associated DNA, hepatitis B surface antigen (HBsAg), and hepatitis B e antigen (HBeAg), thereby playing an inhibitory role during HBV replication. Further studies indicated that SOX2 bound to the EnhII/Cp DNA and repressed the promoter activation. With the deletion of the high mobility group (HMG) domain, SOX2 loses the ability to repress EnhII/Cp activation, viral RNA transcription, HBV core-associated DNA replication, HBsAg and HBeAg production, as well as fails to enter the nucleus, demonstrating that the HMG domain is required for the SOX2-mediated repression of HBV replication. Moreover, SOX2 represses HBsAg and HBeAg secretion in BALB/c mice sera, and attenuates HBV 3.5kb RNA transcription and hepatitis B virus core protein (HBc) production in the liver tissues, demonstrating that SOX2 suppresses HBV replication in mice. Furthermore, the results revealed that the HMG domain was required for SOX2-mediated repression of HBV replication in the mice. Taken together, the above facts indicate that SOX2 acts as a new host restriction factor to repress HBV replication by binding to the viral EnhII/Cp and inhibiting the promoter activation through the HMG domain.

MYSM1 Represses Innate Immunity and Autoimmunity through Suppressing the cGAS-STING Pathway.

The immune system is not only required for preventing threats exerted by pathogens but also essential for developing immune tolerance to avoid tissue damage. This study identifies a distinct mechanism by which MYSM1 suppresses innate immunity and autoimmunity. The expression of MYSM1 is induced upon DNA virus infection and by intracellular DNA stimulation. MYSM1 subsequently interacts with STING and cleaves STING K63-linked ubiquitination to suppress cGAS-STING signaling. Notably, Mysm1-deficient mice exhibit a hyper-inflammatory response, acute tissue damage, and high mortality upon virus infection. Moreover, in the PBMCs of patients with systemic lupus erythematosus (SLE), MYSM1 production decreases, while type I interferons and pro-inflammatory cytokine expressions increase. Importantly, MYSM1 treatment represses the production of IFNs and pro-inflammatory cytokines in the PBMCs of SLE patients. Thus, MYSM1 is a critical repressor of innate immunity and autoimmunity and is thus a potential therapeutic agent for infectious, inflammatory, and autoimmune diseases.