Pyrogallol protects against influenza A virus-triggered lethal lung injury by activating the Nrf2-PPAR-γ-HO-1 signaling axis.

Pyrogallol, a natural polyphenol compound (1,2,3-trihydroxybenzene), has shown efficacy in the therapeutic treatment of disorders associated with inflammation. Nevertheless, the mechanisms underlying the protective properties of pyrogallol against influenza A virus infection are not yet established. We established in this study that pyrogallol effectively alleviated H1N1 influenza A virus-induced lung injury and reduced mortality. Treatment with pyrogallol was found to promote the expression and nuclear translocation of nuclear factor erythroid-2-related factor 2 (Nrf2) and peroxisome proliferator-activated receptor gamma (PPAR-γ). Notably, the activation of Nrf2 by pyrogallol was involved in elevating the expression of PPAR-γ, both of which act synergistically to enhance heme oxygenase-1 (HO-1) synthesis. Blocking HO-1 by zinc protoporphyrin (ZnPP) reduced the suppressive impact of pyrogallol on H1N1 virus-mediated aberrant retinoic acid-inducible gene-I-nuclear factor kappa B (RIG-I-NF-κB) signaling, which thus abolished the dampening effects of pyrogallol on excessive proinflammatory mediators and cell death (including apoptosis, necrosis, and ferroptosis). Furthermore, the HO-1-independent inactivation of janus kinase 1/signal transducers and activators of transcription (JAK1/STATs) and the HO-1-dependent RIG-I-augmented STAT1/2 activation were both abrogated by pyrogallol, resulting in suppression of the enhanced transcriptional activity of interferon-stimulated gene factor 3 (ISGF3) complexes, thus prominently inhibiting the amplification of the H1N1 virus-induced proinflammatory reaction and apoptosis in interferon-beta (IFN-ß)-sensitized cells. The study provides evidence that pyrogallol alleviates excessive proinflammatory responses and abnormal cell death via HO-1 induction, suggesting it could be a potential agent for treating influenza.

Bidirectional Longitudinal Associations between Parental Psychological Control and Peer Victimization among Chinese Adolescents: The Mediating Role of Basic Psychological Need Satisfaction.

Despite evidence indicating a connection between inappropriate parenting styles and peer victimization, the dynamic processes and mechanisms underlying this link and whether it is consistent across genders and different developmental stages have yet to be explored. To address these gaps, the current 2-year longitudinal study explored the potential bidirectional associations between parental psychological control and peer victimization, as well as the mediating role of adolescent basic psychological need satisfaction. A total of 4,990 adolescents (49.4% boys, Mage T1 = 12.21 years, SDage T1 = 2.60) across different developmental stages (early adolescents, N = 1,819, 49.2% boys, Mage T1 = 9.34 years, SDage T1 = 0.62; middle adolescents, N = 1,525, 50.75% boys, Mage T1 = 12.47 years, SDage T1 = 0.69; late adolescents, N = 1,646, 46.5% boys, Mage T1 = 15.26 years, SDage T1 = 0.50) participated in this three-wave longitudinal survey. The results revealed that parental psychological control was bidirectionally associated with peer victimization. Additionally, basic psychological need satisfaction played the meditating role in this vicious cycle. Further analysis demonstrated interesting developmental differences. Parental psychological control was directly associated with subsequent peer victimization at all three developmental stages, and peer victimization was only directly associated with subsequent parental psychological control in the next year among early adolescents and middle adolescents. The mutual mediating role of basic psychological need satisfaction between parental psychological control and peer victimization was observed exclusively in early adolescents. Both male and female adolescents could be equally affected by these dynamics. This research underscores the reciprocal dynamics inherent in parent-child interactions, intervening in either of these processes (i.e., family, peers, and adolescent basic psychological need satisfaction) may break this destructive cycle.

Pyrogallol promotes growth arrest by activating the p53-mediated up-regulation of p21 and p62/SQSTM1-dependent degradation of ß-catenin in nonsmall cell lung cancer cells.

Pyrogallol (1,2,3-trihydroxybenzene), a polyphenolic natural compound, has attracted considerable attention with regard to its potential anticancer activity. However, further study is needed to elucidate the underlying mechanism related to the antiNSCLC activity of pyrogallol and provide a comprehensive theoretical basis for better clinical utilization of pyrogallol. Our current study aims to investigate the effects and potential underlying mechanisms of pyrogallol on the inhibition of NSCLC growth. Our results showed that pyrogallol treatment induced cell cycle arrest at the G2/M phase and apoptosis in two different NSCLC cell lines. Mechanistically, we found that the induction of cell cycle arrest in NSCLC cells at the G2/M phase by pyrogallol was due to the upregulation of p21 in a p53-dependent manner. And blockade of p53 and p21 effectively abolished the cell cycle arrest at the G2/M phase. Meanwhile, p53 inhibition has been found to abrogate the pyrogallol-induced apoptosis of the two NSCLC cells. Moreover, we revealed that the inhibitory effects of pyrogallol on ß-catenin signaling resulted from autophagy initiation depending on p53 activation, accompanied by an increase in p62/SQSTM1 expression, thus p62 subsequently interacting with ubiquitinated ß-catenin and facilitating autophagic destruction of ß-catenin. Furthermore, in vivo experiments demonstrated that pyrogallol exerted growth inhibition on NSCLC with low toxicity through the same molecular mechanism as observed in vitro. Our findings could contribute to the understanding of the mechanism by which pyrogallol negatively regulates NSCLC growth, which could be effective in treating NSCLC.

Rosmarinic acid treatment protects against lethal H1N1 virus-mediated inflammation and lung injury by promoting activation of the h-PGDS-PGD2-HO-1 signal axis.

BACKGROUND: Rosmarinic acid (RosA) is a natural phenolic compound that possesses a wide-range of pharmacological properties. However, the effects of RosA on influenza A virus-mediated acute lung injury remain unknown. In this study, we aimed to explore whether RosA could protect against H1N1 virus-mediated lung injury and elucidate the underlying mechanisms. METHODS: Mice were intragastrically administered with RosA for 2 days before intranasal inoculation of the H1N1 virus (5LD50) for the establishment of an acute lung injury model. At day 7 post-infection (p.i.), gross anatomic lung pathology, lung histopathologic, and lung index (lung weight/body weight) were examined. Luminex assay, multiple immunofluorescence and flow cytometry were performed to detect the levels of pro-inflammatory cytokines and apoptosis, respectively. Western blotting and plasmid transfection with hematopoietic-type PGD2 synthase (h-PGDS) overexpression were conducted to elucidate the mechanisms. RESULTS: RosA effectively attenuated H1N1 virus-triggered deterioration of gross anatomical morphology, worsened lung histopathology, and elevated lung index. Excessive pro-inflammatory reactions, aberrant alveolar epithelial cell apoptosis, and cytotoxic CD8+ T lung recruitment in the lung tissues induced by H1N1 virus infection were observed to be reduced by RosA treatment. In vitro experiments demonstrated that RosA treatment dose-dependently suppressed the increased levels of pro-inflammatory mediators and apoptosis through inhibition of nuclear factor kappa B (NF-κB) and P38 MAPK signaling pathways in H1N1 virus-infected A549 cells, which was accompanied by promoting activation of the h-PGDS-PGD2-HO-1 signal axis. Furthermore, we strikingly found that h-PGDS inhibition significantly abrogated the inhibitory effects of RosA on H1N1 virus-mediated activation of NF-κB and P38 MAPK signaling pathways, resulting in diminishing the suppressive effects on the increased levels of pro-inflammatory cytokines and chemokines as well as apoptosis. Finally, suppressing h-PGDS prominently abolished the protective effects of RosA on H1N1 virus-mediated severe pneumonia and lung injury. CONCLUSIONS: Taken together, our study demonstrates that RosA is a promising compound to alleviate H1N1 virus-induced severe lung injury through prompting the h-PGDS-PGD2-HO-1 signal axis.

An α-hemoglobin-derived peptide (m)VD-hemopressin (α) promotes NREM sleep via the CB1 cannabinoid receptor.

Hemopressin and related peptides have shown to function as the endogenous ligands or the regulator of cannabinoid receptors. The previous studies demonstrated that the endocannabinoid system played important roles in modulating several physiological functions such as sleep, olfaction, emotion, learning and memory, and reward behaviors. Mouse VD-hemopressin (α) [(m)VD-HPα], an 11-residue peptide derived from the α1 chain of hemoglobin, was recently presumed as a selective agonist of the CB1 receptor. The present study was undertaken to investigate the effects of (m)VD-HPα on the sleep-wake cycle and power spectrum of cortical EEG in freely moving rats and the potential neurons in the brain activated by (m)VD-HPα. The results showed that 20.1 nmol of (m)VD-HPα i.c.v. administration increased non-rapid eye movement (NREM) sleep in the first 2 h section accompanied by an increase in EEG delta (0.5-4 Hz) activity. The (m)VD-HPα-induced NREM sleep enhancement was due to extended episode duration instead of the episode number. In addition, the effect of (m)VD-HPα (20.1 nmol) on sleep-wake states was significantly attenuated by an antagonist of the CB1 receptor, AM251 (20 nmol, i.c.v.) but not by the CB2 receptor antagonist, AM630 (20 nmol, i.c.v.). In comparison with vehicle, (m)VD-HPα increased Fos-immunoreactive (-ir) neurons in the ventrolateral preoptic nucleus (VLPO), but reduced Fos-ir neurons in the lateral hypothalamus (LH), tuberomammillary nucleus (TMN), and locus coeruleus (LC). These findings suggest that (m)VD-HPα promotes NREM sleep via the CB1 cannabinoid receptor to probably activate VLPO GABAergic neurons, but inactivates the LH orexinergic, LC noradrenergic, and TMN histaminergic neurons.

Diosmetin alleviates benzo[a]pyrene-exacerbated H1N1 influenza virus-induced acute lung injury and dysregulation of inflammation through modulation of the PPAR-γ-NF-κB/P38 MAPK signaling axis.

The severity of a viral respiratory illness was greatly exacerbated after exposure to a contaminant containing benzo[a]pyrene (B[a]P). Flavonoid-rich fruit intake has gained intense interest due to their health-promoting benefits for viral respiratory diseases, including influenza viruses. In our study, diosmetin (3',5,7-trihydroxy-4'-methoxyflavone), a naturally occurring hydroxylated methoxyflavone that is abundant in Citrus fruits, was explored for its effects on B[a]P-exacerbated H1N1 influenza virus-mediated inflammation and lung injury. Initially, in vivo results demonstrated that diosmetin protected against H1N1 virus-elicited acute lung injury. Simultaneously, H1N1 virus or B[a]P-stimulated A549 cells treated with diosmetin inhibited NF-κB and P-P38 activation, resulting in suppression of pro-inflammatory cytokines and apoptosis. Interestingly, diosmetin obviously promoted the expression of PPAR-γ as well as nuclear translocation of PPAR-γ, whereas, PPAR-γ inhibition by GW9662 weakened the inhibitory effects of diosmetin on H1N1 virus or B[a]P-mediated activation of NF-κB and P-P38, elevated expression of pro-inflammatory mediators as well as apoptosis. Furthermore, it was surprising to discover that mice exposed to both B[a]P and H1N1 viruses contributed to exacerbated acute lung injury, which were significantly ameliorated by diosmetin administration. In vitro studies showed that A549 cells with the combination of B[a]P and H1N1 virus augmented NF-κB and P-P38 activation, accompanied by higher levels of pro-inflammatory mediators and apoptosis, all of which were also significantly reduced by diosmetin treatment. Repressing PPAR-γ abrogated the inhibitory effects of diosmetin on B[a]P-exacerbated H1N1 virus-mediated NF-κB and P-P38 activation, inflammation, and apoptosis in A549 cells. Our findings suggest that diosmetin protected against B[a]P-exacerbated H1N1 virus-mediated lung injury by suppressing the exacerbation of NF-κB and P38 kinase activation in a PPAR-γ-dependent manner, suggesting potential benefits for B[a]P-exacerbated influenza-related illness therapeutics.

Autonomy-relatedness Patterns and their Association with Academic and Psychological Adjustment among Chinese Adolescents.

Establishing autonomy and maintaining relatedness with parents are two of the most crucial goals for adolescents and meeting these goals can be critical for academic and psychological adjustment. A two-dimensional framework was proposed for exploring the integrative synthesis of autonomy and relatedness, but its cultural applicability was limited. To better account for the situations associated with non-Western cultural context, this study extended the prior framework to three dimensions (volition, functional independence, and relatedness) and utilized latent profile analysis to explore the configurations and their concurrent and longitudinal (one year later) associations with adjustment (academic engagement, academic buoyancy, depressive symptoms, and externalizing problems). The study collected data from 3992 Chinese adolescents (51.33% girls, Mage = 15.41, SD = 0.55). Latent profile analyses identified five profiles: High, High Functional Independence, Moderate, Low Functional Independence, and Extremely Low Functional Independence. The High profile was the robust optimal pattern for academic and psychological adjustment, while the Low Functional Independence and Extremely Low Functional Independence were risk patterns over time. The High Functional Independence profile was only conducive to academic areas but not to psychological areas. Findings demonstrated the necessity of the three-dimensional framework in this field.

Longitudinal association between interparental conflict and risk-taking behavior among Chinese adolescents: testing a moderated mediation model.

BACKGROUND: The interparental conflict has been associated with an increased adolescents' engagement in risk-taking behaviors. However, few studies have examined the potential mediation of deviant peer affiliation and the potential moderation of school climate. Grounded in the ecological system theory, this study aimed to explore the mediating role of deviant peer affiliation and the moderating role of school climate between the association of interparental conflict and risk-taking behavior. METHODS: This study conducted a longitudinal design (3 time points, 3 months apart) with the sample comprising 550 middle school students in southeastern China (52.91% males; mean age at Time 1 = 15.37). The performed measurements encompassed interparental conflict (T1), deviant peer affiliation (T2), school climate (T3), risk-taking behavior (T1/T2/T3), and demographic information. RESULTS: The moderated mediation model revealed that after controlling for T1/T2 risk-taking behavior, T1 interparental conflict was longitudinally and positively correlated with T3 risk-taking behavior through T2 deviant peer affiliation. Furthermore, moderated mediation analysis demonstrated that a positive school climate ameliorated the adverse impact of deviant peer affiliation on risk-taking behavior, thereby mitigating the indirect effect of interparental conflict on risk-taking behavior among adolescents. CONCLUSIONS: Our findings propose a nuanced explanation of the processing mechanisms between interparental conflict and risk-taking behaviors among Chinese adolescents. The theoretical and practical implications of the findings are discussed.

5-Methoxyflavone alleviates LPS-mediated lung injury by promoting Nrf2-mediated the suppression of NOX4/TLR4 axis in bronchial epithelial cells and M1 polarization in macrophages.

BACKGROUND: Acute lung injury (ALI) arises from sepsis or bacterial infection, which are life-threatening respiratory disorders that cause the leading cause of death worldwide. 5-Methoxyflavone, a methylated flavonoid, is gaining increased attention for its various health benefits. In the current study, we investigated the potential effects of 5-methoxyflavone against LPS-mediated ALI and elucidated the corresponding possible mechanism. METHODS: A mouse model with ALI was established by intratracheal instillation of LPS, and lung pathological changes, signaling pathway related proteins and apoptosis in lung tissues were estimated by H&E staining, immunofluorescence and TUNEL assay, respectively. Cell viability was evaluated by MTT assay; protein levels of pro-inflammatory mediators were measured by ELISA assay; levels of ROS and M1 macrophage polarization were assayed by flow cytometry; the expression of Nrf2 signaling, NOX4/TLR4 axis and P-STAT1 were detected by western blotting. RESULTS: Our results showed that 5-methoxyflavone treatment inhibited LPS-induced expression of NOX4 and TLR4 as well as the activation of downstream signaling (NF-κB and P38 MAPK), which was accompanied by markedly decreased ROS levels and pro-inflammatory cytokines (IL-6, TNF-α, MCP-1, and IL-8) in BEAS-2B cells. Moreover, we revealed that these effects of 5-methoxyflavone were related to its Nrf2 activating property, and blockade of Nrf2 prevented its inhibitory effects on NOX4/TLR4/NF-κB/P38 MAPK signaling, thus abrogating the anti-inflammatory effects of 5-methoxyflavone. Besides, the Nrf2 activating property of 5-methoxyflavone in RAW264.7 cells led to inhibition of LPS/IFN-γ-mediated STAT1 signaling, resulting in suppression of LPS/IFN-γ-induced M1 macrophage polarization and the repolarization of M2 macrophages to M1. In a mouse model of LPS-induced ALI, 5-methoxyflavone administration ameliorated LPS-mediated lung pathological changes, the increased lung index (lung/body weight ratio), and epithelial cell apoptosis. Meanwhile, we found 5-methoxyflavone effectively suppressed the hyperactive signaling pathways and the production of excessive pro-inflammatory mediators. Moreover, 5-methoxyflavone reduced LPS-mediated M1 macrophage polarization associated with elevated P-STAT1 activation in the lung tissues. In addition, 5-methoxyflavone improved the survival of LPS-challenged mice. CONCLUSION: These results indicated that 5-methoxyflavone might be suitable for the development of a novel drug for ALI therapeutic.

A New Stress-Based Formulation for Modeling Notched Fiber-Reinforced Laminates.

Laminated plates are often modeled with infinite dimensions in terms of the so-called Whitney-Nuismer (WN) stress criteria, which form a theoretical basis for predicting the residual properties of open-hole structures. Based upon the WN stress criteria, this study derived a new formulation involving finite width; the effects of notch shape and size on the applicability of new formulae and the tensile properties of carbon-fiber-reinforced plastic (CFRP) laminates were investigated via experimental and theoretical analyses. The specimens were prepared by using laminates reinforced by plain woven carbon fiber fabrics and machined with or without an open circular hole or a straight notch. Standard tensile tests were performed and measured using the digital image correlation (DIC) technique, aiming to characterize the full-field surface strain. Continuum damage mechanics (CDMs)-based finite element models were developed to predict the stress concentration factors and failure processes of notched specimens. The characteristic distances in the stress criterion models were calibrated using the experimental results of un-notched and notched specimens, such that the failure of carbon fiber laminates with or without straight notches could be analytically predicted. The experimental results demonstrated well the effectiveness of the present formulations. The new formula provides an effective approach to implementing a finite-width stress criterion for evaluating the tensile properties of notched fiber-reinforced laminates. In addition, the notch size has a great effect on strength prediction while the fiber direction has a great influence on the fracture mode.

The Association between Peer Victimization and Risk-Taking Behavior among Chinese Adolescents: Testing a Moderated Mediation Model.

Peer victimization has been considered a main source of risk-taking behavior among adolescents, but little is known about the mechanisms underlying this association. Based on the social-cognitive theory and the person-environment interactions model, the current study built a moderated mediation model to explore whether self-control mediated the link between peer victimization and adolescent risk-taking behavior and whether positive parenting moderated this link. We used a 2-time longitudinal design (6 months apart) to investigate 488 adolescents (Mage = 15.63 years, SD = 1.64) from 3 middle schools in Guangzhou. The results were as follows: (1) There were significant correlations among peer victimization, adolescent risk-taking behavior, self-control, and positive parenting when controlling for demographic variables. (2) Peer victimization not only influenced risk-taking behavior directly, but also indirectly through self-control. (3) Positive parenting moderated the influence of self-control on risk-taking behavior. In other words, positive parenting could enhance the inhibitory effect of self-control on risk-taking behavior. The results help reveal the mechanism by which adolescent risk-taking behavior forms and may help inform interventions against adolescent risk-taking behavior.

5-Methoxyflavone-induced AMPKα activation inhibits NF-κB and P38 MAPK signaling to attenuate influenza A virus-mediated inflammation and lung injury in vitro and in vivo.

Influenza-related acute lung injury (ALI) is a life-threatening condition that results mostly from uncontrolled replication of influenza virus (IV) and severe proinflammatory responses. The methoxy flavonoid compound 5-methoxyflavone (5-MF) is believed to have superior biological activity in the treatment of cancer. However, the effects and underlying mechanism of 5-MF on IV-mediated ALI are still unclear. Here, we showed that 5-MF significantly improved the survival of mice with lethal IV infection and ameliorated IV-mediated lung edema, lung histological changes, and inflammatory cell lung recruitment. We found that 5-MF has antiviral activity against influenza A virus (IAV), which was probably associated with increased expression of radical S-adenosyl methionine domain containing 2 (RSAD2) and suppression of endosomal acidification. Moreover, IV-infected A549 cells with 5-MF treatment markedly reduced proinflammatory mediator expression (IL-6, CXCL8, TNF-α, CXCL10, CCL2, CCL3, CCL4, GM-CSF, COX-2, and PGE2) and prevented P-IKBα, P-P65, and P-P38 activation. Interestingly, we demonstrated that 5-MF treatment could trigger activation of AMP-activated protein kinase (AMPK)α in IV-infected A549 cells, as evidenced by activation of the AMPKα downstream molecule P53. Importantly, the addition of AMPKα blocker compound C dramatically abolished 5-MF-mediated increased levels of RSAD2, the inhibitory effects on H1N1 virus-elicited endosomal acidification, and the suppression expression of proinflammatory mediators (IL-6, TNF-α, CXCL10, COX-2 and PGE2), as well as the inactivation of P-IKBα, P-P65, and P-P38 MAPK signaling pathways. Furthermore, inhibition of AMPKα abrogated the protective effects of 5-MF on H1N1 virus-mediated lung injury and excessive inflammation in vivo. Taken together, these results indicate that 5-MF alleviated IV-mediated ALI and suppressed excessive inflammatory responses through activation of AMPKα signaling.

Longitudinal association between parental involvement and internet gaming disorder among Chinese adolescents: Consideration of future consequences as a mediator and peer victimization as a moderator.

Background and aims: Internet gaming disorder (IGD) in adolescents is a concerning issue. Positive parenting has been found to protect against adolescent IGD, but the underlying mechanisms await further investigation. As such, this study examined the longitudinal association between parental involvement (PI) - a specific type of positive parenting understudied in the literature of adolescent gaming disorder - and IGD. Moreover, this study also tested consideration of future consequences (CFC) as a mediator and peer victimization (PV) as a moderator. Methods: A two-wave longitudinal research spanning 6 months apart was conducted. Participants were Chinese adolescents (final N = 434; 222 females; Mage = 14.44 years, SD = 1.56). They provided ratings on PI, PV, and IGD at Wave 1, and CFC-immediate, CFC-future, and IGD at Wave 2. Results: Descriptive statistics showed that the prevalence rate of IGD was 10.81% and 9.45% at Waves 1 and 2, respectively. Moreover, results of moderated mediation model found that after controlling for Wave 1 IGD and covariates, Wave 1 PI was associated with Wave 2 IGD via preventing adolescents who had higher levels of PV from developing a tendence of CFC-immediate and via promoting adolescents who had lower levels of PV to develop a tendence of CFC-future. Discussion and Conclusions: Altogether, these results suggest that facilitative ecological systems (e.g., positive parenting and good relationships with peers) and personal strengths (e.g., positive future orientation) jointly contribute to the mitigation of adolescent IGD.

Theory of planned behavior explains males' and females' intention to receive COVID-19 vaccines differently.

Uptake of COVID-19 vaccines is an important measure to curb the transmission of the coronavirus. Before the vaccines were available, numerous studies found that people had a moderate-to-high intention to receive the vaccines. Several studies have also used the theory of planned behavior (TPB) to predict people's COVID-19 vaccination intention with three elements (i.e. attitudes, subjective norms, and perceived behavioral control) . However, the vaccination rate falters after the vaccines became available, and there were few updated data documenting people's vaccination intention and how well TPB can explain their intention. In addition, studies investigating other outcomes found that the predictive utilities of TPB often varied across gender, but such gender differences received little consideration in the literature of COVID-19 vaccination intention. To help fill these gaps, we examined the associations between TPB elements and people's intention to receive COVID-19 vaccines and the moderation of gender in the context of vaccination campaign. Participants were 405 Chinese citizens. They reported on the three TPB elements and intention to receive vaccines in the coming months. Descriptive results showed that participants' vaccination intention was moderate. Results of path analysis showed that subjective norms and perceived behavioral control were positively related to vaccination intention for the whole sample. Furthermore, results of multigroup path analysis showed that attitudes were only related to males', while subjective norms were only related to females', intention. These findings enhance the utility of TPB in explaining people's COVID-19 vaccination intention and inform gender-specific strategies to boost males' and females' vaccination intention.

Longitudinal association between poor parental supervision and risk-taking behavior: The role of self-control and school climate.

INTRODUCTION: Although poor parental supervision has been associated with an increased adolescents' propensity for risk-taking behavior, few researchers have investigated nuanced mechanisms of how and for whom from the perspective of "family × school." Inspired by ecological system theory and self-control theory, this study aimed to investigate the mediating role of self-control and the moderating role of school climate between the link between poor parental supervision and risk-taking behavior. METHODS: Four hundred and ninety-one Chinese adolescents (231 females, Mage = 15.39 ± 1.36) were recruited to participate in a three-wave longitudinal study (3 months apart) and complete questionnaires regarding poor parental supervision (W1), school climate (W1), self-control (W2), and risk-taking behavior (W1/W3). RESULTS: After controlling for W1 risk-taking behavior, our moderated mediation model indicated that W1 poor parental supervision was positively related to W3 risk-taking behavior by restraining the development of W2 self-control. Additionally, a high level of school climate as a protective factor buffered the negative impact of poor parental supervision on adolescents' self-control, further reducing risk-taking behavior. CONCLUSION: Our findings shed light on the processing mechanisms between poor parental supervision and risk-taking behavior among Chinese adolescents and underscore the importance of effective preventions and interventions to facilitate adolescents' healthy development.

Sonodynamic Therapy Promotes Efferocytosis via CD47 Down-Regulation in Advanced Atherosclerotic Plaque.

Atherosclerotic cerebrocardiovascular disease is the major cause of acute ischemic diseases in humans. Impaired efferocytosis contributes to the progression of atherosclerosis. Pathological and apoptotic cells fail to undergo effective phagocytic clearance, leading to increased inflammation and necrotic core formation. Previously, we reported that 5-aminolevulinic acid-mediated sonodynamic therapy (SDT) promotes apoptotic cell efferocytosis via ATP release in atherosclerotic plaques. However, the exact signaling molecule involved in this process is still unknown. In the present study, sinoporphyrin sodium-mediated SDT (DVDMS-SDT) was applied to balloon-denuded rabbits in vivo to observe changes in the composition of atherosclerotic lesions. Cultured human THP-1-derived and mouse peritoneal macrophage-derived foam cells were used for in vitro mechanistic studies. Three days after DVDMS-SDT treatment, macrophage efferocytosis was significantly enhanced whereas local inflammation was attenuated in rabbit atherosclerotic lesions. At days 7 and 28, the histopathological analysis showed that DVDMS-SDT inhibited the progression of atherosclerosis, reduced the macrophage content, and increased the smooth muscle cell content in a time-dependent manner. Mechanistically, DVDMS-SDT activated mitochondria-caspase apoptosis in foam cells. Interestingly, activated by DVDMS-SDT, caspase-3 a key factor of apoptosis, reduced the expression of the anti-phagocytic molecule CD47 in foam cells. Of great importance, the promotion of macrophage efferocytosis by DVDMS-SDT can be eliminated by the overexpression of CD47. Overall, these results demonstrated that DVDMS-SDT effectively boosted efferocytosis via deactivation of CD47 expression, thereby reducing inflammation in advanced atherosclerotic plaques.

Chinese public's panic buying at the beginning of COVID-19 outbreak: The contribution of perceived risk, social media use, and connection with close others.

Panic buying is a globally witnessed behavior during the outbreak of COVID-19. This consumer behavior is related to many undesirable consequences, ranging from disrupting economic stability to hindering timely provision of supplies to those in dire need. As such, to understand the causes and underlying mechanisms of panic buying is crucial. Based on terror management theory, this study examined the contribution of perceived risk, social media use, and connection with close others to panic buying. Data were collected through an online survey from 972 Chinese citizens (65.9% female, M age = 33.69 years) at the beginning period of COVID-19 in early February 2020. The results found that individuals with a higher level of perceived risk were more prone to engage in panic buying, but this link was mitigated by connection with close others when individuals less used social media. Theoretically, this study advances the understandings of the psychological processes of panic buying during health crisis. Practically, alleviating individuals' perceived risk, establishing a healthy habit of social media use, and strengthening social ties are important to circumventing panic buying in times of COVID-19.

Arctiin suppresses H9N2 avian influenza virus-mediated inflammation via activation of Nrf2/HO-1 signaling.

BACKGROUND: H9N2 avian influenza viruses (AIVs) infect avian and mammalian hosts and provide internal genes for new emerging highly pathogenic avian viruses that cause severe pneumonia with high mortality, for which few medications are available. Arctiin, a bioactive lignan glycoside, has been reported to possess multiple pharmacological properties. However, the effect of arctiin on H9N2 virus infection is unclear. In the current study, we analyzed the effect of arctiin on H9N2 virus infection and the underlying molecular mechanism in vitro. METHODS: The antiviral effect against H9N2 virus was determined by plaque reduction assay (PRA) and progeny virus reduction assay. We employed MTT assay, qRT-PCR, ELISA, immunofluorescence and Western blotting to better understand the anti-inflammatory effect and corresponding mechanism of arctiin on H9N2 virus-infected cells. RESULTS: The results showed that arctiin had antiviral activity against H9N2 virus. Arctiin treatment reduced H9N2 virus-triggered proinflammatory cytokines, such as IL-6, and TNF-α. Moreover, arctiin significantly suppressed H9N2 virus-mediated expression of COX-2 and PGE2. Furthermore, we found that arctiin inhibited H9N2 virus-mediated activation of RIG-I/JNK MAPK signaling. Interestingly, arctiin treatment obviously reversed H9N2 virus-induced reduction of Nrf2, increased the nuclear translocation of Nrf2, and upregulated Nrf2 signaling target genes (HO-1 and SOD2). Zinc protoporphyrin (Znpp)-an HO-1 inhibitor-weakened the inhibitory effect of arctiin on H9N2 virus-induced RIG-I/JNK MAPK and proinflammatory mediators. CONCLUSION: Taken together, these results suggested that the anti-inflammatory effects of arctiin on H9N2 virus infection may be due to the activation of Nrf2/HO-1 and blocked RIG-I/JNK MAPK signaling; thus, arctiin may be a promising agent for prevention and treatment of H9N2 virus infections.

Optimisation of oral anticoagulants for patients with atrial fibrillation within 12 months after percutaneous coronary intervention: A meta-analysis and systematic review.

BACKGROUND: The optimal antithrombotic strategy, especially regarding oral anticoagulants (OACs) for atrial fibrillation (AF) patients with bleeding and thrombosis risk after percutaneous coronary intervention (PCI), remains unknown. This study explored the optimal oral anticoagulants for AF patients after PCI using a meta-analysis. METHODS: Randomised controlled trials were identified from PubMed, Embase, and the Cochrane Library through December 2020. Risk ratios, 95% confidence intervals, and random-effects models were used to compare different antithrombotic strategies through network meta-analysis, and the combination of antithrombotic agents was ranked according to the surface under the cumulative ranking curve and rankograms. Interval plots were drawn to observe pairwise comparisons between the different strategies. RESULTS: Five studies of 11,532 patients were included. Factor IIa inhibitor 110 mg bid plus a P2Y12 inhibitor had the greatest advantage for reducing Thrombolysis In Myocardial Infarction (TIMI) major or minor bleeding; Factor Xa inhibitor plus a P2Y12 inhibitor had the greatest advantage for reducing International Society on Thrombosis and Hemostasis major bleeding. For patients at risk of stroke plus all-cause death, factor IIa inhibitor 150 mg bid plus a P2Y12 inhibitor should be prioritised, and for those at risk of myocardial infarction and stent thrombosis, vitamin K antagonists plus a P2Y12 inhibitor were preferred. CONCLUSION: Factor IIa inhibitor 110 mg, factor IIa inhibitor 150 mg, factor Xa inhibitor and vitamin K antagonists should be selected in different situations.