The relationship between mindfulness, anxiety and depression during the COVID-19 pandemic: A meta-analysis of correlational studies.

Background: The emergence of the COVID-19 pandemic has created an environment in which numerous determinants of poor mental health are intensified. Lockdown, re-lockdown, and media coverage of the spread of the virus, have the potential to contribute to increased levels of anxiety and depression. Mindfulness may act as a buffer against COVID-19-related depressive and anxiety disorders. Methods: We conducted a systematic review and meta-analysis by searching PubMed, PsycINFO, Web of Science, and Google Scholar for any study published between January 2020 and March 2022. In this study, Comprehensive Meta-Analysis Version 3.3 software was applied to evaluate the effect size by random effect model. In addition, the heterogeneity analysis was evaluated using indicators Q and I2 indicators. Three methods were used to test for publication bias: funnel plot, Classic Fail-safe N, and Egger's linear regression. According to the features of the included articles, subgroup analysis was utilized for the moderator analysis of this study. Results: The analysis finally included 12 articles (16 samples, N = 10,940) and obtained 26 independent effect sizes. In accordance with the meta-analysis, in the random effect model, the correlation between mindfulness and anxiety was -0.330 (p < 0.001), and the correlation between mindfulness and depression was -0.353 (p < 0.001), which supported the effect of mindfulness on anxiety and depression. In the meta-analysis of the correlation between mindfulness and anxiety, study region had an essential moderating effect (p < 0.001). The Sample type did not produce a significant moderating effect (p = 0.190). The mode of action of mindfulness was a significant moderator (p = 0.038). In the meta-analysis of the linkage between mindfulness and depression, regional differences had a significant moderating effect (p < 0.001). The sample type had no discernible moderating impact (p = 0.213). The mode of action of mindfulness was a significant moderator (p = 0.003). Conclusion: Our meta-analysis indicated that there was an essential correlation between public mindfulness and mental health. Our systematic review added evidence supporting the beneficial nature of mindfulness. A cascading development of beneficial traits that improve mental health may start with mindfulness.

High-performance broadband photoresponse of self-powered Mg2Si/Si photodetectors.

Infrared optoelectronic devices are capable of operating in harsh environments with outstanding confidentiality and reliability. Nevertheless, suffering from the large band gap value, most semiconductor materials are difficult to detect infrared light signals. Here, Mg2Si/Si heterojunction photodetectors (PDs), which possess the advantages of low-cost, easy process, environmental friendliness, and compatibility with silicon CMOS technology, have been reported with a broadband spectral response as tested from 532 to 1550 nm under zero-bias. When the incident light wavelength is 808 nm, the Mg2Si/Si photodetector (PD) has a responsivity of 1.04 A W-1and a specific detectivity of 1.51 × 1012Jones. Furthermore, we find that the Ag nanoparticles (Ag_NPs) assembled on the Mg2Si layer can greatly improve the performance of the Mg2Si/Si PD. The responsivity and specific detectivity of Mg2Si/Si device with Ag_NPs under 808 nm illumination are 2.55 A W-1and 2.60 × 1012Jones, respectively. These excellent photodetection performances can be attributed to the high-quality of our grown Mg2Si material and the strong built-in electric field effect in the heterojunction, which can be further enhanced by the local surface plasmon effect and local electromagnetic field induced by Ag_NPs. Our study would provide significant guidance for the development of new self-powered infrared PDs based on silicon materials.

The saponin D39 blocks dissociation of non-muscular myosin heavy chain IIA from TNF receptor 2, suppressing tissue factor expression and venous thrombosis.

BACKGROUND AND PURPOSE: Non-muscular myosin heavy chain IIA (NMMHC IIA) plays a key role in tissue factor expression and venous thrombosis. Natural products might inhibit thrombosis through effects on NMMHC IIA. Here, we have shown that a natural saponin, D39, from Liriope muscari exerted anti-thrombotic activity in vivo, by targeting NMMHC IIA. EXPERIMENTAL APPROACH: Expression and activity of tissue factor in endothelial cells were analysed in vitro by Western blot and simplified chromogenic assays. Interactions between D39 and NMMHC IIA were assessed by serial affinity chromatography and molecular docking analysis. D39-dependent interactions between NMMHC IIA and TNF receptor 2 (TNFR2) were measured by immunofluorescence, co-immunoprecipitation and proximity ligation assays. Anti-thrombotic activity of D39 in vivo was evaluated with a model of inferior vena cava ligation injury in mice. KEY RESULTS: D39 inhibited tissue factor expression and procoagulant activities in HUVECs and decreased thrombus weight in inferior vena cava-ligated mice dose-dependently. Serial affinity chromatography and molecular docking analysis suggested that D39 bound to NMMHC IIA. In HEK293T cells, D39 inhibited tissue factor expression evoked by NMMHC IIA overexpression. This effect was blocked by NMMHC IIA knockdown in HUVECs. D39 inhibited dissociation of NMMHC IIA from TNFR2, which subsequently modulated the Akt/GSK3ß-NF-κB signalling pathways. CONCLUSIONS AND IMPLICATIONS: D39 inhibited tissue factor expression and thrombus formation by modulating the Akt/GSK3ß and NF-κB signalling pathways through NMMHC IIA. We identified a new natural product that targeted NMMHC IIA, as a potential treatment for thrombotic disorders and other vasculopathies.

Enhanced Neuroprotection of Minimally Invasive Surgery Joint Local Cooling Lavage against ICH-induced Inflammation Injury and Apoptosis in Rats.

Hypothermia treatment is one of the neuroprotective strategies that improve neurological outcomes effectively after brain damage. Minimally invasive surgery (MIS) has been an important treatment of intracerebral hemorrhage (ICH). Herein, we evaluated the neuroprotective effect and mechanism of MIS joint local cooling lavage (LCL) treatment on ICH via detecting the inflammatory responses, oxidative injury, and neuronal apoptosis around the hematoma cavity in rats. ICH model was established by type IV collagenase caudatum infusion. The rats were treated with MIS 6 h after injection, and then were lavaged by normothermic (37 °C) and hypothermic (33 °C) normal saline in brain separately. The results indicated that MIS joint LCL treatment showed enhanced therapeutic effects against ICH-induced inflammation injury and apoptosis in rats, as convinced by the decline of TUNEL-positive cells, followed by the decrease of IL-1ß and LDH and increase of IL-10 and SOD. This study demonstrated that the strategy of using MIS joint LCL may achieve enhanced neuroprotection against ICH-induced inflammation injury and apoptosis in rats with potential clinic application.

Advances in the pharmacological activities and mechanisms of diosgenin.

Diosgenin, a well-known steroid sapogenin derived from plants, has been used as a starting material for production of steroidal hormones. The present review will summarize published literature concerning pharmacological potential of diosgenin, and the underlying mechanisms of actions. Diosgenin has shown a vast range of pharmacological activities in preclinical studies. It exhibits anticancer, cardiovascular protective, anti-diabetes, neuroprotective, immunomodulatory, estrogenic, and skin protective effects, mainly by inducing apoptosis, suppressing malignant transformation, decreasing oxidative stress, preventing inflammatory events, promoting cellular differentiation/proliferation, and regulating T-cell immune response, etc. It interferes with cell death pathways and their regulators to induce apoptosis. Diosgenin antagonizes tumor metastasis by modulating epithelial-mesenchymal transition and actin cytoskeleton to change cellular motility, suppressing degradation of matrix barrier, and inhibiting angiogenesis. Additionally, diosgenin improves antioxidant status and inhibits lipid peroxidation. Its anti-inflammatory activity is through inhibiting production of pro-inflammatory cytokines, enzymes and adhesion molecules. Furthermore, diosgenin drives cellular growth/differentiation through the estrogen receptor (ER) cascade and transcriptional factor PPARγ. In summary, these mechanistic studies provide a basis for further development of this compound for pharmacotherapy of various diseases.

The saponin DT-13 attenuates tumor necrosis factor-α-induced vascular inflammation associated with Src/NF-кB/MAPK pathway modulation.

This study aimed to explore the effect of DT-13 (25(R,S)-ruscogenin- 1-O- [ß-d-glucopyranosyl- (1→2)][ß-d-xylopyranosyl-(1→3)]-ß -d- fucopyranoside) on tumor necrosis factor (TNF)-α-induced vascular inflammation and the potential molecular mechanisms. In vitro, DT-13 suppressed TNF-α-induced adhesion and migration of human umbilical vein endothelial cells (HUVECs) by inhibiting the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). DT-13 markedly suppressed NF-кB p65 phosphorylation, and when NF-кB p65 was over-expressed, the inhibitory effect of DT-13 on adhesion molecular decreased. DT-13 also suppressed TNF-α induced luciferase activities of ICAM-1 and VCAM-1 promoter containing NF-κB binding sites. Furthermore, DT-13 markedly suppressed p38 phosphorylation and Src degradation induced by TNF-α, whereas had no significant effect on ERK and JNK activation. In vivo, DT-13 at 4 mg/kg prevented vascular inflammation and the expression of adhesion molecules induced by TNF-α in mice. These findings suggest that DT-13 abrogates vascular inflammation by down-regulating adhesion molecules associated with modulating the NF-кB, p38MAPK, Src signaling pathways, and NF-κB binding site is at least one of the targets of DT-13. This study provides novel information regarding the mechanism by which DT-13 exerts its effects on vascular inflammation, which is important for the onset and progression of various diseases.

NMMHC IIA inhibition impedes tissue factor expression and venous thrombosis via Akt/GSK3ß-NF-κB signalling pathways in the endothelium.

Non-muscle myosin heavy chain IIA (NMMHC IIA) has been shown to be involved in thrombus formation and inflammatory microparticle release in endothelial cells. However, the role of NMMHC IIA in regulating the expression of tissue factor (TF) and deep venous thrombosis remains to be elucidated. In the present study, endothelial cells were stimulated with tumour necrosis factor-α (TNF-α) to induce TF expression. Pretreatment with the NMMHC II inhibitor blebbistatin suppressed the mRNA and protein expressions as well as the procoagulant activity of TF in a dose-dependent manner. Blebbistatin enhanced Akt and GSK3ß phosphorylation and inhibited NF-κB p65 nuclear translocation and IκBα degradation. These observations were similar to the effect of CHIR99021, a GSK3ß inhibitor. TF downregulation by blebbistatin was antagonised by the PI3K inhibitor, wortmannin. Furthermore, siRNA knockdown of NMMHC IIA, but not IIB or IIC, inhibited TF expression, activated Akt/GSK3ß and suppressed NF-κB signalling pathways, whereas the overexpression of NMMHC IIA increased TF expression. The binding of NMMHC IIA and TNF receptor 2 mediated signal internalisation in TNF-α-stimulated endothelial cells. Importantly, blebbistatin decreased endothelium NMMHC IIA and TF expression, deactivated GSK3ß by inducing its phosphorylation, suppressed p65 nuclear translocation, and inhibited thrombus formation in a mouse deep venous thrombosis model.Our findings provide solid evidence that inhibition of NMMHC II, most likely NMMHC IIA, impedes TF expression and venous thrombosis via Akt/GSK3ß-NF-κB signalling pathways in the endothelium both in vitro and in vivo. NMMHC IIA might be a potential novel target for the treatment of thrombotic disorders.