Background: To quantitatively summarize the available epidemiological evidence on the survival rate of out-of-hospital cardiac arrest (OHCA) patients who received cardiopulmonary resuscitation (CPR). Methods: We systematically searched the PubMed, Embase, and Web of Science databases, and the references of retrieved articles were manually reviewed to identify studies reporting the outcome of OHCA patients who received CPR. The overall incidence and outcome of OHCA were assessed using a random-effects meta-analysis. Results: A total of 141 eligible studies were included in this meta-analysis. The pooled incidence of return of spontaneous circulation (ROSC) was 29.7% (95% CI 27.6–31.7%), the rate of survival to hospital admission was 22.0% (95% CI 20.7–23.4%), the rate of survival to hospital discharge was 8.8% (95% CI 8.2–9.4%), the pooled 1-month survival rate was 10.7% (95% CI 9.1–13.3%), and the 1-year survival rate was 7.7% (95% CI 5.8–9.5%). Subgroup analysis showed that survival to hospital discharge was more likely among OHCA patients whose cardiac arrest was witnessed by a bystander or emergency medical services (EMS) (10.5%; 95% CI 9.2–11.7%), who received bystander CPR (11.3%, 95% CI 9.3–13.2%), and who were living in Europe and North America (Europe 11.7%; 95% CI 10.5–13.0%; North America: 7.7%; 95% CI 6.9–8.6%). The survival to discharge (8.6% in 1976–1999 vs. 9.9% in 2010–2019), 1-month survival (8.0% in 2000–2009 vs. 13.3% in 2010–2019), and 1-year survival (8.0% in 2000–2009 vs. 13.3% in 2010–2019) rates of OHCA patients who underwent CPR significantly increased throughout the study period. The Egger’s test did not indicate evidence of publication bias for the outcomes of OHCA patients who underwent CPR. Conclusions: The global survival rate of OHCA patients who received CPR has increased in the past 40 years. A higher survival rate post-OHCA is more likely among patients who receive bystander CPR and who live in Western countries.

1 What is the primary question addressed by this study? To assess the psychological status of college students in China during the COVID-19 outbreak, and offer some theoretical evidence for psychological intervention of college students. 2 What is the main finding of this study? (1) A total of 89,588 college students participated in the current study, among which 36,865 students (41.1%) reported anxiety symptoms. (2) Multivariate logistic regression analysis revealed that the risk factors for anxiety symptoms included the age of 26-30 college students, sophomore students, junior students, senior students, father have a higher education level, bad economic status, and low social support. 3 What is the meaning of the finding? (1) About two-fifths of Chinese college students have anxiety symptoms during the COVID-19 epidemic. (2) Timely and appropriate psychological interventions for college students should be implemented to reduce the psychological harm caused by COVID-19 epidemic. (3)Meanwhile, psychological skills training should be strengthened to better regulate the psychological status of college students as well as to mitigate the psychological problems of patients.

Background: Andrographolide (Andro), a diterpenoid lactone, has been used for treatment of various cancers with less adverse effects. However, the underlying mechanisms regarding its anti-tumor mechanism still remain unclear. Methods: Cell viability and proliferation were measured by CCK8 and CFSE dilution assay. The localization of p50/p65 or cytochrome c was determined using confocal immunofluorescence. Streptavidin-agarose pulldown or ChIP assays were used to detect the binding of multiple transactivators to COX-2 promoter. The promoter activity was examined by a dual-Luciferase reporter assay. The functions of Andro on COX-2-mediated angiogenesis were also investigated using human HUVEC cells through tube formation and spheroids sprouting assay. The in vivo anti-tumor efficacy of Andro was analyzed in xenografts nude mice. Results: The results indicated that Andro could significantly inhibit the proliferation of human breast cancers, and suppress COX-2 expression at both protein and mRNA levels. Furthermore, Andro could dose-dependently inhibit COX-2-mediated angiogenesis in human endothelial cells. We have also found that Andro significantly promoted the activation of cytochrome c and activated caspase-dependent apoptotic signaling pathway. Our further explorations demonstrated that Andro inhibited the binding of the transactivators CREB2, C-Fos and NF-κB and blocked the recruitment of coactivator p300 to COX-2 promoter. Moreover, Andro could effectively inhibit the activity of p300 histone acetyltransferase (HAT), thereby attenuating the p300-mediated acetylation of NF-κB. Besides, Andro could also dramatically inhibit the migration, invasion and tubulogenesis of HUVECs in vitro. In addition, Andro also exhibited effective anti-tumor efficacy as well as angiogenesis inhibition in vivo. Conclusion: In current study, we explore the potential effects of Andro in suppressing breast cancer growth and tumor angiogenesis, as well as the precise mechanisms. This work demonstrated the potential anti-cancer effects of Andro, indicating that Andro could inhibit COX-2 expression through attenuating p300 HAT activity and suppress angiogenesis via VEGF pathway, and thereby could be developed as an antitumor agent for the treatment of breast cancer.

An increasing number of original studies suggest that sedentary behavior is associated with the risk of dementia, but the results remain inconsistent and inconclusive. In this meta-analysis, we analyzed available observational epidemiological evidence to identify the association between sedentary behavior and the risk of dementia. We searched PubMed and Embase from their inception to March 2019 to identify observational studies examining the association between sedentary behavior and risk of dementia. Two authors independently extracted data and assessed study quality using predefined criteria. The Q statistics and I² methods were used to test for heterogeneity. The publication bias of the included studies was also estimated using Begg’s and Egger’s tests. We identified 18 relevant cohort studies involving 250,063 participants and 2269 patients with dementia. Pooled result showed that sedentary behavior was significantly associated with increased risk of dementia (RR = 1.30; 95% CI: 1.12–1.51). In addition, subgroup analyses by state, and controlling for the concomitant effects of age, sex, education were conducted for the increase of dementia risk, relating to sedentary, respectively. In general, these subgroup analyses showed no statistically significant differences. The results of our meta-analysis suggested that sedentary behavior was independently associated with a significantly increased risk of dementia, which might have important implications in conducting etiological studies for dementia and developing strategies for dementia prevention.

Background: Sepsis is a severe syndrome of organ dysfunction that often leads to cardiac dysfunction and endangers life. The role of mitochondrial aldehyde dehydrogenase 2 (ALDH2) in LPS-induced myocardial injury is unclear. The purpose of this study was to assess the role of ALDH2 in lipopolysaccharide (LPS)-induced myocardial injury and the regulatory mechanism and to identify potential therapeutic strategies for treating this condition. Methods: An in vivo model was established by 12 h of LPS (10 mg/kg, intraperitoneal injection) stimulation, and an in vitro model was generated by stimulating H9C2 cells with LPS (10 μg/ml) for 12 h. We then used the ALDH2 activator Alda-1 and the ALDH2 inhibitor daidzin to assess their effects on LPS-induced cardiac injury. Cardiac function in mice was evaluated by using cardiac ultrasound. We used various methods to evaluate inflammation, apoptosis, and oxidative stress, including ELISA, flow cytometry, JC-1 staining, Western blotting, and DCFH-DA staining. Additionally, we used a small interfering RNA (siRNA) to knock down cyclic GMP-AMP synthase (cGAS) to further investigate the relationship between ALDH2 and cGAS in LPS-induced cardiac injury. Results: LPS-induced cardiac dysfunction and increased the levels of the cardiac injury markers creatine kinase-MB (CKMB) and lactate dehydrogenase (LDH) in vivo. This change was accompanied by an increase in reactive oxygen species (ROS) levels, which exacerbated the oxidative stress response and regulated apoptosis through cleaved caspase-3, BAX, BCL-2. The expression of inflammatory cytokines such as IL-6/IL-1β/TNF-α was also upregulated. However, these effects were reversed by pretreatment with Alda-1 via the inhibition of cGAS/stimulator of interferon genes (STING) signaling pathway. Interestingly, LPS, Alda-1 and daidzin altered the activity of ALDH2 but did not regulate its protein expression. Knocking down cGAS in H9C2 cardiomyocytes alleviated LPS-induced cardiac inflammation, apoptosis, and ROS production and weakened the synergistic effect of daidzin. Conclusion: We demonstrated that ALDH2 alleviated LPS-induced cardiac dysfunction, inflammation, and apoptosis through the cGAS/STING signaling pathway, thereby protecting against LPS-induced cardiac injury. This study identifies a novel therapeutic approach for treating sepsis-induced cardiomyopathy (SIC).