Effects of different types of exercise on hypertension in middle-aged and older adults: a network meta-analysis.

Objective: This study mainly used network meta-analysis to explore the effect of different types of exercise on hypertension in middle-aged and older adults. Methods: Several databases (e.g., PubMed, Embase, and the Cochrane Library) were used to search for randomized controlled trials on the effects of different types of exercise on hypertension in middle-aged and older adults. Results: A total of 19 articles and 2,385 participants were included in the analysis. Aerobic exercise interventions [MD = -9.254, P < 0.05, 95% CI (-14.810, -3.698)] and static exercise interventions [MD = -10.465, P < 0.05, 95% CI (-18.135, -2.794)] had a significant effect on the improvement in systolic blood pressure (SBP). For diastolic blood pressure (DBP), aerobic exercise interventions [MD = -1.4096; P > 0.05, 95% CI (-8.2395, 5.4201)] and static exercise interventions [MD = -4.5206, P > 0.05, 95% CI (-14.0436, 5.0023)] were not statistically significant. The results of the surface under the cumulative ranking curve (SUCRA) showed that static exercise improved hypertension better than aerobic exercise. Conclusion: Aerobic exercise and static exercise have been shown to have a good effect on the improvement of hypertension, but the effect on DBP is not significant.

Proteome Analysis in a Mammalian Cell line Reveals that PLK2 is Involved in Avian Metapneumovirus Type C (aMPV/C)-Induced Apoptosis.

Avian metapneumovirus subtype C (aMPV/C) causes an acute respiratory disease that has caused serious economic losses in the Chinese poultry industry. In the present study, we first explored the protein profile in aMPV/C-infected Vero cells using iTRAQ quantitative proteomics. A total of 921 of 7034 proteins were identified as significantly altered by aMPV/C infection. Three selected proteins were confirmed by Western blot analysis. Bioinformatics GO analysis revealed multiple signaling pathways involving cell cycle, endocytosis, and PI3K-Akt, mTOR, MAPK and p53 signaling pathways, which might participate in viral infection. In this analysis, we found that PLK2 expression was upregulated by aMPV/C infection and investigated whether it contributed to aMPV/C-mediated cellular dysfunction. Suppressing PLK2 attenuated aMPV/C-induced reactive oxygen species (ROS) production and p53-dependent apoptosis and reduced virus release. These results in a mammalian cell line suggest that high PLK2 expression correlates with aMPV/C-induced apoptosis and viral replication, providing new insight into the potential avian host cellular response to aMPV/C infection and antiviral targets.

Seneca valley virus activates autophagy through the PERK and ATF6 UPR pathways.

Diverse effects on autophagy, a cell degradation pathway, have been associated with the infectious mechanisms of different pathogens. Here, we demonstrated that Seneca valley virus (SVV), an important emerging porcine virus characterized by vesicular lesions and neonatal mortality, can induce autophagy in cultured PK-15 and BHK-21 cells by detecting autophagosome formation, GFP-LC3 puncta and accumulation of LC3-II proteins. Treatment with pharmacological inducers/inhibitors and small interfering RNA sequences targeting genes critical for autophagosome formation affected autophagy induction and viral yields. SVV induced a complete autophagic process to enhance its replication. The PERK and ATF6 pathways, two components of the endoplasmic reticulum (ER)-related unfolded protein response (UPR), were also activated in SVV-infected cells and downregulation of their expression suppressed SVV-induced autophagy and viral yields. Overall, these results reveal that SVV induces autophagy in cultured cells through the PERK and ATF6 pathways, thereby contributing to understanding of the molecular mechanisms underlying SVV pathogenesis.