No abstract

This study reports the corrective reaction time (tcr) of individuals using a novel methodology. The estimated tcr ranged from 87 to 441 ms, helping model hand control movements, such as aiming and tracking. The methodology can be continuously applied to study tcr under conditions with various performers and movements.

Acute myocardial infarction (AMI) and the following heart failure are public health problems faced all over the globe. The current study set out to investigate the role of B-cell lymphoma 6 (BCL-6) in cardiac protection after AMI.Initially, AMI mouse models and H9c2 cell oxygen-glucose deprivation (OGD) models were established. The cell models were transfected with the vectors containing oe-BCL-6, oe-EZH2, sh-EZH2, miR-34a mimic, and miR-34a inhibitor. RT-qPCR and Western blot analysis were applied to detect the expression patterns of microRNA-34a (miR-34a), BCL-6, enhancer of zeste homolog 2 (EZH2), and C1q tumor necrosis factor-related protein 9 (CTRP9) in the treated cell models. ChIP-qPCR and co-immunoprecipitation assay were performed to detect EZH2 enrichment and H3K27me3 levels in the miR-34a promoter region and the interaction between BCL-2 and EZH2, respectively. EdU staining, TUNEL staining, and flow cytometry were performed to detect cell proliferation and apoptosis, while ELISA was conducted to detect the oxidative stress levels. It was found that miR-34a was highly expressed in heart tissues of AMI models, while BCL-6 and EZH2 were poorly expressed. BCL-2 overexpression increased the recruitment of EZH2, upregulated H3K27me3 level in the miR-34a promoter region, and inhibited the miR-34a expression. Ctrp9, the downstream negative-regulatory molecule of miR-34a, was upregulated. Besides, miR-34a/CTRP9 expression changes were found to affect cardiomyocyte apoptosis, oxidation stress, and proliferation, and prevent myocardial injury in AMI mice. Our findings indicate that BCL-6 increases the level of H3K27me3 in the promoter region of miR-34a via EZH2 recruitment and CTRP9 upregulation, which inhibits the apoptosis of myocardial cells.

Purpose The purpose of this paper is to investigate volatility spillovers across the interest rate swap markets of the G7 economies, and then the authors investigate whether spillovers of swap markets contain useful information to explain subsequent stock price movements. Design/methodology/approach This study uses the short- and long-term swap spread volatility of the G7 countries to explore the spillover effects of international swap markets, and then investigates the relationship between swap and stock markets. The authors use the generalized VAR approach suggested by Diebold and Yilmaz (2012) to study spillovers of international swap markets. The Granger-causality tests are employed to examine the linkage of interest rate swap and stock markets. Findings This paper shows that a moderate spillover effect exists for the short- and long-term swap markets. Moreover, the results show that the short- and long-term swap markets of France and Germany have a larger impact on other countries’ swap markets than that of other countries’ swap markets on the French and German swap markets. Finally, the results indicate that the total volatility spillovers for the long-term swap markets have a larger influence on the total volatility spillover index of stock markets and the global stock market volatility than that of the short-term swap markets. Originality/value Prior literature has used impulse response and variance decomposition analyses to investigate international swap markets linkages. However, the results depend on the ordering of variables. This study uses the framework of Diebold and Yilmaz (2012) to overcome the ordering issue, and thus the authors can compute directional spillovers. This paper is the first study to explore the linkage of the total volatility spillover of swap markets and the stock markets.