ABSTRACT
This research analyses the relative efficacy of gold price, financial market, and stock exchange hedging against sectoral and industry-level global stock market returns. Incorporating Gold into equity-based asset allocation techniques and assessing the stock market and financial sector during the COVID-19 epidemic is one way to diversify your portfolio and reduce risk. After orthogonalizing raw returns concerning a robust collection of relevant universal variables, we conduct our analysis inside a bivariate GARCH(p, q) framework. To further assess ideal portfolio proportions and the efficacy of hedging methods, we expand the volatility spillovers study by calculating the optimal weights for a minimal risk portfolio and determining the hedge ratio. In high-volatility environments, our results show which financial market and stock exchange sectors and industries investors should prioritize to minimize the risk and maximize reward. Use of country-specific macroeconomic variables indices to supplement the worldwide index, (3) separate analysis for the COVID-19 first wave due to the existing argument that the pandemic raises unexpected market events and our early data showing co-movement among the three unpredictability metrics during the pandemic. These findings have important implications for portfolio entrepreneurs and business investors looking to buy international equities.
ABSTRACT
Transmissible gastroenteritis virus (TGEV), a member of the coronavirus family, is the pathogen responsible for transmissible gastroenteritis, which results in mitochondrial dysfunction in host cells. Previously, we identified 123 differentially expressed circular RNAs (cRNA)from the TGEV-infected porcine intestinal epithelial cell line jejunum 2 (IPEC-J2). Previous bioinformatics analysis suggested that, of these, circBIRC6 had the potential to regulate mitochondrial function. Furthermore, mitochondrial permeability transition, a key step in the process of mitochondrial dysfunction, is known to be caused by abnormal opening of mitochondrial permeability transition pores (mPTPs) regulated by the voltage-dependent anion-selective channel protein 1 (VDAC)-Cyclophilin D (CypD) complex. Therefore, in the present study, we investigated the effects of circBIRC6-2 on mitochondrial dysfunction and opening of mPTPs. We found that TGEV infection reduced circBIRC6-2 levels, which in turn reduced mitochondrial calcium (Ca2+) levels, the decrease of mitochondrial membrane potential, and opening of mPTPs. In addition, we also identified ORFs and internal ribosomal entrance sites within the circBIRC6-2 RNA. We demonstrate circBIRC6-2 encodes a novel protein, BIRC6-236aa, which we show inhibits TGEV-induced opening of mPTPs during TGEV infection. Mechanistically, we identified an interaction between BIRC6-236aa and VDAC1, suggesting that BIRC6-236aa destabilizes the VDAC1-CypD complex. Taken together, the results suggest that the novel protein BIRC6-236aa encoded by cRNA circBIRC6-2 inhibits mPTP opening and subsequent mitochondrial dysfunction by interacting with VDAC1.