Association Between Phenotypic Age and the Risk of Mortality in Patients With Heart Failure: A Retrospective Cohort Study.

BACKGROUND: Chronological age (CA) is an imperfect proxy for the true biological aging state of the body. As novel measures of biological aging, Phenotypic age (PhenoAge) and Phenotypic age acceleration (PhenoAgeAccel), have been shown to identify morbidity and mortality risks in the general population. HYPOTHESIS: PhenoAge and PhenoAgeAccel might be associated with mortality in heart failure (HF) patients. METHODS: This cohort study extracted adult data from the National Health and Nutrition Examination Survey (NHANES) databases. Weighted univariable and multivariable Cox models were performed to analyze the effect of PhenoAge and PhenoAgeAccel on all-cause mortality in HF patients, and hazard ratio (HR) with 95% confidence intervals (CI) was calculated. RESULTS: In total, 845 HF patients were identified, with 626 all-cause mortality patients. The findings suggested that (1) each 1- and 10-year increase in PhenoAge were associated with a 3% (HR = 1.03, 95% CI: 1.03-1.04) and 41% (HR = 1.41, 95% CI: 1.29-1.54) increased risk of all-cause mortality, respectively; (2) when the PhenoAgeAccel < 0 as reference, the ≥ 0 group was associated with higher risk of all-cause mortality (HR = 1.91, 95% CI = 1.49-2.45). Subgroup analyses showed that (1) older PhenoAge was associated with an increased risk of all-cause mortality in all subgroups; (2) when the PhenoAgeAccel < 0 as a reference, PhenoAgeAccel ≥ 0 was associated with a higher risk of all-cause mortality in all subgroups. CONCLUSION: Older PhenoAge was associated with an increased risk of all-cause mortality in HF patients. PhenoAge and PhenoAgeAccel can be used as convenient tools to facilitate the identification of at-risk individuals with HF and the evaluation of intervention efficacy.

Pricing of Shanghai stock exchange 50 ETF options based on different volatility models.

On March 15, 2022, the volume of trade of the Shanghai Stock Exchange (SSE) 50 ETF option contracts and the CSI 300 ETF option contracts exceeded 10 million for the first time, of which 5,707,400 50 ETF options were traded, and SSE 50 ETF options, as the main force, has become one of the most active ETF option varieties in the world after seven years of vigorous development. The SSE 50 ETF options receive highlights in risk-free arbitrage, hedging, risk management and other aspects. In order to give full play to the function of the SSE 50 ETF options, it is necessary to conduct studies on their pricing. This paper adopts the traditional classical models for pricing European-style options, the BSM model and the volatility model, to price call options and put options of the SSE ETF, and meanwhile analyzes the volatility of the SSE 50 ETF. The empirical results suggest that (1) the volatility of SSE 50 ETF has a weak leverage effect or no leverage effect, which converges with the existence of the inverse leverage effect of the SSE index; (2) the BSM model will underestimate the price of SSE 50 ETF options and is only ideal for pricing in-the-money (ITM) options; while out-of-the-money (OTM) options are highly influenced by time value and therefore cannot be accurately priced.

MicroRNA-494-3p facilitates the progression of bladder cancer by mediating the KLF9/RGS2 axis.

Bladder cancer (BC) is a familiar malignancy with high morbidity and mortality. The effect of treatment is unsatisfactory after the metastasis and invasion of BC. Hence, more studies should be carried out to explore the metastasis of BC. RT-qPCR or/and western blot was conducted to evaluate miR-494-3p, KLF9, and RGS2 expression. Cell proliferation and invasion were estimated by MTT assay and transwell assay, respectively. Cell migration was tested by wound healing assay and transwell assay. Dual-luciferase reporter gene assay was employed to validate the interplay between miR-494-3p and KLF9 mRNA. The interaction between KLF9 and RGS2 promoter was verified using dual-luciferase reporter gene assay and chromatin immunoprecipitation (ChIP) assay. miR-494-3p expression was upregulated, whereas KLF9 and RGS2 were downregulated in BC cells. miR-494-3p inhibition was competent to limit the growth of BC cells. KLF9 knockdown abolished the miR-494-3p depletion-mediated inhibitory growth of BC cells. Mechanistically, we found that KLF9 was a downstream gene of miR-494-3p and could bind to the promoter region of RGS2 to promote the expression of RGS2. Moreover, RGS2 knockdown abrogated the suppressive effects of miR-494-3p knockdown on the proliferation, migration, and invasion of BC cells. Notably, miR-494-3p inhibition obstructed the tumor growth in nude mice. miR-494-3p silencing inhibited the progression of BC by regulating the KLF9/RGS2 axis in vitro and in vivo, which laid the foundation for experiments of miR-494-3p in BC and provided therapeutic targets for BC.