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压力系统是机体在压力源刺激下做出的一系列跨系统复杂性综合反应, 参与调节睡眠-觉醒周期、维持 正常生物钟及昼夜节律。2019 冠状病毒病 (COVID-19) 作为慢性压力性生活事件, 长期过度激活压力系统, 造成睡 眠结构的改变, 并以慢性压力、强压力源的形式影响记忆过程, 长期应激下压力记忆与恐惧记忆得到加强巩固, 加之 心理因素对睡眠压力的附加, 导致长期睡眠障碍。同时, 有别于其他压力, 严重急性呼吸综合征 (SARS) 相关冠状病 毒感染包括严重急性呼吸综合征冠状病毒2 (SARS-CoV-2) 可能是由于其可造成下丘脑-垂体-肾上腺 (HPA) 轴长期 无法恢复、大脑区域的直接靶向性损伤等因素, 使得压力系统产生特殊的长期效应, 从而参与了 “长新冠”-睡眠障 碍的发生。 [ABSTRACT FROM AUTHOR]

BACKGROUND: Osteoporosis is often accompanied by sarcopenia and an increased risk of fractures from falls. Recent studies have indicated a close relationship between lipid metabolism and sarcopenia. Abnormal lipid metabolism may directly impact muscle physiological function and metabolism. OBJECTIVE: To investigate the relationship between lipid metabolism and sarcopenia and evaluate their causal relationship using Mendelian randomization. METHODS: Mendelian randomization was used to explore the causal relationship between low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, and muscle mass. Research data from genome-wide association studies were used and a sensitivity analysis was conducted to verify the reliability of the results. Approximate indicators of muscle mass, including trunk lean mass and appendicular lean mass, were used as outcome measures. RESULTS AND CONCLUSION: The study found a negative correlation of low-density lipoprotein cholesterol and triglycerides with muscle mass, while no correlation was observed between high-density lipoprotein cholesterol and muscle mass. The results of the sensitivity analysis indicated a robust causal relationship. Using Mendelian randomization, this study provides evidence of a causal relationship between low-density lipoprotein cholesterol and triglycerides and muscle mass. This finding deepens our understanding of the effects of lipids on sarcopenia and has important clinical implications for the prevention and treatment of sarcopenia and osteoporosis. [ABSTRACT FROM AUTHOR]

Objective To study the effect of VD3 and its metabolites on the osteoblast differentiation and biomineralization in different concentrations. Methods Osteoblasts were isolated with collagenase digestion method . The control group, VDJ treatment group, 25(0H)VD3 treatment group, and la, 25(0H) 2VD3 treatment group were established, respectively. CCK-8 test was used to detect the proliferation rate of osteoblasts. PNPP method was used for the determination of alkaline phosphatase activity. Calcium content determination, ELISA, and real-time quantitative polymerase chain reaction were used to evaluate the response of osteoblasts to VD3, 25 (OH) VDJ, or la, 25 (OH) 2 VDJ. The effects of VD3 and its metabolites on the differentiation and biomineralization of osteoblasts were evaluated with osteoblast marker analysis. Results The experimental result confirmed that VD3 and its metabolites had no cytotoxicity to osteoblasts. The proliferation of osteoblasts was promoted significantly with 200 nmol/L of VD3 only. It was not promoted significantly with 25 ( OH) VD3 and 1 a, 25 (OH) 2 VD,. Moreover, 25 (OH) VDJ and 1 a, 25 (OH) 2 VDJ up-regulated the transcription activity of CYP24Al gene in osteoblasts, but did not metabolize VD3 and 25 (OH) VD3 directly. The expression of osteogenic markers (Runx2, ALP, etc.) was promoted by 25 (OH) VDJ and la, 25 (OH) 2 VD3 in a dose-dependent manner. More importantly, the gene and protein expressions of osteocalcin and the biomineralization level of osteoblasts were promoted by 25 (OH) VDJ only. Conclusion In vitro, 25 ( OH) VD3 induces osteoblast differentiation and biomineralization, which can provide evidence for its application in clinical osteoporosis and bone tissue engineering. [ABSTRACT FROM AUTHOR]