真实世界数据相关标准体系研究与应用进展

阐述真实世界数据标准体系和研究进展,分析国内真实世界数据标准面临的挑战并提出相关建议,包括在行业内整体全面规划医学语义标准和数据模型、进一步细化个人数据使用和调用的管理方式等,为我国真实世界数据相关标准制定提供有力依据。     

DRG/DIP付费下中医药医保支付改革的现实困境、典型经验及政策建议

中医药是中华民族的传统瑰宝,具有独特诊疗优势和疗效价值。医保支付方式改革要与中医药事业发展协同共进,兼容并蓄发展。基于国家当前正在推进的医保按疾病诊断相关分组（DRG）和按病种分值付费（DIP）付费的改革背景,剖析了中医医保支付面临的困境与挑战,将已经出台了中医倾斜支付政策的滨州、柳州、南京和杭州作为医保倾斜中医支付的典型案例,从病种遴选范围、医疗机构管理制度、费用结算倾斜机制3个方面,对比分析了各自的政策特点与改革经验。单纯的DRG/DIP付费方式改革并不能有效支持中医药传承创新发展的现实问题,各地应基于本地中医药发展实际,因地制宜地打出一套倾斜支付的政策“组合拳”。     

Aconitum carmichaelii protects against acetaminophen-induced hepatotoxicity via B-cell lymphoma-2 protein-mediated inhibition of mitochondrial dysfunction

We previously reported the clinical profile of processed Aconitum carmichaelii (AC, Aconibal^®), which included inhibition of cytochrome P450 (CYP) 2E1 activity in healthy male adults. CYP2E1 is recognized as the enzyme that initiates the cascade of events leading to acetaminophen (APAP)-induced toxicity. However, no studies have characterized its role in APAP-induced hepatic injury. Here, we investigated the protective effects of AC on APAP-induced hepatotoxicity via mitochondrial dysfunction. AC (5–500 μg/mL) significantly inhibited APAP-induced reduction of glutathione. In addition, AC decreased mitochondrial membrane potential (Δψm) and B-cell lymphoma 2 (Bcl-2)-associated X protein levels (% change 46.63) in mitochondria. Moreover, it increased Bcl-2 (% change 55.39) and cytochrome C levels (% change 38.33) in mitochondria, measured using immunofluorescence or a commercial kit. Furthermore, cell membrane integrity was preserved and nuclear fragmentation inhibited by AC. These results demonstrate that AC protects hepatocytes against APAP-induced toxicity by inhibiting mitochondrial dysfunction.     

Decabromodiphenyl ether-induced PRKACA hypermethylation contributed to glycolipid metabolism disorder via regulating PKA/AMPK pathway in rat and L-02 cells

BDE-209 is the most prevalent congener of polybrominated diphenyl ethers and has high bioaccumulation in humans and animals. BDE-209 has been reported to disrupt glycolipid metabolism, but the mechanisms are still unclear. In this study, we found that BDE-209 induced liver tissue injury and hepatotoxicity, increased the glucose and total cholesterol levels in the serum of rats, and increased glucose and triglyceride levels in L-02 cells. BDE-209 exposure changed the PKA, p-PKA, AMPK, p-AMPK, ACC, and FAS expression in rats’ liver and L-02 cells. Moreover, BDE-209 induced PRKACA-1 hypermethylation in L-02 cells. AMPK activator (AICAR) inhibited the changes of p-AMPK, ACC, and FAS expression and elevation of glucose and triglyceride levels induced by BDE-209. DNA methylation inhibitor (5-Aza-CdR) reversed BDE-209 induced alters of PKA/AMPK/ACC/FAS signaling pathway. These results demonstrated that BDE-209 could disrupt the glycolipid metabolism by causing PRKACA-1 hypermethylation to regulate the PKA/AMPK signaling pathway in hepatocytes.