Effects of 2,6-di-tert-butyl-hydroxytotulene and mineral-lubricant base oils on microbial communities during lubricants biodegradation.

2,6-Di-tert-butyl-hydroxytotulene (BHT) is an additive commonly used in the manufacturing of lubricants to improve their antioxidant properties. However, in this study, we found that BHT affects the biodegradation of bio-lubricants by influencing the microbial community during the degradation of bio-lubricants. Specifically, BHT was found to reduce bacterial richness in activated sludge, but it increased the relative abundance of Actinobacteria (from 21.24% to 40.89%), Rhodococcus (from 17.15% to 31.25%), Dietzia (from 0.069% to 6.49%), and Aequorivita (from 0.90% to 1.85%). LEfSe analysis and co-occurrence network analysis suggested that Actinobacteria could be potential biomarkers and keystone taxa in microbial communities. Using the MetaCyc pathway database, the study found that BHT interfered with cellular biosynthetic processes. Additionally, the study also showed that mineral-lubricant base oils, which are difficult to degrade, significantly altered the diversity and composition of the microbiome. Overall, the findings demonstrate that BHT and mineral-lubricant base oils can substantially alter bacterial richness, structure, and function, potentially contributing to the difficulty in degrading lubricants. These findings have implications for the development of more biodegradable lubricants and the management of industrial waste containing lubricants.

Epigenetic modifications in abdominal aortic aneurysms: from basic to clinical.

Abdominal Aortic Aneurysm (AAA) is a disease characterized by localized dilation of the abdominal aorta, involving multiple factors in its occurrence and development, ultimately leading to vessel rupture and severe bleeding. AAA has a high mortality rate, and there is a lack of targeted therapeutic drugs. Epigenetic regulation plays a crucial role in AAA, and the treatment of AAA in the epigenetic field may involve a series of related genes and pathways. Abnormal expression of these genes may be a key factor in the occurrence of the disease and could potentially serve as promising therapeutic targets. Understanding the epigenetic regulation of AAA is of significant importance in revealing the mechanisms underlying the disease and identifying new therapeutic targets. This knowledge can contribute to offering AAA patients better clinical treatment options beyond surgery. This review systematically explores various aspects of epigenetic regulation in AAA, including DNA methylation, histone modification, non-coding RNA, and RNA modification. The analysis of the roles of these regulatory mechanisms, along with the identification of relevant genes and pathways associated with AAA, is discussed comprehensively. Additionally, a comprehensive discussion is provided on existing treatment strategies and prospects for epigenetics-based treatments, offering insights for future clinical interventions.