Equine infectious anemia is an equine disease caused by equine infectious anemia virus, which was first reported in 1840. Equine infectious anemia virus research in China started in the 1960s, focusing on etiology, pathology, diagnosis, and immunology. Notably, in 1978 an attenuated vaccine was successfully developed for equine infectious anemia virus, effectively preventing equine infectious anemia virus in China. This article will review equine infectious anemia virus in China, including past and recent research, and commemorate scientists who have made great contributions to equine infectious anemia virus prevention.

The genome is transcriptionally inert at fertilization and must be activated through a remarkable developmental process called zygotic genome activation (ZGA). Epigenetic reprogramming contributes significantly to the dynamic gene expression during ZGA, however the mechanism has yet to be resolved. Here, we find histone deacetylase 1 and 2 (HDAC1/2) can regulate ZGA through the lysine deacetylase activity. Notably, in mouse embryos, overexpression of HDAC1/2 dominant negative mutant leads to a developmental arrest at 2-cell stage. RNA-seq reveals that 64% of down-regulated genes are ZGA genes and 49% of up-regulated genes are developmental genes. Inhibition of the deacetylase activity of HDAC1/2 causes a failure of histone deacetylation at multiple sites including H4K5, H4K16, H3K14, H3K18, and H3K27. ChIP-seq analysis exhibits an increase and decrease of H3K27ac enrichment at promoters of up- and down-regulated genes, respectively. Moreover, HDAC1 mutants prohibited the removal of H3K4me3 via impeding KDM5s. Importantly, the developmental block can be greatly rescued through Kdm5b injection and expression of the majority of dysregulated genes partially corrected. Similar functional significance of HDAC1/2 is conserved in cattle embryos. Overall, we propose that HDAC1/2 is indispensable for ZGA via creating correct transcriptional repressive and active states in mouse and bovine embryos.

Biomimetic total syntheses of Festuclavine and Pyroclavine were achieved by a sequential radical coupling. The key steps include intramolecular decarboxylative Giese reaction to form the central C ring and 4-nitrobenzenesulfonyl (Ns)-directed indole C4–H olefination to introduce the indole C4 component. In addition, D-ring formation was completed by decarboxylative alkenylation and intramolecular SN2 reaction.

Mitochondrial dysfunction plays an important role in gamma-radiation-induced mediating oxidative stress. Scavenging radiation-induced reactive oxygen species (ROS) can help mitochondria to maintain their physiological function. Rosmarinic acid is a polyphenol antioxidant that can scavenge radiation-induced ROS, but the structure prevents it from accumulating in mitochondria. In this study, we designed and synthesized a novel rosmarinic acid derivative (Mito-RA) that could use the mitochondrial membrane potential to enter the organelle and scavenge ROS. The DCFH-DA assay revealed that Mito-RA was more effective than rosmarinic acid at scavenging ROS. DNA double-strand breaks, chromosomal aberration, micronucleus and comet assays demonstrated the ability of Mito-RA to protect against radiation-induced oxidative stress in vitro. These findings demonstrate the potential of Mito-RA as an antioxidant, which can penetrate mitochondria, scavenge ROS and protect cells against radiation-induced oxidative damage.