Lignin is a major component of plant cell walls that is essential to their function. However, the strong bonds that bind the various subunits of lignin, and its cross-linking with other plant cell wall polymers, make it one of the most important factors in the recalcitrance of plant cell walls against polysaccharide utilization. Plants make lignin from a variety of monolignols including p-coumaryl, coniferyl, and sinapyl alcohols to produce the three primary lignin units: p-hydroxyphenyl, guaiacyl, and syringyl, respectively, when incorporated into the lignin polymer. In grasses, these monolignols can be enzymatically preacylated by p-coumarates prior to their incorporation into lignin, and these monolignol conjugates can also be "monomer" precursors of lignin. Although monolignol p-coumarate-derived units may comprise up to 40% of the lignin in some grass tissues, the p-coumarate moiety from such conjugates does not enter into the radical coupling (polymerization) reactions of lignification. With a greater understanding of monolignol p-coumarate conjugates, grass lignins could be engineered to contain fewer pendent p-coumarate groups and more monolignol conjugates that improve lignin cleavage. We have cloned and expressed an enzyme from rice that has p-coumarate monolignol transferase activity and determined its kinetic parameters.

Wastewater emissions from textile factories cause serious environmental problems. Manganese peroxidase (MnP) is an oxidoreductase with ligninolytic activity and is a promising biocatalyst for the biodegradation of hazardous environmental contaminants, and especially for dye wastewater decolorization. This article first summarizes the origin, crystal structure, and catalytic cycle of MnP, and then reviews the recent literature on its application to dye wastewater decolorization. In addition, the application of new technologies such as enzyme immobilization and genetic engineering that could improve the stability, durability, adaptability, and operating costs of the enzyme are highlighted. Finally, we discuss and propose future strategies to improve the performance of MnP-assisted dye decolorization in industrial applications.

Previous studies reveal that combining non-thermal plasma with cheap metal catalysts achieved a significant synergy of enhancing performance of NH₃ decomposition, and this synergy strongly depended on the properties of the catalyst used. In this study, techniques of vacuum-freeze drying and plasma calcination were employed to improve the conventional preparation method of catalyst, aiming to enhance the activity of plasma-catalytic NH₃ decomposition. Compared with the activity of the catalyst prepared by a conventional method, the conversion of NH₃ significantly increased by 47% when Co/fumed SiO₂ was prepared by the improved method, and the energy efficiency of H₂ production increased from 2.3 to 5.7 mol(kW·h)⁻¹ as well. So far, the highest energy efficiency of H₂ formation of 15.9 mol(kW·h)⁻¹ was achieved on improved prepared Co/fumed SiO₂ with 98.0% ammonia conversion at the optimal conditions. The improved preparation method enables cobalt species to be highly dispersed on fumed SiO₂ support, which creates more active sites. Besides, interaction of Co with fumed SiO₂ and acidity of the catalyst were strengthened according to results of H₂-TPR and NH₃-probe experiments, respectively. These results demonstrate that employing vacuum-freeze drying and plasma calcination during catalyst preparation is an effective approach to manipulate the properties of catalyst, and enables the catalyst to display high activity towards plasma-catalytic NH₃ decomposition to produce H₂.

Alcohol intake is thought to be a risk factor for breast cancer, but the causal relationship and carcinogenic mechanisms are not clear. We performed an up-to-date meta-analysis of prospective studies to assess observational association, and then conducted MR analysis to make causal inference based on the genetic predisposition to alcohol consumption (“drinks per week”) and pathological drinking behaviours (“alcohol use disorder” and “problematic alcohol use”), as well as genetically predicted DNA methylation at by alcohol-related CpG sites in blood. We found an observational dose–response association between alcohol intake and breast cancer incidence with an additional risk of 4% for per 10 g/day increase in alcohol consumption. Genetic predisposition to alcohol consumption (“drinks per week”) was not causally associated with breast cancer incidence at the OR of 1.01 (95% CI 0.84, 1.23), but problematic alcohol use (PAU) was linked to a higher breast cancer risk at the OR of 1.76 (95% CI 1.04, 2.99) when conditioning on alcohol consumption. Epigenetic MR analysis identified four CpG sites, cg03260624 near CDC7 gene, cg10816169 near ZNF318 gene, cg03345232 near RIN3 gene, and cg26312998 near RP11-867G23.13 gene, where genetically predicted epigenetic modifications were associated with an increased breast cancer incidence risk. Our findings re-affirmed that alcohol consumption is of high risk for breast cancer incidence even at a very low dose, and the pathogenic effect of alcohol on breast cancer could be due to pathological drinking behaviour and epigenetic modification at several CpG sites, which could be potential intervention targets for breast cancer prevention.