Improved computational modeling of the kinetics of the acetylperoxy + HO2 reaction.

The acetylperoxy + HO2 reaction has multiple impacts on the troposphere, with a triplet pathway leading to peracetic acid + O2 (reaction (1a)) competing with singlet pathways leading to acetic acid + O3 (reaction (1b)) and acetoxy + OH + O2 (reaction (1c)). A recent experimental study has reported branching fractions for these three pathways (α1a, α1b, and α1c) from 229 K to 294 K. We constructed a theoretical model for predicting α1a, α1b, and α1c using quantum chemical and Rice-Ramsperger-Kassel-Marcus/master equation (RRKM/ME) simulations. Our main quantum chemical method was Weizmann-1 Brueckner Doubles (W1BD) theory; we combined W1BD and equation-of-motion spin-flip coupled cluster (SF) theory to treat open-shell singlet structures. Using RRKM/ME simulations that included all conformers of acetylperoxy-HO2 pre-reactive complexes led to a 298 K triplet rate constant, k1a = 5.11 × 10-12 cm3 per molecule per s, and values of α1a in excellent agreement with experiment. Increasing the energies of all singlet structures by 0.9 kcal mol-1 led to a combined singlet rate constant, k1b+1c = 1.20 × 10-11 cm3 per molecule per s, in good agreement with experiment. However, our predicted variations in α1b and α1c with temperature are not nearly as large as those measured, perhaps due to the inadequacy of SF theory in treating the transition structures controlling acetic acid + O3 formation vs. acetoxy + OH + O2 formation.

Conditional Vitamin D Receptor Deletion Induces Fungal and Archaeal Dysbiosis and Altered Metabolites.

A vitamin D receptor (VDR) deficiency leads to the dysbiosis of intestinal bacteria and is associated with various diseases, including cancer, infections, and inflammatory bowel disease. However, the impact of a VDR deficiency on fungi and archaea is unknown. We conditionally deleted the VDR in Paneth cells (VDRΔPC), intestinal epithelial cells (VDRΔIEC), or myeloid cells (VDRΔLyz) in mice and collected feces for shotgun metagenomic sequencing and untargeted metabolomics. We found that fungi were significantly altered in each knockout (KO) group compared to the VDRLoxp control. The VDRΔLyz mice had the most altered fungi species (three depleted and seven enriched), followed by the VDRΔPC mice (six depleted and two enriched), and the VDRΔIEC mice (one depleted and one enriched). The methanogen Methanofollis liminatans was enriched in the VDRΔPC and VDRΔLyz mice and two further archaeal species (Thermococcus piezophilus and Sulfolobus acidocaldarius) were enriched in the VDRΔLyz mice compared to the Loxp group. Significant correlations existed among altered fungi, archaea, bacteria, and viruses in the KO mice. Functional metagenomics showed changes in several biologic functions, including decreased sulfate reduction and increased biosynthesis of cobalamin (vitamin B12) in VDRΔLyz mice relative to VDRLoxp mice. Fecal metabolites were analyzed to examine the involvement of sulfate reduction and other pathways. In conclusion, a VDR deficiency caused the formation of altered fungi and archaea in a tissue- and sex-dependent manner. These results provide a foundation about the impact of a host factor (e.g., VDR deficiency) on fungi and archaea. It opens the door for further studies to determine how mycobiome and cross-kingdom interactions in the microbiome community and metabolites contribute to the risk of certain diseases.