Synthesis, characterisation and electronic structure of SnS, SnS2 and Sn2S3

Tin sulfide is being widely investigated as an earth-abundant light harvesting material, but recorded efficiencies for SnS fall far below theoretical limits. We describe the synthesis and characterization of the single-crystal tin sulfides (SnS, SnS2, and Sn2S3) through chemical vapor transport, and combine electronic structure calculations with time-resolved microwave conductivity measurements to shed light on the underlying electrical properties of each material. We show that the coexistence of the Sn(II) and Sn(IV) oxidation states would limit the performance of SnS in photovoltaic devices due to the valence band alignment of the respective phases and the ''asymmetry'' in the underlying point defect behavior. Furthermore, our results suggest that Sn2S3, in addition to SnS, is a candidate material for low-cost thin-film solar cells

The chromatin landscape of healthy and injured cell types in the human kidney

There is a need to define regions of gene activation or repression that control human kidney cells in states of health, injury, and repair to understand the molecular pathogenesis of kidney disease and design therapeutic strategies. Comprehensive integration of gene expression with epigenetic features that define regulatory elements remains a significant challenge. We measure dual single nucleus RNA expression and chromatin accessibility, DNA methylation, and H3K27ac, H3K4me1, H3K4me3, and H3K27me3 histone modifications to decipher the chromatin landscape and gene regulation of the kidney in reference and adaptive injury states. We establish a spatially-anchored epigenomic atlas to define the kidney’s active, silent, and regulatory accessible chromatin regions across the genome. Using this atlas, we note distinct control of adaptive injury in different epithelial cell types. A proximal tubule cell transcription factor network of ELF3, KLF6, and KLF10 regulates the transition between health and injury, while in thick ascending limb cells this transition is regulated by NR2F1. Further, combined perturbation of ELF3, KLF6, and KLF10 distinguishes two adaptive proximal tubular cell subtypes, one of which manifested a repair trajectory after knockout. This atlas will serve as a foundation to facilitate targeted cell-specific therapeutics by reprogramming gene regulatory networks. © 2024, The Author(s).Open access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]