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Adipose-derived mesenchymal stem cells (ADSCs) show considerable promise for clinical applications in regenerative medicine. We performed a large-scale single-cell transcriptomic sequencing of 24,358 cultured human ADSCs from three donors. We provide a high-quality dataset, which would be a valuable resource for dissecting the intrapopulation heterogeneity of cultured ADSCs as well as interrogating lineage priming patterns for any interested lineages at single-cell resolution.

Highlights d Single-cell transcriptomes of 55,611 cells from developing cardiac OFT in mice d Molecular signatures of six cell lineages and their subpopulations d Myocardial-to-VSMC trans-differentiation occurs during OFT development d Convergent development of VSMCs from myocardial and mesenchymal cells

We describe sonication-assisted liquid-phase exfoliation of rhombohedral germanium telluride (α-GeTe) to obtain a good dispersion of α-GeTe nanosheets in ethanol. The thickness of the α-GeTe nanosheets is dependent on the exfoliation conditions, and few-layer α-GeTe nanosheets of 2-4 layers and even monolayer α-GeTe were obtained. We use first-principles calculations to investigate the structural, electronic, and optical properties of monolayer and bulk α-GeTe and compare the optical band gap of centrifugally fractionated α-GeTe nanosheet dispersions with the computational predictions. We demonstrate that few layer α-GeTe nanosheets are purified selectively through centrifugation, and they exhibit high sensitivity to Fe3+. The scalable production of two-dimensional α-GeTe nanosheets can be used in the future optoelectronic industry.

Thoracic aortic aneurysm and dissection (TAAD) is a life-threatening condition characterized by medial layer degeneration of the thoracic aorta. A thorough understanding of the regulator changes during pathogenesis is essential for medical therapy development. To delineate the cellular and molecular changes during the development of TAAD, we performed single-cell RNA sequencing of thoracic aortic cells from β-aminopropionitrile-induced TAAD mouse models at three time points that spanned from the early to the advanced stages of the disease. Comparative analyses were performed to delineate the temporal dynamics of changes in cellular composition, lineage-specific regulation, and cell–cell communications. Excessive activation of stress-responsive and Toll-like receptor signaling pathways contributed to the smooth muscle cell senescence at the early stage. Three subpopulations of aortic macrophages were identified, i.e., Lyve1+ resident-like, Cd74high antigen-presenting, and Il1rn+/Trem1+ pro-inflammatory macrophages. In both mice and humans, the pro-inflammatory macrophage subpopulation was found to represent the predominant source of most detrimental molecules. Suppression of macrophage accumulation in the aorta with Ki20227 could significantly decrease the incidence of TAAD and aortic rupture in mice. Targeting the Il1rn+/Trem1+ macrophage subpopulation via blockade of Trem1 using mLR12 could significantly decrease the aortic rupture rate in mice. We present the first comprehensive analysis of the cellular and molecular changes during the development of TAAD at single-cell resolution. Our results highlight the importance of anti-inflammation therapy in TAAD, and pinpoint the macrophage subpopulation as the predominant source of detrimental molecules for TAAD. Targeting the IL1RN+/TREM1+ macrophage subpopulation via blockade of TREM1 may represent a promising medical treatment.