a b s t r a c tNanocomposite engineering has been proved effective in diverse regimes of material research to attain a performance beyond each constituent phase. In this work, Yb-filled CoSb 3 (bulk matrix/host)-Bi 0.4 Sb 1.6 Te 3 (secondary inclusion) thermoelectric nanocomposites have been synthesized via an ex situ process. Bi 0.4 Sb 1.6 Te 3 inclusions are mainly distributed at the grain boundaries of Yb 0.2 Co 4 Sb 12 matrix in the composites. In particular, Te diffuses in situ from Bi 0.4 Sb 1.6 Te 3 through Yb 0.2 Co 4 Sb 12 matrix during the hot pressing process. This, combined with the grain boundary effect, results in favorable changes in the carrier concentration, carrier mobility, electrical resistivity, Seebeck coefficient, and thermal conductivity. Such synergistic changes are notably absent in the stand-alone Te-doped Yb-filled CoSb 3 , suggesting the key role of diffusion and grain boundaries. As a result, a maximum ZT value of 0.96 has been attained for Yb 0.2 Co 4 Sb 12 -2 wt% Bi 0.4 Sb 1.6 Te 3 at 650 K. The present work opens a new avenue towards high performance thermoelectric composites via controlled inter-constituent diffusion and grain boundary effect.

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Nanocomposites are becoming a new paradigm in thermoelectric study: by incorporating nanophase(s) into a bulk matrix, a nanocomposite often exhibits unusual thermoelectric properties beyond its constituent phases. To date most nanophases are binary, while reports on ternary nanoinclusions are scarce. In this work, we conducted an exploratory study of introducing ternary (Ag2Te)x(Sb2Te3)1−x inclusions in the host matrix of Yb0.25Co4Sb12. Yb0.25Co4Sb12-4wt% (Ag2Te)x(Sb2Te3)1−x nanocomposites were prepared by a melting-milling-hot-pressing process. Microstructural analysis showed that poly-dispersed nanosized Ag-Sb-Te inclusions are distributed on the grain boundaries of Yb0.25Co4Sb12 coarse grains. Compared to the pristine nanoinclusion-free sample, the electrical conductivity, Seebeck coefficient, and thermal conductivity were optimized simultaneously upon nanocompositing, while the carrier mobility was largely remained. A maximum ZT of 1.3 was obtained in Yb0.25Co4Sb12-4wt% (Ag2Te)0.42(Sb2Te3)0.58 at 773 K, a ~ 40% increase compared to the pristine sample. The electron and phonon mean-free-path were estimated to help quantify the observed changes in the carrier mobility and lattice thermal conductivity.

Endothelial cell senescence has a vital implication for vascular dysfunction, leading to age-related cardiovascular disease, especially hypertension and atherosclerosis. E2F transcription factor 2 (E2F2) plays a critical role in cell proliferation, differentiation, and DNA damage response. Up to date, no study has ever connected E2F2 to vascular endothelial cell senescence. Here, we demonstrate that E2F2 is involved in endothelial cellular senescence. We found that E2F2 expression is decreased during the replicative senescence of human umbilical vein endothelial cells (HUVECs) and the aortas of aged mice. The knockdown of E2F2 in young HUVECs induces premature senescence characterized by an increase in senescence-associated β-galactosidase (SA-β-gal) activity, a reduction in phosphorylated endothelial nitric oxide synthase (p-eNOS) and sirtuin 1 (SIRT1), and the upregulation of senescence-associated secretory phenotype (SASP) IL-6 and IL-8. The lack of E2F2 promoted cell cycle arrest, DNA damage, and cell proliferation inhibition. Conversely, E2F2 overexpression reversed the senescence phenotype and enhanced the cellular function in the senescent cells. Furthermore, E2F2 deficiency downregulated downstream target genes including CNNA2, CDK1, and FOXM1, and overexpression restored the expression of these genes. Our findings demonstrate that E2F2 plays an indispensable role in endothelial cell senescence.

Natriuretic peptide receptor 1 (NPR1) serves as a modulator of vascular endothelial homeostasis. Interactions between monocytes and endothelial cells may initiate endothelium dysfunction, which is known as an early hallmark of atherosclerosis. In this study, we performed RNA-sequencing analysis for the aorta of Npr1 knockout (Npr1+/−) mice and found that differentially expressed genes were significantly related to cell adhesion. This result was supported by an increased expression of intercellular adhesion molecule 1 (ICAM-1) in the aortic endothelium of Npr1+/− mice. Moreover, we observed that the knockdown of NPR1 increased ICAM-1 expression and promoted THP-1 monocyte adhesion to human umbilical vein endothelial cells (HUVECs). NPR1 overexpression decreased ICAM-1 expression and inhibited the adhesion of monocytes to HUVECs treated by TNF-α (a cell adhesion inducer). Further analysis showed that adhesion-related genes were enriched in the focal adhesion signaling pathway, in which integrin beta 4 (Itgb4) was determined as a key gene. Notably, ITGB4 expression increased in vascular endothelium of Npr1+/− mice and in NPR1-knockdown HUVECs. The deficiency of ITGB4 decreased ICAM-1 expression and attenuated monocyte adhesion to NPR1-knockdown endothelial cells. Additionally, a reduced NPR1 and an increased ITGB4 expression level were found in an atherosclerosis mouse model. In conclusion, our findings demonstrate that NPR1 deficiency increases vascular endothelial cell adhesion by stimulating ITGB4 expression, which may contribute to the development of atherosclerosis.