Typical Raman spectra of transition metal dichalcogenides (TMDs) display two prominent peaks, E2g and A1g, that are well separated from each other. We find that these modes are degenerate in bulk WSe2 yielding one single Raman peak. As the dimensionality is lowered, the observed peak splits in two as a result of broken degeneracy. In contrast to our experimental findings, our phonon dispersion calculations reveal that these modes remain degenerate independent of the number of layers. Interestingly, for minuscule biaxial strain the degeneracy is preserved but once the crystal symmetry is broken by uniaxial strain, the degeneracy is lifted. Our calculated phonon dispersion for uniaxially strained WSe2 shows a perfect match to the measured Raman spectrum which suggests that uniaxial strain exists in WSe2 flakes possibly induced during the sample preparation and/or as a result of interaction between WSe2 and the substrate. Furthermore, we find that WSe2 undergoes an indirect to direct bandgap transition from bulk to monolayers which is ubiquitous for semiconducting TMDs. These results not only allow us to understand the vibrational properties of WSe2 but also provides detailed insight to their physical properties.
Dexamethasone (Dex)-induced osteoporosis has been described as the most severe side effect in long-term glucocorticoid therapy. The decreased bone mass and the increased marrow fat suggest that Dex possibly shifts the differentiation of bone marrow stromal cells (BMSCs) to favor adipocyte over osteoblast, but the underlying mechanisms are still unknown. In this paper, we established a Dex-induced osteoporotic mouse model, and found that BMSCs from Dex-treated mice are more likely to differentiate into adipocyte than those from control mice, even under the induction of bone morphogenetic protein-2 (BMP2). We also discovered both in vitro and in vivo that the expression level of adipocyte regulator CCAAT/enhancer-binding protein alpha (C/EBPalpha) is significantly upregulated in Dex-induced osteoporotic BMSCs during osteoblastogenesis by a mechanism that involves inhibited DNA hypermethylation of its promoter. Knockdown of C/EBPalpha in Dex-induced osteoporotic cells rescues their differentiation potential, suggesting that Dex shifts BMSC differentiation by inhibiting C/EBPalpha promoter methylation and upregulating its expression level. We further found that the Wnt/beta-catenin pathway is involved in Dex-induced osteoporosis and C/EBPalpha promoter methylation, and its activation by LiCl rescues the effect of Dex on C/EBPalpha promoter methylation and osteoblast/adipocyte balance. This study revealed the C/EBPalpha promoter methylation mechanism and evaluated the function of Wnt/beta-catenin pathway in Dex-induced osteoporosis, providing a useful therapeutic target for this type of osteoporosis.
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