Atomically thin PtSe 2 films have attracted extensive research interests for potential applications in high-speed electronics, spintronics and photodetectors. Obtaining high quality, single crystalline thin films with large size is critical. Here we report the first successful layer-by-layer growth of high quality PtSe 2 films by molecular beam † The authors declare no competing financial interest. 1 arXiv:1703.04279v2 [cond-mat.mtrl-sci] 15 Mar 2017 epitaxy. Atomically thin films from 1 ML to 22 ML have been grown and characterized by low-energy electron diffraction, Raman spectroscopy and X-ray photoemission spectroscopy. Moreover, a systematic thickness dependent study of the electronic structure is revealed by angle-resolved photoemission spectroscopy (ARPES), and helical spin texture is revealed by spin-ARPES. Our work provides new opportunities for growing large size single crystalline films for investigating the physical properties and potential applications of PtSe 2 . KeywordsPtSe 2 , Molecular beam epitaxy (MBE), Raman, ARPES, Transition metal dichalcogenide (TMDC) Layered transition metal dichalcogenides (TMDCs) have attracted extensive interests for applications in electronics, optoelectronics and valleytronics due to the strong spin-orbit coupling, sizable band gap and tunability of the electronic structure by quantum confinement effect. [1][2][3][4] In the past decade, this has been witnessed by the significant efforts conducted on the atomically thin MoS 2 film. 5-7 However, its low mobility has limited applications, for inbstance, in high speed electronics. 8,9 Finding thin films of other TMDC with better properties is highly desirable. PtSe 2 has emerged as an interesting compound that belongs to TMDC.Although the bulk crystal is a semimetal, 10,11 monolayer (ML) platinum diselenide (PtSe 2 ) has been revealed to be a semiconductor with a band gap of ≈ 1.2 eV. 12 Importantly, the charge-carrier mobility of PtSe 2 has been predicted among the highest in TMDCs 9 and has been experimentally shown to be comparable to black phosphorene 13 yet with the advantage of much improved stability. 14 This makes PtSe 2 a promising candidate for high-speed electronics. Moreover, the hidden helical spin texture with spin-layer locking in monolayer PtSe 2 has been recently revealed, 15 and such spin physics induced by a local Rashba effect has great potential for electric field tunable spintronic devices. 16 In addition, remarkable performance

Arsenic (As) is a well-characterized human carcinogen but is generally not mutagenic. The evidence that As induces both loss of global DNA methylation and gene promoter DNA hypermethylation has suggested that epigenetic mechanisms may play an important role in As-induced carcinogenesis. In the present study, we examined the change in histone methylation by As exposure. In human lung carcinoma A549 cells, exposure to inorganic trivalent As (arsenite) increased H3K9 dimethylation (H3K9me2) and decreased H3K27 trimethylation (H3K27me3), both of which represent gene silencing marks, while increasing the global levels of the H3K4 trimethylation (H3K4me3), a gene-activating mark. The increase in H3K9me2 was mediated by an increase in the histone methyltransferase G9a protein and messenger RNA levels. We also observed strikingly significant altered histone modifications induced by very low-dose (0.1 microM) arsenite. Taken together, these results suggest a potential mechanism by which As induces carcinogenesis through the alteration of specific histone methylations that represent both gene silencing and activating marks. Furthermore, these marks are known to affect DNA methylation, and it is likely that arsenic's effect is not limited to histone modifications alone, but extends, perhaps by them, to DNA methylations as well. Future studies in our laboratory will address the genomic location of these silencing and activating marks using ChIP-on-chip technology.

The regeneration of bone tissue is regulated by both osteogenic and angiogenic growth factors which are expressed in a coordinated cascade of events. The aim of this study was to create a dual growth factor-release system that allows for time-controlled release to facilitate bone regeneration. We fabricated core−shell SF/PCL/PVA nanofibrous mats using coaxial electrospinning and layer-by-layer (LBL) techniques, where bone morphogenetic protein 2 (BMP2) was incorporated into the core of the nanofibers and connective tissue growth factor (CTGF) was attached onto the surface. Our study confirmed the sustained release of BMP2 and a rapid release of CTGF. Both in vitro and in vivo experiments demonstrated improvements in bone tissue recovery with the dual-drug release system. In vivo studies showed improvement in bone regeneration by 43% compared with single BMP2 release systems. Time-controlled release enabled by the core−shell nanofiber assembly provides a promising strategy to facilitate bone healing.

Histone H3 lysine 4 (H3K4) trimethylation (H3K4me3) at the promoter region of genes has been linked to transcriptional activation. In the present study, we found that hypoxia (1% oxygen) increased H3K4me3 in both normal human bronchial epithelial Beas-2B cells and human lung carcinoma A549 cells. The increase of H3K4me3 from hypoxia was likely caused by the inhibition of H3K4 demethylating activity, as hypoxia still increased H3K4me3 in methionine-deficient medium. Furthermore, an in vitro histone demethylation assay showed that 1% oxygen decreased the activity of H3K4 demethylases in Beas-2B nuclear extracts because ambient oxygen tensions were required for the demethylation reaction to proceed. Hypoxia only minimally increased H3K4me3 in the BEAS-2B cells with knockdown of JARID1A, which is the major histone H3K4 demethylase in this cell line. However, the mRNA and protein levels of JARID1A were not affected by hypoxia. GeneChip and pathway analysis in JARID1A knockdown Beas-2B cells revealed that JARID1A regulates the expression of hundreds of genes involved in different cellular functions, including tumorigenesis. Knocking down of JARID1A increased H3K4me3 at the promoters of HMOX1 and DAF genes. Thus, these results indicate that hypoxia might target JARID1A activity, which in turn increases H3K4me3 at both the global and genespecific levels, leading to the altered programs of gene expression and tumor progression.

Occupational exposure to nickel(Ni), chromium(Cr), and arsenic(As) containing compounds has been associated with lung cancer and other adverse health effects. Their carcinogenic properties may be attributable in part, to activation and/or repression of gene expression induced by changes in the DNA methylation status and histone tail post-translational modifications. Here we show that individual treatment with nickel, chromate, and arsenite all affect the gene activating mark H3K4 methylation. We found that nickel(1 mM), chromate(10 μM), and arsenite(1 μM) significantly increase tri-methyl H3K4 after 24 h exposure in human lung carcinoma A549 cells. Seven days of exposure to lower levels of nickel(50 and 100 μM), chromate(0.5 and 1 μM) or arsenite(0.1 0.5 and 1 μM) also increased tri-methylated H3K4 in A549 cells. This mark still remained elevated and inherited through cell division seven days following removal of 1 μM arsenite. We also demonstrate by dual staining immunofluorescence microscopy that both H3K4 tri-methyl and H3K9 di-methyl marks increase globally after 24 h exposure to each metal treatment in A549 cells. However, the trimethyl H3K4 and di-methyl H3K9 marks localize in different regions in the nucleus of the cell. Thus, our study provides further evidence that a mechanism(s) of carcinogenicity of nickel, chromate, and arsenite metal compounds may involve alterations of various histone tail modifications that may in turn affect the expression of genes that may cause transformation.