Graphene and hexagonal boron nitride (h-BN) have similar crystal structures with a lattice constant difference of only 2%. However, graphene is a zero-bandgap semiconductor with remarkably high carrier mobility at room temperature, whereas an atomically thin layer of h-BN is a dielectric with a wide bandgap of ∼5.9 eV. Accordingly, if precise two-dimensional domains of graphene and h-BN can be seamlessly stitched together, hybrid atomic layers with interesting electronic applications could be created. Here, we show that planar graphene/h-BN heterostructures can be formed by growing graphene in lithographically patterned h-BN atomic layers. Our approach can create periodic arrangements of domains with size ranging from tens of nanometres to millimetres. The resulting graphene/h-BN atomic layers can be peeled off the growth substrate and transferred to various platforms including flexible substrates. We also show that the technique can be used to fabricate two-dimensional devices, such as a split closed-loop resonator that works as a bandpass filter.

Perfect graphene is believed to be the strongest material. However, the useful strength of large-area graphene with engineering relevance is usually determined by its fracture toughness, rather than the intrinsic strength that governs a uniform breaking of atomic bonds in perfect graphene. To date, the fracture toughness of graphene has not been measured. Here we report an in situ tensile testing of suspended graphene using a nanomechanical device in a scanning electron microscope. During tensile loading, the pre-cracked graphene sample fractures in a brittle manner with sharp edges, at a breaking stress substantially lower than the intrinsic strength of graphene. Our combined experiment and modelling verify the applicability of the classic Griffith theory of brittle fracture to graphene. The fracture toughness of graphene is measured as the critical stress intensity factor of 4:0 AE 0:6 MPa ffiffiffiffi m p and the equivalent critical strain energy release rate of 15.9 J m À 2 . Our work quantifies the essential fracture properties of graphene and provides mechanistic insights into the mechanical failure of graphene.

Graphene (G) and atomic layers of hexagonal boron nitride (h-BN) are complementary two-dimensional materials, structurally very similar but with vastly different electronic properties. Recent studies indicate that h-BN atomic layers would be excellent dielectric layers to complement graphene electronics. Graphene on h-BN has been realized via peeling of layers from bulk material to create G/h-BN stacks. Considering that both these layers can be independently grown via chemical vapor deposition (CVD) of their precursors on metal substrates, it is feasible that these can be sequentially grown on substrates to create the G/h-BN stacked layers useful for applications. Here we demonstrate the direct CVD growth of h-BN on highly oriented pyrolytic graphite and on mechanically exfoliated graphene, as well as the large area growth of G/h-BN stacks, consisting of few layers of graphene and h-BN, via a two-step CVD process. The G/h-BN film is uniform and continuous and could be transferred onto different substrates for further characterization and device fabrication.

SummaryHere we describe a proteomic data resource for the NCI-60 cell lines generated by pressure cycling technology and SWATH mass spectrometry. We developed the DIA-expert software to curate and visualize the SWATH data, leading to reproducible detection of over 3,100 SwissProt proteotypic proteins and systematic quantification of pathway activities. Stoichiometric relationships of interacting proteins for DNA replication, repair, the chromatin remodeling NuRD complex, β-catenin, RNA metabolism, and prefoldins are more evident than that at the mRNA level. The data are available in CellMiner (discover.nci.nih.gov/cellminercdb and discover.nci.nih.gov/cellminer), allowing casual users to test hypotheses and perform integrative, cross-database analyses of multi-omic drug response correlations for over 20,000 drugs. We demonstrate the value of proteome data in predicting drug response for over 240 clinically relevant chemotherapeutic and targeted therapies. In summary, we present a novel proteome resource for the NCI-60, together with relevant software tools, and demonstrate the benefit of proteome analyses.

MicroRNAs (miRNAs/miRs) are small non-coding RNAs, which serve important roles in tumor progression. The present study analyzed the role of miR-19a-3p in the chemosensitivity of osteosarcoma (OS) cells. Overexpression of miR-19a-3p was observed in OS cells and a cisplatin-resistant MG63 cell line was subsequently constructed. It was observed that miR-19a-3p inhibitor transfection suppressed cell proliferation and decreased the expression of Ki67 and PCNA compared with the cisplatin treatment group. miR-19a-3p inhibitor transfection also promoted apoptotic rate, increased the expression of Bcl-2 associated X, apoptosis regulator (Bax) and markedly decreased the expression of Bcl-2 compared with the cisplatin treatment group. These results elucidated that silencing of miR-19a-3p enhanced chemosensitivity of OS cells to Cisplatin, through suppressing cell proliferation and promoting cell apoptosis during treatment with Cisplatin. Bioinformatics study and luciferase reporter assays indicated that PTEN was a target of miR-19a-3p, and western blotting demonstrated that PTEN expression was negatively regulated by miR-19a-3p in OS cells. In addition, overexpression of PTEN decreased cell proliferation, but increased apoptotic rate compared with the cisplatin treatment group. It was observed that inhibition of PTEN by BpV(HOpic) upregulated cell proliferation and downregulated apoptotic rate compared with the Cisplatintreated miR-19a-3p inhibitor group, indicating that inhibition of PTEN expression counteracted the effect of the miR-19a-3p inhibitor on the regulation of chemosensitivity in OS cells. Taken together, overexpression of miR-19a-3p was observed in OS cell lines and that downregulation of miR-19a-3p enhanced the chemosensitivity of OS cells to Cisplatin, by elevating the expression of the tumor suppressor, PTEN.