Confined states in quantum dots defined within finite flakes of bilayer graphene: Coupling to the edge, ionization threshold, and valley degeneracy

We study quantum dots defined by external potentials within finite flakes of bilayer graphene using the tight-binding approach. We find that in the limit of large flakes containing zigzag edges the dot-localized energy levels appear within the energy continuum formed by extended states. As a consequence no ionization threshold for the carriers contained within the dot exists. For smaller flakes with zigzag boundaries the dot-localized energy levels appear interlaced with the energy levels outside the flake, so in a charging experiment the electrons will be added alternately to the dot area and to its neighborhood. We demonstrate that for flakes with armchair boundaries only, an energy window accessible uniquely to the dot-localized states is opened. Then a number of electrons can be added to the dot before the external states start to be occupied. We also discuss coupling of the dot-localized states to the edge states in the context of the valley degeneracy lifting. Moreover, we extract smooth envelope wave functions from the tight-binding solution and discuss their spatial symmetries. The coupling of the dot localized energy levels with reconstructed zigzag edges and atomic vacancies present within the layers is also considered.Comment: 9 pages,13 figure

A multichannel magnetic probe system for analysing magnetic fluctuations in helical axis plasmas

The need to understand the structure of magnetic fluctuations in H-1NF heliac [S. Hamberger et al., Fusion Technol. 17, 123 (1990)] plasmas has motivated the installation of a sixteen former, tri-axis helical magnetic probe Mirnov array (HMA). The new array complements two existing poloidal Mirnov arrays by providing polarisation information, higher frequency response, and improved toroidal resolution. The helical placement is ideal for helical axis plasmas because it positions the array as close as possible to the plasma in regions of varying degrees of favourable curvature in the magnetohydrodynamic sense, but almost constant magnetic angle. This makes phase variation with probe position near linear, greatly simplifying the analysis of the data. Several of the issues involved in the design, installation, data analysis, and calibration of this unique array are presented including probe coil design, frequency response measurements, mode number identification, orientation calculations, and mapping probe coil positions to magnetic coordinates. Details of specially designed digitally programmable pre-amplifiers, which allow gains and filters to be changed as part of the data acquisition initialisation sequence and stored with the probe signals, are also presented. The low shear heliac geometry [R. Jiménez-Gómez et al., Nucl. Fusion 51, 033001 (2011)], flexibility of the H-1NF heliac, and wealth of information provided by the HMA create a unique opportunity for detailed study of Alfvén eigenmodes, which could be a serious issue for future fusion reactors.This work was supported by the Education Investment Fund under the Super Science Initiative of the Australian Government. S.R.H. wishes to thank AINSE Ltd. for providing financial assistance to enable this work on H-1NF to be conducted

Melanoma cells break down LPA to establish local gradients that drive chemotactic dispersal.

The high mortality of melanoma is caused by rapid spread of cancer cells, which occurs unusually early in tumour evolution. Unlike most solid tumours, thickness rather than cytological markers or differentiation is the best guide to metastatic potential. Multiple stimuli that drive melanoma cell migration have been described, but it is not clear which are responsible for invasion, nor if chemotactic gradients exist in real tumours. In a chamber-based assay for melanoma dispersal, we find that cells migrate efficiently away from one another, even in initially homogeneous medium. This dispersal is driven by positive chemotaxis rather than chemorepulsion or contact inhibition. The principal chemoattractant, unexpectedly active across all tumour stages, is the lipid agonist lysophosphatidic acid (LPA) acting through the LPA receptor LPAR1. LPA induces chemotaxis of remarkable accuracy, and is both necessary and sufficient for chemotaxis and invasion in 2-D and 3-D assays. Growth factors, often described as tumour attractants, cause negligible chemotaxis themselves, but potentiate chemotaxis to LPA. Cells rapidly break down LPA present at substantial levels in culture medium and normal skin to generate outward-facing gradients. We measure LPA gradients across the margins of melanomas in vivo, confirming the physiological importance of our results. We conclude that LPA chemotaxis provides a strong drive for melanoma cells to invade outwards. Cells create their own gradients by acting as a sink, breaking down locally present LPA, and thus forming a gradient that is low in the tumour and high in the surrounding areas. The key step is not acquisition of sensitivity to the chemoattractant, but rather the tumour growing to break down enough LPA to form a gradient. Thus the stimulus that drives cell dispersal is not the presence of LPA itself, but the self-generated, outward-directed gradient

An Integrated TCGA Pan-Cancer Clinical Data Resource to Drive High-Quality Survival Outcome Analytics

For a decade, The Cancer Genome Atlas (TCGA) program collected clinicopathologic annotation data along with multi-platform molecular profiles of more than 11,000 human tumors across 33 different cancer types. TCGA clinical data contain key features representing the democratized nature of the data collection process. To ensure proper use of this large clinical dataset associated with genomic features, we developed a standardized dataset named the TCGA Pan-Cancer Clinical Data Resource (TCGA-CDR), which includes four major clinical outcome endpoints. In addition to detailing major challenges and statistical limitations encountered during the effort of integrating the acquired clinical data, we present a summary that includes endpoint usage recommendations for each cancer type. These TCGA-CDR findings appear to be consistent with cancer genomics studies independent of the TCGA effort and provide opportunities for investigating cancer biology using clinical correlates at an unprecedented scale. Analysis of clinicopathologic annotations for over 11,000 cancer patients in the TCGA program leads to the generation of TCGA Clinical Data Resource, which provides recommendations of clinical outcome endpoint usage for 33 cancer types

Characterization of paralic paleoenvironments using benthic foraminifera from early Cretaceous deposits (Scotian Shelf)

Abstrac

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts