Anisotropic behavior of quantum transport in graphene superlattices:Coexistence of ballistic conduction with Anderson insulating regime

Under the terms of the Creative Commons Attribution License 3.0 (CC-BY).We report on the possibility to generate highly anisotropic quantum conductivity in disordered graphene-based superlattices. Our quantum simulations, based on an efficient real-space implementation of the Kubo-Greenwood formula, show that in disordered graphene superlattices the strength of multiple scattering phenomena can strongly depend on the transport measurement geometry. This eventually yields the coexistence of a ballistic waveguide and a highly resistive channel (Anderson insulator) in the same two-dimensional platform, evidenced by a σyy/σxx ratio varying over several orders of magnitude, and suggesting the possibility of building graphene electronic circuits based on the unique properties of chiral massless Dirac fermions in graphene. © 2014 American Physical Society.The work by J.G.P. is financially supported by the Danish Council for Independent Research, FTP Grants No. 11-105204 and No. 11-120941. S.R. and A.W.C. acknowledge the Spanish Ministry of Economy and Competitiveness for national project funding (MAT2012-33911) and SAMSUNG for support within the Global Innovation Program. The research leading to these results has received funding from the European Union Seventh Framework Programme under Grant No. 604391 Graphene Flagship.Peer Reviewe

Spin qubits in antidot lattices

We suggest and study designed defects in an otherwise periodic potential modulation of a two-dimensional electron gas as an alternative approach to electron spin based quantum information processing in the solid-state using conventional gate-defined quantum dots. We calculate the band structure and density of states for a periodic potential modulation, referred to as an antidot lattice, and find that localized states appear, when designed defects are introduced in the lattice. Such defect states may form the building blocks for quantum computing in a large antidot lattice, allowing for coherent electron transport between distant defect states in the lattice and tunnel coupling of neighboring defect states with corresponding electrostatically controllable exchange coupling between different electron spins.Comment: 9 pages, 9 figure

Widespread erosion on high plateaus during recent glaciations in Scandinavia

Glaciers create some of Earth’s steepest topography; yet, many areas that were repeatedly overridden by ice sheets in the last few million years include extensive plateaus. The distinct geomorphic contrast between plateaus and the glacial troughs that dissect them has sustained two long-held hypotheses: first, that ice sheets perform insignificant erosion beyond glacial troughs, and, second, that the plateaus represent ancient pre-glacial landforms bearing information of tectonic and geomorphic history prior to Pliocene–Pleistocene global cooling (~3.5 Myr ago). Here we show that the Fennoscandian ice sheets drove widespread erosion across plateaus far beyond glacial troughs. We apply inverse modelling to 118 new cosmogenic 10Be and 26Al measurements to quantify ice sheet erosion on the plateaus fringing the Sognefjorden glacial trough in western Norway. Our findings demonstrate substantial modification of the pre-glacial landscape during the Quaternary, and that glacial erosion of plateaus is important when estimating the global sediment flux to the oceans

Evolution of the leukotoxin promoter in genus Mannheimia

<b>Background</b>: The <i>Mannheimia</i> species encompass a wide variety of bacterial lifestyles, including opportunistic pathogens and commensals of the ruminant respiratory tract, commensals of the ovine rumen, and pathogens of the ruminant integument. Here we present a scenario for the evolution of the leukotoxin promoter among representatives of the five species within genus <i>Mannheimia</i>. We also consider how the evolution of the leukotoxin operon fits with the evolution and maintenance of virulence. <b>Results</b>: The alignment of the intergenic regions upstream of the leukotoxin genes showed significant sequence and positional conservation over a 225-bp stretch immediately proximal to the transcriptional start site of the <i>lktC</i> gene among all <i>Mannheimia</i> strains. However, in the course of the <i>Mannheimia</i> genome evolution, the acquisition of individual noncoding regions upstream of the conserved promoter region has occurred. The rate of evolution estimated branch by branch suggests that the conserved promoter may be affected to different extents by the types of natural selection that potentially operate in regulatory regions. Tandem repeats upstream of the core promoter were confined to <i>M. haemolytica</i> with a strong association between the sequence of the repeat units, the number of repeat units per promoter, and the phylogenetic history of this species. <b>Conclusion</b>: The mode of evolution of the intergenic regions upstream of the leukotoxin genes appears to be highly dependent on the lifestyle of the bacterium. Transition from avirulence to virulence has occurred at least once in <i>M. haemolytica</i> with some evolutionary success of bovine serotype A1/A6 strains. Our analysis suggests that changes in <i>cis</i>-regulatory systems have contributed to the derived virulence phenotype by allowing phase-variable expression of the leukotoxin protein. We propose models for how phase shifting and the associated virulence could facilitate transmission to the nasopharynx of new hosts

Molecular Basis of Enhanced Activity in Factor VIIa-Trypsin Variants Conveys Insights into Tissue Factor-mediated Allosteric Regulation of Factor VIIa Activity

The complex of coagulation factor VIIa (FVIIa), a trypsin-like serine protease, and membrane-bound tissue factor (TF) initiates blood coagulation upon vascular injury. Binding of TF to FVIIa promotes allosteric conformational changes in the FVIIa protease domain and improves its catalytic properties. Extensive studies have revealed two putative pathways for this allosteric communication. Here we provide further details of this allosteric communication by investigating FVIIa loop swap variants containing the 170 loop of trypsin that display TF-independent enhanced activity. Using x-ray crystallography, we show that the introduced 170 loop from trypsin directly interacts with the FVIIa active site, stabilizing segment 215–217 and activation loop 3, leading to enhanced activity. Molecular dynamics simulations and novel fluorescence quenching studies support that segment 215–217 conformation is pivotal to the enhanced activity of the FVIIa variants. We speculate that the allosteric regulation of FVIIa activity by TF binding follows a similar path in conjunction with protease domain N terminus insertion, suggesting a more complete molecular basis of TF-mediated allosteric enhancement of FVIIa activity