150 research outputs found
Electric Field Effects on Graphene Materials
Understanding the effect of electric fields on the physical and chemical
properties of two-dimensional (2D) nanostructures is instrumental in the design
of novel electronic and optoelectronic devices. Several of those properties are
characterized in terms of the dielectric constant which play an important role
on capacitance, conductivity, screening, dielectric losses and refractive
index. Here we review our recent theoretical studies using density functional
calculations including van der Waals interactions on two types of layered
materials of similar two-dimensional molecular geometry but remarkably
different electronic structures, that is, graphene and molybdenum disulphide
(MoS). We focus on such two-dimensional crystals because of they
complementary physical and chemical properties, and the appealing interest to
incorporate them in the next generation of electronic and optoelectronic
devices. We predict that the effective dielectric constant () of
few-layer graphene and MoS is tunable by external electric fields (). We show that at low fields ( V/\AA)
assumes a nearly constant value 4 for both materials, but increases at
higher fields to values that depend on the layer thickness. The thicker the
structure the stronger is the modulation of with the electric
field. Increasing of the external field perpendicular to the layer surface
above a critical value can drive the systems to an unstable state where the
layers are weakly coupled and can be easily separated. The observed dependence
of on the external field is due to charge polarization driven by
the bias, which show several similar characteristics despite of the layer
considered.Comment: Invited book chapter on Exotic Properties of Carbon Nanomatter:
Advances in Physics and Chemistry, Springer Series on Carbon Materials.
Editors: Mihai V. Putz and Ottorino Ori (11 pages, 4 figures, 30 references
Dirac cones reshaped by interaction effects in suspended graphene
We report measurements of the cyclotron mass in graphene for carrier
concentrations n varying over three orders of magnitude. In contrast to the
single-particle picture, the real spectrum of graphene is profoundly nonlinear
so that the Fermi velocity describing the spectral slope reaches ~3x10^6 m/s at
n <10^10 cm^-2, three times the value commonly used for graphene. The observed
changes are attributed to electron-electron interaction that renormalizes the
Dirac spectrum because of weak screening. Our experiments also put an upper
limit of ~0.1 meV on the possible gap in graphene
Higher-order renormalization of graphene many-body theory
We study the many-body theory of graphene Dirac quasiparticles interacting
via the long-range Coulomb potential, taking as a starting point the ladder
approximation to different vertex functions. We test in this way the low-energy
behavior of the electron system beyond the simple logarithmic dependence of
electronic correlators on the high-energy cutoff, which is characteristic of
the large-N approximation. We show that the graphene many-body theory is
perfectly renormalizable in the ladder approximation, as all higher powers in
the cutoff dependence can be absorbed into the redefinition of a finite number
of parameters (namely, the Fermi velocity and the weight of the fields) that
remain free of infrared divergences even at the charge neutrality point. We
illustrate this fact in the case of the vertex for the current density, where a
complete cancellation between the cutoff dependences of vertex and electron
self-energy corrections becomes crucial for the preservation of the gauge
invariance of the theory. The other potentially divergent vertex corresponds to
the staggered (sublattice odd) charge density, which is made cutoff independent
by a redefinition in the scale of the density operator. This allows to compute
a well-defined, scale invariant anomalous dimension to all orders in the ladder
series, which becomes singular at a value of the interaction strength marking
the onset of chiral symmetry breaking (and gap opening) in the Dirac field
theory. The critical coupling we obtain in this way matches with great accuracy
the value found with a quite different method, based on the resolution of the
gap equation, thus reassuring the predictability of our renormalization
approach.Comment: 27 pages, 7 figures, references adde
Investigation of the Genes Involved in Antigenic Switching at the vlsE Locus in Borrelia burgdorferi: An Essential Role for the RuvAB Branch Migrase
Persistent infection by pathogenic organisms requires effective strategies for the defense of these organisms against the host immune response. A common strategy employed by many pathogens to escape immune recognition and clearance is to continually vary surface epitopes through recombinational shuffling of genetic information. Borrelia burgdorferi, a causative agent of Lyme borreliosis, encodes a surface-bound lipoprotein, VlsE. This protein is encoded by the vlsE locus carried at the right end of the linear plasmid lp28-1. Adjacent to the expression locus are 15 silent cassettes carrying information that is moved into the vlsE locus through segmental gene conversion events. The protein players and molecular mechanism of recombinational switching at vlsE have not been characterized. In this study, we analyzed the effect of the independent disruption of 17 genes that encode factors involved in DNA recombination, repair or replication on recombinational switching at the vlsE locus during murine infection. In Neisseria gonorrhoeae, 10 such genes have been implicated in recombinational switching at the pilE locus. Eight of these genes, including recA, are either absent from B. burgdorferi, or do not show an obvious requirement for switching at vlsE. The only genes that are required in both organisms are ruvA and ruvB, which encode subunits of a Holliday junction branch migrase. Disruption of these genes results in a dramatic decrease in vlsE recombination with a phenotype similar to that observed for lp28-1 or vls-minus spirochetes: productive infection at week 1 with clearance by day 21. In SCID mice, the persistence defect observed with ruvA and ruvB mutants was fully rescued as previously observed for vlsE-deficient B. burgdorferi. We report the requirement of the RuvAB branch migrase in recombinational switching at vlsE, the first essential factor to be identified in this process. These findings are supported by the independent work of Lin et al. in the accompanying article, who also found a requirement for the RuvAB branch migrase. Our results also indicate that the mechanism of switching at vlsE in B. burgdorferi is distinct from switching at pilE in N. gonorrhoeae, which is the only other organism analyzed genetically in detail. Finally, our findings suggest a unique mechanism for switching at vlsE and a role for currently unidentified B. burgdorferi proteins in this process
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Changing pattern in the basal ganglia: motor switching under reduced dopaminergic drive
Action selection in the basal ganglia is often described within the framework of a standard model, associating low dopaminergic drive with motor suppression. Whilst powerful, this model does not explain several clinical and experimental data, including varying therapeutic efficacy across movement disorders. We tested the predictions of this model in patients with Parkinson’s disease, on and off subthalamic deep brain stimulation (DBS), focussing on adaptive sensory-motor responses to a changing environment and maintenance of an action until it is no longer suitable. Surprisingly, we observed prolonged perseverance under on-stimulation, and high inter-individual variability in terms of the motor selections performed when comparing the two conditions. To account for these data, we revised the standard model exploring its space of parameters and associated motor functions and found that, depending on effective connectivity between external and internal parts of the globus pallidus and saliency of the sensory input, a low dopaminergic drive can result in increased, dysfunctional, motor switching, besides motor suppression. This new framework provides insight into the biophysical mechanisms underlying DBS, allowing a description in terms of alteration of the signal-to-baseline ratio in the indirect pathway, which better account of known electrophysiological data in comparison with the standard model
Mixed Th1 and Th2 Mycobacterium tuberculosis-specific CD4 T cell responses in patients with active pulmonary tuberculosis from Tanzania.
Mycobacterium tuberculosis (Mtb) and helminth infections elicit antagonistic immune effector functions and are co-endemic in several regions of the world. We therefore hypothesized that helminth infection may influence Mtb-specific T-cell immune responses. We evaluated the cytokine profile of Mtb-specific T cells in 72 individuals with pulmonary TB disease recruited from two Sub-Saharan regions with high and moderate helminth burden i.e. 55 from Tanzania (TZ) and 17 from South Africa (SA), respectively. We showed that Mtb-specific CD4 T-cell functional profile of TB patients from Tanzania are primarily composed of polyfunctional Th1 and Th2 cells, associated with increased expression of Gata-3 and reduced expression of T-bet in memory CD4 T cells. In contrast, the cytokine profile of Mtb-specific CD4 T cells of TB patients from SA was dominated by single IFN-γ and dual IFN-γ/TNF-α and associated with TB-induced systemic inflammation and elevated serum levels of type I IFNs. Of note, the proportion of patients with Mtb-specific CD8 T cells was significantly reduced in Mtb/helminth co-infected patients from TZ. It is likely that the underlying helminth infection and possibly genetic and other unknown environmental factors may have caused the induction of mixed Th1/Th2 Mtb-specific CD4 T cell responses in patients from TZ. Taken together, these results indicate that the generation of Mtb-specific CD4 and CD8 T cell responses may be substantially influenced by environmental factors in vivo. These observations may have major impact in the identification of immune biomarkers of disease status and correlates of protection
Co-Orientation of Replication and Transcription Preserves Genome Integrity
In many bacteria, there is a genome-wide bias towards co-orientation of replication and transcription, with essential and/or highly-expressed genes further enriched co-directionally. We previously found that reversing this bias in the bacterium Bacillus subtilis slows replication elongation, and we proposed that this effect contributes to the evolutionary pressure selecting the transcription-replication co-orientation bias. This selection might have been based purely on selection for speedy replication; alternatively, the slowed replication might actually represent an average of individual replication-disruption events, each of which is counter-selected independently because genome integrity is selected. To differentiate these possibilities and define the precise forces driving this aspect of genome organization, we generated new strains with inversions either over ∼1/4 of the chromosome or at ribosomal RNA (rRNA) operons. Applying mathematical analysis to genomic microarray snapshots, we found that replication rates vary dramatically within the inverted genome. Replication is moderately impeded throughout the inverted region, which results in a small but significant competitive disadvantage in minimal medium. Importantly, replication is strongly obstructed at inverted rRNA loci in rich medium. This obstruction results in disruption of DNA replication, activation of DNA damage responses, loss of genome integrity, and cell death. Our results strongly suggest that preservation of genome integrity drives the evolution of co-orientation of replication and transcription, a conserved feature of genome organization
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