Unconventional Integer Quantum Hall effect in graphene

Monolayer graphite films, or graphene, have quasiparticle excitations that can be described by 2+1 dimensional Dirac theory. We demonstrate that this produces an unconventional form of the quantized Hall conductivity $\sigma_{xy} = - (2 e^2/h)(2n+1)$ with $n=0,1,...$, that notably distinguishes graphene from other materials where the integer quantum Hall effect was observed. This unconventional quantization is caused by the quantum anomaly of the $n=0$ Landau level and was discovered in recent experiments on ultrathin graphite films.Comment: 4 pages, RevTeX4, 2 EPS figures; version accepted for publication in Physical Review Letter

Transport of Dirac quasiparticles in graphene: Hall and optical conductivities

The analytical expressions for both diagonal and off-diagonal ac and dc conductivities of graphene placed in an external magnetic field are derived. These conductivities exhibit rather unusual behavior as functions of frequency, chemical potential and applied field which is caused by the fact that the quasiparticle excitations in graphene are Dirac-like. One of the most striking effects observed in graphene is the odd integer quantum Hall effect. We argue that it is caused by the anomalous properties of the Dirac quasiparticles from the lowest Landau level. Other quantities such as Hall angle and Nernst signal also exhibit rather unusual behavior, in particular when there is an excitonic gap in the spectrum of the Dirac quasiparticle excitations.Comment: 25 pages, RevTeX4, 8 EPS figures; final version published in PR

Localization and conductance fluctuations in the integer quantum Hall effect: Real--space renormalization group approach

We consider the network model of the integer quantum Hall effect transition. By generalizing the real--space renormalization group procedure for the classical percolation to the case of quantum percolation, we derive a closed renormalization group (RG) equation for the universal distribution of conductance of the quantum Hall sample at the transition. We find an approximate solution of the RG equation and use it to calculate the critical exponent of the localization length and the central moments of the conductance distribution. The results obtained are compared with the results of recent numerical simulations.Comment: 17 pages, RevTex, 7 figure

Signature-Tagged Mutagenesis in a Chicken Infection Model Leads to the Identification of a Novel Avian Pathogenic Escherichia coli Fimbrial Adhesin

The extraintestinal pathogen, avian pathogenic E. coli (APEC), known to cause systemic infections in chickens, is responsible for large economic losses in the poultry industry worldwide. In order to identify genes involved in the early essential stages of pathogenesis, namely adhesion and colonization, Signature-tagged mutagenesis (STM) was applied to a previously established lung colonization model of infection by generating and screening a total of 1,800 mutants of an APEC strain IMT5155 (O2:K1:H5; Sequence type complex 95). The study led to the identification of new genes of interest, including two adhesins, one of which coded for a novel APEC fimbrial adhesin (Yqi) not described for its role in APEC pathogenesis to date. Its gene product has been temporarily designated ExPEC Adhesin I (EA/I) until the adhesin-specific receptor is identified. Deletion of the ExPEC adhesin I gene resulted in reduced colonization ability by APEC strain IMT5155 both in vitro and in vivo. Furthermore, complementation of the adhesin gene restored its ability to colonize epithelial cells in vitro. The ExPEC adhesin I protein was successfully expressed in vitro. Electron microscopy of an afimbriate strain E. coli AAEC189 over-expressed with the putative EA/I gene cluster revealed short fimbrial-like appendages protruding out of the bacterial outer membrane. We observed that this adhesin coding gene yqi is prevalent among extraintestinal pathogenic E. coli (ExPEC) isolates, including APEC (54.4%), uropathogenic E. coli (UPEC) (65.9%) and newborn meningitic E. coli (NMEC) (60.0%), and absent in all of the 153 intestinal pathogenic E. coli strains tested, thereby validating the designation of the adhesin as ExPEC Adhesin I. In addition, prevalence of EA/I was most frequently associated with the B2 group of the EcoR classification and ST95 complex of the multi locus sequence typing (MLST) scheme, with evidence of a positive selection within this highly pathogenic complex. This is the first report of the newly identified and functionally characterized ExPEC adhesin I and its significant role during APEC infection in chickens

The Size, Shape, and Scattering of Sagittarius A* at 86GHz: First VLBI with ALMA

Contains fulltext : 200904.pdf (preprint version ) (Open Access) Contains fulltext : 200904.pdf (publisher's version ) (Open Access

Effect of ABCG2, OCT1, and ABCB1 (MDR1) Gene Expression on Treatment-Free Remission in a EURO-SKI Subtrial

Within the EURO-SKI trial, 132 chronic phase CML patients discontinued imatinib treatment. RNA was isolated from peripheral blood in order to analyze the expression of MDR1, ABCG2 and OCT1. ABCG2 was predictive for treatment-free remission in Cox regression analysis. High transcript levels of the ABCG2 efflux transporter (>4.5‰) were associated with a twofold higher risk of relapse. Introduction: Tyrosine kinase inhibitors (TKIs) can safely be discontinued in chronic myeloid leukemia (CML) patients with sustained deep molecular response. ABCG2 (breast cancer resistance protein), OCT1 (organic cation transporter 1), and ABCB1 (multidrug resistance protein 1) gene products are known to play a crucial role in acquired pharmacogenetic TKI resistance. Their influence on treatment-free remission (TFR) has not yet been investigated. Materials and Methods: RNA was isolated on the last day of TKI intake from peripheral blood leukocytes of 132 chronic phase CML patients who discontinued TKI treatment within the European Stop Tyrosine Kinase Inhibitor Study trial. Plasmid standards were designed including subgenic inserts of OCT1, ABCG2, and ABCB1 together with GUSB as reference gene. For expression analyses, quantitative real-time polymerase chain reaction was used. Multiple Cox regression analysis was performed. In addition, gene expression cutoffs for patient risk stratification were investigated. Results: The TFR rate of 132 patients, 12 months after TKI discontinuation, was 54% (95% confidence interval [CI], 46%-62%). ABCG2 expression (‰) was retained as the only significant variable (P =.02; hazard ratio, 1.04; 95% CI, 1.01-1.07) in multiple Cox regression analysis. Only for the ABCG2 efflux transporter, a significant cutoff was found (P =.04). Patients with an ABCG2/GUSB transcript level >4.5‰ (n = 93) showed a 12-month TFR rate of 47% (95% CI, 37%-57%), whereas patients with low ABCG2 expression (≤4.5‰; n = 39) had a 12-month TFR rate of 72% (95% CI, 55%-82%). Conclusion: In this study, we investigated the effect of pharmacogenetics in the context of a CML treatment discontinuation trial. The transcript levels of the efflux transporter ABCG2 predicted TFR after TKI discontinuation. © 2018 The Author