Quantum Hall effect in narrow graphene ribbons

The edge states in the integer quantum Hall effect are known to be significantly affected by electrostatic interactions leading to the formation of compressible and incompressible strips at the boundaries of Hall bars. We show here, in a combined experimental and theoretical analysis, that this does not hold for the quantum Hall effect in narrow graphene ribbons. In our graphene Hall bar, which is only 60 nm wide, we observe the quantum Hall effect up to Landau level index k=2 and show within a zero free-parameter model that the spatial extent of the compressible and incompressible strips is of a similar magnitude as the magnetic length. We conclude that in narrow graphene ribbons the single-particle picture is a more appropriate description of the quantum Hall effect and that electrostatic effects are of minor importance.Comment: RevTex, 5 pages, 4 figures (matches published version

Group 2 Innate Lymphoid Cells in Respiratory Allergic Inflammation

Millions of people worldwide are suffering from allergic inflammatory airway disorders. These conditions are regarded as a consequence of multiple imbalanced immune events resulting in an inadequate response with the exact underlying mechanisms still being a subject of ongoing research. Several cell populations have been proposed to be involved but it is becoming increasingly evident that group 2 innate lymphoid cells (ILC2s) play a key role in the initiation and orchestration of respiratory allergic inflammation. ILC2s are important mediators of inflammation but also tissue remodeling by secreting large amounts of signature cytokines within a short time period. Thereby, ILC2s instruct innate but also adaptive immune responses. Here, we will discuss the recent literature on allergic inflammation of the respiratory tract with a focus on ILC2 biology. Furthermore, we will highlight different therapeutic strategies to treat pulmonary allergic inflammation and their potential influence on ILC2 function as well as discuss the perspective of using human ILC2s for diagnostic purposes

PTGER4 expression-modulating polymorphisms in the 5p13.1 region predispose to Crohn's disease and affect NF-κB and XBP1 binding sites.

Genome-wide association studies identified a PTGER4 expression-modulating region on chromosome 5p13.1 as Crohn's disease (CD) susceptibility region. The study aim was to test this association in a large cohort of patients with inflammatory bowel disease (IBD) and to elucidate genotypic and phenotypic interactions with other IBD genes. A total of 7073 patients and controls were genotyped: 844 CD and 471 patients with ulcerative colitis and 1488 controls were analyzed for the single nucleotide polymorphisms (SNPs) rs4495224 and rs7720838 on chromosome 5p13.1. The study included two replication cohorts of North American (CD: n = 684; controls: n = 1440) and of German origin (CD: n = 1098; controls: n = 1048). Genotype-phenotype, epistasis and transcription factor binding analyses were performed. In the discovery cohort, an association of rs4495224 (p = 4.10×10⁻⁵; 0.76 [0.67-0.87]) and of rs7720838 (p = 6.91×10⁻⁴; 0.81 [0.71-0.91]) with susceptibility to CD was demonstrated. These associations were confirmed in both replication cohorts. In silico analysis predicted rs4495224 and rs7720838 as essential parts of binding sites for the transcription factors NF-κB and XBP1 with higher binding scores for carriers of the CD risk alleles, providing an explanation of how these SNPs might contribute to increased PTGER4 expression. There was no association of the PTGER4 SNPs with IBD phenotypes. Epistasis detected between 5p13.1 and ATG16L1 for CD susceptibility in the discovery cohort (p = 5.99×10⁻⁷ for rs7720838 and rs2241880) could not be replicated in both replication cohorts arguing against a major role of this gene-gene interaction in the susceptibility to CD. We confirmed 5p13.1 as a major CD susceptibility locus and demonstrate by in silico analysis rs4495224 and rs7720838 as part of binding sites for NF-κB and XBP1. Further functional studies are necessary to confirm the results of our in silico analysis and to analyze if changes in PTGER4 expression modulate CD susceptibility

A relativistically covariant version of Bohm's quantum field theory for the scalar field

We give a relativistically covariant, wave-functional formulation of Bohm's quantum field theory for the scalar field based on a general foliation of space-time by space-like hypersurfaces. The wave functional, which guides the evolution of the field, is space-time-foliation independent but the field itself is not. Hence, in order to have a theory in which the field may be considered a beable, some extra rule must be given to determine the foliation. We suggest one such rule based on the eigen vectors of the energy-momentum tensor of the field itself.Comment: 1 figure. Submitted to J Phys A. 20/05/04 replacement has additional references and a few minor changes made for clarity. Accepted by J Phys

Dirac Sea Effects on Superfluidity in Nuclear Matter

We study two kinds of Dirac sea effects on the $^1S_0$ pairing gap in nuclear matter based on the relativistic Hartree approximation to quantum hadrodynamics and the Gor'kov formalism. We show that the vacuum fluctuation effect on the nucleon effective mass is more important than the direct coupling between the Fermi sea and the Dirac sea due to the pairing interaction. The effects of the high-momentum cutoff are also discussed.Comment: 11 pages, 3 eps figures included, uses REVTeX (with \tightenlines

DNA tumor virus oncoproteins and retinoblastoma gene mutations share the ability to relieve the cells requirement for cyclin D1 function in G1

The retinoblastoma gene product (pRB) participates in the regulation of the cell division cycle through complex formation with numerous cellular regulatory proteins including the potentially oncogenic cyclin D1. Extending the current view of the emerging functional interplay between pRB and D-type cyclins, we now report that cyclin D1 expression is positively regulated by pRB. Cyclin D1 mRNA and protein is specifically downregulated in cells expressing SV40 large T antigen, adenovirus E1A, and papillomavirus E7/E6 oncogene products and this effect requires intact RB-binding, CR2 domain of E1A. Exceptionally low expression of cyclin D1 is also seen in genetically RB-deficient cell lines, in which ectopically expressed wild-type pRB results in specific induction of this G1 cyclin. At the functional level, antibody-mediated cyclin D1 knockout experiments demonstrate that the cyclin D1 protein, normally required for G1 progression, is dispensable for passage through the cell cycle in cell lines whose pRB is inactivated through complex formation with T antigen, E1A, or E7 oncoproteins as well as in cells which have suffered loss-of-function mutations of the RB gene. The requirement for cyclin D1 function is not regained upon experimental elevation of cyclin D1 expression in cells with mutant RB, while reintroduction of wild-type RB into RB-deficient cells leads to restoration of the cyclin D1 checkpoint. These results strongly suggest that pRB serves as a major target of cyclin D1 whose cell cycle regulatory function becomes dispensable in cells lacking functional RB. Based on available data including this study, we propose a model for an autoregulatory feedback loop mechanism that regulates both the expression of the cyclin D1 gene and the activity of pRB, thereby contributing to a G1 phase checkpoint control in cycling mammalian cells