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

IL-33 signaling regulates innate and adaptive immunity to Cryptococcus neoformans.

Susceptibility to progressive infection with the fungus Cryptococcus neoformans is associated with an allergic pattern of lung inflammation, yet the factors that govern this host response are not clearly understood. Using a clinically relevant mouse model of inhalational infection with virulent C. neoformans H99, we demonstrate a role for IL-33-dependent signaling in host immune defense. Infection of BALB/c mice with 10(4) CFU of C. neoformans H99 caused a time-dependent induction of IL-33 with accumulation of type 2 pulmonary innate lymphoid cells and alternatively activated macrophages in the lungs as well as Th2-polarized CD4(+) T cells in draining lymph nodes. IL-33R subunit T1/ST2-deficient (T1/ST2(-/-)) mice infected with C. neoformans H99 had improved survival with a decreased fungal burden in the lungs, spleen, and brain, compared with wild-type mice. Signaling through T1/ST2 was required for the accumulation and early production of IL-5 and IL-13 by lung type 2 pulmonary innate lymphoid cells. Further analysis of T1/ST2(-/-) mice revealed increased fungicidal exudate macrophages in the lungs and decreased C. neoformans-specific Th2 cells in the mediastinal lymph nodes. T1/ST2 deficiency also diminished goblet cell hyperplasia, mucus hypersecretion, bronchoalveolar lavage eosinophilia, alternative activation of macrophages, and serum IgE. These observations demonstrate that IL-33-dependent signaling contributes to the expansion of innate type 2 immunity and subsequent Th2-biased lung immunopathology that facilitates C. neoformans growth and dissemination

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

On the Quantitative Impact of the Schechter-Valle Theorem

We evaluate the Schechter-Valle (Black Box) theorem quantitatively by considering the most general Lorentz invariant Lagrangian consisting of point-like operators for neutrinoless double beta decay. It is well known that the Black Box operators induce Majorana neutrino masses at four-loop level. This warrants the statement that an observation of neutrinoless double beta decay guarantees the Majorana nature of neutrinos. We calculate these radiatively generated masses and find that they are many orders of magnitude smaller than the observed neutrino masses and splittings. Thus, some lepton number violating New Physics (which may at tree-level not be related to neutrino masses) may induce Black Box operators which can explain an observed rate of neutrinoless double beta decay. Although these operators guarantee finite Majorana neutrino masses, the smallness of the Black Box contributions implies that other neutrino mass terms (Dirac or Majorana) must exist. If neutrino masses have a significant Majorana contribution then this will become the dominant part of the Black Box operator. However, neutrinos might also be predominantly Dirac particles, while other lepton number violating New Physics dominates neutrinoless double beta decay. Translating an observed rate of neutrinoless double beta decay into neutrino masses would then be completely misleading. Although the principal statement of the Schechter-Valle theorem remains valid, we conclude that the Black Box diagram itself generates radiatively only mass terms which are many orders of magnitude too small to explain neutrino masses. Therefore, other operators must give the leading contributions to neutrino masses, which could be of Dirac or Majorana nature.Comment: 18 pages, 4 figures; v2: minor corrections, reference added, matches journal version; v3: typo corrected, physics result and conclusions unchange

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

Receptors and Other Signaling Proteins Required for Serotonin Control of Locomotion in Caenorhabditis elegans

A better understanding of the molecular mechanisms of signaling by the neurotransmitter serotonin is required to assess the hypothesis that defects in serotonin signaling underlie depression in humans. Caenorhabditis elegans uses serotonin as a neurotransmitter to regulate locomotion, providing a genetic system to analyze serotonin signaling. From large-scale genetic screens we identified 36 mutants of C. elegans in which serotonin fails to have its normal effect of slowing locomotion, and we molecularly identified eight genes affected by 19 of the mutations. Two of the genes encode the serotonin-gated ion channel MOD-1 and the G-protein-coupled serotonin receptor SER-4. mod-1 is expressed in the neurons and muscles that directly control locomotion, while ser-4 is expressed in an almost entirely non-overlapping set of sensory and interneurons. The cells expressing the two receptors are largely not direct postsynaptic targets of serotonergic neurons. We analyzed animals lacking or overexpressing the receptors in various combinations using several assays for serotonin response. We found that the two receptors act in parallel to affect locomotion. Our results show that serotonin functions as an extrasynaptic signal that independently activates multiple receptors at a distance from its release sites and identify at least six additional proteins that appear to act with serotonin receptors to mediate serotonin response.National Institutes of Health (U.S.) (Grant GM24663