Classical and quantum q-deformed physical systems

On the basis of the non-commutative q-calculus, we investigate a q-deformation of the classical Poisson bracket in order to formulate a generalized q-deformed dynamics in the classical regime. The obtained q-deformed Poisson bracket appears invariant under the action of the q-symplectic group of transformations. In this framework we introduce the q-deformed Hamilton's equations and we derive the evolution equation for some simple q-deformed mechanical systems governed by a scalar potential dependent only on the coordinate variable. It appears that the q-deformed Hamiltonian, which is the generator of the equation of motion, is generally not conserved in time but, in correspondence, a new constant of motion is generated. Finally, by following the standard canonical quantization rule, we compare the well known q-deformed Heisenberg algebra with the algebra generated by the q-deformed Poisson bracket.Comment: 9 pages, accepted for publication in "The European Physical Journal C

Albert Pierrepoint and the cultural persona of the twentieth-century hangman

Albert Pierrepoint was Britain’s most famous 20th-century hangman. This article utilises diverse sources in order to chart his public representation, or cultural persona, as hangman from his rise to prominence in the mid-1940s to his portrayal in the biopic Pierrepoint(2005). It argues that Pierrepoint exercised agency in shaping this persona through publishing his autobiography and engagement with the media, although there were also representations that he did not influence. In particular, it explores three iterations of his cultural persona – the Professional Hangman, the Reformed Hangman and the Haunted Hangman. Each of these built on and reworked historical antecedents and also communicated wider understandings and contested meanings in relation to capital punishment. As a hangman who remained in the public eye after the death penalty in Britain was abolished, Pierrepoint was an important, authentic link to the practice of execution and a symbolic figure in debates over reintroduction. In the 21st century, he was portrayed as a victim of the ‘secondary trauma’ of the death penalty, which resonated with worldwide campaigns for abolition

The ALICE Transition Radiation Detector: Construction, operation, and performance

The Transition Radiation Detector (TRD) was designed and built to enhance the capabilities of the ALICE detector at the Large Hadron Collider (LHC). While aimed at providing electron identification and triggering, the TRD also contributes significantly to the track reconstruction and calibration in the central barrel of ALICE. In this paper the design, construction, operation, and performance of this detector are discussed. A pion rejection factor of up to 410 is achieved at a momentum of 1 GeV/c in p-Pb collisions and the resolution at high transverse momentum improves by about 40% when including the TRD information in track reconstruction. The triggering capability is demonstrated both for jet, light nuclei, and electron selection. (c) 2017 CERN for the benefit of the Authors. Published by Elsevier B.V

Widespread non-additive and interaction effects within HLA loci modulate the risk of autoimmune diseases

Human leukocyte antigen (HLA) genes confer substantial risk for autoimmune diseases on a log-additive scale. Here we speculated that differences in autoantigen-binding repertoires between a heterozygote\u27s two expressed HLA variants might result in additional non-additive risk effects. We tested the non-additive disease contributions of classical HLA alleles in patients and matched controls for five common autoimmune diseases: rheumatoid arthritis (ncases = 5,337), type 1 diabetes (T1D; ncases = 5,567), psoriasis vulgaris (ncases = 3,089), idiopathic achalasia (ncases = 727) and celiac disease (ncases = 11,115). In four of the five diseases, we observed highly significant, non-additive dominance effects (rheumatoid arthritis, P = 2.5 x 10(-12); T1D, P = 2.4 x 10(-10); psoriasis, P = 5.9 x 10(-6); celiac disease, P = 1.2 x 10(-87)). In three of these diseases, the non-additive dominance effects were explained by interactions between specific classical HLA alleles (rheumatoid arthritis, P = 1.8 x 10(-3); T1D, P = 8.6 x 10(-27); celiac disease, P = 6.0 x 10(-100)). These interactions generally increased disease risk and explained moderate but significant fractions of phenotypic variance (rheumatoid arthritis, 1.4%; T1D, 4.0%; celiac disease, 4.1%) beyond a simple additive model

Long ncRNA Landscape in the Ileum of Treatment-Naive Early-Onset Crohn Disease.

Long noncoding RNAs (lncRNA) are key regulators of gene transcription and many show tissue-specific expression. We previously defined a novel inflammatory and metabolic ileal gene signature in treatment-naive pediatric Crohn disease (CD). We now extend our analyses to include potential regulatory lncRNA.Using RNAseq, we systematically profiled lncRNAs and protein-coding gene expression in 177 ileal biopsies. Co-expression analysis was used to identify functions and tissue-specific expression. RNA in situ hybridization was used to validate expression. Real-time polymerase chain reaction was used to test lncRNA regulation by IL-1β in Caco-2 enterocytes.We characterize widespread dysregulation of 459 lncRNAs in the ileum of CD patients. Using only the lncRNA in discovery and independent validation cohorts showed patient classification as accurate as the protein-coding genes, linking lncRNA to CD pathogenesis. Co-expression and functional annotation enrichment analyses across several tissues and cell types 1showed that the upregulated LINC01272 is associated with a myeloid pro-inflammatory signature, whereas the downregulated HNF4A-AS1 exhibits association with an epithelial metabolic signature. We confirmed tissue-specific expression in biopsies using in situ hybridization, and validated regulation of prioritized lncRNA upon IL-1β exposure in differentiated Caco-2 cells. Finally, we identified significant correlations between LINC01272 and HNF4A-AS1 expression and more severe mucosal injury.We systematically define differentially expressed lncRNA in the ileum of newly diagnosed pediatric CD. We show lncRNA utility to correctly classify disease or healthy states and demonstrate their regulation in response to an inflammatory signal. These lncRNAs, after mechanistic exploration, may serve as potential new tissue-specific targets for RNA-based interventions

Functional biology of the Steel syndrome founder allele and evidence for clan genomics derivation of COL27A1 pathogenic alleles worldwide

© 2020, The Author(s). Previously we reported the identification of a homozygous COL27A1 (c.2089G\u3eC; p.Gly697Arg) missense variant and proposed it as a founder allele in Puerto Rico segregating with Steel syndrome (STLS, MIM #615155); a rare osteochondrodysplasia characterized by short stature, congenital bilateral hip dysplasia, carpal coalitions, and scoliosis. We now report segregation of this variant in five probands from the initial clinical report defining the syndrome and an additional family of Puerto Rican descent with multiple affected adult individuals. We modeled the orthologous variant in murine Col27a1 and found it recapitulates some of the major Steel syndrome associated skeletal features including reduced body length, scoliosis, and a more rounded skull shape. Characterization of the in vivo murine model shows abnormal collagen deposition in the extracellular matrix and disorganization of the proliferative zone of the growth plate. We report additional COL27A1 pathogenic variant alleles identified in unrelated consanguineous Turkish kindreds suggesting Clan Genomics and identity-by-descent homozygosity contributing to disease in this population. The hypothesis that carrier states for this autosomal recessive osteochondrodysplasia may contribute to common complex traits is further explored in a large clinical population cohort. Our findings auNorthwell Healthnt our understanding of COL27A1 biology and its role in skeletal development; and expand the functional allelic architecture in this gene underlying both rare and common disease phenotypes

K Kbar photoproduction and S-P wave interference

Results of a new analysis of the $K^+K^-$ photoproduction at two photon energies $E_\gamma = 4{GeV}$ and $5.65{GeV}$ with a particular emphasis on the $S$-wave production are presented. We show that the proper treatment of all the helicity components of the $S$- and $P$-waves enables one to eliminate the reported discrepancies in extraction of the $S$-wave photoproduction cross section from experimental data.Comment: 25 pages, 5 figures, new predictions at 8 GeV added in Fig.