221 research outputs found

    Entanglement of photons

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    It is argued that the title of this paper represents a misconception. Contrary to widespread beliefs it is electromagnetic field modes that are ``systems'' and can be entangled, not photons. The amount of entanglement in a given state is shown to depend on redefinitions of the modes; we calculate the minimum and maximum over all such redefinitions for several examples.Comment: 5 pages ReVTe

    Megahertz dynamics in skyrmion systems probed with muon-spin relaxation

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    We present longitudinal-field muon-spin relaxation (LF μ SR ) measurements on two systems that stabilize a skyrmion lattice (SkL): Cu 2 OSeO 3 , and Co x Zn y Mn 20 − x − y for ( x , y ) = ( 10 , 10 ) , (8, 9), and (8, 8). We find that the SkL phase of Cu 2 OSeO 3 exhibits emergent dynamic behavior at megahertz frequencies, likely due to collective excitations, allowing the SkL to be identified from the μ SR response. From measurements following different cooling protocols and calculations of the muon stopping site, we suggest that the metastable SkL is not the majority phase throughout the bulk of this material at the fields and temperatures where it is often observed. The dynamics of bulk Co 8 Zn 9 Mn 3 are well described by ≃ 2 GHz excitations that reduce in frequency near the critical temperature, while in Co 8 Zn 8 Mn 4 we observe similar behavior over a wide range of temperatures, implying that dynamics of this kind persist beyond the SkL phase

    The Hamiltonian formulation of General Relativity: myths and reality

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    A conventional wisdom often perpetuated in the literature states that: (i) a 3+1 decomposition of space-time into space and time is synonymous with the canonical treatment and this decomposition is essential for any Hamiltonian formulation of General Relativity (GR); (ii) the canonical treatment unavoidably breaks the symmetry between space and time in GR and the resulting algebra of constraints is not the algebra of four-dimensional diffeomorphism; (iii) according to some authors this algebra allows one to derive only spatial diffeomorphism or, according to others, a specific field-dependent and non-covariant four-dimensional diffeomorphism; (iv) the analyses of Dirac [Proc. Roy. Soc. A 246 (1958) 333] and of ADM [Arnowitt, Deser and Misner, in "Gravitation: An Introduction to Current Research" (1962) 227] of the canonical structure of GR are equivalent. We provide some general reasons why these statements should be questioned. Points (i-iii) have been shown to be incorrect in [Kiriushcheva et al., Phys. Lett. A 372 (2008) 5101] and now we thoroughly re-examine all steps of the Dirac Hamiltonian formulation of GR. We show that points (i-iii) above cannot be attributed to the Dirac Hamiltonian formulation of GR. We also demonstrate that ADM and Dirac formulations are related by a transformation of phase-space variables from the metric gμνg_{\mu\nu} to lapse and shift functions and the three-metric gkmg_{km}, which is not canonical. This proves that point (iv) is incorrect. Points (i-iii) are mere consequences of using a non-canonical change of variables and are not an intrinsic property of either the Hamilton-Dirac approach to constrained systems or Einstein's theory itself.Comment: References are added and updated, Introduction is extended, Subsection 3.5 is added, 83 pages; corresponds to the published versio

    Informal and formal reconciliation strategies of older peoples’ working carers: the European carers@work project

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    Faced with a historically unprecedented process of demographic ageing, many European societies implemented pension reforms in recent years to extend working lives. Although aimed at rebalancing public pension systems, this approach has the unintended side effect that it also extends the number of years in which working carers have to juggle the conflicting demands of employment and caregiving. This not only impinges on working carers’ well-being and ability to continue providing care but also affects European enterprises’ capacity to generate growth which increasingly relies on ageing workforces. The focus of this paper will thus be a cross-national comparison of individual reconciliation strategies and workplace-related company policies aimed at enabling working carers to reconcile both conflicting roles in four different European welfare states: Germany, Italy, Poland, and the United Kingdom

    Pooled resequencing of 122 ulcerative colitis genes in a large Dutch cohort suggests population-Specific associations of rare variants in MUC2

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    Genome-wide association studies have revealed several common genetic risk variants for ulcerative colitis (UC). However, little is known about the contribution of rare, large effect genetic variants to UC susceptibility. In this study, we performed a deep targeted resequencing of 122 genes in Dutch UC patients in order to investigate the contribution of rare variants to the genetic susceptibility to UC. The selection of genes consists of 111 established human UC susceptibility genes and 11 genes that lead to spontaneous colitis when knocked-out in mice. In addition, we sequenced the promoter regions of 45 genes where known variants exert cis-eQTL-effects. Targeted pooled re-sequencing was performed on DNA of 790 Dutch UC cases. The Genome of the Netherlands project provided sequence data of 500 healthy controls. After quality control and prioritization based on allele frequency and pathogenicity probability, follow-up genotyping of 171 rare variants was performed on 1021 Dutch UC cases and 1166 Dutch controls. Single-variant association and gene-based analyses identified an association of rare variants in the MUC2 gene with UC. The associated variants in the Dutch population could not be replicated in a German replication cohort (1026 UC cases, 3532 controls). In conclusion, this study has identified a putative role for MUC2 on UC susceptibility in the Dutch population and suggests a populationspecific contribution of rare variants to UC

    Transfer origins in the conjugative Enterococcus faecalis plasmids pAD1 and pAM373: identification of the pAD1 nic site, a specific relaxase and a possible TraG-like protein

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    The Enterococcus faecalis conjugative plasmids pAD1 and pAM373 encode a mating response to the peptide sex pheromones cAD1 and cAM373 respectively. Sequence determination of both plasmids has recently been completed with strong similarity evident over many of the structural genes related to conjugation. pAD1 has two origins of transfer, with oriT1 being located within the repA determinant, whereas the more efficiently utilized oriT2 is located between orf53 and orf57 , two genes found in the present study to be essential for conjugation. We have found a similarly located oriT to be present in pAM373. oriT2 corresponds to about 285 bp based on its ability to facilitate mobilization by pAD1 when ligated to the shuttle vector pAM401; however, it was not mobilized by pAM373. In contrast, a similarly ligated fragment containing the oriT of pAM373 did not facilitate mobilization by pAD1 but was efficiently mobilized by pAM373. The oriT sites of the two plasmids each contained a homologous large inverted repeat (spanning about 140 bp) adjacent to a series of non-homologous short (6 bp) direct repeats. A hybrid construction containing the inverted repeat of pAM373 and direct repeats of pAD1 was mobilized efficiently by pAD1 but not by pAM373, indicating a significantly greater degree of specificity is associated with the direct repeats. Mutational (deletion) analyses of the pAD1 oriT2 inverted repeat structure suggested its importance in facilitating transfer or perhaps ligation of the ends of the newly transferred DNA strand. Analyses showed that Orf57 (to be called TraX) is the relaxase, which was found to induce a specific nick in the large inverted repeat inside oriT ; the protein also facilitated site-specific recombination between two oriT2 sites. Orf53 (to be called TraW) exhibits certain structural similarities to TraG-like proteins, although there is little overall homology.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72536/1/j.1365-2958.2002.03007.x.pd

    Molecular ontogeny of larval immunity in European eel at increasing temperatures

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    Temperature is a major factor that modulates the development and reactivity of the immune system. Only limited knowledge exists regarding the immune system of the catadromous European eel, Anguilla anguilla, especially during the oceanic early life history stages. Thus, a new molecular toolbox was developed, involving tissue specific characterisation of 3 housekeeping genes, 9 genes from the innate and 3 genes from the adaptive immune system of this species. The spatial pattern of immune genes reflected their function, e.g. complement component c3 was mainly produced in liver and il10 in the head kidney. Subsequently, the ontogeny of the immune system was studied in larvae reared from hatch to first-feeding at four temperatures, spanning their thermal tolerance range (16, 18, 20, and 22 °C). Expression of some genes (c3 and igm) declined post hatch, whilst expression of most other genes (mhc2, tlr2, il1β, irf3, irf7) increased with larval age. At the optimal temperature, 18 °C, this pattern of immune-gene expression revealed an immunocompromised phase between hatch (0 dph) and teeth-development (8 dph). The expression of two of the studied genes (mhc2, lysc) was temperature dependent, leading to increased mRNA levels at 22 °C. Additionally, at the lower end of the thermal spectrum (16 °C) immune competency appeared reduced, whilst close to the upper thermal limit (22 °C) larvae showed signs of thermal stress. Thus, protection against pathogens is probably impaired at temperatures close to the critical thermal maximum (CTmax), impacting survival and productivity in hatcheries and natural recruitment

    Susceptibility to chronic mucus hypersecretion, a genome wide association study

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    Background: Chronic mucus hypersecretion (CMH) is associated with an increased frequency of respiratory infections, excess lung function decline, and increased hospitalisation and mortality rates in the general population. It is associated with smoking, but it is unknown why only a minority of smokers develops CMH. A plausible explanation for this phenomenon is a predisposing genetic constitution. Therefore, we performed a genome wide association (GWA) study of CMH in Caucasian populations. Methods: GWA analysis was performed in the NELSON-study using the Illumina 610 array, followed by replication and meta-analysis in 11 additional cohorts. In total 2,704 subjects with, and 7,624 subjects without CMH were included, all current or former heavy smokers (≥20 pack-years). Additional studies were performed to test the functional relevance of the most significant single nucleotide polymorphism (SNP). Results: A strong association with CMH, consistent across all cohorts, was observed with rs6577641 (p = 4.25x10-6, OR = 1.17), located in intron 9 of the special AT-rich sequence-binding protein 1 locus (SATB1) on chromosome 3. The risk allele (G) was associated with higher mRNA expression of SATB1 (4.3x10 -9) in lung tissue. Presence of CMH was associated with increased SATB1 mRNA expression in bronchial biopsies from COPD patients. SATB1 expression was induced during differentiation of primary human bronchial epithelial cells in culture. Conclusions: Our findings, that SNP rs6577641 is associated with CMH in multiple cohorts and is a cis-eQTL for SATB1, together with our additional observation that SATB1 expression increases during epithelial differentiation provide suggestive evidence that SATB1 is a gene that affects CMH

    GWAS for Systemic Sclerosis Identifies Multiple Risk Loci and Highlights Fibrotic and Vasculopathy Pathways

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    Systemic sclerosis (SSc) is an autoimmune disease that shows one of the highest mortality rates among rheumatic diseases. We perform a large genome-wide association study (GWAS), and meta-analysis with previous GWASs, in 26,679 individuals and identify 27 independent genome-wide associated signals, including 13 new risk loci. The novel associations nearly double the number of genome-wide hits reported for SSc thus far. We define 95% credible sets of less than 5 likely causal variants in 12 loci. Additionally, we identify specific SSc subtype-associated signals. Functional analysis of high-priority variants shows the potential function of SSc signals, with the identification of 43 robust target genes through HiChIP. Our results point towards molecular pathways potentially involved in vasculopathy and fibrosis, two main hallmarks in SSc, and highlight the spectrum of critical cell types for the disease. This work supports a better understanding of the genetic basis of SSc and provides directions for future functional experiments.Funding: This work was supported by Spanish Ministry of Economy and Competitiveness (grant ref. SAF2015-66761-P), Consejeria de Innovacion, Ciencia y Tecnologia, Junta de Andalucía (P12-BIO-1395), Ministerio de Educación, Cultura y Deporte through the program FPU, Juan de la Cierva fellowship (FJCI-2015-24028), Red de Investigación en Inflamación y Enfermadades Reumaticas (RIER) from Instituto de Salud Carlos III (RD16/0012/0013), and Scleroderma Research Foundation and NIH P50-HG007735 (to H.Y.C.). H.Y.C. is an Investigator of the Howard Hughes Medical Institute. PopGen 2.0 is supported by a grant from the German Ministry for Education and Research (01EY1103). M.D.M and S.A. are supported by grant DoD W81XWH-18-1-0423 and DoD W81XWH-16-1-0296, respectively
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