98 research outputs found

    The Dependence of the Superconducting Transition Temperature of Organic Molecular Crystals on Intrinsically Non-Magnetic Disorder: a Signature of either Unconventional Superconductivity or Novel Local Magnetic Moment Formation

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    We give a theoretical analysis of published experimental studies of the effects of impurities and disorder on the superconducting transition temperature, T_c, of the organic molecular crystals kappa-ET_2X and beta-ET_2X (where ET is bis(ethylenedithio)tetrathiafulvalene and X is an anion eg I_3). The Abrikosov-Gorkov (AG) formula describes the suppression of T_c both by magnetic impurities in singlet superconductors, including s-wave superconductors and by non-magnetic impurities in a non-s-wave superconductor. We show that various sources of disorder lead to the suppression of T_c as described by the AG formula. This is confirmed by the excellent fit to the data, the fact that these materials are in the clean limit and the excellent agreement between the value of the interlayer hopping integral, t_perp, calculated from this fit and the value of t_perp found from angular-dependant magnetoresistance and quantum oscillation experiments. If the disorder is, as seems most likely, non-magnetic then the pairing state cannot be s-wave. We show that the cooling rate dependence of the magnetisation is inconsistent with paramagnetic impurities. Triplet pairing is ruled out by several experiments. If the disorder is non-magnetic then this implies that l>=2, in which case Occam's razor suggests that d-wave pairing is realised. Given the proximity of these materials to an antiferromagnetic Mott transition, it is possible that the disorder leads to the formation of local magnetic moments via some novel mechanism. Thus we conclude that either kappa-ET_2X and beta-ET_2X are d-wave superconductors or else they display a novel mechanism for the formation of localised moments. We suggest systematic experiments to differentiate between these scenarios.Comment: 18 pages, 5 figure

    TDP-43 in the hypoglossal nucleus identifies amyotrophic lateral sclerosis in behavioral variant frontotemporal dementia

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    The hypoglossal nucleus was recently identified as a key brain region in which the presence of TDP-43 pathology could accurately discriminate TDP-43 proteinopathy cases with clinical amyotrophic lateral sclerosis (ALS). The objective of the present study was to assess the hypoglossal nucleus in behavioral variant frontotemporal dementia (bvFTD), and determine whether TDP-43 in this region is associated with clinical ALS. Twenty-nine cases with neuropathological FTLD-TDP and clinical bvFTD that had not been previously assessed for hypoglossal TDP-43 pathology were included in this study. Of these 29 cases, 41% (n = 12) had a dual diagnosis of bvFTD-ALS at presentation, all 100% (n = 12) of which demonstrated hypoglossal TDP-43 pathology. Of the 59% (n = 17) cohort that presented with pure bvFTD, 35% (n = 6) were identified with hypoglossal TDP-43 pathology. Review of the case files of all pure bvFTD cases revealed evidence of possible or probable ALS in 5 of the 6 hypoglossal-positive cases (83%) towards the end of disease, and this was absent from all cases without such pathology. In conclusion, the present study validates grading the presence of TDP-43 in the hypoglossal nucleus for the pathological identification of bvFTD cases with clinical ALS, and extends this to include the identification of cases with possible ALS at end-stage

    Immune-related genetic enrichment in frontotemporal dementia:An analysis of genome-wide association studies

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    Background: Converging evidence suggests that immune-mediated dysfunction plays an important role in the pathogenesis of frontotemporal dementia (FTD). Although genetic studies have shown that immune-associated loci are associated with increased FTD risk, a systematic investigation of genetic overlap between immune-mediated diseases and the spectrum of FTD-related disorders has not been performed. Methods and findings: Using large genome-wide association studies (GWASs) (total n = 192,886 cases and controls) and recently developed tools to quantify genetic overlap/pleiotropy, we systematically identified single nucleotide polymorphisms (SNPs) jointly associated with FTD-related disorders—namely, FTD, corticobasal degeneration (CBD), progressive supranuclear palsy (PSP), and amyotrophic lateral sclerosis (ALS)—and 1 or more immune-mediated diseases including Crohn disease, ulcerative colitis (UC), rheumatoid arthritis (RA), type 1 diabetes (T1D), celiac disease (CeD), and psoriasis. We found up to 270-fold genetic enrichment between FTD and RA, up to 160-fold genetic enrichment between FTD and UC, up to 180-fold genetic enrichment between FTD and T1D, and up to 175-fold genetic enrichment between FTD and CeD. In contrast, for CBD and PSP, only 1 of the 6 immune-mediated diseases produced genetic enrichment comparable to that seen for FTD, with up to 150-fold genetic enrichment between CBD and CeD and up to 180-fold enrichment between PSP and RA. Further, we found minimal enrichment between ALS and the immune-mediated diseases tested, with the highest levels of enrichment between ALS and RA (up to 20-fold). For FTD, at a conjunction false discovery rate < 0.05 and after excluding SNPs in linkage disequilibrium, we found that 8 of the 15 identified loci mapped to the human leukocyte antigen (HLA) region on Chromosome (Chr) 6. We also found novel candidate FTD susceptibility loci within LRRK2 (leucine rich repeat kinase 2), TBKBP1 (TBK1 binding protein 1), and PGBD5 (piggyBac transposable element derived 5). Functionally, we found that the expression of FTD–immune pleiotropic genes (particularly within the HLA region) is altered in postmortem brain tissue from patients with FTD and is enriched in microglia/macrophages compared to other central nervous system cell types. The main study limitation is that the results represent only clinically diagnosed individuals. Also, given the complex interconnectedness of the HLA region, we were not able to define the specific gene or genes on Chr 6 responsible for our pleiotropic signal. Conclusions: We show immune-mediated genetic enrichment specifically in FTD, particularly within the HLA region. Our genetic results suggest that for a subset of patients, immune dysfunction may contribute to FTD risk. These findings have potential implications for clinical trials targeting immune dysfunction in patients with FTD

    A JWST near- and mid-infrared nebular spectrum of the type Ia supernova 2021aefx

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    We present JWST near-infrared (NIR) and mid-infrared (MIR) spectroscopic observations of the nearby normal Type Ia supernova (SN) SN 2021aefx in the nebular phase at +255 days past maximum light. Our Near Infrared Spectrograph (NIRSpec) and Mid Infrared Instrument observations, combined with ground-based optical data from the South African Large Telescope, constitute the first complete optical+NIR+MIR nebular SN Ia spectrum covering 0.3–14 μm. This spectrum unveils the previously unobserved 2.5−5 μm region, revealing strong nebular iron and stable nickel emission, indicative of high-density burning that can constrain the progenitor mass. The data show a significant improvement in sensitivity and resolution compared to previous Spitzer MIR data. We identify numerous NIR and MIR nebular emission lines from iron-group elements as well as lines from the intermediate-mass element argon. The argon lines extend to higher velocities than the iron-group elements, suggesting stratified ejecta that are a hallmark of delayed-detonation or double-detonation SN Ia models. We present fits to simple geometric line profiles to features beyond 1.2 μm and find that most lines are consistent with Gaussian or spherical emission distributions, while the [Ar iii] 8.99 μm line has a distinctively flat-topped profile indicating a thick spherical shell of emission. Using our line profile fits, we investigate the emissivity structure of SN 2021aefx and measure kinematic properties. Continued observations of SN 2021aefx and other SNe Ia with JWST will be transformative to the study of SN Ia composition, ionization structure, density, and temperature, and will provide important constraints on SN Ia progenitor and explosion models

    Ground-based and JWST Observations of SN 2022pul. II. Evidence from nebular spectroscopy for a violent merger in a peculiar type Ia supernova

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    We present an analysis of ground-based and JWST observations of SN 2022pul, a peculiar "03fg-like" (or "super-Chandrasekhar") Type Ia supernova (SN Ia), in the nebular phase at 338 days postexplosion. Our combined spectrum continuously covers 0.4–14 μm and includes the first mid-infrared spectrum of a 03fg-like SN Ia. Compared to normal SN Ia 2021aefx, SN 2022pul exhibits a lower mean ionization state, asymmetric emission-line profiles, stronger emission from the intermediate-mass elements (IMEs) argon and calcium, weaker emission from iron-group elements (IGEs), and the first unambiguous detection of neon in a SN Ia. A strong, broad, centrally peaked [Ne ii] line at 12.81 μm was previously predicted as a hallmark of "violent merger" SN Ia models, where dynamical interaction between two sub-MCh white dwarfs (WDs) causes disruption of the lower-mass WD and detonation of the other. The violent merger scenario was already a leading hypothesis for 03fg-like SNe Ia; in SN 2022pul it can explain the large-scale ejecta asymmetries seen between the IMEs and IGEs and the central location of narrow oxygen and broad neon. We modify extant models to add clumping of the ejecta to reproduce the optical iron emission better, and add mass in the innermost region (<2000 km s−1) to account for the observed narrow [O i] λλ6300, 6364 emission. A violent WD–WD merger explains many of the observations of SN 2022pul, and our results favor this model interpretation for the subclass of 03fg-like SNe Ia

    Mendelian randomization implies no direct causal association between leukocyte telomere length and amyotrophic lateral sclerosis

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    Funder: QingLan Research Project of Jiangsu for Outstanding Young TeachersFunder: Project funded by Postdoctoral Science Foundation of Xuzhou Medical UniversityFunder: Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD) for Xuzhou Medical UniversityAbstract: We employed Mendelian randomization (MR) to evaluate the causal relationship between leukocyte telomere length (LTL) and amyotrophic lateral sclerosis (ALS) with summary statistics from genome-wide association studies (n = ~ 38,000 for LTL and ~ 81,000 for ALS in the European population; n = ~ 23,000 for LTL and ~ 4,100 for ALS in the Asian population). We further evaluated mediation roles of lipids in the pathway from LTL to ALS. The odds ratio per standard deviation decrease of LTL on ALS was 1.10 (95% CI 0.93–1.31, p = 0.274) in the European population and 0.75 (95% CI 0.53–1.07, p = 0.116) in the Asian population. This null association was also detected between LTL and frontotemporal dementia in the European population. However, we found that an indirect effect of LTL on ALS might be mediated by low density lipoprotein (LDL) or total cholesterol (TC) in the European population. These results were robust against extensive sensitivity analyses. Overall, our MR study did not support the direct causal association between LTL and the ALS risk in neither population, but provided suggestive evidence for the mediation role of LDL or TC on the influence of LTL and ALS in the European population

    Search for heavy resonances decaying into a Z or W boson and a Higgs boson in final states with leptons and b-jets in 139 fb−1 of pp collisions at s√ = 13 TeV with the ATLAS detector

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    This article presents a search for new resonances decaying into a Z or W boson and a 125 GeV Higgs boson h, and it targets the νν¯¯¯bb¯¯, ℓ+ℓ−bb¯¯, or ℓ±νbb¯¯ final states, where ℓ = e or μ, in proton-proton collisions at s√ = 13 TeV. The data used correspond to a total integrated luminosity of 139 fb−1 collected by the ATLAS detector during Run 2 of the LHC at CERN. The search is conducted by examining the reconstructed invariant or transverse mass distributions of Zh or Wh candidates for evidence of a localised excess in the mass range from 220 GeV to 5 TeV. No significant excess is observed and 95% confidence-level upper limits between 1.3 pb and 0.3 fb are placed on the production cross section times branching fraction of neutral and charged spin-1 resonances and CP-odd scalar bosons. These limits are converted into constraints on the parameter space of the Heavy Vector Triplet model and the two-Higgs-doublet model

    Search for boosted diphoton resonances in the 10 to 70 GeV mass range using 138 fb−1 of 13 TeV pp collisions with the ATLAS detector

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    A search for diphoton resonances in the mass range between 10 and 70 GeV with the ATLAS experiment at the Large Hadron Collider (LHC) is presented. The analysis is based on pp collision data corresponding to an integrated luminosity of 138 fb−1 at a centre-of-mass energy of 13 TeV recorded from 2015 to 2018. Previous searches for diphoton resonances at the LHC have explored masses down to 65 GeV, finding no evidence of new particles. This search exploits the particular kinematics of events with pairs of closely spaced photons reconstructed in the detector, allowing examination of invariant masses down to 10 GeV. The presented strategy covers a region previously unexplored at hadron colliders because of the experimental challenges of recording low-energy photons and estimating the backgrounds. No significant excess is observed and the reported limits provide the strongest bound on promptly decaying axion-like particles coupling to gluons and photons for masses between 10 and 70 GeV
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