Multi-gap superconductivity in a BaFe1.84Co0.16As2 film from optical measurements at terahertz frequencies

We measured the THz reflectance properties of a high quality epitaxial thin film of the Fe-based superconductor BaFe$_{1.84}$Co$_{0.16}$As$_2$ with T$_c$=22.5 K. The film was grown by pulsed laser deposition on a DyScO$_3$ substrate with an epitaxial SrTiO$_3$ intermediate layer. The measured $R_S/R_N$ spectrum, i.e. the reflectivity ratio between the superconducting and normal state reflectance, provides clear evidence of a superconducting gap $\Delta_A$ close to 15 cm$^{-1}$. A detailed data analysis shows that a two-band, two-gap model is absolutely necessary to obtain a good description of the measured $R_S/R_N$ spectrum. The low-energy $\Delta_A$ gap results to be well determined ($\Delta_A$=15.5$\pm$0.5 cm$^{-1}$), while the value of the high-energy gap $\Delta_B$ is more uncertain ($\Delta_B$=55$\pm$7 cm$^{-1}$). Our results provide evidence of a nodeless isotropic double-gap scenario, with the presence of two optical gaps corresponding to 2$\Delta/kT_c$ values close to 2 and 7.Comment: Published Versio

Large-angle production of charged pions by 3 GeV/c - 12.9 GeV/c protons on beryllium, aluminium and lead targets

Measurements of the double-differential $\pi^{\pm}$ production cross-section in the range of momentum 100 \MeVc \leq p < 800 \MeVc and angle 0.35 \rad \leq \theta < 2.15 \rad in proton--beryllium, proton--aluminium and proton--lead collisions are presented. The data were taken with the HARP detector in the T9 beam line of the CERN PS. The pions were produced by proton beams in a momentum range from 3 \GeVc to 12.9 \GeVc hitting a target with a thickness of 5% of a nuclear interaction length. The tracking and identification of the produced particles was performed using a small-radius cylindrical time projection chamber (TPC) placed inside a solenoidal magnet. Incident particles were identified by an elaborate system of beam detectors. Results are obtained for the double-differential cross-sections at six incident proton beam momenta (3 \GeVc, 5 \GeVc, 8 \GeVc, 8.9 \GeVc (Be only), 12 \GeVc and 12.9 \GeVc (Al only)) and compared to previously available data

Observation of exclusive DVCS in polarized electron beam asymmetry measurements

We report the first results of the beam spin asymmetry measured in the reaction e + p -> e + p + gamma at a beam energy of 4.25 GeV. A large asymmetry with a sin(phi) modulation is observed, as predicted for the interference term of Deeply Virtual Compton Scattering and the Bethe-Heitler process. The amplitude of this modulation is alpha = 0.202 +/- 0.028. In leading-order and leading-twist pQCD, the alpha is directly proportional to the imaginary part of the DVCS amplitude.Comment: 6 pages, 5 figure

Physics with charm particles produced in neutrino interactions. A historical recollection

Results obtained in neutrino unteractions on charm particles are presented

UK Eutrophying and Acidifying Atmospheric Pollutants Monitoring networks UKEAP

In 2012 the complete dataset from the Defra funded UK Eutrophying and Acidifying Atmospheric Pollutants National Ammonia MOnitoring Network and the Acid Gas and aerosol network was prepared and submitted to EMEP for publication in the EMEP database. The talk gave an overview of the measurements being made and the scientific purpose of them

Age at symptom onset and death and disease duration in genetic frontotemporal dementia : an international retrospective cohort study

Background: Frontotemporal dementia is a heterogenous neurodegenerative disorder, with about a third of cases being genetic. Most of this genetic component is accounted for by mutations in GRN, MAPT, and C9orf72. In this study, we aimed to complement previous phenotypic studies by doing an international study of age at symptom onset, age at death, and disease duration in individuals with mutations in GRN, MAPT, and C9orf72. Methods: In this international, retrospective cohort study, we collected data on age at symptom onset, age at death, and disease duration for patients with pathogenic mutations in the GRN and MAPT genes and pathological expansions in the C9orf72 gene through the Frontotemporal Dementia Prevention Initiative and from published papers. We used mixed effects models to explore differences in age at onset, age at death, and disease duration between genetic groups and individual mutations. We also assessed correlations between the age at onset and at death of each individual and the age at onset and at death of their parents and the mean age at onset and at death of their family members. Lastly, we used mixed effects models to investigate the extent to which variability in age at onset and at death could be accounted for by family membership and the specific mutation carried. Findings: Data were available from 3403 individuals from 1492 families: 1433 with C9orf72 expansions (755 families), 1179 with GRN mutations (483 families, 130 different mutations), and 791 with MAPT mutations (254 families, 67 different mutations). Mean age at symptom onset and at death was 49\ub75 years (SD 10\ub70; onset) and 58\ub75 years (11\ub73; death) in the MAPT group, 58\ub72 years (9\ub78; onset) and 65\ub73 years (10\ub79; death) in the C9orf72 group, and 61\ub73 years (8\ub78; onset) and 68\ub78 years (9\ub77; death) in the GRN group. Mean disease duration was 6\ub74 years (SD 4\ub79) in the C9orf72 group, 7\ub71 years (3\ub79) in the GRN group, and 9\ub73 years (6\ub74) in the MAPT group. Individual age at onset and at death was significantly correlated with both parental age at onset and at death and with mean family age at onset and at death in all three groups, with a stronger correlation observed in the MAPT group (r=0\ub745 between individual and parental age at onset, r=0\ub763 between individual and mean family age at onset, r=0\ub758 between individual and parental age at death, and r=0\ub769 between individual and mean family age at death) than in either the C9orf72 group (r=0\ub732 individual and parental age at onset, r=0\ub736 individual and mean family age at onset, r=0\ub738 individual and parental age at death, and r=0\ub740 individual and mean family age at death) or the GRN group (r=0\ub722 individual and parental age at onset, r=0\ub718 individual and mean family age at onset, r=0\ub722 individual and parental age at death, and r=0\ub732 individual and mean family age at death). Modelling showed that the variability in age at onset and at death in the MAPT group was explained partly by the specific mutation (48%, 95% CI 35\u201362, for age at onset; 61%, 47\u201373, for age at death), and even more by family membership (66%, 56\u201375, for age at onset; 74%, 65\u201382, for age at death). In the GRN group, only 2% (0\u201310) of the variability of age at onset and 9% (3\u201321) of that of age of death was explained by the specific mutation, whereas 14% (9\u201322) of the variability of age at onset and 20% (12\u201330) of that of age at death was explained by family membership. In the C9orf72 group, family membership explained 17% (11\u201326) of the variability of age at onset and 19% (12\u201329) of that of age at death. Interpretation: Our study showed that age at symptom onset and at death of people with genetic frontotemporal dementia is influenced by genetic group and, particularly for MAPT mutations, by the specific mutation carried and by family membership. Although estimation of age at onset will be an important factor in future pre-symptomatic therapeutic trials for all three genetic groups, our study suggests that data from other members of the family will be particularly helpful only for individuals with MAPT mutations. Further work in identifying both genetic and environmental factors that modify phenotype in all groups will be important to improve such estimates. Funding: UK Medical Research Council, National Institute for Health Research, and Alzheimer's Society

Comprehensive analysis of epigenetic clocks reveals associations between disproportionate biological ageing and hippocampal volume

The concept of age acceleration, the difference between biological age and chronological age, is of growing interest, particularly with respect to age-related disorders, such as Alzheimer’s Disease (AD). Whilst studies have reported associations with AD risk and related phenotypes, there remains a lack of consensus on these associations. Here we aimed to comprehensively investigate the relationship between five recognised measures of age acceleration, based on DNA methylation patterns (DNAm age), and cross-sectional and longitudinal cognition and AD-related neuroimaging phenotypes (volumetric MRI and Amyloid-β PET) in the Australian Imaging, Biomarkers and Lifestyle (AIBL) and the Alzheimer’s Disease Neuroimaging Initiative (ADNI). Significant associations were observed between age acceleration using the Hannum epigenetic clock and cross-sectional hippocampal volume in AIBL and replicated in ADNI. In AIBL, several other findings were observed cross-sectionally, including a significant association between hippocampal volume and the Hannum and Phenoage epigenetic clocks. Further, significant associations were also observed between hippocampal volume and the Zhang and Phenoage epigenetic clocks within Amyloid-β positive individuals. However, these were not validated within the ADNI cohort. No associations between age acceleration and other Alzheimer’s disease-related phenotypes, including measures of cognition or brain Amyloid-β burden, were observed, and there was no association with longitudinal change in any phenotype. This study presents a link between age acceleration, as determined using DNA methylation, and hippocampal volume that was statistically significant across two highly characterised cohorts. The results presented in this study contribute to a growing literature that supports the role of epigenetic modifications in ageing and AD-related phenotypes