First characterisation of the PADME electromagnetic calorimeter

The PADME experiment, hosted at the LNF Beam Test Facility, is searching for a dark photon that decays into dark matter particles. This search is performed looking for the reaction e+ + e− → A0 + γ, where A' is the dark photon, which cannot be observed directly or via its decay products. A key role in the experiment is played by the electromagnetic calorimeter, which measures the energy and the position of the γ in the final state. From this, the missing four-momentum carried away by the A' can be evaluated and the particle mass can be inferred. This article will present the process followed for the construction and calibration of the electromagnetic calorimeter of the experiment. The results achieved in terms of equalisation, detection efficiency and energy resolution during the first phase of the experiment, demonstrate the effectiveness of the various devices used to improve the calorimeter performance with respect to first prototypes

Dark Photon Search with PADME at LNF

Dark Matter elusiveness could be explained by speculating that it lives in a separate sector with respect to the Standard Model and that interacts with it only by means of messengers. The simplest model foresees just one messenger: a, possibly massive, vector boson given by a new U(1) symmetry. This mediator can faintly mix with the photon and, hence, interact with SM charged particles, seeing an effective charge equal to [Formula: see text], with [Formula: see text] SM charge. The PADME experiment, hosted at Laboratori Nazionali di Frascati, is designed to search for such kind of particle, looking for its production in [Formula: see text] annihilations. Exploiting the DA[Formula: see text]NE linac, the collaboration aims to collect [Formula: see text] positrons on target by the end of 2018, reaching a sensitivity of [Formula: see text] for masses up to [Formula: see text][Formula: see text]Mev

Trigger and Analysis Tools for Dark Matter Search in CUORE-0☆

Abstract The CUORE and CUORE-0 experiments have the possibility to search for Dark Matter interactions. To reach this goal is necessary to use a dedicated trigger, the Optimum Trigger, based on the matched filter technique, that pushes the energy threshold down to the keV region, where the signal is expected to lie. In addition, new low energy analysis tools are described

Genetic lineage tracing reveals poor angiogenic potential of cardiac endothelial cells.

Abstract Aims Cardiac ischaemia does not elicit an efficient angiogenic response. Indeed, lack of surgical revascularization upon myocardial infarction results in cardiomyocyte death, scarring, and loss of contractile function. Clinical trials aimed at inducing therapeutic revascularization through the delivery of pro-angiogenic molecules after cardiac ischaemia have invariably failed, suggesting that endothelial cells in the heart cannot mount an efficient angiogenic response. To understand why the heart is a poorly angiogenic environment, here we compare the angiogenic response of the cardiac and skeletal muscle using a lineage tracing approach to genetically label sprouting endothelial cells. Methods and results We observed that overexpression of the vascular endothelial growth factor in the skeletal muscle potently stimulated angiogenesis, resulting in the formation of a massive number of new capillaries and arterioles. In contrast, response to the same dose of the same factor in the heart was blunted and consisted in a modest increase in the number of new arterioles. By using Apelin-CreER mice to genetically label sprouting endothelial cells we observed that different pro-angiogenic stimuli activated Apelin expression in both muscle types to a similar extent, however, only in the skeletal muscle, these cells were able to sprout, form elongated vascular tubes activating Notch signalling, and became incorporated into arteries. In the heart, Apelin-positive cells transiently persisted and failed to give rise to new vessels. When we implanted cancer cells in different organs, the abortive angiogenic response in the heart resulted in a reduced expansion of the tumour mass. Conclusion Our genetic lineage tracing indicates that cardiac endothelial cells activate Apelin expression in response to pro-angiogenic stimuli but, different from those of the skeletal muscle, fail to proliferate and form mature and structured vessels. The poor angiogenic potential of the heart is associated with reduced tumour angiogenesis and growth of cancer cells

Discovery of the 151^{151}Eu α\alpha decay

We report on the first compelling observation of $\alpha$ decay of $^{151}$Eu to the ground state of $^{147}$Pm. The measurement was performed using a 6.15 g Li$_6$Eu(BO$_3$)$_3$ crystal operated as a scintillating bolometer. The Q-value and half-life measured are: Q = 1948.9$\pm 6.9(stat.) \pm 5.1(syst.)$ keV, and T$_{1/2}=\left( 4.62\pm0.95(stat.)\pm0.68(syst.)\right) \times 10^{18}$ y . The half-life prediction of nuclear theory using the Coulomb and proximity potential model are in good agreement with this experimental result

Distribution of Exonic Variants in Glycogen Synthesis and Catabolism Genes in Late Onset Pompe Disease (LOPD)

Pompe disease (PD) is a monogenic autosomal recessive disorder caused by biallelic pathogenic variants of the GAA gene encoding lysosomal alpha-glucosidase; its loss causes glycogen storage in lysosomes, mainly in the muscular tissue. The genotype-phenotype correlation has been extensively discussed, and caution is recommended when interpreting the clinical significance of any mutation in a single patient. As there is no evidence that environmental factors can modulate the phenotype, the observed clinical variability in PD suggests that genetic variants other than pathogenic GAA mutations influence the mechanisms of muscle damage/repair and the overall clinical picture. Genes encoding proteins involved in glycogen synthesis and catabolism may represent excellent candidates as phenotypic modifiers of PD. The genes analyzed for glycogen synthesis included UGP2, glycogenin (GYG1-muscle, GYG2, and other tissues), glycogen synthase (GYS1-muscle and GYS2-liver), GBE1, EPM2A, NHLRC1, GSK3A, and GSK3B. The only enzyme involved in glycogen catabolism in lysosomes is alpha-glucosidase, which is encoded by GAA, while two cytoplasmic enzymes, phosphorylase (PYGB-brain, PGL-liver, and PYGM-muscle) and glycogen debranching (AGL) are needed to obtain glucose 1-phosphate or free glucose. Here, we report the potentially relevant variants in genes related to glycogen synthesis and catabolism, identified by whole exome sequencing in a group of 30 patients with late-onset Pompe disease (LOPD). In our exploratory analysis, we observed a reduced number of variants in the genes expressed in muscles versus the genes expressed in other tissues, but we did not find a single variant that strongly affected the phenotype. From our work, it also appears that the current clinical scores used in LOPD do not describe muscle impairment with enough qualitative/quantitative details to correlate it with genes that, even with a slightly reduced function due to genetic variants, impact the phenotype

Shedding light on X17: community report

The workshop “Shedding light on X17” brings together scientists looking for the existence of a possible new light particle, often referred to as X17. This hypothetical particle can explain the resonant structure observed at ∼ 17 MeV in the invariant mass of electron-positron pairs, produced after excitation of nuclei such as 8Be and 4He by means of proton beams at the Atomki Laboratory in Debrecen. The purpose of the workshop is to discuss implications of this anomaly, in particular theoretical interpretations as well as present and future experiments aiming at confirming the result and/or at providing experimental evidence for its interpretation

Initial performance of the CUORE-0 experiment

CUORE-0 is a cryogenic detector that uses an array of tellurium dioxide bolometers to search for neutrinoless double-beta decay of ^{130}Te. We present the first data analysis with 7.1 kg y of total TeO_2 exposure focusing on background measurements and energy resolution. The background rates in the neutrinoless double-beta decay region of interest (2.47 to 2.57 MeV) and in the {\alpha} background-dominated region (2.70 to 3.90 MeV) have been measured to be 0.071 \pm 0.011 and 0.019 \pm 0.002 counts/keV/kg/y, respectively. The latter result represents a factor of 6 improvement from a predecessor experiment, Cuoricino. The results verify our understanding of the background sources in CUORE-0, which is the basis of extrapolations to the full CUORE detector. The obtained energy resolution (full width at half maximum) in the region of interest is 5.7 keV. Based on the measured background rate and energy resolution in the region of interest, CUORE-0 half-life sensitivity is expected to surpass the observed lower bound of Cuoricino with one year of live time.Comment: 8 pages, 5 figures, version 2 as published in Eur. Phys. J.

Neutrinoless double-beta decay search with CUORE and CUORE-0 experiments

The Cryogenic Underground Observatory for Rare Events (CUORE) is an upcoming experiment designed to search for the neutrinoless double-beta decays. Observation of the process would unambiguously establish that neutrinos are Majorana particles and provide information on their absolute mass scale hierarchy. CUORE is now under construction and will consist of an array of 988 TeO2 crystal bolometers operated at 10 mK, but the first tower (CUORE-0) is already taking data. The experimental techniques used will be presented as well as the preliminary CUORE-0 results. The current status of the full-mass experiment and its expected sensitivity will then be discussed