Exploring nu signals in dark matter detectors

We investigate standard and non-standard solar neutrino signals in direct dark matter detection experiments. It is well known that even without new physics, scattering of solar neutrinos on nuclei or electrons is an irreducible background for direct dark matter searches, once these experiments each the ton scale. Here, we entertain the possibility that neutrino interactions are enhanced by new physics, such as new light force carriers (for instance a "dark photon") or neutrino magnetic moments. We consider models with only the three standard neutrino flavors, as well as scenarios with extra sterile neutrinos. We find that low-energy neutrino--electron and neutrino--nucleus scattering rates can be enhanced by several orders of magnitude, potentially enough to explain the event excesses observed in CoGeNT and CRESST. We also investigate temporal modulation in these neutrino signals, which can arise from geometric effects, oscillation physics, non-standard neutrino energy loss, and direction-dependent detection efficiencies. We emphasize that, in addition to providing potential explanations for existing signals, models featuring new physics in the neutrino sector can also be very relevant to future dark matter searches, where, on the one hand, they can be probed and constrained, but on the other hand, their signatures could also be confused with dark matter signals.Comment: 38 pages, 8 figures, 1 table; v3: eq 3 and nuclear recoil plots corrected, footnote added, conclusions unchange

A new measurement of the Collins and Sivers asymmetries on a transversely polarised deuteron target

New high precision measurements of the Collins and Sivers asymmetries of charged hadrons produced in deep-inelastic scattering of muons on a transversely polarised 6LiD target are presented. The data were taken in 2003 and 2004 with the COMPASS spectrometer using the muon beam of the CERN SPS at 160 GeV/c. Both the Collins and Sivers asymmetries turn out to be compatible with zero, within the present statistical errors, which are more than a factor of 2 smaller than those of the published COMPASS results from the 2002 data. The final results from the 2002, 2003 and 2004 runs are compared with naive expectations and with existing model calculations.Comment: 40 pages, 28 figure

Burosumab treatment in adults with X-linked hypophosphataemia: 96-week patient-reported outcomes and ambulatory function from a randomised phase 3 trial and open-label extension

Objectives To report the impact of burosumab on patient-reported outcomes (PROs) and ambulatory function in adults with X-linked hypophosphataemia (XLH) through 96 weeks. Methods Adults diagnosed with XLH were randomised 1:1 in a double-blinded trial to receive subcutaneous burosumab 1 mg/kg or placebo every 4 weeks for 24 weeks (NCT02526160). Thereafter, all subjects received burosumab every 4 weeks until week 96. PROs were measured using the Western Ontario and the McMaster Universities Osteoarthritis Index (WOMAC), Brief Pain Inventory-Short Form (BPI-SF) and Brief Fatigue Inventory (BFI), and ambulatory function was measured with the 6 min walk test (6MWT). Results Subjects (N=134) were randomised to burosumab (n=68) or placebo (n=66) for 24 weeks. At baseline, subjects experienced pain, stiffness, and impaired physical and ambulatory function. At week 24, subjects receiving burosumab achieved statistically significant improvement in some BPI-SF scores, BFI worst fatigue (average and greatest) and WOMAC stiffness. At week 48, all WOMAC and BPI-SF scores achieved statistically significant improvement, with some WOMAC and BFI scores achieving meaningful and significant change from baseline. At week 96, all WOMAC, BPI-SF and BFI achieved statistically significant improvement, with selected scores in all measures also achieving meaningful change. Improvement in 6MWT distance and percent predicted were statistically significant at all time points from 24 weeks. Conclusions Adults with XLH have substantial burden of disease as assessed by PROs and 6MWT. Burosumab treatment improved phosphate homoeostasis and was associated with a steady and consistent improvement in PROs and ambulatory function. Trial registration number NCT02526160

Prospects for e+e- physics at Frascati between the phi and the psi

We present a detailed study, done in the framework of the INFN 2006 Roadmap, of the prospects for e+e- physics at the Frascati National Laboratories. The physics case for an e+e- collider running at high luminosity at the phi resonance energy and also reaching a maximum center of mass energy of 2.5 GeV is discussed, together with the specific aspects of a very high luminosity tau-charm factory. Subjects connected to Kaon decay physics are not discussed here, being part of another INFN Roadmap working group. The significance of the project and the impact on INFN are also discussed. All the documentation related to the activities of the working group can be found in http://www.roma1.infn.it/people/bini/roadmap.html.Comment: INFN Roadmap Report: 86 pages, 25 figures, 9 table

Zoledronate in the prevention of Paget's (ZiPP) : protocol for a randomised trial of genetic testing and targeted zoledronic acid therapy to prevent SQSTM1-mediated Paget's disease of bone.

Introduction Paget’s disease of bone (PDB) is characterised by increased and disorganised bone remodelling affecting one or more skeletal sites. Complications include bone pain, deformity, deafness and pathological fractures. Mutations in sequestosome-1 (SQSTM1) are strongly associated with the development of PDB. Bisphosphonate therapy can improve bone pain in PDB, but there is no evidence that treatment alters the natural history of PDB or prevents complications. The Zoledronate in the Prevention of Paget’s disease trial (ZiPP) will determine if prophylactic therapy with the bisphosphonate zoledronic acid (ZA) can delay or prevent the development of PDB in people who carry SQSTM1 mutations. Methods and analysis People with a family history of PDB aged >30 years who test positive for SQSTM1 mutations are eligible to take part. At the baseline visit, participants will be screened for the presence of bone lesions by radionuclide bone scan. Biochemical markers of bone turnover will be measured and questionnaires completed to assess pain, health-related quality of life (HRQoL), anxiety and depression. Participants will be randomised to receive a single intravenous infusion of 5 mg ZA or placebo and followed up annually for between 4 and 8 years at which point baseline assessments will be repeated. The primary endpoint will be new bone lesions assessed by radionuclide bone scan. Secondary endpoints will include changes in biochemical markers of bone turnover, pain, HRQoL, anxiety, depression and PDB-related skeletal events

Genetic Sharing with Cardiovascular Disease Risk Factors and Diabetes Reveals Novel Bone Mineral Density Loci.

Bone Mineral Density (BMD) is a highly heritable trait, but genome-wide association studies have identified few genetic risk factors. Epidemiological studies suggest associations between BMD and several traits and diseases, but the nature of the suggestive comorbidity is still unknown. We used a novel genetic pleiotropy-informed conditional False Discovery Rate (FDR) method to identify single nucleotide polymorphisms (SNPs) associated with BMD by leveraging cardiovascular disease (CVD) associated disorders and metabolic traits. By conditioning on SNPs associated with the CVD-related phenotypes, type 1 diabetes, type 2 diabetes, systolic blood pressure, diastolic blood pressure, high density lipoprotein, low density lipoprotein, triglycerides and waist hip ratio, we identified 65 novel independent BMD loci (26 with femoral neck BMD and 47 with lumbar spine BMD) at conditional FDR < 0.01. Many of the loci were confirmed in genetic expression studies. Genes validated at the mRNA levels were characteristic for the osteoblast/osteocyte lineage, Wnt signaling pathway and bone metabolism. The results provide new insight into genetic mechanisms of variability in BMD, and a better understanding of the genetic underpinnings of clinical comorbidity