Testing creation of matter with neutrinoless double beta decay

In this brief review, the importance of the so called neutrinoless double beta decay transition in the search for physics beyond the Standard Model is emphasized. The expectations for the transition rate are examined in the assumption that ordinary neutrinos have Majorana masses. We stress the relevance of cosmological measurements and discuss the uncertainties implied by nuclear physics.Comment: 9 pages. Based on the review paper Neutrinoless double beta decay: 2015 review, Adv.High Energy Phys. 2016 (2016) 2162659. To appear in the proceedings of the XVII International Workshop on Neutrino Telescopes 13-17 March 2017, Venice, Ital

Is the Eureka cluster a collisional family of Mars Trojan asteroids?

We explore the hypothesis that the Eureka family of sub-km asteroids in the L5 region of Mars could have formed in a collision. We estimate the size distribution index from available information on family members; model the orbital dispersion of collisional fragments; and carry out a formal calculation of the collisional lifetime as a function of size. We find that, as initially conjectured by Rivkin et al (2003), the collisional lifetime of objects the size of (5261) Eureka is at least a few Gyr, significantly longer than for similar-sized Main Belt asteroids. In contrast, the observed degree of orbital compactness is inconsistent with all but the least energetic family-forming collisions. Therefore, the family asteroids may be ejecta from a cratering event sometime in the past ~1 Gyr if the orbits are gradually dispersed by gravitational diffusion and the Yarkovsky effect (Cuk et al, 2015). The comparable sizes of the largest family members require either negligible target strength or a particular impact geometry under this scenario (Durda et al, 2007; Benavidez et al, 2012). Alternatively, the family may have formed by a series of YORP-induced fission events (Pravec.et.al, 2010). The shallow size distribution of the family is similar to that of small MBAs (Gladman et al, 2009) interpreted as due to the dominance of this mechanism for Eureka-family-sized asteroids (Jacobson et al, 2014). However, our population index estimate is likely a lower limit due to the small available number of family asteroids and observational incompleteness. Future searches for fainter family members, further observational characterisation of the known Trojans' physical properties as well as orbital and rotational evolution modelling will help distinguish between different formation models.Comment: 3 Tables, 13 Figures, Accepted for publication in Icaru

Neutrinoless Double Beta Decay Experiments With TeO2 Low-Temperature Detectors

Neutrinoless double beta decay (0νββ) is a powerful tool to investigate Lepton Number Violation (LNV), and the only practical way to assess the nature of the neutrinos. It can therefore provide unique information about the Physics Beyond the Standard Model. If observed, 0νββ would unambiguously demonstrate that neutrinos are Majorana particles and would provide a precise measurement of their mass. Among the many experimental techniques used in the search for this rare process, low-temperature detectors represent one of the most promising choices: they show an excellent energy resolution and can scale to very large masses. In this work, we review the most relevant experiments based on TeO2 bolometers that have been developed and taking data at the Laboratori Nazionali del Gran Sasso (LNGS), Italy, since the early 90's. This 30-years-old effort has led to the design and construction of the CUORE detector, currently taking data at LNGS. The use of low-temperature detectors allows to study the 0νββ of 130Te on both ground and excited states, and to explore different decay mechanisms ("standard" light neutrino exchange, Majoron emission, …). At the same time, the investigation of other rare nuclear physics processes is also possible, such as the two-neutrino double beta decay of 130Te as well as the rare decays (120Te and 123Te). Next generation bolometric experiments anticipate top leading sensitivities. The corresponding challenges in the development of ton-scale, low background detectors are highlighted

The Results of the URRAH (Uric Acid Right for Heart Health) Project: A Focus on Hyperuricemia in Relation to Cardiovascular and Kidney Disease and its Role in Metabolic Dysregulation

The relationship between Serum Uric Acid (UA) and Cardiovascular (CV) diseases has already been extensively evaluated, and it was found to be an independent predictor of all-cause and cardiovascular mortality but also acute coronary syndrome, stroke and heart failure. Similarly, also many papers have been published on the association between UA and kidney function, while less is known on the role of UA in metabolic derangement and, particularly, in metabolic syndrome. Despite the substantial number of publications on the topic, there are still some elements of doubt: (1) the better cut-off to be used to refine CV risk (also called CV cut-off); (2) the needing for a correction of UA values for kidney function; and (3) the better definition of its role in metabolic syndrome: is UA simply a marker, a bystander or a key pathological element of metabolic dysregulation?. The Uric acid Right for heArt Health (URRAH) project was designed by the Working Group on uric acid and CV risk of the Italian Society of Hypertension to answer the first question. After the first papers that individuates specific cut-off for different CV disease, subsequent articles have been published responding to the other relevant questions. This review will summarise most of the results obtained so far from the URRAH research project

Serum Uric Acid Predicts All-Cause and Cardiovascular Mortality Independently of Hypertriglyceridemia in Cardiometabolic Patients without Established CV Disease: A Sub-Analysis of the URic acid Right for heArt Health (URRAH) Study

High serum uric acid (SUA) and triglyceride (TG) levels might promote high-cardiovascular risk phenotypes across the cardiometabolic spectrum. However, SUA predictive power in the presence of normal and high TG levels has never been investigated. We included 8124 patients from the URic acid Right for heArt Health (URRAH) study cohort who were followed for over 20 years and had no established cardiovascular disease or uncontrolled metabolic disease. All-cause mortality (ACM) and cardiovascular mortality (CVM) were explored by the Kaplan-Meier estimator and Cox multivariable regression, adopting recently defined SUA cut-offs for ACM (≥4.7 mg/dL) and CVM (≥5.6 mg/dL). Exploratory analysis across cardiometabolic subgroups and a sensitivity analysis using SUA/serum creatinine were performed as validation. SUA predicted ACM (HR 1.25 [1.12-1.40], p < 0.001) and CVM (1.31 [1.11-1.74], p < 0.001) in the whole study population, and according to TG strata: ACM in normotriglyceridemia (HR 1.26 [1.12-1.43], p < 0.001) and hypertriglyceridemia (1.31 [1.02-1.68], p = 0.033), and CVM in normotriglyceridemia (HR 1.46 [1.23-1.73], p < 0.001) and hypertriglyceridemia (HR 1.31 [0.99-1.64], p = 0.060). Exploratory and sensitivity analyses confirmed our findings, suggesting a substantial role of SUA in normotriglyceridemia and hypertriglyceridemia. In conclusion, we report that SUA can predict ACM and CVM in cardiometabolic patients without established cardiovascular disease, independent of TG levels

The importance of microvascular inflammation in ageing and age-related diseases: a position paper from the ESH working group on small arteries, section of microvascular inflammation

Microcirculation is pervasive and orchestrates a profound regulatory cross-talk with the surrounding tissue and organs. Similarly, it is one of the earliest biological systems targeted by environmental stressors and consequently involved in the development and progression of ageing and age-related disease. Microvascular dysfunction, if not targeted, leads to a steady derangement of the phenotype, which cumulates comorbidities and eventually results in a nonrescuable, very high-cardiovascular risk. Along the broad spectrum of pathologies, both shared and distinct molecular pathways and pathophysiological alteration are involved in the disruption of microvascular homeostasis, all pointing to microvascular inflammation as the putative primary culprit. This position paper explores the presence and the detrimental contribution of microvascular inflammation across the whole spectrum of chronic age-related diseases, which characterise the 21st-century healthcare landscape. The manuscript aims to strongly affirm the centrality of microvascular inflammation by recapitulating the current evidence and providing a clear synoptic view of the whole cardiometabolic derangement. Indeed, there is an urgent need for further mechanistic exploration to identify clear, very early or disease-specific molecular targets to provide an effective therapeutic strategy against the otherwise unstoppable rising prevalence of age-related diseases