State-dependent Jastrow correlation functions for 4He nuclei

We calculate the ground-state energy for the nucleus 4He with V4 nucleon interactions, making use of a Jastrow description of the corresponding wavefunction with state-dependent correlation factors. The effect related to the state dependence of the correlation is quite important, lowering the upper bound for the ground-state energy by some 2 MeV.Comment: 10 pages, REVTeX, to be published in J. Phys. G: Nucl. Part. Phy

Projected multicluster model with Jastrow and linear state dependent correlations for 12≤A≤1612 \leq A \leq 16 nuclei

Variational wave functions based on a Margenau-Brink cluster model with short range and state dependent correlations, and angular momentum projection are obtained for some nuclei with $12 \leq A \leq 16$. The calculations have been carried out starting from the nucleon-nucleon interaction by using the Variational Monte Carlo method. The configuration used consists of three alpha clusters located at the apexes of an equilateral triangle, and an additional cluster, not necessarily of alpha type, forming a tetrahedron. This cluster is located at the top of its height. Short-range and state dependent correlations are included by means of a central Jastrow factor and a linear operatorial correlation factor respectively. Angular momentum projection is performed by using the Peierls-Yoccoz operators. Optimal structures are obtained for all the nuclei studied. Some aspects of our methodology have been tested by comparing with previous calculations carried out without short range correlations. The binding energy, the root mean square radius, and the one- and two-body densities are reported. The effects of correlations on both the energy and the nucleon distribution are analyzed systematically.Comment: 19 pages, 6 figure

NOD1 deficiency promotes an imbalance of thyroid hormones and microbiota homeostasis in mice fed high fat diet

The contribution of the nucleotide-binding oligomerization domain protein NOD1 to obesity has been investigated in mice fed a high fat diet (HFD). Absence of NOD1 accelerates obesity as early as 2 weeks after feeding a HFD. The obesity was due to increases in abdominal and inguinal adipose tissues. Analysis of the resting energy expenditure showed an impaired function in NOD1-deficient animals, compatible with an alteration in thyroid hormone homeostasis. Interestingly, free thyroidal T4 increased in NOD1-deficient mice fed a HFD and the expression levels of UCP1 in brown adipose tissue were significantly lower in NOD1-deficient mice than in the wild type animals eating a HFD, thus contributing to the observed adiposity in NOD1-deficient mice. Feeding a HFD resulted in an alteration of the proinflammatory profile of these animals, with an increase in the infiltration of inflammatory cells in the liver and in the white adipose tissue, and an elevation of the circulating levels of TNF-α. In addition, alterations in the gut microbiota in NOD1-deficient mice correlate with increased vulnerability of their ecosystem to the HFD challenge and affect the immune-metabolic phenotype of obese mice. Together, the data are compatible with a protective function of NOD1 against low-grade inflammation and obesity under nutritional conditions enriched in saturated lipids. Moreover, one of the key players of this early obesity onset is a dysregulation in the metabolism and release of thyroid hormones leading to reduced energy expenditure, which represents a new role for these hormones in the metabolic actions controlled by NOD1.This work was supported by Grants SAF2017-82436R, AGL2017-88801-P and SAF2016-75004R from MINECO/AEI/FEDER/EU, S2017/BMD-3686 from Comunidad de Madrid, CIVP18A3864 from Fundación Ramón Areces and CIBERCV and CIBERHED (funded by the Instituto de Salud Carlos III) and Fondos FEDER.Peer reviewe

Mild and short-term caloric restriction prevents obesity-induced cardiomyopathy in young zucker rats without changing in metabolites and fatty acids cardiac profile

Caloric restriction (CR) ameliorates cardiac dysfunction associated with obesity. However, most of the studies have been performed under severe CR (30-65% caloric intake decrease) for several months or even years in aged animals. Here, we investigated whether mild (20% food intake reduction) and short-term (2-weeks) CR prevented the obese cardiomyopathy phenotype and improved the metabolic profile of young (14 weeks of age) genetically obese Zucker fa/fa rats. Heart weight (HW) and HW/tibia length ratio was significantly lower in fa/fa rats after 2 weeks of CR than in counterparts fed ad libitum. Invasive pressure measurements showed that systolic blood pressure, maximal rate of positive left ventricle (LV) pressure, LV systolic pressure and LV end-diastolic pressure were all significantly higher in obese fa/fa rats than in lean counterparts, which were prevented by CR. Magnetic resonance imaging revealed that the increase in LV end-systolic volume, stroke volume and LV wall thickness observed in fa/fa rats was significantly lower in animals on CR diet. Histological analysis also revealed that CR blocked the significant increase in cardiomyocyte diameter in obese fa/fa rats. High resolution magic angle spinning magnetic resonance spectroscopy analysis of the LV revealed a global decrease in metabolites such as taurine, creatine and phosphocreatine, glutamate, glutamine and glutathione, in obese fa/fa rats, whereas lactate concentration was increased. By contrast, fatty acid concentrations in LV tissue were significantly elevated in obese fa/fa rats. CR failed to restore the LV metabolomic profile of obese fa/fa rats. In conclusion, mild and short-term CR prevented an obesity-induced cardiomyopathy phenotype in young obese fa/fa rats independently of the cardiac metabolic profile.This study was supported by grants from Spanish Ministry of Science and Innovation (BFU2011-25303), Spanish Institute of Health Carlos III (CP15/00129), UCM groups (GR-921641), SESCAMET, Fundación Mutua Madrileña, Fundación Eugenio Rodríguez Pascual and Fondos FEDER.Peer Reviewe

Neutrino physics with the PTOLEMY project: active neutrino properties and the light sterile case

The PTOLEMY project aims to develop a scalable design for a Cosmic NeutrinoBackground (CNB) detector, the first of its kind and the only one conceivedthat can look directly at the image of the Universe encoded in neutrinobackground produced in the first second after the Big Bang. The scope of thework for the next three years is to complete the conceptual design of thisdetector and to validate with direct measurements that the non-neutrinobackgrounds are below the expected cosmological signal. In this paper wediscuss in details the theoretical aspects of the experiment and its physicsgoals. In particular, we mainly address three issues. First we discuss thesensitivity of PTOLEMY to the standard neutrino mass scale. We then study theperspectives of the experiment to detect the CNB via neutrino capture ontritium as a function of the neutrino mass scale and the energy resolution ofthe apparatus. Finally, we consider an extra sterile neutrino with mass in theeV range, coupled to the active states via oscillations, which has beenadvocated in view of neutrino oscillation anomalies. This extra state wouldcontribute to the tritium decay spectrum, and its properties, mass and mixingangle, could be studied by analyzing the features in the beta decay electronspectrum

Targeted reprogramming of H3K27me3 resets epigenetic memory in plant paternal chromatin

Epigenetic marks are reprogrammed in the gametes to reset genomic potential in the next generation. In mammals, paternal chromatin is extensively reprogrammed through the global erasure of DNA methylation and the exchange of histones with protamines(1,2). Precisely how the paternal epigenome is reprogrammed in flowering plants has remained unclear since DNA is not demethylated and histones are retained in sperm(3,4). Here, we describe a multi-layered mechanism by which H3K27me3 is globally lost from histone-based sperm chromatin in Arabidopsis. This mechanism involves the silencing of H3K27me3 writers, activity of H3K27me3 erasers and deposition of a sperm-specific histone, H3.10 (ref. (5)), which we show is immune to lysine 27 methylation. The loss of H3K27me3 facilitates the transcription of genes essential for spermatogenesis and pre-configures sperm with a chromatin state that forecasts gene expression in the next generation. Thus, plants have evolved a specific mechanism to simultaneously differentiate male gametes and reprogram the paternal epigenome