Role of Landau-Rabi quantization of electron motion on the crust of magnetars within the nuclear energy density functional theory

Magnetic fields of order $10^{15}$ G have been measured at the surface of some neutron stars, and much stronger magnetic fields are expected to be present in the solid region beneath the surface. The effects of the magnetic field on the equation of state and on the composition of the crust due to Landau-Rabi quantization of electron motion are studied. Both the outer and inner crustal regions are described in a unified and consistent way within the nuclear-energy density functional theory.Comment: 23 pages, 11 figure

Landau quantization and neutron emissions by nuclei in the crust of a magnetar

Magnetars are neutron stars endowed with surface magnetic fields of the order of $10^{14}-10^{15}$~G, and with presumably much stronger fields in their interior. As a result of Landau quantization of electron motion, the neutron-drip transition in the crust of a magnetar is shifted to either higher or lower densities depending on the magnetic field strength. The impact of nuclear uncertainties is explored considering the recent series of Brussels-Montreal microscopic nuclear mass models. All these models are based on the Hartree-Fock-Bogoliubov method with generalized Skyrme functionals. They differ in their predictions for the symmetry energy coefficient at saturation, and for the stiffness of the neutron-matter equation of state. For comparison, we have also considered the very accurate but more phenomenological model of Duflo and Zuker. Although the equilibrium composition of the crust of a magnetar and the onset of neutron emission are found to be model dependent, the quantum oscillations of the threshold density are essentially universal.Comment: 7 pages, 2 figure

Superfluid to normal phase transition and extreme regularity of superdeformed bands

We derive the exact semiclassical expression for the second inertial parameter $\cal B$ for the superfluid and normal phases. Interpolation between these limiting values shows that the function ${\cal B}(I)$ changes sign at the spin $I_c$, which is critical for a rotational spectrum. The quantity $\cal B$ turns out to be a sensitive measure of the change in static pairing correlations. The superfluid-to-normal transition reveals itself in the specific variation of the ratio ${\cal B}/{\cal A}$ versus spin $I$ with the plateau characteristic of the normal phase. We find this dependence to be universal for normal deformed and superdeformed bands. The long plateau with a small value ${\cal B}/{\cal A}\sim A^{-8/3}$ explains the extreme regularity of superdeformed bands.Comment: 30 pages in LaTeX, 6 figures (PostScript). To be published in Yadernaya Fizika (Physics of Atomic Nuclei), special edition dedecated to the 90th birthday of Prof. I. I. Gurevit

Collisional and thermal ionization of sodium Rydberg atoms I. Experiment for nS and nD atoms with n=8-20

Collisional and thermal ionization of sodium nS and nD Rydberg atoms with n=8-20 has been studied. The experiments were performed using a two-step pulsed laser excitation in an effusive atomic beam at atom density of about 2 10^{10} cm^{-3}. Molecular and atomic ions from associative, Penning, and thermal ionization processes were detected. It has been found that the atomic ions were created mainly due to photoionization of Rydberg atoms by photons of blackbody radiation at the ambient temperature of 300K. Blackbody ionization rates and effective lifetimes of Rydberg states of interest were determined. The molecular ions were found to be from associative ionization in Na(nL)+Na(3S) collisions. Rate constants of associative ionization have been measured using an original method based on relative measurements of Na_{2}^{+} and Na^{+} ion signals.Comment: 23 pages, 10 figure

Copy number variations and cognitive phenotypes in unselected populations

IMPORTANCE: The association of copy number variations (CNVs), differing numbers of copies of genetic sequence at locations in the genome, with phenotypes such as intellectual disability has been almost exclusively evaluated using clinically ascertained cohorts. The contribution of these genetic variants to cognitive phenotypes in the general population remains unclear. OBJECTIVE: To investigate the clinical features conferred by CNVs associated with known syndromes in adult carriers without clinical preselection and to assess the genome-wide consequences of rare CNVs (frequency ≤0.05%; size ≥250 kilobase pairs [kb]) on carriers' educational attainment and intellectual disability prevalence in the general population. DESIGN, SETTING, AND PARTICIPANTS: The population biobank of Estonia contains 52,000 participants enrolled from 2002 through 2010. General practitioners examined participants and filled out a questionnaire of health- and lifestyle-related questions, as well as reported diagnoses. Copy number variant analysis was conducted on a random sample of 7877 individuals and genotype-phenotype associations with education and disease traits were evaluated. Our results were replicated on a high-functioning group of 993 Estonians and 3 geographically distinct populations in the United Kingdom, the United States, and Italy. MAIN OUTCOMES AND MEASURES: Phenotypes of genomic disorders in the general population, prevalence of autosomal CNVs, and association of these variants with educational attainment (from less than primary school through scientific degree) and prevalence of intellectual disability. RESULTS: Of the 7877 in the Estonian cohort, we identified 56 carriers of CNVs associated with known syndromes. Their phenotypes, including cognitive and psychiatric problems, epilepsy, neuropathies, obesity, and congenital malformations are similar to those described for carriers of identical rearrangements ascertained in clinical cohorts. A genome-wide evaluation of rare autosomal CNVs (frequency, ≤0.05%; ≥250 kb) identified 831 carriers (10.5%) of the screened general population. Eleven of 216 (5.1%) carriers of a deletion of at least 250 kb (odds ratio [OR], 3.16; 95% CI, 1.51-5.98; P = 1.5e-03) and 6 of 102 (5.9%) carriers of a duplication of at least 1 Mb (OR, 3.67; 95% CI, 1.29-8.54; P = .008) had an intellectual disability compared with 114 of 6819 (1.7%) in the Estonian cohort. The mean education attainment was 3.81 (P = 1.06e-04) among 248 (≥250 kb) deletion carriers and 3.69 (P = 5.024e-05) among 115 duplication carriers (≥1 Mb). Of the deletion carriers, 33.5% did not graduate from high school (OR, 1.48; 95% CI, 1.12-1.95; P = .005) and 39.1% of duplication carriers did not graduate high school (OR, 1.89; 95% CI, 1.27-2.8; P = 1.6e-03). Evidence for an association between rare CNVs and lower educational attainment was supported by analyses of cohorts of adults from Italy and the United States and adolescents from the United Kingdom. CONCLUSIONS AND RELEVANCE: Known pathogenic CNVs in unselected, but assumed to be healthy, adult populations may be associated with unrecognized clinical sequelae. Additionally, individually rare but collectively common intermediate-size CNVs may be negatively associated with educational attainment. Replication of these findings in additional population groups is warranted given the potential implications of this observation for genomics research, clinical care, and public health

A comprehensive 1000 Genomes-based genome-wide association meta-analysis of coronary artery disease

Existing knowledge of genetic variants affecting risk of coronary artery disease (CAD) is largely based on genome-wide association studies (GWAS) analysis of common SNPs. Leveraging phased haplotypes from the 1000 Genomes Project, we report a GWAS meta-analysis of 185 thousand CAD cases and controls, interrogating 6.7 million common (MAF>0.05) as well as 2.7 million low frequency (0.005<MAF<0.05) variants. In addition to confirmation of most known CAD loci, we identified 10 novel loci, eight additive and two recessive, that contain candidate genes that newly implicate biological processes in vessel walls. We observed intra-locus allelic heterogeneity but little evidence of low frequency variants with larger effects and no evidence of synthetic association. Our analysis provides a comprehensive survey of the fine genetic architecture of CAD showing that genetic susceptibility to this common disease is largely determined by common SNPs of small effect siz