301 research outputs found

    The Stern-Gerlach Experiment Revisited

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    The Stern-Gerlach-Experiment (SGE) of 1922 is a seminal benchmark experiment of quantum physics providing evidence for several fundamental properties of quantum systems. Based on today's knowledge we illustrate the different benchmark results of the SGE for the development of modern quantum physics and chemistry. The SGE provided the first direct experimental evidence for angular momentum quantization in the quantum world and thus also for the existence of directional quantization of all angular momenta in the process of measurement. It measured for the first time a ground state property of an atom, it produced for the first time a `spin-polarized' atomic beam, it almost revealed the electron spin. The SGE was the first fully successful molecular beam experiment with high momentum-resolution by beam measurements in vacuum. This technique provided a new kinematic microscope with which inner atomic or nuclear properties could be investigated. The original SGE is described together with early attempts by Einstein, Ehrenfest, Heisenberg, and others to understand directional quantization in the SGE. Heisenberg's and Einstein's proposals of an improved multi-stage SGE are presented. The first realization of these proposals by Stern, Phipps, Frisch and Segr\`e is described. The set-up suggested by Einstein can be considered an anticipation of a Rabi-apparatus. Recent theoretical work is mentioned in which the directional quantization process and possible interference effects of the two different spin states are investigated. In full agreement with the results of the new quantum theory directional quantization appears as a general and universal feature of quantum measurements. One experimental example for such directional quantization in scattering processes is shown. Last not least, the early history of the `almost' discovery of the electron spin in the SGE is revisited.Comment: 50pp, 17 fig

    Pairing in nuclear systems: from neutron stars to finite nuclei

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    We discuss several pairing-related phenomena in nuclear systems, ranging from superfluidity in neutron stars to the gradual breaking of pairs in finite nuclei. We focus on the links between many-body pairing as it evolves from the underlying nucleon-nucleon interaction and the eventual experimental and theoretical manifestations of superfluidity in infinite nuclear matter and of pairing in finite nuclei. We analyse the nature of pair correlations in nuclei and their potential impact on nuclear structure experiments. We also describe recent experimental evidence that points to a relation between pairing and phase transitions (or transformations) in finite nuclear systems. Finally, we discuss recent investigations of ground-state properties of random two-body interactions where pairing plays little role although the interactions yield interesting nuclear properties such as 0+ ground states in even-even nuclei.Comment: 74 pages, 33 figs, uses revtex4. Submitted to Reviews of Modern Physic

    Lindblad master equation approach to superconductivity in open quantum systems

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    We consider an open quantum Fermi-system which consists of a single degenerate level with pairing interactions embedded into a superconducting bath. The time evolution of the reduced density matrix for the system is given by Linblad master equation, where the dissipators describe exchange of Bogoliubov quasiparticles with the bath. We obtain fixed points of the time evolution equation for the covariance matrix and study their stability by analyzing full dynamics of the order parameter.Comment: 7 pages, 2 pdf figure

    The first transcriptome of Italian wall lizard, a new tool to infer about the Island Syndrome

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    Some insular lizards show a high degree of differentiation from their conspecific mainland populations, like Licosa island lizards, which are described as affected by Reversed Island Syndrome (RIS). In previous works, we demonstrated that some traits of RIS, as melanization, depend on a differential expression of gene encoding melanocortin receptors. To better understand the basis of syndrome, and providing raw data for future investigations, we generate the first de novo transcriptome of the Italian wall lizard. Comparing mainland and island transcriptomes, we link differences in life-traits to differential gene expression. Our results, taking together testis and brain sequences, generated 275,310 and 269,885 transcripts, 18,434 and 21,606 proteins in Gene Ontology annotation, for mainland and island respectively. Variant calling analysis identified about the same number of SNPs in island and mainland population. Instead, through a differential gene expression analysis we found some putative genes involved in syndrome more expressed in insular samples like Major Histocompatibility Complex class I, Immunoglobulins, Melanocortin 4 receptor, Neuropeptide Y and Proliferating Cell Nuclear Antigen

    Common Genetic Variation And Age at Onset Of Anorexia Nervosa

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    Background Genetics and biology may influence the age at onset of anorexia nervosa (AN). The aims of this study were to determine whether common genetic variation contributes to AN age at onset and to investigate the genetic associations between age at onset of AN and age at menarche. Methods A secondary analysis of the Psychiatric Genomics Consortium genome-wide association study (GWAS) of AN was performed which included 9,335 cases and 31,981 screened controls, all from European ancestries. We conducted GWASs of age at onset, early-onset AN (< 13 years), and typical-onset AN, and genetic correlation, genetic risk score, and Mendelian randomization analyses. Results Two loci were genome-wide significant in the typical-onset AN GWAS. Heritability estimates (SNP-h2) were 0.01-0.04 for age at onset, 0.16-0.25 for early-onset AN, and 0.17-0.25 for typical-onset AN. Early- and typical-onset AN showed distinct genetic correlation patterns with putative risk factors for AN. Specifically, early-onset AN was significantly genetically correlated with younger age at menarche, and typical-onset AN was significantly negatively genetically correlated with anthropometric traits. Genetic risk scores for age at onset and early-onset AN estimated from independent GWASs significantly predicted age at onset. Mendelian randomization analysis suggested a causal link between younger age at menarche and early-onset AN. Conclusions Our results provide evidence consistent with a common variant genetic basis for age at onset and implicate biological pathways regulating menarche and reproduction.Peer reviewe

    Dermatite seborreica

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    Shared genetic risk between eating disorder- and substance-use-related phenotypes:Evidence from genome-wide association studies

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    First published: 16 February 202

    Genomic Relationships, Novel Loci, and Pleiotropic Mechanisms across Eight Psychiatric Disorders

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    Genetic influences on psychiatric disorders transcend diagnostic boundaries, suggesting substantial pleiotropy of contributing loci. However, the nature and mechanisms of these pleiotropic effects remain unclear. We performed analyses of 232,964 cases and 494,162 controls from genome-wide studies of anorexia nervosa, attention-deficit/hyper-activity disorder, autism spectrum disorder, bipolar disorder, major depression, obsessive-compulsive disorder, schizophrenia, and Tourette syndrome. Genetic correlation analyses revealed a meaningful structure within the eight disorders, identifying three groups of inter-related disorders. Meta-analysis across these eight disorders detected 109 loci associated with at least two psychiatric disorders, including 23 loci with pleiotropic effects on four or more disorders and 11 loci with antagonistic effects on multiple disorders. The pleiotropic loci are located within genes that show heightened expression in the brain throughout the lifespan, beginning prenatally in the second trimester, and play prominent roles in neurodevelopmental processes. These findings have important implications for psychiatric nosology, drug development, and risk prediction.Peer reviewe

    Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors

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    Background Suicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders. Methods We conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors. Results Two loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged. Conclusions Our results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders.Peer reviewe
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