Single and vertically coupled type II quantum dots in a perpendicular magnetic field: exciton groundstate properties

The properties of an exciton in a type II quantum dot are studied under the influence of a perpendicular applied magnetic field. The dot is modelled by a quantum disk with radius $R$, thickness $d$ and the electron is confined in the disk, whereas the hole is located in the barrier. The exciton energy and wavefunctions are calculated using a Hartree-Fock mesh method. We distinguish two different regimes, namely $d<<2R$ (the hole is located at the radial boundary of the disk) and $d>>2R$ (the hole is located above and below the disk), for which angular momentum $(l)$ transitions are predicted with increasing magnetic field. We also considered a system of two vertically coupled dots where now an extra parameter is introduced, namely the interdot distance $d_{z}$. For each $l_{h}$ and for a sufficient large magnetic field, the ground state becomes spontaneous symmetry broken in which the electron and the hole move towards one of the dots. This transition is induced by the Coulomb interaction and leads to a magnetic field induced dipole moment. No such symmetry broken ground states are found for a single dot (and for three vertically coupled symmetric quantum disks). For a system of two vertically coupled truncated cones, which is asymmetric from the start, we still find angular momentum transitions. For a symmetric system of three vertically coupled quantum disks, the system resembles for small $d_{z}$ the pillar-like regime of a single dot, where the hole tends to stay at the radial boundary, which induces angular momentum transitions with increasing magnetic field. For larger $d_{z}$ the hole can sit between the disks and the $l_{h}=0$ state remains the groundstate for the whole $B$-region.Comment: 11 pages, 16 figure

Magnetic field dependence of the exciton energy in a quantum disk

The groundstate energy and binding energy of an exciton, confined in a^M quantum disk, are calculated as a function of an external magnetic field. The confinement potential is a hard wall of finite height. The diamagnetic shift is investigated for magnetic fields up to 40$T$. Our results are applied to $In_{y}Al_{1-y}As/Al_{x}Ga_{1-x}As$ self-assembled quantum dots and very good agreement with experiments is obtained. Furthermore, we investigated the influence of the dot size on the diamagnetic shift by changing the disk radius. The exciton excited states are found as a function of the magnetic field. The relative angular momentum is not a quantum number and changes with the magnetic field strength.Comment: 10 pages, 17 figure

Analysis of shared heritability in common disorders of the brain

ience, this issue p. eaap8757 Structured Abstract INTRODUCTION Brain disorders may exhibit shared symptoms and substantial epidemiological comorbidity, inciting debate about their etiologic overlap. However, detailed study of phenotypes with different ages of onset, severity, and presentation poses a considerable challenge. Recently developed heritability methods allow us to accurately measure correlation of genome-wide common variant risk between two phenotypes from pools of different individuals and assess how connected they, or at least their genetic risks, are on the genomic level. We used genome-wide association data for 265,218 patients and 784,643 control participants, as well as 17 phenotypes from a total of 1,191,588 individuals, to quantify the degree of overlap for genetic risk factors of 25 common brain disorders. RATIONALE Over the past century, the classification of brain disorders has evolved to reflect the medical and scientific communities' assessments of the presumed root causes of clinical phenomena such as behavioral change, loss of motor function, or alterations of consciousness. Directly observable phenomena (such as the presence of emboli, protein tangles, or unusual electrical activity patterns) generally define and separate neurological disorders from psychiatric disorders. Understanding the genetic underpinnings and categorical distinctions for brain disorders and related phenotypes may inform the search for their biological mechanisms. RESULTS Common variant risk for psychiatric disorders was shown to correlate significantly, especially among attention deficit hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder (MDD), and schizophrenia. By contrast, neurological disorders appear more distinct from one another and from the psychiatric disorders, except for migraine, which was significantly correlated to ADHD, MDD, and Tourette syndrome. We demonstrate that, in the general population, the personality trait neuroticism is significantly correlated with almost every psychiatric disorder and migraine. We also identify significant genetic sharing between disorders and early life cognitive measures (e.g., years of education and college attainment) in the general population, demonstrating positive correlation with several psychiatric disorders (e.g., anorexia nervosa and bipolar disorder) and negative correlation with several neurological phenotypes (e.g., Alzheimer's disease and ischemic stroke), even though the latter are considered to result from specific processes that occur later in life. Extensive simulations were also performed to inform how statistical power, diagnostic misclassification, and phenotypic heterogeneity influence genetic correlations. CONCLUSION The high degree of genetic correlation among many of the psychiatric disorders adds further evidence that their current clinical boundaries do not reflect distinct underlying pathogenic processes, at least on the genetic level. This suggests a deeply interconnected nature for psychiatric disorders, in contrast to neurological disorders, and underscores the need to refine psychiatric diagnostics. Genetically informed analyses may provide important "scaffolding" to support such restructuring of psychiatric nosology, which likely requires incorporating many levels of information. By contrast, we find limited evidence for widespread common genetic risk sharing among neurological disorders or across neurological and psychiatric disorders. We show that both psychiatric and neurological disorders have robust correlations with cognitive and personality measures. Further study is needed to evaluate whether overlapping genetic contributions to psychiatric pathology may influence treatment choices. Ultimately, such developments may pave the way toward reduced heterogeneity and improved diagnosis and treatment of psychiatric disorders

New insights into the genetic etiology of Alzheimer's disease and related dementias

Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele