Dephasing and Measurement Efficiency via a Quantum Dot Detector

We study charge detection and controlled dephasing of a mesoscopic system via a quantum dot detector (QDD), where the mesoscopic system and the QDD are capacitively coupled. The QDD is considered to have coherent resonant tunnelling via a single level. It is found that the dephasing rate is proportional to the square of the conductance of the QDD for the Breit-Wigner model, showing that the dephasing is completely different from the shot noise of the detector. The measurement rate, on the other hand, shows a dip near the resonance. Our findings are peculiar especially for a symmetric detector in the following aspect: The dephasing rate is maximum at resonance of the QDD where the detector conductance is insensitive to the charge state of the mesoscopic system. As a result, the efficiency of the detector shows a dip and vanishes at resonance, in contrast to the single-channel symmetric non-resonant detector that has always a maximum efficiency. We find that this difference originates from a very general property of the scattering matrix: The abrupt phase change exists in the scattering amplitudes in the presence of the symmetry, which is insensitive to the detector current but {\em stores} the information of the quantum state of the mesoscopic system.Comment: 7 pages, 3 figure

Crossover from mesoscopic to universal phase for electron transmission in quantum dots

Measuring phase in coherent electron systems (mesoscopic systems) provides ample information not easily revealed by conductance measurements. Phase measurements in relatively large quantum dots (QDs) recently demonstrated a universal like phase evolution independent of dot size, shape, and occupancy. Explicitly, in Coulomb blockaded QDs the transmission phase increased monotonically by pi throughout each conductance peak, thereafter, in the conductance valleys the phase returned sharply to its base value. Expected mesoscopic features in the phase, related to spin degeneracy or to exchange effects, were never observed. Presently, there is no satisfactory full explanation for the observed phase universality. Unfortunately, the phase in a few-electron QDs, where it can be better understood was never measured. Here we report on such measurements on a small QD that occupy only 1-20 electrons. Such dot was embedded in one arm of a two path electron interferometer, with an electron counter near the dot. Unlike the repetitive behavior found in larger dots we found now mesoscopic features for dot occupation of less than some 10 electrons. An unexpected feature in this regime is a clear observation of the occupation of two different orbital states by the first two electrons - contrary to the recent publications. As the occupation increased the phase evolved and turned universal like for some 14 electrons and higher. The present measurements allowed us to determine level occupancy and parity. More importantly, they suggest that QDs go through a phase transition, from mesoscopic to universal like behavior, as the occupancy increases. These measurements help in singling out potential few theoretical models among the many proposed.Comment: 12 pages, 6 figure

Nonequilibrium transport in quantum impurity models: Exact path integral simulations

We simulate the nonequilibrium dynamics of two generic many-body quantum impurity models by employing the recently developed iterative influence-functional path integral method [Phys. Rev. B {\bf 82}, 205323 (2010)]. This general approach is presented here in the context of quantum transport in molecular electronic junctions. Models of particular interest include the single impurity Anderson model and the related spinless two-state Anderson dot. In both cases we study the time evolution of the dot occupation and the current characteristics at finite temperature. A comparison to mean-field results is presented, when applicable

Avpr1a variant associated with preschoolers' lower altruistic behavior

10.1371/journal.pone.0025274PLoS ONE69

Differential Genetic Susceptibility to Child Risk at Birth in Predicting Observed Maternal Behavior

This study examined parenting as a function of child medical risks at birth and parental genotype (dopamine D4 receptor; DRD4). Our hypothesis was that the relation between child risks and later maternal sensitivity would depend on the presence/absence of a genetic variant in the mothers, thus revealing a gene by environment interaction (GXE). Risk at birth was defined by combining risk indices of children's gestational age at birth, birth weight, and admission to the neonatal intensive care unit. The DRD4-III 7-repeat allele was chosen as a relevant genotype as it was recently shown to moderate the effect of environmental stress on parental sensitivity. Mothers of 104 twin pairs provided DNA samples and were observed with their children in a laboratory play session when the children were 3.5 years old. Results indicate that higher levels of risk at birth were associated with less sensitive parenting only among mothers carrying the 7-repeat allele, but not among mothers carrying shorter alleles. Moreover, mothers who are carriers of the 7-repeat allele and whose children scored low on the risk index were observed to have the highest levels of sensitivity. These findings provide evidence for the interactive effects of genes and environment (in this study, children born at higher risk) on parenting, and are consistent with a genetic differential susceptibility model of parenting by demonstrating that some parents are inherently more susceptible to environmental influences, both good and bad, than are others

Genetic variants for head size share genes and pathways with cancer

The size of the human head is highly heritable, but genetic drivers of its variation within the general population remain unmapped. We perform a genome-wide association study on head size (N = 80,890) and identify 67 genetic loci, of which 50 are novel. Neuroimaging studies show that 17 variants affect specific brain areas, but most have widespread effects. Gene set enrichment is observed for various cancers and the p53, Wnt, and ErbB signaling pathways. Genes harboring lead variants are enriched for macrocephaly syndrome genes (37-fold) and high-fidelity cancer genes (9-fold), which is not seen for human height variants. Head size variants are also near genes preferentially expressed in intermediate progenitor cells, neural cells linked to evolutionary brain expansion. Our results indicate that genes regulating early brain and cranial growth incline to neoplasia later in life, irrespective of height. This warrants investigation of clinical implications of the link between head size and cancer.</p

Genetic variants for head size share genes and pathways with cancer

The size of the human head is determined by growth in the first years of life, while the rest of the body typically grows until early adulthood1. Such complex developmental processes are regulated by various genes and growth pathways2. Rare genetic syndromes have revealed genes that affect head size3, but the genetic drivers of variation in head size within the general population remain largely unknown. To elucidate biological pathways underlying the growth of the human head, we performed the largest genome-wide association study on human head size to date (N = 79,107). We identified 67 genetic loci, 50 of which are novel, and found that these loci are preferentially associated with head size and mostly independent from height. In subsequent neuroimaging analyses, the majority of genetic variants demonstrated widespread effects on the brain, whereas the effects of 17 variants could be localized to one or two specific brain regions. Through hypothesis-free approaches, we find a strong overlap of head size variants with both cancer pathways and cancer genes. Gene set analyses showed enrichment for different types of cancer and the p53, Wnt and ErbB signalling pathway. Genes overlapping or close to lead variants – such as TP53, PTEN and APC – were enriched for genes involved in macrocephaly syndromes (up to 37-fold) and high-fidelity cancer genes (up to 9-fold), whereas this enrichment was not seen for human height variants. This indicates that genes regulating early brain and cranial growth are associated with a propensity to neoplasia later in life, irrespective of height. Our results warrant further investigations of the link between head size and cancer, as well as its clinical implications in the general population

Genetic Variants For Head Size Share Genes and Pathways With Cancer

The size of the human head is highly heritable, but genetic drivers of its variation within the general population remain unmapped. We perform a genome-wide association study on head size (N = 80,890) and identify 67 genetic loci, of which 50 are novel. Neuroimaging studies show that 17 variants affect specific brain areas, but most have widespread effects. Gene set enrichment is observed for various cancers and the p53, Wnt, and ErbB signaling pathways. Genes harboring lead variants are enriched for macrocephaly syndrome genes (37-fold) and high-fidelity cancer genes (9-fold), which is not seen for human height variants. Head size variants are also near genes preferentially expressed in intermediate progenitor cells, neural cells linked to evolutionary brain expansion. Our results indicate that genes regulating early brain and cranial growth incline to neoplasia later in life, irrespective of height. This warrants investigation of clinical implications of the link between head size and cancer

Physiological Correlates of Volunteering

We review research on physiological correlates of volunteering, a neglected but promising research field. Some of these correlates seem to be causal factors influencing volunteering. Volunteers tend to have better physical health, both self-reported and expert-assessed, better mental health, and perform better on cognitive tasks. Research thus far has rarely examined neurological, neurochemical, hormonal, and genetic correlates of volunteering to any significant extent, especially controlling for other factors as potential confounds. Evolutionary theory and behavioral genetic research suggest the importance of such physiological factors in humans. Basically, many aspects of social relationships and social activities have effects on health (e.g., Newman and Roberts 2013; Uchino 2004), as the widely used biopsychosocial (BPS) model suggests (Institute of Medicine 2001). Studies of formal volunteering (FV), charitable giving, and altruistic behavior suggest that physiological characteristics are related to volunteering, including specific genes (such as oxytocin receptor [OXTR] genes, Arginine vasopressin receptor [AVPR] genes, dopamine D4 receptor [DRD4] genes, and 5-HTTLPR). We recommend that future research on physiological factors be extended to non-Western populations, focusing specifically on volunteering, and differentiating between different forms and types of volunteering and civic participation