124 research outputs found

    Beating of exciton-dressed states in a single semiconductor InGaAs/GaAs quantum dot

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    We report picosecond control of excitonic dressed states in a single semiconductor quantum dot. A strong laser pulse couples the exciton and biexciton states, to form an Autler-Townes doublet of the neutral exciton transition. The Rabi-splitting, and hence the admixture of the dressed states follows the envelope of the picosecond control laser. We create a superposition of dressed states, and observe the resulting beat: a direct measurement of a Rabi oscillation in time delay rather than the usual power domain

    Boost operators in Coulomb-gauge QCD: the pion form factor and Fock expansions in phi radiative decays

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    In this article we rederive the Boost operators in Coulomb-Gauge Yang-Mills theory employing the path-integral formalism and write down the complete operators for QCD. We immediately apply them to note that what are usually called the pion square, quartic... charge radii, defined from derivatives of the pion form factor at zero squared momentum transfer, are completely blurred out by relativistic and interaction corrections, so that it is not clear at all how to interpret these quantities in terms of the pion charge distribution. The form factor therefore measures matrix elements of powers of the QCD boost and Moeller operators, weighted by the charge density in the target's rest frame. In addition we remark that the decomposition of the eta' wavefunction in quarkonium, gluonium, ... components attempted by the KLOE collaboration combining data from phi radiative decays, requires corrections due to the velocity of the final state meson recoiling against a photon. This will be especially important if such decompositions are to be attempted with data from J/psi decays.Comment: 14 pages, 4 figure

    Prenatal exposure to per-and polyfluoroalkyl substances, umbilical cord blood DNA methylation, and cardio-metabolic indicators in newborns: The healthy start study

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    BACKGROUND: Per-and polyfluoroalkyl substances (PFAS) are environmentally persistent chemicals widely detected in women of reproductive age. Prenatal PFAS exposure is associated with adverse health outcomes in children. We hypothesized that DNA methylation changes may result from prenatal PFAS exposure and may be linked to offspring cardio-metabolic phenotype. OBJECTIVES: We estimated associations of prenatal PFAS with DNA methylation in umbilical cord blood. We evaluated associations of methylation at selected sites with neonatal cardio-metabolic indicators. METHODS: Among 583 mother–infant pairs in a prospective cohort, five PFAS were quantified in maternal serum (median 27 wk of gestation). Umbilical cord blood DNA methylation was evaluated using the Illumina HumanMethylation450 array. Differentially methylated positions (DMPs) were evaluated at a false discovery rate (FDR) <0:05 and differentially methylated regions (DMRs) were identified using comb-p (Šidák-adjusted p <0:05). We estimated associations between methylation at candidate DMPs and DMR sites and the following outcomes: newborn weight, adiposity, and cord blood glucose, insulin, lipids, and leptin. RESULTS: Maternal serum PFAS concentrations were below the median for females in the U.S. general population. Moderate to high pairwise correla-tions were observed between PFAS concentrations (q =0:28 − 0:76). Methylation at one DMP (cg18587484), annotated to the gene TJAP1, was associated with perfluorooctanoate (PFOA) at FDR < 0:05. Comb-p detected between 4 and 15 DMRs for each PFAS. Associated genes, some common across multiple PFAS, were implicated in growth (RPTOR), lipid homeostasis (PON1, PON3, CIDEB, NR1H2), inflammation and immune activity (RASL11B, RNF39), among other functions. There was suggestive evidence that two PFAS-associated loci (cg09093485, cg09637273) were associated with cord blood triglycerides and birth weight, respectively (FDR < 0:1). DISCUSSION: DNA methylation in umbilical cord blood was associated with maternal serum PFAS concentrations during pregnancy, suggesting potential associations with offspring growth, metabolism, and immune function. Future research should explore whether DNA methylation changes mediate associations between prenatal PFAS exposures and child health outcomes. https://doi.org/10.1289/EHP6888

    A CHIME/FRB Study of Burst Rate and Morphological Evolution of the Periodically Repeating FRB 20180916B

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    FRB 20180916B is a repeating fast radio burst (FRB) with a 16.3 day periodicity in its activity. In this study, we present morphological properties of 60 FRB 20180916B bursts detected by CHIME/FRB between 2018 August and 2021 December. We recorded raw voltage data for 45 of these bursts, enabling microseconds time resolution in some cases. We studied variation of spectro-temporal properties with time and activity phase. We find that the variation in dispersion measure (DM) is ≲1 pc cm−3 and that there is burst-to-burst variation in scattering time estimates ranging from ∼0.16 to over 2 ms, with no discernible trend with activity phase for either property. Furthermore, we find no DM and scattering variability corresponding to the recent change in rotation measure from the source, which has implications for the immediate environment of the source. We find that FRB 20180916B has thus far shown no epochs of heightened activity as have been seen in other active repeaters by CHIME/FRB, with its burst count consistent with originating from a Poissonian process. We also observe no change in the value of the activity period over the duration of our observations and set a 1σ upper limit of 1.5 × 10−4 day day−1 on the absolute period derivative. Finally, we discuss constraints on progenitor models yielded by our results, noting that our upper limits on changes in scattering and DM as a function of phase do not support models invoking a massive binary companion star as the origin of the 16.3 day periodicity.</p

    Whole-genome sequencing reveals host factors underlying critical COVID-19

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    Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

    ATLAS detector and physics performance: Technical Design Report, 1

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