30 research outputs found
Chaos in a double driven dissipative nonlinear oscillator
We propose an anharmonic oscillator driven by two periodic forces of
different frequencies as a new time-dependent model for investigating quantum
dissipative chaos. Our analysis is done in the frame of statistical ensemble of
quantum trajectories in quantum state diffusion approach. Quantum dynamical
manifestation of chaotic behavior, including the emergence of chaos, properties
of strange attractors, and quantum entanglement are studied by numerical
simulation of ensemble averaged Wigner function and von Neumann entropy.Comment: 9 pages, 18 figure
Sub-Poissonian statistics in order-to-chaos transition
We study the phenomena at the overlap of quantum chaos and nonclassical
statistics for the time-dependent model of nonlinear oscillator. It is shown in
the framework of Mandel Q-parameter and Wigner function that the statistics of
oscillatory excitation number is drastically changed in order-to chaos
transition. The essential improvement of sub-Poissonian statistics in
comparison with an analogous one for the standard model of driven anharmonic
oscillator is observed for the regular operational regime. It is shown that in
the chaotic regime the system exhibits the range of sub- and super-Poissonian
statistics which alternate one to other depending on time intervals. Unusual
dependence of the variance of oscillatory number on the external noise level
for the chaotic dynamics is observed.Comment: 9 pages, RevTeX, 14 figure
Giant Planet Formation and Migration
© 2018, The Author(s). Planets form in circumstellar discs around young stars. Starting with sub-micron sized dust particles, giant planet formation is all about growing 14 orders of magnitude in size. It has become increasingly clear over the past decades that during all stages of giant planet formation, the building blocks are extremely mobile and can change their semimajor axis by substantial amounts. In this chapter, we aim to give a basic overview of the physical processes thought to govern giant planet formation and migration, and to highlight possible links to water delivery.S.-J. Paardekooper is supported by a Royal Society University Research Fellowship. A. Johansen is supported by the Knut and Alice Wallenberg Foundation, the Swedish Research Council (grant 2014-5775) and the European Research Council (ERC Starting Grant 278675-PEBBLE2PLANET)
Integrative analysis of genomic variants reveals new associations of candidate haploinsufficient genes with congenital heart disease
Congenital Heart Disease (CHD) affects approximately 7-9 children per 1000 live births. Numerous genetic studies have established a role for rare genomic variants at the copy number variation (CNV) and single nucleotide variant level. In particular, the role of de novo mutations (DNM) has been highlighted in syndromic and non-syndromic CHD. To identify novel haploinsufficient CHD disease genes we performed an integrative analysis of CNVs and DNMs identified in probands with CHD including cases with sporadic thoracic aortic aneurysm (TAA). We assembled CNV data from 7,958 cases and 14,082 controls and performed a gene-wise analysis of the burden of rare genomic deletions in cases versus controls. In addition, we performed mutation rate testing for DNMs identified in 2,489 parent-offspring trios. Our combined analysis revealed 21 genes which were significantly affected by rare genomic deletions and/or constrained non-synonymous de novo mutations in probands. Fourteen of these genes have previously been associated with CHD while the remaining genes (FEZ1, MYO16, ARID1B, NALCN, WAC, KDM5B and WHSC1) have only been associated in singletons and small cases series, or show new associations with CHD. In addition, a systems level analysis revealed shared contribution of CNV deletions and DNMs in CHD probands, affecting protein-protein interaction networks involved in Notch signaling pathway, heart morphogenesis, DNA repair and cilia/centrosome function. Taken together, this approach highlights the importance of re-analyzing existing datasets to strengthen disease association and identify novel disease genes