Soliton dynamics in the Gross–Pitaevskii equation: splitting, collisions and interferometry

Bose–Einstein condensates with attractive interactions have stable 1D solutions in the form of bright solitary-waves. These solitary waves behave, in the absence of external potentials, like macroscopic quantum particles. This opens up a wide array of applications for the testing of quantum mechanical behaviours and precision measurement. Here we investigate these applications with particular focus on the interactions of bright solitary-waves with narrow potential barriers. We first study bright solitons in the Gross–Pitaevskii equation as they are split on Gaussian and δ-function barriers, and then on Gaussian barriers in a low energy system. We present analytic and numerical results determining the general region in which a soliton may not be split on a finite width potential barrier. Furthermore, we test the sensitivity of the system to quantum fluctuations. We then study fast-moving bright solitons colliding at a narrow Gaussian potential barrier. In the limiting case of a δ-function barrier, we show analytically that the relative norms of the outgoing waves depends sinusoidally on the relative phase of the incoming waves, and determine whether the outgoing waves are bright solitons. We use numerical simulations to show that outside the high velocity limit nonlinear effects introduce a skew to the phase-dependence. Finally, we use these results to analyse the process of soliton interferometry. We develop analyses of both toroidal and harmonic trapping geometries for Mach–Zehnder interferometry, and then two implementations of a toroidal Sagnac inter- ferometer, also giving the analytical determination of the Sagnac phase in such systems. These results are again verified numerically. In the Mach–Zehnder case, we again probe the systems sensitivity to quantum fluctuations

Living God Pandeism: Evidential Support

Pandeism is the belief that God chose to wholly become our Universe, imposing principles at this Becoming that have fostered the lawful evolution of multifarious structures, including life and consciousness. This article describes and defends a particular form of pandeism: living God pandeism (LGP). On LGP, our Universe inherits all of God's unsurpassable attributes—reality, unity, consciousness, knowledge, intelligence, and effectiveness—and includes as much reality, conscious and unconscious, as is possible consistent with retaining those attributes. God and the Universe, together “God-and-Universe,” is also eternal into the future and the past. The article derives testable hypotheses from these claims and shows that the evidence to date confirms some of these while falsifying none. Theism cannot be tested in the same way

2017 HRS/EHRA/ECAS/APHRS/SOLAECE expert consensus statement on catheter and surgical ablation of atrial fibrillation: executive summary.

S

2017 HRS/EHRA/ECAS/APHRS/SOLAECE expert consensus statement on catheter and surgical ablation of atrial fibrillation: executive summary.

S

withdrawn 2017 hrs ehra ecas aphrs solaece expert consensus statement on catheter and surgical ablation of atrial fibrillation

n/

Recombination and Annealing Pathways Compete for Substrates in Making rrn

Tandem genetic duplications arise frequently between the seven directly repeated 5.5-kb rrn loci that encode ribosomal RNAs in Salmonella enterica. The closest rrn genes, rrnB and rrnE, flank a 40-kb region that includes the purHD operon. Duplications of purHD arise by exchanges between rrn loci and form at a high rate (10(−3)/cell/division) that remains high in strains blocked for early steps in recombination (recA, recB, and/or recF), but drops 30-fold in mutants blocked for later Holliday junction resolution (ruvC recG). The duplication defect of a ruvC recG mutant was fully corrected by an added mutation in any one of the recA, recB, or recF genes. To explain these results, we propose that early recombination defects activate an alternative single-strand annealing pathway for duplication formation. In wild-type cells, rrn duplications form primarily by the action of RecFORA on single-strand gaps. Double-strand breaks cannot initiate rrn duplications because rrn loci lack Chi sites, which are essential for recombination between two separated rrn sequences. A recA or recF mutation allows unrepaired gaps to accumulate such that different rrn loci can provide single-strand rrn sequences that lack the RecA coating that normally inhibits annealing. A recB mutation activates annealing by allowing double-strand ends within rrn to avoid digestion by RecBCD and provide a new source of rrn ends for use in annealing. The equivalent high rates of rrn duplication by recombination and annealing pathways may reflect a limiting economy of gaps and breaks arising in heavily transcribed, palindrome-rich rrn sequences