Low-lying excitations of a trapped rotating Bose-Einstein condensate

We investigate the low-lying excitations of a weakly-interacting, harmonically-trapped Bose-Einstein condensed gas under rotation, in the limit where the angular mometum $L$ of the system is much less than the number of the atoms $N$ in the trap. We show that in the asymptotic limit $N \to \infty$ the excitation energy, measured from the energy of the lowest state, is given by $27 N_{3}(N_{3}-1) v_0 /68$, where $N_{3}$ is the number of octupole excitations and $v_{0}$ is the unit of the interaction energy.Comment: 3 pages, RevTex, 2 ps figures, submitted to PR

Long-Time Behavior of Macroscopic Quantum Systems: Commentary Accompanying the English Translation of John von Neumann's 1929 Article on the Quantum Ergodic Theorem

The renewed interest in the foundations of quantum statistical mechanics in recent years has led us to study John von Neumann's 1929 article on the quantum ergodic theorem. We have found this almost forgotten article, which until now has been available only in German, to be a treasure chest, and to be much misunderstood. In it, von Neumann studied the long-time behavior of macroscopic quantum systems. While one of the two theorems announced in his title, the one he calls the "quantum H-theorem", is actually a much weaker statement than Boltzmann's classical H-theorem, the other theorem, which he calls the "quantum ergodic theorem", is a beautiful and very non-trivial result. It expresses a fact we call "normal typicality" and can be summarized as follows: For a "typical" finite family of commuting macroscopic observables, every initial wave function $\psi_0$ from a micro-canonical energy shell so evolves that for most times $t$ in the long run, the joint probability distribution of these observables obtained from $\psi_t$ is close to their micro-canonical distribution.Comment: 34 pages LaTeX, no figures; v2: minor improvements and additions. The English translation of von Neumann's article is available as arXiv:1003.213

Persistent currents in a Bose-Einstein condensate in the presence of disorder

We examine bosonic atoms that are confined in a toroidal, quasi-one-dimensional trap, subjected to a random potential. The resulting inhomogeneous atomic density is smoothened for sufficiently strong, repulsive interatomic interactions. Statistical analysis of our simulations show that the gas supports persistent currents, which become more fragile due to the disorder.Comment: 5 pages, RevTex, 3 figures, revised version, to appear in JLT

Lung purinoceptor activation triggers ventilator-induced brain injury

OBJECTIVES: Mechanical ventilation can cause ventilator-induced brain injury via afferent vagal signaling and hippocampal neurotransmitter imbalances. The triggering mechanisms for vagal signaling during mechanical ventilation are unknown. The objective of this study was to assess whether pulmonary transient receptor potential vanilloid type-4 (TRPV4) mechanoreceptors and vagal afferent purinergic receptors (P2X) act as triggers of ventilator-induced brain injury. DESIGN: Controlled, human in vitro and ex vivo studies, as well as murine in vivo laboratory studies. SETTING: Research laboratory. SUBJECTS: Wild-type, TRPV4-deficient C57BL/6J mice, 8-10 weeks old. Human postmortem lung tissue and human lung epithelial cell line BEAS-2B. INTERVENTION: Mice subjected to mechanical ventilation were studied using functional MRI to assess hippocampal activity. The effects of lidocaine (a nonselective ion-channel inhibitor), P2X-purinoceptor antagonist (iso-PPADS), or genetic TRPV4 deficiency on hippocampal dopamine-dependent pro-apoptotic signaling were studied in mechanically ventilated mice. Human lung epithelial cells (BEAS-2B) were used to study the effects of mechanical stretch on TRPV4 and P2X expression and activation. TRPV4 levels were measured in postmortem lung tissue from ventilated and nonventilated patients. MEASUREMENTS AND MAIN RESULTS: Hippocampus functional MRI analysis revealed considerable changes in response to the increase in tidal volume during mechanical ventilation. Intratracheal lidocaine, iso-PPADS, and TRPV4 genetic deficiency protected mice against ventilationinduced hippocampal pro-apoptotic signaling. Mechanical stretch in both, BEAS-2B cells and ventilated wild-type mice, resulted in TRPV4 activation and reduced Trpv4 and P2x expression. Intratracheal replenishment of adenosine triphosphate in Trpv4 mice abrogated the protective effect of TRPV4 deficiency. Autopsy lung tissue from ventilated patients showed decreased lung TRPV4 levels compared with nonventilated patients. CONCLUSIONS: TRPV4 mechanosensors and purinergic receptors are involved in the mechanisms of ventilator-induced brain injury. Inhibition of this neural signaling, either using nonspecific or specific inhibitors targeting the TRPV4/adenosine triphosphate/P2X signaling axis, may represent a novel strategy to prevent or treat ventilator-induced brain injury

Magnetism of quantum dot clusters: A Hubbard model study

Magnetic properties of two and three-dimensional clusters of quantum dots are studied with exact diagonalization of a generalized Hubbard model. We study the weak coupling limit, where the electrons interact only within a quantum dot and consider cases where the second or third harmonic oscillator shell is partially filled. The results show that in the case of half-filled shell the magnetism is determined by the antiferromagnetic Heisenberg model with spin 1/2, 1 or 3/2, depending on the number of electrons in the open shell. For other fillings the system in most cases favors a large total spin, indicating a ferromagnetic coupling between the dots.Comment: 9 pages, 9 figure

Neutrino oscillation studies with IceCube-DeepCore

AbstractIceCube, a gigaton-scale neutrino detector located at the South Pole, was primarily designed to search for astrophysical neutrinos with energies of PeV and higher. This goal has been achieved with the detection of the highest energy neutrinos to date. At the other end of the energy spectrum, the DeepCore extension lowers the energy threshold of the detector to approximately 10 GeV and opens the door for oscillation studies using atmospheric neutrinos. An analysis of the disappearance of these neutrinos has been completed, with the results produced being complementary with dedicated oscillation experiments. Following a review of the detector principle and performance, the method used to make these calculations, as well as the results, is detailed. Finally, the future prospects of IceCube-DeepCore and the next generation of neutrino experiments at the South Pole (IceCube-Gen2, specifically the PINGU sub-detector) are briefly discussed

A muon-track reconstruction exploiting stochastic losses for large-scale Cherenkov detectors

IceCube is a cubic-kilometer Cherenkov telescope operating at the South Pole. The main goal of IceCube is the detection of astrophysical neutrinos and the identification of their sources. High-energy muon neutrinos are observed via the secondary muons produced in charge current interactions with nuclei in the ice. Currently, the best performing muon track directional reconstruction is based on a maximum likelihood method using the arrival time distribution of Cherenkov photons registered by the experiment\u27s photomultipliers. A known systematic shortcoming of the prevailing method is to assume a continuous energy loss along the muon track. However at energies >1 TeV the light yield from muons is dominated by stochastic showers. This paper discusses a generalized ansatz where the expected arrival time distribution is parametrized by a stochastic muon energy loss pattern. This more realistic parametrization of the loss profile leads to an improvement of the muon angular resolution of up to 20% for through-going tracks and up to a factor 2 for starting tracks over existing algorithms. Additionally, the procedure to estimate the directional reconstruction uncertainty has been improved to be more robust against numerical errors

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

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