Quantum Metrology with Cold Atoms

Quantum metrology is the science that aims to achieve precision measurements by making use of quantum principles. Attribute to the well-developed techniques of manipulating and detecting cold atoms, cold atomic systems provide an excellent platform for implementing precision quantum metrology. In this chapter, we review the general procedures of quantum metrology and some experimental progresses in quantum metrology with cold atoms. Firstly, we give the general framework of quantum metrology and the calculation of quantum Fisher information, which is the core of quantum parameter estimation. Then, we introduce the quantum interferometry with single and multiparticle states. In particular, for some typical multiparticle states, we analyze their ultimate precision limits and show how quantum entanglement could enhance the measurement precision beyond the standard quantum limit. Further, we review some experimental progresses in quantum metrology with cold atomic systems.Comment: 53 pages, 9 figures, revised versio

Kibble-Zurek dynamics in an array of coupled binary Bose condensates

Universal dynamics of spontaneous symmetry breaking is central to understanding the universal behavior of spontaneous defect formation in various system from the early universe, condensed-matter systems to ultracold atomic systems. We explore the universal real-time dynamics in an array of coupled binary atomic Bose-Einstein condensates in optical lattices, which undergo a spontaneous symmetry breaking from the symmetric Rabi oscillation to the broken-symmetry self-trapping. In addition to Goldstone modes, there exist gapped Higgs mode whose excitation gap vanishes at the critical point. In the slow passage through the critical point, we analytically find that the symmetry-breaking dynamics obeys the Kibble-Zurek mechanism. From the scalings of bifurcation delay and domain formation, we numerically extract two Kibble-Zurek exponents $b_{1}=\nu/(1+\nu z)$ and $b_{2}=1/(1+\nu z)$, which give the static correlation-length critical exponent $\nu$ and the dynamic critical exponent $z$. Our approach provides an efficient way to simultaneous determination of the critical exponents $\nu$ and $z$ for a continuous phase transition.Comment: 6 pages, 4 figures, accepted for publication in EPL (Europhysics Letters

N-WASP Is Essential for the Negative Regulation of B Cell Receptor Signaling

Negative regulation of receptor signaling is essential for controlling cell activation and differentiation. In B-lymphocytes, the down-regulation of B-cell antigen receptor (BCR) signaling is critical for suppressing the activation of self-reactive B cells; however, the mechanism underlying the negative regulation of signaling remains elusive. Using genetically manipulated mouse models and total internal reflection fluorescence microscopy, we demonstrate that neuronal Wiskott–Aldrich syndrome protein (N-WASP), which is coexpressed with WASP in all immune cells, is a critical negative regulator of B-cell signaling. B-cell–specific N-WASP gene deletion causes enhanced and prolonged BCR signaling and elevated levels of autoantibodies in the mouse serum. The increased signaling in N-WASP knockout B cells is concurrent with increased accumulation of F-actin at the B-cell surface, enhanced B-cell spreading on the antigen-presenting membrane, delayed B-cell contraction, inhibition in the merger of signaling active BCR microclusters into signaling inactive central clusters, and a blockage of BCR internalization. Upon BCR activation, WASP is activated first, followed by N-WASP in mouse and human primary B cells. The activation of N-WASP is suppressed by Bruton's tyrosine kinase-induced WASP activation, and is restored by the activation of SH2 domain-containing inositol 5-phosphatase that inhibits WASP activation. Our results reveal a new mechanism for the negative regulation of BCR signaling and broadly suggest an actin-mediated mechanism for signaling down-regulation

Quasi-spin Model for Macroscopic Quantum Tunnelling between Two Coupled Bose-Einstein Condensates

The macroscopic quantum tunneling between two coupled Bose-Einstein condensates (BEC) (radio-frequency coupled two-component BECs or two BECs confined in a double-well potential) is mapped onto the tunneling of an uniaxial spin with an applied magnetic field. The tunneling exponent is calculated with an imaginary-time path-integral method. In the limit of low barrier, the dependence of tunneling exponent on the system parameters is obtained, and the crossover temperature from thermal regime to quantum regime is estimated. The detailed information about the tunnelling will give help to control population conversion between coupled BECs and realize quantum computation with coupled BECs.Comment: 20 pages, 4 figures, accepted by Phys.Rev.

Automatic Robust Neurite Detection and Morphological Analysis of Neuronal Cell Cultures in High-content Screening

Cell-based high content screening (HCS) is becoming an important and increasingly favored approach in therapeutic drug discovery and functional genomics. In HCS, changes in cellular morphology and biomarker distributions provide an information-rich profile of cellular responses to experimental treatments such as small molecules or gene knockdown probes. One obstacle that currently exists with such cell-based assays is the availability of image processing algorithms that are capable of reliably and automatically analyzing large HCS image sets. HCS images of primary neuronal cell cultures are particularly challenging to analyze due to complex cellular morphology. Here we present a robust method for quantifying and statistically analyzing the morphology of neuronal cells in HCS images. The major advantages of our method over existing software lie in its capability to correct non-uniform illumination using the contrast-limited adaptive histogram equalization method; segment neuromeres using Gabor-wavelet texture analysis; and detect faint neurites by a novel phase-based neurite extraction algorithm that is invariant to changes in illumination and contrast and can accurately localize neurites. Our method was successfully applied to analyze a large HCS image set generated in a morphology screen for polyglutaminemediated neuronal toxicity using primary neuronal cell cultures derived from embryos of a Drosophila Huntington’s Disease (HD) model.National Institutes of Health (U.S.) (Grant

Single-cell profiling reveals distinct immune response landscapes in tuberculous pleural effusion and non-TPE

BackgroundTuberculosis (TB) is caused by Mycobacterium tuberculosis (Mtb) and remains a major health threat worldwide. However, a detailed understanding of the immune cells and inflammatory mediators in Mtb-infected tissues is still lacking. Tuberculous pleural effusion (TPE), which is characterized by an influx of immune cells to the pleural space, is thus a suitable platform for dissecting complex tissue responses to Mtb infection.MethodsWe employed singe-cell RNA sequencing to 10 pleural fluid (PF) samples from 6 patients with TPE and 4 non-TPEs including 2 samples from patients with TSPE (transudative pleural effusion) and 2 samples with MPE (malignant pleural effusion).ResultCompared to TSPE and MPE, TPE displayed obvious difference in the abundance of major cell types (e.g., NK, CD4+T, Macrophages), which showed notable associations with disease type. Further analyses revealed that the CD4 lymphocyte population in TPE favored a Th1 and Th17 response. Tumor necrosis factors (TNF)-, and XIAP related factor 1 (XAF1)-pathways induced T cell apoptosis in patients with TPE. Immune exhaustion in NK cells was an important feature in TPE. Myeloid cells in TPE displayed stronger functional capacity for phagocytosis, antigen presentation and IFN-γ response, than TSPE and MPE. Systemic elevation of inflammatory response genes and pro-inflammatory cytokines were mainly driven by macrophages in patients with TPE.ConclusionWe provide a tissue immune landscape of PF immune cells, and revealed a distinct local immune response in TPE and non-TPE (TSPE and MPE). These findings will improve our understanding of local TB immunopathogenesis and provide potential targets for TB therapy