Demonstration of Geometric Landau-Zener Interferometry in a Superconducting Qubit

Geometric quantum manipulation and Landau-Zener interferometry have been separately explored in many quantum systems. In this Letter, we combine these two approaches to study the dynamics of a superconducting phase qubit. We experimentally demonstrate Landau-Zener interferometry based on the pure geometric phases in this solid-state qubit. We observe the interference caused by a pure geometric phase accumulated in the evolution between two consecutive Landau-Zener transitions, while the dynamical phase is canceled out by a spin-echo pulse. The full controllability of the qubit state as a function of the intrinsically robust geometric phase provides a promising approach for quantum state manipulation.Comment: 5 pages + 3 pages supplemental Materia

A Unified Framework for Testing High Dimensional Parameters: A Data-Adaptive Approach

High dimensional hypothesis test deals with models in which the number of parameters is significantly larger than the sample size. Existing literature develops a variety of individual tests. Some of them are sensitive to the dense and small disturbance, and others are sensitive to the sparse and large disturbance. Hence, the powers of these tests depend on the assumption of the alternative scenario. This paper provides a unified framework for developing new tests which are adaptive to a large variety of alternative scenarios in high dimensions. In particular, our framework includes arbitrary hypotheses which can be tested using high dimensional $U$-statistic based vectors. Under this framework, we first develop a broad family of tests based on a novel variant of the $L_p$-norm with $p\in \{1,\dots,\infty\}$. We then combine these tests to construct a data-adaptive test that is simultaneously powerful under various alternative scenarios. To obtain the asymptotic distributions of these tests, we utilize the multiplier bootstrap for $U$-statistics. In addition, we consider the computational aspect of the bootstrap method and propose a novel low-cost scheme. We prove the optimality of the proposed tests. Thorough numerical results on simulated and real datasets are provided to support our theory

Rapid characterization of microscopic two-level systems using Landau-Zener transitions in a superconducting qubit

This is the published version. Copyright 2015 American Institute of PhysicsWe demonstrate a fast method to detect microscopic two-level systems in a superconducting phase qubit. By monitoring the population leak after sweeping the qubit bias flux, we are able to measure the two-level systems that are coupled with the qubit. Compared with the traditional method that detects two-level systems by energy spectroscopy, our method is faster and more sensitive. This method supplies a useful tool to investigate two-level systems in solid-state qubits

Simulating the Kibble-Zurek mechanism of the Ising model with a superconducting qubit system

The Kibble-Zurek mechanism (KZM) predicts the density of topological defects produced in the dynamical processes of phase transitions in systems ranging from cosmology to condensed matter and quantum materials. The similarity between KZM and the Landau-Zener transition (LZT), which is a standard tool to describe the dynamics of some non-equilibrium physics in contemporary physics, is being extensively exploited. Here we demonstrate the equivalence between KZM in the Ising model and LZT in a superconducting qubit system. We develop a time-resolved approach to study quantum dynamics of LZT with nano-second resolution. By using this technique, we simulate the key features of KZM in the Ising model with LZT, e.g., the boundary between the adiabatic and impulse regions, the freeze-out phenomenon in the impulse region, especially, the scaling law of the excited state population as the square root of the quenching rate. Our results supply the experimental evidence of the close connection between KZM and LZT, two textbook paradigms to study the dynamics of the non-equilibrium phenomena.Comment: Title changed, authors added, and some experimental data update

Variants in MME are associated with autosomal-recessive distal hereditary motor neuropathy

© 2019 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals, Inc on behalf of American Neurological Association. Objective: To identify a new genetic cause in patients segregating distal hereditary motor neuropathy (dHMN) with an autosomal recessive pattern. Methods: Whole-exome sequencing was conducted in two siblings and was combined with segregation analysis. Additionally, 83 unrelated dHMN patients with unknown genetic cause were screened. RNA analysis was performed using blood lymphocytes and HEK293 cells transfected with mutant plasmids. Immunohistochemistry and Western blot analysis was applied to the nerve tissue. The enzymatic activities of mutant proteins were measured in the cultured cells to verify the pathogenicity of variants. Results: The clinical features of the patients showed late-onset phenotype of distal motor neuropathy without sensory involvement. We identified that compound heterozygous variants of c.1342C\u27T and c.2071_2072delGCinsTT in the membrane metalloendopeptidase (MME) gene co-segregated with the phenotype in a dHMN family. In an additional group of 83 patients with dHMN, compound heterozygous variants of c.1416+2T\u27C and c.2027C\u27T in MME were identified in one patient. The splice site variant c.1416+2T\u27C results in skipping of exon 13. The stop variant c.1342C\u27T induces mRNA degradation via nonsense-mediated mRNA decay. Transcript levels of MME in the lymphocytes showed no significant differences between the patients and controls. We also identified that MME variants were associated with mild decrease in protein expression in the sural nerve and significant impairments of enzymatic activity. Interpretation: Variants in the MME gene were associated with not only a Charcot-Marie-Tooth neuropathy phenotype but also with an autosomal-recessive dHMN phenotype. Loss of function may play a role in the pathogenesis of dHMN