748 research outputs found

    The Encoding and Decoding Complexities of Entanglement-Assisted Quantum Stabilizer Codes

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    Quantum error-correcting codes are used to protect quantum information from decoherence. A raw state is mapped, by an encoding circuit, to a codeword so that the most likely quantum errors from a noisy quantum channel can be removed after a decoding process. A good encoding circuit should have some desired features, such as low depth, few gates, and so on. In this paper, we show how to practically implement an encoding circuit of gate complexity O(n(nk+c)/logn)O(n(n-k+c)/\log n) for an [[n,k;c]][[n,k;c]] quantum stabilizer code with the help of cc pairs of maximally-entangled states. For the special case of an [[n,k]][[n,k]] stabilizer code with c=0c=0, the encoding complexity is O(n(nk)/logn)O(n(n-k)/\log n), which is previously known to be O(n2/logn)O(n^2/\log n). For c>0,c>0, this suggests that the benefits from shared entanglement come at an additional cost of encoding complexity. Finally we discuss decoding of entanglement-assisted quantum stabilizer codes and extend previously known computational hardness results on decoding quantum stabilizer codes.Comment: accepted by the 2019 IEEE International Symposium on Information Theory (ISIT2019

    Exploiting Degeneracy in Belief Propagation Decoding of Quantum Codes

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    Quantum information needs to be protected by quantum error-correcting codes due to imperfect physical devices and operations. One would like to have an efficient and high-performance decoding procedure for the class of quantum stabilizer codes. A potential candidate is Pearl's belief propagation (BP), but its performance suffers from the many short cycles inherent in a quantum stabilizer code, especially highly-degenerate codes. A general impression exists that BP is not effective for topological codes. In this paper, we propose a decoding algorithm for quantum codes based on quaternary BP with additional memory effects (called MBP). This MBP is like a recursive neural network with inhibitions between neurons (edges with negative weights), which enhance the perception capability of a network. Moreover, MBP exploits the degeneracy of a quantum code so that the most probable error or its degenerate errors can be found with high probability. The decoding performance is significantly improved over the conventional BP for various quantum codes, including quantum bicycle, hypergraph-product, surface and toric codes. For MBP on the surface and toric codes over depolarizing errors, we observe error thresholds of 16% and 17.5%, respectively.Comment: 22 pages, 25 figures, 3 tables, and 3 algorithm

    Correcting phenomenological quantum noise via belief propagation

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    Quantum stabilizer codes often face the challenge of syndrome errors due to error-prone measurements. To address this issue, multiple rounds of syndrome extraction are typically employed to obtain reliable error syndromes. In this paper, we consider phenomenological decoding problems, where data qubit errors may occur between two syndrome extractions, and each syndrome measurement can be faulty. To handle these diverse error sources, we define a generalized check matrix over mixed quaternary and binary alphabets to characterize their error syndromes. This generalized check matrix leads to the creation of a Tanner graph comprising quaternary and binary variable nodes, which facilitates the development of belief propagation (BP) decoding algorithms to tackle phenomenological errors. Importantly, our BP decoders are applicable to general sparse quantum codes. Through simulations of quantum memory protected by rotated toric codes, we demonstrates an error threshold of 3.3% in the phenomenological noise model. Additionally, we propose a method to construct effective redundant stabilizer checks for single-shot error correction. Simulations show that BP decoding performs exceptionally well, even when the syndrome error rate greatly exceeds the data error rate.Comment: 14 pages, 9 figures, 1 tabl

    Terpenoids from the Octocorals Menella sp. (Plexauridae) and Lobophytum crassum (Alcyonacea)

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    A new germacrane-type sesquiterpenoid, menelloide E (1), and a new cembrane-type diterpenoid, lobocrassin F (2), were isolated from the octocorals Menella sp. and Lobophytum crassum, respectively. The structures of terpenoids 1 and 2 were determined by spectroscopic and chemical methods and compound 2 was found to display a significant inhibitory effect on the release of elastase by human neutrophils

    Lobocrassins A–E: New Cembrane-Type Diterpenoids from the Soft Coral Lobophytum crassum

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    Five new cembrane-type diterpenoids, lobocrassins A–E (1–5), were isolated from the soft coral Lobophytum crassum. The structures of cembranes 1–5 were established by spectroscopic and chemical methods and by comparison of the spectral data with those of known cembrane analogues. Lobocrassin A (1) is the first cembranoid possessing an α-chloromethyl-α-hydroxy-γ-lactone functionality and is the first chlorinated cembranoid from soft corals belonging to the genus Lobophytum. Lobocrassins B (2) and C (3) were found to be the stereoisomers of the known cembranes, 14-deoxycrassin (6) and pseudoplexaurol (7), respectively. Lobocrassin B (2) exhibited modest cytotoxicity toward K562, CCRF-CEM, Molt4, and HepG2 tumor cells and displayed significant inhibitory effects on the generation of superoxide anion and the release of elastase by human neutrophils

    Thrombomodulin Regulates Keratinocyte Differentiation and Promotes Wound Healing

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    The membrane glycoprotein thrombomodulin (TM) has been implicated in keratinocyte differentiation and wound healing, but its specific function remains undetermined. The epidermis-specific TM knockout mice were generated to investigate the function of TM in these biological processes. Primary cultured keratinocytes obtained from TMlox/lox; K5-Cre mice, in which TM expression was abrogated, underwent abnormal differentiation in response to calcium induction. Poor epidermal differentiation, as evidenced by downregulation of the terminal differentiation markers loricrin and filaggrin, was observed in TMlox/lox; K5-Cre mice. Silencing TM expression in human epithelial cells impaired calcium-induced extracellular signal–regulated kinase pathway activation and subsequent keratinocyte differentiation. Compared with wild-type mice, the cell spreading area and wound closure rate were lower in keratinocytes from TMlox/lox; K5-Cre mice. In addition, the lower density of neovascularization and smaller area of hyperproliferative epithelium contributed to slower wound healing in TMlox/lox; K5-Cre mice than in wild-type mice. Local administration of recombinant TM (rTM) accelerated healing rates in the TM-null skin. These data suggest that TM has a critical role in skin differentiation and wound healing. Furthermore, rTM may hold therapeutic potential for the treatment of nonhealing chronic wounds

    Enhanced Differentiation of Three-Gene-Reprogrammed Induced Pluripotent Stem Cells into Adipocytes via Adenoviral-Mediated PGC-1α Overexpression

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    Induced pluripotent stem cells formed by the introduction of only three factors, Oct4/Sox2/Klf4 (3-gene iPSCs), may provide a safer option for stem cell-based therapy than iPSCs conventionally introduced with four-gene iPSCs. Peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) plays an important role during brown fat development. However, the potential roles of PGC-1α in regulating mitochondrial biogenesis and the differentiation of iPSCs are still unclear. Here, we investigated the effects of adenovirus-mediated PGC-1α overexpression in 3-gene iPSCs. PGC-1α overexpression resulted in increased mitochondrial mass, reactive oxygen species production, and oxygen consumption. Microarray-based bioinformatics showed that the gene expression pattern of PGC-1α-overexpressing 3-gene iPSCs resembled the expression pattern observed in adipocytes. Furthermore, PGC-1α overexpression enhanced adipogenic differentiation and the expression of several brown fat markers, including uncoupling protein-1, cytochrome C, and nuclear respiratory factor-1, whereas it inhibited the expression of the white fat marker uncoupling protein-2. Furthermore, PGC-1α overexpression significantly suppressed osteogenic differentiation. These data demonstrate that PGC-1α directs the differentiation of 3-gene iPSCs into adipocyte-like cells with features of brown fat cells. This may provide a therapeutic strategy for the treatment of mitochondrial disorders and obesity
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