26 research outputs found

    Quantum arbitrary waveform generator

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    Controlling the waveform of light is the key for a versatile light source in classical and quantum electronics. Although pulse shaping of classical light is a mature technique and has been used in various fields, more advanced applications would be realized by a light source that generates arbitrary quantum light with arbitrary temporal waveform. We call such a device a quantum arbitrary waveform generator (Q-AWG). The Q-AWG must be able to handle versatile quantum states of light, which are fragile. Thus, the Q-AWG requires a radically different methodology from classical pulse shaping. In this paper, we invent an architecture of Q-AWGs that can operate semi-deterministically at a repetition rate over GHz in principal. We demonstrate its core technology via generating highly non-classical states with waveforms that have never been realized before. This result would lead to powerful quantum technologies based on Q-AWGs such as practical optical quantum computing.Comment: 24 pages, 5 figure

    Integrable semi-discretization of the coupled nonlinear Schr\"{o}dinger equations

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    A system of semi-discrete coupled nonlinear Schr\"{o}dinger equations is studied. To show the complete integrability of the model with multiple components, we extend the discrete version of the inverse scattering method for the single-component discrete nonlinear Schr\"{o}dinger equation proposed by Ablowitz and Ladik. By means of the extension, the initial-value problem of the model is solved. Further, the integrals of motion and the soliton solutions are constructed within the framework of the extension of the inverse scattering method.Comment: 27 pages, LaTeX2e (IOP style

    Usefulness of Combined Screening with Conventional Procedure and Screening Mammography in the Detection of Breast Cancer : Results from the Mass Survey for Breast Cancer in Kumamoto Prefecture

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    The aim of this study was to evaluate the usefulness of combined screening with conventional procedure and screening mammography by comparing a number and detection rate of breast cancers between conventional procedure without (CP group) and with screening mammography (MMG group) performed in Kumamoto prefecture from 1999 to 2005

    Stretching Actin Filaments within Cells Enhances their Affinity for the Myosin II Motor Domain

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    To test the hypothesis that the myosin II motor domain (S1) preferentially binds to specific subsets of actin filaments in vivo, we expressed GFP-fused S1 with mutations that enhanced its affinity for actin in Dictyostelium cells. Consistent with the hypothesis, the GFP-S1 mutants were localized along specific portions of the cell cortex. Comparison with rhodamine-phalloidin staining in fixed cells demonstrated that the GFP-S1 probes preferentially bound to actin filaments in the rear cortex and cleavage furrows, where actin filaments are stretched by interaction with endogenous myosin II filaments. The GFP-S1 probes were similarly enriched in the cortex stretched passively by traction forces in the absence of myosin II or by external forces using a microcapillary. The preferential binding of GFP-S1 mutants to stretched actin filaments did not depend on cortexillin I or PTEN, two proteins previously implicated in the recruitment of myosin II filaments to stretched cortex. These results suggested that it is the stretching of the actin filaments itself that increases their affinity for the myosin II motor domain. In contrast, the GFP-fused myosin I motor domain did not localize to stretched actin filaments, which suggests different preferences of the motor domains for different structures of actin filaments play a role in distinct intracellular localizations of myosin I and II. We propose a scheme in which the stretching of actin filaments, the preferential binding of myosin II filaments to stretched actin filaments, and myosin II-dependent contraction form a positive feedback loop that contributes to the stabilization of cell polarity and to the responsiveness of the cells to external mechanical stimuli

    Time-restricted feeding suppresses excess sucrose-induced plasma and liver lipid accumulation in rats.

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    The etiology of metabolic syndrome involves several complicated factors. One of the main factors contributing to metabolic syndrome has been proposed to be excessive intake of sucrose, which disturbs hepatic lipid metabolism, resulting in fatty liver. However, the mechanism by which sucrose induces fatty liver remains to be elucidated. Considering feeding behavior important for metabolism, we investigated whether time-restricted feeding of high sucrose diet (HSD), only in the active phase (the dark phase of the daily light/dark cycle), would ameliorate adverse effects of sucrose on lipid homeostasis in rats. Male Wistar rats, fed either an ad libitum (ad lib.) or time-restricted control starch diet (CD) or HSD were investigated. Rats fed ad lib. (CD and HSD) completed approximately 20% of food intake in the daytime. Time-restricted feeding did not significantly suppress total food intake of rats. However, time-restricted feeding of HSD significantly suppressed the increased plasma triglyceride levels. Moreover, time-restricted feeding also ameliorated HSD-induced liver lipid accumulation, whereas circadian oscillations of liver clock gene or transcriptional factor gene expression for lipid metabolism were not altered significantly. These results demonstrated that restricting sucrose intake only during the active phase in rats ameliorates the abnormal lipid metabolism caused by excess sucrose intake

    Delayed first active-phase meal, a breakfast-skipping model, led to increased body weight and shifted the circadian oscillation of the hepatic clock and lipid metabolism-related genes in rats fed a high-fat diet.

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    The circadian clock is closely related to human health, such as metabolic syndrome and cardiovascular disease. Our previous study revealed that irregular feeding induced abnormal lipid metabolism with disruption of the hepatic circadian clock. We hypothesized that breakfast skipping induces lipid abnormalities, such as adiposity, by altering the hepatic circadian oscillation of clock and lipid metabolism-related genes. Here, we established a delayed first active-phase meal (DFAM) protocol as a breakfast-skipping model. Briefly, rats were fed a high-fat diet during zeitgeber time (ZT) 12-24 in a control group and ZT 16-4 in the DFAM group. The DFAM group showed increased body weight gain and perirenal adipose tissue weight without a change in total food intake. The circadian oscillations of hepatic clock and de novo fatty acid synthesis genes were delayed by 2-4 h because of DFAM. The peaks of serum insulin, a synchronizer for the liver clock, bile acids, and non-esterified fatty acid (NEFA) were delayed by 4-6 h because of DFAM. Moreover, DFAM delayed the surge in body temperature by 4 h and may have contributed to the increase in body weight gain and adipose tissue weight because of decreased energy expenditure. These data indicated a potential molecular mechanism by which breakfast skipping induces abnormal lipid metabolism, which is related to the altered circadian oscillation of hepatic gene expression. The results also suggested that the delayed peaks of serum NEFA, bile acids, and insulin entrain the circadian rhythm of hepatic clock and lipid metabolism-related genes

    Freshwater Clam Extract Ameliorates Triglyceride and Cholesterol Metabolism through the Expression of Genes Involved in Hepatic Lipogenesis and Cholesterol Degradation in Rats

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    The freshwater clam (Corbicula spp.) is a popular edible bivalve and has been used as a folk remedy for liver disease in Asia. As a Chinese traditional medicine, it is said that freshwater clam ameliorates alcoholic intoxication and cholestasis. In this study, to estimate the practical benefit of freshwater clam extract (FCE), we compared the effects of FCE and soy protein isolate (SPI) on triglyceride and cholesterol metabolism in rats. FCE and SPI lowered serum cholesterol, and FCE tended to reduce serum triglycerides. FCE enhanced fecal sterol excretion and hepatic mRNA levels of CYP7A1 and ABCG5 more substantially than SPI; however, both diets reduced hepatic cholesterol. Both of the diets similarly suppressed liver lipids improved Ξ”9-desaturated fatty acid profile, and FCE was associated with a reduction in FAS and SCD1 mRNA levels. Hepatic transcriptome analysis revealed that inhibition of lipogenesis-related gene expression may contribute to downregulation of hepatic triglycerides by FCE. FCE would have better potential benefits for preventing metabolic disorders, through greater improvement of metabolism of triglycerides and cholesterol, likely through a mechanism similar to SPI

    Generation of Schr\"{o}dinger cat states with Wigner negativity using continuous-wave low-loss waveguide optical parametric amplifier

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    Continuous-wave (CW) squeezed light is used in generation of various optical quantum states thus is a fundamental resource of fault-tolerant universal quantum computation using optical continuous variables. To realize a practical quantum computer, a waveguide optical parametric amplifier (OPA) is an attractive CW squeezed light source in terms of its THz-order bandwidth and suitability for modularization. The usages of a waveguide OPA in quantum applications thus far, however, are limited due to the difficulty of the generation of the squeezed light with a high purity. In this paper, we report the first observation of Wigner negativity of the states generated by a heralding method using a waveguide OPA. We generate Schr\"{o}dinger cat states at the wavelength of 1545 nm with Wigner negativity using a quasi-single-mode ZnO-doped periodically poled LiNbO3{\rm LiNbO_3} waveguide module we developed. Wigner negativity is regarded as an important indicator of the usefulness of the quantum states as it is essential in the fault-tolerant universal quantum computation. Our result shows that our waveguide OPA can be used in wide range of quantum applications leading to a THz-clock optical quantum computer.Comment: 10 pages, 5 figure
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