51 research outputs found

    Comment on `Vacuum Rabi Splitting in a Semiconductor Circuit QED System' by Toida et al., Phys. Rev. Lett. 110, 066802 - Published 6 February 2013

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    Toida et al. claim in their recent article [Phys. Rev. Lett. 110, 066802 (2013)] that they `report a direct observation of vacuum Rabi splitting in a GaAs/AlGaAs double quantum dot (DQD) based charge qubit coupled with a superconducting coplanar waveguide (CPW) resonator'. In this comment, we challenge the main claims made in their paper and show that their results: a) do not provide any evidence of vacuum Rabi oscillations and b) do not provide any direct evidence of vacuum Rabi splitting.Comment: 2 pages, 2 figure

    Strong Coupling Cavity QED with Gate-Defined Double Quantum Dots Enabled by a High Impedance Resonator

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    The strong coupling limit of cavity quantum electrodynamics (QED) implies the capability of a matter-like quantum system to coherently transform an individual excitation into a single photon within a resonant structure. This not only enables essential processes required for quantum information processing but also allows for fundamental studies of matter-light interaction. In this work we demonstrate strong coupling between the charge degree of freedom in a gate-detuned GaAs double quantum dot (DQD) and a frequency-tunable high impedance resonator realized using an array of superconducting quantum interference devices (SQUIDs). In the resonant regime, we resolve the vacuum Rabi mode splitting of size 2g/2π=2382g/2\pi = 238 MHz at a resonator linewidth κ/2π=12\kappa/2\pi = 12 MHz and a DQD charge qubit dephasing rate of γ2/2π=80\gamma_2/2\pi = 80 MHz extracted independently from microwave spectroscopy in the dispersive regime. Our measurements indicate a viable path towards using circuit based cavity QED for quantum information processing in semiconductor nano-structures

    Mesenteric Resistance Arteries in Type 2 Diabetic db/db Mice Undergo Outward Remodeling

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    Resistance vessel remodeling is controlled by myriad of hemodynamic and neurohormonal factors. This study characterized structural and molecular remodeling in mesenteric resistance arteries (MRAs) in diabetic (db/db) and control (Db/db) mice.Structural properties were assessed in isolated MRAs from 12 and 16 wk-old db/db and Db/db mice by pressure myography. Matrix regulatory proteins were measured by Western blot analysis. Mean arterial pressure and superior mesenteric blood flow were measured in 12 wk-old mice by telemetry and a Doppler flow nanoprobe, respectively.Blood pressure was similar between groups. Lumen diameter and medial cross-sectional area were significantly increased in 16 wk-old db/db MRA compared to control, indicating outward hypertrophic remodeling. Moreover, wall stress and cross-sectional compliance were significantly larger in diabetic arteries. These remodeling indices were associated with increased expression of matrix regulatory proteins matrix metalloproteinase (MMP)-9, MMP-12, tissue inhibitors of matrix metalloproteinase (TIMP)-1, TIMP-2, and plasminogen activator inhibitor-1 (PAI-1) in db/db arteries. Finally, superior mesenteric artery blood flow was increased by 46% in 12 wk-old db/db mice, a finding that preceded mesenteric resistance artery remodeling.These data suggest that flow-induced hemodynamic changes may supersede the local neurohormonal and metabolic milieu to culminate in hypertrophic outward remodeling of type 2 DM mesenteric resistance arteries

    Electroluminescence Caused by the Transport of Interacting Electrons through Parallel Quantum Dots in a Photon Cavity

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    This work was financially supported by the Research Fund of the University of Iceland, the Icelandic Research Fund, grant no. 163082-051, and the Icelandic Instruments Fund. HSG acknowledges support from Ministry of Science and Technology of Taiwan, under grant no. 103-2112-M-002-003-MY3.We show that a Rabi-splitting of the states of strongly interacting electrons in parallel quantum dots embedded in a short quantum wire placed in a photon cavity can be produced by either the para- or the dia-magnetic electron-photon interactions when the geometry of the system is properly accounted for and the photon field is tuned close to a resonance with the electron system. We use these two resonances to explore the electroluminescence caused by the transport of electrons through the one- and two-electron ground states of the system and their corresponding conventional and vacuum electroluminescense as the central system is opened up by coupling it to external leads acting as electron reservoirs. Our analysis indicates that high-order electron-photon processes are necessary to adequately construct the cavity-photon dressed electron states needed to describe both types of electroluminescence

    Hyperactive S6K1 Mediates Oxidative Stress and Endothelial Dysfunction in Aging: Inhibition by Resveratrol

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    Mammalian target of rapamycin (mTOR)/S6K1 signalling emerges as a critical regulator of aging. Yet, a role of mTOR/S6K1 in aging-associated vascular endothelial dysfunction remains unknown. In this study, we investigated the role of S6K1 in aging-associated endothelial dysfunction and effects of the polyphenol resveratrol on S6K1 in aging endothelial cells. We show here that senescent endothelial cells displayed higher S6K1 activity, increased superoxide production and decreased bioactive nitric oxide (NO) levels than young endothelial cells, which is contributed by eNOS uncoupling. Silencing S6K1 in senescent cells reduced superoxide generation and enhanced NO production. Conversely, over-expression of a constitutively active S6K1 mutant in young endothelial cells mimicked endothelial dysfunction of the senescent cells through eNOS uncoupling and induced premature cellular senescence. Like the mTOR/S6K1 inhibitor rapamycin, resveratrol inhibited S6K1 signalling, resulting in decreased superoxide generation and enhanced NO levels in the senescent cells. Consistent with the data from cultured cells, an enhanced S6K1 activity, increased superoxide generation, and decreased bioactive NO levels associated with eNOS uncoupling were also detected in aortas of old WKY rats (aged 20–24 months) as compared to the young animals (1–3 months). Treatment of aortas of old rats with resveratrol or rapamycin inhibited S6K1 activity, oxidative stress, and improved endothelial NO production. Our data demonstrate a causal role of the hyperactive S6K1 in eNOS uncoupling leading to endothelial dysfunction and vascular aging. Resveratrol improves endothelial function in aging, at least in part, through inhibition of S6K1. Targeting S6K1 may thus represent a novel therapeutic approach for aging-associated vascular disease
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