499 research outputs found

    Information hiding and retrieval in Rydberg wave packets using half-cycle pulses

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    We demonstrate an information hiding and retrieval scheme with the relative phases between states in a Rydberg wave packet acting as the bits of a data register. We use a terahertz half-cycle pulse (HCP) to transfer phase-encoded information from an optically accessible angular momentum manifold to another manifold which is not directly accessed by our laser pulses, effectively hiding the information from our optical interferometric measurement techniques. A subsequent HCP acting on these wave packets reintroduces the information back into the optically accessible data register manifold which can then be `read' out.Comment: 4 pages, 4 figure

    Phase transitions in open quantum systems

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    We consider the behaviour of open quantum systems in dependence on the coupling to one decay channel by introducing the coupling parameter α\alpha being proportional to the average degree of overlapping. Under critical conditions, a reorganization of the spectrum takes place which creates a bifurcation of the time scales with respect to the lifetimes of the resonance states. We derive analytically the conditions under which the reorganization process can be understood as a second-order phase transition and illustrate our results by numerical investigations. The conditions are fulfilled e.g. for a picket fence with equal coupling of the states to the continuum. Energy dependencies within the system are included. We consider also the generic case of an unfolded Gaussian Orthogonal Ensemble. In all these cases, the reorganization of the spectrum occurs at the critical value αcrit\alpha_{crit} of the control parameter globally over the whole energy range of the spectrum. All states act cooperatively.Comment: 28 pages, 22 Postscript figure

    Time-Frequency Signatures of Electronic Coherence of Colloidal CdSe Quantum Dot Dimer Assemblies Probed at Room Temperature by Two-Dimensional Electronic Spectroscopy

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    Electronic coherence signatures can be directly identified in the time-frequency maps measured in two-dimensional electronic spectroscopy (2DES). Here, we demonstrate the theory and discuss the advantages of this approach via the detailed application to the fast-femtosecond beatings of a wide variety of electronic coherences in ensemble dimers of quantum dots (QDs), assembled from QDs of 3 nm in diameter, with 8% size dispersion in diameter. The observed and computed results can be consistently characterized directly in the time-frequency domain by probing the polarization in the 2DES setup. The experimental and computed time-frequency maps are found in very good agreement, and several electronic coherences are characterized at room temperature in solution, before the extensive dephasing due to the size dispersion begins. As compared to the frequency-frequency maps that are commonly used in 2DES, the time-frequency maps allow exploiting electronic coherences without additional post-processing and with fewer 2DES measurements. Towards quantum technology applications, we also report on the modeling of the time-frequency photocurrent response of these electronic coherences, which paves the way to integrating QD devices with classical architectures, thereby enhancing the quantum advantage of such technologies for parallel information processing at room temperature

    Assay of matrix metalloproteinases types 1, 2, 3 and 9 in breast cancer.

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    Matrix metalloproteinases (MMPs) are zinc dependent endopeptidases implicated in cancer invasion and metastasis. Gelatin zymography was performed on 84 human breast carcinomas and seven normal breast tissues. The precursor form of MMP-2 (72 kDa) was found in 11 (12%) samples, while its two activated forms, i.e. 62 kDa and 59 kDa, were found in three (6%) and 34 (40%) samples respectively. In contrast to MMP-2, most of the samples (52%) contained MMP-9 in its precursor form. Using ELISA, MMP-1 levels were found in 12% of the samples while MMP-3 levels were found in only 2% of the samples. Levels of MMP-2, -3 and -9 correlated inversely with numbers of nodal metastases. Neither MMP-2 nor -9 levels were significantly related to patient outcome. However, patients with high levels of a 50-kDa gelatinase band after zymography had a significantly better survival than patients with low levels. This species was never observed in normal breast tissue

    Ammonium accumulation is a primary effect of 2-methylcitrate exposure in an in vitro model for brain damage in methylmalonic aciduria.

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    Using 3D organotypic rat brain cell cultures in aggregates we recently identified 2-methylcitrate (2-MCA) as the main toxic metabolite for developing brain cells in methylmalonic aciduria. Exposure to 2-MCA triggered morphological changes and apoptosis of brain cells. This was accompanied by increased ammonium and decreased glutamine levels. However, the sequence and causal relationship between these phenomena remained unclear. To understand the sequence and time course of pathogenic events, we exposed 3D rat brain cell aggregates to different concentrations of 2-MCA (0.1, 0.33 and 1.0mM) from day in vitro (DIV) 11 to 14. Aggregates were harvested at different time points from DIV 12 to 19. We compared the effects of a single dose of 1mM 2-MCA administered on DIV 11 to the effects of repeated doses of 1mM 2-MCA. Pan-caspase inhibitors Z-VAD FMK or Q-VD-OPh were used to block apoptosis. Ammonium accumulation in the culture medium started within few hours after the first 2-MCA exposure. Morphological changes of the developing brain cells were already visible after 17h. The highest rate of cleaved caspase-3 was observed after 72h. A dose-response relationship was observed for all effects. Surprisingly, a single dose of 1mM 2-MCA was sufficient to induce all of the biochemical and morphological changes in this model. 2-MCA-induced ammonium accumulation and morphological changes were not prevented by concomitant treatment of the cultures with pan-caspase inhibitors Z-VAD FMK or Q-VD-OPh: ammonium increased rapidly after a single 1mM 2-MCA administration even after apoptosis blockade. We conclude that following exposure to 2-MCA, ammonium production in brain cell cultures is an early phenomenon, preceding cell degeneration and apoptosis, and may actually be the cause of the other changes observed. The fact that a single dose of 1mM 2-MCA is sufficient to induce deleterious effects over several days highlights the potential damaging effects of even short-lasting metabolic decompensations in children affected by methylmalonic aciduria

    Resonance trapping and saturation of decay widths

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    Resonance trapping appears in open many-particle quantum systems at high level density when the coupling to the continuum of decay channels reaches a critical strength. Here a reorganization of the system takes place and a separation of different time scales appears. We investigate it under the influence of additional weakly coupled channels as well as by taking into account the real part of the coupling term between system and continuum. We observe a saturation of the mean width of the trapped states. Also the decay rates saturate as a function of the coupling strength. The mechanism of the saturation is studied in detail. In any case, the critical region of reorganization is enlarged. When the transmission coefficients for the different channels are different, the width distribution is broadened as compared to a chi_K^2 distribution where K is the number of channels. Resonance trapping takes place before the broad state overlaps regions beyond the extension of the spectrum of the closed system.Comment: 18 pages, 8 figures, accepted by Phys. Rev.

    Doorway states in nuclear reactions as a manifestation of the "super-radiant" mechanism

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    A mechanism is considered for generating doorway states and intermediate structure in low-energy nuclear reactions as a result of collectivization of widths of unstable intrinsic states coupled to common decay channels. At the limit of strong continuum coupling, the segregation of broad (''super-radiating") and narrow (''trapped") states occurs revealing the separation of direct and compound processes. We discuss the conditions for the appearance of intermediate structure in this process and doorways related to certain decay channels.Comment: 16 page

    Nomenclature proposal to describe vocal fold motion impairment

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    The terms used to describe vocal fold motion impairment are confusing and not standardized. This results in a failure to communicate accurately and to major limitations of interpreting research studies involving vocal fold impairment. We propose standard nomenclature for reporting vocal fold impairment. Overarching terms of vocal fold immobility and hypomobility are rigorously defined. This includes assessment techniques and inclusion and exclusion criteria for determining vocal fold immobility and hypomobility. In addition, criteria for use of the following terms have been outlined in detail: vocal fold paralysis, vocal fold paresis, vocal fold immobility/hypomobility associated with mechanical impairment of the crico-arytenoid joint and vocal fold immobility/hypomobility related to laryngeal malignant disease. This represents the first rigorously defined vocal fold motion impairment nomenclature system. This provides detailed definitions to the terms vocal fold paralysis and vocal fold paresis

    The transcription factor Zeb2 regulates development of conventional and plasmacytoid DCs by repressing Id2

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    Plasmacytoid dendritic cells (DCs [pDCs]) develop from pre-pDCs, whereas two lineages of conventional DCs (cDCs; cDC1s and cDC2s) develop from lineage-committed pre-cDCs. Several transcription factors (TFs) have been implicated in regulating the development of pDCs (E2-2 and Id2) and cDC1s (Irf8, Id2, and Batf3); however, those required for the early commitment of pre-cDCs toward the cDC2 lineage are unknown. Here, we identify the TF zinc finger E box-binding homeobox 2 (Zeb2) to play a crucial role in regulating DC development. Zeb2 was expressed from the pre-pDC and pre-cDC stage onward and highly expressed in mature pDCs and cDC2s. Mice conditionally lacking Zeb2 in CD11c(+) cells had a cell-intrinsic reduction in pDCs and cDC2s, coupled with an increase in cDC1s. Conversely, mice in which CD11c(+) cells overexpressed Zeb2 displayed a reduction in cDC1s. This was accompanied by altered expression of Id2, which was up-regulated in cDC2s and pDCs from conditional knock-out mice. Zeb2 chromatin immunoprecipitation analysis revealed Id2 to be a direct target of Zeb2. Thus, we conclude that Zeb2 regulates commitment to both the cDC2 and pDC lineages through repression of Id2
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