Quantum walk of a trapped ion in phase space

We implement the proof of principle for the quantum walk of one ion in a linear ion trap. With a single-step fidelity exceeding 0.99, we perform three steps of an asymmetric walk on the line. We clearly reveal the differences to its classical counterpart if we allow the walker/ion to take all classical paths simultaneously. Quantum interferences enforce asymmetric, non-classical distributions in the highly entangled degrees of freedom (of coin and position states). We theoretically study and experimentally observe the limitation in the number of steps of our approach, that is imposed by motional squeezing. We propose an altered protocol based on methods of impulsive steps to overcome these restrictions, in principal allowing to scale the quantum walk to several hundreds of steps.Comment: 4 pages, 4 figure

Experimental simulation and limitations of quantum walks with trapped ions

We examine the prospects of discrete quantum walks (QWs) with trapped ions. In particular, we analyze in detail the limitations of the protocol of Travaglione and Milburn (PRA 2002) that has been implemented by several experimental groups in recent years. Based on the first realization in our group (PRL 2009), we investigate the consequences of leaving the scope of the approximations originally made, such as the Lamb--Dicke approximation. We explain the consequential deviations from the idealized QW for different experimental realizations and an increasing number of steps by taking into account higher-order terms of the quantum evolution. It turns out that these become dominant after a few steps already, which is confirmed by experimental results and is currently limiting the scalability of this approach. Finally, we propose a new scheme using short laser pulses, derived from a protocol from the field of quantum computation. We show that the new scheme is not subject to the above-mentioned restrictions, and analytically and numerically evaluate its limitations, based on a realistic implementation with our specific setup. Implementing the protocol with state-of-the-art techniques should allow for substantially increasing the number of steps to 100 and beyond and should be extendable to higher-dimensional QWs.Comment: 29 pages, 15 figue

A new tool to ensure the fluorescent dye labeling stability of nanocarriers: A real challenge for fluorescence imaging

International audienceNumerous studies on nanocarriers use fluorescent dye labeling to investigate their biodistribution or cellular trafficking. However, when the fluorescence dye is not grafted to the nanocarrier, the question of the stability of the labeling arises. How can it be validated that the fluorescence observed during an experiment corresponds to the nanocarriers, and not to the free dye released from the nanocarriers? Studying the integrity of the labeling is challenging. Therefore, an innovative approach to confirm the labeling stability was developed, based on the transfer of a fluorescent dye from its hosting nanocarrier to a lipophilic compartment. Lipid nanocapsules (LNC) and triglyceride oil were used as models. The protocol involved mixing of LNC suspension and oil, and then separation by centrifugation. The quality of the separation was controlled by light scattering, using the derived count rate tool. Dye transfer from loaded LNCs to the lipophilic compartment or from a lipophilic compartment containing dye to non-loaded LNC was investigated by varying the nature of the dye and the oil, the oil volume and the LNC dilution. Tensiometry was used to define the dye location in the nanocarrier. Results showed that when dyes such as Nile Red and Coumarin-6 are located in oily core, the transfer occurred in a partition-dependent manner. In contrast, when the dye was entrapped in the surfactant shell of LNCs such as lipophilic indocarbocyanines (i.e. DiO, DiI and DiD), no transfer was observed. Dye diffusion was also observed in cell culture, with Nile Red inside lipid bodies of HEI-OC1 cells, without uptake of LNCs. In contrast, DiO-loaded LNCs had to be internalized to observe fluorescence inside the cells, providing a further confirmation of the absence of transfer in this case, and the stability of fluorescence labeling of the LNCs

Murine malaria is associated with significant hearing impairment

<p>Abstract</p> <p>Background</p> <p><it>Plasmodium falciparum </it>malaria has been suspected to cause hearing loss. Developmental, cognitive and language disorders have been observed in children, surviving cerebral malaria. This prospective study aims to evaluate whether malaria influences hearing in mice.</p> <p>Methods</p> <p>Twenty mice were included in a standardized murine cerebral malaria model. Auditory evoked brainstem responses were assessed before infection and at the peak of the illness.</p> <p>Results</p> <p>A significant hearing impairment could be demonstrated in mice with malaria, especially the cerebral form. The control group did not show any alterations. No therapy was used.</p> <p>Conclusion</p> <p>This suggests that malaria itself leads to a hearing impairment in mice.</p

Apoptosis of the fibrocytes type 1 in the spiral ligament and blood labyrinth barrier disturbance cause hearing impairment in murine cerebral malaria

<p>Abstract</p> <p>Background</p> <p>Experimental murine malaria has been shown to result in significant hearing impairment. Microscopic evaluation of the temporal bones of these animals has revealed regular morphology of the cochlea duct. Furthermore, the known vascular pathologic changes being associated with malaria could not be found. Immunohistochemistry for ICAM1 showed a strong marking in the <it>stria vascularis</it>, indicating a disturbance of the endocochlear potential. The aim of this study was to evaluate the role of apoptosis and the disturbance of the blood labyrinth barrier in the murine malaria associated hearing impairment.</p> <p>Methods</p> <p>The temporal bones of seven mice with cerebral malaria-four with hearing impairment, three without hearing impairment-were evaluated with immunohistochemistry for cleaved caspase 3 to detect apoptosis and connexin 26, a gap junction protein being a cornerstone in the endocochlear potassium recirculation. Furthermore five animals with cerebral malaria were treated with Evans blue prior to sacrification to detect disturbances of the blood labyrinth barrier.</p> <p>Results</p> <p>Cleaved caspase 3 could clearly be detected by immunohistochemistry in the fibrocytes of the spiral ligament, more intensively in animals with hearing impairment, less intensively in those without. Apoptosis signal was equally distributed in the spiral ligament as was the connexin 26 gap junction protein. The Evans blue testing revealed a strong signal in the malaria animals and no signal in the healthy control animals.</p> <p>Conclusion</p> <p>Malfunction of the fibrocytes type 1 in the spiral ligament and disruption of the blood labyrinth barrier, resulting in a breakdown of the endocochlear potential, are major causes for hearing impairment in murine cerebral malaria.</p

Quantitative X-ray Tomography of the Mouse Cochlea

Imaging with hard X-rays allows visualizing cochlear structures while maintaining intrinsic qualities of the tissue, including structure and size. With coherent X-rays, soft tissues, including membranes, can be imaged as well as cells making use of the so-called in-line phase contrast. In the present experiments, partially coherent synchrotron radiation has been used for micro-tomography. Three-dimensional reconstructions of the mouse cochlea have been created using the EM3D software and the volume has been segmented in the Amira Software Suite. The structures that have been reconstructed include scala tympani, scala media, scala vestibuli, Reissner's membrane, basilar membrane, tectorial membrane, organ of Corti, spiral limbus, spiral ganglion and cochlear nerve. Cross-sectional areas of the scalae were measured. The results provide a realistic and quantitative reconstruction of the cochlea