Mapping photonic entanglement into and out of a quantum memory

Recent developments of quantum information science critically rely on entanglement, an intriguing aspect of quantum mechanics where parts of a composite system can exhibit correlations stronger than any classical counterpart. In particular, scalable quantum networks require capabilities to create, store, and distribute entanglement among distant matter nodes via photonic channels. Atomic ensembles can play the role of such nodes. So far, in the photon counting regime, heralded entanglement between atomic ensembles has been successfully demonstrated via probabilistic protocols. However, an inherent drawback of this approach is the compromise between the amount of entanglement and its preparation probability, leading intrinsically to low count rate for high entanglement. Here we report a protocol where entanglement between two atomic ensembles is created by coherent mapping of an entangled state of light. By splitting a single-photon and subsequent state transfer, we separate the generation of entanglement and its storage. After a programmable delay, the stored entanglement is mapped back into photonic modes with overall efficiency of 17 %. Improvements of single-photon sources together with our protocol will enable "on demand" entanglement of atomic ensembles, a powerful resource for quantum networking.Comment: 7 pages, and 3 figure

Evanescent light-matter Interactions in Atomic Cladding Wave Guides

Alkali vapors, and in particular rubidium, are being used extensively in several important fields of research such as slow and stored light non-linear optics3 and quantum computation. Additionally, the technology of alkali vapors plays a major role in realizing myriad industrial applications including for example atomic clocks magentometers8 and optical frequency stabilization. Lately, there is a growing effort towards miniaturizing traditional centimeter-size alkali vapor cells. Owing to the significant reduction in device dimensions, light matter interactions are greatly enhanced, enabling new functionalities due to the low power threshold needed for non-linear interactions. Here, taking advantage of the mature Complimentary Metal-Oxide-Semiconductor (CMOS) compatible platform of silicon photonics, we construct an efficient and flexible platform for tailored light vapor interactions on a chip. Specifically, we demonstrate light matter interactions in an atomic cladding wave guide (ACWG), consisting of CMOS compatible silicon nitride nano wave-guide core with a Rubidium (Rb) vapor cladding. We observe the highly efficient interaction of the electromagnetic guided mode with the thermal Rb cladding. The nature of such interactions is explained by a model which predicts the transmission spectrum of the system taking into account Doppler and transit time broadening. We show, that due to the high confinement of the optical mode (with a mode area of 0.3{\lambda}2), the Rb absorption saturates at powers in the nW regime.Comment: 10 Pages 4 Figures. 1 Supplementar

Elimination, reversal, and directional bias of optical diffraction

We experimentally demonstrate the manipulation of optical diffraction, utilizing the atomic thermal motion in a hot vapor medium of electromagnetically-induced transparency (EIT). By properly tuning the EIT parameters, the refraction induced by the atomic motion may completely counterbalance the paraxial free-space diffraction and by that eliminates the effect of diffraction for arbitrary images. By further manipulation, the diffraction can be doubled, biased asymmetrically to induced deflection, or even reversed. The latter allows an experimental implementation of an analogy to a negative-index lens

Pleiotropic effects of levofloxacin, fluoroquinolone antibiotics, against influenza virus-induced lung injury

© 2015 Enoki et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Reactive oxygen species (ROS) and nitric oxide (NO) are major pathogenic molecules produced during viral lung infections, including influenza. While fluoroquinolones are widely used as antimicrobial agents for treating a variety of bacterial infections, including secondary infections associated with the influenza virus, it has been reported that they also function as anti-oxidants against ROS and as a NO regulator. Therefore, we hypothesized that levofloxacin (LVFX), one of the most frequently used fluoroquinolone derivatives, may attenuate pulmonary injuries associated with influenza virus infections by inhibiting the production of ROS species such as hydroxyl radicals and neutrophil-derived NO that is produced during an influenza viral infection. The therapeutic impact of LVFX was examined in a PR8 (H1N1) influenza virus-induced lung injury mouse model. ESR spin-trapping experiments indicated that LVFX showed scavenging activity against neutrophil-derived hydroxyl radicals. LVFX markedly improved the survival rate of mice that were infected with the influenza virus in a dose-dependent manner. In addition, the LVFX treatment resulted in a dose-dependent decrease in the level of 8-hydroxy-2'-deoxyguanosine (a marker of oxidative stress) and nitrotyrosine (a nitrative marker) in the lungs of virus-infected mice, and the nitrite/nitrate ratio (NO metabolites) and IFN-? in BALF. These results indicate that LVFX may be of substantial benefit in the treatment of various acute inflammatory disorders such as influenza virus-induced pneumonia, by inhibiting inflammatory cell responses and suppressing the overproduction of NO in the lungs

Cavity electromagnetically induced transparency and all-optical switching using ion Coulomb crystals

The control of one light field by another, ultimately at the single photon level, is a challenging task which has numerous interesting applications within nonlinear optics and quantum information science. Due to the extremely weak direct interactions between optical photons in vacuum, this type of control can in practice only be achieved through highly nonlinear interactions within a medium. Electromagnetic induced transparency (EIT) constitutes one such means to obtain the extremely strong nonlinear coupling needed to facilitate interactions between two faint light fields. Here, we demonstrate for the first time EIT as well as all-optical EIT-based light switching using ion Coulomb crystals situated in an optical cavity. Unprecedented narrow cavity EIT feature widths down to a few kHz and a change from essentially full transmission to full absorption of the probe field within a window of only ~100 kHz are achieved. By applying a weak switching field, we furthermore demonstrate nearly perfect switching of the transmission of the probe field. These results represent important milestones for future realizations of quantum information processing devices, such as high-efficiency quantum memories, single-photon transistors and single-photon gates

Controlling photons using electromagnetically induced transparency

It is well known that a dielectric medium can be used to manipulate properties of light pulses. However, optical absorption limits the extent of possible control: this is especially important for weak light pulses. Absorption in an opaque medium can be eliminated via quantum mechanical interference, an effect known as electromagnetically induced transparency. Theoretical and experimental work has demonstrated that this phenomenon can be used to slow down light pulses dramatically, or even bring them to a complete halt. Interactions between photons in such an atomic medium can be many orders of magnitude stronger than in conventional optical materials

Conformational changes in α7 acetylcholine receptors underlying allosteric modulation by divalent cations

Allosteric modulation of membrane receptors is a widespread mechanism by which endogenous and exogenous agents regulate receptor function. For example, several members of the nicotinic receptor family are modulated by physiological concentrations of extracellular calcium ions. In this paper, we examined conformational changes underlying this modulation and compare these with changes evoked by ACh. Two sets of residues in the α7 acetylcholine receptor extracellular domain were mutated to cysteine and analyzed by measuring the rates of modification by the thiol-specific reagent 2-aminoethylmethane thiosulfonate. Using Ba2+ as a surrogate for Ca2+, we found a divalent-dependent decrease the modification rates of cysteine substitutions at M37 and M40, residues at which rates were also slowed by ACh. In contrast, Ba2+ had no significant effect at N52C, a residue where ACh increased the rate of modification. Thus divalent modulators cause some but not all of the conformational effects elicited by agonist. Cysteine substitution of either of two glutamates (E44 or E172), thought to participate in the divalent cation binding site, caused a loss of allosteric modulation, yet Ba2+ still had a significant effect on modification rates of these residues. In addition, the effect of Ba2+ at these residues did not appear to be due to direct occlusion. Our data demonstrate that modulation by divalent cations involves substantial conformational changes in the receptor extracellular domain. Our evidence also suggests the modulation occurs via a binding site distinct from one which includes either (or both) of the conserved glutamates at E44 or E172

Acute Respiratory Distress Syndrome Induced by a Swine 2009 H1N1 Variant in Mice

Background: Acute respiratory distress syndrome (ARDS) induced by pandemic 2009 H1N1 influenza virus has been widely reported and was considered the main cause of death in critically ill patients with 2009 H1N1 infection. However, no animal model has been developed for ARDS caused by infection with 2009 H1N1 virus. Here, we present a mouse model of ARDS induced by 2009 H1N1 virus. Methodology Principal Findings: Mice were inoculated with A/swine/Shandong/731/2009 (SD/09), which was a 2009 H1N1 influenza variant with a G222D mutation in the hemagglutinin. Clinical symptoms were recorded every day. Lung injury was assessed by lung water content and histopathological observation. Arterial blood gas, leukocyte count in the bronchial alveolar lavage fluid and blood, virus titers, and cytokine levels in the lung were measured at various times post-inoculation. Mice infected with SD/09 virus showed typical ARDS symptoms characterized by 60 % lethality on days 8–10 postinoculation, highly edematous lungs, inflammatory cellular infiltration, alveolar and interstitial edema, lung hemorrhage, progressive and severe hypoxemia, and elevated levels of proinflammatory cytokines and chemokines. Conclusions/Significance: These results suggested that we successfully established an ARDS mouse model induced by a virulent 2009 H1N1 variant without previous adaptation, which may be of benefit for evaluating the pathogenesis or therapy of human ARDS caused by 2009 H1N1 virus

Using C. elegans to decipher the cellular and molecular mechanisms underlying neurodevelopmental disorders

Prova tipográfica (uncorrected proof)Neurodevelopmental disorders such as epilepsy, intellectual disability (ID), and autism spectrum disorders (ASDs) occur in over 2 % of the population, as the result of genetic mutations, environmental factors, or combination of both. In the last years, use of large-scale genomic techniques allowed important advances in the identification of genes/loci associated with these disorders. Nevertheless, following association of novel genes with a given disease, interpretation of findings is often difficult due to lack of information on gene function and effect of a given mutation in the corresponding protein. This brings the need to validate genetic associations from a functional perspective in model systems in a relatively fast but effective manner. In this context, the small nematode, Caenorhabditis elegans, presents a good compromise between the simplicity of cell models and the complexity of rodent nervous systems. In this article, we review the features that make C. elegans a good model for the study of neurodevelopmental diseases. We discuss its nervous system architecture and function as well as the molecular basis of behaviors that seem important in the context of different neurodevelopmental disorders. We review methodologies used to assess memory, learning, and social behavior as well as susceptibility to seizures in this organism. We will also discuss technological progresses applied in C. elegans neurobiology research, such as use of microfluidics and optogenetic tools. Finally, we will present some interesting examples of the functional analysis of genes associated with human neurodevelopmental disorders and how we can move from genes to therapies using this simple model organism.The authors would like to acknowledge Fundação para a Ciência e Tecnologia (FCT) (PTDC/SAU-GMG/112577/2009). AJR and CB are recipients of FCT fellowships: SFRH/BPD/33611/2009 and SFRH/BPD/74452/2010, respectively