Quasi-Superactivation of Classical Capacity of Zero-Capacity Quantum Channels

One of the most surprising recent results in quantum Shannon theory is the superactivation of the quantum capacity of a quantum channel. This phenomenon has its roots in the extreme violation of additivity of the channel capacity and enables to reliably transmit quantum information over zero-capacity quantum channels. In this work we demonstrate a similar effect for the classical capacity of a quantum channel which previously was thought to be impossible. We show that a nonzero classical capacity can be achieved for all zero-capacity quantum channels and it only requires the assistance of an elementary photon-atom interaction process - the stimulated emission.Comment: 52 pages, 6 figures, Journal-ref: Journal of Modern Optics, published version (minor typo fixed

Experimental linear-optical implementation of a multifunctional optimal qubit cloner

We present the first experimental implementation of a multifunctional device for the optimal cloning of one to two qubits. Previous implementations have always been designed to optimize the cloning procedure with respect to one single type of a priori information about the cloned state. In contrast, our "all-in-one" implementation is optimal for several prominent regimes such as universal cloning, phase-covariant cloning, and also the first ever realized mirror phase-covariant cloning, when the square of the expected value of Pauli's Z operator is known in advance. In all these regimes the experimental device yields clones with almost maximum achievable average fidelity (97.5% of theoretical limit). Our device has a wide range of possible applications in quantum information processing, especially in quantum communication. For instance, one can use it for incoherent and coherent attacks against a variety of cryptographic protocols, including the Bennett-Brassard 1984 protocol of quantum key distribution through the Pauli damping channels. It can be also applied as a state-dependent photon multiplier in practical quantum networks.Comment: 9 pages, 6 figures, accepted to Phys. Rev. A (Rapid Communications

Gene expression analysis indicates CB1 receptor upregulation in the hippocampus and neurotoxic effects in the frontal cortex 3 weeks after single-dose MDMA administration in Dark Agouti rats.

BACKGROUND: 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy") is a widely used recreational drug known to impair cognitive functions on the long-run. Both hippocampal and frontal cortical regions have well established roles in behavior, memory formation and other cognitive tasks and damage of these regions is associated with altered behavior and cognitive functions, impairments frequently described in heavy MDMA users. The aim of this study was to examine the hippocampus, frontal cortex and dorsal raphe of Dark Agouti rats with gene expression arrays (Illumina RatRef bead arrays) looking for possible mechanisms and new candidates contributing to the effects of a single dose of MDMA (15 mg/kg) 3 weeks earlier. RESULTS: The number of differentially expressed genes in the hippocampus, frontal cortex and the dorsal raphe were 481, 155, and 15, respectively. Gene set enrichment analysis of the microarray data revealed reduced expression of 'memory' and 'cognition', 'dendrite development' and 'regulation of synaptic plasticity' gene sets in the hippocampus, parallel to the upregulation of the CB1 cannabinoid- and Epha4, Epha5, Epha6 ephrin receptors. Downregulated gene sets in the frontal cortex were related to protein synthesis, chromatin organization, transmembrane transport processes, while 'dendrite development', 'regulation of synaptic plasticity' and 'positive regulation of synapse assembly' gene sets were upregulated. Changes in the dorsal raphe region were mild and in most cases not significant. CONCLUSION: The present data raise the possibility of new synapse formation/synaptic reorganization in the frontal cortex three weeks after a single neurotoxic dose of MDMA. In contrast, a prolonged depression of new neurite formation in the hippocampus is suggested by the data, which underlines the particular vulnerability of this brain region after the drug treatment. Finally, our results also suggest the substantial contribution of CB1 receptor and endocannabinoid mediated pathways in the hippocampal impairments. Taken together the present study provides evidence for the participation of new molecular candidates in the long-term effects of MDMA

Carboxypeptidase-M is regulated by lipids and CSFs in macrophages and dendritic cells and expressed selectively in tissue granulomas and foam cells

Granulomatous inflammations, characterized by the presence of activated macrophages (MAs) forming epithelioid cell (EPC) clusters, are usually easy to recognize. However, in ambiguous cases the use of a MA marker that expresses selectively in EPCs may be needed. Here, we report that carboxypeptidase-M (CPM), a MA-differentiation marker, is preferentially induced in EPCs of all granuloma types studied, but not in resting MAs. As CPM is not expressed constitutively in MAs, this allows utilization of CPM-immunohistochemistry in diagnostics of minute granuloma detection when dense non-granulomatous MAs are also present. Despite this rule, hardly any detectable CPM was found in advanced/active tubercle caseous disease, albeit in early tuberculosis granuloma, MAs still expressed CPM. Indeed, in vitro both the CPM-protein and -mRNA became downregulated when MAs were infected with live mycobacteria. In vitro, MA-CPM transcript is neither induced remarkably by interferon-γ, known to cause classical MA activation, nor by IL-4, an alternative MA activator. Instead, CPM is selectively expressed in lipid-laden MAs, including the foam cells of atherosclerotic plaques, xanthomatous lesions and lipid pneumonias. By using serum, rich in lipids, and low-density lipoprotein (LDL) or VLDL, CPM upregulation could be reproduced in vitro in monocyte-derived MAs both at transcriptional and protein levels, and the increase is repressed under lipid-depleted conditions. The microarray analyses support the notion that CPM induction correlates with a robust progressive increase in CPM gene expression during monocyte to MA maturation and dendritic cell (DC) differentiation mediated by granulocyte–MA-colony-stimulating factor+IL-4. M-CSF alone also induced CPM. These results collectively indicate that CPM upregulation in MAs is preferentially associated with increased lipid uptake, and exposure to CSF, features of EPCs, also. Therefore, CPM-immunohistochemistry is useful for granuloma and foam MA detections in tissue sections. Furthermore, the present data offer CPM for the first time to be a novel marker and cellular player in lipid uptake and/or metabolism of MAs by promoting foam cell formation

Stem Cell Therapy: Pieces of the Puzzle

Acute ischemic injury and chronic cardiomyopathies can cause irreversible loss of cardiac tissue leading to heart failure. Cellular therapy offers a new paradigm for treatment of heart disease. Stem cell therapies in animal models show that transplantation of various cell preparations improves ventricular function after injury. The first clinical trials in patients produced some encouraging results, despite limited evidence for the long-term survival of transplanted cells. Ongoing research at the bench and the bedside aims to compare sources of donor cells, test methods of cell delivery, improve myocardial homing, bolster cell survival, and promote cardiomyocyte differentiation. This article reviews progress toward these goals

Dynamic topology resilience for quantum networks

In quantum repeater networks, the varying stability of entangled quantum links makes dynamic topology resilience an emerging issue. Here we define an efficient topology adaption method for quantum repeater networks. The model assumes the random failures of entangled links and several parallel demands from legal users. The shortest path defines a set of entangled links for which the probability of stability is above a critical threshold. The scheme is utilized in a base-graph of the overlay quantum network to provide an efficient shortest path selection for the demands of all users of the network. We study the problem of entanglement assignment in a quantum repeater network, prove its computational complexity, and show an optimization procedure. The results are particularly convenient for future quantum networking, quantum-internet, and experimental long-distance quantum communications.</p