Feasibility of free space quantum key distribution with coherent polarization states

We demonstrate for the first time the feasibility of free space quantum key distribution with continuous variables under real atmospheric conditions. More specifically, we transmit coherent polarization states over a 100m free space channel on the roof of our institute's building. In our scheme, signal and local oscillator are combined in a single spatial mode which auto-compensates atmospheric fluctuations and results in an excellent interference. Furthermore, the local oscillator acts as spatial and spectral filter thus allowing unrestrained daylight operation.Comment: 12 pages, 8 figures, extensions in sections 2, 3.1, 3.2 and 4. This is an author-created, un-copyedited version of an article accepted for publication in New Journal of Physics (Special Issue on Quantum Cryptography: Theory and Practice). IOP Publishing Ltd is not responsible for any errors or omissions in this version of the manuscript or any version derived from i

Quantum optical coherence can survive photon losses: a continuous-variable quantum erasure correcting code

A fundamental requirement for enabling fault-tolerant quantum information processing is an efficient quantum error-correcting code (QECC) that robustly protects the involved fragile quantum states from their environment. Just as classical error-correcting codes are indispensible in today's information technologies, it is believed that QECC will play a similarly crucial role in tomorrow's quantum information systems. Here, we report on the first experimental demonstration of a quantum erasure-correcting code that overcomes the devastating effect of photon losses. Whereas {\it errors} translate, in an information theoretic language, the noise affecting a transmission line, {\it erasures} correspond to the in-line probabilistic loss of photons. Our quantum code protects a four-mode entangled mesoscopic state of light against erasures, and its associated encoding and decoding operations only require linear optics and Gaussian resources. Since in-line attenuation is generally the strongest limitation to quantum communication, much more than noise, such an erasure-correcting code provides a new tool for establishing quantum optical coherence over longer distances. We investigate two approaches for circumventing in-line losses using this code, and demonstrate that both approaches exhibit transmission fidelities beyond what is possible by classical means.Comment: 5 pages, 4 figure

Genetic Determinants of Time Perception Mediated by the Serotonergic System

Background: The present study investigates neurobiological underpinnings of individual differences in time perception. Methodology: Forty-four right-handed Russian Caucasian males (18–35 years old) participated in the experiment. The polymorphism of the genes related to the activity of serotonin (5-HT) and dopamine (DA)-systems (such as 5-HTT, 5HT2a, MAOA, DAT, DRD2, COMT) was determined upon the basis of DNA analysis according to a standard procedure. Time perception in the supra-second range (mean duration 4.8 s) was studied, using the duration discrimination task and parametric fitting of psychometric functions, resulting in individual determination of the point of subjective equality (PSE). Assuming the ‘dual klepsydra model ’ of internal duration representation, the PSE values were transformed into equivalent values of the parameter k (kappa), which is a measure of the ‘loss rate ’ of the duration representation. An association between time representation parameters (PSE and k, respectively) and 5-HT-related genes was found, but not with DArelated genes. Higher ‘loss rate ’ (k) of the cumulative duration representation were found for the carriers of genotypes characterized by higher 5-HT transmission, i.e., 1) lower 5-HT reuptake, known for the 5-HTTLPR SS polymorphism compared with LL, 2) lower 5-HT degradation, described for the ‘low expression ’ variant of MAOA VNTR gene compared with ‘high expression ’ variant, and 3) higher 5-HT2a receptor density, proposed for the TT polymorphism of 5-HT2a T102C gene compared with CC

13C-assisted metabolic flux analysis to investigate heterotrophic and mixotrophic metabolism in Cupriavidus necator H16

Introduction. Cupriavidus necator H16 is a gram-negative bacterium, capable of lithoautotrophic growth by utilizing hydrogen as an energy source and fixing carbon dioxide (CO2) through Calvin-Benson-Bassham (CBB) cycle. The potential to utilize synthesis gas (Syngas) and the prospects of rerouting carbon from polyhydroxybutyrate synthesis to value-added compounds makes C. necator an excellent chassis for industrial application. Objectives. In the context of lack of sufficient quantitative information of the metabolic pathways and to advance in rational metabolic engineering for optimized product synthesis in C. necator H16, we carried out a metabolic flux analysis based on steady-state 13C-labelling. Methods. In this study, steady-state carbon labelling experiments, using either D-[1-13C]fructose or [1,2-13C]glycerol, were undertaken to investigate the carbon flux through the central carbon metabolism in C. necator H16 under heterotrophic and mixotrophic growth conditions, respectively. Results. We found that the CBB cycle is active even under heterotrophic condition, and growth is indeed mixotrophic. While Entner-Doudoroff (ED) pathway is shown to be the major route for sugar degradation, tricarboxylic acid (TCA) cycle is highly active in mixotrophic condition. Enhanced flux is observed in reductive pentose phosphate pathway (redPPP) under the mixotrophic condition to supplement the precursor requirement for CBB cycle. The flux distribution was compared to the mRNA abundance of genes encoding enzymes involved in key enzymatic reactions of the central carbon metabolism. Conclusion. This study leads the way to establishing 13C-based quantitative fluxomics for rational pathway engineering in C. necator H16

Hadron Production in Diffractive Deep-Inelastic Scattering

Characteristics of hadron production in diffractive deep-inelastic positron-proton scattering are studied using data collected in 1994 by the H1 experiment at HERA. The following distributions are measured in the centre-of-mass frame of the photon dissociation system: the hadronic energy flow, the Feynman-x (x_F) variable for charged particles, the squared transverse momentum of charged particles (p_T^{*2}), and the mean p_T^{*2} as a function of x_F. These distributions are compared with results in the gamma^* p centre-of-mass frame from inclusive deep-inelastic scattering in the fixed-target experiment EMC, and also with the predictions of several Monte Carlo calculations. The data are consistent with a picture in which the partonic structure of the diffractive exchange is dominated at low Q^2 by hard gluons.Comment: 16 pages, 6 figures, submitted to Phys. Lett.

Measurement of D* Meson Cross Sections at HERA and Determination of the Gluon Density in the Proton using NLO QCD

With the H1 detector at the ep collider HERA, D* meson production cross sections have been measured in deep inelastic scattering with four-momentum transfers Q^2>2 GeV2 and in photoproduction at energies around W(gamma p)~ 88 GeV and 194 GeV. Next-to-Leading Order QCD calculations are found to describe the differential cross sections within theoretical and experimental uncertainties. Using these calculations, the NLO gluon momentum distribution in the proton, x_g g(x_g), has been extracted in the momentum fraction range 7.5x10^{-4}< x_g <4x10^{-2} at average scales mu^2 =25 to 50 GeV2. The gluon momentum fraction x_g has been obtained from the measured kinematics of the scattered electron and the D* meson in the final state. The results compare well with the gluon distribution obtained from the analysis of scaling violations of the proton structure function F_2.Comment: 27 pages, 9 figures, 2 tables, submitted to Nucl. Phys.

Role of miR-10b in breast cancer metastasis

Ninety percent of cancer-related mortality is caused by metastasis. Current cancer treatments can control many primary tumors but rarely stop the metastatic spread. Accumulating evidence demonstrates that miRNAs are involved in cancer initiation and progression. Furthermore, several miRNAs have been found to regulate metastasis. In particular, recent studies provide the first functional evidence that overexpression of a specific miRNA, miR-10b, can contribute to the development of metastasis, which can be exploited therapeutically in treating breast cancer metastasis in mice. Further in-depth analysis should provide more precise evaluation of the roles, mechanisms, and therapeutic utility of this miRNA in breast cancer

Homo-PROTACs:bivalent small-molecule dimerizers of the VHL E3 ubiquitin ligase to induce self-degradation

E3 ubiquitin ligases are key enzymes within the ubiquitin proteasome system which catalyze the ubiquitination of proteins, targeting them for proteasomal degradation. E3 ligases are gaining importance as targets to small molecules, both for direct inhibition and to be hijacked to induce the degradation of non-native neo-substrates using bivalent compounds known as PROTACs (for 'proteolysis-targeting chimeras'). We describe Homo-PROTACs as an approach to dimerize an E3 ligase to trigger its suicide-type chemical knockdown inside cells. We provide proof-of-concept of Homo-PROTACs using diverse molecules composed of two instances of a ligand for the von Hippel-Lindau (VHL) E3 ligase. The most active compound, CM11, dimerizes VHL with high avidity in vitro and induces potent, rapid and proteasome-dependent self-degradation of VHL in different cell lines, in a highly isoform-selective fashion and without triggering a hypoxic response. This approach offers a novel chemical probe for selective VHL knockdown, and demonstrates the potential for a new modality of chemical intervention on E3 ligases.Targeting the ubiquitin proteasome system to modulate protein homeostasis using small molecules has promising therapeutic potential. Here the authors describe Homo-PROTACS: small molecules that can induce the homo-dimerization of E3 ubiquitin ligases and cause their proteasome-dependent degradation