Rate-Adaptive LDPC-based key reconciliation for high performance quantum key distribution

The postprocessing or secret-key distillation process in quantum key distribution (QKD) mainly involves two well-known procedures: information reconciliation and privacy amplification. Information or key reconciliation has been customarily studied in terms of efficiency. During this, some information needs to be disclosed for reconciling discrepancies in the exchanged keys. The leakage of information is lower bounded by a theoretical limit, and is usually parameterized by the reconciliation efficiency (or inefficiency), i.e. the ratio of additional information disclosed over the Shannon limit. Most techniques for reconciling errors in QKD try to optimize this parameter. For instance, the well-known Cascade (probably the most widely used procedure for reconciling errors in QKD) was recently shown to have an average efficiency of 1.05 at the cost of a high interactivity (number of exchanged messages). Modern coding techniques, such as rate-adaptive low-density parity-check (LDPC) codes were also shown to achieve similar efficiency values exchanging only one message, or even better values with few interactivity and shorter block-length codes.

Comparing the Luttinger–Kohn–Pikus–Bir and the Empiric K·P Hamiltonians in quantum dot intermediate band solar cells manufactured in zincblende semiconductors

The calculation of the energy spectrum and absorption coefficients of quantum dot nanostructured intermediate band solar cells using the Empiric K·P Hamiltonian method and its agreement with experimental data are summarized. The well established Luttinger Kohn Hamiltonian modified by Pikus and Bir for strained material, such as quantum dot arrays, is presented using a simplified strain field that allows for square band offsets. The energy spectrum and absorption coefficients are calculated with this new Hamiltonian. With the approximations made the energy spectrum results to be exactly the same but the absorption coefficient fits experiments less accurately. The computer time using the latter Hamiltonian is much longer than the former one.

Quantum dot parameters determination from quantum-efficiency measurements

The energy spectrum of the confined states of a quantum dot intermediate band (IB) solar cell is calculated with a simplified model. Two peaks are usually visible at the lowest energy side of the subbandgap quantum-efficiency spectrum in these solar cells. They can be attributed to photon absorption between well-defined states. As a consequence, the horizontal size of the quantum dots can be determined, and the conduction (valence) band offset is also determined if the valence (conduction) offset is known.

DNA double-strand break repair proteins are required to cap the ends of mammalian chromosomes

Recent findings intriguingly place DNA double-strand break repair proteins at chromosome ends in yeast, where they help maintain normal telomere length and structure. In the present study, an essential telomere function, the ability to cap and thereby protect chromosomes from end-to-end fusions, was assessed in repair-deficient mouse cell lines. By using fluorescence in situ hybridization with a probe to telomeric DNA, spontaneously occurring chromosome aberrations were examined for telomere signal at the points of fusion, a clear indication of impaired end-capping. Telomeric fusions were not observed in any of the repair-proficient controls and occurred only rarely in a p53 null mutant. In striking contrast, chromosomal end fusions that retained telomeric sequence were observed in nontransformed DNA-PKcs-deficient cells, where they were a major source of chromosomal instability. Metacentric chromosomes created by telomeric fusion became even more abundant in these cells after spontaneous immortalization. Restoration of repair proficiency through transfection with a functional cDNA copy of the human DNA-PKcs gene reduced the number of fusions compared with a negative transfection control. Virally transformed cells derived from Ku70 and Ku80 knockout mice also displayed end-to-end fusions. These studies demonstrate that DNA double-strand break repair genes play a dual role in maintaining chromosomal stability in mammalian cells, the known role in repairing incidental DNA damage, as well as a new protective role in telomeric end-capping.

Multiple quantum solid-state NMR indicates a parallel, not antiparallel, organization of β-sheets in Alzheimer's β-amyloid fibrils

Senile plaques associated with Alzheimer's disease contain deposits of fibrils formed by 39- to 43-residue β-amyloid peptides with possible neurotoxic effects. X-ray diffraction measurements on oriented fibril bundles have indicated an extended β-sheet structure for Alzheimer's β-amyloid fibrils and other amyloid fibrils, but the supramolecular organization of the β-sheets and other structural details are not well established because of the intrinsically noncrystalline, insoluble nature of amyloid fibrils. Here we report solid-state NMR measurements, using a multiple quantum (MQ) 13C NMR technique, that probe the β-sheet organization in fibrils formed by the full-length, 40-residue β-amyloid peptide (Aβ1–40). Although an antiparallel β-sheet organization often is assumed and is invoked in recent structural models for full-length β-amyloid fibrils, the MQNMR data indicate an in-register, parallel organization. This work provides site-specific, atomic-level structural constraints on full-length β-amyloid fibrils and applies MQNMR to a significant problem in structural biology.

Toward a quantum-mechanical description of metal-assisted phosphoryl transfer in pyrophosphatase

The wealth of kinetic and structural information makes inorganic pyrophosphatases (PPases) a good model system to study the details of enzymatic phosphoryl transfer. The enzyme accelerates metal-complexed phosphoryl transfer 1010-fold: but how? Our structures of the yeast PPase product complex at 1.15 Å and fluoride-inhibited complex at 1.9 Å visualize the active site in three different states: substrate-bound, immediate product bound, and relaxed product bound. These span the steps around chemical catalysis and provide strong evidence that a water molecule (Onu) directly attacks PPi with a pKa vastly lowered by coordination to two metal ions and D117. They also suggest that a low-barrier hydrogen bond (LBHB) forms between D117 and Onu, in part because of steric crowding by W100 and N116. Direct visualization of the double bonds on the phosphates appears possible. The flexible side chains at the top of the active site absorb the motion involved in the reaction, which may help accelerate catalysis. Relaxation of the product allows a new nucleophile to be generated and creates symmetry in the elementary catalytic steps on the enzyme. We are thus moving closer to understanding phosphoryl transfer in PPases at the quantum mechanical level. Ultra-high resolution structures can thus tease out overlapping complexes and so are as relevant to discussion of enzyme mechanism as structures produced by time-resolved crystallography.

Increase in the Quantum Yield of Photoinhibition Contributes to Copper Toxicity in Vivo1

The effect of copper on photoinhibition of photosystem II in vivo was studied in bean (Phaseolus vulgaris L. cv Dufrix). The plants were grown hydroponically in the presence of various concentrations of Cu2+ ranging from the optimum 0.3 μm (control) to 15 μm. The copper concentration of leaves varied according to the nutrient medium from a control value of 13 mg kg−1 dry weight to 76 mg kg−1 dry weight. Leaf samples were illuminated in the presence and absence of lincomycin at different light intensities (500–1500 μmol photons m−2 s−1). Lincomycin prevents the concurrent repair of photoinhibitory damage by blocking chloroplast protein synthesis. The photoinhibitory decrease in the light-saturated rate of O2 evolution measured from thylakoids isolated from treated leaves correlated well with the decrease in the ratio of variable to maximum fluorescence measured from the leaf discs; therefore, the fluorescence ratio was used as a routine measurement of photoinhibition in vivo. Excess copper was found to affect the equilibrium between photoinhibition and repair, resulting in a decrease in the steady-state concentration of active photosystem II centers of illuminated leaves. This shift in equilibrium apparently resulted from an increase in the quantum yield of photoinhibition (ΦPI) induced by excess copper. The kinetic pattern of photoinhibition and the independence of ΦPI on photon flux density were not affected by excess copper. An increase in ΦPI may contribute substantially to Cu2+ toxicity in certain plant species.

An essential role for the interferon-inducible, double-stranded RNA-activated protein kinase PKR in the tumor necrosis factor-induced apoptosis in U937 cells.

Tumor necrosis factor alpha (TNF-alpha) is well-characterized for its necrotic action against tumor cells; however, it has been increasingly associated with an apoptosis-inducing potential on target cells. While the signaling events and the actual cytolytic mechanism(s) for both TNF-alpha-induced necrosis and apoptosis remain to be fully elucidated, we report here on (i) the ability of TNF-alpha to induce apoptosis in the promonocytic U937 cells, (ii) the discovery of a cross-talk between the TNF-alpha and the interferon signaling pathways, and (iii) the pivotal role of interferon-inducible, double-stranded RNA-activated protein kinase (PKR) in the induction of apoptosis by TNF-alpha. Our data from microscopy studies, trypan blue exclusion staining, and apoptotic DNA ladder electrophoresis revealed that a subclone derived from U937 and carrying a PKR antisense expression vector was resistant to TNF-alpha-induced apoptosis. Further, TNF-alpha initiated a generalized RNA degradation process in which the participation of PKR was required. Finally, the PKR gene is a candidate "death gene" since overexpression of this gene could bring about apoptosis in U937 cells.

Involvement of the double-stranded-RNA-dependent kinase PKR in interferon expression and interferon-mediated antiviral activity.

The signaling mechanisms responsible for the induced expression of interferon (IFN) genes by viral infection or double-stranded RNA (dsRNA) are not well understood. Here we investigate the role of the interferon-induced dsRNA-dependent protein kinase PKR in the regulation of IFN induction. Biological activities attributed to PKR include regulating protein synthesis, mediating IFN actions, and functioning as a possible tumor suppressor. Since binding of dsRNA is required for its activation, PKR has been considered as a candidate signal transducer for regulating IFN expression. To examine this role of PKR, loss-of-function phenotypes in stable transformants of promonocytic U-937 cells were achieved by two different strategies, overexpression of an antisense PKR transcript or a dominant negative PKR mutant gene. Both types of PKR-deficient cells were more permissive for viral replication than the control U-937 cells. As the result of PKR loss, they also showed impaired induction of IFN-alpha and IFN-beta genes in response to several inducers--specifically, encephalomyocarditis virus, lipopolysaccharide, and phorbol 12-myristate 13-acetate. Interestingly, while IFN-alpha induction by dsRNA was impaired in PKR-deficient cells, IFN-beta induction remained intact. Loss of PKR function also resulted in decreased antiviral activity as elicited by IFN-alpha and, to a greater extent, by IFN-gamma. These results implicate PKR in the regulation of several antiviral activities.

Complex formation in yeast double-strand break repair: participation of Rad51, Rad52, Rad55, and Rad57 proteins.

The repair of DNA double-strand breaks in Saccharomyces cerevisiae requires genes of the RAD52 epistasis group, of which RAD55 and RAD57 are members. Here, we show that the x-ray sensitivity of rad55 and rad57 mutant strains is suppressible by overexpression of RAD51 or RAD52. Virtually complete suppression is provided by the simultaneous overexpression of RAD51 and RAD52. This suppression occurs at 23 degrees C, where these mutants are more sensitive to x-rays, as well as at 30 degrees C and 36 degrees C. In addition, a recombination defect of rad55 and rad57 mutants is similarly suppressed. Direct in vivo interactions between the Rad51 and Rad55 proteins, and between Rad55 and Rad57, have also been identified by using the two-hybrid system. These results indicate that these four proteins constitute part of a complex, a "recombinosome," to effect the recombinational repair of double-strand breaks.

Mutational analysis of the conserved region 2 site of adenovirus E1A and its effect on binding to the retinoblastoma gene product: use of the "double-tagging" assay.

We have explored the feasibility of using a "double-tagging" assay for assessing which amino acids of a protein are responsible for its binding to another protein. We have chosen the adenovirus E1A-retinoblastoma gene product (pRB) proteins for a model system, and we focused on the high-affinity conserved region 2 of adenovirus E1A (CR2). We used site-specific mutagenesis to generate a mutant E1A gene with a lysine instead of an aspartic acid at position 121 within the CR2 site. We demonstrated that this mutant exhibited little binding to pRB by the double-tagging assay. We also have shown that this lack of binding is not due to any significant decrease in the level of expression of the beta-galactosidase-E1A fusion protein. We then created a "library" of phage expressing beta-galactosidase-E1A fusion proteins with a variety of different mutations within CR2. This library of E1A mutations was used in a double-tagging screening to identify mutant clones that bound to pRB. Three classes of phage were identified: the vast majority of clones were negative and exhibited no binding to pRB. Approximately 1 in 10,000 bound to pRB but not to E1A ("true positives"). A variable number of clones appeared to bind equally well to both pRB and E1A ("false positives"). The DNA sequence of 10 true positive clones yielded the following consensus sequence: DLTCXEX, where X = any amino acid. The recovery of positive clones with only one of several allowed amino acids at each position suggests that most, if not all, of the conserved residues play an important role in binding to pRB. On the other hand, the DNA sequence of the negative clones appeared random. These results are consistent with those obtained from other sources. These data suggest that a double-tagging assay can be employed for determining which amino acids of a protein are important for specifying its interaction with another protein if the complex forms within bacteria. This assay is rapid and up to 1 x 10(6) mutations can be screened at one time.

Sampling Quantum Nonlocal Correlations with High Probability

It is well known that quantum correlations for bipartite dichotomic measurements are those of the form (Formula presented.), where the vectors ui and vj are in the unit ball of a real Hilbert space. In this work we study the probability of the nonlocal nature of these correlations as a function of (Formula presented.), where the previous vectors are sampled according to the Haar measure in the unit sphere of (Formula presented.). In particular, we prove the existence of an (Formula presented.) such that if (Formula presented.), (Formula presented.) is nonlocal with probability tending to 1 as (Formula presented.), while for (Formula presented.), (Formula presented.) is local with probability tending to 1 as (Formula presented.).

Single-exciton spectroscopy of semimagnetic quantum dots

A photoexcited II-VI semiconductor quantum dots doped with a few Mn spins is considered. The effects of spin-exciton interactions and the resulting multispin correlations on the photoluminescence are calculated by numerical diagonalization of the Hamiltonian, including exchange interaction between electrons, holes, and Mn spins, as well as spin-orbit interaction. The results provide a unified description of recent experiments on the photoluminesnce of dots with one and many Mn atoms as well as optically induced ferromagnetism in semimagnetic quantum dots.

Impurity states in the quantum spin Hall phase in graphene

Two-dimensional insulators with time-reversal symmetry can have two topologically different phases, the quantum spin Hall and the normal phase. The former is revealed by the existence of conducting edge states that are topologically protected. Here we show that the reaction to impurity, in bulk, is radically different in the two phases and can be used as a marker for the topological phase. Within the context of the Kane-Mele model for graphene, we find that strictly normalizable in-gap impurity states only occur in the quantum spin Hall phase and carry a dissipationless current whose chirality is determined by the spin and pseudospin of the residing electron.

Quantum Hall effect in gapped graphene heterojunctions

We model the quantum Hall effect in heterostructures made of two gapped graphene stripes with different gaps, Δ1 and Δ2. We consider two main situations, Δ1=0,Δ2≠0, and Δ1=−Δ2. They are different in a fundamental aspect: only the latter features kink states that, when intervalley coupling is absent, are protected against backscattering. We compute the two-terminal conductance of heterostructures with channel length up to 430 nm, in two transport configurations, parallel and perpendicular to the interface. By studying the effect of disorder on the transport along the boundary, we quantify the robustness of kink states with respect to backscattering. Transport perpendicular to the boundary shows how interface states open a backscattering channel for the conducting edge states, spoiling the perfect conductance quantization featured by the homogeneously gapped graphene Hall bars. Our results can be relevant for the study of graphene deposited on hexagonal boron-nitride, as well as to model graphene with an interaction-driven gapped phase with two equivalent phases separated by a domain wall.