Controlled Quantum Secret Sharing

We present a new protocol in which a secret multiqubit quantum state $\ket{\Psi}$ is shared by $n$ players and $m$ controllers, where $\ket{\Psi}$ is the encoding state of a quantum secret sharing scheme. The players may be considered as field agents responsible for carrying out a task, using the secret information encrypted in $\ket{\Psi}$, while the controllers are superiors who decide if and when the task should be carried out and who to do it. Our protocol only requires ancillary Bell states and Bell-basis measurements.Comment: 6 pages, 0 figure, RevTeX4; published version with minor change

How to share a quantum secret

We investigate the concept of quantum secret sharing. In a ((k,n)) threshold scheme, a secret quantum state is divided into n shares such that any k of those shares can be used to reconstruct the secret, but any set of k-1 or fewer shares contains absolutely no information about the secret. We show that the only constraint on the existence of threshold schemes comes from the quantum "no-cloning theorem", which requires that n < 2k, and, in all such cases, we give an efficient construction of a ((k,n)) threshold scheme. We also explore similarities and differences between quantum secret sharing schemes and quantum error-correcting codes. One remarkable difference is that, while most existing quantum codes encode pure states as pure states, quantum secret sharing schemes must use mixed states in some cases. For example, if k <= n < 2k-1 then any ((k,n)) threshold scheme must distribute information that is globally in a mixed state.Comment: 5 pages, REVTeX, submitted to PR

Some Directions beyond Traditional Quantum Secret Sharing

We investigate two directions beyond the traditional quantum secret sharing (QSS). First, a restriction on QSS that comes from the no-cloning theorem is that any pair of authorized sets in an access structure should overlap. From the viewpoint of application, this places an unnatural constraint on secret sharing. We present a generalization, called assisted QSS (AQSS), where access structures without pairwise overlap of authorized sets is permissible, provided some shares are withheld by the share dealer. We show that no more than $\lambda-1$ withheld shares are required, where $\lambda$ is the minimum number of {\em partially linked classes} among the authorized sets for the QSS. Our result means that such applications of QSS need not be thwarted by the no-cloning theorem. Secondly, we point out a way of combining the features of QSS and quantum key distribution (QKD) for applications where a classical information is shared by quantum means. We observe that in such case, it is often possible to reduce the security proof of QSS to that of QKD.Comment: To appear in Physica Scripta, 7 pages, 1 figure, subsumes arXiv:quant-ph/040720

Discovery of Stable and Selective Antibody Mimetics from Combinatorial Libraries of Polyvalent, Loop-Functionalized Peptoid Nanosheets.

The ability of antibodies to bind a wide variety of analytes with high specificity and high affinity makes them ideal candidates for therapeutic and diagnostic applications. However, the poor stability and high production cost of antibodies have prompted exploration of a variety of synthetic materials capable of specific molecular recognition. Unfortunately, it remains a fundamental challenge to create a chemically diverse population of protein-like, folded synthetic nanostructures with defined molecular conformations in water. Here we report the synthesis and screening of combinatorial libraries of sequence-defined peptoid polymers engineered to fold into ordered, supramolecular nanosheets displaying a high spatial density of diverse, conformationally constrained peptoid loops on their surface. These polyvalent, loop-functionalized nanosheets were screened using a homogeneous Förster resonance energy transfer (FRET) assay for binding to a variety of protein targets. Peptoid sequences were identified that bound to the heptameric protein, anthrax protective antigen, with high avidity and selectivity. These nanosheets were shown to be resistant to proteolytic degradation, and the binding was shown to be dependent on the loop display density. This work demonstrates that key aspects of antibody structure and function-the creation of multivalent, combinatorial chemical diversity within a well-defined folded structure-can be realized with completely synthetic materials. This approach enables the rapid discovery of biomimetic affinity reagents that combine the durability of synthetic materials with the specificity of biomolecular materials

A recessive homozygous p.Asp92Gly SDHD mutation causes prenatal cardiomyopathy and a severe mitochondrial complex II deficiency

Succinate dehydrogenase (SDH) is a crucial metabolic enzyme complex that is involved in ATP production, playing roles in both the tricarboxylic cycle and the mitochondrial respiratory chain (complex II). Isolated complex II deficiency is one of the rarest oxidative phosphorylation disorders with mutations described in three structural subunits and one of the assembly factors; just one case is attributed to recessively inherited SDHD mutations. We report the pathological, biochemical, histochemical and molecular genetic investigations of a male neonate who had left ventricular hypertrophy detected on antenatal scan and died on day one of life. Subsequent postmortem examination confirmed hypertrophic cardiomyopathy with left ventricular non-compaction. Biochemical analysis of his skeletal muscle biopsy revealed evidence of a severe isolated complex II deficiency and candidate gene sequencing revealed a novel homozygous c.275A>G, p.(Asp92Gly) SDHD mutation which was shown to be recessively inherited through segregation studies. The affected amino acid has been reported as a Dutch founder mutation p.(Asp92Tyr) in families with hereditary head and neck paraganglioma. By introducing both mutations into Saccharomyces cerevisiae, we were able to confirm that the p.(Asp92Gly) mutation causes a more severe oxidative growth phenotype than the p.(Asp92Tyr) mutant, and provides functional evidence to support the pathogenicity of the patient’s SDHD mutation. This is only the second case of mitochondrial complex II deficiency due to inherited SDHD mutations and highlights the importance of sequencing all SDH genes in patients with biochemical and histochemical evidence of isolated mitochondrial complex II deficiency

Mathematical Constraint on Functions with Continuous Second Partial Derivatives

A new integral identity for functions with continuous second partial derivatives is derived. It is shown that the value of any function f(r,t) at position r and time t is completely determined by its previous values at all other locations r' and retarded times t'<t, provided that the function vanishes at infinity and has continuous second partial derivatives. Functions of this kind occur in many areas of physics and it seems somewhat surprising that they are constrained in this way.Comment: 10 pages, 6 figure

The local economic development processes in low-income countries: the case of the metropolis of Chegutu in Zimbabwe

Local authorities are widely regarded as catalysts accelerating localised processes of economic development in industrialised countries but in low-income countries they are perceived as dysfunctional, inefficient and ineffective in meeting and addressing societal demands. This abstract view is however, not grounded in empirical research. As such, utilising the case of the metropolis of Chegutu a survey was designed to empirically explicate the economic processes militating its economic development. The findings are useful to policy-makers, local government authorities and management scholars. The study's unique contribution lies in its examination of the processes of local economic development in a low-income country

Aurora kinase A drives the evolution of resistance to third-generation EGFR inhibitors in lung cancer.

Although targeted therapies often elicit profound initial patient responses, these effects are transient due to residual disease leading to acquired resistance. How tumors transition between drug responsiveness, tolerance and resistance, especially in the absence of preexisting subclones, remains unclear. In epidermal growth factor receptor (EGFR)-mutant lung adenocarcinoma cells, we demonstrate that residual disease and acquired resistance in response to EGFR inhibitors requires Aurora kinase A (AURKA) activity. Nongenetic resistance through the activation of AURKA by its coactivator TPX2 emerges in response to chronic EGFR inhibition where it mitigates drug-induced apoptosis. Aurora kinase inhibitors suppress this adaptive survival program, increasing the magnitude and duration of EGFR inhibitor response in preclinical models. Treatment-induced activation of AURKA is associated with resistance to EGFR inhibitors in vitro, in vivo and in most individuals with EGFR-mutant lung adenocarcinoma. These findings delineate a molecular path whereby drug resistance emerges from drug-tolerant cells and unveils a synthetic lethal strategy for enhancing responses to EGFR inhibitors by suppressing AURKA-driven residual disease and acquired resistance