Secrecy extraction from no-signalling correlations

Quantum cryptography shows that one can guarantee the secrecy of correlation on the sole basis of the laws of physics, that is without limiting the computational power of the eavesdropper. The usual security proofs suppose that the authorized partners, Alice and Bob, have a perfect knowledge and control of their quantum systems and devices; for instance, they must be sure that the logical bits have been encoded in true qubits, and not in higher-dimensional systems. In this paper, we present an approach that circumvents this strong assumption. We define protocols, both for the case of bits and for generic $d$-dimensional outcomes, in which the security is guaranteed by the very structure of the Alice-Bob correlations, under the no-signalling condition. The idea is that, if the correlations cannot be produced by shared randomness, then Eve has poor knowledge of Alice's and Bob's symbols. The present study assumes, on the one hand that the eavesdropper Eve performs only individual attacks (this is a limitation to be removed in further work), on the other hand that Eve can distribute any correlation compatible with the no-signalling condition (in this sense her power is greater than what quantum physics allows). Under these assumptions, we prove that the protocols defined here allow extracting secrecy from noisy correlations, when these correlations violate a Bell-type inequality by a sufficiently large amount. The region, in which secrecy extraction is possible, extends within the region of correlations achievable by measurements on entangled quantum states.Comment: 23 pages, 4 figure

Reexamination of a multisetting Bell inequality for qudits

The class of d-setting, d-outcome Bell inequalities proposed by Ji and collaborators [Phys. Rev. A 78, 052103] are reexamined. For every positive integer d > 2, we show that the corresponding non-trivial Bell inequality for probabilities provides the maximum classical winning probability of the Clauser-Horne-Shimony-Holt-like game with d inputs and d outputs. We also demonstrate that the general classical upper bounds given by Ji et al. are underestimated, which invalidates many of the corresponding correlation inequalities presented thereof. We remedy this problem, partially, by providing the actual classical upper bound for d less than or equal to 13 (including non-prime values of d). We further determine that for prime value d in this range, most of these probability and correlation inequalities are tight, i.e., facet-inducing for the respective classical correlation polytope. Stronger lower and upper bounds on the quantum violation of these inequalities are obtained. In particular, we prove that once the probability inequalities are given, their correlation counterparts given by Ji and co-workers are no longer relevant in terms of detecting the entanglement of a quantum state.Comment: v3: Published version (minor rewordings, typos corrected, upper bounds in Table III improved/corrected); v2: 7 pages, 1 figure, 4 tables (substantially revised with new results on the tightness of the correlation inequalities included); v1: 7.5 pages, 1 figure, 4 tables (Comments are welcome

Inhibition of the Nuclear Import of Cubitus Interruptus by Roadkill in the Presence of Strong Hedgehog Signal

Hedgehog (Hh) signalling plays an important role in various developmental processes by activating the Cubitus interruptus (Ci)/Glioblastoma (Gli) family of transcription factors. In the process of proper pattern formation, Ci activity is regulated by multiple mechanisms, including processing, trafficking, and degradation. However, it remains elusive how Ci distinctly recognizes the strong and moderate Hh signals. Roadkill (Rdx) induces Ci degradation in the anterior region of the Drosophila wing disc. Here, we report that Rdx inhibited Ci activity by two different mechanisms. In the region abutting the anterior/posterior boundary, which receives strong Hh signal, Rdx inhibited the nuclear import of Ci by releasing importin α3 from Ci. In this region, Rdx negatively regulated the expression of transcription factor Knot/Collier. In farther anterior regions receiving moderate levels of Hh signal, Rdx induced Ci degradation, as reported previously. Thus, two different mechanisms by which Rdx negatively regulates Ci may play an important role in the fine-tuning of Hh responses

R497K polymorphism in epidermal growth factor receptor gene is associated with the risk of acute coronary syndrome

<p>Abstract</p> <p>Background</p> <p>Previous studies suggested that genetic polymorphisms in the epidermal growth factor receptor (EGFR) gene had been implicated in the susceptibility to some tumors and inflammatory diseases. EGFR has been recently implicated in vascular pathophysiological processes associated with excessive remodeling and atherosclerosis. Acute coronary syndrome (ACS) is a clinical manifestation of preceding atherosclerosis. Our purpose was to investigate the association of the EGFR polymorphism with the risk of ACS. In this context, we analyzed the HER-1 R497K and EGFR intron 1 (CA)_nrepeat polymorphisms in 191 patients with ACS and 210 age- and sex-matched controls in a Chinese population, using a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) strategy and direct sequencing.</p> <p>Results</p> <p>There were significant differences in the genotype and allele distribution of R497K polymorphism of the EGFR gene between cases and controls. The <it>Lys </it>allele had a significantly increased risk of ACS compared with the <it>Arg </it>allele (adjusted OR = 1.49, 95% CI: 1.12–1.98, adjusted <it>P </it>= 0.006). However, no significant relationship between the number of (CA)_nrepeats of EGFR intron 1 (both alleles < 20 or any allele ≥ 20) and the risk of ACS was observed (adjusted OR = 0.97, 95% CI: 0.58–1.64, adjusted <it>P </it>= 0.911). Considering these two polymorphisms together, there was no statistically significant difference between the two groups.</p> <p>Conclusion</p> <p>R497K polymorphism of the EGFR gene is significantly associated with the risk of ACS. Our data suggests that R497K polymorphism may be used as a genetic susceptibility marker of the ACS.</p

Suppressor of fused opposes hedgehog signal transduction by impeding nuclear accumulation of the activator form of Cubitus interruptus.

Hedgehog controls the expression of key developmental genes through the conversion of the transcription factor Cubitus interruptus (Ci) into either an activator (Ci[act]) or a repressor (Ci[rep]) form. Proteolytic cleavage of full-length Ci is important for the generation of Ci[rep], but little is known about how Ci[act] arises in response to Hh. Here we examine Hh signal transduction components for their role in the conversion of full-length Ci into either Ci[act] or Ci[rep]. We report that Cos2, PKA and Fused are necessary for the generation of Ci[rep], whereas the inhibition of either Cos2 or PKA activity is a prerequisite for Ci[act] formation. Fused (Fu) kinase stimulates a constitutively active form of Ci in a Hh-dependent manner, suggesting that Fu enhances the activity rather than the formation of Ci[act]. Su(fu) reduces the nuclear accumulation of the constitutively active form of Ci, arguing that Su(fu) can function subsequent to Ci[act] formation. We propose that Hh induces target gene expression by a two-step mechanism in which Ci[act] is first formed and then accumulates in the nucleus via Fu-induced neutralization of Su(fu) activity

An absolute requirement for Cubitus interruptus in Hedgehog signaling.

Hedgehog (Hh) proteins play diverse organizing roles in animal development by regulating gene expression in responding cells. Several components of the Hh signal transduction pathway have been identified, yet their precise role in mediating the various outputs of the pathway is still poorly understood. The Gli homolog Cubitus interruptus (Ci) is involved in controlling the transcription of Drosophila Hh target genes and thus represents the most downstream component known in this pathway. We address the question of whether the Hh pathway is distally branched or, in other words, whether the regulation of Ci activity is the sole output of Hh signaling. Putative Ci-independent branches of Hh signaling are explored by analyzing the behavior of cells that lack Ci but have undergone maximal activation of the Hh transduction pathway due to the removal of Patched (Ptc). The analysis of target gene expression and morphogenetic read-outs of Hh in embryonic, larval and adult stages indicates that Ci is absolutely required for all examined aspects of Hh outputs. We interpret this as evidence against the existence of Ci-independent branches in the Hh signal transduction pathway and propose that most cases of apparent Ci/Gli-independent Hh output can be attributed to the derepression of target gene expression in the absence of Ci/Gli repressor function

Hedgehog controls limb development by regulating the activities of distinct transcriptional activator and repressor forms of Cubitus interruptus.

Hedgehog (Hh) proteins play diverse organizing roles in development by regulating gene expression in responding cells. The Gli homolog Cubitus interruptus (Ci) is involved in controlling the transcription of Hh target genes. A repressor form of Ci arises in the absence of Hh signaling by proteolytic cleavage of intact Ci. We show that this cleavage is essential for limb patterning and is regulated by Hh in vivo. We provide evidence for the existence of a distinct activator form of Ci, which does not arise by mere prevention of Ci proteolysis, but rather depends on a separate regulatory step subject to Hh control. These different activities of Ci regulate overlapping but distinct subsets of Hh target genes. Thus, limb development is organized by the integration of different transcriptional outputs of Hh signaling