Fermi Velocity Spectrum and Incipient Magnetism in TiBe2

We address the origin of the incipient magnetism in TiBe$_2$ through precise first principles calculations, which overestimate the ferromagnetic tendency and therefore require correction to account for spin fluctuations. TiBe$_2$ has sharp fine structure in its electronic density of states, with a van Hove singularity only 3 meV above the Fermi level. Similarly to the isovalent weak ferromagnet ZrZn$_2$, it is flat bands along the K-W-U lines of hexagonal face of the fcc Brillouin zone make the system prone to magnetism, and more so if electrons are added. We find that the Moriya $B$ coefficient (multiplying $\frac{\omega}{q}$ in the fluctuation susceptibility $\Delta \chi(q,\omega)$) is divergent when the velocity vanishes at a point on the Fermi surface, which is very close (3 meV) to occurring in TiBe$_2$. In exploring how the FM instability (the $q$=0 Stoner enhancement is $S\approx 60$) might be suppressed by fluctuations in TiBe$_2$, we calculate that the Moriya A coefficient (of $q^2$) is negative, so $q$=0 is not the primary instability. Explicit calculation of $\chi_o(q)$ shows that its maximum occurs at the X point $(1,0,0)\frac{2\pi}{a}$; TiBe$_2$ is thus an incipient {\it anti}ferromagnet rather than ferromagnet as has been supposed. We further show that simple temperature smearing of the peak accounts for most of the temperature dependence of the susceptibility, which previously had been attributed to local moments (via a Curie-Weiss fit), and that energy dependence of the density of states also strongly affects the magnetic field variation of $\chi$

Security of practical private randomness generation

Measurements on entangled quantum systems necessarily yield outcomes that are intrinsically unpredictable if they violate a Bell inequality. This property can be used to generate certified randomness in a device-independent way, i.e., without making detailed assumptions about the internal working of the quantum devices used to generate the random numbers. Furthermore these numbers are also private, i.e., they appear random not only to the user, but also to any adversary that might possess a perfect description of the devices. Since this process requires a small initial random seed, one usually speaks of device-independent randomness expansion. The purpose of this paper is twofold. First, we point out that in most real, practical situations, where the concept of device-independence is used as a protection against unintentional flaws or failures of the quantum apparatuses, it is sufficient to show that the generated string is random with respect to an adversary that holds only classical-side information, i.e., proving randomness against quantum-side information is not necessary. Furthermore, the initial random seed does not need to be private with respect to the adversary, provided that it is generated in a way that is independent from the measured systems. The devices, though, will generate cryptographically-secure randomness that cannot be predicted by the adversary and thus one can, given access to free public randomness, talk about private randomness generation. The theoretical tools to quantify the generated randomness according to these criteria were already introduced in [S. Pironio et al, Nature 464, 1021 (2010)], but the final results were improperly formulated. The second aim of this paper is to correct this inaccurate formulation and therefore lay out a precise theoretical framework for practical device-independent randomness expansion.Comment: 18 pages. v3: important changes: the present version focuses on security against classical side-information and a discussion about the significance of these results has been added. v4: minor changes. v5: small typos correcte

Перспективи розвитку експортоорієнтованої стратегії підприємств

Рассмотрен вопрос стратегического развития экспортноориентрованной политики предприятий. Раскрыты перспективы развития международных торговых отношений Украины.Розглянуто питання стратегічного розвитку експортноорієнтовної політики підприємств. Розкрито перспективи розвитку міжнародних торгівельних відносин України

Constructive Dimension and Turing Degrees

This paper examines the constructive Hausdorff and packing dimensions of Turing degrees. The main result is that every infinite sequence S with constructive Hausdorff dimension dim_H(S) and constructive packing dimension dim_P(S) is Turing equivalent to a sequence R with dim_H(R) <= (dim_H(S) / dim_P(S)) - epsilon, for arbitrary epsilon > 0. Furthermore, if dim_P(S) > 0, then dim_P(R) >= 1 - epsilon. The reduction thus serves as a *randomness extractor* that increases the algorithmic randomness of S, as measured by constructive dimension. A number of applications of this result shed new light on the constructive dimensions of Turing degrees. A lower bound of dim_H(S) / dim_P(S) is shown to hold for the Turing degree of any sequence S. A new proof is given of a previously-known zero-one law for the constructive packing dimension of Turing degrees. It is also shown that, for any regular sequence S (that is, dim_H(S) = dim_P(S)) such that dim_H(S) > 0, the Turing degree of S has constructive Hausdorff and packing dimension equal to 1. Finally, it is shown that no single Turing reduction can be a universal constructive Hausdorff dimension extractor, and that bounded Turing reductions cannot extract constructive Hausdorff dimension. We also exhibit sequences on which weak truth-table and bounded Turing reductions differ in their ability to extract dimension.Comment: The version of this paper appearing in Theory of Computing Systems, 45(4):740-755, 2009, had an error in the proof of Theorem 2.4, due to insufficient care with the choice of delta. This version modifies that proof to fix the error

From Low-Distortion Norm Embeddings to Explicit Uncertainty Relations and Efficient Information Locking

The existence of quantum uncertainty relations is the essential reason that some classically impossible cryptographic primitives become possible when quantum communication is allowed. One direct operational manifestation of these uncertainty relations is a purely quantum effect referred to as information locking. A locking scheme can be viewed as a cryptographic protocol in which a uniformly random n-bit message is encoded in a quantum system using a classical key of size much smaller than n. Without the key, no measurement of this quantum state can extract more than a negligible amount of information about the message, in which case the message is said to be "locked". Furthermore, knowing the key, it is possible to recover, that is "unlock", the message. In this paper, we make the following contributions by exploiting a connection between uncertainty relations and low-distortion embeddings of L2 into L1. We introduce the notion of metric uncertainty relations and connect it to low-distortion embeddings of L2 into L1. A metric uncertainty relation also implies an entropic uncertainty relation. We prove that random bases satisfy uncertainty relations with a stronger definition and better parameters than previously known. Our proof is also considerably simpler than earlier proofs. We apply this result to show the existence of locking schemes with key size independent of the message length. We give efficient constructions of metric uncertainty relations. The bases defining these metric uncertainty relations are computable by quantum circuits of almost linear size. This leads to the first explicit construction of a strong information locking scheme. Moreover, we present a locking scheme that is close to being implementable with current technology. We apply our metric uncertainty relations to exhibit communication protocols that perform quantum equality testing.Comment: 60 pages, 5 figures. v4: published versio

Efficient and Provable White-Box Primitives

International audienceIn recent years there have been several attempts to build white-box block ciphers whose implementations aim to be incompress-ible. This includes the weak white-box ASASA construction by Bouil-laguet, Biryukov and Khovratovich from Asiacrypt 2014, and the recent space-hard construction by Bogdanov and Isobe from CCS 2015. In this article we propose the first constructions aiming at the same goal while offering provable security guarantees. Moreover we propose concrete instantiations of our constructions, which prove to be quite efficient and competitive with prior work. Thus provable security comes with a surprisingly low overhead

Distinct phosphatases antagonize the p53 response in different phases of the cell cycle

The basic machinery that detects DNA damage is the same throughout the cell cycle. Here, we show, in contrast, that reversal of DNA damage responses (DDRs) and recovery are fundamentally different in G1 and G2 phases of the cell cycle. We find that distinct phosphatases are required to counteract the checkpoint response in G1 vs. G2. Whereas WT p53-induced phosphatase 1 (Wip1) promotes recovery in G2-arrested cells by antagonizing p53, it is dispensable for recovery from a G1 arrest. Instead, we identify phosphoprotein phosphatase 4 catalytic subunit (PP4) to be specifically required for cell cycle restart after DNA damage in G1. PP4 dephosphorylates Krüppel-associated box domain-associated protein 1-S473 to repress p53-dependent transcriptional activation of p21 when the DDR is silenced. Taken together, our results show that PP4 and Wip1 are differentially required to counteract the p53-dependent cell cycle arrest in G1 and G2, by antagonizing early or late p53-mediated responses, respectively

Towards the clinical implementation of pharmacogenetics in bipolar disorder.

BackgroundBipolar disorder (BD) is a psychiatric illness defined by pathological alterations between the mood states of mania and depression, causing disability, imposing healthcare costs and elevating the risk of suicide. Although effective treatments for BD exist, variability in outcomes leads to a large number of treatment failures, typically followed by a trial and error process of medication switches that can take years. Pharmacogenetic testing (PGT), by tailoring drug choice to an individual, may personalize and expedite treatment so as to identify more rapidly medications well suited to individual BD patients.DiscussionA number of associations have been made in BD between medication response phenotypes and specific genetic markers. However, to date clinical adoption of PGT has been limited, often citing questions that must be answered before it can be widely utilized. These include: What are the requirements of supporting evidence? How large is a clinically relevant effect? What degree of specificity and sensitivity are required? Does a given marker influence decision making and have clinical utility? In many cases, the answers to these questions remain unknown, and ultimately, the question of whether PGT is valid and useful must be determined empirically. Towards this aim, we have reviewed the literature and selected drug-genotype associations with the strongest evidence for utility in BD.SummaryBased upon these findings, we propose a preliminary panel for use in PGT, and a method by which the results of a PGT panel can be integrated for clinical interpretation. Finally, we argue that based on the sufficiency of accumulated evidence, PGT implementation studies are now warranted. We propose and discuss the design for a randomized clinical trial to test the use of PGT in the treatment of BD

Tipping the scales:Lessons from simple model systems on inositol imbalance in neurological disorders

Inositol and inositol-containing compounds have signalling and regulatory roles in many cellular processes, suggesting that inositol imbalance may lead to wide-ranging changes in cellular functions. Indeed, changes in inositol-dependent signalling have been implicated in various diseases and cellular functions such as autophagy, and these changes have often been proposed as therapeutic targets. However, few studies have highlighted the links between inositol depletion and the downstream effects on inositol phosphates and phosphoinositides in disease states. For this research, many advances have employed simple model systems that include the social amoeba D. discoideum and the yeast S. cerevisiae, since these models enable a range of experimental approaches that are not possible in mammalian models. In this review, we discuss recent findings initiated in simple model systems and translated to higher model organisms where the effect of altered inositol, inositol phosphate and phosphoinositide levels impact on bipolar disorder, Alzheimer disease, epilepsy and autophagy