On some developments and evaluation of an Eulerian-Lagrangian method for the transport equation

The modelling of typical engineering problems in industry, such as water-jet cooling of hot-rolled steel strip products, directly involves the solution of a transport (advection-diffusion) equation for the cooling characteristics of the strip. The non-linear nature of the heat conduction involved aggravates the difficulty of the problem. Traditional Finite Difference techniques for the solution of this advection dominated transport equation incur severe Courant number stability restrictions as well as instabilities in the presence of temperature discontinuities. Eulerian-Lagrangian Methods (ELM's) solve the transport equation in Lagrangian form `along' backward characteristics effectively decoupling the advection and diffusion terms but retaining the convenience of fixed computational grids. Typical interpolation methods used to obtain the values at the feet of characteristic lines lead to spurious oscillations, numerical diffusion, peak clipping and phase errors. Through the use of `peak tracking', by the forward-tracking of Eulerian nodal points, this paper attempts to alleviate these errors. A comparison of 1-D benchmark tests from the Convection-Diffusion Forum as well as appropriate error measures, are shown to produce appreciable improvements over the standard methods for a range of time steps, very large Peclet numbers and Courant numbers in excess of one

Critical illness polyneuropathy in ICU patients is related to reduced motor nerve excitability caused by reduced sodium permeability

Background: Reduced motor and sensory nerve amplitudes in critical illness polyneuropathy (CIP) are characteristic features described in electrophysiological studies and due to dysfunction of voltage-gated sodium channels. Yet, faulty membrane depolarization as reported in various tissues of critically ill patients may cause reduced membrane excitability as well. The aim of this study was to compare the pathophysiological differences in motor nerve membrane polarization and voltage-gated sodium channel function between CIP patients and critically ill patients not developing CIP during their ICU stay (ICU controls). Methods: ICU patients underwent electrophysiological nerve conduction studies and were categorized as either ICU controls or CIP patients. Subsequently, excitability parameters were recorded as current-threshold relationship, stimulus-response behavior, threshold electrotonus, and recovery of excitability from the abductor pollicis brevis following median nerve stimulation. Results: Twenty-six critically ill patients were enrolled and categorized as 12 ICU controls and 14 CIP patients. When compared to 31 healthy subjects, the ICU controls exhibited signs of membrane depolarization as shown by reduced superexcitability (p = 0.003), depolarized threshold electrotonus (p = 0.007), increased current-threshold relationship (p = 0.03), and slightly prolonged strength-duration time constant. In contrast, the CIP patients displayed a significantly reduced strength-duration time constant (p < 0.0001), which indicates an increased inactivation of voltage-gated sodium channels. Conclusions: Abnormal motor nerve membrane depolarization is a general finding in critically ill patients whereas voltage-gated sodium channel dysfunction is a characteristic of CIP patients

Perfect Secrecy Systems Immune to Spoofing Attacks

We present novel perfect secrecy systems that provide immunity to spoofing attacks under equiprobable source probability distributions. On the theoretical side, relying on an existence result for $t$-designs by Teirlinck, our construction method constructively generates systems that can reach an arbitrary high level of security. On the practical side, we obtain, via cyclic difference families, very efficient constructions of new optimal systems that are onefold secure against spoofing. Moreover, we construct, by means of $t$-designs for large values of $t$, the first near-optimal systems that are 5- and 6-fold secure as well as further systems with a feasible number of keys that are 7-fold secure against spoofing. We apply our results furthermore to a recently extended authentication model, where the opponent has access to a verification oracle. We obtain this way novel perfect secrecy systems with immunity to spoofing in the verification oracle model.Comment: 10 pages (double-column); to appear in "International Journal of Information Security

Attacks on quantum key distribution protocols that employ non-ITS authentication

We demonstrate how adversaries with unbounded computing resources can break Quantum Key Distribution (QKD) protocols which employ a particular message authentication code suggested previously. This authentication code, featuring low key consumption, is not Information-Theoretically Secure (ITS) since for each message the eavesdropper has intercepted she is able to send a different message from a set of messages that she can calculate by finding collisions of a cryptographic hash function. However, when this authentication code was introduced it was shown to prevent straightforward Man-In-The-Middle (MITM) attacks against QKD protocols. In this paper, we prove that the set of messages that collide with any given message under this authentication code contains with high probability a message that has small Hamming distance to any other given message. Based on this fact we present extended MITM attacks against different versions of BB84 QKD protocols using the addressed authentication code; for three protocols we describe every single action taken by the adversary. For all protocols the adversary can obtain complete knowledge of the key, and for most protocols her success probability in doing so approaches unity. Since the attacks work against all authentication methods which allow to calculate colliding messages, the underlying building blocks of the presented attacks expose the potential pitfalls arising as a consequence of non-ITS authentication in QKD-postprocessing. We propose countermeasures, increasing the eavesdroppers demand for computational power, and also prove necessary and sufficient conditions for upgrading the discussed authentication code to the ITS level.Comment: 34 page

The Threat of Capital Drain: A Rationale for Public Banks?

This paper yields a rationale for why subsidized public banks may be desirable from a regional perspective in a financially integrated economy. We present a model with credit rationing and heterogeneous regions in which public banks prevent a capital drain from poorer to richer regions by subsidizing local depositors, for example, through a public guarantee. Under some conditions, cooperative banks can perform the same function without any subsidization; however, they may be crowded out by public banks. We also discuss the impact of the political structure on the emergence of public banks in a political-economy setting and the role of interregional mobility

Comment on "Arbitrated quantum-signature scheme"

We investigate the quantum signature scheme proposed by Zeng and Keitel [Phys. Rev. A 65, 042312 (2002)]. It uses Greenberger-Horne-Zeilinger (GHZ) states and the availability of a trusted arbitrator. However, in our opinion the protocol is not clearly operationally defined and several steps are ambiguous. Moreover, we argue that the security statements claimed by the authors are incorrect.Comment: 4 page

On Weak Keys and Forgery Attacks Against Polynomial-Based MAC Schemes

Abstract. Universal hash functions are commonly used primitives for fast and secure message authentication in the form of Message Authentication Codes (MACs) or Authenticated Encryption with Associated Data (AEAD) schemes. These schemes are widely used and standardised, the most well known being McGrew and Viega’s Galois/Counter Mode (GCM). In this paper we identify some properties of hash functions based on polynomial evaluation that arise from the underlying algebraic structure. As a result we are able to describe a general forgery attack, of which Saarinen’s cycling attack from FSE 2012 is a special case. Our attack removes the requirement for long messages and applies regardless of the field in which the hash function is evaluated. Furthermore we provide a common description of all published attacks against GCM, by showing that the existing attacks are the result of these algebraic properties of the polynomial-based hash function. We also greatly expand the number of known weak GCM keys and show that almost every subset of the keyspace is a weak key class. Finally, we demonstrate that these algebraic properties and corresponding attacks are highly relevant to GCM/2 +, a variant of GCM designed to increase the efficiency in software

Deletion of Nlrp3 protects from inflammation-induced skeletal muscle atrophy

BACKGROUND: Critically ill patients develop atrophic muscle failure, which increases morbidity and mortality. Interleukin-1β (IL-1β) is activated early in sepsis. Whether IL-1β acts directly on muscle cells and whether its inhibition prevents atrophy is unknown. We aimed to investigate if IL-1β activation via the Nlrp3 inflammasome is involved in inflammation-induced atrophy. METHODS: We performed an experimental study and prospective animal trial. The effect of IL-1β on differentiated C2C12 muscle cells was investigated by analyzing gene-and-protein expression, and atrophy response. Polymicrobial sepsis was induced by cecum ligation and puncture surgery in Nlrp3 knockout and wild type mice. Skeletal muscle morphology, gene and protein expression, and atrophy markers were used to analyze the atrophy response. Immunostaining and reporter-gene assays showed that IL-1β signaling is contained and active in myocytes. RESULTS: Immunostaining and reporter gene assays showed that IL-1β signaling is contained and active in myocytes. IL-1β increased Il6 and atrogene gene expression resulting in myocyte atrophy. Nlrp3 knockout mice showed reduced IL-1β serum levels in sepsis. As determined by muscle morphology, organ weights, gene expression, and protein content, muscle atrophy was attenuated in septic Nlrp3 knockout mice, compared to septic wild-type mice 96 h after surgery. CONCLUSIONS: IL-1β directly acts on myocytes to cause atrophy in sepsis. Inhibition of IL-1β activation by targeting Nlrp3 could be useful to prevent inflammation-induced muscle failure in critically ill patients