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Mensch-Roboter-Kollaboration
(2016)
Eine enge Zusammenarbeit von Mensch und Roboter, die sogenannte Mensch-Roboter-Kollaboration (MRK), könnte eine bisher beispielslose Produktivität entstehen lassen. Bis zur allgemeinen Nutzung der Technologie sind noch zahlreiche Probleme zu lösen, insbesondere die des Arbeits- und Gesundheitsschutzes. Am Institut für Sicherheitsforschung der Hochschule Bonn-Rhein-Sieg wurde in den vergangenen Jahren eine Reihe von Projekten zur Entwicklung von optischen Sensorsystemen für Schutzeinrichtungen durchgeführt. Im Projekt SPAI (Sichere Personendetektion im Arbeitsbereich von Industrierobotern durch ein aktives NIR-Kamerasystem) wurde ein spezielles Kamerasystem für den nahinfraroten (NIR) Spektralbereich entwickelt.
Nicht im Elfenbeinturm
(2016)
Recent years have seen extensive adoption of domain generation algorithms (DGA) by modern botnets. The main goal is to generate a large number of domain names and then use a small subset for actual C&C communication. This makes DGAs very compelling for botmasters to harden the infrastructure of their botnets and make it resilient to blacklisting and attacks such as takedown efforts. While early DGAs were used as a backup communication mechanism, several new botnets use them as their primary communication method, making it extremely important to study DGAs in detail.
In this paper, we perform a comprehensive measurement study of the DGA landscape by analyzing 43 DGAbased malware families and variants. We also present a taxonomy for DGAs and use it to characterize and compare the properties of the studied families. By reimplementing the algorithms, we pre-compute all possible domains they generate, covering the majority of known and active DGAs. Then, we study the registration status of over 18 million DGA domains and show that corresponding malware families and related campaigns can be reliably identified by pre-computing future DGA domains. We also give insights into botmasters’ strategies regarding domain registration and identify several pitfalls in previous takedown efforts of DGA-based botnets. We will share the dataset for future research and will also provide a web service to check domains for potential DGA identity.
Helping Johnny to Analyze Malware: A Usability-Optimized Decompiler and Malware Analysis User Study
(2016)
The Fifth International Conference on Advances in Vehicular Systems, Technologies and Applications (VEHICULAR 2016), held between November 13-17, 2016 - Barcelona, Spain, continued the inaugural event considering the state-of-the-art technologies for information dissemination in vehicle-to-vehicle and vehicle-to-infrastructure and focusing on advances in vehicular systems, technologies and applications.
We demonstrated previously that phosphocholine and phosphocholine-modified macromolecules efficiently inhibit ATP-dependent release of interleukin-1β from human and murine monocytes by a mechanism involving nicotinic acetylcholine receptors (nAChR). Interleukin-1β is a potent pro-inflammatory cytokine of innate immunity that plays pivotal roles in host defence. Control of interleukin-1β release is vital as excessively high systemic levels cause life threatening inflammatory diseases. In spite of its structural similarity to acetylcholine, there are no other reports on interactions of phosphocholine with nAChR. In this study, we demonstrate that phosphocholine inhibits ion-channel function of ATP receptor P2X7 in monocytic cells via nAChR containing α9 and α10 subunits. In stark contrast to choline, phosphocholine does not evoke ion current responses in Xenopus laevis oocytes, which heterologously express functional homomeric nAChR composed of α9 subunits or heteromeric receptors containing α9 and α10 subunits. Preincubation of these oocytes with phosphocholine, however, attenuated choline-induced ion current changes, suggesting that phosphocholine may act as a silent agonist. We conclude that phophocholine activates immuno-modulatory nAChR expressed by monocytes but does not stimulate canonical ionotropic receptor functions.
Hydrogen sulfide (H2S) is a well-known environmental chemical threat with an unpleasant smell of rotten eggs. Aside from the established toxic effects of high-dose H2S, research over the past decade revealed that cells endogenously produce small amounts of H2S with physiological functions. H2S has therefore been classified as a gasotransmitter. A major challenge for cells and tissues is the maintenance of low physiological concentrations of H2S in order to prevent potential toxicity. Epithelia of the respiratory and gastrointestinal tract are especially faced with this problem, since these barriers are predominantly exposed to exogenous H2S from environmental sources or sulfur-metabolising microbiota. In this paper, we review the cellular mechanisms by which epithelial cells maintain physiological, endogenous H2S concentrations. Furthermore, we suggest a concept by which epithelia use their electrolyte and liquid transport machinery as defence mechanisms in order to eliminate exogenous sources for potentially harmful H2S concentrations.
Hydrogen sulfide contributes to hypoxic inhibition of airway transepithelial sodium absorption
(2016)