Lightweight Protocols and Applications for Memory-Based Intrinsic Physically Unclonable Functions on Commercial Off-The-Shelve Devices

We are currently living in the era in which through the ever-increasing dissemination of inter-connected embedded devices, the Internet-of-Things manifests. Although such end-point devices are commonly labeled as ``smart gadgets'' and hence they suggest to implement some sort of intelligence, from a cyber-security point of view, more then often the opposite holds. The market force in the branch of commercial embedded devices leads to minimizing production costs and time-to-market. This widespread trend has a direct, disastrous impact on the security properties of such devices. The majority of currently used devices or those that will be produced in the future do not implement any or insufficient security mechanisms. Foremost the lack of secure hardware components often mitigates the application of secure protocols and applications. This work is dedicated to a fundamental solution statement, which allows to retroactively secure commercial off-the-shelf devices, which otherwise are exposed to various attacks due to the lack of secure hardware components. In particular, we leverage the concept of Physically Unclonable Functions (PUFs), to create hardware-based security anchors in standard hardware components. For this purpose, we exploit manufacturing variations in Static Random-Access Memory (SRAM) and Dynamic Random-Access Memory modules to extract intrinsic memory-based PUF instances and building on that, to develop secure and lightweight protocols and applications. For this purpose, we empirically evaluate selected and representative device types towards their PUF characteristics. In a further step, we use those device types, which qualify due to the existence of desired PUF instances for subsequent development of security applications and protocols. Subsequently, we present various software-based security solutions which are specially tailored towards to the characteristic properties of embedded devices. More precisely, the proposed solutions comprise a secure boot architecture as well as an approach to protect the integrity of the firmware by binding it to the underlying hardware. Furthermore, we present a lightweight authentication protocol which leverages a novel DRAM-based PUF type. Finally, we propose a protocol, which allows to securely verify the software state of remote embedded devices

Physiologic cold shock of Moraxella catarrhalis affects the expression of genes involved in the iron acquisition, serum resistance and immune evasion

<p>Abstract</p> <p>Background</p> <p><it>Moraxella catarrhalis</it>, a major nasopharyngeal pathogen of the human respiratory tract, is exposed to rapid downshifts of environmental temperature when humans breathe cold air. It was previously shown that the prevalence of pharyngeal colonization and respiratory tract infections caused by <it>M. catarrhalis </it>are greatest in winter. The aim of this study was to investigate how <it>M. catarrhalis </it>uses the physiologic exposure to cold air to upregulate pivotal survival systems in the pharynx that may contribute to <it>M. catarrhalis </it>virulence.</p> <p>Results</p> <p>A 26°C cold shock induces the expression of genes involved in transferrin and lactoferrin acquisition, and enhances binding of these proteins on the surface of <it>M. catarrhalis</it>. Exposure of <it>M. catarrhalis </it>to 26°C upregulates the expression of UspA2, a major outer membrane protein involved in serum resistance, leading to improved binding of vitronectin which neutralizes the lethal effect of human complement. In contrast, cold shock decreases the expression of Hemagglutinin, a major adhesin, which mediates B cell response, and reduces immunoglobulin D-binding on the surface of <it>M. catarrhalis</it>.</p> <p>Conclusion</p> <p>Cold shock of <it>M. catarrhalis </it>induces the expression of genes involved in iron acquisition, serum resistance and immune evasion. Thus, cold shock at a physiologically relevant temperature of 26°C induces in <it>M. catarrhalis </it>a complex of adaptive mechanisms that enables the bacterium to target their host cellular receptors or soluble effectors and may contribute to enhanced growth, colonization and virulence.</p

Outer membrane porin M35 of Moraxella catarrhalis mediates susceptibility to aminopenicillins

<p>Abstract</p> <p>Background</p> <p>The outer membrane protein M35 is a conserved porin of type 1 strains of the respiratory pathogen <it>Moraxella catarrhalis</it>. It was previously shown that M35 is involved in the uptake of essential nutrients required for bacterial growth and for nasal colonization in mice. The aim of this study was (i) to characterize the potential roles of M35 in the host-pathogen interactions considering the known multifunctionality of porins and (ii) to characterize the degree of conservation in the phylogenetic older subpopulation (type 2) of <it>M. catarrhalis</it>.</p> <p>Results</p> <p>Isogenic <it>m35 </it>mutants of the type 1 strains O35E, 300 and 415 were tested for their antimicrobial susceptibility against 15 different agents. Differences in the MIC (Minimum Inhibitory Concentration) between wild-type and mutant strains were found for eight antibiotics. For ampicillin and amoxicillin, we observed a statistically significant 2.5 to 2.9-fold MIC increase (p < 0.03) in the <it>m35 </it>mutants. Immunoblot analysis demonstrated that human saliva contains anti-M35 IgA. Wild-type strains and their respective <it>m35 </it>mutants were indistinguishable with respect to the phenotypes of autoagglutination, serum resistance, iron acquisition from human lactoferrin, adherence to and invasion of respiratory tract epithelial cells, and proinflammatory stimulation of human monocytes. DNA sequencing of <it>m35 </it>from the phylogenetic subpopulation type 2 strain 287 revealed 94.2% and 92.8% identity on the DNA and amino acid levels, respectively, in comparison with type 1 strains.</p> <p>Conclusion</p> <p>The increase in MIC for ampicillin and amoxicillin, respectively, in the M35-deficient mutants indicates that this porin affects the outer membrane permeability for aminopenicillins in a clinically relevant manner. The presence of IgA antibodies in healthy human donors indicates that M35 is expressed <it>in vivo </it>and recognized as a mucosal antigen by the human host. However, immunoblot analysis of human saliva suggests the possibility of antigenic variation of immunoreactive epitopes, which warrants further analysis before M35 can be considered a potential vaccine candidate.</p

Models for Pop I stars: implications for age determinations

Starting from a few topical astrophysical questions which require the knowledge of the age of Pop I stars, we discuss the needed precision on the age in order to make progresses in these areas of research. Then we review the effects of various inputs of the stellar models on the age determination and try to identify those affecting the most the lifetimes of stars.Comment: 10 pages, 6 figures, 2 tables, IAU Symp. 258, D. Soderblom et al. ed

L'élevage, un atout pour le développement durable des territoires dans les régions de polyculture-élevage

Comment l’élevage peut-il contribuer au développement durable des territoires en région de polyculture-élevage ? A l’inverse, les objectifs de développement rural peuvent-ils conforter la durabilité de l’élevage dans ces situations ? Notre réflexion est fondée sur des recherches interdisciplinaires sur l’agriculture et l’environnement dans différentes régions françaises (Coteaux de Gascogne, Plaine de Niort, Bretagne, Pays de Caux et Lorraine). Nos recherches appréhendent les relations entre transformations des activités agricoles et changements de l’utilisation des terres en lien avec les services écosystémiques. Ces questions exigent d’aborder de multiples dimensions de la gestion de l’espace et des ressources naturelles par l’élevage. Nos résultats illustrent la complexité et l’imbrication des questions de gestion de l’espace, de la parcelle au paysage, soulevées par le développement durable de l’élevage en milieu de polyculture-élevage. Au niveau de l’exploitation, ils éclairent les stratégies décisionnelles des agriculteurs. Au niveau du tissu d’exploitations, ils soulignent l’importance des relations et des échanges entre exploitations. L’expérimentation de systèmes innovants contribue à évaluer la compatibilité des enjeux territoriaux et de durabilité des exploitations. Enfin, nous proposons des pistes de recherche et d’actions pour conforter la contribution de l’élevage au développement durable des territoires ruraux

Mitochondrial tRNALeu(UUR) mutation m.3302A > G presenting as childhood-onset severe myopathy: threshold determination through segregation study

Mitochondrial tRNALeu(UUR) mutation m.3302A > G is associated with respiratory chain complex I deficiency and has been described as a rare cause of mostly adult-onset slowly progressive myopathy. Five families with 11 patients have been described so far; 5 of them died young due to cardiorespiratory failure. Here, we report on a segregation study in a family with an index patient who already presented at the age of 18months with proximal muscular hypotonia, abnormal fatigability, and lactic acidosis. This early-onset myopathy was rapidly progressive. At 8years, the patient is wheel-chair bound, requires nocturnal assisted ventilation, and suffers from recurrent respiratory infections. Severe complex I deficiency and nearly homoplasmy for m.3302A > G were found in muscle. We collected blood, hair, buccal swabs and muscle biopsies from asymptomatic adults in this pedigree and determined heteroplasmy levels in these tissues as well as OXPHOS activities in muscle. All participating asymptomatic adults had normal OXPHOS activities. In contrast to earlier reports, we found surprisingly little variation of heteroplasmy levels in different tissues of the same individual. Up to 45% mutation load in muscle and up to 38% mutation load in other tissues were found in non-affected adults. The phenotypic spectrum of tRNALeu(UUR) m.3302A > G mutation seems to be wider than previously described. A threshold of more than 45% heteroplasmy in muscle seems to be necessary to alter complex I activity leading to clinical manifestation. The presented data may be helpful for prognostic considerations and counseling in affected familie

Abusing Commodity DRAMs in IoT Devices to Remotely Spy on Temperature

The ubiquity and pervasiveness of modern Internet of Things (IoT) devices opens up vast possibilities for novel applications, but simultaneously also allows spying on, and collecting data from, unsuspecting users to a previously unseen extent. This paper details a new attack form in this vein, in which the decay properties of widespread, off-the-shelf DRAM modules are exploited to accurately sense the temperature in the vicinity of the DRAM-carrying device. Among others, this enables adversaries to remotely and purely digitally spy on personal behavior in users' private homes, or to collect security-critical data in server farms, cloud storage centers, or commercial production lines. We demonstrate that our attack can be performed by merely compromising the software of an IoT device and does not require hardware modifications or physical access at attack time. It can achieve temperature resolutions of up to 0.5{\deg}C over a range of 0{\deg}C to 70{\deg}C in practice. Perhaps most interestingly, it even works in devices that do not have a dedicated temperature sensor on board. To complete our work, we discuss practical attack scenarios as well as possible countermeasures against our temperature espionage attacks.Comment: Submitted to IEEE TIFS and currently under revie

Direct Association of Protein-tyrosine Phosphatase PTP-PEST with Paxillin

Tyrosine phosphorylation of focal adhesion-associated proteins may be involved in the regulation of the cytoskeleton and in the control of signals for growth and survival. The focal adhesion kinase (FAK) functions in regulating tyrosine phosphorylation of several of these proteins, including paxillin, tensin, and p130(cas). Protein- tyrosine phosphatases, the counterparts of protein-tyrosine kinases, also presumably regulate phosphorylation of these proteins. We have tested the hypothesis that FAK intimately associates with a protein-tyrosine phosphatase. Protein-tyrosine phosphatase activity associated with the recombinant C-terminal domain of FAK in vitro and could be coimmunoprecipitated with both FAK and paxillin from lysates of chicken embryo cells. However, the interaction with FAK appeared to be indirect and mediated via paxillin. The protein-tyrosine phosphatase was subsequently identified as protein-tyrosine phosphatase-PEST, a nonreceptor protein-tyrosine phosphatase. The C-terminal noncatalytic domain of protein-tyrosine phosphatase-PEST directly bound to paxillin in vitro. The association of both a protein-tyrosine kinase and a protein-tyrosine phosphatase with paxillin suggests that paxillin may play a critical role in the regulation of the phosphotyrosine content of proteins in focal adhesions

Effects of endurance training on skeletal muscle mitochondrial function in Huntington disease patients

BACKGROUND Mitochondrial dysfunction may represent a pathogenic factor in Huntington disease (HD). Physical exercise leads to enhanced mitochondrial function in healthy participants. However, data on effects of physical exercise on HD skeletal muscle remains scarce. We aimed at investigating adaptations of the skeletal muscle mitochondria to endurance training in HD patients. METHODS Thirteen HD patients and 11 healthy controls completed 26 weeks of endurance training. Before and after the training phase muscle biopsies were obtained from M. vastus lateralis. Mitochondrial respiratory chain complex activities, mitochondrial respiratory capacity, capillarization, and muscle fiber type distribution were determined from muscle samples. RESULTS Citrate synthase activity increased during the training intervention in the whole cohort (P = 0.006). There was no group x time interaction for citrate synthase activity during the training intervention (P = 0.522). Complex III (P = 0.008), Complex V (P = 0.043), and succinate cytochrome c reductase (P = 0.008) activities increased in HD patients and controls by endurance training. An increase in mass-specific mitochondrial respiratory capacity was present in HD patients during the endurance training intervention. Overall capillary-to-fiber ratio increased in HD patients by 8.4% and in healthy controls by 6.4% during the endurance training intervention. CONCLUSIONS Skeletal muscle mitochondria of HD patients are equally responsive to an endurance-training stimulus as in healthy controls. Endurance training is a safe and feasible option to enhance indices of energy metabolism in skeletal muscle of HD patients and may represent a potential therapeutic approach to delay the onset and/or progression of muscular dysfunction. TRIAL REGISTRATION ClinicalTrials.gov NCT01879267 . Registered May 24, 2012