Formal Enforcement of Security Policies : An Algebraic Approach

La sécurité des systèmes d’information est l’une des préoccupations les plus importantes du domaine de la science informatique d’aujourd’hui. Les particuliers et les entreprises sont de plus en plus touchés par des failles de sécurité et des milliards de dollars ont été perdus en raison de cyberattaques. Cette thèse présente une approche formelle basée sur la réécriture de programmes permettant d’appliquer automatiquement des politiques de sécurité sur des programmes non sécuritaires. Pour un programme P et une politique de sécurité Q, nous générons un autre programme P’ qui respecte une politique de sécurité Q et qui se comporte comme P, sauf si la politique est sur le point d’être violée. L’approche présentée utilise l’algèbre [symbol] qui est une variante de [symbol] (Basic Process Algebra) étendue avec des variables, des environnements et des conditions pour formaliser et résoudre le problème. Le problème de trouver la version sécuritaire P’ à partir de P et de Q se transforme en un problème de résolution d’un système linéaire pour lequel nous savons déjà comment extraire la solution par un algorithme polynomial. Cette thèse présente progressivement notre approche en montrant comment la solution évolue lorsqu’on passe de l’algèbre de [symbol] à [symbol].The security of information systems is one of the most important preoccupations of today’s computer science field. Individuals and companies are more and more affected by security flaws and billions of dollars have been lost because of cyber-attacks. This thesis introduces a formal program-rewriting approach that can automatically enforce security policies on non-trusted programs. For a program P and a security policy Q, we generate another program P’ that respects the security policy Q and behaves like P except when the enforced security policy is about to be violated. The presented approach uses the [symbol] algebra that is a variant of the BPA (Basic Process Algebra) algebra extended with variables, environments and conditions to formalize and resolve the problem. The problem of computing the expected enforced program [symbol] is transformed to a problem of resolving a linear system for which we already know how to extract the solution by a polynomial algorithm. This thesis presents our approach progressively and shows how the solution evolves when we move from the [symbol] algebra to the [symbol] algebra

Neuroprotectants attenuate hypobaric hypoxia-induced brain injuries in cynomolgus monkeys

Hypobaric hypoxia (HH) exposure can cause serious brain injury as well as life-threatening cerebral edema in severe cases. Previous studies on the mechanisms of HH-induced brain injury have been conducted primarily using non-primate animal models that are genetically distant to humans, thus hindering the development of disease treatment. Here, we report that cynomolgus monkeys (Macaca fascicularis) exposed to acute HH developed human-like HH syndrome involving severe brain injury and abnormal behavior. Transcriptome profiling of white blood cells and brain tissue from monkeys exposed to increasing altitude revealed the central role of the HIF-1 and other novel signaling pathways, such as the vitamin D receptor (VDR) signaling pathway, in co-regulating HH-induced inflammation processes. We also observed profound transcriptomic alterations in brains after exposure to acute HH, including the activation of angiogenesis and impairment of aerobic respiration and protein folding processes, which likely underlie the pathological effects of HH-induced brain injury. Administration of progesterone (PROG) and steroid neuroprotectant 5α-androst-3β,5,6β-triol (TRIOL) significantly attenuated brain injuries and rescued the transcriptomic changes induced by acute HH. Functional investigation of the affected genes suggested that these two neuroprotectants protect the brain by targeting different pathways, with PROG enhancing erythropoiesis and TRIOL suppressing glutamate-induced excitotoxicity. Thus, this study advances our understanding of the pathology induced by acute HH and provides potential compounds for the development of neuroprotectant drugs for therapeutic treatment

Reactivity tests for supplementary cementitious materials: RILEM TC 267-TRM phase 1

A primary aim of RILEM TC 267-TRM: “Tests for Reactivity of Supplementary Cementitious Materials (SCMs)” is to compare and evaluate the performance of conventional and novel SCM reactivity test methods across a wide range of SCMs. To this purpose, a round robin campaign was organized to investigate 10 different tests for reactivity and 11 SCMs covering the main classes of materials in use, such as granulated blast furnace slag, fly ash, natural pozzolan and calcined clays. The methods were evaluated based on the correlation to the 28 days relative compressive strength of standard mortar bars containing 30% of SCM as cement replacement and the interlaboratory reproducibility of the test results. It was found that only a few test methods showed acceptable correlation to the 28 days relative strength over the whole range of SCMs. The methods that showed the best reproducibility and gave good correlations used the R3 model system of the SCM and Ca(OH)2, supplemented with alkali sulfate/carbonate. The use of this simplified model system isolates the reaction of the SCM and the reactivity can be easily quantified from the heat release or bound water content. Later age (90 days) strength results also correlated well with the results of the IS 1727 (Indian standard) reactivity test, an accelerated strength test using an SCM/Ca(OH)2-based model system. The current standardized tests did not show acceptable correlations across all SCMs, although they performed better when latently hydraulic materials (blast furnace slag) were excluded. However, the Frattini test, Chapelle and modified Chapelle test showed poor interlaboratory reproducibility, demonstrating experimental difficulties. The TC 267-TRM will pursue the development of test protocols based on the R3 model systems. Acceleration and improvement of the reproducibility of the IS 1727 test will be attempted as well

Establishment and transfer of classical eyeblink conditioning using electrical microstimulation of the hippocampus as the conditioned stimulus.

The present experiment was designed to determine whether classical eyeblink conditioning (EBC) can be established by using electrical microstimulation of the hippocampus as a conditioned stimulus (CS) paired with an air-puff unconditioned stimulus (US). We intended to examine whether EBC transfer could occur when a CS was shifted between microstimulation of the hippocampus as a CS (Hip-CS) and tone as a CS (tone-CS) and to compare the difference in transfer effectiveness between delay EBC (dEBC) and trace EBC (tEBC). Eight groups of guinea pigs, including 4 experimental groups and 4 control groups, were included in the study. First, the experimental groups received either a Hip-CS or a tone-CS paired with a US; then, these groups were exposed to a shifted CS (tone-CS or Hip-CS) paired with the US. The control groups received the corresponding Hip-CS or tone-CS, which was, however, pseudo-paired with the US. The control groups were then shifted to the tone-CS (or Hip-CS) paired with the US. The results show that EBC can be successfully established when using microstimulation of the hippocampus as a CS paired with an air-puff US, and that the acquisition rates of EBC are higher in the experimental groups than in the control groups after switching from the Hip-CS to the tone-CS or vice versa, indicating the occurrence of learning transfer between EBC established with the Hip-CS and tone-CS. The present study also demonstrated that the EBC re-acquisition rates were remarkably higher in dEBC than in tEBC with both types of transfer, which suggests that the saving effect was more evident in dEBC than tEBC. These results significantly expand our knowledge of EBC transfer as well as the functional neural circuit underlying EBC transfer

Locations of the electrode tips in the hippocampus of guinea pigs.

<p>(A) A representative of toluidine blue-stained coronal hippocampus section (30 μm) from a guinea pig that received hippocampal electrical stimulation as the CS. Scale bar represents 1.0 mm; (B, C) Schematic illustration of the locations of all electrode tips. (B) For delay paradigm: (□ group of from Hip-CS (paired) to tone-CS (paired), n = 6; ■ group of from Hip-CS (pseudo-paired) to tone-CS (paired), n = 4; ○ group of from tone-CS (paired) to Hip-CS (paired), n = 7; ● group of from tone-CS (pseudo-paired) to Hip-CS (paired), n = 4); (C) For trace paradigm: (△ group of from Hip-CS (paired) to tone-CS (paired), n = 6; ▲ group of from Hip-CS (pseudo-paired) to tone-CS (paired), n = 4; ◇ group of from tone-CS (paired) to Hip-CS (paired), n = 5; ◆ group of from tone-CS (pseudo-paired) to Hip-CS (paired), n = 4). The coronal brain plates are adapted from the atlas of Rapisarda and Bacchelli [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0178502#pone.0178502.ref039" target="_blank">39</a>].</p

La Modiste universelle : édition de chapeaux-modèles

01 novembre 18761876/11/01 (A1,N2)

Comparisons of post-shift CR acquisition rates between dEBC and tEBC, and between with Hip-CS and with tone-CS.

<p>Four curves depicting post-shift CR acquisition rates in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0178502#pone.0178502.g003" target="_blank">Fig 3</a> were rearranged and illustrated (for comparison, pre-shift CR acquisition rate in the last day of stage I was also demonstrated). Data represent mean ± SEM. (A, B) comparison of CR acquisition between paradigms of dEBC and tEBC (n = 6, for tone-CS/dEBC; n = 6, for tone-CS/tEBC; n = 7, for Hip-CS/dEBC; n = 5, for Hip-CS/tEBC). For post-shift learning with both tone-CS (A) and Hip-CS (B), establishment of dEBC (square, space or black) showed higher acquisition rates than of tEBC (roundness, space or black), confirmed by statistically significant main effects of group [Fig 5A and 5F(1, 10) = 53.918, *p < 0.05; Fig 5B and 5F(1, 10) = 92.772, *p < 0.05], a two-way repeated measures ANOVA, followed by the LSD post hoc test. (C, D) comparison of CR acquisition between with Hip-CS and with tone-CS (n = 6, for tone-CS/dEBC; n = 7, for hip-CS/dEBC; n = 6, for tone-CS/tEBC; n = 5, for Hip-CS/tEBC). Post-shift learning with Hip-CS (black square) showed significant difference relative to with tone-CS (space roundness) for establishment of dEBC (Fig 5C and 5F(1, 11) = 26.796, *p < 0.05), but not of tEBC (Fig 5D and 5F(1, 9) = 0.113, p = 0.745), confirmed by a two-way repeated measures ANOVA, followed by the LSD post hoc test.</p

Acquisition curves of eyelid conditioned responses in delay and trace paradigms when CS shifted from central (Hip–CS) to peripheral (tone-CS) or vice versa.

<p>(A, B) Learning curves of dEBC (A) and tEBC (B) for groups of experiment (square, n = 6, for both dEBC and tEBC) and control (roundness, n = 4, for both dEBC and tEBC) when CS shifted from central to peripheral. Central CS (black in A, B) was presented during first 6 (dEBC) or 12 (tEBC) sessions in stage I and paired (black square in A and B) or pseudo-paired (black roundness in A, B) with US, then CS was switched to peripheral and paired with US (space square and space roundness, A and B) in sessions 7–12 (dEBC) or 13–18 (tEBC) of stage II. (C, D) Learning curves of dEBC (C) and tEBC (D) for groups of experiment (square, n = 7, for dEBC; n = 5, for tEBC) and control (roundness, n = 4, for both dEBC and tEBC) when CS shifted from peripheral to central (C, D). Central CS (space in C, D) was presented during first 6 (dEBC) or 12 (tEBC) sessions in stage I and paired (space square in C and D) or pseudo-paired (space roundness in C, D) with US, then CS was switched to central and paired with US (black square and black roundness, C, D) in sessions 7–12 (dEBC) or 13–18 (tEBC) of stage II. Data represent mean ± SEM. A two-way repeated measures ANOVA followed by the LSD post hoc test showed that there were significant differences in the percentages of the conditioned responses (CR) between groups of experiment and control in stage II in both delay and trace paradigms, either shifting CS from central to peripheral or vice versa. [Fig 3A and 3F (1, 8) = 40.028, *p < 0.05; Fig 3B and 3F (1, 8) = 8.905, *p < 0.05; Fig 3C and 3F (1, 9) = 154.691, *p < 0.05; Fig 3D and 3F (1, 7) = 16.299, *p < 0.05]. In recognition tests of stage III in the above 4 conditions, animals were all able to recall the original CR% to CS1.</p

MicroRNA-205-5p regulates the chemotherapeutic resistance of hepatocellular carcinoma cells by targeting PTEN/JNK/ANXA3 pathway

Hepatocellular carcinoma (HCC) is a common malignant tumor of the digestive system, and patients with advanced HCC have a poor outlook, partly due to resistance to chemotherapeutic drugs. Previous studies have implicated microRNAs in the regulation of chemoresistance, and we have previously shown that microRNA (miR)-205- 5p is down-regulated in multiple hepatoma cell lines. Here, we investigate whether miR-205-5p is involved in chemotherapeutic resistance in HCC. Expression of miR-205-5p was measured by real-time quantitative reverse transcription PCR and cell viability was determined using a CCK-8 cell viability assay. Expression of proteins in the PTEN/JNK/ANXA3 pathway were assessed via Western blotting. We found that miR-205-5p expression was down-regulated in all HCC cell lines investigated. In addition, miR-205-5p expression was upregulated by 5-fluorouracil (5-Fu) treatment in Bel-7402 (Bel) cells. Interestingly, miR-205-5p expression was increased in multidrug-resistant Bel-7402/5-Fu (Bel/Fu) cells, compared with Bel cells. We next demonstrated that sensitivity to 5-Fu was increased in Bel/Fu cells after treatment with a miR-205-5p inhibitor. Similarly, increased resistance to 5-Fu was observed in Bel cells after transfection with a miR-205-5p mimic. We injected nude mice with Bel/5-Fu cells to promote tumor growth, and found that co-treatment with a miR-205-5p antagomir and 5-Fu slowed tumor growth more than either treatment alone. Finally, we found that these effects were all associated with changes in the PTEN/JNK/ANXA3 pathway. In conclusion, inhibition of miR-205-5p may reverse chemotherapeutic resistance to 5-Fu, and this may occur via the PTEN/JNK/ANXA3 pathway