Safe abstractions of data encodings in formal security protocol models

When using formal methods, security protocols are usually modeled at a high level of abstraction. In particular, data encoding and decoding transformations are often abstracted away. However, if no assumptions at all are made on the behavior of such transformations, they could trivially lead to security faults, for example leaking secrets or breaking freshness by collapsing nonces into constants. In order to address this issue, this paper formally states sufficient conditions, checkable on sequential code, such that if an abstract protocol model is secure under a Dolev-Yao adversary, then a refined model, which takes into account a wide class of possible implementations of the encoding/decoding operations, is implied to be secure too under the same adversary model. The paper also indicates possible exploitations of this result in the context of methods based on formal model extraction from implementation code and of methods based on automated code generation from formally verified model

Effect of Ferric Sodium EDTA administration, in combination with vitamin C, folic acid, copper gluconate, zinc gluconate and selenomethionine, on cardiovascular risk evaluation: exploration of the HRV frequency domain

diseases. Using the Heart Rate Variability (HRV) analysis is possible to provide an evaluation of the safety and the effectiveness of intervention. Objective: To evaluate the efficacy and safety of Ferric Sodium EDTA in combination with vitamin C, folic acid, copper gluconate, zinc gluconate and selenomethionine (Ferachel forte®) 2 tabs/day for 24 days in elderly patients with secondary anaemia, by exploring the HRV frequency domain. Methods: In 45 elderly patients with secondary anaemia and/or low-moderate kidney failure, laboratory values after administration of Ferric Sodium EDTA, 2 tabs a day, in combination with vitamin C, folic acid, copper gluconate, zinc gluconate and selenomethionine (Ferachel forte®) for 24 days (N=16 patients) or ferrous gluconate 63 mg/day added to saline solution, administered using intravenous access during the hospitalization period of 15 ± 5 days (N=29 patients) were evaluated. Also, ECG signals and bioelectrical impedance (BIA) were measured. Results: Oral iron supplementation with Ferric Sodium EDTA, in combination with vitamin C, folic acid, copper gluconate, zinc gluconate and selenomethionine (Ferachel forte®) confirmed to be effective and safe about the cardiovascular risk in old patients. This study showed the real superiority of the oral administration about the cardiovascular risk in elderly patients in comparison with intravenous administration of ferrous gluconate. Conclusion: This study confirms that Ferric Sodium EDTA combination (Ferachel forte®) can be a valid alternative to ferrous gluconate intravenous therapy (gold standard) in the treatment of secondary anaemia in elderly patients. In fact, during the treatment, efficacy results have been maintained without statistically significant variations about cardiovascular risk, evaluated by exploring the HRV frequency domain

Formal Verification of Security Protocol Implementations: A Survey

Automated formal verification of security protocols has been mostly focused on analyzing high-level abstract models which, however, are significantly different from real protocol implementations written in programming languages. Recently, some researchers have started investigating techniques that bring automated formal proofs closer to real implementations. This paper surveys these attempts, focusing on approaches that target the application code that implements protocol logic, rather than the libraries that implement cryptography. According to these approaches, libraries are assumed to correctly implement some models. The aim is to derive formal proofs that, under this assumption, give assurance about the application code that implements the protocol logic. The two main approaches of model extraction and code generation are presented, along with the main techniques adopted for each approac

De novo mutation in SLC25A22 gene: expansion of the clinical and electroencephalographic phenotype

The SLC25A22 (Solute Carrier Family 25, Member 22) gene encodes for a mitochondrial glutamate/H+ symporter and is involved in the mitochondrial transport of metabolites across the mitochondrial membrane. We hereby report a 12-year-old girl presenting with early-onset epileptic encephalopathy, hypotonia, and global developmental delay. Whole exome sequencing identified a novel homozygous missense mutation in SLC25A22 gene (c.97A>G; p.Lys33Glu), as the likely cause of the disease. The phenotype of our patient and EEG recordings do not completely overlap with the phenotypes previously described, leading to a new and more complex form of disease associated with SLC25A22 variants, characterized by dyskinetic movements and oculogyric crisis

Near term perspectives for fusion research and new contributions by the Ignitor program

The main advances made within the Ignitor program, that is aimed at investigating the physics of fusion burning plasmas near ignition, are described. In particular, the operation of the machine in the H and I regimes at the 10 MA plasma current levels has been considered and analyzed. The unique properties of the plasmas that can be generated by operating the machine with reduced parameters (lower magnetic fields and plasma currents) relative to those needed to achieve ignition are identified. A key feature of this operation is the relatively fast duty cycle that can be maintained. The Ideal Ignition Conditions, under which the density barrier due to bremsstrahlung emission in high density plasmas is removed, can be attained in this case. The plasma heating cycles are identified for which the contribution of ICRH is used both to enter the H-regime and to optimize the time needed for ignition. The on going effort to set up a test ICRH facility is described. The initial results (2 km/sec) of the high speed pellet injection system developed for Ignitor and operated at Oak Ridge are reported. The combined structural analysis and integration of the entire machine core (Load Assembly) is discussed. The adopted control system for both the machine and the plasma column has been designed and is described. The design solutions of the vertical field coils made of MgB2 and operating at 10 K have been identified and the relevant R&D program is underway. The analysis of the Caorso site and of its facility for the operation of the Ignitor with approved safety standards is completed. The relevant results are being made available for the operation of Ignitor at the Triniti site within the framework of the Italy-Russia agreement on the joint construction and operation of the Ignitor facility. A development effort concerning the advanced diagnostic systems that is being carried out for fusion burning plasma regimes is described. An initial analysis of the characteristics of a neutron source based on a system of Ignitor-like machines is reported

Development of a concept and basis for the DEMO diagnostic and control system

An initial concept for the plasma diagnostic and control (D&C) system has been developed as part of European studies towards the development of a demonstration tokamak fusion reactor (DEMO). The main objective is to develop a feasible, integrated concept design of the DEMO D&C system that can provide reliable plasma control and high performance (electricity output) over extended periods of operation. While the fusion power is maximized when operating near to the operational limits of the tokamak, the reliability of operation typically improves when choosing parameters significantly distant from these limits. In addition to these conflicting requirements, the D&C development has to cope with strong adverse effects acting on all in vessel components on DEMO (harsh neutron environment, particle fluxes, temperatures, electromagnetic forces, etc.). Moreover, space allocation and plasma access are constrained by the needs for first wall integrity and optimization of tritium breeding. Taking into account these boundary conditions, the main DEMO plasma control issues have been formulated, and a list of diagnostic systems and channels needed for plasma control has been developed, which were selected for their robustness and the required coverage of control issues. For a validation and refinement of this concept, simulation tools are being refined and applied for equilibrium, kinetic and mode control studies

Epigenetic switch at Atp2a2 and Myh7 gene promoters in pressure overload-induced heart failure

Re-induction of fetal genes and/or re-expression of postnatal genes represent hallmarks of pathological cardiac remodeling, and are considered important in the progression of the normal heart towards heart failure (HF). Whether epigenetic modifications are involved in these processes is currently under investigation. Here we hypothesized that histone chromatin modifications may underlie changes in the gene expression program during pressure overload-induced HF. We evaluated chromatin marks at the promoter regions of the sarcoplasmic reticulum Ca(2+)ATPase (SERCA-2A) and β-myosin-heavy chain (β-MHC) genes (Atp2a2 and Myh7, respectively) in murine hearts after one or eight weeks of pressure overload induced by transverse aortic constriction (TAC). As expected, all TAC hearts displayed a significant reduction in SERCA-2A and a significant induction of β-MHC mRNA levels. Interestingly, opposite histone H3 modifications were identified in the promoter regions of these genes after TAC, including H3 dimethylation (me2) at lysine (K) 4 (H3K4me2) and K9 (H3K9me2), H3 trimethylation (me3) at K27 (H3K27me3) and dimethylation (me2) at K36 (H3K36me2). Consistently, a significant reduction of lysine-specific demethylase KDM2A could be found after eight weeks of TAC at the Atp2a2 promoter. Moreover, opposite changes in the recruitment of DNA methylation machinery components (DNA methyltransferases DNMT1 and DNMT3b, and methyl CpG binding protein 2 MeCp2) were found at the Atp2a2 or Myh7 promoters after TAC. Taken together, these results suggest that epigenetic modifications may underlie gene expression reprogramming in the adult murine heart under conditions of pressure overload, and might be involved in the progression of the normal heart towards HF

Genetic deletion of uncoupling protein 3 exaggerates apoptotic cell death in the ischemic heart leading to heart failure

BACKGROUND: Uncoupling protein 3 (ucp3) is a member of the mitochondrial anion carrier superfamily of proteins uncoupling mitochondrial respiration. In this study, we investigated the effects of ucp3 genetic deletion on mitochondrial function and cell survival under low oxygen conditions in vitro and in vivo. METHODS AND RESULTS: To test the effects of ucp3 deletion in vitro, murine embryonic fibroblasts and adult cardiomyocytes were isolated from wild-type (WT, n=67) and ucp3 knockout mice (ucp3(-/-), n=70). To test the effects of ucp3 genetic deletion in vivo, myocardial infarction (MI) was induced by permanent coronary artery ligation in WT and ucp3(-/-) mice. Compared with WT, ucp3(-/-) murine embryonic fibroblasts and cardiomyocytes exhibited mitochondrial dysfunction and increased mitochondrial reactive oxygen species generation and apoptotic cell death under hypoxic conditions in vitro (terminal deoxynucleotidyl transferase-dUTP nick end labeling-positive nuclei: WT hypoxia, 70.3 ± 1.2%; ucp3(-/-) hypoxia, 85.3 ± 0.9%; P<0.05). After MI, despite similar areas at risk in the 2 groups, ucp3(-/-) hearts demonstrated a significantly larger infarct size compared with WT (infarct area/area at risk: WT, 48.2 ± 3.7%; ucp3(-/-), 65.0 ± 2.9%; P<0.05). Eight weeks after MI, cardiac function was significantly decreased in ucp3(-/-) mice compared with WT (fractional shortening: WT MI, 42.7 ± 3.1%; ucp3(-/-) MI, 24.4 ± 2.9; P<0.05), and this was associated with heightened apoptotic cell death (terminal deoxynucleotidyl transferase-dUTP nick end labeling-positive nuclei: WT MI, 0.7 ± 0.04%; ucp3(-/-) MI, 1.1 ± 0.09%, P<0.05). CONCLUSIONS: Our data indicate that ucp3 levels regulate reactive oxygen species levels and cell survival during hypoxia, modulating infarct size in the ischemic heart