International audienceThe AVANTSSAR Platform is an integrated toolset for the formal specification and automated validation of trust and security of service-oriented architectures and other applications in the Internet of Services. The platform supports application-level specification languages (such as BPMN and our custom languages) and features three validation backends (CL-AtSe, OFMC, and SATMC), which provide a range of complementary automated reasoning techniques (including service orchestration, compositional reasoning, model checking, and abstract interpretation). We have applied the platform to a large number of industrial case studies, collected into the AVANTSSAR Library of validated problem cases. In doing so, we unveiled a number of problems and vulnerabilities in deployed services. These include, most notably, a serious flaw in the SAML-based Single Sign-On for Google Apps (now corrected by Google as a result of our findings). We also report on the migration of the platform to industry

Evidence underlines the importance of microRNAs (miRNAs) in the pathogenesis of multiple sclerosis (MS). Based on the fact that miRNAs are present in human biological fluids, we previously showed that miR-223, miR-23a and miR-15b levels were downregulated in the sera of MS patients versus controls. Here, the expression levels of these candidate miRNAs were determined in peripheral blood mononuclear cells (PBMCs) and the serum of MS patients, in addition to three genotyped single nucleotide polymorphisms (SNPs). Mapping in the genomic regions of miR-223, miR-23a and miR-15b genes, 399 cases and 420 controls were tested. Expression levels of miR-223 and miR-23a were altered in PBMCs from MS patients versus controls. Conversely, there were no differences in the expression levels of miR-15b. A significantly decreased genotypic frequency of miR-223 rs1044165 T/T genotype was observed in MS patients. Moreover, the allelic frequency of miR-23a rs3745453 C allele was significantly increased in patients versus controls. In contrast, there were no differences in the distribution of miR-15b SNP. In conclusion, our results suggest that miR-223 and miR-23a could play a role in the pathogenesis of MS. Moreover, miR-223 rs1044165 polymorphism likely acts as a protective factor, while miR-23a rs3745453 variant seems to act as a risk factor for MS.