Embedded Systems Requirements Verification Using HiLeS Designer

International audienceOne of the issues related to systems design is the early verification in first design steps: system specifications verification. Nowadays, it is common to use text-based specifications to begin a system design. However, these specifications cannot be verified until a software model is made. In this work, we show how can we use HiLeS Designer to model and verify, formally and by simulation an embedded system specification. This tool makes easier to build the model, using graphical concepts which are familiar to designers. It also helps to verify formally the structure and some logical behavior, and by simulation, it is possible to verify the consistence of the embedded system specification. We model and verify System Display Selector Requirements applying HiLeS Designer

Serine residue 115 of MAPK-activated protein kinase MK5 is crucial for its PKA-regulated nuclear export and biological function

The mitogen-activated protein kinase-activated protein kinase-5 (MK5) resides predominantly in the nucleus of resting cells, but p38MAPK, extracellular signal-regulated kinases-3 and -4 (ERK3 and ERK4), and protein kinase A (PKA) induce nucleocytoplasmic redistribution of MK5. The mechanism by which PKA causes nuclear export remains unsolved. In the study reported here we demonstrated that Ser-115 is an in vitro PKA phosphoacceptor site, and that PKA, but not p38MAPK, ERK3 or ERK4, is unable to redistribute MK5 S115A to the cytoplasm. However, the phosphomimicking MK5 S115D mutant resides in the cytoplasm in untreated cells. While p38MAPK, ERK3 and ERK4 fail to trigger nuclear export of the kinase dead T182A and K51E MK5 mutants, S115D/T182A and K51E/S115D mutants were able to enter the cytoplasm of resting cells. Finally, we demonstrated that mutations in Ser-115 affect the biological properties of MK5. Taken together, our results suggest that Ser-115 plays an essential role in PKA-regulated nuclear export of MK5, and that it also may regulate the biological functions of MK5

Comportement d’une réparation en escalier obtenue par Jet d’Eau Abrasif

National audienceDes éprouvettes carbone/époxy pour évaluer la qualité d’une réparation en escalier sont usinées, réparées puis testées mécaniquement. L’usinage préalable à la phase de réparation est effectué par Jet d’Eau abrasif, sous forme de marches régulières de ratio 1/30, et dont la profondeur correspond à l’épaisseur d’un pli. Le relâchement des contraintes résiduelles observé pendant la phase d’usinage est quantifié grâce à la technique de mesure de champs par stéréovision, et simulé par EF. La plaque usinée est ensuite reconstruite par remplacement des plis usinés, et cocuit en autoclave. Le schéma de stratification de la partie réparée est décalé d’un pli par rapport à la zone initiale, de manière à restituer le transfert de charges. Des éprouvettes sont découpées dans les plaques réparées, et sollicitées en traction. Les résultats montrent que les charges à rupture obtenues atteignent 70 % des charges à rupture d’éprouvettes «vierges». L’analyse des fragments des éprouvettes démontre que la rupture de la zone de collage dans les interfaces 0/0 est à l’origine de la rupture finale de toutes les éprouvettes. Le croisement essais/calcul conduit à l’évaluation d’un critère de rupture en contrainte de cisaillement admissible pour l’interface zone parent/patch

The function, mechanisms, and role of the genes PTEN and TP53 and the effects of asbestos in the development of malignant mesothelioma : a review focused on the genes' molecular mechanisms.

The malignant mesothelioma is an aggressive form of cancer with a mean survival rate of less than a year. Moreover, environmental exposure to minerals is an important factor in the development of malignant mesothelioma (MM), especially the mineral asbestos, which has a well-documented role in MM, and more recently, the mineral erionite has been proven to be a strong carcinogenic inducer of MM. In addition, the virus simian virus 40 has been implicated as a cocarcinogenic player in MM. However, the molecular mechanisms involved in the pathogenesis of this cancer are still not fully understood. Indeed, it is known that several genes are altered ormutated inMM, among those are p16INK4A, p14ARF, and neurofibromatosis type II. Furthermore, TP53 has been reported to be mutated in the majority of the cancers; however, inMM, it is very uncommon mutations in this gene. Also, the PTEN gene has been shown to play an important role in endometrial cancer and glioblastoma, although the role of PTEN in MM has yet to be established. Taken altogether, this review focuses on the historical aspects, molecular mechanisms, interaction with other genes and proteins, and the role of these genes inMM. Lastly, this review questions the cancer theory of the two hits because the functions of both PTEN and TP53 are not fully explained by this theory