Automatic control of an active vibration damping system

This work deals with the automatic control of an active vibration damping system . The basic mechanical system is made of two motors driving two unbalanced masses. This equipment, tied to the axe, creates an antagonistic vibration . This torque can be tuned to be exactly opposite to the initial vibration . However, a direct measure of the characteristics of the initial vibration is not available . Thus, it is crucial to get a real time estimation of the vibration parameters (frequency and phase) from the residual torque . The identification is performed by means of extended Kalman filtering based on a special convenient model. At the same Lime, the control law of the motors is implemented .L'étude présentée ici consiste à définir le pilotage d'un étouffeur actif de vibrations constitué par deux ensembles supportant chacun deux moteurs qui entraînent des balourds en rotation. Ces ensembles sont fixés sur la structure vibrante et le mouvement des balourds crée une vibration antagoniste. En réglant correctement la vitesse de rotation et le déphasage des différentes masses excentrées, il est possible de créer un couple qui s'oppose exactement au couple perturbateur inconnu, ce qui revient à annuler le couple résiduel. Une contrainte technique impose cependant de se passer de toute mesure directe de la vibration à atténuer. Il est donc fondamental d'estimer le plus précisément possible en temps réel, les caractéristiques (fréquences et phases) du couple perturbateur à partir de la simple mesure de l'accélération induite par la vibration résiduelle mesurée sur un bâti solidaire de l'axe en rotatio

Separation of Recombination and SOS Response in Escherichia coli RecA Suggests LexA Interaction Sites

RecA plays a key role in homologous recombination, the induction of the DNA damage response through LexA cleavage and the activity of error-prone polymerase in Escherichia coli. RecA interacts with multiple partners to achieve this pleiotropic role, but the structural location and sequence determinants involved in these multiple interactions remain mostly unknown. Here, in a first application to prokaryotes, Evolutionary Trace (ET) analysis identifies clusters of evolutionarily important surface amino acids involved in RecA functions. Some of these clusters match the known ATP binding, DNA binding, and RecA-RecA homo-dimerization sites, but others are novel. Mutation analysis at these sites disrupted either recombination or LexA cleavage. This highlights distinct functional sites specific for recombination and DNA damage response induction. Finally, our analysis reveals a composite site for LexA binding and cleavage, which is formed only on the active RecA filament. These new sites can provide new drug targets to modulate one or more RecA functions, with the potential to address the problem of evolution of antibiotic resistance at its root

Rad51 Inhibits Translocation Formation by Non-Conservative Homologous Recombination in Saccharomyces cerevisiae

Chromosomal translocations are a primary biological response to ionizing radiation (IR) exposure, and are likely to result from the inappropriate repair of the DNA double-strand breaks (DSBs) that are created. An abundance of repetitive sequences in eukaryotic genomes provides ample opportunity for such breaks to be repaired by homologous recombination (HR) between non-allelic repeats. Interestingly, in the budding yeast, Saccharomyces cerevisiae the central strand exchange protein, Rad51 that is required for DSB repair by gene conversion between unlinked repeats that conserves genomic structure also suppresses translocation formation by several HR mechanisms. In particular, Rad51 suppresses translocation formation by single-strand annealing (SSA), perhaps the most efficient mechanism for translocation formation by HR in both yeast and mammalian cells. Further, the enhanced translocation formation that emerges in the absence of Rad51 displays a distinct pattern of genetic control, suggesting that this occurs by a separate mechanism. Since hypomorphic mutations in RAD51 in mammalian cells also reduce DSB repair by conservative gene conversion and stimulate non-conservative repair by SSA, this mechanism may also operate in humans and, perhaps contribute to the genome instability that propels the development of cancer