Abnormal social behaviors and altered gene expression rates in a mouse model for Potocki-Lupski syndrome

The Potocki-Lupski syndrome (PTLS) is associated with a microduplication of 17p11.2. Clinical features include multiple congenital and neurobehavioral abnormalities and autistic features. We have generated a PTLS mouse model, Dp(11)17/+, that recapitulates some of the physical and neurobehavioral phenotypes present in patients. Here, we investigated the social behavior and gene expression pattern of this mouse model in a pure C57BL/6-Tyrc-Brd genetic background. Dp(11)17/+ male mice displayed normal home-cage behavior but increased anxiety and increased dominant behavior in specific tests. A subtle impairment in the preference for a social target versus an inanimate target and abnormal preference for social novelty (the preference to explore an unfamiliar mouse versus a familiar one) was also observed. Our results indicate that these animals could provide a valuable model to identify the specific gene(s) that confer abnormal social behaviors and that map within this delimited genomic deletion interval. In a first attempt to identify candidate genes and for elucidating the mechanisms of regulation of these important phenotypes, we directly assessed the relative transcription of genes within and around this genomic interval. In this mouse model, we found that candidates genes include not only most of the duplicated genes, but also normal-copy genes that flank the engineered interval; both categories of genes showed altered expression levels in the hippocampus of Dp(11)17/+ mic

DESARROLLO DE UN INSTRUMENTO VIRTUAL PARA EL BALANCEAMIENTO DINAMICO DE ROTORES DEVELOPMENT OF A VIRTUAL INSTRUMENT FOR ROTOR DYNAMICS BALANCING

El presente trabajo resalta la importancia del balanceamiento de rotores como principal herramienta dentro de las tareas correctivas del mantenimiento predictivo, con el fin de que se reduzcan las vibraciones y sus efectos secundarios en las máquinas rotatorias. Se ha desarrollado un instrumento virtual para el balanceamiento dinámico de rotores, basado en un sistema de adquisición de datos (SAD). El instrumento tiene incluidos todos los cálculos necesarios para balancear rotores en un plano y en dos planos, a partir de la medición de los datos de vibración, utilizando el procedimiento de los coeficientes de influencia o utilizando un procedimiento de medición sin fase. También se ha incluido un módulo para determinar la severidad vibratoria del rotor y un módulo de análisis de vibraciones, que incluye análisis espectral y de la forma de onda. Este instrumento virtual es una herramienta útil para el balanceamiento de rotores en laboratorio así como también en la industria.<br>This article highlights the importance of rotor balancing like the most important corrective action included in a predictive maintenance program, whose main objective is reducing the vibrations level and its secondary effect in rotary machines. A virtual instrument, based in a data acquisition system has been developed for rotor balancing. With this instrument it is possible to balance rotors in a single or two-plane, using the influence coefficient method or a no phase method. Also the instrument includes a function to determine the vibration severity and a function of vibration analysis with spectral and waveform analysis included. This virtual instrument is useful for rotor balancing in the laboratory as well as in the industry

Desarrollo de un instrumento virtual para el balanceamiento dinámico de rotores

El presente trabajo resalta la importancia del balanceamiento de rotores como principal herramienta dentro de las tareas correctivas del mantenimiento predictivo, con el fin de que se reduzcan las vibraciones y sus efectos secundarios en las máquinas rotatorias. Se ha desarrollado un instrumento virtual para el balanceamiento dinámico de rotores, basado en un sistema de adquisición de datos (SAD). El instrumento tiene incluidos todos los cálculos necesarios para balancear rotores en un plano y en dos planos, a partir de la medición de los datos de vibración, utilizando el procedimiento de los coeficientes de influencia o utilizando un procedimiento de medición sin fase. También se ha incluido un módulo para determinar la severidad vibratoria del rotor y un módulo de análisis de vibraciones, que incluye análisis espectral y de la forma de onda. Este instrumento virtual es una herramienta útil para el balanceamiento de rotores en laboratorio así como también en la industria

Abnormal social behaviors and altered gene expression rates in a mouse model for Potocki-Lupski syndrome.

The Potocki-Lupski syndrome (PTLS) is associated with a microduplication of 17p11.2. Clinical features include multiple congenital and neurobehavioral abnormalities and autistic features. We have generated a PTLS mouse model, Dp(11)17/+, that recapitulates some of the physical and neurobehavioral phenotypes present in patients. Here, we investigated the social behavior and gene expression pattern of this mouse model in a pure C57BL/6-Tyr(c-Brd) genetic background. Dp(11)17/+ male mice displayed normal home-cage behavior but increased anxiety and increased dominant behavior in specific tests. A subtle impairment in the preference for a social target versus an inanimate target and abnormal preference for social novelty (the preference to explore an unfamiliar mouse versus a familiar one) was also observed. Our results indicate that these animals could provide a valuable model to identify the specific gene(s) that confer abnormal social behaviors and that map within this delimited genomic deletion interval. In a first attempt to identify candidate genes and for elucidating the mechanisms of regulation of these important phenotypes, we directly assessed the relative transcription of genes within and around this genomic interval. In this mouse model, we found that candidates genes include not only most of the duplicated genes, but also normal-copy genes that flank the engineered interval; both categories of genes showed altered expression levels in the hippocampus of Dp(11)17/+ mice