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La norma UNE-EN 13374 “Sistemas provisionales de protección de borde. Especificaciones del producto, métodos de ensayo” (1) clasifica los sistemas provisionales de protección de borde (SPPB) en tres clases (A, B y C), en función del ángulo de la superficie de trabajo y de la altura de caída de la persona a proteger. Los sistemas clase A son los indicados cuando la inclinación de la superficie de trabajo es menor de 10º. La norma establece los requisitos de flecha y de resistencia de los SPPB. Los requisitos se pueden comprobar tanto analítica como experimentalmente. El objetivo del trabajo ha sido la evaluación del comportamiento de los SPPB utilizados habitualmente en las obras y establecer los cambios necesarios para que cumplan con la norma UNE-EN 13374. Para ello se han evaluado analítica y experimentalmente tres SPPB clase A, fabricados con acero S235. Los resultados obtenidos muestran que, el sistema empleado de forma habitual en obras no supera los requisitos de la norma ni analítica ni experimentalmente. El tercer sistema supera los requisitos con las dos metodologías de análisis. El segundo sistema supera los requisitos cuando la evaluación se realiza analíticamente pero no cuando la vía utilizada es la experimental.

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Mechanically stressed cells display increased levels of fos message and protein. Although the intracellular signaling pathways responsible for FOS induction have been extensively characterized, we still do not understand the nature of the primary cell mechanotransduction event responsible for converting an externally acting mechanical stressor into an intracellular signal cascade. We now report that plasma membrane disruption (PMD) is quantitatively correlated on a cell-by-cell basis with fos protein levels expressed in mechanically injured monolayers. When the population of PMD-affected cells in injured monolayers was selectively prevented from responding to the injury, the fos response was completely ablated, demonstrating that PMD is a requisite event. This PMD-dependent expression of fos protein did not require cell exposure to cues inherent in release from cell–cell contact inhibition or presented by denuded substratum, because it also occurred in subconfluent monolayers. Fos expression also could not be explained by factors released through PMD, because cell injury conditioned medium failed to elicit fos expression. Translocation of the transcription factor NF-κB into the nucleus may also be regulated by PMD, based on a quantitative correlation similar to that found with fos. We propose that PMD, by allowing a flux of normally impermeant molecules across the plasma membrane, mediates a previously unrecognized form of cell mechanotransduction. PMD may thereby lead to cell growth or hypertrophy responses such as those that are present normally in mechanically stressed skeletal muscle and pathologically in the cardiovascular system.