Recently, slab track systems have arisen as a safer and more sustainable option for high speed railway infrastructures, compared to traditional ballasted tracks. Integrating Wireless Sensor Networks within these infrastructures can provide structural health related data that can be used to evaluate their degradation and to not only detect failures but also to predict them. The design of such systems has to deal with a scenario of large areas with inaccessible zones, where neither Internet coverage nor electricity supply is guaranteed.
View Article and Find Full Text PDFWe recently identified that the MEK/ERK1/2 pathway synergized with retinoic acid (RA) to restore both transcriptional activity and RA-induced differentiation in RA-resistant acute promyelocytic leukemia (APL) cells. To target the MEK/ERK pathway, we identified glycogen synthase kinase-3β (GSK-3β) inhibitors including lithium chloride (LiCl) as activators of this pathway in APL cells. Using NB4 (RA-sensitive) and UF-1 (RA-resistant) APL cell lines, we observed that LiCl as well as synthetic GSK-3β inhibitors decreased proliferation, induced apoptosis and restored, in RA-resistant cells, the expression of RA target genes and the RA-induced differentiation.
View Article and Find Full Text PDFWireless Sensor Networks constitute pervasive and distributed computing systems and are potentially one of the most important technologies of this century. They have been specifically identified as a good candidate to become an integral part of the protection of critical infrastructures. In this paper we focus on railway infrastructure protection and we present the details of a sensor platform designed to be integrated into a slab track system in order to carry out both installation and maintenance monitoring activities.
View Article and Find Full Text PDFThe induction of the granulocytic differentiation of leukemic cells by all-trans retinoic acid (RA) has been a major breakthrough in terms of survival for acute promyelocytic leukemia (APL) patients. Here we highlight the synergism and the underlying novel mechanism between RA and the granulocyte colony-stimulating factor (G-CSF) to restore differentiation of RA-refractory APL blasts. First, we show that in RA-refractory APL cells (UF-1 cell line), PML-RA receptor alpha (RARα) is not released from target promoters in response to RA, resulting in the maintenance of chromatin repression.
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