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La falta de estandarización en los sistemas de telecontrol de regadío dificulta enormemente la gestión y el mantenimiento de los mismos, pero no menos importante es reconocer que dificulta la explotación de las propias infraestructuras modernizadas. El proyecto MEGA define los criterios para establecer interoperabilidad entre los diferentes sistemas de control y gestión que se emplean en el regadío. Dicha interoperabilidad se basa en el establecimiento de una nueva arquitectura de control a través de la cual se comuniquen los diferentes sistemas mediante un lenguaje de modelización desarrollado exprofeso. El desarrollo teórico de la modelización y el diseño de la nueva arquitectura tienen un largo recorrido y son conocidos por todo el sector. Se pretende presentar a continuación cómo se ha procedido a la validación empírica de esas bases teóricas estableciéndose una interoperabilidad real entre diferentes sistemas, participando en las pruebas diferentes agentes del sector del regadío., The lack of standardization of telecontrol systems for irrigation complicates their management and maintenance as well as the exploitation of modernized infrastructures. The MEGA project defines the criteria for establishing interoperability between different control and management systems used in irrigation. Such interoperability is based on the establishment of a new control architecture enabling the communication of various systems by a modeling language developed for this purpose. The theoretical development of modeling and design of the new architecture have a long way and are known throughout the sector. In this work we present the procedure to empirical validation of these theoretical bases, establishing a real interoperability between different systems, participating different operators from the irrigation sector in the testing.

Triple-negative breast cancer (TNBC) is an aggressive form of breast cancer. Despite response to chemotherapy, relapses are frequent and resistance to available treatments is often seen in the metastatic setting. Therefore, identification of new therapeutic targets is required. With this aim, we have profiled the activation status of 44 receptor tyrosine kinases (RTKs) and their major signaling pathways in patient-derived TNBC tumors. Frequent co-activation of several RTKs as well as the extracellular signal-regulated protein kinases 1 and 2 (Erk1/2) and mammalian target of rapamycin (mTOR) routes was found. Pharmacologic targeting of the activated kinases indicated that agents that attack the mTOR route are more potent and efficient antitumoral treatments than agents targeting RTKs. mTOR signals through two multiprotein complexes, mTORC1 and mTORC2. We used a genetic approach to explore the contribution of each of the two mTOR branches to the regulation of cell number of TNBC cells. RNA interference experiments indicated that mTORC1 predominated over mTORC2 in the control of TNBC cell proliferation. Moreover, RNA interference of mTOR had a superior antiproliferative action than separately acting on mTORC1 or mTORC2. To analyze the relevance of mTOR targeting in vivo, we used mice with TNBC. Treatment of these mice with BEZ235, a drug that targets mTOR, slowed tumor growth. Mechanistically, BEZ235 delayed cell cycle progression without affecting cell viability. Our results show that TNBCs are particularly sensitive to inhibition of the mTOR pathway, and indicate that mTOR targeting may be a more efficient anti-TNBC therapy than exclusively acting on the mTORC1 branch of the pathway. This is relevant as most mTOR inhibitors used in the clinic act on mTORC1. Collectively with the fact that BEZ235 synergized with drugs commonly used in the treatment of TNBC, our data support the clinical development of agents that act on mTOR as a therapy for this disease.