Design and implementation of an interoperable architecture for integrating building legacy systems into scalable energy management systems

The building sector is responsible for a significant amount of energy consumption and greenhouse gas (GHG) emissions. Thus, the monitoring, control and optimization of energy consumption in buildings will play a critical role in the coming years in improving energy efficiency in the building sector and in reducing greenhouse gas emissions. However, while there are a significant number of studies on how to make buildings smarter and manage energy through smart devices, there is a need for more research on integrating buildings with legacy equipment and systems. It is therefore vital to define mechanisms to improve the use of energy efficiency in existing buildings. This study proposes a new architecture (PHOENIX architecture) for integrating legacy building systems into scalable energy management systems with focus also on user comfort in the concept of interoperability layers. This interoperable and intelligent architecture relies on Artificial Intelligence/Machine Learning (AI/ML) and Internet of Things (IoT) technologies to increase building efficiency, grid flexibility and occupant well-being. To validate the architecture and demonstrate the impact and replication potential of the proposed solution, five demonstration pilots have been utilized across Europe. As a result, by implementing the proposed architecture in the pilot sites, 30 apartments and four commercial buildings with more than 400 devices have been integrated into the architecture and have been communicating successfully. In addition, six Trials were performed in a commercial building and five key performance indicators (KPIs) were measured in order to evaluate the robust operation of the architecture. Work is still ongoing for the trials and the KPIs’ analysis after the implementation of PHOENIX architecture at the rest of the pilot sites

Angiotensin II Requires Zinc and Downregulation of the Zinc Transporters ZnT3 and ZnT10 to Induce Senescence of Vascular Smooth Muscle Cells

Senescence, a hallmark of mammalian aging, is associated with the onset and progression of cardiovascular disease. Angiotensin II (Ang II) signaling and zinc homeostasis dysfunction are increased with age and are linked to cardiovascular disease, but the relationship among these processes has not been investigated. We used a model of cellular senescence induced by Ang II in vascular smooth muscle cells (VSMCs) to explore the role of zinc in vascular dysfunction. We found that Ang II-induced senescence is a zinc-dependent pathway mediated by the downregulation of the zinc transporters ZnT3 and ZnT10, which work to reduce cytosolic zinc. Zinc mimics Ang II by increasing reactive oxygen species (ROS), activating NADPH oxidase activity and Akt, and by downregulating ZnT3 and ZnT10 and inducing senescence. Zinc increases Ang II-induced senescence, while the zinc chelator TPEN, as well as overexpression of ZnT3 or ZnT10, decreases ROS and prevents senescence. Using HEK293 cells, we found that ZnT10 localizes in recycling endosomes and transports zinc into vesicles to prevent zinc toxicity. Zinc and ZnT3/ZnT10 downregulation induces senescence by decreasing the expression of catalase. Consistently, ZnT3 and ZnT10 downregulation by siRNA increases ROS while downregulation of catalase by siRNA induces senescence. Zinc, siZnT3 and siZnT10 downregulate catalase by a post-transcriptional mechanism mediated by decreased phosphorylation of ERK1/2. These data demonstrate that zinc homeostasis dysfunction by decreased expression of ZnT3 or ZnT10 promotes senescence and that Ang II-induced senescence is a zinc and ROS-dependent process. Our studies suggest that zinc might also affect other ROS-dependent processes induced by Ang II, such as hypertrophy and migration of smooth muscle cells