A hierarchical architecture for an energy management system

This paper introduces an innovative energy management system architecture for Smart Grids, designed in the European 7th framework program project e-balance. The architecture is hierarchical and fractal-like, which results in better scalability and reuse of algorithms and programming code for energy management. It supports both micro-grids and distributed energy resources. The system is structured into two main parts – the communication platform and the energy management platform. The former provides a common data exchange layer, while the latter provides the local energy management logic, currently supporting energy balancing and grid resilience services. The system is being deployed in two pilots: in Portugal and in the Netherlands, where use cases on energy balancing, grid monitoring and grid reliability will be demonstrated

Innate immune response to viral infections in primary bronchial epithelial cells is modified by the atopic status of asthmatic patients

Purpose: In order to gain an insight into determinants of reported variability in immune responses to respiratory viruses in human bronchial epithelial cells (HBECs) from asthmatics, the responses of HBEC to viral infections were evaluated in HBECs from phenotypically heterogeneous groups of asthmatics and in healthy controls. Methods: HBECs were obtained during bronchoscopy from 10 patients with asthma (6 atopic and 4 non-atopic) and from healthy controls (n=9) and grown as undifferentiated cultures. HBECs were infected with parainfluenza virus (PIV)-3 (MOI 0.1) and rhinovirus (RV)-1B (MOI 0.1), or treated with medium alone. The cell supernatants were harvested at 8, 24, and 48 hours. IFN-α, CXCL10 (IP-10), and RANTES (CCL5) were analyzed by using Cytometric Bead Array (CBA), and interferon (IFN)-β and IFN-γ1 by ELISA. Gene expression of IFNs, chemokines, and IFN-regulatory factors (IRF-3 and IRF-7) was determined by using quantitative PCR. Results: PIV3 and RV1B infections increased IFN-γ1 mRNA expression in HBECs from asthmatics and healthy controls to a similar extent, and virus-induced IFN-γ1 expression correlated positively with IRF-7 expression. Following PIV3 infection, IP-10 protein release and mRNA expression were significantly higher in asthmatics compared to healthy controls (median 36.03-fold). No differences in the release or expression of RANTES, IFN-γ1 protein and mRNA, or IFN-α and IFN-β mRNA between asthmatics and healthy controls were observed. However, when asthmatics were divided according to their atopic status, HBECs from atopic asthmatics (n=6) generated significantly more IFN-γ1 protein and demonstrated higher IFN-α, IFN-β, and IRF-7 mRNA expressions in response to PIV3 compared to non-atopic asthmatics (n=4) and healthy controls (n=9). In response to RV1B infection, IFN-β mRNA expression was lower (12.39-fold at 24 hours and 19.37-fold at 48 hours) in non-atopic asthmatics compared to atopic asthmatics. Conclusions: The immune response of HBECs to virus infections may not be deficient in asthmatics, but seems to be modified by atopic status. © The Korean Academy of Asthma, Allergy and Clinical Immunology • The Korean Academy of Pediatric Allergy and Respiratory Disease

Inhibition of mast cell-dependent anaphylaxis by sodium salicylate

Sodium salicylate (NaSal) is a commonly used agent with a wide pharmacological spectrum. The objective of the present study was to investigate the effect of NaSal on anaphylaxis. NaSal (10−1 and 1 mm) significantly inhibited systemic anaphylaxis induced by compound 48/80 in rats. NaSal also significantly inhibited local anaphylaxis activated by anti-dinitrophenyl (DNP) immunoglobulin E (IgE). NaSal (10−1 and 1 mm) significantly inhibited histamine release from rat peritoneal mast cells (RPMC) activated by compound 48/80 or anti-DNP IgE. Northern-blot analysis demonstrated that a significantly reduced level of the mRNA of l-histidine decarboxylase was expressed in mast cells treated with NaSal, compared with that without NaSal. NaSal (10−2 and 10−1 mm) had a significant inhibitory effect on anti-DNP IgE-induced tumour necrosis factor-α secretion from RPMC. The level of cyclic AMP in RPMC, when NaSal (1 mm) was added, transiently and significantly increased about sixfold compared with that of basal cells. These results suggest a possible use of NaSal in managing mast cell-dependent anaphylaxis