Architecting the IoT Paradigm: A Middleware for Autonomous Distributed Sensor Networks

Actualizing Internet of Things undoubtedly constitutes a major challenge of modern computing and is a promising next step in realizing the unification of all seamlessly interacting entities, either human users or participating machines, under a shared, coherent architecture. While it has now become common belief that the related solutions should be based on compatible network infrastructure employing widely accepted communication schemes, the specifics of the intermediate system that would act as global interface for all involved “things” are yet to be determined. A rising trend to define such machine-based entities is through cyber-physical systems, in terms of collaborating elements with physical input and output. Certainly, sensor networks constitute the most representative realization of such systems. Taking these issues and opportunities under consideration, this work proposes a bioinspired distributed architecture for an Internet of Things that exhibits self-organization properties to enable efficient interaction between entities modeled as cyber-physical systems, mainly focusing on sensor networks. Furthermore, a middleware has been implemented according to the proposed architecture, which serves the role of the backbone of this network as a multiagent and autonomous distributed system. The evaluation results demonstrate the self-optimization properties of the introduced scheme and indicate global network convergence

Activation of the Fas/Fas ligand pathway in hypertensive renal disease in Dahl/Rapp rats

BACKGROUND: Hypertensive nephrosclerosis is the second most common cause of end-stage renal failure in the United States. The mechanism by which hypertension produces renal failure is incompletely understood. Recent evidence demonstrated that an unscheduled and inappropriate increase in apoptosis occurred in the Dahl/Rapp rat, an inbred strain of rat that uniformly develops hypertension and hypertensive nephrosclerosis; early correction of the hypertension prevents the renal injury. The present study examined the role of the Fas/FasL pathway in this process. METHODS: Young male Dahl/Rapp salt-sensitive (S) and Sprague-Dawley rats were fed diets that contained 0.3% or 8.0% NaCl diets. Kidneys were examined at days 7 and 21 of the study. RESULTS: An increase in Fas and FasL expression was observed in glomerular and tubular compartments of kidneys of hypertensive S rats, whereas dietary salt did not change expression of either of these molecules in normotensive Sprague-Dawley rats. Associated with this increase was cleavage of Bid and activation of caspase-8, the initiator caspase in this apoptotic pathway, by day 21 of the study. CONCLUSIONS: Augmented expression of apoptotic signaling by the Fas/FasL pathway occurred during development of end-stage renal failure in this model of hypertensive nephrosclerosis

Collaborative environment for energy-efficient buildings at an early design stage

This paper provides an approach for creating a collaborative environment for energy efficient buildings highlighting the issues required to be addressed at an early design phase. The paper will discuss a design scenario for a new built and suggest system architecture for implementing such scenario through the use of advanced simulation tools and modelling techniques to improve current practice in an early design phase. The suggested system architecture will allow multi-disciplinary teams to collectively and individually explore various energy solutions in a 3D interactive workspace to achieve optimum energy efficiency at building level

Essential Role of TGF-β/Smad Pathway on Statin Dependent Vascular Smooth Muscle Cell Regulation

BACKGROUND: The 3-hydroxy-3-methylglutaryl CoA reductase inhibitors (also called statins) exert proven beneficial effects on cardiovascular diseases. Recent data suggest a protective role for Transforming Growth Factor-beta (TGF-beta) in atherosclerosis by regulating the balance between inflammation and extracellular matrix accumulation. However, there are no studies about the effect of statins on TGF-beta/Smad pathway in atherosclerosis and vascular cells. METHODOLOGY: In cultured vascular smooth muscle cells (VSMCs) statins enhanced Smad pathway activation caused by TGF-beta. In addition, statins upregulated TGF-beta receptor type II (TRII), and increased TGF-beta synthesis and TGF-beta/Smad-dependent actions. In this sense, statins, through Smad activation, render VSMCs more susceptible to TGF-beta induced apoptosis and increased TGF-beta-mediated ECM production. It is well documented that high doses of statins induce apoptosis in cultured VSMC in the presence of serum; however the precise mechanism of this effect remains to be elucidated. We have found that statins-induced apoptosis was mediated by TGF-beta/Smad pathway. Finally, we have described that RhoA inhibition is a common intracellular mechanisms involved in statins effects. The in vivo relevance of these findings was assessed in an experimental model of atherosclerosis in apolipoprotein E deficient mice: Treatment with Atorvastatin increased Smad3 phosphorylation and TRII overexpression, associated to elevated ECM deposition in the VSMCs within atheroma plaques, while apoptosis was not detected. CONCLUSIONS: Statins enhance TGF-beta/Smad pathway, regulating ligand levels, receptor, main signaling pathway and cellular responses of VSMC, including apoptosis and ECM accumulation. Our findings show that TGF-beta/Smad pathway is essential for statins-dependent actions in VSMCs