When a FILTER Makes the Difference in Continuously Answering SPARQL Queries on Streaming and Quasi-Static Linked Data

We are witnessing a growing interest for Web applications that (i) require to continuously combine highly dynamic data stream with background data and (ii) have reactivity as key performance indicator. The Semantic Web community showed that RDF Stream Processing (RSP) is an adequate framework to develop this type of applications. However, when the background data is distributed over theWeb, even RSP engines risk losing reactiveness due to the time necessary to access the background data. State-of-the-art RSP engines remain reactive using a local replica of the background data, but such a replica progressively become stale if not updated to reflect the changes in the remote background data. For this reason, recently, the RSP community investigated maintenance policies (collectively named Acqua) that guarantee reactiveness while maximizing the freshness of the replica. Acquaâ\u80\u99s policies apply to queries that join a basic graph pattern in a window clause with another basic graph pattern in a service clause. In this paper, we extend the class of queries considered in Acqua adding a FILTER clause that selects mapping in the background data. We propose a new maintenance policy (namely, the Filter Update Policy) and we show how to combine it with Acqua policies. A set of experimental evaluations empirically proves the ability of the proposed policies to guarantee reactiveness while keeping the replica fresher than with the Acqua policies

ConnecTown...ConnecToMi

Urban computing project originated from the aim to apply and experiment a new analytical approach to the city of Turin and Milan by improving different kinds of social connections through the use of widespread technologies such as Wi-Fi and smartphones

Malattie cardiovascolari e anafilassi: Il ruolo del mastocita cardiaco

Anaphylaxis is a clinical syndrome often presenting as a medical emergency requiring immediate recognition of symptoms, proper treatment and, if possible, the identification and elimination of risk factors. The symptoms of anaphylaxis are mainly determined by chemicals mediators released upon activation of the immune cells. Mast cells which are abundant in cardiovascular tissues, are the main cells activated during anaphylaxis. Human cardiac mast cells have been identified at the site of sarcolemma, within perivascular tissues, in the adventitia of large coronary arteries, and within coronary plaques. Cardiac mast cells display unique immunological and functional features that make them distinct from mast cells in other tissues. Mast cells play a complex role in the development of several pathological processes in the heart. High affinity receptors for IgE (FcṘI) and for C5a anaphylatoxin are involved in development of systemic and cardiac anaphylactic reactions. Furthermore, in myocardial ischemia, mast cell mediators contribute to coronary vasoconstriction, arhythmias, leukocyte recruitment, and tissue injury and repair. In coronary atherosclerosis, mast cell mediators facilitate cholesterol accumulation and plaque destabilization. In cardiac failure, mast cell chymase causes myocyte apoptosis and fibroblast proliferation, leading to ventricular dysfunction. Chymase and tryptase also contribute to fibrosis in cardiomyopathies and myocarditis. In addition, mast cell-derived TNF-α promotes myocardial remodeling. Cardiac mast cells might contribute to the evolution of atherosclerosis, dilated cardiomyopathy, cardiac and systemic anaphylaxis through the release of cytokines and vasoactive and proinflammatory mediators. It has recently been reported that cardiac mast cells contain and release renin, which initiates local angiotensin formation. Angiotensin causes coronary vasoconstriction, arrhythmias, fibrosis, apoptosis, and endothelin release. In addition, preexisting cardiovascular disease as well as mastocytosis with elevated serum tryptase levels are risk factors for fatal anaphylaxis and for the occurrence of myocardial or cerebrovascular ischemia associated with anaphylaxis. Thus, cardiac mast cells play a primary role not only in anaphylaxis but also in determining the severity and outcome of ischemic heart disease