Reliability-based optimal design of water distribution networks

A considerable amount of research has been carried out on the reliability analysis and optimal design of water distribution systems, and it has been reported that each of the above problems is very difficult to solve (Eiger et al. 1994; Wagner et al. 1988). The authors are therefore to be commended for their work, which directly incorporated a sophisticated probabilistic reliability model into an optimization routine. The paper had other interesting and useful aspects, which, unfortunately, will not be elaborated upon here

Reliability and tolerance comparison in water supply networks

The final publication is available at Springer via http://dx.doi.org/10.1007/s11269-010-9753-2Urban water supply is a high priority service and so looped networks are extensively used in order to considerably reduce the number of consumers affected by a failure. Looped networks may be redundant in connectivity and capacity. The concept of reliability has been introduced in an attempt to quantitatively measure the possibility of maintaining an adequate service for a given period. Numerous researchers have considered reliability as a measure of redundancy. This concept is usually implicit, but some researchers have even stated it explicitly. This paper shows why reliability cannot be considered a measure of redundancy given that branched networks can achieve high values of reliability and this would deny the fact that a looped network is more reliable than a branched network with a similar layout and size. To this end the paper discusses two quantitative indices for measuring expected network behavior: reliability and tolerance. These indices are calculated and a comparison is made between looped, branched, and mixed networks. © 2011 Springer Science+Business Media B.V.The authors wish to acknowledge the support received from project IDAWAS, DPI2009-11591, of the Directorate-General of Research at the Spanish Ministry of Education, the grant PAID-02-09 for a stay at the Universidad Politecnica de Valencia by the first author, and a grant MAEC-AECI 0000202066 awarded to the second author by the Ministerio de Asuntos Exteriores y Cooperacion of Spain. The use of English in this paper was revised by John Rawlins; and the revision was funded by the Universidad Politecnica de Valencia, Spain.Martínez-Rodríguez, JB.; Montalvo Arango, I.; Izquierdo Sebastián, J.; Pérez García, R. (2011). Reliability and tolerance comparison in water supply networks. 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Paraoxonase-1 is related to inflammation, fibrosis and PPAR delta in experimental liver disease

<p>Abstract</p> <p>Background</p> <p>Paraoxonase-1 (PON1) is an antioxidant enzyme synthesized by the liver. It protects against liver impairment and attenuates the production of the pro-inflammatory monocyte chemoattractant protein-1 (MCP-1). We investigated the relationships between hepatic PON1 and MCP-1 expression in rats with liver disease and explored the possible molecular mechanisms involved.</p> <p>Methods</p> <p>CCl₄was administered for up to 12 weeks to induce liver damage. Serum and hepatic levels of PON1 and MCP-1, their gene and protein expression, nuclear transcription factors, and histological and biochemical markers of liver impairment were measured.</p> <p>Results</p> <p>High levels of PON1 and MCP-1 expression were observed at 12^thweek in the hepatocytes surrounding the fibrous septa and inflammatory areas. CCl₄-administered rats had an increased hepatic PON1 concentration that was related to decreased gene transcription and inhibited protein degradation. Decreased PON1 gene transcription was associated with PPARδ expression. These changes were accompanied by increased hepatic MCP-1 concentration and gene expression. There were significant direct relationships between hepatic PON1 and MCP-1 concentrations (P = 0.005) and between PON1 and the amount of activated stellate cells (P = 0.001).</p> <p>Conclusion</p> <p>Our results from this experimental model suggest a hepato-protective role for PON1 against inflammation, fibrosis and liver disease mediated by MCP-1.</p