28 research outputs found

    Faecal contamination of water and sediment in the rivers of the Scheldt drainage network

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    The Scheldt watershed is characterized by a high population density, intense industrial activities and intensive agriculture and breeding. A monthly monitoring (n = 16) of the abundance of two faecal indicator bacteria (FIB), Escherichia coli and intestinal enterococci (IE), showed that microbiological water quality of the main rivers of the Scheldt drainage network was poor (median values ranging between 1.4 × 103 and 4.0 × 105 E. coli (100 mL)−1 and between 3.4 × 102 and 7.6 × 104 IE (100 mL)−1). The Zenne River downstream from Brussels was particularly contaminated. Glucuronidase activity was measured in parallel and was demonstrated to be a valid surrogate for a rapid evaluation of E. coli concentration in the river waters. FIB were also investigated in the river sediments; their abundance was sometimes high (average values ranging between 2.1 × 102 and 3.3 × 105 E. coli g−1 and between 1.0 × 102 and 1.7 × 105 IE g−1) but was not sufficient to contribute significantly to the river water contamination during resuspension events, except for the Scheldt and the Nethe Rivers. FIB were also quantified in representative point sources (wastewater treatment plants) and non-point sources (runoff water and soil leaching on different types of land use) of faecal contamination. The comparison of the respective contribution of point and non-point sources at the scale of the Scheldt watershed showed that point sources were largely predominant.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

    Copy number polymorphism in Fcgr3 predisposes to glomerulonephritis in rats and humans.

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    Identification of the genes underlying complex phenotypes and the definition of the evolutionary forces that have shaped eukaryotic genomes are among the current challenges in molecular genetics. Variation in gene copy number is increasingly recognized as a source of inter-individual differences in genome sequence and has been proposed as a driving force for genome evolution and phenotypic variation. Here we show that copy number variation of the orthologous rat and human Fcgr3 genes is a determinant of susceptibility to immunologically mediated glomerulonephritis. Positional cloning identified loss of the newly described, rat-specific Fcgr3 paralogue, Fcgr3-related sequence (Fcgr3-rs), as a determinant of macrophage overactivity and glomerulonephritis in Wistar Kyoto rats. In humans, low copy number of FCGR3B, an orthologue of rat Fcgr3, was associated with glomerulonephritis in the autoimmune disease systemic lupus erythematosus. The finding that gene copy number polymorphism predisposes to immunologically mediated renal disease in two mammalian species provides direct evidence for the importance of genome plasticity in the evolution of genetically complex phenotypes, including susceptibility to common human disease
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