In Situ Contaminated Sediments Project – Work Package 1A Report

Project aims Defra is seeking to understand the magnitude of risks (e.g. to aquatic ecology and human health) or impacts (e.g. on the way that water bodies are managed) posed by contaminated sediment in England, as part of its work towards meeting its environmental objectives. In the context of this project, in-situ contaminated sediment is defined as: Chemically contaminated sediment within the water column, bed, banks and floodplain of a surface water body that has been transported alongside the normal sediment load and deposited by fluvial or coastal processes. This project considers the risk posed by non-agricultural diffuse pollution sources in England that result in the contamination of in-situ sediments (for example, contamination from toxic metals, hydrocarbons and surfactants). The scope encompasses both freshwater and marine sediments in England and extends to one nautical mile off-shore (the seaward limit of coastal waters under the Water Framework Directive (WFD) in England). Previous national strategies, including the 2007 Defra UK Strategy for Managing Contaminated Marine Sediments (CDMS), focussed on characterising the risks associated with contaminated sediments in the marine environment. However, while extensive research has been carried out in many locations (including as part of WFD implementation studies) and for particular sources of contamination (e.g. historical metal mining; Environment Agency, 2008) there has not been a comprehensive overview of sediment contamination on a national scale. This project seeks to build on the existing evidence base, drawing together information on the freshwater environment to complement that already gathered for marine waters. This project’s overall aim is to provide a sound evidence base on the contamination of in-situ sediments, which can underpin the development of tools and methods that will help Defra, the Environment Agency and other bodies engaged in regulation and protection of water quality

Genomic analysis of human and mouse TCL1 loci reveals a complex of tightly clustered genes

TCL1 and TCL1b genes on human chromosome 14q23.1 are activated in T cell leukemias by translocations and inversions at 14q32.1, juxtaposing them to regulatory elements of T cell receptor genes. In this report we present the cloning, mapping, and expression analysis of the human and murine TCL1/Tcl1 locus. In addition to TCL1 and TCL1b, the human locus contains two additional genes, TCL1-neighboring genes (TNG) 1 and 2, encoding proteins of 141 and 110 aa, respectively. Both genes show no homology to any known genes, but their expression profiles are very similar to those of TCL1 and TCL1b. TNG1 and TNG2 also are activated in T cell leukemias with rearrangements at 14q32.1. To aid in the development of a mouse model we also have characterized the murine Tcl1 locus and found five genes homologous to human TCL1b. Tcl1b1- Tcl1b5 proteins range from 117 to 123 aa and are 65-80% similar, but they show only a 30-40% similarity to human TCL1b. All five mouse Tcl1b and murine Tcl1 mRNAs are abundant in mouse oocytes and two-cell embryos but rare in various adult tissues and lymphoid cell lines. These data suggest a similar or complementary function of these proteins in early embryogenesis

Use of a Prescribed Ephedrine/Caffeine Combination and the Risk of Serious Cardiovascular Events: A Registry-based Case-Crossover Study

Ephedrine and herbal ephedra preparations have been shown to induce a small-to-moderate weight loss. Owing to reports on serious cardiovascular events, they were banned from the US market in 2004. There have been no large controlled studies on the possible association between prescribed ephedrine/caffeine and cardiovascular events in general. The authors linked data from four different sources within Statistics Denmark, using data on 257,364 users of prescribed ephedrine/caffeine for the period 1995–2002. The data were analyzed using a case-crossover technique with a composite endpoint: death outside of a hospital, myocardial infarction, or stroke. To account for effects of chronic exposure and effects in naïve users, the authors performed a secondary case-control study nested within the cohort of ephedrine/caffeine ever users. Among 2,316 case subjects, 282 (12.2%) were current users of ephedrine/caffeine. The case-crossover analysis yielded an odds ratio of 0.84 (95% confidence interval: 0.71, 1.00); after adjustment for trends in ephedrine/caffeine use, it was 0.95 (95% confidence interval: 0.79, 1.16). Subgroup analyses revealed no strata with significantly elevated risk. In the case-control substudy, there was no increased risk among naïve users or users with large cumulative doses. Prescribed ephedrine/caffeine was not associated with a substantially increased risk of adverse cardiovascular outcomes in this study