4 research outputs found

    Finishing the euchromatic sequence of the human genome

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    The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

    Modelling the initiation and spread of infectious pancreatic necrosis virus (ipnv) in the irish salmon farming industry: the role of inputs

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    Peer-reviewed.Released with a Creative Commons Attribution Non-Commercial No Derivatives LicenseObserved emergence of IPNV in farmed Irish salmon is simulated using a model originally developed to analyse the spread of the virus in Scotland [Murray, A.G., 2006a. A model of the spread of infectious pancreatic necrosis virus in Scottish salmon farms 1996–2003. Ecol. Model. 199, 64–72]. IPNV appears to have become established relatively recently in Ireland and the model is altered to explicitly simulate the origin of the spread of the virus. Input to freshwater farms was key to initiation of infection, but modelling suggests that endogenous spread was responsible for much of the subsequent increase in prevalence of IPNV. From the modelling, it is unlikely that direct imports accounted for most IPNV cases. If this is the case, cessation of imports, without a substantial improvement in biosecurity, would be likely to be of only limited effect in controlling IPNV. Marine IPNV prevalence appears to be insensitive to direct interventions in the marine environment (as in the Scottish model). A multi-element control strategy, targeting both endogenous spread and external input of infection and prioritising freshwater sites, but extending to marine sites, would probably now be required to eradicate IPNV from Ireland
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