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    <title>Nature Precedings - Tag feed for mouse</title>
    <link>http://precedings.nature.com/tags/mouse</link>
    <description>Recently posted documents tagged with 'mouse'</description>
    <dc:publisher>Nature Publishing Group</dc:publisher>
    <dc:language>en</dc:language>
    <prism:publicationName>Nature Precedings</prism:publicationName>
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      <title>Developing a Mammalian Behaviour Ontology</title>
      <link>http://dx.doi.org/10.1038/npre.2009.3565.1</link>
      <description>The use of the Entity + Quality (EQ) model in phenotypic descriptions is dependent on the use of specialised domain ontologies to define the entity under observation.  A domain currently lacking a specialised ontology is mammalian behaviour, and so the Mammalian Behaviour Ontology is being constructed to address this.  Top-level class distinctions are made between behavioural activities and behavioural functions of individuals, and those between two or more individuals.  The ontology is manually developed and encourages contributions from domain experts.</description>
      <guid>http://dx.doi.org/10.1038/npre.2009.3565.1</guid>
      <pubDate>Fri, 07 Aug 2009 10:05:09 UTC</pubDate>
      <dc:title>Developing a Mammalian Behaviour Ontology</dc:title>
      <dc:identifier>doi:10.1038/npre.2009.3565.1</dc:identifier>
      <dc:date>2009-08-07</dc:date>
      <dc:creator>Tim Beck</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-08-07T10:05:09Z</prism:publicationDate>
      <prism:category>Poster</prism:category>
      <prism:section>Bioinformatics</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/3565/version/1/files/npre20093565-1.pdf.thumb.png"/>
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      <title>Standard operating procedures (SOP) in experimental stroke research: SOP for middle cerebral artery occlusion in the mouse</title>
      <link>http://precedings.nature.com/documents/3492/version/1</link>
      <description>Recently, systematic reviews have found quantitative evidence that low study quality may have introduced a bias into preclinical stroke research. Monitoring, auditing, and standard operating procedures (SOPs) are already key elements of quality control in randomized clinical trials and will hopefully be widely adopted by preclinical stroke research in the near future. Increasingly, funding bodies and review boards overseeing animal experiments are taking a proactive stance, and demand auditable quality control measures in preclinical research. Every good quality control system is based on its SOPs. This article introduces the concept of quality control and presents for the first time an SOP in experimental stroke research. </description>
      <guid>http://precedings.nature.com/documents/3492/version/1</guid>
      <pubDate>Tue, 28 Jul 2009 17:50:21 UTC</pubDate>
      <dc:title>Standard operating procedures (SOP) in experimental stroke research: SOP for middle cerebral artery occlusion in the mouse</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3492.1</dc:identifier>
      <dc:date>2009-07-28</dc:date>
      <dc:creator>Ulrich Dirnagl</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-07-28T17:50:21Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Neuroscience</prism:section>
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      <title>GUDMAP &amp;#8211; An Online GenitoUrinary Resource</title>
      <link>http://dx.doi.org/10.1038/npre.2009.3297.1</link>
      <description>The GenitoUrinary Development Molecular Anatomy Project (GUDMAP) is a consortium of laboratories working to provide the scientific and medical community with gene expression data and tools to facilitate research (see www.gudmap.org). The data provided by GUDMAP includes large in situ hybridization screens (wholemount and section) and expression microarray analysis of components of the developing mouse urogenital system (including laser-captured material and FACS-isolated cells from transgenic reporter mice). In addition, a high-resolution anatomy ontology has been developed by members of the GUDMAP consortium to describe the subcompartments of the developing murine genitourinary tract. The GUDMAP Database Development Team and Editorial Office &amp;#8211; both based in Edinburgh &amp;#8211; function to ensure submission, curation, storage and presentation of the data submitted by the GUDMAP consortium. Our collective aim is twofold: 1) to simplify the process of submission so that data is publically available as soon as it is produced; and 2) to organize this information in a database and ensure that the online interface is continuously available and easy to use. Thus far, we have developed a range of tools that help both the submitter and the end user. These include: an online annotation tool that simplifies in situ data submission through an ontology-based graphical user interface; a database interface that allows users to browse and query expression data, and to filter data by organ system; a heat-map display of microarray data and analyses. Furthermore, the Edinburgh team has developed a GUDMAP Disease Database that queries associations between genes, genitourinary diseases, and renal/urinary and reproductive phenotypes. In collaboration with GUDMAP consortium members at the CCHMC (Cincinnati Children&amp;#8217;s Hospital Medical Center), the Disease Database is being extended to include mammalian phenotypes mapped to OMIM entries. By virtue of its impressive dataset and its ease of use we hope that the GUDMAP Website will continue to serve as a powerful resource for biologists, clinicians and bioinformaticians with an interest in the urogenital system.</description>
      <guid>http://dx.doi.org/10.1038/npre.2009.3297.1</guid>
      <pubDate>Sat, 30 May 2009 14:17:58 UTC</pubDate>
      <dc:title>GUDMAP &amp;#8211; An Online GenitoUrinary Resource</dc:title>
      <dc:identifier>doi:10.1038/npre.2009.3297.1</dc:identifier>
      <dc:date>2009-05-30</dc:date>
      <dc:creator>Simon Harding</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-05-30T14:17:58Z</prism:publicationDate>
      <prism:category>Poster</prism:category>
      <prism:section>Developmental Biology</prism:section>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Bioinformatics</prism:section>
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      <title>IMGT/GENE-DB: genomic reference sequences for human and mouse IG and TR genes and alleles</title>
      <link>http://dx.doi.org/10.1038/npre.2009.3158.1</link>
      <description>The immunoglobulin (IG) and T cell receptor (TR) major loci span about 6 Megabases (Mb) of the human genome on chromosomes 2, 7, 14 and 22, and 9 Mb in mouse on chromosomes 6, 12, 13, 14 and 16. There are seven major loci: three IG loci (IGH, IGK, IGL) and four TR loci (TRA, TRB, TRG, TRD), with a distinct repartition of the variable (V), diversity (D), joining (J) and constant (C) genes. The human genome comprises a total number of 608-665 IG and TR genes (371-422 IG and 237-243 TR), depending on the haplotypes, per haploid genome 1, 2 of which 531-588 genes are located in the major loci (distributed in 369-418 V, 32 D, 105-109 J and 25-29 C genes). There are also 77 orphons (68 IG and 9 TR) including two processed IG genes, outside the major loci. The number of functional IG and TR genes is 308-356 (136-171 IG and 172-185 TR) per haploid genome. The mouse genome comprises an approximate number of 876 IG and TR genes (624 IG and 252 TR). All these genomic data are available in the IMGT&#174; gene database, IMGT/GENE-DB 3. The major contribution of IMGT/GENE-DB has been to establish, for the first time, a standardized nomenclature of the IG and TR genes and alleles of humans and other vertebrates. In April 2009, IMGT/GENE-DB manages 1999 genes and 3026 alleles. [1] Lefranc M.-P. and Lefranc G., The Immunoglobulin FactsBook, Academic Press, London, 458 pages (2001).[2] Lefranc M.-P. and Lefranc G., The T cell receptor FactsBook, Academic Press, London, 398 pages (2001).[3] Giudicelli V. et al. Nucleic Acids Res., 33, D256-261 (2005).</description>
      <guid>http://dx.doi.org/10.1038/npre.2009.3158.1</guid>
      <pubDate>Thu, 23 Apr 2009 17:57:23 UTC</pubDate>
      <dc:title>IMGT/GENE-DB: genomic reference sequences for human and mouse IG and TR genes and alleles</dc:title>
      <dc:identifier>doi:10.1038/npre.2009.3158.1</dc:identifier>
      <dc:date>2009-04-23</dc:date>
      <dc:creator>Fatena Bellahcene</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-04-23T17:57:23Z</prism:publicationDate>
      <prism:category>Poster</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Immunology</prism:section>
      <prism:section>Bioinformatics</prism:section>
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      <title>Introduction of Transmembrane Inner Ear (tmie) Gene Can Recover the Hearing Impairment and Abnormal Behavior in the Circling Mouse</title>
      <link>http://precedings.nature.com/documents/2106/version/1</link>
      <description>The spontaneous mutant circling mouse (cir/cir) shows a circling behavior and hearing loss. We produced transgenic mice overexpressing the causative gene, transmembrane inner ear (tmie), for the phenotypic rescue of the circling mouse. Through the continuous breeding with circling mice, the cir/cir homozygous mice carrying the transgene (cir/cir-tg) were produced. The rescued cir/cir -tg mice were able to swim in the water with proper orientation and did not show any circling behavior like wild type mice. Western blot and immunohistochemical analysis exhibited that the transgenic tmie was expressed in the inner ear. Inner and outer hair cells were recovered in the cochlea and spiral ganglion neurons were also recovered in the rescued mice. Auditory brainstem response (ABR) test demonstrated that the cir/cir -tg mice are able to respond to sound. This study demonstrates that tmie transgene can recover the hearing impairment and abnormal behavior in the circling mouse.</description>
      <guid>http://precedings.nature.com/documents/2106/version/1</guid>
      <pubDate>Mon, 28 Jul 2008 19:23:59 UTC</pubDate>
      <dc:title>Introduction of Transmembrane Inner Ear (tmie) Gene Can Recover the Hearing Impairment and Abnormal Behavior in the Circling Mouse</dc:title>
      <dc:identifier>hdl:10101/npre.2008.2106.1</dc:identifier>
      <dc:date>2008-07-28</dc:date>
      <dc:creator>Zae Young Ryoo</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2008-07-28T19:23:59Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Developmental Biology</prism:section>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Neuroscience</prism:section>
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      <title>Intra- and inter-individual genetic differences in gene expression</title>
      <link>http://precedings.nature.com/documents/1799/version/1</link>
      <description>Genetic variation is known to influence the amount of mRNA produced by a gene. Given that the molecular machines control mRNA levels of multiple genes, we expect genetic variation in the components of these machines would influence multiple genes in a similar fashion. In this study we show that this assumption is correct by using correlation of mRNA levels measured independently in the brain, kidney or liver of multiple, genetically typed, mice strains to detect shared genetic influences. These correlating groups of genes (CGG) have collective properties that account for 40-90% of the variability of their constituent genes and in some cases, but not all, contain genes encoding functionally related proteins. Critically, we show that the genetic influences are essentially tissue specific and consequently the same genetic variations in the one animal may up-regulate a CGG in one tissue but down-regulate the same CGG in a second tissue. We further show similarly paradoxical behaviour of CGGs within the same tissues of different individuals. The implication of this study is that this class of genetic variation can result in complex inter- and intra-individual and tissue differences and that this will create substantial challenges to the investigation of phenotypic outcomes, particularly in humans where multiple tissues are not readily available.</description>
      <guid>http://precedings.nature.com/documents/1799/version/1</guid>
      <pubDate>Tue, 15 Apr 2008 12:55:56 UTC</pubDate>
      <dc:title>Intra- and inter-individual genetic differences in gene expression</dc:title>
      <dc:identifier>hdl:10101/npre.2008.1799.1</dc:identifier>
      <dc:date>2008-04-15</dc:date>
      <dc:creator>Mark J. Cowley</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2008-04-15T12:55:56Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Bioinformatics</prism:section>
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