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    <title>Nature Precedings - Tag feed for microarray</title>
    <link>http://precedings.nature.com/tags/microarray</link>
    <description>Recently posted documents tagged with 'microarray'</description>
    <dc:publisher>Nature Publishing Group</dc:publisher>
    <dc:language>en</dc:language>
    <prism:publicationName>Nature Precedings</prism:publicationName>
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      <title>Nature Precedings</title>
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    <item>
      <title>Annotation-based meta-analysis of microarray experiments</title>
      <link>http://dx.doi.org/10.1038/npre.2009.3569.1</link>
      <description>We are developing software applications to perform meta-analysis of microarray experiments based on standardized experiment annotations aiming to identify similar experiments and cluster experiments. The applications were tested on files obtained from the ArrayExpress public repository. Annotation terms were used to compute experiment dissimilarities to find experiments related to a query experiment. These applications may motivate efforts of bench biologists to better annotate experiments.</description>
      <guid>http://dx.doi.org/10.1038/npre.2009.3569.1</guid>
      <pubDate>Thu, 06 Aug 2009 20:01:12 UTC</pubDate>
      <dc:title>Annotation-based meta-analysis of microarray experiments</dc:title>
      <dc:identifier>doi:10.1038/npre.2009.3569.1</dc:identifier>
      <dc:date>2009-08-06</dc:date>
      <dc:creator>Jie Zheng</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-08-06T20:01:12Z</prism:publicationDate>
      <prism:category>Poster</prism:category>
      <prism:section>Bioinformatics</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/3569/version/1/files/npre20093569-1.pdf.thumb.png"/>
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      <title>A Drosophila systems model of withdrawal from chronic pentylenetetrazole relevant in post-epileptogenesis  </title>
      <link>http://precedings.nature.com/documents/3447/version/1</link>
      <description>Rodent kindling induced by pentylenetetrazole (PTZ) is an established model of epileptogenesis and antiepileptic drug (AED) testing. Recently, a Drosophila systems model has been described in which chronic PTZ causes a decreased climbing speed in adult males on 7th day. Some AEDs ameliorate development of this locomotor deficit. Time-series of microarray expression profiles of heads of flies treated with PTZ has been found to resemble transcriptomic alterations associated with epileptogenesis. In the fly model, withdrawal from seven day long PTZ treatment causes an increased climbing speed on 7th consequent day. Here, we present a systems model of the post-PTZ withdrawal regime. Unlike AED-untreated individuals, flies treated with any of the five AEDs after PTZ discontinuation exhibited normal climbing speed on 7th day, i.e., 14th day from the beginning of PTZ treatment. Time-series of microarray expression profiles of fly heads comparing control PTZ- and AED-untreated, and AED-untreated post PTZ withdrawal groups showed differentially expressed genes throughout. These genes enriched gene ontology (GO) molecular functions including transcription regulator and GTPase regulator activities. Interestingly, expression profiles of fly heads comparing control PTZ- and AED-untreated, and AED-treated post PTZ withdrawal groups showed neutralization of transcription regulator and GTPase regulator activities by the AEDs. Further transcriptomic analysis based on overinteraction in protein interactome and enrichment of miRNA targets implicated axon guidance and neuronal remodeling related perturbations in the fly model. Differential expression of genes belonging to transcription regulator and GTPase regulator activities have previously been reported in post-epileptogenesis in established rodent models. Also, axon guidance and neuronal remodeling related alterations have been implicated in epilepsy. The Drosophila model thus provides a unique opportunity to dissect long-term plasticity relevant in epileptogenesis at cellular and molecular levels. Besides, the model also offers an excellent system to efficiently screen agents with potential therapeutic activity.</description>
      <guid>http://precedings.nature.com/documents/3447/version/1</guid>
      <pubDate>Tue, 21 Jul 2009 16:40:03 UTC</pubDate>
      <dc:title>A Drosophila systems model of withdrawal from chronic pentylenetetrazole relevant in post-epileptogenesis  </dc:title>
      <dc:identifier>hdl:10101/npre.2009.3447.1</dc:identifier>
      <dc:date>2009-07-21</dc:date>
      <dc:creator>Abhay Sharma</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-07-21T16:40:03Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Neuroscience</prism:section>
      <prism:section>Pharmacology</prism:section>
      <prism:section>Bioinformatics</prism:section>
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      <title>A novel Drosophila transcriptomic and behavioral model detects potassium chloride with therapeutic potential</title>
      <link>http://precedings.nature.com/documents/3429/version/1</link>
      <description>In a newly described Drosophila model, two of the five antiepileptic drugs (AEDs) tested, sodium valproate (NaVP) and levetiracetam (LEV), not ethosuximide (ETH), gabapentin (GBP) and vigabatrin (VGB), ameliorate development of chronic pentylenetetrazole (PTZ) induced locomotor alteration. To further characterize the model, we analyze here the microarray expression profile of heads of flies treated with depolarizing compound potassium chloride (KCl). Surprisingly, microarray clustering showed unexpected similarity among KCl, LEV and NaVP. Further, like the two effective AEDs in the fly model, KCl regulated genes overrepresented ribosomal pathway. Interestingly, KCl also ameliorated development of locomotor deficit in the chronic PTZ model. Both transcriptomic and behavioral analyses thus showed LEV- and NaVP- like neuroprotective effect of KCl. This is consistent with neuroprotective effect of KCl observed previously in mammalian system. The Drosophila model thus provides a unique opportunity to understand long term mechanisms of neuroactive compounds.</description>
      <guid>http://precedings.nature.com/documents/3429/version/1</guid>
      <pubDate>Fri, 17 Jul 2009 14:41:20 UTC</pubDate>
      <dc:title>A novel Drosophila transcriptomic and behavioral model detects potassium chloride with therapeutic potential</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3429.1</dc:identifier>
      <dc:date>2009-07-17</dc:date>
      <dc:creator>Abhay Sharma</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-07-17T14:41:20Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Neuroscience</prism:section>
      <prism:section>Pharmacology</prism:section>
      <prism:section>Bioinformatics</prism:section>
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    <item>
      <title>Transcriptomic analysis implicates ribosomal and energy metabolic pathways in antiepileptic drug action in a Drosophila model</title>
      <link>http://precedings.nature.com/documents/3396/version/1</link>
      <description>Mechanisms of long term action of antiepileptic drugs (AEDs), used in treating epilepsy and many other neurological and psychiatric disorders, are poorly understood. Recently, a novel Drosophila transcriptomic model of locomotor plasticity induced by chronic pentylenetetrazole (PTZ), a chemoconvulsant commonly used to model epileptogenesis and test AEDs in rodents, has been described. In this model, two of the five AEDs tested, sodium valproate (NaVP) and levetiracetam (LEV), not ethosuximide (ETH), gabapentin (GBP) and vigabatrin (VGB), ameliorate development of chronic PTZ induced locomotor alteration. Here, we describe transcriptomic effect of the AEDs in the fly model. Singular treatment with ETH, GBP and VGB in general caused downregulation of genes. In contrast, similar treatment with NaVP and LEV caused upregulation. The GBP and NaVP gene sets showed enrichment of the ribosomal and energy metabolic pathways. The network partners of ETH, VGB and LEV regulated genes in the available interactome map were also found to overrepresent the ribosomal pathway. Unlike PTZ alone, PTZ and LEV combination treatment was found to cause differential regulation of genes that too enriched the ribosomal and energy metabolic pathways. Cumulatively, we provide transcriptomic evidence that suggests involvement of ribosomal and energy metabolic mechanisms in AED action. The Drosophila model provides an excellent opportunity to further understand mechanisms of AED action in molecular details.</description>
      <guid>http://precedings.nature.com/documents/3396/version/1</guid>
      <pubDate>Tue, 07 Jul 2009 16:27:35 UTC</pubDate>
      <dc:title>Transcriptomic analysis implicates ribosomal and energy metabolic pathways in antiepileptic drug action in a Drosophila model</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3396.1</dc:identifier>
      <dc:date>2009-07-07</dc:date>
      <dc:creator>Abhay Sharma</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-07-07T16:27:35Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Neuroscience</prism:section>
      <prism:section>Pharmacology</prism:section>
      <prism:section>Bioinformatics</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/3396/version/1/files/npre20093396-1.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
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    <item>
      <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>
      <media:thumbnail url="http://precedings.nature.com/documents/3297/version/1/files/npre20093297-1.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
    </item>
    <item>
      <title>The Gene Ontology Annotation (GOA) Database</title>
      <link>http://dx.doi.org/10.1038/npre.2009.3154.1</link>
      <description>The Gene Ontology (GO) is a well-established, structured vocabulary that has been successfully used for 10 years in the annotation of proteins. GO terms, created in consultation with the biology community, are used to replace the multiple nomenclatures used by scientific databases that can hamper data integration. Currently GO consists of more than 26,500 terms distributed over three ontologies that describe the molecular function, biological process and subcellular location of a protein in a generic cell.The Gene Ontology Annotation (GOA) database (http://www.ebi.ac.uk/GOA) aims to provide high-quality manual and electronic GO annotations to proteins within the UniProt Knowledgebase (UniProtKB). By annotating all &#8216;known&#8217; proteins with GO terms and transferring this knowledge to highly similar &#8216;unknown&#8217; proteins, GOA offers a valuable contribution to the understanding of all proteomes.As well as generating manual annotation, made by extracting experimental evidence from full text peer-reviewed publications, GOA produces electronic annotation by making large-scale assignments of GO terms to proteins using computational methods. To date we have six electronic annotation methods including; InterPro2GO, Swiss-Prot Keyword2GO and the projection of annotations between orthologous species using Ensembl Compara.GOA provides annotated entries for over 180,000 species and is the largest and most comprehensive open-source contributor of annotations to the GO Consortium annotation effort. In addition, by integrating GO annotations from model organism groups (e.g. FlyBase, GeneDB, MGI, RGD, SGD and TAIR), GOA ensures the dataset remains a key reference. GOA prioritises the annotation of the human proteome and provides this annotation to the GO Consortium&#8217;s Reference Genome project.GOA produces monthly releases of annotations to the human, mouse, rat, zebrafish, cow, chicken and Arabidopsis proteomes as well as a file for the multiple species within UniProtKB. The GOA dataset can be queried through a user-friendly web interface via our QuickGO browser(http://www.ebi.ac.uk/QuickGO) or downloaded in a parsable format via the EBI(ftp://ftp.ebi.ac.uk/pub/databases/GO/goa) and GO FTP sites. The GOA dataset has increasingly been integrated into tools that aid in the analysis of large datasets resulting from high-throughput experiments thus assisting researchers in biological interpretation of their results.</description>
      <guid>http://dx.doi.org/10.1038/npre.2009.3154.1</guid>
      <pubDate>Thu, 23 Apr 2009 14:55:40 UTC</pubDate>
      <dc:title>The Gene Ontology Annotation (GOA) Database</dc:title>
      <dc:identifier>doi:10.1038/npre.2009.3154.1</dc:identifier>
      <dc:date>2009-04-23</dc:date>
      <dc:creator>Rachael Huntley</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-04-23T14:55:40Z</prism:publicationDate>
      <prism:category>Poster</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Bioinformatics</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/3154/version/1/files/npre20093154-1.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
    </item>
    <item>
      <title>Data submission and curation for caArray, a standard based microarray data repository system </title>
      <link>http://dx.doi.org/10.1038/npre.2009.3138.1</link>
      <description>caArray is an open-source, open development, web and programmatically accessible array data management system developed at National Cancer Institute. It was developed to support the exchange of array data across the Cancer Biomedical Informatics Grid (caBIG&#8482;), a collaborative information network that connect scientists and practitioners through a shareable and interoperable infrastructure to share data and knowledge.  caArray adopts a federated model of local installations, in which data deposited are shareable across caBIG&#8482;.  Comprehensive in annotation yet easy to use has always been a challenge to any data repository system. To alleviate this difficulty, caArray accepts data upload using the MAGE-TAB, a spreadsheet-based format for annotating and communicating microarray data in a MIAME-compliant fashion (http://www.mged.org/mage-tab).  MAGE-TAB is built on community standards &#8211; MAGE, MIAME, and Ontology. The components and work flow of MAGE-TAB files are organized in such a way which is already familiar to bench scientists and thus minimize the time and frustration of reorganizing their data before submission. The MAGE-TAB files are also structured to be machine readable so that they can be easily parsed into database.  Users can control public access to experiment- and sample-level data and can create collaboration groups to support data exchange among a defined set of partners. All data submitted to caArray at NCI will go through strict curation by a group of scientists against these standards to make sure that the data are correctly annotated using proper controlled vocabulary terms and all required information are provided. Two of mostly used ontology sources are MGED ontology (http://mged.sourceforge.net/ontologies/MGEDontology.php) and NCI thesaurus (http://nciterms.nci.nih.gov/NCIBrowser/Dictionary.do). The purpose of data curation is to ensure easy comparison of results from different labs and unambiguous report of results. Data will also undergo automatic validation process before parsed into database, in which minimum information requirement and data consistency with the array designs are checked. Files with error found during validation are flagged with error message. Curators will re-examine those files and make necessary corrections before re-load the files. The iteration repeats until files are validated successfully. Data are then imported into the system and ready for access through the portal or through API. Interested parties are encouraged to review the installation package, documentation, and source code available from http://caarray.nci.nih.gov.  </description>
      <guid>http://dx.doi.org/10.1038/npre.2009.3138.1</guid>
      <pubDate>Wed, 22 Apr 2009 21:17:19 UTC</pubDate>
      <dc:title>Data submission and curation for caArray, a standard based microarray data repository system </dc:title>
      <dc:identifier>doi:10.1038/npre.2009.3138.1</dc:identifier>
      <dc:date>2009-04-22</dc:date>
      <dc:creator>X Bian</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-04-22T21:17:19Z</prism:publicationDate>
      <prism:category>Poster</prism:category>
      <prism:section>Cancer</prism:section>
      <prism:section>Bioinformatics</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/3138/version/1/files/npre20093138-1.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
    </item>
    <item>
      <title>Evaluation of diversity, specialization, and gene specificity in transcriptomes</title>
      <link>http://dx.doi.org/10.1038/npre.2009.3012.1</link>
      <description>The transcriptome is a set of genes transcribed in a given tissue under specific conditions and can be characterized by a list of genes with their corresponding frequencies of transcription. Transcriptome changes can be measured by counting gene tags from mRNA libraries or by measuring light signals in DNA microarrays. Recently we proposed an approach to define and estimate the diversity and specialization of transcriptomes and gene specificity. This approach can be useful for the determination and measure of transcriptional networks. We defined transcriptome diversity as the Shannon entropy of its frequency distribution. Gene specificity is defined as the mutual information between the tissues and the corresponding transcript, allowing detection of either housekeeping or highly specific genes and clarifying the meaning of these concepts in the literature. Tissue specialization is measured by average gene specificity. Visualization of the positions of transcriptomes in a system of diversity and specialization coordinates makes it possible to understand at a glance their interrelations, summarizing in a powerful way which transcriptomes are richer in diversity of expressed genes, or which are relatively more specialized. This enlightens the relation among transcriptomes, allowing a better understanding of their changes through the development of the organism or in response to environmental stimuli. We present statistical tools based on resampling procedures to obtain confidence intervals for the parameters as well as perform statistical test. These approaches are illustrated with a human dataset.</description>
      <guid>http://dx.doi.org/10.1038/npre.2009.3012.1</guid>
      <pubDate>Thu, 02 Apr 2009 08:00:34 UTC</pubDate>
      <dc:title>Evaluation of diversity, specialization, and gene specificity in transcriptomes</dc:title>
      <dc:identifier>doi:10.1038/npre.2009.3012.1</dc:identifier>
      <dc:date>2009-04-02</dc:date>
      <dc:creator>Octavio Martinez</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-04-02T08:00:34Z</prism:publicationDate>
      <prism:category>Poster</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Bioinformatics</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/3012/version/1/files/npre20093012-1.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
    </item>
    <item>
      <title>Far-infrared rays control prostate cancer cells in vitro and in vivo</title>
      <link>http://precedings.nature.com/documents/1980/version/2</link>
      <description>We introduce a new effective method to control hormone refractory prostate cancer cells by using an activated rubber/resin form (RB), far-infrared ray emitter, with or without sodium butyrate (SB). The growth of three human prostate cancer cell lines (Du145, PC-3 and LNCaP) was suppressed in vitro and in vivo by using RB, and the cells were eradicated with RB + 3 mM SB. G1 arrest and apoptotic pathway proteins were induced by RB with intensified expressions of apoptosis &amp;#8211; related mRNA on cDNA microarray. RB radiates far-infrared rays of the 4 to 25 &amp;#956;m wavelengths to an object which exert a favorable influence on a cancer control. These results may render us a new therapeutic modality in hormone refractory prostate cancer.</description>
      <guid>http://precedings.nature.com/documents/1980/version/2</guid>
      <pubDate>Fri, 20 Mar 2009 12:43:46 UTC</pubDate>
      <dc:title>Far-infrared rays control prostate cancer cells in vitro and in vivo</dc:title>
      <dc:identifier>hdl:10101/npre.2009.1980.2</dc:identifier>
      <dc:date>2009-03-20</dc:date>
      <dc:creator>Hiroki Shima</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-03-20T12:43:46Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Cancer</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/1980/version/2/files/npre20091980-2.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
    </item>
    <item>
      <title>Analysis of Endocrine Disruption in Southern California Coastal Fish using an Aquatic Multi-Species Microarray</title>
      <link>http://precedings.nature.com/documents/2823/version/1</link>
      <description>BACKGROUND:  Endocrine disruptors include plasticizers, pesticides, detergents and pharmaceuticals.  Turbot and other flatfish are used to characterize the presence of chemicals in the marine environment.  Unfortunately, there are relatively few genes of turbot and other flatfish in GenBank, which limits the use of molecular tools such as microarrays and qRT-PCR to study disruption of endocrine responses in sentinel fish captured by regulatory agencies.OBJECTIVES:  A multi-gene cross species microarray was fabricated as a diagnostic tool to screen the effects of environmental chemicals in fish, for which there is minimal genomic information.  The array included genes that are involved in the actions of adrenal and sex steroids, thyroid hormone, and xenobiotic responses.  This will provide a sensitive tool for screening for the presence of chemicals with adverse effects on endocrine responses in coastal fish species.METHODS:  A custom multi-species microarray was used to study gene expression in wild hornyhead turbot, collected from polluted and clean coastal waters and in laboratory male zebrafish following exposure to estradiol and 4-nonylphenol.  Gene-specific expression in turbot liver was measured by qRT-PCR and correlated to microarray data.RESULTS:  Microarray and qRT-PCR analyses of livers from turbot collected near municipal wastewater discharge areas revealed altered gene expression profiles compared to those from reference areas.  CONCLUSIONS:  The agreement between the array data and qRT-PCR analyses validates this multi-species microarray.  The microarray measurement of gene expression in zebrafish, which are phylogenetically distant from turbot, indicates that this multi-species microarray will be useful for measuring endocrine responses in other fish.</description>
      <guid>http://precedings.nature.com/documents/2823/version/1</guid>
      <pubDate>Mon, 02 Feb 2009 09:24:52 UTC</pubDate>
      <dc:title>Analysis of Endocrine Disruption in Southern California Coastal Fish using an Aquatic Multi-Species Microarray</dc:title>
      <dc:identifier>hdl:10101/npre.2009.2823.1</dc:identifier>
      <dc:date>2009-02-02</dc:date>
      <dc:creator>Michael E. Baker</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-02-02T09:24:52Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Developmental Biology</prism:section>
      <prism:section>Ecology</prism:section>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Earth &amp; Environment</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/2823/version/1/files/npre20092823-1.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
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