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<pubDate>Sat, 26 Jul 2008 06:36:37 BST</pubDate>


	<title>CiteULike: jonsta247's library [127 articles]</title>
	<description>CiteULike: jonsta247's library [127 articles]</description>


	<link>http://www.citeulike.org/user/jonsta247</link>
	<dc:publisher>CiteULike.org</dc:publisher>
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	<dc:rights>Copyright &#169; 2004-2008 citeulike.org</dc:rights>
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        <rdf:li rdf:resource="http://www.citeulike.org/user/jonsta247/article/2350781"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/jonsta247/article/2983691"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/jonsta247/article/2998698"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/jonsta247/article/2998696"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/jonsta247/article/2998695"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/jonsta247/article/2998694"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/jonsta247/article/2914784"/>
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<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2350781">
    <title>Haematopoietic stem cell release is regulated by circadian oscillations</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2350781</link>
    <description>&lt;i&gt;Nature (06 February 2008)&lt;/i&gt;</description>
    <dc:title>Haematopoietic stem cell release is regulated by circadian oscillations</dc:title>

    <dc:creator>Simón Méndez-Ferrer</dc:creator>
    <dc:creator>Daniel Lucas</dc:creator>
    <dc:creator>Michela Battista</dc:creator>
    <dc:creator>Paul Frenette</dc:creator>
    <dc:identifier>doi:10.1038/nature06685</dc:identifier>
    <dc:source>Nature (06 February 2008)</dc:source>
    <dc:date>2008-02-08T00:40:40-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Nature</prism:publicationName>
    <prism:issn>0028-0836</prism:issn>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>temptemp</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2983691">
    <title>Protein-Protein Interactions in the Membrane: Sequence, Structural, and Biological Motifs</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2983691</link>
    <description>&lt;i&gt;Structure, Vol. 16, No. 7. (9 July 2008), pp. 991-1001.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Summary Single-span transmembrane (TM) helices have structural and functional roles well beyond serving as mere anchors to tether water-soluble domains in the vicinity of the membrane. They frequently direct the assembly of protein complexes and mediate signal transduction in ways analogous to small modular domains in water-soluble proteins. This review highlights different sequence and structural motifs that direct TM assembly and discusses their roles in diverse biological processes. We believe that TM interactions are potential therapeutic targets, as evidenced by natural proteins that modulate other TM interactions and recent developments in the design of TM-targeting peptides.</description>
    <dc:title>Protein-Protein Interactions in the Membrane: Sequence, Structural, and Biological Motifs</dc:title>

    <dc:creator>David Moore</dc:creator>
    <dc:creator>Bryan Berger</dc:creator>
    <dc:creator>William Degrado</dc:creator>
    <dc:identifier>doi:10.1016/j.str.2008.05.007</dc:identifier>
    <dc:source>Structure, Vol. 16, No. 7. (9 July 2008), pp. 991-1001.</dc:source>
    <dc:date>2008-07-10T03:35:58-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Structure</prism:publicationName>
    <prism:volume>16</prism:volume>
    <prism:number>7</prism:number>
    <prism:startingPage>991</prism:startingPage>
    <prism:endingPage>1001</prism:endingPage>
    <prism:category>temptemp</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2998698">
    <title>Current Biology -- Obbard and Finnegan</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2998698</link>
    <description>&lt;i&gt;&lt;/i&gt;</description>
    <dc:title>Current Biology -- Obbard and Finnegan</dc:title>

    <dc:date>2008-07-14T12:04:41-00:00</dc:date>
    <prism:category>temptemp</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2998696">
    <title>Stem Cells: Time to Check Our Premises</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2998696</link>
    <description>&lt;i&gt;Cell Stem Cell, Vol. 3, No. 1. (3 July 2008), pp. 25-29.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Summary A recent meeting titled &#34;Conserved Mechanisms of Stem Cell Control and Regeneration&#34; was held at the Biopharmaceutical Technology Center Institute (BTCI) in Madison, Wisconsin. The diversity of stem cells and biological contexts discussed highlight the field's rapid progress in deciphering the molecular basis of stem cell functions and emphasize the challenges facing the future exploitation of these cells as therapeutic vectors.</description>
    <dc:title>Stem Cells: Time to Check Our Premises</dc:title>

    <dc:creator>Sánchez</dc:creator>
    <dc:identifier>doi:10.1016/j.stem.2008.06.013</dc:identifier>
    <dc:source>Cell Stem Cell, Vol. 3, No. 1. (3 July 2008), pp. 25-29.</dc:source>
    <dc:date>2008-07-14T12:04:01-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Cell Stem Cell</prism:publicationName>
    <prism:volume>3</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>25</prism:startingPage>
    <prism:endingPage>29</prism:endingPage>
    <prism:category>temptemp</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2998695">
    <title>Stem Cells for Spinal Cord Repair</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2998695</link>
    <description>&lt;i&gt;Cell Stem Cell, Vol. 3, No. 1. (3 July 2008), pp. 16-24.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Summary Spinal cord injury typically results in permanent disability. Many studies have indicated that transplantation of several different types of stem cells promotes functional recovery in animal models of spinal cord injury. A conceptually different approach to utilize stem cells for regenerative therapies may be recruitment of endogenous neural stem cells resident in the adult spinal cord. We discuss the possibilities, risks, and mechanisms for stem cells in spinal cord repair.</description>
    <dc:title>Stem Cells for Spinal Cord Repair</dc:title>

    <dc:creator>Fanie Barnabé-Heider</dc:creator>
    <dc:creator>Jonas Frisén</dc:creator>
    <dc:identifier>doi:10.1016/j.stem.2008.06.011</dc:identifier>
    <dc:source>Cell Stem Cell, Vol. 3, No. 1. (3 July 2008), pp. 16-24.</dc:source>
    <dc:date>2008-07-14T12:04:01-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Cell Stem Cell</prism:publicationName>
    <prism:volume>3</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>16</prism:startingPage>
    <prism:endingPage>24</prism:endingPage>
    <prism:category>temptemp</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2998694">
    <title>In Childhood Acute Lymphoblastic Leukemia, Blasts at Different Stages of Immunophenotypic Maturation Have Stem Cell Properties</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2998694</link>
    <description>&lt;i&gt;Cancer Cell, Vol. 14, No. 1. (8 July 2008), pp. 47-58.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Summary We examined the leukemic stem cell potential of blasts at different stages of maturation in childhood acute lymphoblastic leukemia (ALL). Human leukemic bone marrow was transplanted intrafemorally into NOD/scid mice. Cells sorted using the B precursor differentiation markers CD19, CD20, and CD34 were isolated from patient samples and engrafted mice before serial transplantation into primary or subsequent (up to quaternary) recipients. Surprisingly, blasts representative of all of the different maturational stages were able to reconstitute and reestablish the complete leukemic phenotype in vivo. Sorted blast populations mirrored normal B precursor cells with transcription of a number of stage-appropriate genes. These observations inform a model for leukemia-propagating stem cells in childhood ALL.</description>
    <dc:title>In Childhood Acute Lymphoblastic Leukemia, Blasts at Different Stages of Immunophenotypic Maturation Have Stem Cell Properties</dc:title>

    <dc:creator>Le</dc:creator>
    <dc:creator>Marc Hotfilder</dc:creator>
    <dc:creator>Simon Bomken</dc:creator>
    <dc:creator>Kerrie Wilson</dc:creator>
    <dc:creator>Silja Röttgers</dc:creator>
    <dc:creator>André Schrauder</dc:creator>
    <dc:creator>Annegret Rosemann</dc:creator>
    <dc:creator>Julie Irving</dc:creator>
    <dc:creator>Ronald Stam</dc:creator>
    <dc:creator>Leonard Shultz</dc:creator>
    <dc:creator>Jochen Harbott</dc:creator>
    <dc:creator>Heribert Jürgens</dc:creator>
    <dc:creator>Martin Schrappe</dc:creator>
    <dc:creator>Rob Pieters</dc:creator>
    <dc:creator>Josef Vormoor</dc:creator>
    <dc:identifier>doi:10.1016/j.ccr.2008.05.015</dc:identifier>
    <dc:source>Cancer Cell, Vol. 14, No. 1. (8 July 2008), pp. 47-58.</dc:source>
    <dc:date>2008-07-14T12:03:52-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Cancer Cell</prism:publicationName>
    <prism:volume>14</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>47</prism:startingPage>
    <prism:endingPage>58</prism:endingPage>
    <prism:category>temptemp</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2914784">
    <title>Chemistry &#38; Biology -- Yoshikuni et al.</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2914784</link>
    <description>&lt;i&gt;&lt;/i&gt;</description>
    <dc:title>Chemistry &#38; Biology -- Yoshikuni et al.</dc:title>

    <dc:date>2008-06-22T08:48:26-00:00</dc:date>
    <prism:category>temptemp</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2998689">
    <title>Current Biology -- Gomis-Rüth et al.</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2998689</link>
    <description>&lt;i&gt;&lt;/i&gt;</description>
    <dc:title>Current Biology -- Gomis-Rüth et al.</dc:title>

    <dc:date>2008-07-14T12:02:24-00:00</dc:date>
    <prism:category>temptemp</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/1586652">
    <title>Development of a high resolution three-dimensional surgical atlas of the murine head for strains 129S1/SvImJ and C57Bl/6J using magnetic resonance imaging and micro-computed tomography.</title>
    <link>http://www.citeulike.org/user/jonsta247/article/1586652</link>
    <description>&lt;i&gt;Neuroscience, Vol. 144, No. 2. (19 January 2007), pp. 604-615.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The mouse has emerged as a major experimental model system for examining the functional properties of the mammalian CNS; both during development and following CNS injury. Histologic procedures currently used to determine the relative position of structures within the CNS are presently limited in their ability to take full advantage of this system for surgical and morphometric procedures. We present here the first three-dimensional interactive digital atlas of the murine brain and skull for two genetically important strains of mice; 129S1/SvImJ and C57Bl/6J. The final resolution of these digital atlases is 54 micro m(3). These representations of the murine brain and skull, in conjunction with our development of a new, more dynamic master coordinate system, provide improved accuracy with respect to targeting CNS structures during surgery compared with previous systems. The interactive three-dimensional nature of these atlases also provide users with stereotactic information necessary to perform accurate &#34;off-axis&#34; surgical procedures, as is commonly required for experiments such as in vivo micro-electroporation. In addition, three-dimensional analysis of the brain and skull shape in C57Bl, 129Sv, CD1, and additional murine strains, suggests that a stereotactic coordinate system based upon the lambda and rostral confluence of the sinuses at the sagittal midline, provides improved accuracy compared with the traditional lambda-bregma landmark system. These findings demonstrate the utility of developing highly accurate and robust three-dimensional representations of the murine brain and skull, in which experimental outputs can be directly compared using a unified coordinate system. The aim of these studies is to enhance comparative morphometric analyses and stereotactic surgical procedures in mice.</description>
    <dc:title>Development of a high resolution three-dimensional surgical atlas of the murine head for strains 129S1/SvImJ and C57Bl/6J using magnetic resonance imaging and micro-computed tomography.</dc:title>

    <dc:creator>E Chan</dc:creator>
    <dc:creator>N Kovacevíc</dc:creator>
    <dc:creator>SK Ho</dc:creator>
    <dc:creator>RM Henkelman</dc:creator>
    <dc:creator>JT Henderson</dc:creator>
    <dc:identifier>doi:10.1016/j.neuroscience.2006.08.080</dc:identifier>
    <dc:source>Neuroscience, Vol. 144, No. 2. (19 January 2007), pp. 604-615.</dc:source>
    <dc:date>2007-08-23T19:12:49-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Neuroscience</prism:publicationName>
    <prism:issn>0306-4522</prism:issn>
    <prism:volume>144</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>604</prism:startingPage>
    <prism:endingPage>615</prism:endingPage>
    <prism:category>3d_mouse_brain_atlas</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2997057">
    <title>Three-dimensional atlas system for mouse and rat brain imaging data</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2997057</link>
    <description>&lt;i&gt;Frontiers in Neuroinformatics (2007)&lt;/i&gt;</description>
    <dc:title>Three-dimensional atlas system for mouse and rat brain imaging data</dc:title>

    <dc:creator>Trine Hjornevik</dc:creator>
    <dc:creator>Trygve Leergaard</dc:creator>
    <dc:creator>Dmitri Darine</dc:creator>
    <dc:creator>Olve Moldestad</dc:creator>
    <dc:creator>Anders Dale</dc:creator>
    <dc:creator>Frode Willoch</dc:creator>
    <dc:creator>Jan Bjaalie</dc:creator>
    <dc:source>Frontiers in Neuroinformatics (2007)</dc:source>
    <dc:date>2008-07-13T11:36:55-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>Frontiers in Neuroinformatics</prism:publicationName>
    <prism:category>3d_mouse_brain_atlas</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/714039">
    <title>Opinion: Localization in the brain: new solutions emerging.</title>
    <link>http://www.citeulike.org/user/jonsta247/article/714039</link>
    <description>&lt;i&gt;Nat Rev Neurosci, Vol. 3, No. 4. (April 2002), pp. 322-325.&lt;/i&gt;</description>
    <dc:title>Opinion: Localization in the brain: new solutions emerging.</dc:title>

    <dc:creator>JG Bjaalie</dc:creator>
    <dc:identifier>doi:10.1038/nrn790</dc:identifier>
    <dc:source>Nat Rev Neurosci, Vol. 3, No. 4. (April 2002), pp. 322-325.</dc:source>
    <dc:date>2006-06-28T15:29:24-00:00</dc:date>
    <prism:publicationYear>2002</prism:publicationYear>
    <prism:publicationName>Nat Rev Neurosci</prism:publicationName>
    <prism:issn>1471-003X</prism:issn>
    <prism:volume>3</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>322</prism:startingPage>
    <prism:endingPage>325</prism:endingPage>
    <prism:category>3d_mouse_brain_atlas</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/144342">
    <title>The role of calmodulin as a signal integrator for synaptic plasticity</title>
    <link>http://www.citeulike.org/user/jonsta247/article/144342</link>
    <description>&lt;i&gt;Nature Reviews Neuroscience, Vol. 6, No. 4. (01 April 2005), pp. 267-276.&lt;/i&gt;</description>
    <dc:title>The role of calmodulin as a signal integrator for synaptic plasticity</dc:title>

    <dc:creator>Zhengui Xia</dc:creator>
    <dc:creator>Daniel Storm</dc:creator>
    <dc:identifier>doi:10.1038/nrn1647</dc:identifier>
    <dc:source>Nature Reviews Neuroscience, Vol. 6, No. 4. (01 April 2005), pp. 267-276.</dc:source>
    <dc:date>2005-04-01T15:58:11-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>Nature Reviews Neuroscience</prism:publicationName>
    <prism:issn>1471-003X</prism:issn>
    <prism:volume>6</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>267</prism:startingPage>
    <prism:endingPage>276</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>calmodulin</prism:category>
    <prism:category>ltd</prism:category>
    <prism:category>ltp</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2984024">
    <title>A novel human disease with abnormal prion protein sensitive to protease</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2984024</link>
    <description>&lt;i&gt;Annals of Neurology, Vol. 63, No. 6. (2008), pp. 697-708.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;To report a novel prion disease characterized by distinct histopathological and immunostaining features, and associated with an abnormal isoform of the prion protein (PrP) that, contrary to the common prion diseases, is predominantly sensitive to protease digestion.Eleven subjects were investigated at the National Prion Disease Pathology Surveillance Center for clinical, histopathological, immunohistochemical, genotypical, and PrP characteristics.Patients presented with behavioral and psychiatric manifestations on average at 62 years, whereas mean disease duration was 20 months. The type of spongiform degeneration, the PrP immunostaining pattern, and the presence of microplaques distinguished these cases from those with known prion diseases. Typical protease-resistant PrP was undetectable in the cerebral neocortex with standard diagnostic procedures. After enrichment, abnormal PrP was detected at concentrations 16 times lower than common prion diseases; it included nearly 4 times less protease-resistant PrP, which formed a distinct electrophoretic profile. The subjects examined comprised about 3% of sporadic cases evaluated by the National Prion Disease Pathology Surveillance Center. Although several subjects had family histories of dementia, no mutations were found in the PrP gene open reading frame.The distinct histopathological, PrP immunohistochemical, and physicochemical features, together with the homogeneous genotype, indicate that this is a previously unidentified type of disease involving the PrP, which we designated ldquoprotease-sensitive prionopathyrdquo (or PSPr). Protease-sensitive prionopathy is not rare among prion diseases, and it may be even more prevalent than our data indicate because protease-sensitive prionopathy cases are likely also to be classified within the group of non-Alzheimer's dementias. Ann Neurol 2008;63:697-708</description>
    <dc:title>A novel human disease with abnormal prion protein sensitive to protease</dc:title>

    <dc:creator>Pierluigi Gambetti</dc:creator>
    <dc:creator>Zhiqian Dong</dc:creator>
    <dc:creator>Jue Yuan</dc:creator>
    <dc:creator>Xiangzhu Xiao</dc:creator>
    <dc:creator>Mengjie Zheng</dc:creator>
    <dc:creator>Amer Alshekhlee</dc:creator>
    <dc:creator>Rudy Castellani</dc:creator>
    <dc:creator>Mark Cohen</dc:creator>
    <dc:creator>Marcelo Barria</dc:creator>
    <dc:creator>D Gonzalez-Romero</dc:creator>
    <dc:creator>Ermias Belay</dc:creator>
    <dc:creator>Lawrence Schonberger</dc:creator>
    <dc:creator>Karen Marder</dc:creator>
    <dc:creator>Carrie Harris</dc:creator>
    <dc:creator>James Burke</dc:creator>
    <dc:creator>Thomas Montine</dc:creator>
    <dc:creator>Thomas Wisniewski</dc:creator>
    <dc:creator>Dennis Dickson</dc:creator>
    <dc:creator>Claudio Soto</dc:creator>
    <dc:creator>Christine Hulette</dc:creator>
    <dc:creator>James Mastrianni</dc:creator>
    <dc:creator>Qingzhong Kong</dc:creator>
    <dc:creator>Wen-Quan Zou</dc:creator>
    <dc:identifier>doi:10.1002/ana.21420</dc:identifier>
    <dc:source>Annals of Neurology, Vol. 63, No. 6. (2008), pp. 697-708.</dc:source>
    <dc:date>2008-07-10T07:34:26-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Annals of Neurology</prism:publicationName>
    <prism:volume>63</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>697</prism:startingPage>
    <prism:endingPage>708</prism:endingPage>
    <prism:category>neurodegeneration</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2758509">
    <title>Sleep-dependent learning and memory consolidation.</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2758509</link>
    <description>&lt;i&gt;Neuron, Vol. 44, No. 1. (30 September 2004), pp. 121-133.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;While the functions of sleep remain largely unknown, one of the most exciting and contentious hypotheses is that sleep contributes importantly to memory. A large number of studies offer a substantive body of evidence supporting this role of sleep in what is becoming known as sleep-dependent memory processing. This review will provide evidence of sleep-dependent memory consolidation and sleep-dependent brain plasticity and is divided into five sections: (1) an overview of sleep stages, memory categories, and the distinct stages of memory development; (2) a review of the specific relationships between sleep and memory, both in humans and animals; (3) a survey of evidence describing sleep-dependent brain plasticity, including human brain imaging studies as well as animal studies of cellular neurophysiology and molecular biology. We close (4) with a consideration of unanswered questions as well as existing arguments against the role of sleep in learning and memory and (5) a concluding summary.</description>
    <dc:title>Sleep-dependent learning and memory consolidation.</dc:title>

    <dc:creator>MP Walker</dc:creator>
    <dc:creator>R Stickgold</dc:creator>
    <dc:identifier>doi:10.1016/j.neuron.2004.08.031</dc:identifier>
    <dc:source>Neuron, Vol. 44, No. 1. (30 September 2004), pp. 121-133.</dc:source>
    <dc:date>2008-05-05T18:05:04-00:00</dc:date>
    <prism:publicationYear>2004</prism:publicationYear>
    <prism:publicationName>Neuron</prism:publicationName>
    <prism:issn>0896-6273</prism:issn>
    <prism:volume>44</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>121</prism:startingPage>
    <prism:endingPage>133</prism:endingPage>
    <prism:category>sleep</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2967449">
    <title>Gene expression in the brain across the sleep-waking cycle</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2967449</link>
    <description>&lt;i&gt;Brain Research, Vol. 885, No. 2. (8 December 2000), pp. 303-321.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Sleep and waking differ significantly in terms of behavior, metabolism, and neuronal activity. Recent evidence indicates that sleep and waking also differ with respect to the expression of certain genes. To systematically investigate such changes, we used mRNA differential display and cDNA microarrays to screen ~10[punctuation space]000 transcripts expressed in the cerebral cortex of rats after 8 h of sleep, spontaneous waking, or sleep deprivation. We found that 44 genes had higher mRNA levels after waking and/or sleep deprivation relative to sleep, while 10 were upregulated after sleep. Known genes that were upregulated in waking and sleep deprivation can be grouped into the following categories: immediate early genes/transcription factors (Arc, CHOP, IER5, NGFI-A, NGFI-B, N-Ras, Stat3), genes related to energy metabolism (glucose type I transporter Glut1, Vgf), growth factors/adhesion molecules (BDNF, TrkB, F3 adhesion molecule), chaperones/heat shock proteins (BiP, ERP72, GRP75, HSP60, HSP70), vesicle- and synapse-related genes (chromogranin C, synaptotagmin IV), neurotransmitter/hormone receptors (adrenergic receptor [alpha]1A and [beta]2, GABAA receptor [beta]3, glutamate NMDA receptor 2A, glutamate AMPA receptor GluR2 and GluR3, nicotinic acetylcholine receptor [beta]2, thyroid hormone receptor TR[beta]), neurotransmitter transporters (glutamate/aspartate transporter GLAST, Na+/Cl- transporter NTT4/Rxt1), enzymes (aryl sulfotransferase, c-jun N-terminal kinase 1, serum/glucocorticoid-induced serine/threonine kinase), and a miscellaneous group (calmodulin, cyclin D2, LMO-4, metallothionein 3). Several other genes that were upregulated in waking and all the genes upregulated in sleep, with the exception of the one coding for membrane protein E25, did not match any known sequence. Thus, significant changes in gene expression occur across behavioral states, which are likely to affect basic cellular functions such as RNA and protein synthesis, neural plasticity, neurotransmission, and metabolism.</description>
    <dc:title>Gene expression in the brain across the sleep-waking cycle</dc:title>

    <dc:creator>Chiara Cirelli</dc:creator>
    <dc:creator>Giulio Tononi</dc:creator>
    <dc:identifier>doi:10.1016/S0006-8993(00)03008-0</dc:identifier>
    <dc:source>Brain Research, Vol. 885, No. 2. (8 December 2000), pp. 303-321.</dc:source>
    <dc:date>2008-07-06T15:45:49-00:00</dc:date>
    <prism:publicationYear>2000</prism:publicationYear>
    <prism:publicationName>Brain Research</prism:publicationName>
    <prism:volume>885</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>303</prism:startingPage>
    <prism:endingPage>321</prism:endingPage>
    <prism:category>sleep</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2714486">
    <title>The Role of Sleep in Memory Consolidation and Brain Plasticity: Dream or Reality?</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2714486</link>
    <description>&lt;i&gt;Neuroscientist, Vol. 12, No. 6. (1 December 2006), pp. 477-488.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The notion that a good night of sleep improves memory is widely accepted by the general public. Among sleep scientists, however, the idea has been hotly debated for decades. In this review, the authors consider current evidence for and against the hypothesis that sleep facilitates memory consolidation and promotes plastic changes in the brain. They find that despite a steady accumulation of positive findings over the past decade, the precise role of sleep in memory and brain plasticity remains elusive. This impasse may be resolved by more integrated approaches that combine behavioral and neurophysiological measurements in well-described in vivo models of synaptic plasticity. 10.1177/1073858406293552</description>
    <dc:title>The Role of Sleep in Memory Consolidation and Brain Plasticity: Dream or Reality?</dc:title>

    <dc:creator>Marcos Frank</dc:creator>
    <dc:creator>Joel Benington</dc:creator>
    <dc:identifier>doi:10.1177/1073858406293552</dc:identifier>
    <dc:source>Neuroscientist, Vol. 12, No. 6. (1 December 2006), pp. 477-488.</dc:source>
    <dc:date>2008-04-24T22:13:23-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Neuroscientist</prism:publicationName>
    <prism:volume>12</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>477</prism:startingPage>
    <prism:endingPage>488</prism:endingPage>
    <prism:category>sleep</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/210673">
    <title>Shaking up sleep research</title>
    <link>http://www.citeulike.org/user/jonsta247/article/210673</link>
    <description>&lt;i&gt;Nature Neuroscience, Vol. 8, No. 6., pp. 703-705.&lt;/i&gt;</description>
    <dc:title>Shaking up sleep research</dc:title>

    <dc:creator>Joan Hendricks</dc:creator>
    <dc:identifier>doi:10.1038/nn0605-703</dc:identifier>
    <dc:source>Nature Neuroscience, Vol. 8, No. 6., pp. 703-705.</dc:source>
    <dc:date>2005-05-25T19:50:19-00:00</dc:date>
    <prism:publicationName>Nature Neuroscience</prism:publicationName>
    <prism:issn>1097-6256</prism:issn>
    <prism:volume>8</prism:volume>
    <prism:number>6</prism:number>
    <prism:startingPage>703</prism:startingPage>
    <prism:endingPage>705</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>sleep</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2967038">
    <title>Identifying Genetic Influences on Sleep: An Approach to Discovering the Mechanisms of Sleep Regulation</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2967038</link>
    <description>&lt;i&gt;Behavior Genetics, Vol. 31, No. 1. (1 January 2001), pp. 39-46.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Comparisons of sleep patterns of various inbred strains of mice have revealed differences in daily amounts of slow-wave sleep and rapid-eye movement sleep, in circadian patterns of sleep, and in some parameters of the electroencephalograms both in healthy mice and in mice undergoing microbial infections. Technical considerations will probably be an important variable in achieving consensus between different independent studies that use a genetic approach to identify sleep-regulatory genes or mechanisms. However, despite such differences, current data suggest that both normal sleep and various sleep disorders either have a genetic basis or are influenced by genetically determined physiologic or environmental predispositions. Excessive sleepiness, abnormal sleep patterns, nonrestorative sleep, and fatigue are becoming increasingly pervasive in modern society. Identifying genes that influence vigilance may ultimately contribute to a better understanding of the processes that control normal sleep and contribute to sleep disorders and may eventually promote the development of interventions to prevent or alleviate these disabling medical conditions.</description>
    <dc:title>Identifying Genetic Influences on Sleep: An Approach to Discovering the Mechanisms of Sleep Regulation</dc:title>

    <dc:creator>Linda Toth</dc:creator>
    <dc:identifier>doi:10.1023/A:1010205824874</dc:identifier>
    <dc:source>Behavior Genetics, Vol. 31, No. 1. (1 January 2001), pp. 39-46.</dc:source>
    <dc:date>2008-07-06T09:05:09-00:00</dc:date>
    <prism:publicationYear>2001</prism:publicationYear>
    <prism:publicationName>Behavior Genetics</prism:publicationName>
    <prism:volume>31</prism:volume>
    <prism:number>1</prism:number>
    <prism:startingPage>39</prism:startingPage>
    <prism:endingPage>46</prism:endingPage>
    <prism:category>sleep</prism:category>
    <prism:category>sleeping_mouse</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2967035">
    <title>An automated system for recording and analysis of sleep in mice</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2967035</link>
    <description>&lt;i&gt;&lt;/i&gt;</description>
    <dc:title>An automated system for recording and analysis of sleep in mice</dc:title>

    <dc:date>2008-07-06T09:04:30-00:00</dc:date>
    <prism:category>sleep</prism:category>
    <prism:category>sleeping_mouse</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2967027">
    <title>Animal models for information processing during sleep</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2967027</link>
    <description>&lt;i&gt;International Journal of Psychophysiology, Vol. 46, No. 3. (December 2002), pp. 163-175.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Information provided by external stimuli does reach the brain during sleep, although the amount of information is reduced during sleep compared to wakefulness. The process controlling this reduction is called [`]sensory' gating and evidence exists that the underlying neurophysiological processes take place in the thalamus. Furthermore, it is clear that stimuli given during sleep can alter the functional state of the brain. Two factors have been shown to play a crucial role in causing changes in the sleeping brain: the intensity and the relevance of the stimulus. Intensive stimuli arouse the brain, as well as stimuli having a high informational impact on the sleeping person. The arousal threshold for important stimuli is quite low compared to neutral stimuli. A central question in sleep research is whether associative learning, or in other words the formation of new associations between stimuli, can take place in a sleeping brain. It has been shown that simple forms of learning are still possible during sleep. In sleeping rats, it is proven that habituation, an active, simple form of learning not to respond to irrelevant stimuli, can occur. Moreover, there is evidence for the view that more complex associations can be modulated and newly formed during sleep. This is shown by two experimental approaches: an extinction paradigm and a latent inhibition (pre-exposure) paradigm. The presentation of non-reinforced stimuli during sleep causes slower extinction compared to the same presentation of these stimuli during wakefulness. Consistently, the suppressive capacity of a stimulus in the latent inhibition paradigm is less when previously pre-exposed during sleep, as compared to pre-exposure during wakefulness. Thus, while associative learning is not completely blocked during sleep, aspects of association formation are clearly altered. However, animal studies also clearly indicate that complex forms of learning are not possible during sleep. It is hypothesised that this restriction in information processing during sleep is due to the considerable reduction of incoming information by the sleeping brain. This reduction may serve to protect the sleep process.</description>
    <dc:title>Animal models for information processing during sleep</dc:title>

    <dc:creator>AML Coenen</dc:creator>
    <dc:creator>WHIM Drinkenburg</dc:creator>
    <dc:identifier>doi:10.1016/S0167-8760(02)00110-1</dc:identifier>
    <dc:source>International Journal of Psychophysiology, Vol. 46, No. 3. (December 2002), pp. 163-175.</dc:source>
    <dc:date>2008-07-06T08:46:27-00:00</dc:date>
    <prism:publicationYear>2002</prism:publicationYear>
    <prism:publicationName>International Journal of Psychophysiology</prism:publicationName>
    <prism:volume>46</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>163</prism:startingPage>
    <prism:endingPage>175</prism:endingPage>
    <prism:category>sleep</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2967022">
    <title>The mouse brain adenosine A1 receptor: functional expression and pharmacology</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2967022</link>
    <description>&lt;i&gt;European Journal of Pharmacology, Vol. 487, No. 1-3. (8 March 2004), pp. 73-79.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The adenosinergic system is involved in many important physiological functions. Adenosine exerts its extracellular effects through four types of G-protein-coupled receptors: A1, A2A, A2B and A3. Adenosine acts as an important regulator of metabolic processes. In the brain adenosine mediates prominent neuroprotective functions via the adenosine A1 receptor. Whereas the pharmacological characteristics of the rat and human adenosine A1 receptor have been intensively studied, the mouse adenosine A1 receptor has not yet been characterised. Accordingly, we have cloned the mouse brain adenosine A1 receptor and present here a pharmacological characterisation of the mouse adenosine A1 receptor using functional studies and radioligand binding assays. The results show that the binding affinities of several ligands for the mouse adenosine A1 receptor are similar to the affinities for the rat and human adenosine A1 receptor with some exceptions.</description>
    <dc:title>The mouse brain adenosine A1 receptor: functional expression and pharmacology</dc:title>

    <dc:creator>Maria Wittendorp</dc:creator>
    <dc:creator>von Frijtag</dc:creator>
    <dc:creator>Adriaan Ijzerman</dc:creator>
    <dc:creator>Hendrikus Boddeke</dc:creator>
    <dc:creator>Knut Biber</dc:creator>
    <dc:identifier>doi:10.1016/j.ejphar.2004.01.034</dc:identifier>
    <dc:source>European Journal of Pharmacology, Vol. 487, No. 1-3. (8 March 2004), pp. 73-79.</dc:source>
    <dc:date>2008-07-06T08:39:48-00:00</dc:date>
    <prism:publicationYear>2004</prism:publicationYear>
    <prism:publicationName>European Journal of Pharmacology</prism:publicationName>
    <prism:volume>487</prism:volume>
    <prism:number>1-3</prism:number>
    <prism:startingPage>73</prism:startingPage>
    <prism:endingPage>79</prism:endingPage>
    <prism:category>sleep</prism:category>
    <prism:category>sleeping_mouse</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2967023">
    <title>Brain oxidation is an initial process in sleep induction</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2967023</link>
    <description>&lt;i&gt;Neuroscience, Vol. 130, No. 4. (2005), pp. 1029-1040.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;CNS activity is generally coupled to the vigilance state, being primarily active during wakefulness and primarily inactive during deep sleep. During periods of high neuronal activity, a significant volume of oxygen is used to maintain neuronal membrane potentials, which subsequently produces cytotoxic reactive oxygen species (ROS). Glutathione, a major endogenous antioxidant, is an important factor protecting against ROS-mediated neuronal degeneration. Glutathione has also been proposed to be a sleep-promoting substance, yet the relationship between sleep and cerebral oxidation remains unclear. Here we report that i.c.v. infusion of the organic peroxide t-butyl-hydroperoxide at a concentration below that triggering neurodegeneration (0.1 [mu]mol/100 [mu]l/10 h) promotes sleep in rats. Also, microinjection (2 nmol, 2 [mu]l) or microdialysis (100 [mu]M, 20 min) oft-butyl-hydroperoxide into the preoptic/anterior hypothalamus (POAH) induces the release of the sleep-inducing neuromodulators, nitric oxide and adenosine, without causing neurodegeneration. Nitric oxide and adenosine release was inhibited by co-dialysis of the N-methyl-d-aspartate receptor antagonist, d(-)-2-amino-5-phosphonopentanoic acid (D-AP5; 1 mM), suggesting that glutamate-induced neuronal excitation mediates the peroxide-induced release of nitric oxide and adenosine. Indeed, Ca2+ release from mitochondria and delayed-onset Ca2+ influx via N-methyl-d-aspartate receptors was visualized during peroxide exposure using Ca2+ indicator proteins (YC-2.1 and mitochondrial-targeted Pericam) expressed in organotypic cultures of the POAH. In the in vitro models, t-butyl-hydroperoxide (50 [mu]M) causes dendritic swelling followed by the intracellular Ca2+ mobilization, and D-AP5 (100 [mu]M) or glutathione (500 [mu]M) inhibited t-butyl-hydroperoxide-induced intracellular Ca2+ mobilization and protected POAH neurons from oxidative stress. These data suggest that low-level subcortical oxidation under the control of an antioxidant system may trigger sleep via the Ca2+-dependent release of sleep-inducing neuromodulators in the POAH, and thus we propose that a moderate increase of ROS during wakefulness in the neuronal circuits regulating sleep may be an initial trigger in sleep induction.</description>
    <dc:title>Brain oxidation is an initial process in sleep induction</dc:title>

    <dc:creator>M Ikeda</dc:creator>
    <dc:creator>M Ikeda-Sagara</dc:creator>
    <dc:creator>T Okada</dc:creator>
    <dc:creator>P Clement</dc:creator>
    <dc:creator>Y Urade</dc:creator>
    <dc:creator>T Nagai</dc:creator>
    <dc:creator>T Sugiyama</dc:creator>
    <dc:creator>T Yoshioka</dc:creator>
    <dc:creator>K Honda</dc:creator>
    <dc:creator>S Inoué</dc:creator>
    <dc:identifier>doi:10.1016/j.neuroscience.2004.09.057</dc:identifier>
    <dc:source>Neuroscience, Vol. 130, No. 4. (2005), pp. 1029-1040.</dc:source>
    <dc:date>2008-07-06T08:39:57-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>Neuroscience</prism:publicationName>
    <prism:volume>130</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>1029</prism:startingPage>
    <prism:endingPage>1040</prism:endingPage>
    <prism:category>sleep</prism:category>
    <prism:category>sleeping_mouse</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2967020">
    <title>The dreaming sleep stage: A new neurobiological model of schizophrenia?</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2967020</link>
    <description>&lt;i&gt;Neuroscience, Vol. 140, No. 4. (2006), pp. 1105-1115.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The rapid eye movement dreaming sleep stage and schizophrenia are both characterized by common intracerebral disconnections, disturbed responsiveness and sensory deafferentation processes. Moreover, in both states, there is dorsolateral prefrontal deactivation as shown by the decrease of blood flow. Finally, identical pharmacological and neurochemical variations are observed for acetylcholine, dopamine, noradrenaline, serotonin and glutamate concentrations. Consequently, rapid eye movement sleep could become a useful new neurobiological model of this mental disease since more functional than current rat models using stimulation, lesion or drugs.</description>
    <dc:title>The dreaming sleep stage: A new neurobiological model of schizophrenia?</dc:title>

    <dc:creator>C Gottesmann</dc:creator>
    <dc:identifier>doi:10.1016/j.neuroscience.2006.02.082</dc:identifier>
    <dc:source>Neuroscience, Vol. 140, No. 4. (2006), pp. 1105-1115.</dc:source>
    <dc:date>2008-07-06T08:36:17-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Neuroscience</prism:publicationName>
    <prism:volume>140</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>1105</prism:startingPage>
    <prism:endingPage>1115</prism:endingPage>
    <prism:category>sleep</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2967019">
    <title>Journal of Neurochemistry - Abstract: Volume 92(5) March 2005 p 1150-1157 Sleep deprivation induces the unfolded protein response in mouse cerebral cortex.</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2967019</link>
    <description>&lt;i&gt;&lt;/i&gt;</description>
    <dc:title>Journal of Neurochemistry - Abstract: Volume 92(5) March 2005 p 1150-1157 Sleep deprivation induces the unfolded protein response in mouse cerebral cortex.</dc:title>

    <dc:date>2008-07-06T08:33:27-00:00</dc:date>
    <prism:category>sleep</prism:category>
    <prism:category>sleeping_mouse</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/1113184">
    <title>HOW DID ALTERNATIVE SPLICING EVOLVE?</title>
    <link>http://www.citeulike.org/user/jonsta247/article/1113184</link>
    <description>&lt;i&gt;Nat Rev Genet, Vol. 5, No. 10. (October 2004), pp. 773-782.&lt;/i&gt;</description>
    <dc:title>HOW DID ALTERNATIVE SPLICING EVOLVE?</dc:title>

    <dc:creator>Gil Ast</dc:creator>
    <dc:identifier>doi:10.1038/nrg1451 </dc:identifier>
    <dc:source>Nat Rev Genet, Vol. 5, No. 10. (October 2004), pp. 773-782.</dc:source>
    <dc:date>2007-02-19T18:13:26-00:00</dc:date>
    <prism:publicationYear>2004</prism:publicationYear>
    <prism:publicationName>Nat Rev Genet</prism:publicationName>
    <prism:volume>5</prism:volume>
    <prism:number>10</prism:number>
    <prism:startingPage>773</prism:startingPage>
    <prism:endingPage>782</prism:endingPage>
    <prism:category>alternative_splicing</prism:category>
    <prism:category>splicing</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/509592">
    <title>The evolution of spliceosomal introns: patterns, puzzles and progress</title>
    <link>http://www.citeulike.org/user/jonsta247/article/509592</link>
    <description>&lt;i&gt;Nature Reviews Genetics, Vol. 7, No. 3., pp. 211-221.&lt;/i&gt;</description>
    <dc:title>The evolution of spliceosomal introns: patterns, puzzles and progress</dc:title>

    <dc:creator>Scott Roy</dc:creator>
    <dc:creator>Walter Gilbert</dc:creator>
    <dc:identifier>doi:10.1038/nrg1807</dc:identifier>
    <dc:source>Nature Reviews Genetics, Vol. 7, No. 3., pp. 211-221.</dc:source>
    <dc:date>2006-02-18T12:44:53-00:00</dc:date>
    <prism:publicationName>Nature Reviews Genetics</prism:publicationName>
    <prism:issn>1471-0056</prism:issn>
    <prism:volume>7</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>211</prism:startingPage>
    <prism:endingPage>221</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>splicing</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2240994">
    <title>Translational control of intron splicing in eukaryotes</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2240994</link>
    <description>&lt;i&gt;Nature, Vol. 451, No. 7176. (17 January 2008), pp. 359-362.&lt;/i&gt;</description>
    <dc:title>Translational control of intron splicing in eukaryotes</dc:title>

    <dc:creator>Olivier Jaillon</dc:creator>
    <dc:creator>Khaled Bouhouche</dc:creator>
    <dc:creator>Jean-Francois Gout</dc:creator>
    <dc:creator>Jean-Marc Aury</dc:creator>
    <dc:creator>Benjamin Noel</dc:creator>
    <dc:creator>Baptiste Saudemont</dc:creator>
    <dc:creator>Mariusz Nowacki</dc:creator>
    <dc:creator>Vincent Serrano</dc:creator>
    <dc:creator>Betina Porcel</dc:creator>
    <dc:creator>Beatrice Segurens</dc:creator>
    <dc:creator>Anne Le Mouel</dc:creator>
    <dc:creator>Gersende Lepere</dc:creator>
    <dc:creator>Vincent Schachter</dc:creator>
    <dc:creator>Mireille Betermier</dc:creator>
    <dc:creator>Jean Cohen</dc:creator>
    <dc:creator>Patrick Wincker</dc:creator>
    <dc:creator>Linda Sperling</dc:creator>
    <dc:creator>Laurent Duret</dc:creator>
    <dc:creator>Eric Meyer</dc:creator>
    <dc:identifier>doi:10.1038/nature06495</dc:identifier>
    <dc:source>Nature, Vol. 451, No. 7176. (17 January 2008), pp. 359-362.</dc:source>
    <dc:date>2008-01-16T20:57:48-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Nature</prism:publicationName>
    <prism:volume>451</prism:volume>
    <prism:number>7176</prism:number>
    <prism:startingPage>359</prism:startingPage>
    <prism:endingPage>362</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>splicing</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/241496">
    <title>In vivo auditory brain mapping in mice with Mn-enhanced MRI</title>
    <link>http://www.citeulike.org/user/jonsta247/article/241496</link>
    <description>&lt;i&gt;Nature Neuroscience, Vol. 8, No. 7. (29 May 2005), pp. 961-968.&lt;/i&gt;</description>
    <dc:title>In vivo auditory brain mapping in mice with Mn-enhanced MRI</dc:title>

    <dc:creator>Xin Yu</dc:creator>
    <dc:creator>Youssef Wadghiri</dc:creator>
    <dc:creator>Dan Sanes</dc:creator>
    <dc:creator>Daniel Turnbull</dc:creator>
    <dc:identifier>doi:10.1038/nn1477</dc:identifier>
    <dc:source>Nature Neuroscience, Vol. 8, No. 7. (29 May 2005), pp. 961-968.</dc:source>
    <dc:date>2005-07-01T19:24:03-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>Nature Neuroscience</prism:publicationName>
    <prism:issn>1097-6256</prism:issn>
    <prism:volume>8</prism:volume>
    <prism:number>7</prism:number>
    <prism:startingPage>961</prism:startingPage>
    <prism:endingPage>968</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>3d_mouse_brain_atlas</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2965884">
    <title>Three-Dimensional Visualization of Protein Expression in Mouse Brain Structures Using Imaging Mass Spectrometry</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2965884</link>
    <description>&lt;i&gt;Journal of the American Society for Mass Spectrometry, Vol. 16, No. 7. (July 2005), pp. 1093-1099.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;We have developed a method to visualize matrix-assisted laser desorption ionization imaging mass spectrometry (MALDI IMS) data aligned with optically determinable tissue structures in three dimensions. Details of the methodology are exemplified using the 3-D reconstruction of myelin basic protein (MBP) in the corpus callosum of a mouse brain. In this procedure, optical images obtained from serial coronal sections are first aligned to each other to reconstruct a surface of the corpus callosum from segmented contours of the aligned images. The MALDI IMS data are then coregistered to the optical images and superimposed into the surface to create the final 3-D visualization. Correlating proteomic data with anatomical structures provides a more comprehensive understanding of healthy and pathological brain functions, and holds promise to be utilized in more complex anatomical arrangements.</description>
    <dc:title>Three-Dimensional Visualization of Protein Expression in Mouse Brain Structures Using Imaging Mass Spectrometry</dc:title>

    <dc:creator>Anna Crecelius</dc:creator>
    <dc:creator>Shannon Cornett</dc:creator>
    <dc:creator>Richard Caprioli</dc:creator>
    <dc:creator>Betsy Williams</dc:creator>
    <dc:creator>Benoit Dawant</dc:creator>
    <dc:creator>Bobby Bodenheimer</dc:creator>
    <dc:identifier>doi:10.1016/j.jasms.2005.02.026</dc:identifier>
    <dc:source>Journal of the American Society for Mass Spectrometry, Vol. 16, No. 7. (July 2005), pp. 1093-1099.</dc:source>
    <dc:date>2008-07-05T12:56:20-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>Journal of the American Society for Mass Spectrometry</prism:publicationName>
    <prism:volume>16</prism:volume>
    <prism:number>7</prism:number>
    <prism:startingPage>1093</prism:startingPage>
    <prism:endingPage>1099</prism:endingPage>
    <prism:category>3d_mouse_brain_atlas</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/567041">
    <title>A three-dimensional digital atlas database of the adult C57BL/6J mouse brain by magnetic resonance microscopy.</title>
    <link>http://www.citeulike.org/user/jonsta247/article/567041</link>
    <description>&lt;i&gt;Neuroscience, Vol. 135, No. 4. (2005), pp. 1203-1215.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;A comprehensive three-dimensional digital atlas database of the C57BL/6J mouse brain was developed based on magnetic resonance microscopy images acquired on a 17.6-T superconducting magnet. By using both manual tracing and an atlas-based semi-automatic segmentation approach, T2-weighted magnetic resonance microscopy images of 10 adult male formalin-fixed, excised C57BL/6J mouse brains were segmented into 20 anatomical structures. These structures included the neocortex, hippocampus, amygdala, olfactory bulbs, basal forebrain and septum, caudate-putamen, globus pallidus, thalamus, hypothalamus, central gray, superior colliculi, inferior colliculi, the rest of midbrain, cerebellum, brainstem, corpus callosum/external capsule, internal capsule, anterior commissure, fimbria, and ventricles. The segmentation data were formatted and stored into a database containing three different atlas types: 10 single-specimen brain atlases, an average brain atlas and a probabilistic atlas. Additionally, quantitative group information, such as variations in structural volume, surface area, magnetic resonance microscopy image intensity and local geometry, were computed and stored as an integral part of the database. The database augments ongoing efforts with other high priority strains as defined by the Mouse Phenome Database focused on providing a quantitative framework for accurate mapping of functional, genetic and protein expression patterns acquired by a myriad of technologies and imaging modalities.</description>
    <dc:title>A three-dimensional digital atlas database of the adult C57BL/6J mouse brain by magnetic resonance microscopy.</dc:title>

    <dc:creator>Y Ma</dc:creator>
    <dc:creator>PR Hof</dc:creator>
    <dc:creator>SC Grant</dc:creator>
    <dc:creator>SJ Blackband</dc:creator>
    <dc:creator>R Bennett</dc:creator>
    <dc:creator>L Slatest</dc:creator>
    <dc:creator>MD McGuigan</dc:creator>
    <dc:creator>H Benveniste</dc:creator>
    <dc:identifier>doi:10.1016/j.neuroscience.2005.07.014</dc:identifier>
    <dc:source>Neuroscience, Vol. 135, No. 4. (2005), pp. 1203-1215.</dc:source>
    <dc:date>2006-03-28T22:39:57-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>Neuroscience</prism:publicationName>
    <prism:issn>0306-4522</prism:issn>
    <prism:volume>135</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>1203</prism:startingPage>
    <prism:endingPage>1215</prism:endingPage>
    <prism:category>3d_mouse_brain_atlas</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/977247">
    <title>Genome-wide atlas of gene expression in the adult mouse brain</title>
    <link>http://www.citeulike.org/user/jonsta247/article/977247</link>
    <description>&lt;i&gt;Nature&lt;/i&gt;</description>
    <dc:title>Genome-wide atlas of gene expression in the adult mouse brain</dc:title>

    <dc:creator>Ed Lein</dc:creator>
    <dc:creator>Michael Hawrylycz</dc:creator>
    <dc:creator>Nancy Ao</dc:creator>
    <dc:creator>Mikael Ayres</dc:creator>
    <dc:creator>Amy Bensinger</dc:creator>
    <dc:creator>Amy Bernard</dc:creator>
    <dc:creator>Andrew Boe</dc:creator>
    <dc:creator>Mark Boguski</dc:creator>
    <dc:creator>Kevin Brockway</dc:creator>
    <dc:creator>Emi Byrnes</dc:creator>
    <dc:creator>Lin Chen</dc:creator>
    <dc:creator>Li Chen</dc:creator>
    <dc:creator>Tsuey-Ming Chen</dc:creator>
    <dc:creator>Mei Chin</dc:creator>
    <dc:creator>Jimmy Chong</dc:creator>
    <dc:creator>Brian Crook</dc:creator>
    <dc:creator>Aneta Czaplinska</dc:creator>
    <dc:creator>Chinh Dang</dc:creator>
    <dc:creator>Suvro Datta</dc:creator>
    <dc:creator>Nick Dee</dc:creator>
    <dc:creator>Aimee Desaki</dc:creator>
    <dc:creator>Tsega Desta</dc:creator>
    <dc:creator>Ellen Diep</dc:creator>
    <dc:creator>Tim Dolbeare</dc:creator>
    <dc:creator>Matthew Donelan</dc:creator>
    <dc:creator>Hong-Wei Dong</dc:creator>
    <dc:creator>Jennifer Dougherty</dc:creator>
    <dc:creator>Ben Duncan</dc:creator>
    <dc:creator>Amanda Ebbert</dc:creator>
    <dc:creator>Gregor Eichele</dc:creator>
    <dc:creator>Lili Estin</dc:creator>
    <dc:creator>Casey Faber</dc:creator>
    <dc:creator>Benjamin Facer</dc:creator>
    <dc:creator>Rick Fields</dc:creator>
    <dc:creator>Shanna Fischer</dc:creator>
    <dc:creator>Tim Fliss</dc:creator>
    <dc:creator>Cliff Frensley</dc:creator>
    <dc:creator>Sabrina Gates</dc:creator>
    <dc:creator>Katie Glattfelder</dc:creator>
    <dc:creator>Kevin Halverson</dc:creator>
    <dc:creator>Matthew Hart</dc:creator>
    <dc:creator>John Hohmann</dc:creator>
    <dc:creator>Maureen Howell</dc:creator>
    <dc:creator>Darren Jeung</dc:creator>
    <dc:creator>Rebecca Johnson</dc:creator>
    <dc:creator>Patrick Karr</dc:creator>
    <dc:creator>Reena Kawal</dc:creator>
    <dc:creator>Jolene Kidney</dc:creator>
    <dc:creator>Rachel Knapik</dc:creator>
    <dc:creator>Chihchau Kuan</dc:creator>
    <dc:creator>James Lake</dc:creator>
    <dc:creator>Annabel Laramee</dc:creator>
    <dc:creator>Kirk Larsen</dc:creator>
    <dc:creator>Christopher Lau</dc:creator>
    <dc:creator>Tracy Lemon</dc:creator>
    <dc:creator>Agnes Liang</dc:creator>
    <dc:creator>Ying Liu</dc:creator>
    <dc:creator>Lon Luong</dc:creator>
    <dc:creator>Jesse Michaels</dc:creator>
    <dc:creator>Judith Morgan</dc:creator>
    <dc:creator>Rebecca Morgan</dc:creator>
    <dc:creator>Marty Mortrud</dc:creator>
    <dc:creator>Nerick Mosqueda</dc:creator>
    <dc:creator>Lydia Ng</dc:creator>
    <dc:creator>Randy Ng</dc:creator>
    <dc:creator>Geralyn Orta</dc:creator>
    <dc:creator>Caroline Overly</dc:creator>
    <dc:creator>Tu Pak</dc:creator>
    <dc:creator>Sheana Parry</dc:creator>
    <dc:creator>Sayan Pathak</dc:creator>
    <dc:creator>Owen Pearson</dc:creator>
    <dc:creator>Ralph Puchalski</dc:creator>
    <dc:creator>Zackery Riley</dc:creator>
    <dc:creator>Hannah Rockett</dc:creator>
    <dc:creator>Stephen Rowland</dc:creator>
    <dc:creator>Joshua Royall</dc:creator>
    <dc:creator>Marcos Ruiz</dc:creator>
    <dc:creator>Nadia Sarno</dc:creator>
    <dc:creator>Katherine Schaffnit</dc:creator>
    <dc:creator>Nadiya Shapovalova</dc:creator>
    <dc:creator>Taz Sivisay</dc:creator>
    <dc:creator>Clifford Slaughterbeck</dc:creator>
    <dc:creator>Simon Smith</dc:creator>
    <dc:creator>Kimberly Smith</dc:creator>
    <dc:creator>Bryan Smith</dc:creator>
    <dc:creator>Andy Sodt</dc:creator>
    <dc:creator>Nick Stewart</dc:creator>
    <dc:creator>Kenda-Ruth Stumpf</dc:creator>
    <dc:creator>Susan Sunkin</dc:creator>
    <dc:creator>Madhavi Sutram</dc:creator>
    <dc:creator>Angelene Tam</dc:creator>
    <dc:creator>Carey Teemer</dc:creator>
    <dc:creator>Christina Thaller</dc:creator>
    <dc:creator>Carol Thompson</dc:creator>
    <dc:creator>Lee Varnam</dc:creator>
    <dc:creator>Axel Visel</dc:creator>
    <dc:creator>Ray Whitlock</dc:creator>
    <dc:creator>Paul Wohnoutka</dc:creator>
    <dc:creator>Crissa Wolkey</dc:creator>
    <dc:creator>Victoria Wong</dc:creator>
    <dc:creator>Matthew Wood</dc:creator>
    <dc:creator>Murat Yaylaoglu</dc:creator>
    <dc:creator>Rob Young</dc:creator>
    <dc:creator>Brian Youngstrom</dc:creator>
    <dc:creator>Xu Yuan</dc:creator>
    <dc:creator>Bin Zhang</dc:creator>
    <dc:creator>Theresa Zwingman</dc:creator>
    <dc:creator>Allan Jones</dc:creator>
    <dc:identifier>doi:10.1038/nature05453</dc:identifier>
    <dc:source>Nature</dc:source>
    <dc:date>2006-12-06T23:59:44-00:00</dc:date>
    <prism:publicationName>Nature</prism:publicationName>
    <prism:issn>0028-0836</prism:issn>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>3d_mouse_brain_atlas</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2965881">
    <title>Building a 3D Atlas of the Mouse Brain</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2965881</link>
    <description>&lt;i&gt;(2005)&lt;/i&gt;</description>
    <dc:title>Building a 3D Atlas of the Mouse Brain</dc:title>

    <dc:creator>Tao Ju</dc:creator>
    <dc:source>(2005)</dc:source>
    <dc:date>2008-07-05T12:50:22-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:category>3d_mouse_brain_atlas</prism:category>
    <prism:category>phd</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2910862">
    <title>The Spread of Ras Activity Triggered by Activation of a Single Dendritic Spine</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2910862</link>
    <description>&lt;i&gt;Science (12 June 2008), 1159675.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;In neurons, individual dendritic spines isolate NMDA receptor-mediated Ca2+ accumulations from the dendrite and other spines. However, it is not known to what extent spines compartmentalize signaling events downstream of Ca2+ influx. We combined two-photon fluorescence lifetime imaging (FLIM) with two-photon glutamate uncaging to image the activity of the small GTPase Ras following NMDA receptor activation at individual spines. Induction of long-term potentiation (LTP) triggered robust Ca2+-dependent Ras activation in single spines that decayed in approximately 5 minutes. Ras activity spread over approximately 10 micrometers of dendrite and invaded neighboring spines by diffusion. The spread of Ras-dependent signaling was necessary for the local regulation of the threshold for LTP induction. Thus Ca2+-dependent synaptic signals can spread to couple multiple synapses on short stretches of dendrite. 10.1126/science.1159675</description>
    <dc:title>The Spread of Ras Activity Triggered by Activation of a Single Dendritic Spine</dc:title>

    <dc:creator>Christopher Harvey</dc:creator>
    <dc:creator>Ryohei Yasuda</dc:creator>
    <dc:creator>Haining Zhong</dc:creator>
    <dc:creator>Karel Svoboda</dc:creator>
    <dc:identifier>doi:10.1126/science.1159675</dc:identifier>
    <dc:source>Science (12 June 2008), 1159675.</dc:source>
    <dc:date>2008-06-20T15:28:22-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Science</prism:publicationName>
    <prism:startingPage>1159675</prism:startingPage>
    <prism:category>dendritic_spine</prism:category>
    <prism:category>flim_fret</prism:category>
    <prism:category>ras</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2953511">
    <title>Highly sensitive and quantitative FRET–FLIM imaging in single dendritic spines using improved non-radiative YFP</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2953511</link>
    <description>&lt;i&gt;Brain Cell Biology&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Abstract&#160;&#160;Two-photon fluorescence lifetime imaging microscopy (TPFLIM) enables the quantitative measurements of fluorescence resonance energy transfer (FRET) in small subcellular compartments in light scattering tissue. We evaluated and optimized the FRET pair of mEGFP (monomeric EGFP with the A206K mutation) and REACh (non-radiative YFP variants) for TPFLIM. We characterized several mutants of REACh in terms of their “darkness,” and their ability to act as a FRET acceptor for mEGFP in HeLa cells and hippocampal neurons. Since the commonly used monomeric mutation A206K increases the brightness of REACh, we introduced a different monomeric mutation (F223R) which does not affect the brightness. Also, we found that the folding efficiency of original REACh, as measured by the fluorescence lifetime of a mEGFP–REACh tandem dimer, was low and variable from cell to cell. Introducing two folding mutations (F46L, Q69M) into REACh increased the folding efficiency by ∼50%, and reduced the variability of FRET signal. Pairing mEGFP with the new REACh (super-REACh, or sREACh) improved the signal-to-noise ratio compared to the mEGFP–mRFP or mEGFP–original REACh pair by ∼50%. Using this new pair, we demonstrated that the fraction of actin monomers in filamentous and globular forms in single dendritic spines can be quantitatively measured with high sensitivity. Thus, the mEGFP–sREACh pair is suited for quantitative FRET measurement by TPFLIM, and enables us to measure protein–protein interactions in individual dendritic spines in brain slices with high sensitivity.</description>
    <dc:title>Highly sensitive and quantitative FRET–FLIM imaging in single dendritic spines using improved non-radiative YFP</dc:title>

    <dc:creator>Hideji Murakoshi</dc:creator>
    <dc:creator>Seok-Jin Lee</dc:creator>
    <dc:creator>Ryohei Yasuda</dc:creator>
    <dc:identifier>doi:10.1007/s11068-008-9024-9</dc:identifier>
    <dc:source>Brain Cell Biology</dc:source>
    <dc:date>2008-07-02T20:24:35-00:00</dc:date>
    <prism:publicationName>Brain Cell Biology</prism:publicationName>
    <prism:category>dendritic_spine</prism:category>
    <prism:category>flim_fret</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2894985">
    <title>Extraterrestrial nucleobases in the Murchison meteorite</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2894985</link>
    <description>&lt;i&gt;Earth and Planetary Science Letters, Vol. 270, No. 1-2. (15 June 2008), pp. 130-136.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Carbon-rich meteorites, carbonaceous chondrites, contain many biologically relevant organic molecules and delivered prebiotic material to the young Earth. We present compound-specific carbon isotope data indicating that measured purine and pyrimidine compounds are indigenous components of the Murchison meteorite. Carbon isotope ratios for uracil and xanthine of [delta]13C = + 44.5[per mille sign] and + 37.7[per mille sign], respectively, indicate a non-terrestrial origin for these compounds. These new results demonstrate that organic compounds, which are components of the genetic code in modern biochemistry, were already present in the early solar system and may have played a key role in life's origin.</description>
    <dc:title>Extraterrestrial nucleobases in the Murchison meteorite</dc:title>

    <dc:creator>Zita Martins</dc:creator>
    <dc:creator>Oliver Botta</dc:creator>
    <dc:creator>Marilyn Fogel</dc:creator>
    <dc:creator>Mark Sephton</dc:creator>
    <dc:creator>Daniel Glavin</dc:creator>
    <dc:creator>Jonathan Watson</dc:creator>
    <dc:creator>Jason Dworkin</dc:creator>
    <dc:creator>Alan Schwartz</dc:creator>
    <dc:creator>Pascale Ehrenfreund</dc:creator>
    <dc:identifier>doi:10.1016/j.epsl.2008.03.026</dc:identifier>
    <dc:source>Earth and Planetary Science Letters, Vol. 270, No. 1-2. (15 June 2008), pp. 130-136.</dc:source>
    <dc:date>2008-06-14T18:43:33-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Earth and Planetary Science Letters</prism:publicationName>
    <prism:volume>270</prism:volume>
    <prism:number>1-2</prism:number>
    <prism:startingPage>130</prism:startingPage>
    <prism:endingPage>136</prism:endingPage>
    <prism:category>life_origin</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2870072">
    <title>Subdiffraction Multicolor Imaging of the Nuclear Periphery with 3D Structured Illumination Microscopy</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2870072</link>
    <description>&lt;i&gt;Science, Vol. 320, No. 5881. (6 June 2008), pp. 1332-1336.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Fluorescence light microscopy allows multicolor visualization of cellular components with high specificity, but its utility has until recently been constrained by the intrinsic limit of spatial resolution. We applied three-dimensional structured illumination microscopy (3D-SIM) to circumvent this limit and to study the mammalian nucleus. By simultaneously imaging chromatin, nuclear lamina, and the nuclear pore complex (NPC), we observed several features that escape detection by conventional microscopy. We could resolve single NPCs that colocalized with channels in the lamin network and peripheral heterochromatin. We could differentially localize distinct NPC components and detect double-layered invaginations of the nuclear envelope in prophase as previously seen only by electron microscopy. Multicolor 3D-SIM opens new and facile possibilities to analyze subcellular structures beyond the diffraction limit of the emitted light. 10.1126/science.1156947</description>
    <dc:title>Subdiffraction Multicolor Imaging of the Nuclear Periphery with 3D Structured Illumination Microscopy</dc:title>

    <dc:creator>Lothar Schermelleh</dc:creator>
    <dc:creator>Peter Carlton</dc:creator>
    <dc:creator>Sebastian Haase</dc:creator>
    <dc:creator>Lin Shao</dc:creator>
    <dc:creator>Lukman Winoto</dc:creator>
    <dc:creator>Peter Kner</dc:creator>
    <dc:creator>Brian Burke</dc:creator>
    <dc:creator>Cristina Cardoso</dc:creator>
    <dc:creator>David Agard</dc:creator>
    <dc:creator>Mats Gustafsson</dc:creator>
    <dc:creator>Heinrich Leonhardt</dc:creator>
    <dc:creator>John Sedat</dc:creator>
    <dc:identifier>doi:10.1126/science.1156947</dc:identifier>
    <dc:source>Science, Vol. 320, No. 5881. (6 June 2008), pp. 1332-1336.</dc:source>
    <dc:date>2008-06-06T16:49:53-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Science</prism:publicationName>
    <prism:volume>320</prism:volume>
    <prism:number>5881</prism:number>
    <prism:startingPage>1332</prism:startingPage>
    <prism:endingPage>1336</prism:endingPage>
    <prism:category>3d_sim</prism:category>
    <prism:category>microscopy</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2867624">
    <title>Protein-DNA Recognition Databse</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2867624</link>
    <description>&lt;i&gt;&lt;/i&gt;</description>
    <dc:title>Protein-DNA Recognition Databse</dc:title>

    <dc:date>2008-06-05T20:20:55-00:00</dc:date>
    <prism:category>protein_dna_interaction</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2867623">
    <title>Cold Spring Harbor Laboratory</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2867623</link>
    <description>&lt;i&gt;&lt;/i&gt;</description>
    <dc:title>Cold Spring Harbor Laboratory</dc:title>

    <dc:date>2008-06-05T20:20:16-00:00</dc:date>
    <prism:category>labs</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2867622">
    <title>HHMI's BioInteractive</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2867622</link>
    <description>&lt;i&gt;&lt;/i&gt;</description>
    <dc:title>HHMI's BioInteractive</dc:title>

    <dc:date>2008-06-05T20:19:37-00:00</dc:date>
    <prism:category>videolectures</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2867606">
    <title>FH Campus Wien - Online-Services für Studierende</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2867606</link>
    <description>&lt;i&gt;&lt;/i&gt;</description>
    <dc:title>FH Campus Wien - Online-Services für Studierende</dc:title>

    <dc:date>2008-06-05T20:08:19-00:00</dc:date>
    <prism:category>aging</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/801862">
    <title>Mechanisms of gene silencing by double-stranded RNA</title>
    <link>http://www.citeulike.org/user/jonsta247/article/801862</link>
    <description>&lt;i&gt;Nature, Vol. 431, No. 7006. (2004), pp. 343-349.&lt;/i&gt;</description>
    <dc:title>Mechanisms of gene silencing by double-stranded RNA</dc:title>

    <dc:creator>Gunter Meister</dc:creator>
    <dc:creator>Thomas Tuschl</dc:creator>
    <dc:identifier>doi:10.1038/nature02873</dc:identifier>
    <dc:source>Nature, Vol. 431, No. 7006. (2004), pp. 343-349.</dc:source>
    <dc:date>2006-08-15T10:49:21-00:00</dc:date>
    <prism:publicationYear>2004</prism:publicationYear>
    <prism:publicationName>Nature</prism:publicationName>
    <prism:volume>431</prism:volume>
    <prism:number>7006</prism:number>
    <prism:startingPage>343</prism:startingPage>
    <prism:endingPage>349</prism:endingPage>
    <prism:category>review</prism:category>
    <prism:category>rnai</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/171583">
    <title>Trafficking in emotions</title>
    <link>http://www.citeulike.org/user/jonsta247/article/171583</link>
    <description>&lt;i&gt;Nature Neuroscience, Vol. 8, No. 5., pp. 548-550.&lt;/i&gt;</description>
    <dc:title>Trafficking in emotions</dc:title>

    <dc:creator>Dan Ehninger</dc:creator>
    <dc:creator>Anna Matynia</dc:creator>
    <dc:creator>Alcino Silva</dc:creator>
    <dc:identifier>doi:10.1038/nn0505-548</dc:identifier>
    <dc:source>Nature Neuroscience, Vol. 8, No. 5., pp. 548-550.</dc:source>
    <dc:date>2005-04-26T18:40:26-00:00</dc:date>
    <prism:publicationName>Nature Neuroscience</prism:publicationName>
    <prism:issn>1097-6256</prism:issn>
    <prism:volume>8</prism:volume>
    <prism:number>5</prism:number>
    <prism:startingPage>548</prism:startingPage>
    <prism:endingPage>550</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>ampa</prism:category>
    <prism:category>memory</prism:category>
    <prism:category>postsynaptic_receptor_trafficking</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/147952">
    <title>Postsynaptic Receptor Trafficking Underlying a Form of Associative Learning</title>
    <link>http://www.citeulike.org/user/jonsta247/article/147952</link>
    <description>&lt;i&gt;Science, Vol. 308, No. 5718. (01 April 2005), pp. 83-88.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;To elucidate molecular, cellular, and circuit changes that occur in the brain during learning, we investigated the role of a glutamate receptor subtype in fear conditioning. In this form of learning, animals associate two stimuli, such as a tone and a shock. Here we report that fear conditioning drives AMPA-type glutamate receptors into the synapse of a large fraction of postsynaptic neurons in the lateral amygdala, a brain structure essential for this learning process. Furthermore, memory was reduced if AMPA receptor synaptic incorporation was blocked in as few as 10 to 20% of lateral amygdala neurons. Thus, the encoding of memories in the lateral amygdala is mediated by AMPA receptor trafficking, is widely distributed, and displays little redundancy.</description>
    <dc:title>Postsynaptic Receptor Trafficking Underlying a Form of Associative Learning</dc:title>

    <dc:creator>Simon Rumpel</dc:creator>
    <dc:creator>Joseph Ledoux</dc:creator>
    <dc:creator>Anthony Zador</dc:creator>
    <dc:creator>Roberto Malinow</dc:creator>
    <dc:identifier>doi:10.1126/science.1103944</dc:identifier>
    <dc:source>Science, Vol. 308, No. 5718. (01 April 2005), pp. 83-88.</dc:source>
    <dc:date>2005-04-03T08:14:16-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>Science</prism:publicationName>
    <prism:volume>308</prism:volume>
    <prism:number>5718</prism:number>
    <prism:startingPage>83</prism:startingPage>
    <prism:endingPage>88</prism:endingPage>
    <prism:category>ampa</prism:category>
    <prism:category>associative_learning</prism:category>
    <prism:category>glur1</prism:category>
    <prism:category>learning</prism:category>
    <prism:category>memory</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2747036">
    <title>Intermediate filaments are dynamic and motile elements of cellular architecture</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2747036</link>
    <description>&lt;i&gt;J Cell Sci, Vol. 117, No. 2. (15 January 2004), pp. 133-141.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Recent evidence showing that intermediate filaments (IFs) are dynamic, motile elements of the cytoskeletal repertoire of vertebrate cells has overturned the long-standing view that they simply form static `space filling' cytoplasmic networks. In fact, many types of IF are now known to engage in a remarkable array of movements that are closely associated with their assembly, disassembly and subcellular organization. Some of these motile properties are intrinsic to IFs and others are attributable to molecular crosstalk with either microtubules or actin-containing microfilaments. This crosstalk is, to a large extent, mediated by molecular motors, including conventional kinesin and cytoplasmic dynein. These motors are responsible for the high-speed delivery of nonfilamentous IF precursors and short filaments to specific regions of the cytoplasm, where they assemble into long IFs. Interestingly, the patterns and speeds of IF movements vary in different cell types and even within different regions of the same cell. These differences in motility may be related to their interactions with different types of molecular motor and/or other factors, such as IF-associated proteins. 10.1242/jcs.00936</description>
    <dc:title>Intermediate filaments are dynamic and motile elements of cellular architecture</dc:title>

    <dc:creator>Brian Helfand</dc:creator>
    <dc:creator>Lynne Chang</dc:creator>
    <dc:creator>Robert Goldman</dc:creator>
    <dc:identifier>doi:10.1242/jcs.00936</dc:identifier>
    <dc:source>J Cell Sci, Vol. 117, No. 2. (15 January 2004), pp. 133-141.</dc:source>
    <dc:date>2008-05-02T20:40:01-00:00</dc:date>
    <prism:publicationYear>2004</prism:publicationYear>
    <prism:publicationName>J Cell Sci</prism:publicationName>
    <prism:volume>117</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>133</prism:startingPage>
    <prism:endingPage>141</prism:endingPage>
    <prism:category>free_fulltext</prism:category>
    <prism:category>intermediate_filament</prism:category>
    <prism:category>review</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2724535">
    <title>Quantitative cDNA-AFLP analysis for genome-wide expression studies.</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2724535</link>
    <description>&lt;i&gt;Molecular genetics and genomics : MGG, Vol. 269, No. 2. (May 2003), pp. 173-179.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;An improved cDNA-AFLP method for genome-wide expression analysis has been developed. We demonstrate that this method is an efficient tool for quantitative transcript profiling and a valid alternative to microarrays. Unique transcript tags, generated from reverse-transcribed messenger RNA by restriction enzymes, were screened through a series of selective PCR amplifications. Based on in silico analysis, an enzyme combination was chosen that ensures that at least 60% of all the mRNAs were represented by an informative sequence tag. The sensitivity and specificity of the method allows one to detect poorly expressed genes and distinguish between homologous sequences. Accurate gene expression profiles were determined by quantitative analysis of band intensities, and subtle differences in transcriptional activity were revealed. A detailed screen for cell cycle-modulated genes in tobacco demonstrates the usefulness of the technology for genome-wide expression analysis.</description>
    <dc:title>Quantitative cDNA-AFLP analysis for genome-wide expression studies.</dc:title>

    <dc:creator>P Breyne</dc:creator>
    <dc:creator>R Dreesen</dc:creator>
    <dc:creator>B Cannoot</dc:creator>
    <dc:creator>D Rombaut</dc:creator>
    <dc:creator>K Vandepoele</dc:creator>
    <dc:creator>S Rombauts</dc:creator>
    <dc:creator>R Vanderhaeghen</dc:creator>
    <dc:creator>D Inzé</dc:creator>
    <dc:creator>M Zabeau</dc:creator>
    <dc:identifier>doi:10.1007/s00438-003-0830-6</dc:identifier>
    <dc:source>Molecular genetics and genomics : MGG, Vol. 269, No. 2. (May 2003), pp. 173-179.</dc:source>
    <dc:date>2008-04-27T19:15:00-00:00</dc:date>
    <prism:publicationYear>2003</prism:publicationYear>
    <prism:publicationName>Molecular genetics and genomics : MGG</prism:publicationName>
    <prism:issn>1617-4615</prism:issn>
    <prism:volume>269</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>173</prism:startingPage>
    <prism:endingPage>179</prism:endingPage>
    <prism:category>cdna_aflp</prism:category>
    <prism:category>expression</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/515206">
    <title>Depression and cancer: mechanisms and disease progression</title>
    <link>http://www.citeulike.org/user/jonsta247/article/515206</link>
    <description>&lt;i&gt;Biological Psychiatry, Vol. 54, No. 3. (1 August 2003), pp. 269-282.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Depression and cancer commonly co-occur. The prevalence of depression among cancer patients increases with disease severity and symptoms such as pain and fatigue. The literature on depression as a predictor of cancer incidence is mixed, although chronic and severe depression may be associated with elevated cancer risk. There is divided but stronger evidence that depression predicts cancer progression and mortality, although disentangling the deleterious effects of disease progression on mood complicates this research, as does the fact that some symptoms of cancer and its treatment mimic depression. There is evidence that providing psychosocial support reduces depression, anxiety, and pain, and may increase survival time with cancer, although studies in this latter area are also divided. Psychophysiological mechanisms linking depression and cancer progression include dysregulation of the hypothalamic-pituitary-adrenal axis, especially diurnal variation in cortisol and melatonin. Depression also affects components of immune function that may affect cancer surveillance. Thus, there is evidence of a bidirectional relationship between cancer and depression, offering new opportunities for therapeutic intervention.</description>
    <dc:title>Depression and cancer: mechanisms and disease progression</dc:title>

    <dc:creator>David Spiegel</dc:creator>
    <dc:creator>Janine Giese-Davis</dc:creator>
    <dc:identifier>doi:10.1016/S0006-3223(03)00566-3</dc:identifier>
    <dc:source>Biological Psychiatry, Vol. 54, No. 3. (1 August 2003), pp. 269-282.</dc:source>
    <dc:date>2006-02-21T22:33:49-00:00</dc:date>
    <prism:publicationYear>2003</prism:publicationYear>
    <prism:publicationName>Biological Psychiatry</prism:publicationName>
    <prism:volume>54</prism:volume>
    <prism:number>3</prism:number>
    <prism:startingPage>269</prism:startingPage>
    <prism:endingPage>282</prism:endingPage>
    <prism:category>cancer</prism:category>
    <prism:category>depression</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/801865">
    <title>Unlocking the potential of the human genome with RNA interference</title>
    <link>http://www.citeulike.org/user/jonsta247/article/801865</link>
    <description>&lt;i&gt;Nature, Vol. 431, No. 7006. (2004), pp. 371-378.&lt;/i&gt;</description>
    <dc:title>Unlocking the potential of the human genome with RNA interference</dc:title>

    <dc:creator>Gregory Hannon</dc:creator>
    <dc:creator>John Rossi</dc:creator>
    <dc:identifier>doi:10.1038/nature02870</dc:identifier>
    <dc:source>Nature, Vol. 431, No. 7006. (2004), pp. 371-378.</dc:source>
    <dc:date>2006-08-15T10:54:21-00:00</dc:date>
    <prism:publicationYear>2004</prism:publicationYear>
    <prism:publicationName>Nature</prism:publicationName>
    <prism:volume>431</prism:volume>
    <prism:number>7006</prism:number>
    <prism:startingPage>371</prism:startingPage>
    <prism:endingPage>378</prism:endingPage>
    <prism:category>free_fulltext</prism:category>
    <prism:category>review</prism:category>
    <prism:category>rnai</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/1044679">
    <title>Analysis of the C. elegans Argonaute family reveals that distinct Argonautes act sequentially during RNAi.</title>
    <link>http://www.citeulike.org/user/jonsta247/article/1044679</link>
    <description>&lt;i&gt;Cell, Vol. 127, No. 4. (17 November 2006), pp. 747-757.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Argonaute (AGO) proteins interact with small RNAs to mediate gene silencing. C. elegans contains 27 AGO genes, raising the question of what roles these genes play in RNAi and related gene-silencing pathways. Here we describe 31 deletion alleles representing all of the previously uncharacterized AGO genes. Analysis of single- and multiple-AGO mutant strains reveals functions in several pathways, including (1) chromosome segregation, (2) fertility, and (3) at least two separate steps in the RNAi pathway. We show that RDE-1 interacts with trigger-derived sense and antisense RNAs to initiate RNAi, while several other AGO proteins interact with amplified siRNAs to mediate downstream silencing. Overexpression of downstream AGOs enhances silencing, suggesting that these proteins are limiting for RNAi. Interestingly, these AGO proteins lack key residues required for mRNA cleavage. Our findings support a two-step model for RNAi, in which functionally and structurally distinct AGOs act sequentially to direct gene silencing.</description>
    <dc:title>Analysis of the C. elegans Argonaute family reveals that distinct Argonautes act sequentially during RNAi.</dc:title>

    <dc:creator>E Yigit</dc:creator>
    <dc:creator>PJ Batista</dc:creator>
    <dc:creator>Y Bei</dc:creator>
    <dc:creator>KM Pang</dc:creator>
    <dc:creator>CC Chen</dc:creator>
    <dc:creator>NH Tolia</dc:creator>
    <dc:creator>L Joshua-Tor</dc:creator>
    <dc:creator>S Mitani</dc:creator>
    <dc:creator>MJ Simard</dc:creator>
    <dc:creator>CC Mello</dc:creator>
    <dc:identifier>doi:10.1016/j.cell.2006.09.033</dc:identifier>
    <dc:source>Cell, Vol. 127, No. 4. (17 November 2006), pp. 747-757.</dc:source>
    <dc:date>2007-01-16T17:34:48-00:00</dc:date>
    <prism:publicationYear>2006</prism:publicationYear>
    <prism:publicationName>Cell</prism:publicationName>
    <prism:issn>0092-8674</prism:issn>
    <prism:volume>127</prism:volume>
    <prism:number>4</prism:number>
    <prism:startingPage>747</prism:startingPage>
    <prism:endingPage>757</prism:endingPage>
    <prism:category>argonaute</prism:category>
    <prism:category>free_fulltext</prism:category>
    <prism:category>rnai</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/2713594">
    <title>Inducible Systemic RNA Silencing in Caenorhabditis elegans</title>
    <link>http://www.citeulike.org/user/jonsta247/article/2713594</link>
    <description>&lt;i&gt;Mol. Biol. Cell, Vol. 14, No. 7. (1 July 2003), pp. 2972-2983.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Introduction of double-stranded RNA (dsRNA) can elicit a gene-specific RNA interference response in a variety of organisms and cell types. In many cases, this response has a systemic character in that silencing of gene expression is observed in cells distal from the site of dsRNA delivery. The molecular mechanisms underlying the mobile nature of RNA silencing are unknown. For example, although cellular entry of dsRNA is possible, cellular exit of dsRNA from normal animal cells has not been directly observed. We provide evidence that transgenic strains of Caenorhabditis elegans transcribing dsRNA from a tissue-specific promoter do not exhibit comprehensive systemic RNA interference phenotypes. In these same animals, modifications of environmental conditions can result in more robust systemic RNA silencing. Additionally, we find that genetic mutations can influence the systemic character of RNA silencing in C. elegans and can separate mechanisms underlying systemic RNA silencing into tissue-specific components. These data suggest that trafficking of RNA silencing signals in C. elegans is regulated by specific physiological and genetic factors. 10.1091/mbc.E03-01-0858</description>
    <dc:title>Inducible Systemic RNA Silencing in Caenorhabditis elegans</dc:title>

    <dc:creator>Lisa Timmons</dc:creator>
    <dc:creator>Hiroaki Tabara</dc:creator>
    <dc:creator>Craig Mello</dc:creator>
    <dc:creator>Andrew Fire</dc:creator>
    <dc:identifier>doi:10.1091/mbc.E03-01-0858</dc:identifier>
    <dc:source>Mol. Biol. Cell, Vol. 14, No. 7. (1 July 2003), pp. 2972-2983.</dc:source>
    <dc:date>2008-04-24T17:36:43-00:00</dc:date>
    <prism:publicationYear>2003</prism:publicationYear>
    <prism:publicationName>Mol. Biol. Cell</prism:publicationName>
    <prism:volume>14</prism:volume>
    <prism:number>7</prism:number>
    <prism:startingPage>2972</prism:startingPage>
    <prism:endingPage>2983</prism:endingPage>
    <prism:category>free_fulltext</prism:category>
    <prism:category>rnai</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/jonsta247/article/801860">
    <title>Revealing the world of RNA interference</title>
    <link>http://www.citeulike.org/user/jonsta247/article/801860</link>
    <description>&lt;i&gt;Nature, Vol. 431, No. 7006. (2004), pp. 338-342.&lt;/i&gt;</description>
    <dc:title>Revealing the world of RNA interference</dc:title>

    <dc:creator>Craig Mello</dc:creator>
    <dc:creator>Darryl Conte</dc:creator>
    <dc:identifier>doi:10.1038/nature02872</dc:identifier>
    <dc:source>Nature, Vol. 431, No. 7006. (2004), pp. 338-342.</dc:source>
    <dc:date>2006-08-15T10:48:04-00:00</dc:date>
    <prism:publicationYear>2004</prism:publicationYear>
    <prism:publicationName>Nature</prism:publicationName>
    <prism:volume>431</prism:volume>
    <prism:number>7006</prism:number>
    <prism:startingPage>338</prism:startingPage>
    <prism:endingPage>342</prism:endingPage>
    <prism:category>free_fulltext</prism:category>
    <prism:category>review</prism:category>
    <prism:category>rnai</prism:category>
</item>



</rdf:RDF>

