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    <title>Nature Precedings - Subject feed for Neuroscience</title>
    <link>http://precedings.nature.com/subjects/neuroscience/</link>
    <description>Recently posted documents in Neuroscience</description>
    <dc:publisher>Nature Publishing Group</dc:publisher>
    <dc:language>en</dc:language>
    <prism:publicationName>Nature Precedings</prism:publicationName>
    <image>
      <title>Nature Precedings</title>
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      <title>The INCF Digital Atlasing Program: Report on Digital Atlasing Standards in the Rodent Brain</title>
      <link>http://dx.doi.org/10.1038/npre.2009.4000.1</link>
      <description>The goal of the INCF Digital Atlasing Program is to provide the vision and direction necessary to make the rapidly growing collection of multidimensional data of the rodent brain (images, gene expression, etc.) widely accessible and usable to the international research community. This Digital Brain Atlasing Standards Task Force was formed in May 2008 to investigate the state of rodent brain digital atlasing, and formulate standards, guidelines, and policy recommendations.Our first objective has been the preparation of a detailed document that includes the vision and specific description of an infrastructure, systems and methods capable of serving the scientific goals of the community, as well as practical issues for achievingthe goals. This report builds on the 1st INCF Workshop on Mouse and Rat Brain Digital Atlasing Systems (Boline et al., 2007, Nature Preceedings, doi:10.1038/npre.2007.1046.1) and includes a more detailed analysis of both the current state and desired state of digital atlasing along with specific recommendations for achieving these goals.</description>
      <guid>http://dx.doi.org/10.1038/npre.2009.4000.1</guid>
      <pubDate>Tue, 24 Nov 2009 09:43:24 UTC</pubDate>
      <dc:title>The INCF Digital Atlasing Program: Report on Digital Atlasing Standards in the Rodent Brain</dc:title>
      <dc:identifier>doi:10.1038/npre.2009.4000.1</dc:identifier>
      <dc:date>2009-11-24</dc:date>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-11-24T09:43:24Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Neuroscience</prism:section>
      <prism:section>Bioinformatics</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/4000/version/1/files/npre20094000-1.pdf.thumb.png"/>
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    <item>
      <title>An apparent medieval stereogram incorporating a symbol for optical illusion</title>
      <link>http://precedings.nature.com/documents/3994/version/1</link>
      <description>Stereograms mark a threshold in understanding visual perception. Modern study of stereopsis began with Wheatstone&amp;#8217;s invention of the stereogram and stereoscope (~ 1832), important tools in vision research and technical imagery ever since. Stereoscopic images formed with frieze and wallpaper patterns in illuminated Insular manuscripts such as the Book of Durrow (~ 680 CE), Lindisfarne Gospels (~ 700-720), and Book of Kells (~ 800) show that, long before spectacle-quality magnifying lenses (~ 1286), illuminators somehow copied multicolored, microscopically detailed designs freehand with an accuracy unsurpassed in scientific instruments until the Renaissance (but well within the power of normally sighted humans&amp;#8217; stereoscopic discrimination). If the artists accomplished this feat by free fusion using the unaided eyes as a magnifying stereocomparator, as suggested, they should have been able to create autostereograms. Did they? Here I report two examples of an apparent stereopair from the Book of Durrow, which gives a sharp, strongly three-dimensional image that includes, among other symbols, an eye-shaped sign identified with mirages (Fig. 1). Apparently, precocious empirical knowledge of stereopsis played more than a technical role in the creation of some of the world&amp;#8217;s more famous graphic art.</description>
      <guid>http://precedings.nature.com/documents/3994/version/1</guid>
      <pubDate>Mon, 23 Nov 2009 15:57:14 UTC</pubDate>
      <dc:title>An apparent medieval stereogram incorporating a symbol for optical illusion</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3994.1</dc:identifier>
      <dc:date>2009-11-23</dc:date>
      <dc:creator>John L. Cisne</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-11-23T15:57:14Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Neuroscience</prism:section>
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      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
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    <item>
      <title>The genetics of colored sequence synesthesia: Evidence of linkage to chromosome 16q and genetic heterogeneity for the condition</title>
      <link>http://dx.doi.org/10.1038/npre.2009.3987.1</link>
      <description>Synesthesia is a perceptual condition in which normal sensory stimulation can trigger anomalous sensory experiences. For example, synesthetes may experience colors in response to sounds, tastes in response to words, or smells in response to touch. We here focus on colored sequence synesthesia, in which color experiences are triggered by learned ordinal sequences such as letters, numbers, weekdays and months. Although synesthesia has been noted in the scientific literature for over a century, it is understood only at the level of the phenomenology, and not at the molecular and neural levels. We have performed a linkage analysis to identify the first genetic loci responsible for the increased neural crosstalk underlying colored sequence synesthesia. Our analysis has identified a 23 MB region on chromosome 16 as a putative locus for the trait. Our data provide the first step in understanding neural crosstalk from its molecular basis to its behavioral consequences, opening a new inroad into the understanding of the multisensory brain. </description>
      <guid>http://dx.doi.org/10.1038/npre.2009.3987.1</guid>
      <pubDate>Fri, 20 Nov 2009 07:08:42 UTC</pubDate>
      <dc:title>The genetics of colored sequence synesthesia: Evidence of linkage to chromosome 16q and genetic heterogeneity for the condition</dc:title>
      <dc:identifier>doi:10.1038/npre.2009.3987.1</dc:identifier>
      <dc:date>2009-11-20</dc:date>
      <dc:creator>Stephanie S. Nelson</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-11-20T07:08:42Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Neuroscience</prism:section>
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    <item>
      <title>Spherulites of A&amp;#946;42 in vitro and in Alzheimer&amp;#8217;s disease</title>
      <link>http://precedings.nature.com/documents/3982/version/1</link>
      <description>Several amyloid-forming proteins and peptides, including insulin1, &amp;#946;-lactoglobulin2 and albumin3, form spherulites in vitro under non-physiological solution conditions. These micrometer-sized, roughly spherical structures are composed of ordered arrays of &amp;#946; sheets of amyloid fibrils in radial arrangements which, characteristically, show a typical Maltese cross pattern of light extinction under the polarizing microscope. The physiological significance, if any, of these amyloid super assemblies is unknown although in Alzheimer&amp;#8217;s disease there is the suggestion that senile plaques composed primarily of &amp;#946; sheets of A&amp;#946;42 are spherulitic4. Herein we describe the first observation of the formation in vitro of spherulites of A&amp;#946;42. They were formed under near-physiological conditions in which the &amp;#946; sheet conformation of pre-formed aggregates of A&amp;#946;42 had been abolished following the addition of an excess of copper. Incubation of these preparations at 37oC for up to 9 months resulted in the formation of spherulites. These were globular in appearance, 5 &amp;#8211; 20 microns in diameter, and exhibited the typical Maltese cross pattern of light extinction. Similarly to other amyloid spherulites formed in vitro they bound Congo red without giving apple-green birefringence5 while also being thioflavin T-positive when viewed by fluorescence microscopy3. Near-identical spherulitic structures were also observed in abundance in 30 micron thick sections of Alzheimer&amp;#8217;s disease brain tissue. Synchrotron x-ray fluorescence showed that the location of these spherulites in AD tissue coincided with locally elevated concentrations of tissue copper. The formation in vitro of spherulites of A&amp;#946;42 which morphologically appeared analogous to spherulitic structures observed in vivo strongly supports the hypothesis that spherulites and senile plaques in AD tissue are one and the same structures and that their ultimate formation involves copper.</description>
      <guid>http://precedings.nature.com/documents/3982/version/1</guid>
      <pubDate>Wed, 18 Nov 2009 20:13:32 UTC</pubDate>
      <dc:title>Spherulites of A&amp;#946;42 in vitro and in Alzheimer&amp;#8217;s disease</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3982.1</dc:identifier>
      <dc:date>2009-11-18</dc:date>
      <dc:creator>Christopher Exley</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-11-18T20:13:32Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Neuroscience</prism:section>
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      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
    </item>
    <item>
      <title>Magnetoencephalography May Allow the Electromagnetic &amp;apos;Biopsy&amp;apos; of Central Nervous System Neoplastic Tissue</title>
      <link>http://precedings.nature.com/documents/3973/version/1</link>
      <description>Developing a non-invasive method for definitively diagnosing intracranial neoplasms would reduce the risks involved with diagnosis and improve the treatment of such tumors. We used magnetoencephalography to measure the power spectral densities of malignant brain tumor cells in vitro and found that meningioma and medulloblastoma cells produce unique electromagnetic signatures. Our results suggest that non-invasive identification of neoplastic tissue is possible through the use of magnetoencephalography.</description>
      <guid>http://precedings.nature.com/documents/3973/version/1</guid>
      <pubDate>Fri, 13 Nov 2009 11:56:20 UTC</pubDate>
      <dc:title>Magnetoencephalography May Allow the Electromagnetic &amp;apos;Biopsy&amp;apos; of Central Nervous System Neoplastic Tissue</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3973.1</dc:identifier>
      <dc:date>2009-11-13</dc:date>
      <dc:creator>Michael Pearlman</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-11-13T11:56:20Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Neuroscience</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/3973/version/1/files/npre20093973-1.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
    </item>
    <item>
      <title>The cultural epigenetics of psychopathology: The missing heritability of complex diseases found?</title>
      <link>http://precedings.nature.com/documents/3894/version/2</link>
      <description>We extend a cognitive paradigm for gene expression to the epigenetic epidemiology of mental disorders, recognizing the fundamental role that culture plays in human biology as another heritage mechanism parallel to, and interacting with, the more familiar genetic and epigenetic systems. In the mathematical model, culture acts as another tunable epigenetic catalyst that both directs developmental trajectories and becomes convoluted with individual ontology via a mutually interacting crosstalk mediated by a social interaction that is itself culturally driven. We call for the incorporation of embedding culture as an essential component of the epigenetic regulation of human mental development and its dysfunctions, bringing what is perhaps the central reality of human biology into the center of biological psychiatry. The cultural and epigenetic systems of heritage may well provide the &amp;#8216;missing&amp;#8217; heritability of complex diseases now under so much intense discussion.</description>
      <guid>http://precedings.nature.com/documents/3894/version/2</guid>
      <pubDate>Wed, 11 Nov 2009 18:29:58 UTC</pubDate>
      <dc:title>The cultural epigenetics of psychopathology: The missing heritability of complex diseases found?</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3894.2</dc:identifier>
      <dc:date>2009-11-11</dc:date>
      <dc:creator>Rodrick Wallace</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-11-11T18:29:58Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Developmental Biology</prism:section>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Neuroscience</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/3894/version/2/files/npre20093894-2.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
    </item>
    <item>
      <title>Cortical activity modulation of language processing by dynamic optimization of task complexity and functional restrictions</title>
      <link>http://precedings.nature.com/documents/3941/version/1</link>
      <description>Language, regarded as a hierarchical cognitive code activated by functional operational modes of the brain by most neuropsychologists, is characterized by increased cognitive load in successively higher levels of processing. Language comprehension is posited to be executed through symbolic-iconic information being encoded neurally as modulated phenomena, and can be studied in vivo by functional brain imaging. Using a lexical decision-making task in conjunction with syntactic error correction that effectively isolated the regulatory neural substrate of processing structural-functional information, and minimizing the possible confounds of gender and proficiency, functional magnetic resonance imaging (fMRI) was performed on bilingual volunteers to ascertain the attentional modulation of second language lexical and sentence processing. Our results indicate that while a right posterior cingulate gyrus-precuneus-lingual gyrus-cerebellar loop processes lexical information, the left inferior and middle frontal cortices are critically involved in the implementation of a structural-functional decision-making procedural loop in mediating second language comprehension. </description>
      <guid>http://precedings.nature.com/documents/3941/version/1</guid>
      <pubDate>Wed, 04 Nov 2009 13:56:52 UTC</pubDate>
      <dc:title>Cortical activity modulation of language processing by dynamic optimization of task complexity and functional restrictions</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3941.1</dc:identifier>
      <dc:date>2009-11-04</dc:date>
      <dc:creator>Shantanu Ghosh</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-11-04T13:56:52Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Neuroscience</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/3941/version/1/files/npre20093941-1.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
    </item>
    <item>
      <title>Roman roads: The hierarchical endosymbiosis of cognitive modules</title>
      <link>http://precedings.nature.com/documents/3892/version/1</link>
      <description>Serial endosymbiosis theory provides a unifying paradigm for examining the interaction of cognitive modules at vastly different scales of biological, social, and cultural organization. A trivial but not unimportant model associates a dual information source with a broad class of cognitive processes, and punctuated phenomena akin to phase transitions in physical systems, and associated coevolutionary processes, emerge as consequences of the homology between information source uncertainty and free energy density. The dynamics, including patterns of punctuation similar to ecosystem resilience transitions, are largely dominated by the availability of &amp;#8216;Roman roads&amp;#8217; constituting channels for the transmission of information between modules.</description>
      <guid>http://precedings.nature.com/documents/3892/version/1</guid>
      <pubDate>Mon, 02 Nov 2009 09:47:58 UTC</pubDate>
      <dc:title>Roman roads: The hierarchical endosymbiosis of cognitive modules</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3892.1</dc:identifier>
      <dc:date>2009-11-02</dc:date>
      <dc:creator>Rodrick Wallace</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-11-02T09:47:58Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Ecology</prism:section>
      <prism:section>Neuroscience</prism:section>
      <prism:section>Earth &amp; Environment</prism:section>
      <prism:section>Evolutionary Biology</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/3892/version/1/files/npre20093892-1.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
    </item>
    <item>
      <title>Accurate telemonitoring of Parkinson&#8217;s disease progression by non-invasive speech tests</title>
      <link>http://precedings.nature.com/documents/3920/version/1</link>
      <description>Tracking Parkinson&amp;#8217;s disease (PD) symptom progression often uses the Unified Parkinson&#8217;s Disease Rating Scale (UPDRS), which requires the patient&amp;#8217;s presence in clinic, and time-consuming physical examinations by trained medical staff. Thus, symptom monitoring is costly and logistically inconvenient for patient and clinical staff alike, also hindering recruitment for future large-scale clinical trials. Here, for the first time, we demonstrate rapid, remote replication of UPDRS assessment with clinically useful accuracy (about 7.5 UPDRS points difference from the clinicians&#8217; estimates), using only simple, self-administered, and non-invasive speech tests. We characterize speech with signal processing algorithms, extracting clinically useful features of average PD progression. Subsequently, we select the most parsimonious model with a robust feature selection algorithm, and statistically map the selected subset of features to UPDRS using linear and nonlinear regression techniques, which include classical least squares and non-parametric classification and regression trees (CART). We verify our findings on the largest database of PD speech in existence (~6,000 recordings from 42 PD patients, recruited to a six-month, multi-centre trial). These findings support the feasibility of frequent, remote and accurate UPDRS tracking. This technology could play a key part in telemonitoring frameworks that enable large-scale clinical trials into novel PD treatments.</description>
      <guid>http://precedings.nature.com/documents/3920/version/1</guid>
      <pubDate>Thu, 29 Oct 2009 15:21:58 UTC</pubDate>
      <dc:title>Accurate telemonitoring of Parkinson&#8217;s disease progression by non-invasive speech tests</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3920.1</dc:identifier>
      <dc:date>2009-10-29</dc:date>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-10-29T15:21:58Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Neuroscience</prism:section>
      <prism:section>Bioinformatics</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/3920/version/1/files/npre20093920-1.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
    </item>
    <item>
      <title>The Role of Neuregulin 1 in Schizophrenia:  A Bioinformatics Approach</title>
      <link>http://precedings.nature.com/documents/3905/version/1</link>
      <description>Context: Notwithstanding the great number of studies on the etiology and pathophysiology of schizophrenia, both issues remain far from being fully understood. Schizophrenia seems to be related to several biochemical abnormalities, which point to a multi-factor etiology and pathophysiology, as well as to the perspective that several etiologically diverse disorders might coexist within this nosographic entity. On the other hand, identical twins reveal a high concordance for schizophrenia. From that standpoint, the perspective that structurally-related proteins may play an important and yet non-deterministic role seems attractive. Among these proteins, it is suggestive that Neuregulin 1 exerts a pivotal role. Objective: This paper aims to uncover the most prominent relations that Neuregulin 1 establishes with schizophrenia. Method: Several bioinformatical methods are used in order to present: 1. A visual representation of Neuregulin 1&#8217;s main molecular pathways, associated with a discussion about their importance to schizophrenia research; 2. A new heatmap of Neuregulin 1 and its receptor&#8217;s expression in brain tissues  most relevant to the understanding of schizophrenia, created after the development of new R programming scripts (described elsewhere), which facilitate the analysis of gene expression profiles in public datasets; 3. A conceptual map of the literature retrieved using the keywords &#8216;Neuregulin 1 and human&#8217; in PubMed, followed by a discussion of the most relevant sub-topics. Results: Neuregulin 1 polymorphisms affect several brain tissues and contribute to the etiology and pathophysiology of schizophrenia. Suggestively, Neuregulin 1 partially bridges the &amp;#8216;molecular gap&amp;#8217; that schizophrenia establishes in relation to bipolar disorder and Alzheimer disease, which involves genes that affect several brain networks, at the same time that they are highly dependent on noxious environmental variables to be triggered.</description>
      <guid>http://precedings.nature.com/documents/3905/version/1</guid>
      <pubDate>Wed, 28 Oct 2009 11:15:17 UTC</pubDate>
      <dc:title>The Role of Neuregulin 1 in Schizophrenia:  A Bioinformatics Approach</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3905.1</dc:identifier>
      <dc:date>2009-10-28</dc:date>
      <dc:creator>Alvaro M. Dias</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-10-28T11:15:17Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Neuroscience</prism:section>
      <prism:section>Bioinformatics</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/3905/version/1/files/npre20093905-1.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
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