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Author (up) openurl 
  Title Type Miscellaneous
  Year 2016 Publication Abbreviated Journal  
  Volume Issue Pages  
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  Corporate Author Thesis  
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  Notes Approved no  
  Call Number refbase @ user @ ref32 Serial 17168  
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Author (up) openurl 
  Title Type Miscellaneous
  Year 2016 Publication Abbreviated Journal  
  Volume Issue Pages  
  Keywords  
  Abstract  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
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  Area Expedition Conference  
  Notes Approved no  
  Call Number refbase @ user @ ref32 Serial 17284  
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Author (up) Achuta, V.S.; Grym, H.; Putkonen, N.; Louhivuori, V.; Karkkainen, V.; Koistinaho, J.; Roybon, L.; Castren, M.L. url  doi
openurl 
  Title Metabotropic glutamate receptor 5 responses dictate differentiation of neural progenitors to NMDA-responsive cells in fragile X syndrome Type Journal Article
  Year 2016 Publication Developmental Neurobiology Abbreviated Journal Dev Neurobiol  
  Volume Issue Pages  
  Keywords 2-methyl-6-(phenylethynyl)-pyridine; fragile X syndrome; glutamatergic neurons; induced pluripotent stem cells; metabotropic glutamate receptor 5  
  Abstract Disrupted metabotropic glutamate receptor 5 (mGluR5) signaling is implicated in many neuropsychiatric disorders, including autism spectrum disorder, found in fragile X syndrome (FXS). Here we report that intracellular calcium responses to the group I mGluR agonist (S)-3,5-dihydroxyphenylglycine (DHPG) are augmented, and calcium-dependent mGluR5-mediated mechanisms alter the differentiation of neural progenitors in neurospheres derived from human induced pluripotent FXS stem cells and the brains of mouse model of FXS. Treatment with the mGluR5 antagonist 2-methyl-6-(phenylethynyl)-pyridine (MPEP) prevents an abnormal clustering of DHPG-responsive cells that are responsive to activation of ionotropic receptors in mouse FXS neurospheres. MPEP also corrects morphological defects of differentiated cells and enhanced migration of neuron-like cells in mouse FXS neurospheres. Unlike in mouse neurospheres, MPEP increases the differentiation of DHPG-responsive radial glial cells as well as the subpopulation of cells responsive to both DHPG and activation of ionotropic receptors in human neurospheres. However, MPEP normalizes the FXS-specific increase in the differentiation of cells responsive only to N-methyl-d-aspartate (NMDA) present in human neurospheres. Exposure to MPEP prevents the accumulation of intermediate basal progenitors in embryonic FXS mouse brain suggesting that rescue effects of GluR5 antagonist are progenitor type-dependent and species-specific differences of basal progenitors may modify effects of MPEP on the cortical development. (c) 2016 Wiley Periodicals, Inc. Develop Neurobiol, 2016.  
  Address Autism Foundation, Kuortaneenkatu 7B, Helsinki, FI-00520, Finland  
  Corporate Author Thesis  
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  Language English Summary Language Original Title  
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  Series Volume Series Issue Edition  
  ISSN 1932-8451 ISBN Medium  
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  Notes PMID:27411166 Approved no  
  Call Number refbase @ user @ Serial 16666  
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Author (up) Aguilera, C.A.; Aguilera, F.J.; Sappa, A.D.; Aguilera, C.; Toledo, R. openurl 
  Title Learning cross-spectral similarity measures with deep convolutional neural networks Type Conference Article
  Year 2016 Publication Proceedings of the IEEE Conference on Computer Vision and Pattern Recognition Workshops Abbreviated Journal  
  Volume Issue Pages 1-9  
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  Notes Approved no  
  Call Number refbase @ user @ aguilera2016learning Serial 17108  
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Author (up) Andoh-Noda, T.; Inouye, M.O.; Miyake, K.; Kubota, T.; Okano, H.; Akamatsu, W. url  openurl
  Title Modeling Rett Syndrome Using Human Induced Pluripotent Stem Cells Type Journal Article
  Year 2016 Publication CNS & Neurological Disorders Drug Targets Abbreviated Journal CNS Neurol Disord Drug Targets  
  Volume 15 Issue 5 Pages 544-550  
  Keywords  
  Abstract Rett syndrome (RTT) is one of a group of neurodevelopmental disorders typically characterized by deficits in the X-linked gene MECP2 (methyl-CpG binding protein 2). The MECP2 gene encodes a multifunctional protein involved in transcriptional repression, transcriptional activation, chromatin remodeling, and RNA splicing. Genetic deletion of Mecp2 in mice revealed neuronal disabilities including RTT-like phenotypes and provided an excellent platform for understanding the pathogenesis of RTT. So far, there are no effective pharmacological treatments for RTT because the role of MECP2 in RTT is incompletely understood. Recently, human induced pluripotent stem cell (hiPSC) technologies have improved our knowledge of neurological and neurodevelopmental diseases including RTT because neurons derived from RTT-hiPSCs can be used for disease modeling to understand RTT phenotypes and to perform high throughput pharmaceutical drug screening. In this review, we provide an overview of RTT, including MeCP2 function and mouse models of RTT. In addition, we introduce recent advances in disease modeling of RTT using hiPSC-derived neural cells.  
  Address Center for Genomic and Regenerative Medicine, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, Japan. awado@juntendo.ac.jp  
  Corporate Author Thesis  
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  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1871-5273 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:27071793 Approved no  
  Call Number refbase @ user @ Serial 16689  
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