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  • Rats
  • American Association for the Advancement of Science (AAAS)  (21)
  • American Chemical Society (ACS)
  • Copernicus
  • 2010-2014  (21)
  • 1980-1984
  • 2013  (21)
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  • 2010-2014  (21)
  • 1980-1984
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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-12-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 2013 Dec 20;342(6165):1440-1. doi: 10.1126/science.342.6165.1440-b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24357292" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/administration & dosage ; Fusobacterium/physiology ; Gastrointestinal Tract/*microbiology ; *Health ; Humans ; Infant ; Infant Formula/chemistry ; Kidney/metabolism ; Kidney Calculi/chemically induced/etiology ; Klebsiella/drug effects/metabolism ; Malnutrition/microbiology ; Neoplasms/microbiology ; Rats ; Triazines/metabolism/toxicity
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-12-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 2013 Dec 20;342(6165):1434-5. doi: 10.1126/science.342.6165.1434-a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24357285" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Proteins/genetics/metabolism ; Clustered Regularly Interspaced Short Palindromic Repeats/*genetics ; DNA/genetics ; Genetic Diseases, Inborn/*surgery ; Genetic Therapy/*methods ; Humans ; Mice ; Microsurgery/*methods ; *RNA Editing ; RNA, Guide/genetics/metabolism ; Rats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-11-23
    Description: In many mammalian tissues, mature differentiated cells are replaced by self-renewing stem cells, either continuously during homeostasis or in response to challenge and injury. For example, hematopoietic stem cells generate all mature blood cells, including monocytes, which have long been thought to be the major source of tissue macrophages. Recently, however, major macrophage populations were found to be derived from embryonic progenitors and to renew independently of hematopoietic stem cells. This process may not require progenitors, as mature macrophages can proliferate in response to specific stimuli indefinitely and without transformation or loss of functional differentiation. These findings suggest that macrophages are mature differentiated cells that may have a self-renewal potential similar to that of stem cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sieweke, Michael H -- Allen, Judith E -- MR/J001929/1/Medical Research Council/United Kingdom -- MR/K01207X1/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2013 Nov 22;342(6161):1242974. doi: 10.1126/science.1242974.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre d'Immunologie de Marseille-Luminy (CIML), Aix-Marseille Universite, UM2, Campus de Luminy, Case 906, 13288 Marseille Cedex 09, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24264994" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Cell Proliferation ; Cytokines/metabolism ; Embryonic Stem Cells/cytology ; Humans ; Macrophages/*cytology ; Mice ; Monocytes/cytology ; Rats ; Signal Transduction ; Stem Cells/*cytology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-11-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bendor, Daniel -- 1-K99-DC012321-01/DC/NIDCD NIH HHS/ -- 5R01MH061976/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2013 Nov 1;342(6158):574. doi: 10.1126/science.1245966.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University College London, 26 Bedford Way, London WC1H 0AP, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24179215" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cues ; Hippocampus/*physiology ; Humans ; Memory/*physiology/*radiation effects ; Microelectrodes ; Rats ; Sleep Stages/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 5
    Publication Date: 2013-06-01
    Description: Successive contrast effects, in which behavior is dependent on whether conditions are currently better or worse than they were before, are a striking illustration of the fact that animals evaluate the world in relative terms. Existing explanations for these effects are based on descriptive models of psychological and physiological processes, but little attention has been paid to the factors promoting their evolution. Using a simple and general optimality model, we show that contrast effects can result from an adaptive response to uncertainty in a changing, unpredictable world. A wide range of patterns of environmental change will select for sensitivity to past conditions, generating positive and negative contrast effects. Our analysis reveals the importance of incorporating uncertainty and environmental stochasticity into models of adaptive behavior.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McNamara, John M -- Fawcett, Tim W -- Houston, Alasdair I -- New York, N.Y. -- Science. 2013 May 31;340(6136):1084-6. doi: 10.1126/science.1230599.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Mathematics, University of Bristol, University Walk, Bristol, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23723234" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; *Adaptation, Psychological ; Animals ; Cognition ; *Models, Psychological ; Rats ; *Uncertainty
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  • 6
    Publication Date: 2013-05-04
    Description: The hippocampal cognitive map is thought to be driven by distal visual cues and self-motion cues. However, other sensory cues also influence place cells. Hence, we measured rat hippocampal activity in virtual reality (VR), where only distal visual and nonvestibular self-motion cues provided spatial information, and in the real world (RW). In VR, place cells showed robust spatial selectivity; however, only 20% were track active, compared with 45% in the RW. This indicates that distal visual and nonvestibular self-motion cues are sufficient to provide selectivity, but vestibular and other sensory cues present in RW are necessary to fully activate the place-cell population. In addition, bidirectional cells preferentially encoded distance along the track in VR, while encoding absolute position in RW. Taken together, these results suggest the differential contributions of these sensory cues in shaping the hippocampal population code. Theta frequency was reduced, and its speed dependence was abolished in VR, but phase precession was unaffected, constraining mechanisms governing both hippocampal theta oscillations and temporal coding. These results reveal cooperative and competitive interactions between sensory cues for control over hippocampal spatiotemporal selectivity and theta rhythm.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4049564/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4049564/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ravassard, Pascal -- Kees, Ashley -- Willers, Bernard -- Ho, David -- Aharoni, Daniel -- Cushman, Jesse -- Aghajan, Zahra M -- Mehta, Mayank R -- 5R01MH092925-02/MH/NIMH NIH HHS/ -- R01 MH092925/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2013 Jun 14;340(6138):1342-6. doi: 10.1126/science.1232655. Epub 2013 May 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉W. M. Keck Center for Neurophysics, Integrative Center for Learning and Memory, and Brain Research Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23641063" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Mapping ; Cues ; Hippocampus/*physiology ; Male ; Rats ; Rats, Inbred LEC ; *Space Perception ; *Spatial Behavior ; Theta Rhythm ; *Time Perception ; User-Computer Interface
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  • 7
    Publication Date: 2013-04-20
    Description: Both bats and rats exhibit grid cells in medial entorhinal cortex that fire as they visit a regular array of spatial locations. In rats, grid-cell firing field properties correlate with theta-frequency rhythmicity of spiking and membrane-potential resonance; however, bat grid cells do not exhibit theta rhythmic spiking, generating controversy over the role of theta rhythm. To test whether this discrepancy reflects differences in rhythmicity at a cellular level, we performed whole-cell patch recordings from entorhinal neurons in both species to record theta-frequency resonance. Bat neurons showed no theta-frequency resonance, suggesting grid-cell coding via different mechanisms in bats and rats or lack of theta rhythmic contributions to grid-cell firing in either species.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heys, James G -- MacLeod, Katrina M -- Moss, Cynthia F -- Hasselmo, Michael E -- New York, N.Y. -- Science. 2013 Apr 19;340(6130):363-7. doi: 10.1126/science.1233831.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate Program for Neuroscience, Center for Memory and Brain, Boston University, 2 Cummington Street, Boston, MA 02215, USA. jimheys@bu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23599495" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Chiroptera ; Entorhinal Cortex/cytology/*physiology ; Female ; Male ; Membrane Potentials ; Models, Neurological ; Neurons/cytology/*physiology ; Patch-Clamp Techniques ; Rats ; Rats, Long-Evans ; *Theta Rhythm
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  • 8
    Publication Date: 2013-04-06
    Description: We used a combined optogenetic-electrophysiological strategy to determine the functional identity of entorhinal cells with output to the place-cell population in the hippocampus. Channelrhodopsin-2 (ChR2) was expressed selectively in the hippocampus-targeting subset of entorhinal projection neurons by infusing retrogradely transportable ChR2-coding recombinant adeno-associated virus in the hippocampus. Virally transduced ChR2-expressing cells were identified in medial entorhinal cortex as cells that fired at fixed minimal latencies in response to local flashes of light. A large number of responsive cells were grid cells, but short-latency firing was also induced in border cells and head-direction cells, as well as cells with irregular or nonspatial firing correlates, which suggests that place fields may be generated by convergence of signals from a broad spectrum of entorhinal functional cell types.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Sheng-Jia -- Ye, Jing -- Miao, Chenglin -- Tsao, Albert -- Cerniauskas, Ignas -- Ledergerber, Debora -- Moser, May-Britt -- Moser, Edvard I -- New York, N.Y. -- Science. 2013 Apr 5;340(6128):1232627. doi: 10.1126/science.1232627.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Kavli Institute for Systems Neuroscience and Centre for Neural Computation, Norwegian University of Science and Technology, Olav Kyrres gate 9, Norwegian Brain Centre, 7491 Trondheim, Norway. sheng-jia.zhang@ntnu.no〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23559255" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; CA1 Region, Hippocampal/cytology/physiology ; *Cell Communication ; Dependovirus ; Entorhinal Cortex/cytology/*physiology ; Gene Targeting ; Hippocampus/cytology/*physiology ; Neurons/*physiology ; Photic Stimulation ; Rats ; Rhodopsin/biosynthesis/genetics ; Transduction, Genetic
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  • 9
    Publication Date: 2013-08-03
    Description: Robust transmission of information despite the presence of variation is a fundamental problem in cellular functions. However, the capability and characteristics of information transmission in signaling pathways remain poorly understood. We describe robustness and compensation of information transmission of signaling pathways at the cell population level. We calculated the mutual information transmitted through signaling pathways for the growth factor-mediated gene expression. Growth factors appeared to carry only information sufficient for a binary decision. Information transmission was generally more robust than average signal intensity despite pharmacological perturbations, and compensation of information transmission occurred. Information transmission to the biological output of neurite extension appeared robust. Cells may use information entropy as information so that messages can be robustly transmitted despite variation in molecular activities among individual cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Uda, Shinsuke -- Saito, Takeshi H -- Kudo, Takamasa -- Kokaji, Toshiya -- Tsuchiya, Takaho -- Kubota, Hiroyuki -- Komori, Yasunori -- Ozaki, Yu-ichi -- Kuroda, Shinya -- New York, N.Y. -- Science. 2013 Aug 2;341(6145):558-61. doi: 10.1126/science.1234511.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biophysics and Biochemistry, Graduate School of Science, University of Tokyo, Bunkyo-ku, Tokyo, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23908238" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cyclic AMP Response Element-Binding Protein/metabolism ; Early Growth Response Protein 1/metabolism ; Gene Expression/drug effects ; *Information Theory ; Intercellular Signaling Peptides and Proteins/pharmacology ; PC12 Cells ; Proto-Oncogene Proteins c-fos/metabolism ; Rats ; *Signal Transduction
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  • 10
    Publication Date: 2013-08-31
    Description: The lateral habenula (LHb) has recently emerged as a key brain region in the pathophysiology of depression. However, the molecular mechanism by which LHb becomes hyperactive in depression remains unknown. Through a quantitative proteomic screen, we found that expression of the beta form of calcium/calmodulin-dependent protein kinase type II (betaCaMKappaIotaIota) was significantly up-regulated in the LHb of animal models of depression and down-regulated by antidepressants. Increasing beta-, but not alpha-, CaMKII in the LHb strongly enhanced the synaptic efficacy and spike output of LHb neurons and was sufficient to produce profound depressive symptoms, including anhedonia and behavioral despair. Down-regulation of betaCaMKII levels, blocking its activity or its target molecule the glutamate receptor GluR1 reversed the depressive symptoms. These results identify betaCaMKII as a powerful regulator of LHb neuron function and a key molecular determinant of depression.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3932364/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3932364/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Kun -- Zhou, Tao -- Liao, Lujian -- Yang, Zhongfei -- Wong, Catherine -- Henn, Fritz -- Malinow, Roberto -- Yates, John R 3rd -- Hu, Hailan -- P41 GM103533/GM/NIGMS NIH HHS/ -- R01 MH067880/MH/NIMH NIH HHS/ -- R01 MH091119/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2013 Aug 30;341(6149):1016-20. doi: 10.1126/science.1240729.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neuroscience and State Key Laboratory of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, P R China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23990563" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antidepressive Agents/pharmacology ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/antagonists & ; inhibitors/*biosynthesis/genetics ; Depressive Disorder, Major/*enzymology/genetics/psychology ; Disease Models, Animal ; Gene Knockdown Techniques ; Habenula/drug effects/*enzymology ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Neurons/drug effects/enzymology ; Promoter Regions, Genetic ; Proteomics ; Rats ; Rats, Sprague-Dawley
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  • 11
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-07-03
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3749839/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3749839/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nedergaard, Maiken -- R01 MH099578/MH/NIMH NIH HHS/ -- R01 NS075177/NS/NINDS NIH HHS/ -- R01 NS078167/NS/NINDS NIH HHS/ -- R01 NS078304/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2013 Jun 28;340(6140):1529-30. doi: 10.1126/science.1240514.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Medicine and Dentistry, University of Rochester Medical Center, Rochester, NY 14642, USA. nedergaard@urmc.rochester.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23812703" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aquaporin 4/*metabolism ; Brain/*physiopathology ; Cerebrospinal Fluid/metabolism ; Extracellular Fluid/metabolism ; Humans ; Lymphatic Vessels/*metabolism ; Mice ; Neurodegenerative Diseases/cerebrospinal fluid/*physiopathology/*therapy ; Neuroglia/*metabolism ; Neurons/metabolism ; Rats
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  • 12
    Publication Date: 2013-07-28
    Description: The resolution of type 2 diabetes after Roux-en-Y gastric bypass (RYGB) attests to the important role of the gastrointestinal tract in glucose homeostasis. Previous studies in RYGB-treated rats have shown that the Roux limb displays hyperplasia and hypertrophy. Here, we report that the Roux limb of RYGB-treated rats exhibits reprogramming of intestinal glucose metabolism to meet its increased bioenergetic demands; glucose transporter-1 is up-regulated, basolateral glucose uptake is enhanced, aerobic glycolysis is augmented, and glucose is directed toward metabolic pathways that support tissue growth. We show that reprogramming of intestinal glucose metabolism is triggered by the exposure of the Roux limb to undigested nutrients. We demonstrate by positron emission tomography-computed tomography scanning and biodistribution analysis using 2-deoxy-2-[18F]fluoro-D-glucose that reprogramming of intestinal glucose metabolism renders the intestine a major tissue for glucose disposal, contributing to the improvement in glycemic control after RYGB.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4068965/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4068965/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saeidi, Nima -- Meoli, Luca -- Nestoridi, Eirini -- Gupta, Nitin K -- Kvas, Stephanie -- Kucharczyk, John -- Bonab, Ali A -- Fischman, Alan J -- Yarmush, Martin L -- Stylopoulos, Nicholas -- DK089503/DK/NIDDK NIH HHS/ -- F32 DK095558/DK/NIDDK NIH HHS/ -- F32DK095558/DK/NIDDK NIH HHS/ -- P50 GM021700/GM/NIGMS NIH HHS/ -- T32DK007191/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2013 Jul 26;341(6144):406-10. doi: 10.1126/science.1235103.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Basic and Translational Obesity Research, Division of Endocrinology, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23888041" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Animals ; Blood Glucose/*metabolism ; Cholesterol/biosynthesis ; Diabetes Mellitus, Experimental/metabolism/surgery ; Digestion ; Energy Metabolism ; Fluorodeoxyglucose F18/metabolism ; *Gastric Bypass ; Gene Expression Regulation ; Glucose/*metabolism ; Glucose Transporter Type 1/metabolism ; Glycolysis ; Jejunum/*metabolism ; Male ; Metabolic Networks and Pathways ; Metabolomics ; Multimodal Imaging ; Pentose Phosphate Pathway ; Positron-Emission Tomography ; Rats ; Rats, Long-Evans ; Signal Transduction ; Tissue Distribution ; Tomography, X-Ray Computed ; Up-Regulation
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  • 13
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-08-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2013 Aug 23;341(6148):833-6. doi: 10.1126/science.341.6148.833.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23970676" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caspase 9/genetics/*metabolism ; DNA, Bacterial/*genetics ; Disease Models, Animal ; Food Microbiology ; Gene Knockout Techniques/methods ; Gene Targeting/*methods ; Genome/genetics ; Humans ; Mice ; Rats ; *Streptococcus Phages ; Streptococcus thermophilus/*genetics/*immunology/virology
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  • 14
    Publication Date: 2013-05-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balter, Michael -- New York, N.Y. -- Science. 2013 May 24;340(6135):909. doi: 10.1126/science.340.6135.909.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23704541" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior, Animal ; *Cognition ; *Forecasting ; Hippocampus/physiology ; Neurons/physiology ; Neuropsychological Tests ; Rats
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  • 15
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-07-03
    Description: The thalamocortical (TC) projection to layer 4 (L4) is thought to be the main route by which sensory organs communicate with cortex. Sensory information is believed to then propagate through the cortical column along the L4--〉L2/3--〉L5/6 pathway. Here, we show that sensory-evoked responses of L5/6 neurons in rats derive instead from direct TC synapses. Many L5/6 neurons exhibited sensory-evoked postsynaptic potentials with the same latencies as L4. Paired in vivo recordings from L5/6 neurons and thalamic neurons revealed substantial convergence of direct TC synapses onto diverse types of infragranular neurons, particularly in L5B. Pharmacological inactivation of L4 had no effect on sensory-evoked synaptic input to L5/6 neurons. L4 is thus not an obligatory distribution hub for cortical activity, and thalamus activates two separate, independent "strata" of cortex in parallel.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4203320/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4203320/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Constantinople, Christine M -- Bruno, Randy M -- NS069679/NS/NINDS NIH HHS/ -- R01 NS069679/NS/NINDS NIH HHS/ -- T32 HD007430/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2013 Jun 28;340(6140):1591-4. doi: 10.1126/science.1236425.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience and Kavli Institute for Brain Science, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23812718" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Evoked Potentials, Somatosensory ; Neocortex/cytology/drug effects/*physiology ; Neurons/drug effects/physiology ; Rats ; Rats, Wistar ; Synapses/drug effects/physiology ; Thalamus/cytology/drug effects/*physiology
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 16
    Publication Date: 2013-10-26
    Description: The induced pluripotent stem (iPS) cell field holds promise for in vitro disease modeling. However, identifying innate cellular pathologies, particularly for age-related neurodegenerative diseases, has been challenging. Here, we exploited mutation correction of iPS cells and conserved proteotoxic mechanisms from yeast to humans to discover and reverse phenotypic responses to alpha-synuclein (alphasyn), a key protein involved in Parkinson's disease (PD). We generated cortical neurons from iPS cells of patients harboring alphasyn mutations, who are at high risk of developing PD dementia. Genetic modifiers from unbiased screens in a yeast model of alphasyn toxicity led to identification of early pathogenic phenotypes in patient neurons. These included nitrosative stress, accumulation of endoplasmic reticulum (ER)-associated degradation substrates, and ER stress. A small molecule identified in a yeast screen (NAB2), and the ubiquitin ligase Nedd4 it affects, reversed pathologic phenotypes in these neurons.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4022187/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4022187/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chung, Chee Yeun -- Khurana, Vikram -- Auluck, Pavan K -- Tardiff, Daniel F -- Mazzulli, Joseph R -- Soldner, Frank -- Baru, Valeriya -- Lou, Yali -- Freyzon, Yelena -- Cho, Sukhee -- Mungenast, Alison E -- Muffat, Julien -- Mitalipova, Maisam -- Pluth, Michael D -- Jui, Nathan T -- Schule, Birgitt -- Lippard, Stephen J -- Tsai, Li-Huei -- Krainc, Dimitri -- Buchwald, Stephen L -- Jaenisch, Rudolf -- Lindquist, Susan -- 5 R01CA084198/CA/NCI NIH HHS/ -- K01 AG038546/AG/NIA NIH HHS/ -- P50 AG005134/AG/NIA NIH HHS/ -- R01 CA084198/CA/NCI NIH HHS/ -- R01 GM058160/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Nov 22;342(6161):983-7. doi: 10.1126/science.1245296. Epub 2013 Oct 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24158904" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzimidazoles/chemistry/*pharmacology ; Endoplasmic Reticulum Stress/drug effects ; Female ; Humans ; Induced Pluripotent Stem Cells/cytology/metabolism ; Mutation ; Neurogenesis ; Neurons/*drug effects/metabolism/pathology ; Parkinson Disease/genetics/*metabolism ; Rats ; alpha-Synuclein/genetics/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 17
    Publication Date: 2013-10-26
    Description: alpha-Synuclein (alpha-syn) is a small lipid-binding protein implicated in several neurodegenerative diseases, including Parkinson's disease, whose pathobiology is conserved from yeast to man. There are no therapies targeting these underlying cellular pathologies, or indeed those of any major neurodegenerative disease. Using unbiased phenotypic screens as an alternative to target-based approaches, we discovered an N-aryl benzimidazole (NAB) that strongly and selectively protected diverse cell types from alpha-syn toxicity. Three chemical genetic screens in wild-type yeast cells established that NAB promoted endosomal transport events dependent on the E3 ubiquitin ligase Rsp5/Nedd4. These same steps were perturbed by alpha-syn itself. Thus, NAB identifies a druggable node in the biology of alpha-syn that can correct multiple aspects of its underlying pathology, including dysfunctional endosomal and endoplasmic reticulum-to-Golgi vesicle trafficking.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3993916/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3993916/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tardiff, Daniel F -- Jui, Nathan T -- Khurana, Vikram -- Tambe, Mitali A -- Thompson, Michelle L -- Chung, Chee Yeun -- Kamadurai, Hari B -- Kim, Hyoung Tae -- Lancaster, Alex K -- Caldwell, Kim A -- Caldwell, Guy A -- Rochet, Jean-Christophe -- Buchwald, Stephen L -- Lindquist, Susan -- 5R01GM069530/GM/NIGMS NIH HHS/ -- F32GM099817/GM/NIGMS NIH HHS/ -- F32NS061419/NS/NINDS NIH HHS/ -- GM58160/GM/NIGMS NIH HHS/ -- K01 AG038546/AG/NIA NIH HHS/ -- R01 GM058160/GM/NIGMS NIH HHS/ -- R15 NS075684/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Nov 22;342(6161):979-83. doi: 10.1126/science.1245321. Epub 2013 Oct 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research (WIBR), Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24158909" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzimidazoles/chemistry/*pharmacology ; Caenorhabditis elegans ; Cells, Cultured ; *Cytoprotection ; Drug Evaluation, Preclinical ; Endosomal Sorting Complexes Required for Transport/*genetics ; Gene Regulatory Networks/*drug effects ; Neurodegenerative Diseases/*metabolism ; Neurons/*drug effects/metabolism ; Neuroprotective Agents/*pharmacology ; Parkinson Disease/metabolism ; Rats ; Saccharomyces cerevisiae/drug effects ; Saccharomyces cerevisiae Proteins/*genetics ; Small Molecule Libraries/chemistry/pharmacology ; Ubiquitin-Protein Ligase Complexes/*genetics ; Ubiquitin-Protein Ligases/*genetics ; alpha-Synuclein/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 18
    Publication Date: 2013-04-27
    Description: Neurotransmitters have been thought to be fixed throughout life, but whether sensory stimuli alter behaviorally relevant transmitter expression in the mature brain is unknown. We found that populations of interneurons in the adult rat hypothalamus switched between dopamine and somatostatin expression in response to exposure to short- and long-day photoperiods. Changes in postsynaptic dopamine receptor expression matched changes in presynaptic dopamine, whereas somatostatin receptor expression remained constant. Pharmacological blockade or ablation of these dopaminergic neurons led to anxious and depressed behavior, phenocopying performance after exposure to the long-day photoperiod. Induction of newly dopaminergic neurons through exposure to the short-day photoperiod rescued the behavioral consequences of lesions. Natural stimulation of other sensory modalities may cause changes in transmitter expression that regulate different behaviors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dulcis, Davide -- Jamshidi, Pouya -- Leutgeb, Stefan -- Spitzer, Nicholas C -- New York, N.Y. -- Science. 2013 Apr 26;340(6131):449-53. doi: 10.1126/science.1234152.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurobiology Section, Division of Biological Sciences and Center for Neural Circuits and Behavior, University of California-San Diego, La Jolla, CA 92093-0357, USA. ddulcis@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23620046" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/*physiology ; Brain/metabolism/*physiology ; Cell Count ; Dopamine/*metabolism ; Dopaminergic Neurons/metabolism/*physiology ; Hypothalamus/metabolism/physiology ; Male ; Maze Learning ; *Photoperiod ; Rats ; Rats, Long-Evans ; Receptors, Dopamine/metabolism ; Receptors, Somatostatin/metabolism ; Seasons ; Somatostatin/*metabolism ; Stress, Psychological/*psychology ; *Synaptic Transmission
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 19
    Publication Date: 2013-11-30
    Description: The late phase of long-term potentiation (LTP) at glutamatergic synapses, which is thought to underlie long-lasting memory, requires gene transcription in the nucleus. However, the mechanism by which signaling initiated at synapses is transmitted into the nucleus to induce transcription has remained elusive. Here, we found that induction of LTP in only three to seven dendritic spines in rat CA1 pyramidal neurons was sufficient to activate extracellular signal-regulated kinase (ERK) in the nucleus and regulate downstream transcription factors. Signaling from individual spines was integrated over a wide range of time (〉30 minutes) and space (〉80 micrometers). Spatially dispersed inputs over multiple branches activated nuclear ERK much more efficiently than clustered inputs over one branch. Thus, biochemical signals from individual dendritic spines exert profound effects on nuclear signaling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4318497/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4318497/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhai, Shenyu -- Ark, Eugene D -- Parra-Bueno, Paula -- Yasuda, Ryohei -- R01 MH080047/MH/NIMH NIH HHS/ -- R01 NS068410/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Nov 29;342(6162):1107-11. doi: 10.1126/science.1245622.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24288335" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CA1 Region, Hippocampal/enzymology/*physiology ; Cells, Cultured ; Dendritic Spines/enzymology/*physiology ; Extracellular Signal-Regulated MAP Kinases/*metabolism ; Glutamates/metabolism ; *Long-Term Potentiation ; Rats ; Signal Transduction ; Transcription Factors/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 20
    Publication Date: 2013-05-11
    Description: Mutations in the PARK2 (parkin) gene are responsible for an autosomal recessive form of Parkinson's disease. The parkin protein is a RING-in-between-RING E3 ubiquitin ligase that exhibits low basal activity. We describe the crystal structure of full-length rat parkin. The structure shows parkin in an autoinhibited state and provides insight into how it is activated. RING0 occludes the ubiquitin acceptor site Cys(431) in RING2, whereas a repressor element of parkin binds RING1 and blocks its E2-binding site. Mutations that disrupted these inhibitory interactions activated parkin both in vitro and in cells. Parkin is neuroprotective, and these findings may provide a structural and mechanistic framework for enhancing parkin activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trempe, Jean-Francois -- Sauve, Veronique -- Grenier, Karl -- Seirafi, Marjan -- Tang, Matthew Y -- Menade, Marie -- Al-Abdul-Wahid, Sameer -- Krett, Jonathan -- Wong, Kathy -- Kozlov, Guennadi -- Nagar, Bhushan -- Fon, Edward A -- Gehring, Kalle -- MOP-14219/Canadian Institutes of Health Research/Canada -- MOP-62714/Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2013 Jun 21;340(6139):1451-5. doi: 10.1126/science.1237908. Epub 2013 May 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉McGill Parkinson Program, Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23661642" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Catalytic Domain ; Crystallography, X-Ray ; Enzyme Activation ; Hydrophobic and Hydrophilic Interactions ; Models, Molecular ; Molecular Sequence Data ; Mutation ; Parkinson Disease ; Parkinsonian Disorders ; Protein Binding ; Protein Conformation ; Protein Folding ; Protein Structure, Tertiary ; Rats ; Ubiquitin-Protein Ligases/*chemistry/genetics/*metabolism ; Ubiquitination ; Zinc Fingers
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  • 21
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-04-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Birren, Susan J -- Marder, Eve -- New York, N.Y. -- Science. 2013 Apr 26;340(6131):436-7. doi: 10.1126/science.1238518.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biology Department and Volen Center, Brandeis University, Waltham, MA 02454, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23620040" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Cortex Hormones/blood ; Animals ; Anxiety/blood/physiopathology ; Corticotropin-Releasing Hormone/*secretion ; Depression/blood/physiopathology ; Dopamine/*secretion ; Humans ; Hypothalamus/cytology/*physiology/secretion ; *Neuronal Plasticity ; Neurons/secretion ; *Photoperiod ; Rats ; Signal Transduction ; Somatostatin/*secretion ; Stress, Psychological/blood/physiopathology ; *Synaptic Transmission
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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