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  • 1
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    Dysfunction in GABA signalling mediates autism-like stereotypies and Rett syndrome phenotypes (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-11-12
    Description: Mutations in the X-linked MECP2 gene, which encodes the transcriptional regulator methyl-CpG-binding protein 2 (MeCP2), cause Rett syndrome and several neurodevelopmental disorders including cognitive disorders, autism, juvenile-onset schizophrenia and encephalopathy with early lethality. Rett syndrome is characterized by apparently normal early development followed by regression, motor abnormalities, seizures and features of autism, especially stereotyped behaviours. The mechanisms mediating these features are poorly understood. Here we show that mice lacking Mecp2 from GABA (gamma-aminobutyric acid)-releasing neurons recapitulate numerous Rett syndrome and autistic features, including repetitive behaviours. Loss of MeCP2 from a subset of forebrain GABAergic neurons also recapitulates many features of Rett syndrome. MeCP2-deficient GABAergic neurons show reduced inhibitory quantal size, consistent with a presynaptic reduction in glutamic acid decarboxylase 1 (Gad1) and glutamic acid decarboxylase 2 (Gad2) levels, and GABA immunoreactivity. These data demonstrate that MeCP2 is critical for normal function of GABA-releasing neurons and that subtle dysfunction of GABAergic neurons contributes to numerous neuropsychiatric phenotypes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3057962/" 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/PMC3057962/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chao, Hsiao-Tuan -- Chen, Hongmei -- Samaco, Rodney C -- Xue, Mingshan -- Chahrour, Maria -- Yoo, Jong -- Neul, Jeffrey L -- Gong, Shiaoching -- Lu, Hui-Chen -- Heintz, Nathaniel -- Ekker, Marc -- Rubenstein, John L R -- Noebels, Jeffrey L -- Rosenmund, Christian -- Zoghbi, Huda Y -- 29709/PHS HHS/ -- F31MH078678/MH/NIMH NIH HHS/ -- HD024064/HD/NICHD NIH HHS/ -- HD053862/HD/NICHD NIH HHS/ -- K08 NS052240/NS/NINDS NIH HHS/ -- K08 NS052240-01/NS/NINDS NIH HHS/ -- K08 NS052240-02/NS/NINDS NIH HHS/ -- K08 NS052240-03/NS/NINDS NIH HHS/ -- K08 NS052240-04/NS/NINDS NIH HHS/ -- K08 NS052240-05/NS/NINDS NIH HHS/ -- P30 HD024064/HD/NICHD NIH HHS/ -- P30 HD024064-22/HD/NICHD NIH HHS/ -- R01 HD062553/HD/NICHD NIH HHS/ -- R01 NS048884/NS/NINDS NIH HHS/ -- R01 NS057819/NS/NINDS NIH HHS/ -- R01 NS057819-04/NS/NINDS NIH HHS/ -- R01 NS057819-05/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Nov 11;468(7321):263-9. doi: 10.1038/nature09582.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉]Department of Neuroscience, Baylor College of Medicine, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21068835" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/complications/genetics/pathology/*physiopathology ; Brain/cytology ; Compulsive Behavior/complications/genetics/physiopathology ; Disease Models, Animal ; Electroencephalography ; Genotype ; Glutamate Decarboxylase/metabolism ; Hippocampus/pathology/physiopathology ; Homeodomain Proteins/genetics ; Inhibitory Postsynaptic Potentials ; Long-Term Potentiation ; Male ; Methyl-CpG-Binding Protein 2/*deficiency/genetics/*metabolism ; Mice ; Mice, Transgenic ; Neural Inhibition ; Neuronal Plasticity ; Neurons/metabolism ; Phenotype ; Presynaptic Terminals/metabolism ; Psychomotor Disorders/complications/genetics/physiopathology ; Reflex, Startle/genetics ; Respiration ; Rett Syndrome/complications/genetics/pathology/*physiopathology ; Self-Injurious Behavior/complications/genetics/physiopathology ; *Signal Transduction ; Stereotypic Movement Disorder/complications/genetics/pathology/*physiopathology ; Survival Rate ; Synaptic Transmission ; Vesicular Inhibitory Amino Acid Transport Proteins/genetics ; gamma-Aminobutyric Acid/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Reduction of naturally occurring motoneuron death in vivo by a target-derived neurotrophic factor (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-05-13
    Description: Treatment of chick embryos in ovo with crude and partially purified extracts from embryonic hindlimbs (days 8 to 9) during the normal cell death period (days 5 to 10) rescues a significant number of motoneurons from degeneration. The survival activity of partially purified extract was dose-dependent and developmentally regulated. The survival of sensory, sympathetic, parasympathetic, and a population of cholinergic sympathetic preganglionic neurons was unaffected by treatment with hindlimb extract. The massive motoneuron death that occurs after early target (hindlimb) removal was partially ameliorated by daily treatment with the hindlimb extract. These results indicate that a target-derived neurotrophic factor is involved in the regulation of motoneuron survival in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oppenheim, R W -- Haverkamp, L J -- Prevette, D -- McManaman, J L -- Appel, S H -- NS 20402/NS/NINDS NIH HHS/ -- NS 23058/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1988 May 13;240(4854):919-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy, Wake Forest University, Bowman Gray School of Medicine, Winston-Salem, NC 27103.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3363373" target="_blank"〉PubMed〈/a〉
    Keywords: Ammonium Sulfate ; Animals ; Cell Survival ; Chemical Fractionation ; Chick Embryo ; Growth Substances/isolation & purification/*pharmacology ; Hindlimb ; Motor Neurons/*cytology ; Muscles/analysis/embryology/innervation ; Nerve Growth Factors/pharmacology ; Tissue Extracts/isolation & purification/pharmacology
    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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    Formation of accumbens GluR2-lacking AMPA receptors mediates incubation of cocaine craving (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-05-27
    Description: Relapse to cocaine use after prolonged abstinence is an important clinical problem. This relapse is often induced by exposure to cues associated with cocaine use. To account for the persistent propensity for relapse, it has been suggested that cue-induced cocaine craving increases over the first several weeks of abstinence and remains high for extended periods. We and others identified an analogous phenomenon in rats that was termed 'incubation of cocaine craving': time-dependent increases in cue-induced cocaine-seeking over the first months after withdrawal from self-administered cocaine. Cocaine-seeking requires the activation of glutamate projections that excite receptors for alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) in the nucleus accumbens. Here we show that the number of synaptic AMPA receptors in the accumbens is increased after prolonged withdrawal from cocaine self-administration by the addition of new AMPA receptors lacking glutamate receptor 2 (GluR2). Furthermore, we show that these new receptors mediate the incubation of cocaine craving. Our results indicate that GluR2-lacking AMPA receptors could be a new target for drug development for the treatment of cocaine addiction. We propose that after prolonged withdrawal from cocaine, increased numbers of synaptic AMPA receptors combined with the higher conductance of GluR2-lacking AMPA receptors causes increased reactivity of accumbens neurons to cocaine-related cues, leading to an intensification of drug craving and relapse.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2574981/" 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/PMC2574981/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Conrad, Kelly L -- Tseng, Kuei Y -- Uejima, Jamie L -- Reimers, Jeremy M -- Heng, Li-Jun -- Shaham, Yavin -- Marinelli, Michela -- Wolf, Marina E -- DA00453/DA/NIDA NIH HHS/ -- DA015835/DA/NIDA NIH HHS/ -- DA020654/DA/NIDA NIH HHS/ -- DA09621/DA/NIDA NIH HHS/ -- Z01 DA000434-08/Intramural NIH HHS/ -- England -- Nature. 2008 Jul 3;454(7200):118-21. doi: 10.1038/nature06995. Epub 2008 May 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Rosalind Franklin University of Medicine and Science, 3333 Green Bay Road, North Chicago, Illinois 60064, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18500330" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cocaine ; Cocaine-Related Disorders/genetics/metabolism/*physiopathology ; Cues ; Gene Expression Regulation ; Male ; Nucleus Accumbens/*metabolism/physiopathology ; Rats ; Rats, Long-Evans ; Rats, Sprague-Dawley ; Receptors, AMPA/deficiency/genetics/*metabolism ; Self Administration ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    S-glutathionylation uncouples eNOS and regulates its cellular and vascular function (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-12-24
    Description: Endothelial nitric oxide synthase (eNOS) is critical in the regulation of vascular function, and can generate both nitric oxide (NO) and superoxide (O(2)(*-)), which are key mediators of cellular signalling. In the presence of Ca(2+)/calmodulin, eNOS produces NO, endothelial-derived relaxing factor, from l-arginine (l-Arg) by means of electron transfer from NADPH through a flavin containing reductase domain to oxygen bound at the haem of an oxygenase domain, which also contains binding sites for tetrahydrobiopterin (BH(4)) and l-Arg. In the absence of BH(4), NO synthesis is abrogated and instead O(2)(*-) is generated. While NOS dysfunction occurs in diseases with redox stress, BH(4) repletion only partly restores NOS activity and NOS-dependent vasodilation. This suggests that there is an as yet unidentified redox-regulated mechanism controlling NOS function. Protein thiols can undergo S-glutathionylation, a reversible protein modification involved in cellular signalling and adaptation. Under oxidative stress, S-glutathionylation occurs through thiol-disulphide exchange with oxidized glutathione or reaction of oxidant-induced protein thiyl radicals with reduced glutathione. Cysteine residues are critical for the maintenance of eNOS function; we therefore speculated that oxidative stress could alter eNOS activity through S-glutathionylation. Here we show that S-glutathionylation of eNOS reversibly decreases NOS activity with an increase in O(2)(*-) generation primarily from the reductase, in which two highly conserved cysteine residues are identified as sites of S-glutathionylation and found to be critical for redox-regulation of eNOS function. We show that eNOS S-glutathionylation in endothelial cells, with loss of NO and gain of O(2)(*-) generation, is associated with impaired endothelium-dependent vasodilation. In hypertensive vessels, eNOS S-glutathionylation is increased with impaired endothelium-dependent vasodilation that is restored by thiol-specific reducing agents, which reverse this S-glutathionylation. Thus, S-glutathionylation of eNOS is a pivotal switch providing redox regulation of cellular signalling, endothelial function and vascular tone.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3370391/" 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/PMC3370391/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Chun-An -- Wang, Tse-Yao -- Varadharaj, Saradhadevi -- Reyes, Levy A -- Hemann, Craig -- Talukder, M A Hassan -- Chen, Yeong-Renn -- Druhan, Lawrence J -- Zweier, Jay L -- K99 HL103846/HL/NHLBI NIH HHS/ -- K99 HL103846-02/HL/NHLBI NIH HHS/ -- R01 HL038324/HL/NHLBI NIH HHS/ -- R01 HL038324-20/HL/NHLBI NIH HHS/ -- R01 HL063744/HL/NHLBI NIH HHS/ -- R01 HL063744-09/HL/NHLBI NIH HHS/ -- R01HL103846/HL/NHLBI NIH HHS/ -- R01HL38324/HL/NHLBI NIH HHS/ -- R01HL63744/HL/NHLBI NIH HHS/ -- R01HL65608/HL/NHLBI NIH HHS/ -- R01HL83237/HL/NHLBI NIH HHS/ -- England -- Nature. 2010 Dec 23;468(7327):1115-8. doi: 10.1038/nature09599.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Davis Heart and Lung Research Institute and Division of Cardiovascular Medicine, Department of Internal Medicine, College of Medicine, Ohio State University, Columbus, Ohio 43210, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179168" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Cells, Cultured ; Dithiothreitol/pharmacology ; Endothelial Cells/metabolism ; Endothelium, Vascular/*metabolism ; Glutathione/*metabolism ; Humans ; Male ; Mercaptoethanol/pharmacology ; Mutation ; Nitric Oxide Synthase Type III/genetics/*metabolism ; Oxidation-Reduction ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Rats, Sprague-Dawley ; Reducing Agents/pharmacology ; Signal Transduction ; Vasodilation/physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Calibrating the end-Permian mass extinction (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-11-19
    Description: The end-Permian mass extinction was the most severe biodiversity crisis in Earth history. To better constrain the timing, and ultimately the causes of this event, we collected a suite of geochronologic, isotopic, and biostratigraphic data on several well-preserved sedimentary sections in South China. High-precision U-Pb dating reveals that the extinction peak occurred just before 252.28 +/- 0.08 million years ago, after a decline of 2 per mil ( per thousand) in delta(13)C over 90,000 years, and coincided with a delta(13)C excursion of -5 per thousand that is estimated to have lasted 〈/=20,000 years. The extinction interval was less than 200,000 years and synchronous in marine and terrestrial realms; associated charcoal-rich and soot-bearing layers indicate widespread wildfires on land. A massive release of thermogenic carbon dioxide and/or methane may have caused the catastrophic extinction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, Shu-zhong -- Crowley, James L -- Wang, Yue -- Bowring, Samuel A -- Erwin, Douglas H -- Sadler, Peter M -- Cao, Chang-qun -- Rothman, Daniel H -- Henderson, Charles M -- Ramezani, Jahandar -- Zhang, Hua -- Shen, Yanan -- Wang, Xiang-dong -- Wang, Wei -- Mu, Lin -- Li, Wen-zhong -- Tang, Yue-gang -- Liu, Xiao-lei -- Liu, Lu-jun -- Zeng, Yong -- Jiang, Yao-fa -- Jin, Yu-gan -- New York, N.Y. -- Science. 2011 Dec 9;334(6061):1367-72. doi: 10.1126/science.1213454. Epub 2011 Nov 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉State Key Laboratory of Palaeobiology and Stratigraphy, Nanjing Institute of Geology and Palaeontology, Nanjing 210008, China. szshen@nigpas.ac.cn〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22096103" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biodiversity ; Carbon Dioxide ; Carbon Isotopes ; China ; *Ecosystem ; *Extinction, Biological ; Fires ; *Fossils ; Geologic Sediments ; Invertebrates/classification ; Isotopes ; Lead ; Mass Spectrometry ; Methane ; Oceans and Seas ; Plants/classification ; Radioisotope Dilution Technique ; Radiometric Dating ; Seawater/chemistry ; Time ; Uranium ; Vertebrates/classification
    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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  • 6
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    Neandertal roots: Cranial and chronological evidence from Sima de los Huesos (2014)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2014-06-21
    Description: Seventeen Middle Pleistocene crania from the Sima de los Huesos site (Atapuerca, Spain) are analyzed, including seven new specimens. This sample makes it possible to thoroughly characterize a Middle Pleistocene hominin paleodeme and to address hypotheses about the origin and evolution of the Neandertals. Using a variety of techniques, the hominin-bearing layer could be reassigned to a period around 430,000 years ago. The sample shows a consistent morphological pattern with derived Neandertal features present in the face and anterior vault, many of which are related to the masticatory apparatus. This suggests that facial modification was the first step in the evolution of the Neandertal lineage, pointing to a mosaic pattern of evolution, with different anatomical and functional modules evolving at different rates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arsuaga, J L -- Martinez, I -- Arnold, L J -- Aranburu, A -- Gracia-Tellez, A -- Sharp, W D -- Quam, R M -- Falgueres, C -- Pantoja-Perez, A -- Bischoff, J -- Poza-Rey, E -- Pares, J M -- Carretero, J M -- Demuro, M -- Lorenzo, C -- Sala, N -- Martinon-Torres, M -- Garcia, N -- Alcazar de Velasco, A -- Cuenca-Bescos, G -- Gomez-Olivencia, A -- Moreno, D -- Pablos, A -- Shen, C-C -- Rodriguez, L -- Ortega, A I -- Garcia, R -- Bonmati, A -- Bermudez de Castro, J M -- Carbonell, E -- New York, N.Y. -- Science. 2014 Jun 20;344(6190):1358-63. doi: 10.1126/science.1253958.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centro Mixto UCM-ISCIII de Evolucion y Comportamiento Humanos, Madrid, Spain. Departamento de Paleontologia, Facultad Ciencias Geologicas, Universidad Complutense de Madrid, Spain. jlarsuaga@isciii.es. ; Area de Paleontologia, Departamento de Geologia, Geografia y Medio Ambiente, Universidad de Alcala, Spain.Centro Mixto UCM-ISCIII de Evolucion y Comportamiento Humanos, Madrid, Spain. ; Centro Nacional de Investigacion sobre la Evolucion Humana Burgos, Spain. School of Earth and Environmental Sciences, the Environment Institute, and the Institute for Photonics and Advanced Sensing (IPAS), University of Adelaide, Australia. ; Departamento Mineralogia y Petrologia, Facultad de Ciencia y Tecnologia, Universidad del Pais Vasco, Spain. ; Berkeley Geochronology Center, Berkeley, CA, USA. ; Department of Anthropology, Binghamton University (State University of New York), Binghamton, NY, USA. Division of Anthropology, American Museum of Natural History, New York, NY, USA.Centro Mixto UCM-ISCIII de Evolucion y Comportamiento Humanos, Madrid, Spain. ; Departement de Prehistoire, Museum National d'Histoire Naturelle, Paris, France. ; Centro Mixto UCM-ISCIII de Evolucion y Comportamiento Humanos, Madrid, Spain. Departamento de Paleontologia, Facultad Ciencias Geologicas, Universidad Complutense de Madrid, Spain. ; U.S. Geological Survey, Menlo Park, CA,USA. ; Centro Nacional de Investigacion sobre la Evolucion Humana Burgos, Spain. ; Laboratorio de Evolucion Humana, Departamento de Ciencias Historicas y Geografia, Universidad de Burgos, Spain. ; Centro Nacional de Investigacion sobre la Evolucion Humana Burgos, Spain. Institute for Photonics and Advanced Sensing (IPAS), School of Chemistry and Physics, University of Adelaide, Australia. ; Area de Prehistoria, Departamento d'Historia i Historia de l'Art, Universitat Rovira i Virgili (URV), Tarragona, Spain. Institut Catala de Paleoecologia Humana i Evolucio Social, Tarragona, Spain.Centro Mixto UCM-ISCIII de Evolucion y Comportamiento Humanos, Madrid, Spain. ; Centro Mixto UCM-ISCIII de Evolucion y Comportamiento Humanos, Madrid, Spain. ; Paleontologia, Aragosaurus-IUCA and Facultad Ciencias, Universidad de Zaragoza, Spain. ; Centro Mixto UCM-ISCIII de Evolucion y Comportamiento Humanos, Madrid, Spain. Departement de Prehistoire, Museum National d'Histoire Naturelle, Paris, France. PAVE Research Group, Division of Biological Anthropology, Cambridge, UK. ; Departement de Prehistoire, Museum National d'Histoire Naturelle, Paris, France. Laboratorio de Evolucion Humana, Departamento de Ciencias Historicas y Geografia, Universidad de Burgos, Spain. ; Centro Mixto UCM-ISCIII de Evolucion y Comportamiento Humanos, Madrid, Spain. Centro Nacional de Investigacion sobre la Evolucion Humana Burgos, Spain. Laboratorio de Evolucion Humana, Departamento de Ciencias Historicas y Geografia, Universidad de Burgos, Spain. ; High-Precision Mass Spectrometry and Environment Change Laboratory (HISPEC), Department of Geosciences, National Taiwan University, Taiwan ROC. ; Institut Catala de Paleoecologia Humana i Evolucio Social, Tarragona, Spain. Area de Prehistoria, Departamento d'Historia i Historia de l'Art, Universitat Rovira i Virgili (URV), Tarragona, Spain. Institute of Vertebrate Paleontology and Paleoanthropology of Beijing (IVPP), China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24948730" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/anatomy & histology ; Extinction, Biological ; *Fossils ; Genetic Drift ; Humans ; Neanderthals/*anatomy & histology/*genetics ; Organ Size ; Reproductive Isolation ; Skull/*anatomy & histology ; Spain
    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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  • 7
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    Restoring systemic GDF11 levels reverses age-related dysfunction in mouse skeletal muscle (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-05-07
    Description: Parabiosis experiments indicate that impaired regeneration in aged mice is reversible by exposure to a young circulation, suggesting that young blood contains humoral "rejuvenating" factors that can restore regenerative function. Here, we demonstrate that the circulating protein growth differentiation factor 11 (GDF11) is a rejuvenating factor for skeletal muscle. Supplementation of systemic GDF11 levels, which normally decline with age, by heterochronic parabiosis or systemic delivery of recombinant protein, reversed functional impairments and restored genomic integrity in aged muscle stem cells (satellite cells). Increased GDF11 levels in aged mice also improved muscle structural and functional features and increased strength and endurance exercise capacity. These data indicate that GDF11 systemically regulates muscle aging and may be therapeutically useful for reversing age-related skeletal muscle and stem cell dysfunction.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4104429/" 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/PMC4104429/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sinha, Manisha -- Jang, Young C -- Oh, Juhyun -- Khong, Danika -- Wu, Elizabeth Y -- Manohar, Rohan -- Miller, Christine -- Regalado, Samuel G -- Loffredo, Francesco S -- Pancoast, James R -- Hirshman, Michael F -- Lebowitz, Jessica -- Shadrach, Jennifer L -- Cerletti, Massimiliano -- Kim, Mi-Jeong -- Serwold, Thomas -- Goodyear, Laurie J -- Rosner, Bernard -- Lee, Richard T -- Wagers, Amy J -- 1DP2 OD004345/OD/NIH HHS/ -- 1R01 AG033053/AG/NIA NIH HHS/ -- 1R01 AG040019/AG/NIA NIH HHS/ -- 5U01 HL100402/HL/NHLBI NIH HHS/ -- DP2 OD004345/OD/NIH HHS/ -- P30 AG038072/AG/NIA NIH HHS/ -- R01 AG032977/AG/NIA NIH HHS/ -- R01 AG033053/AG/NIA NIH HHS/ -- R01 AG040019/AG/NIA NIH HHS/ -- R01 AR042238/AR/NIAMS NIH HHS/ -- R01 AR42238/AR/NIAMS NIH HHS/ -- T32 DE007057/DE/NIDCR NIH HHS/ -- U01 HL100402/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 May 9;344(6184):649-52. doi: 10.1126/science.1251152. Epub 2014 May 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Harvard Stem Cell Institute and Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24797481" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Aging/blood/drug effects/*physiology ; Animals ; Bone Morphogenetic Proteins/administration & dosage/blood/*physiology ; Growth Differentiation Factors/administration & dosage/blood/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Muscle, Skeletal/*blood supply/drug effects/*physiology ; Myoblasts, Skeletal/drug effects/*physiology ; Parabiosis ; *Regeneration ; *Rejuvenation
    Print ISSN: 0036-8075
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  • 8
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    Expression cloning and signaling properties of the rat glucagon receptor (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-03-12
    Description: Glucagon and the glucagon receptor are a primary source of control over blood glucose concentrations and are especially important to studies of diabetes in which the loss of control over blood glucose concentrations clinically defines the disease. A complementary DNA clone for the glucagon receptor was isolated by an expression cloning strategy, and the receptor protein was expressed in several kidney cell lines. The cloned receptor bound glucagon and caused an increase in the intracellular concentration of adenosine 3', 5'-monophosphate (cAMP). The cloned glucagon receptor also transduced a signal that led to an increased concentration of intracellular calcium. The glucagon receptor is similar to the calcitonin and parathyroid hormone receptors. It can transduce signals leading to the accumulation of two different second messengers, cAMP and calcium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jelinek, L J -- Lok, S -- Rosenberg, G B -- Smith, R A -- Grant, F J -- Biggs, S -- Bensch, P A -- Kuijper, J L -- Sheppard, P O -- Sprecher, C A -- New York, N.Y. -- Science. 1993 Mar 12;259(5101):1614-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ZymoGenetics Inc., Seattle, WA 98105.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8384375" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium/pharmacology ; Cell Line ; Cloning, Molecular ; Cricetinae ; Cyclic AMP/metabolism ; Glucagon/metabolism/*pharmacology ; Kidney ; Kinetics ; Liver/*metabolism ; Molecular Sequence Data ; Rats ; Receptors, Gastrointestinal Hormone/genetics/metabolism/*physiology ; Receptors, Glucagon ; *Signal Transduction ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 9
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    A call for transparent reporting to optimize the predictive value of preclinical research (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-10-13
    Description: The US National Institute of Neurological Disorders and Stroke convened major stakeholders in June 2012 to discuss how to improve the methodological reporting of animal studies in grant applications and publications. The main workshop recommendation is that at a minimum studies should report on sample-size estimation, whether and how animals were randomized, whether investigators were blind to the treatment, and the handling of data. We recognize that achieving a meaningful improvement in the quality of reporting will require a concerted effort by investigators, reviewers, funding agencies and journal editors. Requiring better reporting of animal studies will raise awareness of the importance of rigorous study design to accelerate scientific progress.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3511845/" 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/PMC3511845/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Landis, Story C -- Amara, Susan G -- Asadullah, Khusru -- Austin, Chris P -- Blumenstein, Robi -- Bradley, Eileen W -- Crystal, Ronald G -- Darnell, Robert B -- Ferrante, Robert J -- Fillit, Howard -- Finkelstein, Robert -- Fisher, Marc -- Gendelman, Howard E -- Golub, Robert M -- Goudreau, John L -- Gross, Robert A -- Gubitz, Amelie K -- Hesterlee, Sharon E -- Howells, David W -- Huguenard, John -- Kelner, Katrina -- Koroshetz, Walter -- Krainc, Dimitri -- Lazic, Stanley E -- Levine, Michael S -- Macleod, Malcolm R -- McCall, John M -- Moxley, Richard T 3rd -- Narasimhan, Kalyani -- Noble, Linda J -- Perrin, Steve -- Porter, John D -- Steward, Oswald -- Unger, Ellis -- Utz, Ursula -- Silberberg, Shai D -- P01 NS012151/NS/NINDS NIH HHS/ -- P30 MH062261/MH/NIMH NIH HHS/ -- R01 NS006477/NS/NINDS NIH HHS/ -- R01 NS034774/NS/NINDS NIH HHS/ -- R01 NS041574/NS/NINDS NIH HHS/ -- T32 MH020016/MH/NIMH NIH HHS/ -- T32 NS007280/NS/NINDS NIH HHS/ -- UL1 RR024160/RR/NCRR NIH HHS/ -- Z99 NS999999/Intramural NIH HHS/ -- England -- Nature. 2012 Oct 11;490(7419):187-91. doi: 10.1038/nature11556.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Neurological Disorders and Stroke, NIH, Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23060188" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Publishing/*standards/trends ; Random Allocation ; Research Design/*standards ; Sample Size ; Statistics as Topic
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 10
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    PKM-zeta is not required for hippocampal synaptic plasticity, learning and memory (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-01-04
    Description: Long-term potentiation (LTP), a well-characterized form of synaptic plasticity, has long been postulated as a cellular correlate of learning and memory. Although LTP can persist for long periods of time, the mechanisms underlying LTP maintenance, in the midst of ongoing protein turnover and synaptic activity, remain elusive. Sustained activation of the brain-specific protein kinase C (PKC) isoform protein kinase M-zeta (PKM-zeta) has been reported to be necessary for both LTP maintenance and long-term memory. Inhibiting PKM-zeta activity using a synthetic zeta inhibitory peptide (ZIP) based on the PKC-zeta pseudosubstrate sequence reverses established LTP in vitro and in vivo. More notably, infusion of ZIP eliminates memories for a growing list of experience-dependent behaviours, including active place avoidance, conditioned taste aversion, fear conditioning and spatial learning. However, most of the evidence supporting a role for PKM-zeta in LTP and memory relies heavily on pharmacological inhibition of PKM-zeta by ZIP. To further investigate the involvement of PKM-zeta in the maintenance of LTP and memory, we generated transgenic mice lacking PKC-zeta and PKM-zeta. We find that both conventional and conditional PKC-zeta/PKM-zeta knockout mice show normal synaptic transmission and LTP at Schaffer collateral-CA1 synapses, and have no deficits in several hippocampal-dependent learning and memory tasks. Notably, ZIP still reverses LTP in PKC-zeta/PKM-zeta knockout mice, indicating that the effects of ZIP are independent of PKM-zeta.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3830948/" 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/PMC3830948/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Volk, Lenora J -- Bachman, Julia L -- Johnson, Richard -- Yu, Yilin -- Huganir, Richard L -- NS36715/NS/NINDS NIH HHS/ -- P30 NS050274/NS/NINDS NIH HHS/ -- R01 NS036715/NS/NINDS NIH HHS/ -- T32 EY017203/EY/NEI NIH HHS/ -- T32 MH015330/MH/NIMH NIH HHS/ -- T32MH15330/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Jan 17;493(7432):420-3. doi: 10.1038/nature11802. Epub 2013 Jan 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23283174" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Avoidance Learning/drug effects/physiology ; Behavior, Animal/drug effects/physiology ; Conditioning, Classical ; Fear ; Female ; Hippocampus/drug effects/*physiology ; Isoenzymes/deficiency/genetics/metabolism ; Lipopeptides/pharmacology ; Long-Term Potentiation/drug effects/genetics/physiology ; Male ; Memory, Long-Term/drug effects/*physiology ; Mice ; Mice, Knockout ; Neuronal Plasticity/genetics/*physiology ; Protein Kinase C/antagonists & inhibitors/deficiency/genetics/*metabolism ; Synapses/drug effects/*metabolism ; Synaptic Transmission/drug effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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