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  • 1
    Publication Date: 2015-06-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hussein, Samer M I -- Puri, Mira C -- Tonge, Peter D -- Benevento, Marco -- Corso, Andrew J -- Clancy, Jennifer L -- Mosbergen, Rowland -- Li, Mira -- Lee, Dong-Sung -- Cloonan, Nicole -- Wood, David L A -- Munoz, Javier -- Middleton, Robert -- Korn, Othmar -- Patel, Hardip R -- White, Carl A -- Shin, Jong-Yeon -- Gauthier, Maely E -- Cao, Kim-Anh Le -- Kim, Jong-Il -- Mar, Jessica C -- Shakiba, Nika -- Ritchie, William -- Rasko, John E J -- Grimmond, Sean M -- Zandstra, Peter W -- Wells, Christine A -- Preiss, Thomas -- Seo, Jeong-Sun -- Heck, Albert J R -- Rogers, Ian M -- Nagy, Andras -- England -- Nature. 2015 Jul 30;523(7562):626. doi: 10.1038/nature14606. Epub 2015 Jun 17.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26083747" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2018-06-14
    Description: Influenza B virus (IBV) is one of the human respiratory viruses and one of the targets of seasonal vaccination. However, the bifurcation of two antigenically distinct lineages of IBVs makes it difficult to arrange proper medical countermeasures. Moreover, compared with pathogenicity-related molecular markers known for influenza A virus, little has been known for IBVs. To understand pathogenicity caused by IBVs, we investigated the molecular determinants of IBV pathogenicity in animal models. After serial lung-to-lung passages of Victoria lineage B/Brisbane/60/2008 (Vc_BR60) and Yamagata lineage B/Wisconsin/01/2010 (Ym_WI01) viruses in BALB/c mice, we identified the mouse-adapted Vc_BR60 (maVc_BR60) and Ym_WI01 (maYm_WI01) viruses, respectively. To find a molecular clue(s) to the increased pathogenicity of maVc_BR60 and maYm_WI01, we determined their genetic sequences. Several amino acid mutations were identified in the PB2, PB1, PA, BM2, and/or NS1 protein-coding regions, and one concurrent lysine (K)-to-arginine (R) mutation in PA residue 338 (PA K338R) was found in both maVc_BR60 and maYm_WI01 viruses. When analyzed using viruses rescued through reverse genetics, it was shown that PA K338R alone could increase the pathogenicity of both IBVs in mice and viral replication in the respiratory tracts of ferrets. In a subsequent minireplicon assay, the effect of PA K338R was highlighted by the enhancement of viral polymerase complex activity of both Vc_BR60 and Ym_WI01 viruses. These results suggest that the PA K338R mutation may be a molecular determinant of IBV pathogenicity via modulating the viral polymerase function of IBVs. IMPORTANCE To investigate molecular pathogenic determinants of IBVs, which are one of the targets of seasonal influenza vaccines, we adapted both Victoria and Yamagata lineage IBVs independently in mice. The recovered mouse-adapted viruses exhibited increased virulence, and of the various mutations identified from both mouse-adapted viruses, a concurrent amino acid mutation was found in the PA protein-coding region. When analyzed using viruses rescued through reverse genetics, the PA mutation alone appeared to contribute to viral pathogenicity in mice within the compatible genetic constellation between the IBV lineages and to the replication of IBVs in ferrets. Regarding the potential mechanism of increased viral pathogenicity, it was shown that the PA mutation could upregulate the viral polymerase complex activity of both IBV lineages. These results indicate that the PA mutation could be a newly defined molecular pathogenic determinant of IBVs that substantiates our understanding of the viral pathogenicity and public health risks of IBVs.
    Print ISSN: 0022-538X
    Electronic ISSN: 1098-5514
    Topics: Medicine
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  • 3
    Publication Date: 2014-12-17
    Description: Somatic cell reprogramming to a pluripotent state continues to challenge many of our assumptions about cellular specification, and despite major efforts, we lack a complete molecular characterization of the reprograming process. To address this gap in knowledge, we generated extensive transcriptomic, epigenomic and proteomic data sets describing the reprogramming routes leading from mouse embryonic fibroblasts to induced pluripotency. Through integrative analysis, we reveal that cells transition through distinct gene expression and epigenetic signatures and bifurcate towards reprogramming transgene-dependent and -independent stable pluripotent states. Early transcriptional events, driven by high levels of reprogramming transcription factor expression, are associated with widespread loss of histone H3 lysine 27 (H3K27me3) trimethylation, representing a general opening of the chromatin state. Maintenance of high transgene levels leads to re-acquisition of H3K27me3 and a stable pluripotent state that is alternative to the embryonic stem cell (ESC)-like fate. Lowering transgene levels at an intermediate phase, however, guides the process to the acquisition of ESC-like chromatin and DNA methylation signature. Our data provide a comprehensive molecular description of the reprogramming routes and is accessible through the Project Grandiose portal at http://www.stemformatics.org.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hussein, Samer M I -- Puri, Mira C -- Tonge, Peter D -- Benevento, Marco -- Corso, Andrew J -- Clancy, Jennifer L -- Mosbergen, Rowland -- Li, Mira -- Lee, Dong-Sung -- Cloonan, Nicole -- Wood, David L A -- Munoz, Javier -- Middleton, Robert -- Korn, Othmar -- Patel, Hardip R -- White, Carl A -- Shin, Jong-Yeon -- Gauthier, Maely E -- Le Cao, Kim-Anh -- Kim, Jong-Il -- Mar, Jessica C -- Shakiba, Nika -- Ritchie, William -- Rasko, John E J -- Grimmond, Sean M -- Zandstra, Peter W -- Wells, Christine A -- Preiss, Thomas -- Seo, Jeong-Sun -- Heck, Albert J R -- Rogers, Ian M -- Nagy, Andras -- MOP102575/Canadian Institutes of Health Research/Canada -- England -- Nature. 2014 Dec 11;516(7530):198-206. doi: 10.1038/nature14046.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario M5G 1X5, Canada. ; 1] Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario M5G 1X5, Canada [2] Department of Medical Biophysics, University of Toronto, Toronto, Ontario M5T 3H7, Canada. ; 1] Biomolecular Mass Spectrometry and Proteomics, Bijvoet Center for Biomolecular Research and Utrecht Institute for Pharmaceutical Sciences, Utrecht University, Padualaan 8, 3584 CH Utrecht, The Netherlands [2] Netherlands Proteomics Centre, Padualaan 8, 3584CH Utrecht, The Netherlands. ; 1] Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario M5G 1X5, Canada [2] Institute of Medical Science, University of Toronto, Toronto, Ontario M5T 3H7, Canada. ; Genome Biology Department, The John Curtin School of Medical Research, The Australian National University, Acton (Canberra), ACT 2601, Australia. ; Australian Institute for Bioengineering and Nanotechnology, The University of Queensland, Brisbane, Queensland 4072, Australia. ; 1] Genomic Medicine Institute, Medical Research Center, Seoul National University, Seoul 110-799, South Korea [2] Department of Biomedical Sciences and Biochemistry, Seoul National University College of Medicine, Seoul 110-799, South Korea. ; Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Queensland 4072, Australia. ; Gene and Stem Cell Therapy Program and Bioinformatics Lab, Centenary Institute, Camperdown 2050, NSW, Australia &Sydney Medical School, 31 University of Sydney 2006, New South Wales, Australia. ; 1] Genome Biology Department, The John Curtin School of Medical Research, The Australian National University, Acton (Canberra), ACT 2601, Australia [2] Genome Discovery Unit, The John Curtin School of Medical Research, The Australian National University, Acton (Canberra) 2601, ACT, Australia. ; 1] Institute of Biomaterials and Biomedical Engineering (IBBME), University of Toronto, Toronto M5S-3G9, Canada [2] The Donnelly Centre for Cellular and Biomolecular Research (CCBR), University of Toronto, Toronto M5S 3E1, Canada. ; 1] Genomic Medicine Institute, Medical Research Center, Seoul National University, Seoul 110-799, South Korea [2] Life Science Institute, Macrogen Inc., Seoul 153-781, South Korea. ; Department of Systems &Computational Biology, Albert Einstein College of Medicine of Yeshiva University, Bronx, New York 10461, USA. ; Institute of Biomaterials and Biomedical Engineering (IBBME), University of Toronto, Toronto M5S-3G9, Canada. ; 1] Gene and Stem Cell Therapy Program and Bioinformatics Lab, Centenary Institute, Camperdown 2050, NSW, Australia &Sydney Medical School, 31 University of Sydney 2006, New South Wales, Australia [2] Cell and Molecular Therapies, Royal Prince Alfred Hospital, Camperdown 2050, New South Wales, Australia. ; 1] Australian Institute for Bioengineering and Nanotechnology, The University of Queensland, Brisbane, Queensland 4072, Australia [2] College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8TA, UK. ; 1] Genome Biology Department, The John Curtin School of Medical Research, The Australian National University, Acton (Canberra), ACT 2601, Australia [2] Victor Chang Cardiac Research Institute, Darlinghurst (Sydney), New South Wales 2010, Australia. ; 1] Genomic Medicine Institute, Medical Research Center, Seoul National University, Seoul 110-799, South Korea [2] Department of Biomedical Sciences and Biochemistry, Seoul National University College of Medicine, Seoul 110-799, South Korea [3] Life Science Institute, Macrogen Inc., Seoul 153-781, South Korea. ; 1] Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario M5G 1X5, Canada [2] Department of Physiology, University of Toronto, Toronto, Ontario M5S 1A8, Canada [3] Department of Obstetrics and Gynaecology, University of Toronto, Toronto, Ontario M5S 1E2, Canada. ; 1] Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario M5G 1X5, Canada [2] Institute of Medical Science, University of Toronto, Toronto, Ontario M5T 3H7, Canada [3] Department of Obstetrics and Gynaecology, University of Toronto, Toronto, Ontario M5S 1E2, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25503233" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cellular Reprogramming/*genetics ; Chromatin/chemistry/genetics/metabolism ; Chromatin Assembly and Disassembly ; DNA Methylation ; Embryonic Stem Cells/cytology/metabolism ; Epistasis, Genetic/genetics ; Fibroblasts/cytology/metabolism ; Genome/*genetics ; Histones/chemistry/metabolism ; Induced Pluripotent Stem Cells/*cytology/*metabolism ; Internet ; Mice ; Proteome/genetics ; Proteomics ; RNA, Long Noncoding/genetics ; Transcription Factors/genetics/metabolism ; Transcription, Genetic/genetics ; Transcriptome/genetics ; Transgenes/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2012-06-16
    Description: Autism spectrum disorder (ASD) is a group of conditions characterized by impaired social interaction and communication, and restricted and repetitive behaviours. ASD is a highly heritable disorder involving various genetic determinants. Shank2 (also known as ProSAP1) is a multi-domain scaffolding protein and signalling adaptor enriched at excitatory neuronal synapses, and mutations in the human SHANK2 gene have recently been associated with ASD and intellectual disability. Although ASD-associated genes are being increasingly identified and studied using various approaches, including mouse genetics, further efforts are required to delineate important causal mechanisms with the potential for therapeutic application. Here we show that Shank2-mutant (Shank2(-/-)) mice carrying a mutation identical to the ASD-associated microdeletion in the human SHANK2 gene exhibit ASD-like behaviours including reduced social interaction, reduced social communication by ultrasonic vocalizations, and repetitive jumping. These mice show a marked decrease in NMDA (N-methyl-D-aspartate) glutamate receptor (NMDAR) function. Direct stimulation of NMDARs with D-cycloserine, a partial agonist of NMDARs, normalizes NMDAR function and improves social interaction in Shank2(-/-) mice. Furthermore, treatment of Shank2(-/-) mice with a positive allosteric modulator of metabotropic glutamate receptor 5 (mGluR5), which enhances NMDAR function via mGluR5 activation, also normalizes NMDAR function and markedly enhances social interaction. These results suggest that reduced NMDAR function may contribute to the development of ASD-like phenotypes in Shank2(-/-) mice, and mGluR modulation of NMDARs offers a potential strategy to treat ASD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Won, Hyejung -- Lee, Hye-Ryeon -- Gee, Heon Yung -- Mah, Won -- Kim, Jae-Ick -- Lee, Jiseok -- Ha, Seungmin -- Chung, Changuk -- Jung, Eun Suk -- Cho, Yi Sul -- Park, Sae-Geun -- Lee, Jung-Soo -- Lee, Kyungmin -- Kim, Daesoo -- Bae, Yong Chul -- Kaang, Bong-Kiun -- Lee, Min Goo -- Kim, Eunjoon -- England -- Nature. 2012 Jun 13;486(7402):261-5. doi: 10.1038/nature11208.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, KAIST, Daejeon 305-701, Korea.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22699620" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/*genetics ; Animals ; Antimetabolites/pharmacology ; *Autistic Disorder/genetics/metabolism ; Behavior, Animal/*drug effects/physiology ; Benzamides/*pharmacology ; Cycloserine/*pharmacology ; Disease Models, Animal ; Female ; Male ; Mice ; Mice, Inbred C57BL ; Nerve Tissue Proteins/*genetics ; Pyrazoles/*pharmacology ; Receptors, N-Methyl-D-Aspartate/*agonists/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2014-03-29
    Description: Lignin is a phenylpropanoid-derived heteropolymer important for the strength and rigidity of the plant secondary cell wall. Genetic disruption of lignin biosynthesis has been proposed as a means to improve forage and bioenergy crops, but frequently results in stunted growth and developmental abnormalities, the mechanisms of which are poorly understood. Here we show that the phenotype of a lignin-deficient Arabidopsis mutant is dependent on the transcriptional co-regulatory complex, Mediator. Disruption of the Mediator complex subunits MED5a (also known as REF4) and MED5b (also known as RFR1) rescues the stunted growth, lignin deficiency and widespread changes in gene expression seen in the phenylpropanoid pathway mutant ref8, without restoring the synthesis of guaiacyl and syringyl lignin subunits. Cell walls of rescued med5a/5b ref8 plants instead contain a novel lignin consisting almost exclusively of p-hydroxyphenyl lignin subunits, and moreover exhibit substantially facilitated polysaccharide saccharification. These results demonstrate that guaiacyl and syringyl lignin subunits are largely dispensable for normal growth and development, implicate Mediator in an active transcriptional process responsible for dwarfing and inhibition of lignin biosynthesis, and suggest that the transcription machinery and signalling pathways responding to cell wall defects may be important targets to include in efforts to reduce biomass recalcitrance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonawitz, Nicholas D -- Kim, Jeong Im -- Tobimatsu, Yuki -- Ciesielski, Peter N -- Anderson, Nickolas A -- Ximenes, Eduardo -- Maeda, Junko -- Ralph, John -- Donohoe, Bryon S -- Ladisch, Michael -- Chapple, Clint -- England -- Nature. 2014 May 15;509(7500):376-80. doi: 10.1038/nature13084. Epub 2014 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Biochemistry, Purdue University, West Lafayette, Indiana 47907, USA [2] Dow AgroSciences LLC, 9330 Zionsville Road, Indianapolis, Indiana 46268, USA (N.D.B.); Department of Agronomy, University of Wisconsin-Madison, 1575 Linden Drive, Madison, Wisconsin 53706, USA (J.M.). ; Department of Biochemistry, Purdue University, West Lafayette, Indiana 47907, USA. ; Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin 53706, USA. ; Biosciences Center, National Renewable Energy Laboratory, Golden, Colorado 80401, USA. ; Department of Agricultural and Biological Engineering and the Laboratory of Renewable Resources Engineering, Purdue University, West Lafayette, Indiana 47907, USA. ; 1] Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin 53706, USA [2] Department of Biological Systems Engineering, University of Wisconsin-Madison, Madison, Wisconsin 53706, USA [3] DOE Great Lakes Bioenergy Research Center, and Wisconsin Energy Institute, University of Wisconsin-Madison, Madison, Wisconsin 53726, USA. ; 1] Department of Agricultural and Biological Engineering and the Laboratory of Renewable Resources Engineering, Purdue University, West Lafayette, Indiana 47907, USA [2] Weldon School of Biomedical Engineering, Purdue University, West Lafayette, Indiana 47907, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24670657" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/*genetics/*growth & development/metabolism ; Arabidopsis Proteins/*genetics/metabolism ; Biofuels ; Biomass ; Cell Wall/chemistry/metabolism ; Cellulose/metabolism ; Gene Expression Regulation, Plant/genetics ; Lignin/biosynthesis/chemistry/*metabolism ; Mediator Complex/chemistry/deficiency/*genetics/metabolism ; Mutation/*genetics ; Phenotype ; Plants, Genetically Modified ; Protein Subunits/genetics/metabolism ; Transcription, Genetic/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2015-10-03
    Description: Memory stabilization after learning requires translational and transcriptional regulations in the brain, yet the temporal molecular changes that occur after learning have not been explored at the genomic scale. We used ribosome profiling and RNA sequencing to quantify the translational status and transcript levels in the mouse hippocampus after contextual fear conditioning. We revealed three types of repressive regulations: translational suppression of ribosomal protein-coding genes in the hippocampus, learning-induced early translational repression of specific genes, and late persistent suppression of a subset of genes via inhibition of estrogen receptor 1 (ESR1/ERalpha) signaling. In behavioral analyses, overexpressing Nrsn1, one of the newly identified genes undergoing rapid translational repression, or activating ESR1 in the hippocampus impaired memory formation. Collectively, this study unveils the yet-unappreciated importance of gene repression mechanisms for memory formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cho, Jun -- Yu, Nam-Kyung -- Choi, Jun-Hyeok -- Sim, Su-Eon -- Kang, SukJae Joshua -- Kwak, Chuljung -- Lee, Seung-Woo -- Kim, Ji-il -- Choi, Dong Il -- Kim, V Narry -- Kaang, Bong-Kiun -- New York, N.Y. -- Science. 2015 Oct 2;350(6256):82-7. doi: 10.1126/science.aac7368.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for RNA Research, Institute for Basic Science, Seoul 151-742, Korea. Department of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul 151-747, Korea. ; Department of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul 151-747, Korea. ; Center for RNA Research, Institute for Basic Science, Seoul 151-742, Korea. Department of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul 151-747, Korea. narrykim@snu.ac.kr kaang@snu.ac.kr. ; Department of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul 151-747, Korea. narrykim@snu.ac.kr kaang@snu.ac.kr.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26430118" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conditioning, Classical ; Estrogen Receptor alpha/*genetics ; Fear ; *Gene Expression Regulation ; Hippocampus/*metabolism ; Male ; Membrane Proteins/*genetics ; *Memory ; Mice ; Mice, Inbred C57BL ; Protein Biosynthesis/*genetics ; Ribosomal Proteins/genetics ; Transcription, Genetic
    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
    Publication Date: 2015-10-03
    Description: Midbrain dopamine neurons are an essential component of the basal ganglia circuitry, playing key roles in the control of fine movement and reward. Recently, it has been demonstrated that gamma-aminobutyric acid (GABA), the chief inhibitory neurotransmitter, is co-released by dopamine neurons. Here, we show that GABA co-release in dopamine neurons does not use the conventional GABA-synthesizing enzymes, glutamate decarboxylases GAD65 and GAD67. Our experiments reveal an evolutionarily conserved GABA synthesis pathway mediated by aldehyde dehydrogenase 1a1 (ALDH1a1). Moreover, GABA co-release is modulated by ethanol (EtOH) at concentrations seen in blood alcohol after binge drinking, and diminished ALDH1a1 leads to enhanced alcohol consumption and preference. These findings provide insights into the functional role of GABA co-release in midbrain dopamine neurons, which may be essential for reward-based behavior and addiction.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4725325/" 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/PMC4725325/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Jae-Ick -- Ganesan, Subhashree -- Luo, Sarah X -- Wu, Yu-Wei -- Park, Esther -- Huang, Eric J -- Chen, Lu -- Ding, Jun B -- MH086403/MH/NIMH NIH HHS/ -- MH091193/MH/NIMH NIH HHS/ -- NS075136/NS/NINDS NIH HHS/ -- NS091144/NS/NINDS NIH HHS/ -- R00 NS075136/NS/NINDS NIH HHS/ -- R01 NS091144/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2015 Oct 2;350(6256):102-6. doi: 10.1126/science.aac4690.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurosurgery, Stanford University School of Medicine, Palo Alto, CA 94304, USA. ; Department of Pathology, University of California San Francisco, San Francisco, CA 94143, USA. Neuroscience Graduate Program, University of California San Francisco, San Francisco, CA 94143, USA. ; Department of Pathology, University of California San Francisco, San Francisco, CA 94143, USA. Neuroscience Graduate Program, University of California San Francisco, San Francisco, CA 94143, USA. Pathology Service 113B, San Francisco VA Medical Center, San Francisco, CA 94121, USA. ; Department of Neurosurgery, Stanford University School of Medicine, Palo Alto, CA 94304, USA. Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Palo Alto, CA 94304, USA. dingjun@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26430123" target="_blank"〉PubMed〈/a〉
    Keywords: Aldehyde Dehydrogenase/genetics/*metabolism ; Animals ; *Binge Drinking/blood/enzymology/genetics ; Dopaminergic Neurons/enzymology/*metabolism ; Ethanol/blood/pharmacology ; Evolution, Molecular ; Female ; Gene Knockdown Techniques ; Male ; Mesencephalon/cytology/enzymology/*metabolism ; Metabolic Networks and Pathways ; Mice ; *Reward ; Sequence Deletion ; gamma-Aminobutyric Acid/*biosynthesis
    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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  • 8
    ISSN: 1432-1130
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Gel permeation chromatography (GPC) was applied for recognizing the origin of groundwater humic and fulvic acids. GPC was performed with Fraktogel TSK HW-50 in 0.1 M NaCl, pH 8.5 (0.05 M phosphate buffer), 1 mM EDTA, with 10% by volume methanol added. Humic substances from groundwaters and sediments of four different aquifer systems in Germany were isolated, purified and characterized. Both UV/Vis and fluorescence detection were applied. UV/Vis detection was found to be more powerful in identifying differences between the various humic and fulvic acids. The four aquifer systems investigated (“Gorleben”, “Fuhrberg”, “Franconian Albvorland” and “Munich”) differed from one another with respect to hydrological and geochemical conditions. The results showed that the GPC-elution behavior reflects the geochemical environment and origin (source material and generation process) of aquatic humic and fulvic acids.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-2307
    Keywords: Key words SV40T ; Thymoma ; Thymic carcinoma ; Thymus ; Transgenic mouse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  There have been several reports that thymoma in human is a progressive disease, and that thymoma and thymic carcinoma form a continuum. We established a stable line of SV40T transgenic mice, which consistently produced thymic epithelial tumours progressing to thymic carcinoma within a predictable time span. Using this animal model and a morphological approach, thymic epithelial tumour progression was studied with reference to sequential changes at different time points in animals aged from 3 to 32 weeks. At all ages, SV40T was expressed in the nuclei of thymic epithelial cells; in these transgenic mice we observed the entire spectrum from cortical type thymoma to thymic carcinoma. Thymic size tended to increase with ageing in SV40T TG mice. While younger mice had predominantly cortical (organoid) or cortical thymoma, older mice had well-differentiated thymic carcinoma (WDTC) or poorly differentiated thymic carcinoma. When SV40T TG mice (248 line) reached a certain age, carcinoma of the thymus was present in all of them. Cortical-type thymoma became malignant within a predictable time span, suggesting a cortical thymoma–carcinoma sequence. When the mice were 9 weeks of age, the thymuses formed gross masses compatible with cortical thymoma. At 14 weeks of age, WDTC appeared against the background of cortical thymoma. Poorly differentiated thymic carcinoma was found after 15 weeks and affected all animals over 23 weeks of age. Most thymic carcinomas coexisted in varying proportions with cortical-type thymoma. Medullary thymomas did not develop in the mice, and no transition from medullary-type thymomas to thymic carcinomas was observed. In this SV40T transgenic mouse model, thymic carcinoma is clearly preceded by cortical-type thymoma. These transgenic mice may provide an interesting model for the progression from cortical thymoma to WDTC and/or high-grade carcinoma.
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  • 10
    ISSN: 1432-0649
    Keywords: 78.20.Hp ; 33.90.+h
    Source: Springer Online Journal Archives 1860-2000
    Topics: Physics
    Notes: Abstract By means of photoacoustic spectroscopy it has been possible to detect U(IV) and U(VI) in aqueous solution in the 10−6 M/L range. Piezoelectric transducer detection, pulsed laser radiation and a differential method to reduce solvent and window absorption has been used. Photoacoustic spectroscopy seems to be a suitable method for the low level detection of actinide elements.
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