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  • 1
    Publication Date: 2018-07-19
    Description: China’s livestock industry has experienced a vast transition during the last three decades, with profound effects on domestic and global food provision, resource use, nitrogen and phosphorus losses, and greenhouse gas (GHG) emissions. We provide a comprehensive analysis of the driving forces around this transition and its national and global consequences. The number of livestock units (LUs) tripled in China in less than 30 years, mainly through the growth of landless industrial livestock production systems and the increase in monogastric livestock (from 62 to 74% of total LUs). Changes were fueled through increases in demand as well as, supply of new breeds, new technology, and government support. Production of animal source protein increased 4.9 times, nitrogen use efficiency at herd level tripled, and average feed use and GHG emissions per gram protein produced decreased by a factor of 2 between 1980 and 2010. In the same period, animal feed imports have increased 49 times, total ammonia and GHG emissions to the atmosphere doubled, and nitrogen losses to watercourses tripled. As a consequence, China’s livestock transition has significant global impact. Forecasts for 2050, using the Shared Socio-economic Pathways scenarios, indicate major further changes in livestock production and impacts. On the basis of these possible trajectories, we suggest an alternative transition, which should be implemented by government, processing industries, consumers, and retailers. This new transition is targeted to increase production efficiency and environmental performance at system level, with coupling of crop-livestock production, whole chain manure management, and spatial planning as major components.
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
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  • 2
    Publication Date: 2018-07-07
    Description: Ferroelectric materials for photovoltaics have sparked great interest because of their switchable photoelectric responses and above-bandgap photovoltages that violate conventional photovoltaic theory. However, their relatively low photocurrent and power conversion efficiency limit their potential application in solar cells. To improve performance, conventional strategies focus mainly on narrowing the bandgap to better match the solar spectrum, leaving the fundamental connection between polar order and photovoltaic effect largely overlooked. We report large photovoltaic enhancement by A -site substitutions in a model ferroelectric photovoltaic material, BiFeO 3 . As revealed by optical measurements and supported by theoretical calculations, the enhancement is accompanied by the chemically driven rotational instability of the polarization, which, in turn, affects the charge transfer at the band edges and drives a direct-to-indirect bandgap transition, highlighting the strong coupling between polarization, lattice, and orbital order parameters in ferroelectrics. Polar order engineering thus provides an additional degree of freedom to further boost photovoltaic efficiency in ferroelectrics and related materials.
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
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  • 3
    Publication Date: 2018-08-02
    Description: Titanium (Ti) is an ideal bone substitute due to its superior bio-compatibility and remarkable corrosion resistance. However, in order to improve the osteoconduction and osteoinduction capacities in clinical applications, different kinds of surface modifications are typically applied to Ti alloys. In this study, we fabricated a tightly attached polydopamine-assisted Fe 3 O 4 nanoparticle coating on Ti with magnetic properties, aiming to improve the osteogenesis of the Ti substrates. The PDA-assisted Fe 3 O 4 nanoparticle coatings were characterized by scanning electron microscopy, energy dispersive spectroscopy, atomic force microscopy and water contact angle measurements. The cell attachment and proliferation rate of the human bone mesenchymal stem cells (hBMSCs) on the Ti surface significantly improved with the Fe 3 O 4 /PDA coating when compared with the pure Ti without a coating. Furthermore, the results of in vitro alkaline phosphatase (ALP) activity at 7 and 14 days and alizarin red S staining at 14 days showed that the Fe 3 O 4 /PDA coating on Ti promoted the osteogenic differentiation of hBMSCs. Moreover, hBMSCs co-cultured with the Fe 3 O 4 /PDA-coated Ti for approximately 14 days also exhibited a significantly higher mRNA expression level of ALP, osteocalcin and runt-related transcription factor-2 (RUNX2). Our in vitro results revealed that the present PDA-assisted Fe 3 O 4 nanoparticle surface coating is an innovative method for Ti surface modification and shows great potential for clinical applications.
    Keywords: materials science, biomaterials, cellular biology
    Electronic ISSN: 2054-5703
    Topics: Natural Sciences in General
    Published by Royal Society
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  • 4
    Publication Date: 2014-11-21
    Description: The laboratory mouse shares the majority of its protein-coding genes with humans, making it the premier model organism in biomedical research, yet the two mammals differ in significant ways. To gain greater insights into both shared and species-specific transcriptional and cellular regulatory programs in the mouse, the Mouse ENCODE Consortium has mapped transcription, DNase I hypersensitivity, transcription factor binding, chromatin modifications and replication domains throughout the mouse genome in diverse cell and tissue types. By comparing with the human genome, we not only confirm substantial conservation in the newly annotated potential functional sequences, but also find a large degree of divergence of sequences involved in transcriptional regulation, chromatin state and higher order chromatin organization. Our results illuminate the wide range of evolutionary forces acting on genes and their regulatory regions, and provide a general resource for research into mammalian biology and mechanisms of human diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4266106/" 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/PMC4266106/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yue, Feng -- Cheng, Yong -- Breschi, Alessandra -- Vierstra, Jeff -- Wu, Weisheng -- Ryba, Tyrone -- Sandstrom, Richard -- Ma, Zhihai -- Davis, Carrie -- Pope, Benjamin D -- Shen, Yin -- Pervouchine, Dmitri D -- Djebali, Sarah -- Thurman, Robert E -- Kaul, Rajinder -- Rynes, Eric -- Kirilusha, Anthony -- Marinov, Georgi K -- Williams, Brian A -- Trout, Diane -- Amrhein, Henry -- Fisher-Aylor, Katherine -- Antoshechkin, Igor -- DeSalvo, Gilberto -- See, Lei-Hoon -- Fastuca, Meagan -- Drenkow, Jorg -- Zaleski, Chris -- Dobin, Alex -- Prieto, Pablo -- Lagarde, Julien -- Bussotti, Giovanni -- Tanzer, Andrea -- Denas, Olgert -- Li, Kanwei -- Bender, M A -- Zhang, Miaohua -- Byron, Rachel -- Groudine, Mark T -- McCleary, David -- Pham, Long -- Ye, Zhen -- Kuan, Samantha -- Edsall, Lee -- Wu, Yi-Chieh -- Rasmussen, Matthew D -- Bansal, Mukul S -- Kellis, Manolis -- Keller, Cheryl A -- Morrissey, Christapher S -- Mishra, Tejaswini -- Jain, Deepti -- Dogan, Nergiz -- Harris, Robert S -- Cayting, Philip -- Kawli, Trupti -- Boyle, Alan P -- Euskirchen, Ghia -- Kundaje, Anshul -- Lin, Shin -- Lin, Yiing -- Jansen, Camden -- Malladi, Venkat S -- Cline, Melissa S -- Erickson, Drew T -- Kirkup, Vanessa M -- Learned, Katrina -- Sloan, Cricket A -- Rosenbloom, Kate R -- Lacerda de Sousa, Beatriz -- Beal, Kathryn -- Pignatelli, Miguel -- Flicek, Paul -- Lian, Jin -- Kahveci, Tamer -- Lee, Dongwon -- Kent, W James -- Ramalho Santos, Miguel -- Herrero, Javier -- Notredame, Cedric -- Johnson, Audra -- Vong, Shinny -- Lee, Kristen -- Bates, Daniel -- Neri, Fidencio -- Diegel, Morgan -- Canfield, Theresa -- Sabo, Peter J -- Wilken, Matthew S -- Reh, Thomas A -- Giste, Erika -- Shafer, Anthony -- Kutyavin, Tanya -- Haugen, Eric -- Dunn, Douglas -- Reynolds, Alex P -- Neph, Shane -- Humbert, Richard -- Hansen, R Scott -- De Bruijn, Marella -- Selleri, Licia -- Rudensky, Alexander -- Josefowicz, Steven -- Samstein, Robert -- Eichler, Evan E -- Orkin, Stuart H -- Levasseur, Dana -- Papayannopoulou, Thalia -- Chang, Kai-Hsin -- Skoultchi, Arthur -- Gosh, Srikanta -- Disteche, Christine -- Treuting, Piper -- Wang, Yanli -- Weiss, Mitchell J -- Blobel, Gerd A -- Cao, Xiaoyi -- Zhong, Sheng -- Wang, Ting -- Good, Peter J -- Lowdon, Rebecca F -- Adams, Leslie B -- Zhou, Xiao-Qiao -- Pazin, Michael J -- Feingold, Elise A -- Wold, Barbara -- Taylor, James -- Mortazavi, Ali -- Weissman, Sherman M -- Stamatoyannopoulos, John A -- Snyder, Michael P -- Guigo, Roderic -- Gingeras, Thomas R -- Gilbert, David M -- Hardison, Ross C -- Beer, Michael A -- Ren, Bing -- Mouse ENCODE Consortium -- 095908/Wellcome Trust/United Kingdom -- 1U54HG007004/HG/NHGRI NIH HHS/ -- 3RC2HG005602/HG/NHGRI NIH HHS/ -- F31CA165863/CA/NCI NIH HHS/ -- F32HL110473/HL/NHLBI NIH HHS/ -- GM083337/GM/NIGMS NIH HHS/ -- GM085354/GM/NIGMS NIH HHS/ -- K99HL119617/HL/NHLBI NIH HHS/ -- P01 GM085354/GM/NIGMS NIH HHS/ -- P01 HL064190/HL/NHLBI NIH HHS/ -- P01 HL110860/HL/NHLBI NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- P30 CA045508/CA/NCI NIH HHS/ -- R01 DK065806/DK/NIDDK NIH HHS/ -- R01 DK096266/DK/NIDDK NIH HHS/ -- R01 ES024992/ES/NIEHS NIH HHS/ -- R01 EY021482/EY/NEI NIH HHS/ -- R01 GM083337/GM/NIGMS NIH HHS/ -- R01 HG004037/HG/NHGRI NIH HHS/ -- R01 HG007175/HG/NHGRI NIH HHS/ -- R01 HG007348/HG/NHGRI NIH HHS/ -- R01 HG007354/HG/NHGRI NIH HHS/ -- R01DK065806/DK/NIDDK NIH HHS/ -- R01HD043997-09/HD/NICHD NIH HHS/ -- R01HG003991/HG/NHGRI NIH HHS/ -- R37 DK044746/DK/NIDDK NIH HHS/ -- R56 DK065806/DK/NIDDK NIH HHS/ -- RC2 HG005573/HG/NHGRI NIH HHS/ -- RC2HG005573/HG/NHGRI NIH HHS/ -- T32 GM081739/GM/NIGMS NIH HHS/ -- U01 HL099656/HL/NHLBI NIH HHS/ -- U01 HL099993/HL/NHLBI NIH HHS/ -- U54 HG006997/HG/NHGRI NIH HHS/ -- U54 HG006998/HG/NHGRI NIH HHS/ -- U54 HG007004/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Nov 20;515(7527):355-64. doi: 10.1038/nature13992.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Ludwig Institute for Cancer Research and University of California, San Diego School of Medicine, 9500 Gilman Drive, La Jolla, California 92093, USA. [2] Department of Biochemistry and Molecular Biology, College of Medicine, The Pennsylvania State University, Hershey, Pennsylvania 17033, USA. ; Department of Genetics, Stanford University, 300 Pasteur Drive, MC-5477 Stanford, California 94305, USA. ; Bioinformatics and Genomics, Centre for Genomic Regulation (CRG) and UPF, Doctor Aiguader, 88, 08003 Barcelona, Catalonia, Spain. ; Department of Genome Sciences, University of Washington, Seattle, Washington 98195, USA. ; Center for Comparative Genomics and Bioinformatics, Huck Institutes of the Life Sciences, The Pennsylvania State University, University Park, Pennsylvania 16802, USA. ; Department of Biological Science, 319 Stadium Drive, Florida State University, Tallahassee, Florida 32306-4295, USA. ; Functional Genomics, Cold Spring Harbor Laboratory, Bungtown Road, Cold Spring Harbor, New York 11724, USA. ; Ludwig Institute for Cancer Research and University of California, San Diego School of Medicine, 9500 Gilman Drive, La Jolla, California 92093, USA. ; Division of Biology, California Institute of Technology, Pasadena, California 91125, USA. ; 1] Bioinformatics and Genomics, Centre for Genomic Regulation (CRG) and UPF, Doctor Aiguader, 88, 08003 Barcelona, Catalonia, Spain. [2] Department of Theoretical Chemistry, Faculty of Chemistry, University of Vienna, Waehringerstrasse 17/3/303, A-1090 Vienna, Austria. ; Departments of Biology and Mathematics and Computer Science, Emory University, O. Wayne Rollins Research Center, 1510 Clifton Road NE, Atlanta, Georgia 30322, USA. ; 1] Department of Pediatrics, University of Washington, Seattle, Washington 98195, USA. [2] Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. ; Basic Science Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. ; 1] Basic Science Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. [2] Department of Radiation Oncology, University of Washington, Seattle, Washington 98195, USA. ; Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology (MIT), Cambridge, Massachusetts 02139, USA. ; 1] Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology (MIT), Cambridge, Massachusetts 02139, USA. [2] Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA. ; Department of Developmental and Cell Biology, University of California, Irvine, Irvine, California 92697, USA. ; Center for Biomolecular Science and Engineering, School of Engineering, University of California Santa Cruz (UCSC), Santa Cruz, California 95064, USA. ; Departments of Obstetrics/Gynecology and Pathology, and Center for Reproductive Sciences, University of California San Francisco, San Francisco, California 94143, USA. ; European Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SD, UK. ; Yale University, Department of Genetics, PO Box 208005, 333 Cedar Street, New Haven, Connecticut 06520-8005, USA. ; Computer &Information Sciences &Engineering, University of Florida, Gainesville, Florida 32611, USA. ; McKusick-Nathans Institute of Genetic Medicine and Department of Biomedical Engineering, Johns Hopkins University, 733 N. Broadway, BRB 573 Baltimore, Maryland 21205, USA. ; 1] European Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SD, UK. [2] Bill Lyons Informatics Centre, UCL Cancer Institute, University College London, London WC1E 6DD, UK. ; Department of Biological Structure, University of Washington, HSB I-516, 1959 NE Pacific Street, Seattle, Washington 98195, USA. ; MRC Molecular Haemotology Unit, University of Oxford, Oxford OX3 9DS, UK. ; Department of Cell and Developmental Biology, Weill Cornell Medical College, New York, New York 10065, USA. ; HHMI and Ludwig Center at Memorial Sloan Kettering Cancer Center, Immunology Program, Memorial Sloan Kettering Cancer Canter, New York, New York 10065, USA. ; Dana Farber Cancer Institute, Harvard Medical School, Cambridge, Massachusetts 02138, USA. ; University of Iowa Carver College of Medicine, Department of Internal Medicine, Iowa City, Iowa 52242, USA. ; Division of Hematology, Department of Medicine, University of Washington, Seattle, Washington 98195, USA. ; Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA. ; Department of Pathology, University of Washington, Seattle, Washington 98195, USA. ; Department of Comparative Medicine, University of Washington, Seattle, Washington 98195, USA. ; Bioinformatics and Genomics program, The Pennsylvania State University, University Park, Pennsylvania 16802, USA. ; Department of Hematology, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. ; 1] Division of Hematology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA. [2] Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. ; Department of Bioengineering, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093, USA. ; Department of Genetics, Center for Genome Sciences and Systems Biology, Washington University School of Medicine, St. Louis, Missouri 63108, USA. ; NHGRI, National Institutes of Health, 5635 Fishers Lane, Bethesda, Maryland 20892-9307, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25409824" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Lineage/genetics ; Chromatin/genetics/metabolism ; Conserved Sequence/genetics ; DNA Replication/genetics ; Deoxyribonuclease I/metabolism ; Gene Expression Regulation/genetics ; Gene Regulatory Networks/genetics ; Genome/*genetics ; Genome-Wide Association Study ; *Genomics ; Humans ; Mice/*genetics ; *Molecular Sequence Annotation ; RNA/genetics ; Regulatory Sequences, Nucleic Acid/genetics ; Species Specificity ; Transcription Factors/metabolism ; Transcriptome/genetics
    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: 2014-11-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ma, Zhijun -- Melville, David S -- Liu, Jianguo -- Chen, Ying -- Yang, Hongyan -- Ren, Wenwei -- Zhang, Zhengwang -- Piersma, Theunis -- Li, Bo -- New York, N.Y. -- Science. 2014 Nov 21;346(6212):912-4. doi: 10.1126/science.1257258.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ministry of Education Key Laboratory for Biodiversity Science and Ecological Engineering, Institute of Biodiversity Science, Fudan University, Shanghai 200438, China. No. 1261 Dovedale Road, Rural Delivery 2, Wakefield, Nelson, 7096, New Zealand. Center for Systems Integration and Sustainability, Department of Fisheries and Wildlife, Michigan State University, East Lansing, MI 48823, USA. College of Nature Reserve, Beijing Forestry University, Beijing 100083, China. Chair in Global Flyway Ecology, Centre for Ecological and Evolutionary Studies, University of Groningen, Post Office Box 11103, 9700 CC Groningen, Netherlands. Department of Marine Ecology, Royal Netherlands Institute for Sea Research (NIOZ), Post Office Box 59, 1790 AB Den Burg, Texel, Netherlands. World Wildlife Fund China Shanghai Office, No. 121 Zhongshan North Road, Shanghai 200083, China. Ministry of Education Key Laboratory for Biodiversity Science and Ecological Engineering, College of Life Sciences, Beijing Normal University, Beijing 100875, China. zhijunm@fudan.edu.cn. ; No. 1261 Dovedale Road, Rural Delivery 2, Wakefield, Nelson, 7096, New Zealand. ; Center for Systems Integration and Sustainability, Department of Fisheries and Wildlife, Michigan State University, East Lansing, MI 48823, USA. ; Ministry of Education Key Laboratory for Biodiversity Science and Ecological Engineering, Institute of Biodiversity Science, Fudan University, Shanghai 200438, China. ; College of Nature Reserve, Beijing Forestry University, Beijing 100083, China. Chair in Global Flyway Ecology, Centre for Ecological and Evolutionary Studies, University of Groningen, Post Office Box 11103, 9700 CC Groningen, Netherlands. Department of Marine Ecology, Royal Netherlands Institute for Sea Research (NIOZ), Post Office Box 59, 1790 AB Den Burg, Texel, Netherlands. ; World Wildlife Fund China Shanghai Office, No. 121 Zhongshan North Road, Shanghai 200083, China. ; Ministry of Education Key Laboratory for Biodiversity Science and Ecological Engineering, College of Life Sciences, Beijing Normal University, Beijing 100875, China. ; Chair in Global Flyway Ecology, Centre for Ecological and Evolutionary Studies, University of Groningen, Post Office Box 11103, 9700 CC Groningen, Netherlands. Department of Marine Ecology, Royal Netherlands Institute for Sea Research (NIOZ), Post Office Box 59, 1790 AB Den Burg, Texel, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25414287" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Migration ; Animals ; *Biodiversity ; Birds ; China ; *Conservation of Natural Resources ; *Wetlands
    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
    Publication Date: 2014-10-11
    Description: Cycloaddition is an essential tool in chemical synthesis. Instead of using light or heat as a driving force, marine sponges promote cycloaddition with a more versatile but poorly understood mechanism in producing pyrrole-imidazole alkaloids sceptrin, massadine, and ageliferin. Through de novo synthesis of sceptrin and massadine, we show that sponges may use single-electron oxidation as a central mechanism to promote three different types of cycloaddition. Additionally, we provide surprising evidence that, in contrast to previous reports, sceptrin, massadine, and ageliferin have mismatched chirality. Therefore, massadine cannot be an oxidative rearrangement product of sceptrin or ageliferin, as is commonly believed. Taken together, our results demonstrate unconventional chemical approaches to achieving cycloaddition reactions in synthesis and uncover enantiodivergence as a new biosynthetic paradigm for natural products.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4205478/" 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/PMC4205478/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ma, Zhiqiang -- Wang, Xiaolei -- Wang, Xiao -- Rodriguez, Rodrigo A -- Moore, Curtis E -- Gao, Shuanhu -- Tan, Xianghui -- Ma, Yuyong -- Rheingold, Arnold L -- Baran, Phil S -- Chen, Chuo -- R01 GM073949/GM/NIGMS NIH HHS/ -- R01 GM079554/GM/NIGMS NIH HHS/ -- R01-GM073949/GM/NIGMS NIH HHS/ -- R01-GM079554/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Oct 10;346(6206):219-24. doi: 10.1126/science.1255677.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; Department of Chemistry, The Scripps Research Institute, La Jolla, CA 92037, USA. ; Department of Chemistry and Biochemistry, University of California San Diego, La Jolla, CA 92093, USA. ; Department of Biochemistry, The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. chuo.chen@utsouthwestern.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25301624" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biosynthetic Pathways ; *Cycloaddition Reaction ; Molecular Structure ; Porifera/*metabolism ; Pyrroles/*chemical synthesis/chemistry/metabolism ; Stereoisomerism
    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: 2015-02-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Jing -- Sun, Junping -- Aryal, Achyut -- Raubenheimer, David -- Liu, Deguang -- Sheng, Yan -- Chang, Dunhu -- Shi, Lei -- Wu, Jian -- Ma, Zhong -- Wang, Hongchen -- Meng, Xiuxiang -- New York, N.Y. -- Science. 2015 Feb 27;347(6225):957. doi: 10.1126/science.347.6225.957-a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Environment and Natural Resources, Renmin University of China, Beijing 100872, China. ; Institute of Natural and Mathematical Sciences, Massey University, Auckland, New Zealand. ; Charles Perkins Centre and Faculty of Veterinary Science and School of Biological Sciences, the University of Sydney, Sydney, NSW, Australia. ; College of Plant Protection, Northwest A & F University, Yangling, Shaanxi 712100, China. ; School of Environment and Natural Resources, Renmin University of China, Beijing 100872, China. meng2014@ruc.edu.cn.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25722402" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; China/ethnology ; Climate Change ; Conservation of Natural Resources ; Culture ; *Ethnic Groups ; Human Migration ; Humans ; Life Style/ethnology ; Population Density ; *Reindeer
    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
    Publication Date: 2015-07-15
    Description: Sherman et al. commented on the precedence of enantiodivergence, listing a number of congeneric natural products with opposite chirality. However, these "congeners" are not derived from enantiodivergent biosyntheses. Instead, they are antipodes arising from separate enantiomeric biosyntheses. A distinct feature of the biosynthesis of the cyclic pyrrole-imidazole dimers is the production of antipodal congeners without the corresponding enantiomers.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4536548/" 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/PMC4536548/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ma, Zhiqiang -- Wang, Xiaolei -- Wang, Xiao -- Rodriguez, Rodrigo A -- Moore, Curtis E -- Gao, Shuanhu -- Tan, Xianghui -- Ma, Yuyong -- Rheingold, Arnold L -- Baran, Phil S -- Chen, Chuo -- R01 GM073949/GM/NIGMS NIH HHS/ -- R01 GM079554/GM/NIGMS NIH HHS/ -- R01-GM073949/GM/NIGMS NIH HHS/ -- R01-GM079554/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2015 Jul 10;349(6244):149. doi: 10.1126/science.aaa9626. Epub 2015 Jul 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. chuo.chen@utsouthwestern.edu. ; Department of Biochemistry, The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; Department of Chemistry, The Scripps Research Institute, La Jolla, CA 92037, USA. ; Department of Chemistry and Biochemistry, University of California San Diego, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26160939" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cycloaddition Reaction ; Porifera/*metabolism ; Pyrroles/*chemical synthesis
    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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  • 9
    Publication Date: 2018-03-29
    Description: Respiratory syncytial virus (RSV) is the main cause of acute lower respiratory tract infection (ALRI) in children worldwide. Virus-host interactions affect the progression and prognosis of the infection. Autophagy plays important roles in virus-host interactions. Respiratory epithelial cells serve as the front line of host defense during RSV infection, However, it is still unclear how they interact with RSV. In this study, we found that RSV induced autophagy that favored RSV replication and exacerbated lung pathology in vivo . Mechanistically, RSV induced complete autophagy flux through reactive oxygen species (ROS) generation and activation of the AMP-activated protein kinase/mammalian target of rapamycin (AMPK-MTOR) signaling pathway in HEp-2 cells. Furthermore, we evaluated the functions of autophagy in RSV replication and found that RSV replication was increased in HEp-2 cells treated with rapamycin but decreased remarkably in cells treated with 3-methylademine (3-MA) or wortmannin. Knockdown key molecules in the autophagy pathway with short hairpinp RNA (shRNA) against autophagy-related gene 5 ( ATG5 ), autophagy-related gene 7 ( ATG7 ), or BECN1/Beclin 1 or treatment with ROS scavenger N-acetyl- l -cysteine (NAC) and AMPK inhibitor (compound C) suppressed RSV replication. 3-MA or sh ATG5/BECN1 significantly decreased cell viability and increased cell apoptosis at 48 hours postinfection (hpi). Blocking apoptosis with Z-VAD-FMK partially restored virus replication at 48 hpi. Those results provide strong evidence that autophagy may function as a proviral mechanism in a cell-intrinsic manner during RSV infection. IMPORTANCE An understanding of the mechanisms that respiratory syncytial virus utilizes to interact with respiratory epithelial cells is critical to the development of novel antiviral strategies. In this study, we found that RSV induces autophagy through a ROS-AMPK signaling axis, which in turn promotes viral infection. Autophagy favors RSV replication through blocking cell apoptosis at 48 hpi. Mechanistically, RSV induces mitophagy, which maintains mitochondrial homeostasis and therefore decreases cytochrome c release and apoptosis induction. This study provides a novel insight into this virus-host interaction, which may help to exploit new antiviral treatments targeting autophagy processes.
    Print ISSN: 0022-538X
    Electronic ISSN: 1098-5514
    Topics: Medicine
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  • 10
    Publication Date: 2018-03-29
    Description: The equine infectious anemia virus (EIAV) attenuated vaccine was developed by long-term passaging of a field-isolated virulent strain in cross-species hosts, followed by successive cultivation in cells in vitro . To explore the molecular mechanism underlying the evolution of the EIAV attenuated vaccine, a systematic study focusing on long-terminal-repeat (LTR) variation in numerous virus strains ranging from virulent EIAV to attenuated EIAV was performed over time both in vitro and in vivo . Two hypervariable regions were identified within the U3 region in the enhancer region (EHR) and the negative regulatory element (NRE) and within the R region in the transcription start site (TSS) and the Tat-activating region (TAR). Among these sites, variation in the U3 region resulted in the formation of additional transcription factor binding sites; this variation of the in vitro -adapted strains was consistent with the loss of pathogenicity. Notably, the same LTR variation pattern was observed both in vitro and in vivo . Generally, the LTR variation in both the attenuated virus and the virulent strain fluctuated over time in vivo . Interestingly, the attenuated-virus-specific LTR variation was also detected in horses infected with the virulent strain, supporting the hypothesis that the evolution of an attenuated virus might have involved branching from EIAV quasispecies. This hypothesis was verified by phylogenetic analysis. The present systematic study examining the molecular evolution of attenuated EIAV from EIAV quasispecies may provide an informative model reflecting the evolution of similar lentiviruses. IMPORTANCE The attenuated EIAV vaccine was the first lentiviral vaccine used to successfully control for equine infectious anemia in China. This vaccine provides an important reference for studying the relationship between EIAV gene variation and changes in biological characteristics. Importantly, the vaccine provides a model for the investigation of lentiviral quasispecies evolution. This study followed the "natural" development of the attenuated EIAV vaccine by use of a systematic analysis of LTR evolution in vitro and in vivo . The results revealed that the increase in LTR variation with passaging was accompanied by a decrease in virulence, which indicated that LTR variability might parallel the attenuation of virulence. Interestingly, the attenuated-virus-specific LTR variation was also detected in virulent-strain-infected horses, a finding consistent with those of previous investigations of gp90 and S2 evolution. Therefore, we present a hypothesis that the evolution of the attenuated virus may involve branching from EIAV quasispecies present in vivo .
    Print ISSN: 0022-538X
    Electronic ISSN: 1098-5514
    Topics: Medicine
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