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  • Springer  (117)
  • American Physical Society (APS)  (29)
  • Nature Publishing Group (NPG)  (20)
  • 1
    Publication Date: 2015-06-25
    Description: Author(s): B. Tu, J. Xiao, K. Yao, Y. Shen, Y. Yang, D. Lu, W. X. Li, M. L. Qiu, X. Wang, C. Y. Chen, Y. Fu, B. Wei, C. Zheng, L. Y. Huang, B. H. Zhang, Y. J. Tang, R. Hutton, and Y. Zou Photon absorption spectroscopy is a powerful tool for uncovering the structure of atoms, molecules, and solids. Symmetric Lorentzian and asymmetric Fano line shapes are fundamental spectroscopic signatures related to the structural and dynamical properties. Recently, Ott et al. [ Science 340 , 716 (20... [Phys. Rev. A 91, 060502(R)] Published Mon Jun 22, 2015
    Keywords: Atomic and molecular structure and dynamics
    Print ISSN: 1050-2947
    Electronic ISSN: 1094-1622
    Topics: Physics
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  • 2
    Publication Date: 2016-03-15
    Description: Author(s): B. Tu, J. Xiao, K. Yao, Y. Shen, Y. Yang, D. Lu, W. X. Li, M. L. Qiu, X. Wang, C. Y. Chen, Y. Fu, B. Wei, C. Zheng, L. Y. Huang, B. H. Zhang, Y. J. Tang, R. Hutton, and Y. Zou In this paper, we present experimental and theoretical studies on the interference between resonant and nonresonant photorecombinations for the main resonances of ground-state He-, Be-, B-, C-, N-, and O-like W ions. Experiments were done using a fast electron energy scanning technique at the upgrad… [Phys. Rev. A 93, 032707] Published Mon Mar 14, 2016
    Keywords: Atomic and molecular collisions and interactions
    Print ISSN: 1050-2947
    Electronic ISSN: 1094-1622
    Topics: Physics
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  • 3
    Publication Date: 2017-09-08
    Description: Author(s): B. Tu, K. Yao, Y. Shen, Y. Yang, M. C. Li, T. H. Xu, Q. F. Lu, D. Lu, X. Wang, C. Y. Chen, Y. Fu, B. Wei, C. Zheng, L. Y. Huang, G. Xiong, J. M. Yang, B. H. Zhang, Y. J. Tang, R. Hutton, Y. Zou, and J. Xiao In this paper we report the L -shell dielectronic recombination measurement in highly charged 3 d n ions of tungsten by employing a fast electron beam-energy scanning technique at Shanghai EBIT. The studies of the LMM DR resonance strengths of Ar-like up to Mn-like tungsten were implemented through the... [Phys. Rev. A 96, 032705] Published Thu Sep 07, 2017
    Keywords: Atomic and molecular collisions and interactions
    Print ISSN: 1050-2947
    Electronic ISSN: 1094-1622
    Topics: Physics
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  • 4
    Publication Date: 2012-09-06
    Description: Author(s): Y. K. Li, X. F. Xu, C. Cao, C. Y. Shen, Y. K. Luo, Q. Tao, X. Lin, L. Zhang, G. H. Cao, and Z. A. Xu The magnetic phase diagram has been mapped out via the measurements of electronic resistivity, magnetization, and specific heat in the cobalt-based layered L Co 1− x Fe x AsO ( L =La, Sm) compounds. The ferromagnetic (FM) transition at ∼63 K for LaCoAsO is rapidly suppressed upon Fe doping, and ultimately d... [Phys. Rev. B 86, 104408] Published Wed Sep 05, 2012
    Keywords: Magnetism
    Print ISSN: 1098-0121
    Electronic ISSN: 1095-3795
    Topics: Physics
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  • 5
    Publication Date: 2011-01-13
    Description: Author(s): X. Lin, H. J. Guo, C. Y. Shen, Y. K. Luo, Q. Tao, G. H. Cao, and Z. A. Xu Superconductivity of polycrystalline Sr and Co codoped Pr_{1-y} Sr_{y} Fe_{1-x} Co_{x} AsO samples was investigated by measuring resistivity, dc magnetic susceptibility, thermopower, and Hall effect. In the PrFe_{1-x} Co_{x} AsO samples with only Co doping, T_{c} reaches a maximum of 16 K at x=0.075... [Phys. Rev. B 83, 014503] Published Wed Jan 12, 2011
    Keywords: Superfluidity and superconductivity
    Print ISSN: 1098-0121
    Electronic ISSN: 1095-3795
    Topics: Physics
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  • 6
    Publication Date: 2012-06-23
    Description: All cancers carry somatic mutations in their genomes. A subset, known as driver mutations, confer clonal selective advantage on cancer cells and are causally implicated in oncogenesis, and the remainder are passenger mutations. The driver mutations and mutational processes operative in breast cancer have not yet been comprehensively explored. Here we examine the genomes of 100 tumours for somatic copy number changes and mutations in the coding exons of protein-coding genes. The number of somatic mutations varied markedly between individual tumours. We found strong correlations between mutation number, age at which cancer was diagnosed and cancer histological grade, and observed multiple mutational signatures, including one present in about ten per cent of tumours characterized by numerous mutations of cytosine at TpC dinucleotides. Driver mutations were identified in several new cancer genes including AKT2, ARID1B, CASP8, CDKN1B, MAP3K1, MAP3K13, NCOR1, SMARCD1 and TBX3. Among the 100 tumours, we found driver mutations in at least 40 cancer genes and 73 different combinations of mutated cancer genes. The results highlight the substantial genetic diversity underlying this common disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3428862/" 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/PMC3428862/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stephens, Philip J -- Tarpey, Patrick S -- Davies, Helen -- Van Loo, Peter -- Greenman, Chris -- Wedge, David C -- Nik-Zainal, Serena -- Martin, Sancha -- Varela, Ignacio -- Bignell, Graham R -- Yates, Lucy R -- Papaemmanuil, Elli -- Beare, David -- Butler, Adam -- Cheverton, Angela -- Gamble, John -- Hinton, Jonathan -- Jia, Mingming -- Jayakumar, Alagu -- Jones, David -- Latimer, Calli -- Lau, King Wai -- McLaren, Stuart -- McBride, David J -- Menzies, Andrew -- Mudie, Laura -- Raine, Keiran -- Rad, Roland -- Chapman, Michael Spencer -- Teague, Jon -- Easton, Douglas -- Langerod, Anita -- Oslo Breast Cancer Consortium (OSBREAC) -- Lee, Ming Ta Michael -- Shen, Chen-Yang -- Tee, Benita Tan Kiat -- Huimin, Bernice Wong -- Broeks, Annegien -- Vargas, Ana Cristina -- Turashvili, Gulisa -- Martens, John -- Fatima, Aquila -- Miron, Penelope -- Chin, Suet-Feung -- Thomas, Gilles -- Boyault, Sandrine -- Mariani, Odette -- Lakhani, Sunil R -- van de Vijver, Marc -- van 't Veer, Laura -- Foekens, John -- Desmedt, Christine -- Sotiriou, Christos -- Tutt, Andrew -- Caldas, Carlos -- Reis-Filho, Jorge S -- Aparicio, Samuel A J R -- Salomon, Anne Vincent -- Borresen-Dale, Anne-Lise -- Richardson, Andrea L -- Campbell, Peter J -- Futreal, P Andrew -- Stratton, Michael R -- 077012/Z/05/Z/Wellcome Trust/United Kingdom -- 088340/Wellcome Trust/United Kingdom -- 093867/Wellcome Trust/United Kingdom -- 10118/Cancer Research UK/United Kingdom -- CA089393/CA/NCI NIH HHS/ -- P30 CA016672/CA/NCI NIH HHS/ -- WT088340MA/Wellcome Trust/United Kingdom -- Cancer Research UK/United Kingdom -- Chief Scientist Office/United Kingdom -- Department of Health/United Kingdom -- England -- Nature. 2012 May 16;486(7403):400-4. doi: 10.1038/nature11017.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Genome Project, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22722201" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Breast Neoplasms/classification/*genetics/pathology ; Cell Transformation, Neoplastic/*genetics ; Cytosine/metabolism ; DNA Mutational Analysis ; Female ; Humans ; JNK Mitogen-Activated Protein Kinases/metabolism ; Mutagenesis/*genetics ; Mutation/*genetics ; Neoplasm Grading ; Oncogenes/*genetics ; Reproducibility of Results ; Signal Transduction/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2012-07-20
    Description: Genotypic differences greatly influence susceptibility and resistance to disease. Understanding genotype-phenotype relationships requires that phenotypes be viewed as manifestations of network properties, rather than simply as the result of individual genomic variations. Genome sequencing efforts have identified numerous germline mutations, and large numbers of somatic genomic alterations, associated with a predisposition to cancer. However, it remains difficult to distinguish background, or 'passenger', cancer mutations from causal, or 'driver', mutations in these data sets. Human viruses intrinsically depend on their host cell during the course of infection and can elicit pathological phenotypes similar to those arising from mutations. Here we test the hypothesis that genomic variations and tumour viruses may cause cancer through related mechanisms, by systematically examining host interactome and transcriptome network perturbations caused by DNA tumour virus proteins. The resulting integrated viral perturbation data reflects rewiring of the host cell networks, and highlights pathways, such as Notch signalling and apoptosis, that go awry in cancer. We show that systematic analyses of host targets of viral proteins can identify cancer genes with a success rate on a par with their identification through functional genomics and large-scale cataloguing of tumour mutations. Together, these complementary approaches increase the specificity of cancer gene identification. Combining systems-level studies of pathogen-encoded gene products with genomic approaches will facilitate the prioritization of cancer-causing driver genes to advance the understanding of the genetic basis of human cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3408847/" 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/PMC3408847/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rozenblatt-Rosen, Orit -- Deo, Rahul C -- Padi, Megha -- Adelmant, Guillaume -- Calderwood, Michael A -- Rolland, Thomas -- Grace, Miranda -- Dricot, Amelie -- Askenazi, Manor -- Tavares, Maria -- Pevzner, Samuel J -- Abderazzaq, Fieda -- Byrdsong, Danielle -- Carvunis, Anne-Ruxandra -- Chen, Alyce A -- Cheng, Jingwei -- Correll, Mick -- Duarte, Melissa -- Fan, Changyu -- Feltkamp, Mariet C -- Ficarro, Scott B -- Franchi, Rachel -- Garg, Brijesh K -- Gulbahce, Natali -- Hao, Tong -- Holthaus, Amy M -- James, Robert -- Korkhin, Anna -- Litovchick, Larisa -- Mar, Jessica C -- Pak, Theodore R -- Rabello, Sabrina -- Rubio, Renee -- Shen, Yun -- Singh, Saurav -- Spangle, Jennifer M -- Tasan, Murat -- Wanamaker, Shelly -- Webber, James T -- Roecklein-Canfield, Jennifer -- Johannsen, Eric -- Barabasi, Albert-Laszlo -- Beroukhim, Rameen -- Kieff, Elliott -- Cusick, Michael E -- Hill, David E -- Munger, Karl -- Marto, Jarrod A -- Quackenbush, John -- Roth, Frederick P -- DeCaprio, James A -- Vidal, Marc -- F32 GM095284/GM/NIGMS NIH HHS/ -- F32GM095284/GM/NIGMS NIH HHS/ -- K08 CA122833/CA/NCI NIH HHS/ -- K08 HL098361/HL/NHLBI NIH HHS/ -- K08HL098361/HL/NHLBI NIH HHS/ -- K25 HG006031/HG/NHGRI NIH HHS/ -- K25HG006031/HG/NHGRI NIH HHS/ -- P01 CA050661/CA/NCI NIH HHS/ -- P01CA050661/CA/NCI NIH HHS/ -- P50 HG004233/HG/NHGRI NIH HHS/ -- P50HG004233/HG/NHGRI NIH HHS/ -- R01 CA047006/CA/NCI NIH HHS/ -- R01 CA063113/CA/NCI NIH HHS/ -- R01 CA066980/CA/NCI NIH HHS/ -- R01 CA081135/CA/NCI NIH HHS/ -- R01 CA085180/CA/NCI NIH HHS/ -- R01 CA093804/CA/NCI NIH HHS/ -- R01 CA131354/CA/NCI NIH HHS/ -- R01 HG001715/HG/NHGRI NIH HHS/ -- R01CA047006/CA/NCI NIH HHS/ -- R01CA063113/CA/NCI NIH HHS/ -- R01CA066980/CA/NCI NIH HHS/ -- R01CA081135/CA/NCI NIH HHS/ -- R01CA085180/CA/NCI NIH HHS/ -- R01CA093804/CA/NCI NIH HHS/ -- R01CA131354/CA/NCI NIH HHS/ -- R01HG001715/HG/NHGRI NIH HHS/ -- T32 HL007208/HL/NHLBI NIH HHS/ -- T32HL007208/HL/NHLBI NIH HHS/ -- U01 CA141583/CA/NCI NIH HHS/ -- U01CA141583/CA/NCI NIH HHS/ -- England -- Nature. 2012 Jul 26;487(7408):491-5. doi: 10.1038/nature11288.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genomic Analysis of Network Perturbations Center of Excellence in Genomic Science, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22810586" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics/metabolism/pathogenicity ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genes, Neoplasm/*genetics ; Genome, Human/*genetics ; Herpesvirus 4, Human/genetics/metabolism/pathogenicity ; *Host-Pathogen Interactions/genetics ; Humans ; Neoplasms/*genetics/*metabolism/pathology ; Oncogenic Viruses/genetics/metabolism/*pathogenicity ; Open Reading Frames/genetics ; Papillomaviridae/genetics/metabolism/pathogenicity ; Polyomavirus/genetics/metabolism/pathogenicity ; Receptors, Notch/metabolism ; Signal Transduction ; Two-Hybrid System Techniques ; Viral Proteins/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
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  • 8
    Publication Date: 2014-09-05
    Description: Homologous recombination is a molecular process that has multiple important roles in DNA metabolism, both for DNA repair and genetic variation in all forms of life. Generally, homologous recombination involves the exchange of genetic information between two identical or nearly identical DNA molecules; however, homologous recombination can also occur between RNA molecules, as shown for RNA viruses. Previous research showed that synthetic RNA oligonucleotides can act as templates for DNA double-strand break (DSB) repair in yeast and human cells, and artificial long RNA templates injected in ciliate cells can guide genomic rearrangements. Here we report that endogenous transcript RNA mediates homologous recombination with chromosomal DNA in yeast Saccharomyces cerevisiae. We developed a system to detect the events of homologous recombination initiated by transcript RNA following the repair of a chromosomal DSB occurring either in a homologous but remote locus, or in the same transcript-generating locus in reverse-transcription-defective yeast strains. We found that RNA-DNA recombination is blocked by ribonucleases H1 and H2. In the presence of H-type ribonucleases, DSB repair proceeds through a complementary DNA intermediate, whereas in their absence, it proceeds directly through RNA. The proximity of the transcript to its chromosomal DNA partner in the same locus facilitates Rad52-driven homologous recombination during DSB repair. We demonstrate that yeast and human Rad52 proteins efficiently catalyse annealing of RNA to a DSB-like DNA end in vitro. Our results reveal a novel mechanism of homologous recombination and DNA repair in which transcript RNA is used as a template for DSB repair. Thus, considering the abundance of RNA transcripts in cells, RNA may have a marked impact on genomic stability and plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keskin, Havva -- Shen, Ying -- Huang, Fei -- Patel, Mikir -- Yang, Taehwan -- Ashley, Katie -- Mazin, Alexander V -- Storici, Francesca -- CA100839/CA/NCI NIH HHS/ -- P30 CA056036/CA/NCI NIH HHS/ -- P30CA056036/CA/NCI NIH HHS/ -- R56 CA100839/CA/NCI NIH HHS/ -- England -- Nature. 2014 Nov 20;515(7527):436-9. doi: 10.1038/nature13682. Epub 2014 Sep 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biology, Georgia Institute of Technology, Atlanta, Georgia 30332, USA. ; 1] School of Biology, Georgia Institute of Technology, Atlanta, Georgia 30332, USA [2] Division of Computational Biomedicine, Boston University School of Medicine, Boston, Massachusetts 02118, USA. ; Department of Biochemistry and Molecular Biology, Drexel University College of Medicine, Philadelphia, Pennsylvania 19102, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25186730" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosomes, Fungal/genetics ; DNA Breaks, Double-Stranded ; DNA Repair/*genetics ; Genomic Instability/genetics ; Homologous Recombination/*genetics ; Humans ; Models, Genetic ; RNA/*genetics ; Rad52 DNA Repair and Recombination Protein/metabolism ; Ribonuclease H/metabolism ; Saccharomyces cerevisiae/*genetics ; Saccharomyces cerevisiae Proteins/metabolism ; Templates, Genetic ; 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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  • 9
    Publication Date: 2014-09-12
    Description: Quasars are rapidly accreting supermassive black holes at the centres of massive galaxies. They display a broad range of properties across all wavelengths, reflecting the diversity in the physical conditions of the regions close to the central engine. These properties, however, are not random, but form well-defined trends. The dominant trend is known as 'Eigenvector 1', in which many properties correlate with the strength of optical iron and [O III] emission. The main physical driver of Eigenvector 1 has long been suspected to be the quasar luminosity normalized by the mass of the hole (the 'Eddington ratio'), which is an important parameter of the black hole accretion process. But a definitive proof has been missing. Here we report an analysis of archival data that reveals that the Eddington ratio indeed drives Eigenvector 1. We also find that orientation plays a significant role in determining the observed kinematics of the gas in the broad-line region, implying a flattened, disk-like geometry for the fast-moving clouds close to the black hole. Our results show that most of the diversity of quasar phenomenology can be unified using two simple quantities: Eddington ratio and orientation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, Yue -- Ho, Luis C -- England -- Nature. 2014 Sep 11;513(7517):210-3. doi: 10.1038/nature13712.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Carnegie Observatories, 813 Santa Barbara Street, Pasadena, California 91101, USA [2] Kavli Institute for Astronomy and Astrophysics, Peking University, Beijing 100871, China. ; 1] Kavli Institute for Astronomy and Astrophysics, Peking University, Beijing 100871, China [2] Department of Astronomy, School of Physics, Peking University, Beijing 100871, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25209799" target="_blank"〉PubMed〈/a〉
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  • 10
    Publication Date: 2015-03-13
    Description: Since 2013 the occurrence of human infections by a novel avian H7N9 influenza virus in China has demonstrated the continuing threat posed by zoonotic pathogens. Although the first outbreak wave that was centred on eastern China was seemingly averted, human infections recurred in October 2013 (refs 3-7). It is unclear how the H7N9 virus re-emerged and how it will develop further; potentially it may become a long-term threat to public health. Here we show that H7N9 viruses have spread from eastern to southern China and become persistent in chickens, which has led to the establishment of multiple regionally distinct lineages with different reassortant genotypes. Repeated introductions of viruses from Zhejiang to other provinces and the presence of H7N9 viruses at live poultry markets have fuelled the recurrence of human infections. This rapid expansion of the geographical distribution and genetic diversity of the H7N9 viruses poses a direct challenge to current disease control systems. Our results also suggest that H7N9 viruses have become enzootic in China and may spread beyond the region, following the pattern previously observed with H5N1 and H9N2 influenza viruses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lam, Tommy Tsan-Yuk -- Zhou, Boping -- Wang, Jia -- Chai, Yujuan -- Shen, Yongyi -- Chen, Xinchun -- Ma, Chi -- Hong, Wenshan -- Chen, Yin -- Zhang, Yanjun -- Duan, Lian -- Chen, Peiwen -- Jiang, Junfei -- Zhang, Yu -- Li, Lifeng -- Poon, Leo Lit Man -- Webby, Richard J -- Smith, David K -- Leung, Gabriel M -- Peiris, Joseph S M -- Holmes, Edward C -- Guan, Yi -- Zhu, Huachen -- HHSN272201400006C/PHS HHS/ -- England -- Nature. 2015 Jun 4;522(7554):102-5. doi: 10.1038/nature14348. Epub 2015 Mar 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] State Key Laboratory of Emerging Infectious Diseases (HKU-Shenzhen Branch), Shenzhen Third People's Hospital, Shenzhen 518112, China [2] Joint Influenza Research Centre (SUMC/HKU), Shantou University Medical College (SUMC), Shantou 515041, China [3] Centre of Influenza Research, School of Public Health, The University of Hong Kong (HKU), Hong Kong, China. ; State Key Laboratory of Emerging Infectious Diseases (HKU-Shenzhen Branch), Shenzhen Third People's Hospital, Shenzhen 518112, China. ; 1] Joint Influenza Research Centre (SUMC/HKU), Shantou University Medical College (SUMC), Shantou 515041, China [2] Centre of Influenza Research, School of Public Health, The University of Hong Kong (HKU), Hong Kong, China. ; Joint Influenza Research Centre (SUMC/HKU), Shantou University Medical College (SUMC), Shantou 515041, China. ; Key Laboratory of Emergency Detection for Public Health of Zhejiang Province, Zhejiang Provincial Center for Disease Control and Prevention, Hangzhou, Zhejiang 310051, China. ; 1] State Key Laboratory of Emerging Infectious Diseases (HKU-Shenzhen Branch), Shenzhen Third People's Hospital, Shenzhen 518112, China [2] Joint Influenza Research Centre (SUMC/HKU), Shantou University Medical College (SUMC), Shantou 515041, China. ; 1] State Key Laboratory of Emerging Infectious Diseases (HKU-Shenzhen Branch), Shenzhen Third People's Hospital, Shenzhen 518112, China [2] Centre of Influenza Research, School of Public Health, The University of Hong Kong (HKU), Hong Kong, China. ; Division of Virology, Department of Infectious Diseases, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. ; Centre of Influenza Research, School of Public Health, The University of Hong Kong (HKU), Hong Kong, China. ; Marie Bashir Institute for Infectious Diseases and Biosecurity, Charles Perkins Centre, School of Biological Sciences and Sydney Medical School, University of Sydney, Sydney, New South Wales 2006, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25762140" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chickens/*virology ; China/epidemiology ; Ecosystem ; *Evolution, Molecular ; Genotype ; Humans ; Influenza A Virus, H7N9 Subtype/classification/*genetics/*isolation & ; purification ; Influenza in Birds/*epidemiology/transmission/*virology ; Influenza, Human/epidemiology/transmission/virology ; Molecular Sequence Data ; Reassortant Viruses/genetics/isolation & purification ; Zoonoses/transmission/virology
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