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      Geospatial Resolution of Human and Bacterial Diversity with City-Scale Metagenomics

      research-article
      1 , 2 , 3 , 1 , 2 , 1 , 2 , 4 , 1 , 2 , 1 , 2 , 1 , 2 , 5 , 1 , 2 , 6 , 1 , 2 , 1 , 2 , 1 , 2 , 7 , 1 , 2 , 8 , 8 , 8 , 9 , 10 , 1 , 2 , 1 , 2 , 1 , 2 , 7 , 7 , 1 , 2 , 6 , 1 , 2 , 1 , 2 , 6 , 1 , 2 , 1 , 2 , 11 , 3 , 12 , 13 , 14 , 15 , 16 , 15 , 15 , 16 , 17 , 17 , 7 , 5 , 18 , 13 , 14 , 19 , 5 , 17 , 1 , 2 , 20 , *
      Cell systems

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          SUMMARY

          The panoply of microorganisms and other species present in our environment influence human health and disease, especially in cities, but have not been profiled with metagenomics at a city-wide scale. We sequenced DNA from surfaces across the entire New York City (NYC) subway system, the Gowanus Canal, and public parks. Nearly half of the DNA (48%) does not match any known organism; identified organisms spanned 1,688 bacterial, viral, archaeal, and eukaryotic taxa, which were enriched for harmless genera associated with skin (e.g., Acinetobacter). Predicted ancestry of human DNA left on subway surfaces can recapitulate U.S. Census demographic data, and bacterial signatures can reveal a station’s history, such as marine-associated bacteria in a hurricane-flooded station. Some evidence of pathogens was found ( Bacillus anthracis), but a lack of reported cases in NYC suggests that the pathogens represent a normal, urban microbiome. This baseline metagenomic map of NYC could help long-term disease surveillance, bioterrorism threat mitigation, and health management in the built environment of cities.

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          Greengenes, a Chimera-Checked 16S rRNA Gene Database and Workbench Compatible with ARB

          A 16S rRNA gene database ( http://greengenes.lbl.gov ) addresses limitations of public repositories by providing chimera screening, standard alignment, and taxonomic classification using multiple published taxonomies. It was found that there is incongruent taxonomic nomenclature among curators even at the phylum level. Putative chimeras were identified in 3% of environmental sequences and in 0.2% of records derived from isolates. Environmental sequences were classified into 100 phylum-level lineages in the Archaea and Bacteria .
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            Waves of resistance: Staphylococcus aureus in the antibiotic era.

            Staphylococcus aureus is notorious for its ability to become resistant to antibiotics. Infections that are caused by antibiotic-resistant strains often occur in epidemic waves that are initiated by one or a few successful clones. Methicillin-resistant S. aureus (MRSA) features prominently in these epidemics. Historically associated with hospitals and other health care settings, MRSA has now emerged as a widespread cause of community infections. Community or community-associated MRSA (CA-MRSA) can spread rapidly among healthy individuals. Outbreaks of CA-MRSA infections have been reported worldwide, and CA-MRSA strains are now epidemic in the United States. Here, we review the molecular epidemiology of the epidemic waves of penicillin- and methicillin-resistant strains of S. aureus that have occurred since 1940, with a focus on the clinical and molecular epidemiology of CA-MRSA.
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              Genome sequence of Yersinia pestis, the causative agent of plague.

              The Gram-negative bacterium Yersinia pestis is the causative agent of the systemic invasive infectious disease classically referred to as plague, and has been responsible for three human pandemics: the Justinian plague (sixth to eighth centuries), the Black Death (fourteenth to nineteenth centuries) and modern plague (nineteenth century to the present day). The recent identification of strains resistant to multiple drugs and the potential use of Y. pestis as an agent of biological warfare mean that plague still poses a threat to human health. Here we report the complete genome sequence of Y. pestis strain CO92, consisting of a 4.65-megabase (Mb) chromosome and three plasmids of 96.2 kilobases (kb), 70.3 kb and 9.6 kb. The genome is unusually rich in insertion sequences and displays anomalies in GC base-composition bias, indicating frequent intragenomic recombination. Many genes seem to have been acquired from other bacteria and viruses (including adhesins, secretion systems and insecticidal toxins). The genome contains around 150 pseudogenes, many of which are remnants of a redundant enteropathogenic lifestyle. The evidence of ongoing genome fluidity, expansion and decay suggests Y. pestis is a pathogen that has undergone large-scale genetic flux and provides a unique insight into the ways in which new and highly virulent pathogens evolve.
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                Author and article information

                Journal
                101656080
                43733
                Cell Syst
                Cell Syst
                Cell systems
                2405-4712
                18 April 2015
                3 March 2015
                29 July 2015
                29 July 2016
                : 1
                : 1
                : 72-87
                Affiliations
                [1 ]Department of Physiology and Biophysics, Weill Cornell Medical College, New York, NY 10065, USA
                [2 ]The HRH Prince Alwaleed Bin Talal Bin Abdulaziz Alsaud Institute for Computational Biomedicine, Weill Cornell Medical College, New York, NY 10065, USA
                [3 ]School of Earth and Environmental Sciences, City University of New York (CUNY) Queens College, Flushing, NY 11367, USA
                [4 ]CUNY Hunter College, New York, NY 10065, USA
                [5 ]Center for Genomics, New York University, New York, NY 10003, USA
                [6 ]Tri-Institutional Program on Computational Biology and Medicine (CBM), New York, NY 10065, USA
                [7 ]CUNY Brooklyn College, Department of Biology, Brooklyn, NY 11210, USA
                [8 ]Cornell University, Ithaca, NY 14850, USA
                [9 ]Genspace Community Laboratory, Brooklyn, NY 11238, USA
                [10 ]Department of Biological Sciences, Fordham University, Bronx, NY 10458, USA
                [11 ]State University of New York, Downstate, Brooklyn, NY 11203, USA
                [12 ]University of Vermont, Burlington, VT 05405, USA
                [13 ]Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA
                [14 ]Rockefeller University, New York, NY 10065, USA
                [15 ]Academic Centre on Rare Diseases, School of Medicine and Medical Science, University College Dublin 4, Ireland
                [16 ]National Centre for Medical Genetics, Our Lady’s Children’s Hospital, Dublin 12, Ireland
                [17 ]HudsonAlpha Institute for Biotechnology, Huntsville, AL 35806, USA
                [18 ]CUNY York College, Jamaica, NY 11451, USA
                [19 ]Accelerated Discovery Lab, IBM Almaden Research Center, San Jose, CA 95120, USA
                [20 ]The Feil Family Brain and Mind Research Institute, New York, NY 10065, USA
                Author notes
                [* ]Correspondence: chm2042@ 123456med.cornell.edu
                [21]

                Co-first author

                Article
                NIHMS662921
                10.1016/j.cels.2015.01.001
                4651444
                26594662
                844435d0-38fe-41f7-abc5-c1cc9d543dc8

                This is an open access article under the CC BY license ( http://creativecommons.org/licenses/by/4.0/).

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