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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2002-03-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanchez, Pedro A -- New York, N.Y. -- Science. 2002 Mar 15;295(5562):2019-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉International Center for Research in Agroforestry, Post Office Box 30677, Nairobi, Kenya. P.sanchez@cgiar.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11896257" target="_blank"〉PubMed〈/a〉
    Keywords: Africa South of the Sahara ; Agriculture/*methods ; Biomass ; Crops, Agricultural/*growth & development ; *Ecosystem ; Fertilizers ; *Food Supply ; Forestry ; Humans ; Hunger ; Nitrogen ; Nitrogen Fixation ; Phosphates ; Plant Development ; Public Policy ; *Soil ; Trees/growth & development ; United Nations ; Zea mays/growth & development
    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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  • 2
    Publication Date: 1998-03-07
    Description: The mechanisms by which Ebola virus evades detection and infects cells to cause hemorrhagic fever have not been defined, though its glycoprotein, synthesized in either a secreted or transmembrane form, is likely involved. Here the secreted glycoprotein was found to interact with neutrophils through CD16b, the neutrophil-specific form of the Fc gamma receptor III, whereas the transmembrane glycoprotein was found to interact with endothelial cells but not neutrophils. A murine retroviral vector pseudotyped with the transmembrane glycoprotein preferentially infected endothelial cells. Thus, the secreted glycoprotein inhibits early neutrophil activation, which likely affects the host response to infection, whereas binding of the transmembrane glycoprotein to endothelial cells may contribute to the hemorrhagic symptoms of this disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Z -- Delgado, R -- Xu, L -- Todd, R F -- Nabel, E G -- Sanchez, A -- Nabel, G J -- New York, N.Y. -- Science. 1998 Feb 13;279(5353):1034-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9461435" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line ; Ebolavirus/genetics/metabolism/*pathogenicity/physiology ; Endothelium, Vascular/cytology/*metabolism/virology ; Genes, Viral ; Genetic Vectors ; Glycoproteins/genetics/*metabolism/secretion ; Hemorrhagic Fever, Ebola/virology ; Humans ; L-Selectin/metabolism ; Membrane Glycoproteins/genetics/*metabolism ; Moloney murine leukemia virus/genetics/physiology ; Neutrophil Activation ; Neutrophils/immunology/*metabolism ; Receptors, IgG/metabolism ; Transfection ; Tumor Cells, Cultured ; Viral Matrix Proteins/genetics/*metabolism ; Viral Proteins/genetics/*metabolism/secretion
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Nature Publishing Group (NPG)
    Publication Date: 2009-03-13
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanchez, Pedro A -- England -- Nature. 2009 Mar 12;458(7235):148. doi: 10.1038/458148a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Earth Institute at Columbia University, 61 Route 9W, Palisades, New York 10964, USA. psanchez@ei.columbia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19279615" target="_blank"〉PubMed〈/a〉
    Keywords: *Agriculture/economics/methods ; Food/economics ; Humans ; *Hunger ; *International Cooperation ; *Public Policy ; United Nations
    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: 2009-08-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanchez, Pedro A -- Ahamed, Sonya -- Carre, Florence -- Hartemink, Alfred E -- Hempel, Jonathan -- Huising, Jeroen -- Lagacherie, Philippe -- McBratney, Alex B -- McKenzie, Neil J -- Mendonca-Santos, Maria de Lourdes -- Minasny, Budiman -- Montanarella, Luca -- Okoth, Peter -- Palm, Cheryl A -- Sachs, Jeffrey D -- Shepherd, Keith D -- Vagen, Tor-Gunnar -- Vanlauwe, Bernard -- Walsh, Markus G -- Winowiecki, Leigh A -- Zhang, Gan-Lin -- New York, N.Y. -- Science. 2009 Aug 7;325(5941):680-1. doi: 10.1126/science.1175084.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Earth Institute at Columbia University, 61 Route 9W, Palisades, NY 10964, USA. psanchez@ei.columbia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19661405" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture ; Climate ; *Databases, Factual ; *Ecology ; Ecosystem ; Environment ; Humans ; *Soil/analysis
    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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  • 5
    Publication Date: 2003-05-06
    Description: In March 2003, a novel coronavirus (SARS-CoV) was discovered in association with cases of severe acute respiratory syndrome (SARS). The sequence of the complete genome of SARS-CoV was determined, and the initial characterization of the viral genome is presented in this report. The genome of SARS-CoV is 29,727 nucleotides in length and has 11 open reading frames, and its genome organization is similar to that of other coronaviruses. Phylogenetic analyses and sequence comparisons showed that SARS-CoV is not closely related to any of the previously characterized coronaviruses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rota, Paul A -- Oberste, M Steven -- Monroe, Stephan S -- Nix, W Allan -- Campagnoli, Ray -- Icenogle, Joseph P -- Penaranda, Silvia -- Bankamp, Bettina -- Maher, Kaija -- Chen, Min-Hsin -- Tong, Suxiong -- Tamin, Azaibi -- Lowe, Luis -- Frace, Michael -- DeRisi, Joseph L -- Chen, Qi -- Wang, David -- Erdman, Dean D -- Peret, Teresa C T -- Burns, Cara -- Ksiazek, Thomas G -- Rollin, Pierre E -- Sanchez, Anthony -- Liffick, Stephanie -- Holloway, Brian -- Limor, Josef -- McCaustland, Karen -- Olsen-Rasmussen, Melissa -- Fouchier, Ron -- Gunther, Stephan -- Osterhaus, Albert D M E -- Drosten, Christian -- Pallansch, Mark A -- Anderson, Larry J -- Bellini, William J -- New York, N.Y. -- Science. 2003 May 30;300(5624):1394-9. Epub 2003 May 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30333, USA. prota@cdc.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730500" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Conserved Sequence ; Coronavirus/classification/genetics ; DNA, Complementary ; Endopeptidases/chemistry/genetics ; *Genome, Viral ; Humans ; Membrane Glycoproteins/chemistry/genetics ; Molecular Sequence Data ; Nucleocapsid Proteins/chemistry/genetics ; Open Reading Frames ; Phylogeny ; Polyproteins/chemistry/genetics ; RNA Replicase/chemistry/genetics ; RNA, Messenger/genetics/metabolism ; RNA, Viral/*genetics ; Regulatory Sequences, Nucleic Acid ; SARS Virus/chemistry/classification/*genetics/isolation & purification ; Sequence Analysis, DNA ; Severe Acute Respiratory Syndrome/virology ; Spike Glycoprotein, Coronavirus ; Transcription, Genetic ; Viral Envelope Proteins/chemistry/genetics ; Viral Matrix Proteins/chemistry/genetics ; Viral Proteins/chemistry/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2005-01-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanchez, Pedro A -- Swaminathan, M S -- New York, N.Y. -- Science. 2005 Jan 21;307(5708):357-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Earth Institute at Columbia University, New York, NY 10964, USA. sanchez@iri.columbia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15661994" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture ; Commerce ; *Global Health ; Humans ; *Hunger ; Income ; International Cooperation ; Malnutrition/epidemiology/*prevention & control ; Nutritional Physiological Phenomena ; Politics ; Poverty/prevention & control ; *Public Health ; Public Policy
    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: 2013-03-15
    Description: Tapeworms (Cestoda) cause neglected diseases that can be fatal and are difficult to treat, owing to inefficient drugs. Here we present an analysis of tapeworm genome sequences using the human-infective species Echinococcus multilocularis, E. granulosus, Taenia solium and the laboratory model Hymenolepis microstoma as examples. The 115- to 141-megabase genomes offer insights into the evolution of parasitism. Synteny is maintained with distantly related blood flukes but we find extreme losses of genes and pathways that are ubiquitous in other animals, including 34 homeobox families and several determinants of stem cell fate. Tapeworms have specialized detoxification pathways, metabolism that is finely tuned to rely on nutrients scavenged from their hosts, and species-specific expansions of non-canonical heat shock proteins and families of known antigens. We identify new potential drug targets, including some on which existing pharmaceuticals may act. The genomes provide a rich resource to underpin the development of urgently needed treatments and control.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3964345/" 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/PMC3964345/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsai, Isheng J -- Zarowiecki, Magdalena -- Holroyd, Nancy -- Garciarrubio, Alejandro -- Sanchez-Flores, Alejandro -- Brooks, Karen L -- Tracey, Alan -- Bobes, Raul J -- Fragoso, Gladis -- Sciutto, Edda -- Aslett, Martin -- Beasley, Helen -- Bennett, Hayley M -- Cai, Jianping -- Camicia, Federico -- Clark, Richard -- Cucher, Marcela -- De Silva, Nishadi -- Day, Tim A -- Deplazes, Peter -- Estrada, Karel -- Fernandez, Cecilia -- Holland, Peter W H -- Hou, Junling -- Hu, Songnian -- Huckvale, Thomas -- Hung, Stacy S -- Kamenetzky, Laura -- Keane, Jacqueline A -- Kiss, Ferenc -- Koziol, Uriel -- Lambert, Olivia -- Liu, Kan -- Luo, Xuenong -- Luo, Yingfeng -- Macchiaroli, Natalia -- Nichol, Sarah -- Paps, Jordi -- Parkinson, John -- Pouchkina-Stantcheva, Natasha -- Riddiford, Nick -- Rosenzvit, Mara -- Salinas, Gustavo -- Wasmuth, James D -- Zamanian, Mostafa -- Zheng, Yadong -- Taenia solium Genome Consortium -- Cai, Xuepeng -- Soberon, Xavier -- Olson, Peter D -- Laclette, Juan P -- Brehm, Klaus -- Berriman, Matthew -- 085775/Wellcome Trust/United Kingdom -- 098051/Wellcome Trust/United Kingdom -- BBG0038151/Biotechnology and Biological Sciences Research Council/United Kingdom -- MOP#84556/Canadian Institutes of Health Research/Canada -- TW008588/TW/FIC NIH HHS/ -- England -- Nature. 2013 Apr 4;496(7443):57-63. doi: 10.1038/nature12031. Epub 2013 Mar 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Parasite Genomics, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23485966" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological/*genetics ; Animals ; Biological Evolution ; Cestoda/drug effects/*genetics/physiology ; Cestode Infections/drug therapy/metabolism ; Conserved Sequence/genetics ; Echinococcus granulosus/genetics ; Echinococcus multilocularis/drug effects/genetics/metabolism ; Genes, Helminth/genetics ; Genes, Homeobox/genetics ; Genome, Helminth/*genetics ; HSP70 Heat-Shock Proteins/genetics ; Humans ; Hymenolepis/genetics ; Metabolic Networks and Pathways/genetics ; Molecular Targeted Therapy ; Parasites/drug effects/*genetics/physiology ; Proteome/genetics ; Stem Cells/cytology/metabolism ; Taenia solium/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2014-07-22
    Description: Myeloproliferative neoplasms (MPNs) are diseases caused by mutations in the haematopoietic stem cell (HSC) compartment. Most MPN patients have a common acquired mutation of Janus kinase 2 (JAK2) gene in HSCs that renders this kinase constitutively active, leading to uncontrolled cell expansion. The bone marrow microenvironment might contribute to the clinical outcomes of this common event. We previously showed that bone marrow nestin(+) mesenchymal stem cells (MSCs) innervated by sympathetic nerve fibres regulate normal HSCs. Here we demonstrate that abrogation of this regulatory circuit is essential for MPN pathogenesis. Sympathetic nerve fibres, supporting Schwann cells and nestin(+) MSCs are consistently reduced in the bone marrow of MPN patients and mice expressing the human JAK2(V617F) mutation in HSCs. Unexpectedly, MSC reduction is not due to differentiation but is caused by bone marrow neural damage and Schwann cell death triggered by interleukin-1beta produced by mutant HSCs. In turn, in vivo depletion of nestin(+) cells or their production of CXCL12 expanded mutant HSC number and accelerated MPN progression. In contrast, administration of neuroprotective or sympathomimetic drugs prevented mutant HSC expansion. Treatment with beta3-adrenergic agonists that restored the sympathetic regulation of nestin(+) MSCs prevented the loss of these cells and blocked MPN progression by indirectly reducing the number of leukaemic stem cells. Our results demonstrate that mutant-HSC-driven niche damage critically contributes to disease manifestation in MPN and identify niche-forming MSCs and their neural regulation as promising therapeutic targets.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arranz, Lorena -- Sanchez-Aguilera, Abel -- Martin-Perez, Daniel -- Isern, Joan -- Langa, Xavier -- Tzankov, Alexandar -- Lundberg, Pontus -- Muntion, Sandra -- Tzeng, Yi-Shiuan -- Lai, Dar-Ming -- Schwaller, Jurg -- Skoda, Radek C -- Mendez-Ferrer, Simon -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Aug 7;512(7512):78-81. doi: 10.1038/nature13383. Epub 2014 Jun 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cell Niche Pathophysiology Group, Centro Nacional de Investigaciones Cardiovasculares (CNIC), 28029 Madrid, Spain. ; University Hospital Basel, CH-4031 Basel, Switzerland. ; Department of Haematology, IBSAL-Hospital Universitario de Salamanca, 37007 Salamanca, Spain. ; National Taiwan University, Taipei 10002, Taiwan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25043017" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic beta-3 Receptor Agonists/pharmacology/therapeutic use ; Animals ; Apoptosis/drug effects ; Disease Progression ; Female ; Hematopoietic Stem Cells/drug effects/*pathology ; Humans ; Interleukin-1beta/metabolism ; Janus Kinase 2/genetics ; Mesenchymal Stromal Cells/drug effects/pathology ; Mice ; Myeloproliferative Disorders/drug therapy/*pathology ; Neoplasms/drug therapy/*pathology ; Neoplastic Stem Cells/drug effects/pathology ; Nerve Fibers/drug effects/*pathology ; Nestin/metabolism ; Neuroprotective Agents/pharmacology/therapeutic use ; Receptors, Adrenergic, beta-3/metabolism ; Schwann Cells/drug effects/pathology ; *Stem Cell Niche ; Sympathetic Nervous System/drug effects/*pathology/physiopathology
    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: 2012-01-27
    Description: The concept of disease-specific chemotherapy was developed a century ago. Dyes and arsenical compounds that displayed selectivity against trypanosomes were central to this work, and the drugs that emerged remain in use for treating human African trypanosomiasis (HAT). The importance of understanding the mechanisms underlying selective drug action and resistance for the development of improved HAT therapies has been recognized, but these mechanisms have remained largely unknown. Here we use all five current HAT drugs for genome-scale RNA interference target sequencing (RIT-seq) screens in Trypanosoma brucei, revealing the transporters, organelles, enzymes and metabolic pathways that function to facilitate antitrypanosomal drug action. RIT-seq profiling identifies both known drug importers and the only known pro-drug activator, and links more than fifty additional genes to drug action. A bloodstream stage-specific invariant surface glycoprotein (ISG75) family mediates suramin uptake, and the AP1 adaptin complex, lysosomal proteases and major lysosomal transmembrane protein, as well as spermidine and N-acetylglucosamine biosynthesis, all contribute to suramin action. Further screens link ubiquinone availability to nitro-drug action, plasma membrane P-type H(+)-ATPases to pentamidine action, and trypanothione and several putative kinases to melarsoprol action. We also demonstrate a major role for aquaglyceroporins in pentamidine and melarsoprol cross-resistance. These advances in our understanding of mechanisms of antitrypanosomal drug efficacy and resistance will aid the rational design of new therapies and help to combat drug resistance, and provide unprecedented molecular insight into the mode of action of antitrypanosomal drugs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3303116/" 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/PMC3303116/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alsford, Sam -- Eckert, Sabine -- Baker, Nicola -- Glover, Lucy -- Sanchez-Flores, Alejandro -- Leung, Ka Fai -- Turner, Daniel J -- Field, Mark C -- Berriman, Matthew -- Horn, David -- 085775/Wellcome Trust/United Kingdom -- 085775/Z/08/Z/Wellcome Trust/United Kingdom -- 090007/Wellcome Trust/United Kingdom -- 090007/Z/09/Z/Wellcome Trust/United Kingdom -- 093010/Wellcome Trust/United Kingdom -- 093010/Z/10/Z/Wellcome Trust/United Kingdom -- England -- Nature. 2012 Jan 25;482(7384):232-6. doi: 10.1038/nature10771.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉London School of Hygiene and Tropical Medicine, Keppel Street, London, WC1E 7HT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22278056" target="_blank"〉PubMed〈/a〉
    Keywords: Aquaglyceroporins/deficiency/metabolism ; Drug Resistance/*genetics ; Eflornithine/pharmacology ; Endocytosis/drug effects ; Glycosylation/drug effects ; High-Throughput Screening Assays ; Humans ; Lysosomes/drug effects/metabolism ; Melarsoprol/pharmacology ; Nifurtimox/pharmacology ; Pentamidine/pharmacology ; RNA Interference ; Suramin/pharmacology ; Trypanocidal Agents/*pharmacology/therapeutic use ; Trypanosoma brucei brucei/cytology/*drug effects/enzymology/metabolism ; Trypanosomiasis, African/*drug therapy/genetics
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 1993-11-05
    Description: A mysterious respiratory illness with high mortality was recently reported in the southwestern United States. Serologic studies implicated the hantaviruses, rodent-borne RNA viruses usually associated elsewhere in the world with hemorrhagic fever with renal syndrome. A genetic detection assay amplified hantavirus-specific DNA fragments from RNA extracted from the tissues of patients and deer mice (Peromyscus maniculatus) caught at or near patient residences. Nucleotide sequence analysis revealed the associated virus to be a new hantavirus and provided a direct genetic link between infection in patients and rodents.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nichol, S T -- Spiropoulou, C F -- Morzunov, S -- Rollin, P E -- Ksiazek, T G -- Feldmann, H -- Sanchez, A -- Childs, J -- Zaki, S -- Peters, C J -- New York, N.Y. -- Science. 1993 Nov 5;262(5135):914-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Viral and Rickettsial Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30333.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8235615" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Bunyaviridae Infections/epidemiology/*microbiology/veterinary ; DNA Primers ; *Disease Outbreaks ; *Disease Reservoirs ; *Genome, Viral ; Hantavirus/classification/*genetics/isolation & purification ; Humans ; Lung Diseases/epidemiology/*microbiology ; Molecular Sequence Data ; Peromyscus/*microbiology ; Phylogeny ; Polymerase Chain Reaction ; Rodent Diseases/epidemiology/microbiology ; Sequence Homology, Nucleic Acid ; Southwestern United States/epidemiology
    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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