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  • 1
    Publication Date: 1999-12-22
    Description: In late summer 1999, an outbreak of human encephalitis occurred in the northeastern United States that was concurrent with extensive mortality in crows (Corvus species) as well as the deaths of several exotic birds at a zoological park in the same area. Complete genome sequencing of a flavivirus isolated from the brain of a dead Chilean flamingo (Phoenicopterus chilensis), together with partial sequence analysis of envelope glycoprotein (E-glycoprotein) genes amplified from several other species including mosquitoes and two fatal human cases, revealed that West Nile (WN) virus circulated in natural transmission cycles and was responsible for the human disease. Antigenic mapping with E-glycoprotein-specific monoclonal antibodies and E-glycoprotein phylogenetic analysis confirmed these viruses as WN. This North American WN virus was most closely related to a WN virus isolated from a dead goose in Israel in 1998.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lanciotti, R S -- Roehrig, J T -- Deubel, V -- Smith, J -- Parker, M -- Steele, K -- Crise, B -- Volpe, K E -- Crabtree, M B -- Scherret, J H -- Hall, R A -- MacKenzie, J S -- Cropp, C B -- Panigrahy, B -- Ostlund, E -- Schmitt, B -- Malkinson, M -- Banet, C -- Weissman, J -- Komar, N -- Savage, H M -- Stone, W -- McNamara, T -- Gubler, D J -- New York, N.Y. -- Science. 1999 Dec 17;286(5448):2333-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Vector-Borne Infectious Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Fort Collins, CO 80522, USA. rsl2@cdc.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10600742" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal/immunology ; Antibodies, Viral/immunology ; Base Sequence ; Bird Diseases/epidemiology/virology ; Birds/virology ; *Disease Outbreaks ; Encephalitis Viruses, Japanese/classification/genetics ; Fluorescent Antibody Technique, Indirect ; Genome, Viral ; Humans ; Molecular Sequence Data ; New England/epidemiology ; New York City/epidemiology ; Phylogeny ; Songbirds/virology ; Viral Envelope Proteins/chemistry/genetics/immunology ; West Nile Fever/*epidemiology/veterinary/*virology ; West Nile virus/*classification/*genetics/immunology/isolation & purification
    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
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-06-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mackenzie, D -- New York, N.Y. -- Science. 1999 Jun 4;284(5420):1607, 1609.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10383334" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Vessels/*anatomy & histology ; *Body Constitution ; Body Surface Area ; *Fractals ; Humans ; Life Expectancy ; *Longevity ; Mathematics ; *Metabolism ; *Models, Biological
    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
    Publication Date: 2000-10-13
    Description: Motivated by the rapid increase in atmospheric CO2 due to human activities since the Industrial Revolution, several international scientific research programs have analyzed the role of individual components of the Earth system in the global carbon cycle. Our knowledge of the carbon cycle within the oceans, terrestrial ecosystems, and the atmosphere is sufficiently extensive to permit us to conclude that although natural processes can potentially slow the rate of increase in atmospheric CO2, there is no natural "savior" waiting to assimilate all the anthropogenically produced CO2 in the coming century. Our knowledge is insufficient to describe the interactions between the components of the Earth system and the relationship between the carbon cycle and other biogeochemical and climatological processes. Overcoming this limitation requires a systems approach.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Falkowski, P -- Scholes, R J -- Boyle, E -- Canadell, J -- Canfield, D -- Elser, J -- Gruber, N -- Hibbard, K -- Hogberg, P -- Linder, S -- Mackenzie, F T -- Moore, B 3rd -- Pedersen, T -- Rosenthal, Y -- Seitzinger, S -- Smetacek, V -- Steffen, W -- New York, N.Y. -- Science. 2000 Oct 13;290(5490):291-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Marine and Coastal Sciences, Rutgers University, 71 Dudley Road, New Brunswick, NJ 08901, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11030643" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atmosphere ; *Carbon/metabolism ; *Carbon Dioxide/metabolism ; *Climate ; *Earth (Planet) ; *Ecosystem ; Greenhouse Effect ; Humans
    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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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2004-02-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mackenzie, Dana -- New York, N.Y. -- Science. 2004 Feb 6;303(5659):786-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14764864" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Computer Simulation ; *Electric Countershock ; Electrodes ; Electrophysiology ; Heart/*physiology/physiopathology ; Heart Conduction System/*physiology ; Humans ; Mathematics ; Models, Anatomic ; *Models, Cardiovascular ; Ventricular Fibrillation/*physiopathology/therapy
    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
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    Nature Publishing Group (NPG)
    Publication Date: 2013-03-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉MacKenzie, Brian R -- Payne, Mark R -- England -- Nature. 2013 Mar 21;495(7441):314. doi: 10.1038/495314c.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23518555" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conservation of Natural Resources/*methods/*statistics & numerical data ; Ecology/*methods ; *Ecosystem ; Fisheries/*statistics & numerical data ; Fishes/*physiology
    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: 2011-08-19
    Description: Fumarate hydratase (FH) is an enzyme of the tricarboxylic acid cycle (TCA cycle) that catalyses the hydration of fumarate into malate. Germline mutations of FH are responsible for hereditary leiomyomatosis and renal-cell cancer (HLRCC). It has previously been demonstrated that the absence of FH leads to the accumulation of fumarate, which activates hypoxia-inducible factors (HIFs) at normal oxygen tensions. However, so far no mechanism that explains the ability of cells to survive without a functional TCA cycle has been provided. Here we use newly characterized genetically modified kidney mouse cells in which Fh1 has been deleted, and apply a newly developed computer model of the metabolism of these cells to predict and experimentally validate a linear metabolic pathway beginning with glutamine uptake and ending with bilirubin excretion from Fh1-deficient cells. This pathway, which involves the biosynthesis and degradation of haem, enables Fh1-deficient cells to use the accumulated TCA cycle metabolites and permits partial mitochondrial NADH production. We predicted and confirmed that targeting this pathway would render Fh1-deficient cells non-viable, while sparing wild-type Fh1-containing cells. This work goes beyond identifying a metabolic pathway that is induced in Fh1-deficient cells to demonstrate that inhibition of haem oxygenation is synthetically lethal when combined with Fh1 deficiency, providing a new potential target for treating HLRCC patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frezza, Christian -- Zheng, Liang -- Folger, Ori -- Rajagopalan, Kartik N -- MacKenzie, Elaine D -- Jerby, Livnat -- Micaroni, Massimo -- Chaneton, Barbara -- Adam, Julie -- Hedley, Ann -- Kalna, Gabriela -- Tomlinson, Ian P M -- Pollard, Patrick J -- Watson, Dave G -- Deberardinis, Ralph J -- Shlomi, Tomer -- Ruppin, Eytan -- Gottlieb, Eyal -- 090532/Wellcome Trust/United Kingdom -- DK072565-05/DK/NIDDK NIH HHS/ -- WT091112MA/Wellcome Trust/United Kingdom -- Cancer Research UK/United Kingdom -- England -- Nature. 2011 Aug 17;477(7363):225-8. doi: 10.1038/nature10363.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research UK, Beatson Institute for Cancer Research, Switchback Road, Glasgow G61 1BD, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21849978" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bilirubin/metabolism ; Cell Line ; Cells, Cultured ; Citric Acid Cycle ; Computer Simulation ; Fumarate Hydratase/deficiency/*genetics/*metabolism ; Fumarates/metabolism ; Genes, Lethal/*genetics ; *Genes, Tumor Suppressor ; Glutamine/metabolism ; Heme/metabolism ; Heme Oxygenase (Decyclizing)/antagonists & inhibitors/*genetics/*metabolism ; Kidney Neoplasms/drug therapy/enzymology/genetics/metabolism ; Leiomyomatosis/congenital/drug therapy/enzymology/genetics/metabolism ; Mice ; Mitochondria/metabolism ; Mutation/*genetics ; NAD/metabolism ; Neoplastic Syndromes, Hereditary ; Skin Neoplasms ; Uterine Neoplasms
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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