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  • Humans  (3)
  • Geophysics
  • American Association for the Advancement of Science (AAAS)  (3)
  • 1
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    Evolutionary dynamics of complex networks of HIV drug-resistant strains: the case of San Francisco (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-01-16
    Description: Over the past two decades, HIV resistance to antiretroviral drugs (ARVs) has risen to high levels in the wealthier countries of the world, which are able to afford widespread treatment. We have gained insights into the evolution and transmission dynamics of ARV resistance by designing a biologically complex multistrain network model. With this model, we traced the evolutionary history of ARV resistance in San Francisco and predict its future dynamics. By using classification and regression trees, we identified the key immunologic, virologic, and treatment factors that increase ARV resistance. Our modeling shows that 60% of the currently circulating ARV-resistant strains in San Francisco are capable of causing self-sustaining epidemics, because each individual infected with one of these strains can cause, on average, more than one new resistant infection. It is possible that a new wave of ARV-resistant strains that pose a substantial threat to global public health is emerging.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, Robert J -- Okano, Justin T -- Kahn, James S -- Bodine, Erin N -- Blower, Sally -- K24RR024369/RR/NCRR NIH HHS/ -- P30-AI27763/AI/NIAID NIH HHS/ -- R01 AI041935/AI/NIAID NIH HHS/ -- R18-HS017784/HS/AHRQ HHS/ -- New York, N.Y. -- Science. 2010 Feb 5;327(5966):697-701. doi: 10.1126/science.1180556. Epub 2010 Jan 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Biomedical Modeling, Semel Institute of Neuroscience & Human Behavior, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA 90024, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20075214" target="_blank"〉PubMed〈/a〉
    Keywords: Anti-HIV Agents/*pharmacology/therapeutic use ; Antiretroviral Therapy, Highly Active ; Computer Simulation ; Disease Outbreaks ; Drug Resistance, Multiple, Viral ; *Drug Resistance, Viral ; Drug Therapy, Combination ; Evolution, Molecular ; Forecasting ; HIV/*drug effects/genetics ; HIV Infections/drug therapy/epidemiology/*transmission/*virology ; HIV Protease Inhibitors/pharmacology/therapeutic use ; Homosexuality, Male ; Humans ; Male ; Models, Statistical ; Monte Carlo Method ; Probability ; Reverse Transcriptase Inhibitors/pharmacology/therapeutic use ; San Francisco/epidemiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Evolutionarily dynamic alternative splicing of GPR56 regulates regional cerebral cortical patterning (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-02-18
    Description: The human neocortex has numerous specialized functional areas whose formation is poorly understood. Here, we describe a 15-base pair deletion mutation in a regulatory element of GPR56 that selectively disrupts human cortex surrounding the Sylvian fissure bilaterally including "Broca's area," the primary language area, by disrupting regional GPR56 expression and blocking RFX transcription factor binding. GPR56 encodes a heterotrimeric guanine nucleotide-binding protein (G protein)-coupled receptor required for normal cortical development and is expressed in cortical progenitor cells. GPR56 expression levels regulate progenitor proliferation. GPR56 splice forms are highly variable between mice and humans, and the regulatory element of gyrencephalic mammals directs restricted lateral cortical expression. Our data reveal a mechanism by which control of GPR56 expression pattern by multiple alternative promoters can influence stem cell proliferation, gyral patterning, and, potentially, neocortex evolution.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4480613/" 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/PMC4480613/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bae, Byoung-Il -- Tietjen, Ian -- Atabay, Kutay D -- Evrony, Gilad D -- Johnson, Matthew B -- Asare, Ebenezer -- Wang, Peter P -- Murayama, Ayako Y -- Im, Kiho -- Lisgo, Steven N -- Overman, Lynne -- Sestan, Nenad -- Chang, Bernard S -- Barkovich, A James -- Grant, P Ellen -- Topcu, Meral -- Politsky, Jeffrey -- Okano, Hideyuki -- Piao, Xianhua -- Walsh, Christopher A -- 2R01NS035129/NS/NINDS NIH HHS/ -- G0700089/Medical Research Council/United Kingdom -- GR082557/Wellcome Trust/United Kingdom -- HHSN275200900011C/PHS HHS/ -- N01-HD-9-0011/HD/NICHD NIH HHS/ -- R01 NS035129/NS/NINDS NIH HHS/ -- U01 MH081896/MH/NIMH NIH HHS/ -- U01MH081896/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Feb 14;343(6172):764-8. doi: 10.1126/science.1244392.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Genetics and Genomics, Manton Center for Orphan Disease, and Howard Hughes Medical Institute, Boston Children's Hospital, Broad Institute of MIT and Harvard, and Departments of Pediatrics and Neurology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24531968" target="_blank"〉PubMed〈/a〉
    Keywords: *Alternative Splicing ; Animals ; Base Sequence ; Biological Evolution ; Body Patterning/*genetics ; Cats ; Cell Proliferation ; Cerebral Cortex/anatomy & histology/cytology/*embryology ; Codon, Nonsense ; Frontal Lobe/anatomy & histology/cytology/embryology ; Genetic Variation ; Haplotypes ; Humans ; Mice ; Molecular Sequence Data ; Neural Stem Cells/cytology/*physiology ; Pedigree ; Promoter Regions, Genetic/genetics ; Receptors, G-Protein-Coupled/*genetics ; Sequence Deletion
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Loss of imprinting of Igf2 alters intestinal maturation and tumorigenesis in mice (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-26
    Description: Loss of imprinting (LOI) of the insulin-like growth factor II gene (IGF2) is an epigenetic alteration that results in a modest increase in IGF2 expression, and it is present in the normal colonic mucosa of about 30% of patients with colorectal cancer. To investigate its role in intestinal tumorigenesis, we created a mouse model of Igf2 LOI by crossing female H19+/- mice with male Apc+/Min mice. Mice with LOI developed twice as many intestinal tumors as did control littermates. Notably, these mice also showed a shift toward a less differentiated normal intestinal epithelium, reflected by an increase in crypt length and increased staining with progenitor cell markers. A similar shift in differentiation was seen in the normal colonic mucosa of humans with LOI. Thus, altered maturation of nonneoplastic tissue may be one mechanism by which epigenetic changes affect cancer risk.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sakatani, Takashi -- Kaneda, Atsushi -- Iacobuzio-Donahue, Christine A -- Carter, Mark G -- de Boom Witzel, Sten -- Okano, Hideyuki -- Ko, Minoru S H -- Ohlsson, Rolf -- Longo, Dan L -- Feinberg, Andrew P -- K08CA106610/CA/NCI NIH HHS/ -- R01CA65145/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2005 Mar 25;307(5717):1976-8. Epub 2005 Feb 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15731405" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoma/etiology/pathology ; Animals ; Apoptosis ; Cell Differentiation ; Cell Proliferation ; Colon/cytology/metabolism ; Colonic Neoplasms/etiology/pathology ; Enterocytes/*cytology/metabolism ; Ephrin-B1/analysis ; Epigenesis, Genetic ; Female ; *Genomic Imprinting ; Humans ; Insulin-Like Growth Factor II/*genetics/*metabolism ; Intestinal Mucosa/*cytology/metabolism ; Intestinal Neoplasms/*etiology/pathology ; Intestines/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Microfilament Proteins/analysis ; Nerve Tissue Proteins/analysis ; Nuclear Proteins/analysis ; RNA, Long Noncoding ; RNA, Untranslated/genetics ; RNA-Binding Proteins/analysis ; Stem Cells/cytology ; Transcription Factors/analysis ; Twist Transcription Factor
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
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