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  • Humans  (5)
  • American Association for the Advancement of Science (AAAS)  (5)
  • Springer Nature
  • 2005-2009  (5)
  • 1960-1964
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  • 1
    Publication Date: 2006-01-28
    Description: The spread of H5N1 avian influenza viruses (AIVs) from China to Europe has raised global concern about their potential to infect humans and cause a pandemic. In spite of their substantial threat to human health, remarkably little AIV whole-genome information is available. We report here a preliminary analysis of the first large-scale sequencing of AIVs, including 2196 AIV genes and 169 complete genomes. We combine this new information with public AIV data to identify new gene alleles, persistent genotypes, compensatory mutations, and a potential virulence determinant.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Obenauer, John C -- Denson, Jackie -- Mehta, Perdeep K -- Su, Xiaoping -- Mukatira, Suraj -- Finkelstein, David B -- Xu, Xiequn -- Wang, Jinhua -- Ma, Jing -- Fan, Yiping -- Rakestraw, Karen M -- Webster, Robert G -- Hoffmann, Erich -- Krauss, Scott -- Zheng, Jie -- Zhang, Ziwei -- Naeve, Clayton W -- AI95357/AI/NIAID NIH HHS/ -- CA 21765/CA/NCI NIH HHS/ -- R01 GM061739/GM/NIGMS NIH HHS/ -- R01 GM069916/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2006 Mar 17;311(5767):1576-80. Epub 2006 Jan 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hartwell Center for Bioinformatics and Biotechnology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16439620" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Birds/virology ; Computational Biology ; *Genes, Viral ; Genome, Viral ; Humans ; Influenza A Virus, H1N1 Subtype/genetics ; Influenza A Virus, H2N2 Subtype/genetics ; Influenza A Virus, H3N2 Subtype/genetics ; Influenza A Virus, H3N8 Subtype/genetics ; Influenza A Virus, H5N1 Subtype/chemistry/*genetics/pathogenicity ; Influenza A Virus, H5N2 Subtype/genetics ; Influenza A Virus, H7N7 Subtype/genetics ; Influenza A Virus, H9N2 Subtype/genetics ; Influenza A virus/chemistry/*genetics/isolation & purification/pathogenicity ; Influenza in Birds/virology ; Influenza, Human/virology ; Molecular Sequence Data ; Mutation ; Phylogeny ; RNA, Viral/genetics ; Reassortant Viruses/genetics ; Sequence Analysis, DNA ; Viral Nonstructural Proteins/*chemistry/genetics ; Viral Proteins/chemistry/genetics ; Virulence Factors/*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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  • 2
    Publication Date: 2005-10-15
    Description: During the past two decades, the use of DNA tests has revolutionized court proceedings in criminal and paternity cases. On the horizon is a new challenge for judges--whether to admit or compel genetic tests to confirm or predict genetic diseases and conditions in many more judicial contexts, e.g., decisions regarding culpability, sentencing, liability, causation, and damages. This Policy Forum reports on an empirical study of how judges would analyze these issues. The authors discuss the challenges these types of cases will bring to the court-room and suggest a series of questions that judges should consider in evaluating the need for genetic information in legal cases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoffmann, Diane E -- Rothenberg, Karen H -- New York, N.Y. -- Science. 2005 Oct 14;310(5746):241-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Maryland School of Law, Baltimore, MD 21210, USA. dhoffman@law.umaryland.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16224007" target="_blank"〉PubMed〈/a〉
    Keywords: Data Collection ; Genetic Testing/*legislation & jurisprudence ; Humans ; Jurisprudence
    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: 2005-04-02
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2821939/" 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/PMC2821939/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barken, Derren -- Wang, Chiaochun Joanne -- Kearns, Jeff -- Cheong, Raymond -- Hoffmann, Alexander -- Levchenko, Andre -- GM072024-01/GM/NIGMS NIH HHS/ -- P01 GM071862/GM/NIGMS NIH HHS/ -- P01 GM071862-01A20005/GM/NIGMS NIH HHS/ -- R01 GM071573/GM/NIGMS NIH HHS/ -- R01 GM071573-01A1/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Apr 1;308(5718):52; author reply 52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Signaling Systems Laboratory, Department of Chemistry and Biochemistry and Bioinformatics Graduate Program, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0375, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15802586" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line, Tumor ; Cell Nucleus/metabolism ; Computer Simulation ; Cytoplasm/metabolism ; Feedback, Physiological ; *Gene Expression Regulation ; HeLa Cells ; Humans ; I-kappa B Proteins/metabolism ; Immunohistochemistry ; Models, Biological ; NF-kappa B/*metabolism ; Recombinant Fusion Proteins ; *Signal Transduction ; Transcription Factor RelA ; Transfection ; Tumor Necrosis Factor-alpha/pharmacology
    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
    Publication Date: 2006-07-11
    Description: The location of and threats to biodiversity are distributed unevenly, so prioritization is essential to minimize biodiversity loss. To address this need, biodiversity conservation organizations have proposed nine templates of global priorities over the past decade. Here, we review the concepts, methods, results, impacts, and challenges of these prioritizations of conservation practice within the theoretical irreplaceability/vulnerability framework of systematic conservation planning. Most of the templates prioritize highly irreplaceable regions; some are reactive (prioritizing high vulnerability), and others are proactive (prioritizing low vulnerability). We hope this synthesis improves understanding of these prioritization approaches and that it results in more efficient allocation of geographically flexible conservation funding.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brooks, T M -- Mittermeier, R A -- da Fonseca, G A B -- Gerlach, J -- Hoffmann, M -- Lamoreux, J F -- Mittermeier, C G -- Pilgrim, J D -- Rodrigues, A S L -- New York, N.Y. -- Science. 2006 Jul 7;313(5783):58-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Conservation International, 1919 M Street, NW, Washington, DC 20036, USA. t.brooks@conservation.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16825561" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biodiversity ; *Conservation of Natural Resources/economics ; *Ecosystem ; Environment ; Financial Support ; Geography ; Humans ; Invertebrates ; Mammals ; Plants ; Population Density ; Vertebrates
    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: 2009-02-14
    Description: Deposition of the amyloid-beta peptide is a pathological hallmark of Alzheimer's disease. A high-throughput functional genomics screen identified G protein-coupled receptor 3 (GPR3), a constitutively active orphan G protein-coupled receptor, as a modulator of amyloid-beta production. Overexpression of GPR3 stimulated amyloid-beta production, whereas genetic ablation of GPR3 prevented accumulation of the amyloid-beta peptide in vitro and in an Alzheimer's disease mouse model. GPR3 expression led to increased formation and cell-surface localization of the mature gamma-secretase complex in the absence of an effect on Notch processing. GPR3 is highly expressed in areas of the normal human brain implicated in Alzheimer's disease and is elevated in the sporadic Alzheimer's disease brain. Thus, GPR3 represents a potential therapeutic target for the treatment of Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thathiah, Amantha -- Spittaels, Kurt -- Hoffmann, Marcel -- Staes, Mik -- Cohen, Adrian -- Horre, Katrien -- Vanbrabant, Mieke -- Coun, Frea -- Baekelandt, Veerle -- Delacourte, Andre -- Fischer, David F -- Pollet, Dirk -- De Strooper, Bart -- Merchiers, Pascal -- New York, N.Y. -- Science. 2009 Feb 13;323(5916):946-51. doi: 10.1126/science.1160649.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Developmental Genetics, Vlaams Institute for Biotechnology, Center for Human Genetics, Catholic University of Leuven, Herestraat 49, 3000 Leuven, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19213921" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Amyloid Precursor Protein Secretases/metabolism ; Amyloid beta-Peptides/*biosynthesis ; Animals ; Cell Line ; Cell Line, Tumor ; Cells, Cultured ; Female ; Humans ; Male ; Mice ; Middle Aged ; Neurons/*metabolism ; Protein Structure, Tertiary ; Receptors, G-Protein-Coupled/*metabolism ; Receptors, Notch/metabolism ; Signal Transduction
    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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