ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Humans  (245)
  • American Association for the Advancement of Science (AAAS)  (245)
  • American Institute of Physics
  • American Institute of Physics (AIP)
  • Cell Press
  • Copernicus
  • National Academy of Sciences
  • Wiley
  • 2015-2019
  • 2010-2014  (140)
  • 2000-2004  (105)
  • 1960-1964
  • 1950-1954
  • 2012  (140)
  • 2000  (105)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (245)
  • American Institute of Physics
  • American Institute of Physics (AIP)
  • Cell Press
  • Copernicus
    • +
Years
  • 2015-2019
  • 2010-2014  (140)
  • 2000-2004  (105)
  • 1960-1964
  • 1950-1954
Year
  • 1
    facet.materialart.
    Unknown
    Complete genome sequence of Neisseria meningitidis serogroup B strain MC58 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-10
    Description: The 2,272,351-base pair genome of Neisseria meningitidis strain MC58 (serogroup B), a causative agent of meningitis and septicemia, contains 2158 predicted coding regions, 1158 (53.7%) of which were assigned a biological role. Three major islands of horizontal DNA transfer were identified; two of these contain genes encoding proteins involved in pathogenicity, and the third island contains coding sequences only for hypothetical proteins. Insights into the commensal and virulence behavior of N. meningitidis can be gleaned from the genome, in which sequences for structural proteins of the pilus are clustered and several coding regions unique to serogroup B capsular polysaccharide synthesis can be identified. Finally, N. meningitidis contains more genes that undergo phase variation than any pathogen studied to date, a mechanism that controls their expression and contributes to the evasion of the host immune system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tettelin, H -- Saunders, N J -- Heidelberg, J -- Jeffries, A C -- Nelson, K E -- Eisen, J A -- Ketchum, K A -- Hood, D W -- Peden, J F -- Dodson, R J -- Nelson, W C -- Gwinn, M L -- DeBoy, R -- Peterson, J D -- Hickey, E K -- Haft, D H -- Salzberg, S L -- White, O -- Fleischmann, R D -- Dougherty, B A -- Mason, T -- Ciecko, A -- Parksey, D S -- Blair, E -- Cittone, H -- Clark, E B -- Cotton, M D -- Utterback, T R -- Khouri, H -- Qin, H -- Vamathevan, J -- Gill, J -- Scarlato, V -- Masignani, V -- Pizza, M -- Grandi, G -- Sun, L -- Smith, H O -- Fraser, C M -- Moxon, E R -- Rappuoli, R -- Venter, J C -- New York, N.Y. -- Science. 2000 Mar 10;287(5459):1809-15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Institute for Genomic Research (TIGR), 9712 Medical Center Drive, Rockville, MD 20850, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10710307" target="_blank"〉PubMed〈/a〉
    Keywords: Antigenic Variation ; Antigens, Bacterial/immunology ; Bacteremia/microbiology ; Bacterial Capsules/genetics ; Bacterial Proteins/genetics/physiology ; DNA Transposable Elements ; Evolution, Molecular ; Fimbriae, Bacterial/genetics ; *Genome, Bacterial ; Humans ; Meningitis, Meningococcal/microbiology ; Meningococcal Infections/microbiology ; Molecular Sequence Data ; Mutation ; Neisseria meningitidis/classification/*genetics/*pathogenicity/physiology ; Open Reading Frames ; Operon ; Phylogeny ; Recombination, Genetic ; *Sequence Analysis, DNA ; Serotyping ; Transformation, Bacterial ; Virulence/genetics
    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
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    Conservation. Challenges to the future conservation of the Antarctic (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chown, S L -- Lee, J E -- Hughes, K A -- Barnes, J -- Barrett, P J -- Bergstrom, D M -- Convey, P -- Cowan, D A -- Crosbie, K -- Dyer, G -- Frenot, Y -- Grant, S M -- Herr, D -- Kennicutt, M C 2nd -- Lamers, M -- Murray, A -- Possingham, H P -- Reid, K -- Riddle, M J -- Ryan, P G -- Sanson, L -- Shaw, J D -- Sparrow, M D -- Summerhayes, C -- Terauds, A -- Wall, D H -- New York, N.Y. -- Science. 2012 Jul 13;337(6091):158-9. doi: 10.1126/science.1222821.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Invasion Biology, Stellenbosch University, Matieland, South Africa. steven.chown@monash.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22798586" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antarctic Regions ; Climate Change ; *Conservation of Natural Resources/trends ; *Ecosystem ; Forecasting ; Human Activities ; Humans ; Public Policy ; Travel
    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
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    Evolution and functional impact of rare coding variation from deep sequencing of human exomes (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-19
    Description: As a first step toward understanding how rare variants contribute to risk for complex diseases, we sequenced 15,585 human protein-coding genes to an average median depth of 111x in 2440 individuals of European (n = 1351) and African (n = 1088) ancestry. We identified over 500,000 single-nucleotide variants (SNVs), the majority of which were rare (86% with a minor allele frequency less than 0.5%), previously unknown (82%), and population-specific (82%). On average, 2.3% of the 13,595 SNVs each person carried were predicted to affect protein function of ~313 genes per genome, and ~95.7% of SNVs predicted to be functionally important were rare. This excess of rare functional variants is due to the combined effects of explosive, recent accelerated population growth and weak purifying selection. Furthermore, we show that large sample sizes will be required to associate rare variants with complex traits.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3708544/" 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/PMC3708544/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tennessen, Jacob A -- Bigham, Abigail W -- O'Connor, Timothy D -- Fu, Wenqing -- Kenny, Eimear E -- Gravel, Simon -- McGee, Sean -- Do, Ron -- Liu, Xiaoming -- Jun, Goo -- Kang, Hyun Min -- Jordan, Daniel -- Leal, Suzanne M -- Gabriel, Stacey -- Rieder, Mark J -- Abecasis, Goncalo -- Altshuler, David -- Nickerson, Deborah A -- Boerwinkle, Eric -- Sunyaev, Shamil -- Bustamante, Carlos D -- Bamshad, Michael J -- Akey, Joshua M -- Broad GO -- Seattle GO -- NHLBI Exome Sequencing Project -- R01 HG003229/HG/NHGRI NIH HHS/ -- RC2 HL-102923/HL/NHLBI NIH HHS/ -- RC2 HL-102924/HL/NHLBI NIH HHS/ -- RC2 HL-102925/HL/NHLBI NIH HHS/ -- RC2 HL-102926/HL/NHLBI NIH HHS/ -- RC2 HL-103010/HL/NHLBI NIH HHS/ -- RC2 HL102926/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2012 Jul 6;337(6090):64-9. doi: 10.1126/science.1219240. Epub 2012 May 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genome Sciences, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22604720" target="_blank"〉PubMed〈/a〉
    Keywords: African Americans/*genetics ; Disease/genetics ; European Continental Ancestry Group/*genetics ; *Evolution, Molecular ; *Exome ; Female ; Gene Frequency ; Genetic Association Studies ; Genetic Predisposition to Disease ; *Genetic Variation ; *Genome, Human ; *High-Throughput Nucleotide Sequencing ; Humans ; Male ; *Polymorphism, Single Nucleotide ; Population Growth ; Selection, Genetic
    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
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    A systematic survey of loss-of-function variants in human protein-coding genes (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-02-22
    Description: Genome-sequencing studies indicate that all humans carry many genetic variants predicted to cause loss of function (LoF) of protein-coding genes, suggesting unexpected redundancy in the human genome. Here we apply stringent filters to 2951 putative LoF variants obtained from 185 human genomes to determine their true prevalence and properties. We estimate that human genomes typically contain ~100 genuine LoF variants with ~20 genes completely inactivated. We identify rare and likely deleterious LoF alleles, including 26 known and 21 predicted severe disease-causing variants, as well as common LoF variants in nonessential genes. We describe functional and evolutionary differences between LoF-tolerant and recessive disease genes and a method for using these differences to prioritize candidate genes found in clinical sequencing studies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3299548/" 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/PMC3299548/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉MacArthur, Daniel G -- Balasubramanian, Suganthi -- Frankish, Adam -- Huang, Ni -- Morris, James -- Walter, Klaudia -- Jostins, Luke -- Habegger, Lukas -- Pickrell, Joseph K -- Montgomery, Stephen B -- Albers, Cornelis A -- Zhang, Zhengdong D -- Conrad, Donald F -- Lunter, Gerton -- Zheng, Hancheng -- Ayub, Qasim -- DePristo, Mark A -- Banks, Eric -- Hu, Min -- Handsaker, Robert E -- Rosenfeld, Jeffrey A -- Fromer, Menachem -- Jin, Mike -- Mu, Xinmeng Jasmine -- Khurana, Ekta -- Ye, Kai -- Kay, Mike -- Saunders, Gary Ian -- Suner, Marie-Marthe -- Hunt, Toby -- Barnes, If H A -- Amid, Clara -- Carvalho-Silva, Denise R -- Bignell, Alexandra H -- Snow, Catherine -- Yngvadottir, Bryndis -- Bumpstead, Suzannah -- Cooper, David N -- Xue, Yali -- Romero, Irene Gallego -- 1000 Genomes Project Consortium -- Wang, Jun -- Li, Yingrui -- Gibbs, Richard A -- McCarroll, Steven A -- Dermitzakis, Emmanouil T -- Pritchard, Jonathan K -- Barrett, Jeffrey C -- Harrow, Jennifer -- Hurles, Matthew E -- Gerstein, Mark B -- Tyler-Smith, Chris -- 085532/Wellcome Trust/United Kingdom -- 090532/Wellcome Trust/United Kingdom -- 090532/Z/09/Z/Wellcome Trust/United Kingdom -- 098051/Wellcome Trust/United Kingdom -- BB/I02593X/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- RG/09/012/28096/British Heart Foundation/United Kingdom -- U54 HG003273/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2012 Feb 17;335(6070):823-8. doi: 10.1126/science.1215040.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Hinxton, UK. macarthur@atgu.mgh.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22344438" target="_blank"〉PubMed〈/a〉
    Keywords: Disease/genetics ; Gene Expression ; Gene Frequency ; *Genetic Variation ; *Genome, Human ; Humans ; Phenotype ; Polymorphism, Single Nucleotide ; Proteins/*genetics ; Selection, Genetic
    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
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 5
    facet.materialart.
    Unknown
    Financial costs of meeting global biodiversity conservation targets: current spending and unmet needs (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-10-16
    Description: World governments have committed to halting human-induced extinctions and safeguarding important sites for biodiversity by 2020, but the financial costs of meeting these targets are largely unknown. We estimate the cost of reducing the extinction risk of all globally threatened bird species (by 〉/=1 International Union for Conservation of Nature Red List category) to be U.S. $0.875 to $1.23 billion annually over the next decade, of which 12% is currently funded. Incorporating threatened nonavian species increases this total to U.S. $3.41 to $4.76 billion annually. We estimate that protecting and effectively managing all terrestrial sites of global avian conservation significance (11,731 Important Bird Areas) would cost U.S. $65.1 billion annually. Adding sites for other taxa increases this to U.S. $76.1 billion annually. Meeting these targets will require conservation funding to increase by at least an order of magnitude.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McCarthy, Donal P -- Donald, Paul F -- Scharlemann, Jorn P W -- Buchanan, Graeme M -- Balmford, Andrew -- Green, Jonathan M H -- Bennun, Leon A -- Burgess, Neil D -- Fishpool, Lincoln D C -- Garnett, Stephen T -- Leonard, David L -- Maloney, Richard F -- Morling, Paul -- Schaefer, H Martin -- Symes, Andy -- Wiedenfeld, David A -- Butchart, Stuart H M -- New York, N.Y. -- Science. 2012 Nov 16;338(6109):946-9. doi: 10.1126/science.1229803. Epub 2012 Oct 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉BirdLife International, Wellbrook Court, Cambridge CB3 0NA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23065904" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biodiversity ; *Birds ; *Capital Financing ; Conservation of Natural Resources/*economics ; Costs and Cost Analysis ; *Extinction, Biological ; Humans
    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
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 6
    facet.materialart.
    Unknown
    Interactions between commensal fungi and the C-type lectin receptor Dectin-1 influence colitis (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-08
    Description: The intestinal microflora, typically equated with bacteria, influences diseases such as obesity and inflammatory bowel disease. Here, we show that the mammalian gut contains a rich fungal community that interacts with the immune system through the innate immune receptor Dectin-1. Mice lacking Dectin-1 exhibited increased susceptibility to chemically induced colitis, which was the result of altered responses to indigenous fungi. In humans, we identified a polymorphism in the gene for Dectin-1 (CLEC7A) that is strongly linked to a severe form of ulcerative colitis. Together, our findings reveal a eukaryotic fungal community in the gut (the "mycobiome") that coexists with bacteria and substantially expands the repertoire of organisms interacting with the intestinal immune system to influence health and disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3432565/" 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/PMC3432565/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iliev, Iliyan D -- Funari, Vincent A -- Taylor, Kent D -- Nguyen, Quoclinh -- Reyes, Christopher N -- Strom, Samuel P -- Brown, Jordan -- Becker, Courtney A -- Fleshner, Phillip R -- Dubinsky, Marla -- Rotter, Jerome I -- Wang, Hanlin L -- McGovern, Dermot P B -- Brown, Gordon D -- Underhill, David M -- 086558/Wellcome Trust/United Kingdom -- AI071116/AI/NIAID NIH HHS/ -- P01-DK046763/DK/NIDDK NIH HHS/ -- R01 DK093426/DK/NIDDK NIH HHS/ -- UL1 RR033176/RR/NCRR NIH HHS/ -- UL1 TR000124/TR/NCATS NIH HHS/ -- UL1RR033176/RR/NCRR NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Jun 8;336(6086):1314-7. doi: 10.1126/science.1221789. Epub 2012 Jun 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22674328" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Fungal/blood ; Candida tropicalis/immunology/isolation & purification/pathogenicity/physiology ; Colitis, Ulcerative/chemically induced/*immunology/*microbiology ; Colon/immunology/*microbiology ; Colony Count, Microbial ; Dextran Sulfate ; Disease Susceptibility ; Female ; Fungi/classification/*immunology/isolation & purification/*physiology ; Haplotypes ; Humans ; Immunity, Innate ; Immunity, Mucosal ; Intestinal Mucosa/immunology/*microbiology ; Intestines/immunology/microbiology ; Lectins, C-Type/deficiency/*genetics/*metabolism ; Metagenome ; Mice ; Mice, Inbred C57BL ; Polymorphism, Single Nucleotide
    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
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 7
    facet.materialart.
    Unknown
    Heterozygous germ line hCHK2 mutations in Li-Fraumeni syndrome (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-05
    Description: The hCHK2 gene encodes the human homolog of the yeast Cds1 and Rad53 G2 checkpoint kinases, whose activation in response to DNA damage prevents cellular entry into mitosis. Here, it is shown that heterozygous germ line mutations in hCHK2 occur in Li-Fraumeni syndrome, a highly penetrant familial cancer phenotype usually associated with inherited mutations in the TP53 gene. These observations suggest that hCHK2 is a tumor suppressor gene conferring predisposition to sarcoma, breast cancer, and brain tumors, and they also provide a link between the central role of p53 inactivation in human cancer and the well-defined G2 checkpoint in yeast.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bell, D W -- Varley, J M -- Szydlo, T E -- Kang, D H -- Wahrer, D C -- Shannon, K E -- Lubratovich, M -- Verselis, S J -- Isselbacher, K J -- Fraumeni, J F -- Birch, J M -- Li, F P -- Garber, J E -- Haber, D A -- New York, N.Y. -- Science. 1999 Dec 24;286(5449):2528-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Center for Cancer Risk Analysis and Harvard Medical School, Building 149, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10617473" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Apoptosis ; Brain Neoplasms/genetics ; Breast Neoplasms/genetics ; Checkpoint Kinase 2 ; Female ; G1 Phase ; *G2 Phase ; *Genes, Tumor Suppressor ; Genes, p53 ; Genetic Predisposition to Disease ; *Germ-Line Mutation ; Heterozygote ; Humans ; Li-Fraumeni Syndrome/enzymology/*genetics/pathology ; Male ; Pedigree ; Polymorphism, Genetic ; Protein Kinases/genetics ; Protein-Serine-Threonine Kinases/*genetics/metabolism ; Sarcoma/genetics ; Signal Transduction ; Tumor Cells, Cultured
    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
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 8
    facet.materialart.
    Unknown
    Control of viremia and prevention of clinical AIDS in rhesus monkeys by cytokine-augmented DNA vaccination (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-10-20
    Description: With accumulating evidence indicating the importance of cytotoxic T lymphocytes (CTLs) in containing human immunodeficiency virus-1 (HIV-1) replication in infected individuals, strategies are being pursued to elicit virus-specific CTLs with prototype HIV-1 vaccines. Here, we report the protective efficacy of vaccine-elicited immune responses against a pathogenic SHIV-89.6P challenge in rhesus monkeys. Immune responses were elicited by DNA vaccines expressing SIVmac239 Gag and HIV-1 89.6P Env, augmented by the administration of the purified fusion protein IL-2/Ig, consisting of interleukin-2 (IL-2) and the Fc portion of immunoglobulin G (IgG), or a plasmid encoding IL-2/Ig. After SHIV-89.6P infection, sham-vaccinated monkeys developed weak CTL responses, rapid loss of CD4+ T cells, no virus-specific CD4+ T cell responses, high setpoint viral loads, significant clinical disease progression, and death in half of the animals by day 140 after challenge. In contrast, all monkeys that received the DNA vaccines augmented with IL-2/Ig were infected, but demonstrated potent secondary CTL responses, stable CD4+ T cell counts, preserved virus-specific CD4+ T cell responses, low to undetectable setpoint viral loads, and no evidence of clinical disease or mortality by day 140 after challenge.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barouch, D H -- Santra, S -- Schmitz, J E -- Kuroda, M J -- Fu, T M -- Wagner, W -- Bilska, M -- Craiu, A -- Zheng, X X -- Krivulka, G R -- Beaudry, K -- Lifton, M A -- Nickerson, C E -- Trigona, W L -- Punt, K -- Freed, D C -- Guan, L -- Dubey, S -- Casimiro, D -- Simon, A -- Davies, M E -- Chastain, M -- Strom, T B -- Gelman, R S -- Montefiori, D C -- Lewis, M G -- Emini, E A -- Shiver, J W -- Letvin, N L -- AI-65301/AI/NIAID NIH HHS/ -- AI-85343/AI/NIAID NIH HHS/ -- CA-50139/CA/NCI NIH HHS/ -- P01 AI041521/AI/NIAID NIH HHS/ -- R01 CA050139/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 2000 Oct 20;290(5491):486-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA. dan_barouch@hotmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11039923" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines/*therapeutic use ; Acquired Immunodeficiency Syndrome/*prevention & control ; Animals ; Antibodies, Viral/blood/immunology ; CD4 Lymphocyte Count ; CD4-Positive T-Lymphocytes/immunology ; Disease Progression ; HIV Antibodies/blood/immunology ; HIV Infections/immunology/*therapy/virology ; *HIV-1/genetics/immunology/physiology ; Humans ; Interleukin-2/genetics/immunology/*therapeutic use ; Lymphocyte Activation ; Macaca mulatta ; Neutralization Tests ; Recombinant Fusion Proteins/therapeutic use ; Simian Acquired Immunodeficiency Syndrome/immunology/prevention & ; control/therapy/virology ; Simian Immunodeficiency Virus/genetics/immunology/physiology ; T-Lymphocytes, Cytotoxic/immunology ; Vaccination ; Vaccines, DNA/*therapeutic use ; Viral Load ; Viremia ; Virus Replication
    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
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 9
    facet.materialart.
    Unknown
    The ancient drug salicylate directly activates AMP-activated protein kinase (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-04-21
    Description: Salicylate, a plant product, has been in medicinal use since ancient times. More recently, it has been replaced by synthetic derivatives such as aspirin and salsalate, both of which are rapidly broken down to salicylate in vivo. At concentrations reached in plasma after administration of salsalate or of aspirin at high doses, salicylate activates adenosine monophosphate-activated protein kinase (AMPK), a central regulator of cell growth and metabolism. Salicylate binds at the same site as the synthetic activator A-769662 to cause allosteric activation and inhibition of dephosphorylation of the activating phosphorylation site, threonine-172. In AMPK knockout mice, effects of salicylate to increase fat utilization and to lower plasma fatty acids in vivo were lost. Our results suggest that AMPK activation could explain some beneficial effects of salsalate and aspirin in humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3399766/" 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/PMC3399766/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hawley, Simon A -- Fullerton, Morgan D -- Ross, Fiona A -- Schertzer, Jonathan D -- Chevtzoff, Cyrille -- Walker, Katherine J -- Peggie, Mark W -- Zibrova, Darya -- Green, Kevin A -- Mustard, Kirsty J -- Kemp, Bruce E -- Sakamoto, Kei -- Steinberg, Gregory R -- Hardie, D Grahame -- 080982/Wellcome Trust/United Kingdom -- 097726/Wellcome Trust/United Kingdom -- MC_U127088492/Medical Research Council/United Kingdom -- Canadian Institutes of Health Research/Canada -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2012 May 18;336(6083):918-22. doi: 10.1126/science.1215327. Epub 2012 Apr 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell Signalling and Immunology, College of Life Sciences, University of Dundee, Dundee DD1 5EH, Scotland, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22517326" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/genetics/*metabolism ; Amino Acid Substitution ; Animals ; Aspirin/pharmacology ; Binding Sites ; Carbohydrate Metabolism/drug effects ; Cell Line ; Enzyme Activation ; Enzyme Activators/pharmacology ; HEK293 Cells ; Humans ; Lipid Metabolism/drug effects ; Liver/drug effects/metabolism ; Mice ; Mice, Knockout ; Mutation ; Oxygen Consumption/drug effects ; Phosphorylation ; Pyrones/pharmacology ; Rats ; Salicylates/blood/*metabolism/*pharmacology ; Thiophenes/pharmacology
    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
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 10
    facet.materialart.
    Unknown
    An abundance of rare functional variants in 202 drug target genes sequenced in 14,002 people (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-05-19
    Description: Rare genetic variants contribute to complex disease risk; however, the abundance of rare variants in human populations remains unknown. We explored this spectrum of variation by sequencing 202 genes encoding drug targets in 14,002 individuals. We find rare variants are abundant (1 every 17 bases) and geographically localized, so that even with large sample sizes, rare variant catalogs will be largely incomplete. We used the observed patterns of variation to estimate population growth parameters, the proportion of variants in a given frequency class that are putatively deleterious, and mutation rates for each gene. We conclude that because of rapid population growth and weak purifying selection, human populations harbor an abundance of rare variants, many of which are deleterious and have relevance to understanding disease risk.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4319976/" 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/PMC4319976/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, Matthew R -- Wegmann, Daniel -- Ehm, Margaret G -- Kessner, Darren -- St Jean, Pamela -- Verzilli, Claudio -- Shen, Judong -- Tang, Zhengzheng -- Bacanu, Silviu-Alin -- Fraser, Dana -- Warren, Liling -- Aponte, Jennifer -- Zawistowski, Matthew -- Liu, Xiao -- Zhang, Hao -- Zhang, Yong -- Li, Jun -- Li, Yun -- Li, Li -- Woollard, Peter -- Topp, Simon -- Hall, Matthew D -- Nangle, Keith -- Wang, Jun -- Abecasis, Goncalo -- Cardon, Lon R -- Zollner, Sebastian -- Whittaker, John C -- Chissoe, Stephanie L -- Novembre, John -- Mooser, Vincent -- T32 HG002536/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2012 Jul 6;337(6090):100-4. doi: 10.1126/science.1217876. Epub 2012 May 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Quantitative Sciences, GlaxoSmithKline (GSK), Research Triangle Park, NC 27709, USA. matthew.r.nelson@gsk.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22604722" target="_blank"〉PubMed〈/a〉
    Keywords: African Americans/genetics ; Asian Continental Ancestry Group ; Disease/*genetics ; European Continental Ancestry Group/genetics ; Gene Frequency ; Genetic Association Studies ; Genetic Predisposition to Disease ; *Genetic Variation ; *Genome, Human ; Geography ; High-Throughput Nucleotide Sequencing ; Humans ; Molecular Targeted Therapy ; Multifactorial Inheritance ; Mutation Rate ; Pharmacogenetics ; Phenotype ; Polymorphism, Single Nucleotide ; Population Growth ; Sample Size ; Selection, Genetic
    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
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...