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  • 1
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    Global biodiversity scenarios for the year 2100 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-10
    Description: Scenarios of changes in biodiversity for the year 2100 can now be developed based on scenarios of changes in atmospheric carbon dioxide, climate, vegetation, and land use and the known sensitivity of biodiversity to these changes. This study identified a ranking of the importance of drivers of change, a ranking of the biomes with respect to expected changes, and the major sources of uncertainties. For terrestrial ecosystems, land-use change probably will have the largest effect, followed by climate change, nitrogen deposition, biotic exchange, and elevated carbon dioxide concentration. For freshwater ecosystems, biotic exchange is much more important. Mediterranean climate and grassland ecosystems likely will experience the greatest proportional change in biodiversity because of the substantial influence of all drivers of biodiversity change. Northern temperate ecosystems are estimated to experience the least biodiversity change because major land-use change has already occurred. Plausible changes in biodiversity in other biomes depend on interactions among the causes of biodiversity change. These interactions represent one of the largest uncertainties in projections of future biodiversity change.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sala, O E -- Chapin, F S 3rd -- Armesto, J J -- Berlow, E -- Bloomfield, J -- Dirzo, R -- Huber-Sanwald, E -- Huenneke, L F -- Jackson, R B -- Kinzig, A -- Leemans, R -- Lodge, D M -- Mooney, H A -- Oesterheld, M -- Poff, N L -- Sykes, M T -- Walker, B H -- Walker, M -- Wall, D H -- New York, N.Y. -- Science. 2000 Mar 10;287(5459):1770-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Instituto de Investigaciones Fisiologicas y Ecologicas vinculadas a la Agricultura, Faculty of Agronomy, University of Buenos Aires, Avenida San Martin 4453, Buenos Aires 1417, Argentina. sala@ifeva.edu.ar〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10710299" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture ; Animals ; Atmosphere ; Carbon Dioxide ; Climate ; *Ecosystem ; Fresh Water ; Models, Biological ; Nitrogen
    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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    Induction of mucosal and systemic immunity to a recombinant simian immunodeficiency viral protein (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-11-20
    Description: Heterosexual transmission through the cervico-vaginal mucosa is the principal route of human immunodeficiency virus (HIV) infection in Africa and is increasing in the United States and Europe. Vaginal immunization with simian immunodeficiency virus (SIV) had not yet been studied in nonhuman primates. Immune responses in macaques were investigated by stimulation of the genital and gut-associated lymphoid tissue with a recombinant, particulate SIV antigen. Vaginal, followed by oral, administration of the vaccine elicited three types of immunity: (i) gag protein p27-specific, secretory immunoglobulin A (IgA) and immunoglobulin G (IgG) in the vaginal fluid, (ii) specific CD4+ T cell proliferation and helper function in B cell p27-specific IgA synthesis in the genital lymph nodes, and (iii) specific serum IgA and IgG, with CD4+ T cell proliferative and helper functions in the circulating blood.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lehner, T -- Bergmeier, L A -- Panagiotidi, C -- Tao, L -- Brookes, R -- Klavinskis, L S -- Walker, P -- Walker, J -- Ward, R G -- Hussain, L -- New York, N.Y. -- Science. 1992 Nov 20;258(5086):1365-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunology, United Medical School, Guy's Hospital, London, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1360702" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Oral ; Animals ; Antibodies, Viral/analysis ; CD4-Positive T-Lymphocytes/immunology ; Female ; Gene Products, gag/*immunology ; Immunity ; Immunoglobulin A/immunology ; Immunoglobulin G/immunology ; Macaca mulatta ; Mucous Membrane/immunology ; Recombinant Proteins/immunology ; Saliva/immunology ; Simian Acquired Immunodeficiency Syndrome/*immunology ; Simian Immunodeficiency Virus/*immunology ; T-Lymphocytes, Helper-Inducer/immunology ; Vaccines, Synthetic/administration & dosage/*immunology ; Vagina/immunology
    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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    Linkage disequilibrium and recombination in hominid mitochondrial DNA (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-05
    Description: The assumption that human mitochondrial DNA is inherited from one parent only and therefore does not recombine is questionable. Linkage disequilibrium in human and chimpanzee mitochondrial DNA declines as a function of the distance between sites. This pattern can be attributed to one mechanism only: recombination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Awadalla, P -- Eyre-Walker, A -- Smith, J M -- New York, N.Y. -- Science. 1999 Dec 24;286(5449):2524-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Cell, Animal and Population Biology, University of Edinburgh, Edinburgh EH9 1JT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10617471" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA, Mitochondrial/*genetics ; Evolution, Molecular ; Fathers ; Female ; Hominidae/*genetics ; Humans ; *Linkage Disequilibrium ; Male ; NADH Dehydrogenase/genetics ; Pan troglodytes/*genetics ; Polymorphism, Restriction Fragment Length ; *Recombination, Genetic
    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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    Prevention of chemotherapy-induced alopecia in rats by CDK inhibitors (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-01-06
    Description: Most traditional cytotoxic anticancer agents ablate the rapidly dividing epithelium of the hair follicle and induce alopecia (hair loss). Inhibition of cyclin-dependent kinase 2 (CDK2), a positive regulator of eukaryotic cell cycle progression, may represent a therapeutic strategy for prevention of chemotherapy-induced alopecia (CIA) by arresting the cell cycle and reducing the sensitivity of the epithelium to many cell cycle-active antitumor agents. Potent small-molecule inhibitors of CDK2 were developed using structure-based methods. Topical application of these compounds in a neonatal rat model of CIA reduced hair loss at the site of application in 33 to 50% of the animals. Thus, inhibition of CDK2 represents a potentially useful approach for the prevention of CIA in cancer patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davis, S T -- Benson, B G -- Bramson, H N -- Chapman, D E -- Dickerson, S H -- Dold, K M -- Eberwein, D J -- Edelstein, M -- Frye, S V -- Gampe Jr, R T -- Griffin, R J -- Harris, P A -- Hassell, A M -- Holmes, W D -- Hunter, R N -- Knick, V B -- Lackey, K -- Lovejoy, B -- Luzzio, M J -- Murray, D -- Parker, P -- Rocque, W J -- Shewchuk, L -- Veal, J M -- Walker, D H -- Kuyper, L F -- New York, N.Y. -- Science. 2001 Jan 5;291(5501):134-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Glaxo Wellcome Research and Development, Research Triangle Park, NC 27709, USA. std41085@glaxowellcome.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11141566" target="_blank"〉PubMed〈/a〉
    Keywords: Alopecia/*chemically induced/*prevention & control ; Animals ; Animals, Newborn ; Antineoplastic Agents/*toxicity ; Antineoplastic Combined Chemotherapy Protocols/toxicity ; Apoptosis/drug effects ; *CDC2-CDC28 Kinases ; Cell Cycle/drug effects ; Cell Line ; Cyclin-Dependent Kinase 2 ; Cyclin-Dependent Kinases/*antagonists & inhibitors/metabolism ; Cyclophosphamide/toxicity ; Cytoprotection/drug effects ; DNA/biosynthesis ; Doxorubicin/toxicity ; Drug Design ; Enzyme Inhibitors/chemical synthesis/chemistry/*pharmacology ; Epithelium/drug effects ; Etoposide/toxicity ; Hair Follicle/cytology/*drug effects ; Humans ; Indoles/chemical synthesis/chemistry/*pharmacology ; Mice ; Mice, SCID ; Phosphorylation ; Protein-Serine-Threonine Kinases/*antagonists & inhibitors/metabolism ; Rats ; Retinoblastoma Protein/metabolism ; Scalp/transplantation ; Sulfonamides/chemical synthesis/chemistry/*pharmacology ; Transplantation, Heterologous
    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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    A Drosophila mechanosensory transduction channel (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-04-01
    Description: Mechanosensory transduction underlies a wide range of senses, including proprioception, touch, balance, and hearing. The pivotal element of these senses is a mechanically gated ion channel that transduces sound, pressure, or movement into changes in excitability of specialized sensory cells. Despite the prevalence of mechanosensory systems, little is known about the molecular nature of the transduction channels. To identify such a channel, we analyzed Drosophila melanogaster mechanoreceptive mutants for defects in mechanosensory physiology. Loss-of-function mutations in the no mechanoreceptor potential C (nompC) gene virtually abolished mechanosensory signaling. nompC encodes a new ion channel that is essential for mechanosensory transduction. As expected for a transduction channel, D. melanogaster NOMPC and a Caenorhabditis elegans homolog were selectively expressed in mechanosensory organs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walker, R G -- Willingham, A T -- Zuker, C S -- 5T32GM08107/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Mar 24;287(5461):2229-34.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Howard Hughes Medical Institute, University of California, San Diego,CA 92093-0649, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10744543" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Adaptation, Physiological ; Amino Acid Sequence ; Animals ; Caenorhabditis elegans/genetics/physiology ; Chromosome Mapping ; Cloning, Molecular ; Dendrites/physiology ; *Drosophila Proteins ; Drosophila melanogaster/genetics/*physiology ; Gene Expression Profiling ; Genes, Insect ; Hair Cells, Auditory/physiology ; Insect Proteins/chemistry/genetics/physiology ; Ion Channels/chemistry/*genetics/*physiology ; Mechanoreceptors/*physiology ; Molecular Sequence Data ; Mutation ; Neurons, Afferent/*physiology ; Patch-Clamp Techniques ; Physical Stimulation ; Proprioception ; Sensation/physiology ; Sense Organs/physiology ; Signal Transduction ; Touch ; Transient Receptor Potential Channels
    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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    The glucocorticoid receptor: rapid exchange with regulatory sites in living cells (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-26
    Description: Steroid receptors bind to site-specific response elements in chromatin and modulate gene expression in a hormone-dependent fashion. With the use of a tandem array of mouse mammary tumor virus reporter elements and a form of glucocorticoid receptor labeled with green fluorescent protein, targeting of the receptor to response elements in live mouse cells was observed. Photobleaching experiments provide direct evidence that the hormone-occupied receptor undergoes rapid exchange between chromatin and the nucleoplasmic compartment. Thus, the interaction of regulatory proteins with target sites in chromatin is a more dynamic process than previously believed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McNally, J G -- Muller, W G -- Walker, D -- Wolford, R -- Hager, G L -- New York, N.Y. -- Science. 2000 Feb 18;287(5456):1262-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Receptor Biology and Gene Expression, Building 41, Room B602, National Cancer Institute, Bethesda, MD 20892-5055, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10678832" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Cell Line, Transformed ; Cell Nucleus/metabolism ; Chromatin/*metabolism ; Dexamethasone/metabolism/*pharmacology ; Green Fluorescent Proteins ; In Situ Hybridization, Fluorescence ; Ligands ; Luminescent Proteins ; Mammary Tumor Virus, Mouse/genetics ; Mice ; Microscopy, Confocal ; Microscopy, Fluorescence ; Nucleosomes/metabolism ; Receptors, Glucocorticoid/*metabolism ; *Response Elements ; *Terminal Repeat Sequences
    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
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    Extension of life-span with superoxide dismutase/catalase mimetics (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-09-01
    Description: We tested the theory that reactive oxygen species cause aging. We augmented the natural antioxidant systems of Caenorhabditis elegans with small synthetic superoxide dismutase/catalase mimetics. Treatment of wild-type worms increased their mean life-span by a mean of 44 percent, and treatment of prematurely aging worms resulted in normalization of their life-span (a 67 percent increase). It appears that oxidative stress is a major determinant of life-span and that it can be counteracted by pharmacological intervention.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Melov, S -- Ravenscroft, J -- Malik, S -- Gill, M S -- Walker, D W -- Clayton, P E -- Wallace, D C -- Malfroy, B -- Doctrow, S R -- Lithgow, G J -- AG-13154/AG/NIA NIH HHS/ -- NS21328/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2000 Sep 1;289(5484):1567-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Buck Institute for Age Research, Novato, CA 94949, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10968795" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*drug effects ; Animals ; Antioxidants/*pharmacology ; Caenorhabditis elegans/drug effects/*physiology ; Catalase/*metabolism ; Disorders of Sex Development ; Fertility/drug effects ; Longevity/drug effects ; Molecular Mimicry ; Oxidative Stress ; Reactive Oxygen Species/metabolism ; Superoxide Dismutase/*metabolism
    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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  • 8
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    Similar requirements of a plant symbiont and a mammalian pathogen for prolonged intracellular survival (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-31
    Description: Brucella abortus, a mammalian pathogen, and Rhizobium meliloti, a phylogenetically related plant symbiont, establish chronic infections in their respective hosts. Here a highly conserved B. abortus homolog of the R. meliloti bacA gene, which encodes a putative cytoplasmic membrane transport protein required for symbiosis, was identified. An isogenic B. abortus bacA mutant exhibited decreased survival in macrophages and greatly accelerated clearance from experimentally infected mice compared to the virulent parental strain. Thus, the bacA gene product is critical for the maintenance of two very diverse host-bacterial relationships.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉LeVier, K -- Phillips, R W -- Grippe, V K -- Roop, R M 2nd -- Walker, G C -- GM31030/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Mar 31;287(5462):2492-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10741969" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Bacterial/immunology ; Bacterial Proteins/genetics/*physiology ; Brucella abortus/genetics/*pathogenicity/physiology ; Brucellosis/immunology/*microbiology ; Cells, Cultured ; Female ; Hypersensitivity, Delayed ; Liver/microbiology ; Macrophages/immunology/*microbiology ; Medicago sativa/microbiology ; Membrane Proteins/genetics/*physiology ; *Membrane Transport Proteins ; Mice ; Mice, Inbred BALB C ; Molecular Sequence Data ; Mutagenesis, Insertional ; Sinorhizobium meliloti/genetics/*physiology ; Spleen/microbiology ; Symbiosis ; Virulence
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 9
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    Research ethics. Managing risks of arthropod vector research (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-08-05
    Description: Field research with vectors is an essential aspect of vector biology research and vector-borne disease prevention and control. This type of research, which brings experimental vector manipulations into endemic areas, can present risks to human populations. This paper seeks to stimulate a full discussion within the medical entomology community of the risks associated with vector field research. Such discussions will promote development of a consensus, among investigators, sponsoring agencies and the communities within which the work is done, so that appropriate steps can be taken to minimize and manage the risks, and adequate oversight can be maintained.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aultman, K S -- Walker, E D -- Gifford, F -- Severson, D W -- Beard, C B -- Scott, T W -- New York, N.Y. -- Science. 2000 Jun 30;288(5475):2321-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Parasitology and International Programs Branch, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892-7630, USA. ka6z@nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10917830" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Arthropod Vectors ; *Bioethics ; Biomedical Research ; Ethics, Research ; Humans ; Informed Consent ; Professional Staff Committees ; *Public Health ; Research/*standards ; Research Design ; Research Subjects ; Risk Assessment
    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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  • 10
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    Deleterious mutations and the evolution of sex (2000)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2000-10-13
    Description: It has been suggested that sexual reproduction is maintained because it reduces the load imposed by recurrent deleterious mutations. If rates of deleterious mutation per diploid genome per generation (U) exceed 1, and mutations interact synergistically, then sexuals can overcome their inherent twofold disadvantage. We have tested this hypothesis by estimating genomic point mutation rates for protein-coding genes in a range of animal taxa. We find a positive linear relationship between U and generation time. In species with short generation times, U is predicted to be far below 1, suggesting that sex is not maintained by its capacity to purge the genome of deleterious mutations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keightley, P D -- Eyre-Walker, A -- New York, N.Y. -- Science. 2000 Oct 13;290(5490):331-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Cell, Animal and Population Biology, University of Edinburgh, West Mains Road, Edinburgh EH9 3JT, UK. p.keightley@ed.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11030650" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Birds/genetics/physiology ; Cats/genetics/physiology ; Cattle/genetics/physiology ; DNA Transposable Elements ; Dogs/genetics/physiology ; Drosophila/genetics/physiology ; Female ; Haplorhini/genetics/physiology ; Humans ; Male ; Mutation ; *Point Mutation ; Proteins/genetics ; Rodentia/genetics/physiology ; *Sex ; Sheep/genetics/physiology
    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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