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  • Female  (92)
  • Instrumentation and Photography  (74)
  • 2000-2004  (166)
  • 2003  (89)
  • 2000  (77)
  • 1
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    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
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  • 2
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    Inferring nonneutral evolution from human-chimp-mouse orthologous gene trios (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-13
    Description: Even though human and chimpanzee gene sequences are nearly 99% identical, sequence comparisons can nevertheless be highly informative in identifying biologically important changes that have occurred since our ancestral lineages diverged. We analyzed alignments of 7645 chimpanzee gene sequences to their human and mouse orthologs. These three-species sequence alignments allowed us to identify genes undergoing natural selection along the human and chimp lineage by fitting models that include parameters specifying rates of synonymous and nonsynonymous nucleotide substitution. This evolutionary approach revealed an informative set of genes with significantly different patterns of substitution on the human lineage compared with the chimpanzee and mouse lineages. Partitions of genes into inferred biological classes identified accelerated evolution in several functional classes, including olfaction and nuclear transport. In addition to suggesting adaptive physiological differences between chimps and humans, human-accelerated genes are significantly more likely to underlie major known Mendelian disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clark, Andrew G -- Glanowski, Stephen -- Nielsen, Rasmus -- Thomas, Paul D -- Kejariwal, Anish -- Todd, Melissa A -- Tanenbaum, David M -- Civello, Daniel -- Lu, Fu -- Murphy, Brian -- Ferriera, Steve -- Wang, Gary -- Zheng, Xianqgun -- White, Thomas J -- Sninsky, John J -- Adams, Mark D -- Cargill, Michele -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1960-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671302" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus/genetics ; Amino Acids/metabolism ; Animals ; Biological Evolution ; Computational Biology ; *Evolution, Molecular ; Female ; Genes ; Genetic Diseases, Inborn/genetics ; *Genome ; *Genome, Human ; Humans ; Likelihood Functions ; Male ; Mice/genetics ; Models, Genetic ; Models, Statistical ; Mutation ; Pan troglodytes/*genetics ; Phylogeny ; Proteins/chemistry/genetics ; Pseudogenes ; Receptors, Odorant/genetics ; *Selection, Genetic ; Sequence Alignment ; Sequence Homology, Nucleic Acid ; Signal Transduction/genetics ; Smell/genetics ; Species Specificity
    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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    Inactivation of TNF signaling by rationally designed dominant-negative TNF variants (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-27
    Description: Tumor necrosis factor (TNF) is a key regulator of inflammatory responses and has been implicated in many pathological conditions. We used structure-based design to engineer variant TNF proteins that rapidly form heterotrimers with native TNF to give complexes that neither bind to nor stimulate signaling through TNF receptors. Thus, TNF is inactivated by sequestration. Dominant-negative TNFs represent a possible approach to anti-inflammatory biotherapeutics, and experiments in animal models show that the strategy can attenuate TNF-mediated pathology. Similar rational design could be used to engineer inhibitors of additional TNF superfamily cytokines as well as other multimeric ligands.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steed, Paul M -- Tansey, Malu G -- Zalevsky, Jonathan -- Zhukovsky, Eugene A -- Desjarlais, John R -- Szymkowski, David E -- Abbott, Christina -- Carmichael, David -- Chan, Cheryl -- Cherry, Lisa -- Cheung, Peter -- Chirino, Arthur J -- Chung, Hyo H -- Doberstein, Stephen K -- Eivazi, Araz -- Filikov, Anton V -- Gao, Sarah X -- Hubert, Rene S -- Hwang, Marian -- Hyun, Linus -- Kashi, Sandhya -- Kim, Alice -- Kim, Esther -- Kung, James -- Martinez, Sabrina P -- Muchhal, Umesh S -- Nguyen, Duc-Hanh T -- O'Brien, Christopher -- O'Keefe, Donald -- Singer, Karen -- Vafa, Omid -- Vielmetter, Jost -- Yoder, Sean C -- Dahiyat, Bassil I -- New York, N.Y. -- Science. 2003 Sep 26;301(5641):1895-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Xencor, 111 West Lemon Avenue, Monrovia, CA 91016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14512626" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; Antigens, CD/metabolism ; Apoptosis ; Arthritis, Experimental/drug therapy ; Biopolymers ; Caspases/metabolism ; Cell Line ; Cell Nucleus/metabolism ; Computer Simulation ; Disease Progression ; Enzyme-Linked Immunosorbent Assay ; Female ; Galactosamine/pharmacology ; HeLa Cells ; Humans ; Liver/drug effects ; NF-kappa B/metabolism ; Point Mutation ; *Protein Engineering ; Rats ; Receptors, Tumor Necrosis Factor/metabolism ; Receptors, Tumor Necrosis Factor, Type I ; Receptors, Tumor Necrosis Factor, Type II ; *Signal Transduction ; Transcription Factor RelA ; Transcription, Genetic ; Tumor Necrosis Factor-alpha/*antagonists & ; inhibitors/genetics/metabolism/*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
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    Neurodegeneration prevented by lentiviral vector delivery of GDNF in primate models of Parkinson's disease (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-10-29
    Description: Lentiviral delivery of glial cell line-derived neurotrophic factor (lenti-GDNF) was tested for its trophic effects upon degenerating nigrostriatal neurons in nonhuman primate models of Parkinson's disease (PD). We injected lenti-GDNF into the striatum and substantia nigra of nonlesioned aged rhesus monkeys or young adult rhesus monkeys treated 1 week prior with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Extensive GDNF expression with anterograde and retrograde transport was seen in all animals. In aged monkeys, lenti-GDNF augmented dopaminergic function. In MPTP-treated monkeys, lenti-GDNF reversed functional deficits and completely prevented nigrostriatal degeneration. Additionally, lenti-GDNF injections to intact rhesus monkeys revealed long-term gene expression (8 months). In MPTP-treated monkeys, lenti-GDNF treatment reversed motor deficits in a hand-reach task. These data indicate that GDNF delivery using a lentiviral vector system can prevent nigrostriatal degeneration and induce regeneration in primate models of PD and might be a viable therapeutic strategy for PD patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kordower, J H -- Emborg, M E -- Bloch, J -- Ma, S Y -- Chu, Y -- Leventhal, L -- McBride, J -- Chen, E Y -- Palfi, S -- Roitberg, B Z -- Brown, W D -- Holden, J E -- Pyzalski, R -- Taylor, M D -- Carvey, P -- Ling, Z -- Trono, D -- Hantraye, P -- Deglon, N -- Aebischer, P -- NS40578/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2000 Oct 27;290(5492):767-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurological Sciences, Rush Presbyterian-St. Luke's Medical Center, Chicago, IL 60612, USA. jkordowe@rush.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11052933" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine ; Aging ; Animals ; Antigens, CD/analysis ; Dihydroxyphenylalanine/*analogs & derivatives/metabolism ; Disease Models, Animal ; Dopamine/*metabolism ; Female ; Gene Expression ; *Genetic Therapy ; Genetic Vectors ; Glial Cell Line-Derived Neurotrophic Factor ; Lentivirus/genetics ; Macaca mulatta ; Neostriatum/metabolism/pathology ; Nerve Degeneration/*prevention & control ; *Nerve Growth Factors ; Nerve Tissue Proteins/*genetics/metabolism/therapeutic use ; Neurons/enzymology ; Parkinson Disease/metabolism/pathology/physiopathology/*therapy ; Parkinsonian Disorders/metabolism/pathology/physiopathology/therapy ; Psychomotor Performance ; Substantia Nigra/metabolism/pathology ; Tyrosine 3-Monooxygenase/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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  • 5
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    Role of brain insulin receptor in control of body weight and reproduction (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-09-23
    Description: Insulin receptors (IRs) and insulin signaling proteins are widely distributed throughout the central nervous system (CNS). To study the physiological role of insulin signaling in the brain, we created mice with a neuron-specific disruption of the IR gene (NIRKO mice). Inactivation of the IR had no impact on brain development or neuronal survival. However, female NIRKO mice showed increased food intake, and both male and female mice developed diet-sensitive obesity with increases in body fat and plasma leptin levels, mild insulin resistance, elevated plasma insulin levels, and hypertriglyceridemia. NIRKO mice also exhibited impaired spermatogenesis and ovarian follicle maturation because of hypothalamic dysregulation of luteinizing hormone. Thus, IR signaling in the CNS plays an important role in regulation of energy disposal, fuel metabolism, and reproduction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bruning, J C -- Gautam, D -- Burks, D J -- Gillette, J -- Schubert, M -- Orban, P C -- Klein, R -- Krone, W -- Muller-Wieland, D -- Kahn, C R -- DK31036/DK/NIDDK NIH HHS/ -- DK55326-01A2/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2000 Sep 22;289(5487):2122-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Klinik II und Poliklinik fur Innere Medizin and Center of Molecular Medicine (ZMMK) der Universitat zu Koln, Joseph Stelzmann Strasse 9, 50931 Cologne, Germany. jens.bruening@uni-koeln.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11000114" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue ; Animals ; Blood Glucose/analysis ; *Body Weight ; Brain/*metabolism ; Eating ; Female ; Hypertriglyceridemia/etiology ; Insulin/blood/*physiology ; Insulin Resistance ; Leptin/blood ; Leuprolide/pharmacology ; Luteinizing Hormone/blood ; Male ; Mice ; Mice, Knockout ; Neurons/metabolism ; Obesity/etiology ; Ovarian Follicle/physiology ; Receptor, Insulin/genetics/*physiology ; *Reproduction ; Sex Characteristics ; Signal Transduction ; Spermatogenesis
    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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    Trophoblast L-selectin-mediated adhesion at the maternal-fetal interface (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-18
    Description: Trophoblast adhesion to the uterine wall is the requisite first step of implantation and, subsequently, placentation. At the maternal-fetal interface, we investigated the expression of selectin adhesion systems that enable leukocyte capture from the bloodstream. On the maternal side, human uterine epithelial cells up-regulated selectin oligosaccharide-based ligands during the window of receptivity. On the fetal side, human trophoblasts expressed L-selectin. This ligand-receptor system was functional, because beads coated with the selectin ligand 6-sulfo sLe(x) bound to trophoblasts, and trophoblasts bound to ligand-expressing uterine luminal epithelium in tissue sections. These results suggest that trophoblast L-selectin mediates interactions with the uterus and that this adhesion mechanism may be critical to establishing human pregnancy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Genbacev, Olga D -- Prakobphol, Akraporn -- Foulk, Russell A -- Krtolica, Ana R -- Ilic, Dusko -- Singer, Mark S -- Yang, Zhi-Qiang -- Kiessling, Laura L -- Rosen, Steven D -- Fisher, Susan J -- DE 07244/DE/NIDCR NIH HHS/ -- HL 64597/HL/NHLBI NIH HHS/ -- R37GM23547/GM/NIGMS NIH HHS/ -- U01 HD 42283/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2003 Jan 17;299(5605):405-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Stomatology, Anatomy, and Pharmaceutical Chemistry, University of California, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12532021" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies ; Blastocyst/physiology ; Cell Adhesion ; Cells, Cultured ; *Embryo Implantation ; Endometrium/cytology/metabolism/*physiology ; Epithelial Cells/metabolism ; Female ; Follicular Phase ; Humans ; Immunoblotting ; Jurkat Cells ; L-Selectin/immunology/*metabolism ; Ligands ; Luteal Phase ; Mice ; Microspheres ; Oligosaccharides/*metabolism ; Organ Culture Techniques ; Pregnancy ; Trophoblasts/metabolism/*physiology ; Up-Regulation
    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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    A Low Frequency Radio and Radar Instrument to Explore Jupiter's Icy Moons (2003)
    In:  CASI
    Details
    Publication Date: 2004-10-30
    Description: The addition of a comprehensive wave investigation to the Jupiter Icy Moons Orbiter (JIMO) science payload will provide a broad range of information on the icy moons of Jupiter including the detection of subsurface liquid oceans; mapping of their ionospheres; their interaction with the magnetospheric environment; and on the Jovian magnetosphere. These measurements are obtained through the use of both passive and active (sounding) means over broad frequency ranges. The frequency range of interest extends from less than 1 Hz to 40 MHz for passive measurements, from approximately 1 kHz to a few MHz for magnetospheric and ionospheric sounding, and between 1 and approximately 10 MHz for subsurface radar sounding. An instrument to detect subsurface radar sounding, magnetospheric interactions, and ionospheric sounding is discussed.
    Keywords: Instrumentation and Photography
    Type: Forum on Concepts and Approaches for Jupiter Icy Moons Orbiter; 42; LPI-Contrib-1163
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    NASA TECHNICAL REPORTS
  • 8
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    Mutations in dynein link motor neuron degeneration to defects in retrograde transport (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-06
    Description: Degenerative disorders of motor neurons include a range of progressive fatal diseases such as amyotrophic lateral sclerosis (ALS), spinal-bulbar muscular atrophy (SBMA), and spinal muscular atrophy (SMA). Although the causative genetic alterations are known for some cases, the molecular basis of many SMA and SBMA-like syndromes and most ALS cases is unknown. Here we show that missense point mutations in the cytoplasmic dynein heavy chain result in progressive motor neuron degeneration in heterozygous mice, and in homozygotes this is accompanied by the formation of Lewy-like inclusion bodies, thus resembling key features of human pathology. These mutations exclusively perturb neuron-specific functions of dynein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hafezparast, Majid -- Klocke, Rainer -- Ruhrberg, Christiana -- Marquardt, Andreas -- Ahmad-Annuar, Azlina -- Bowen, Samantha -- Lalli, Giovanna -- Witherden, Abi S -- Hummerich, Holger -- Nicholson, Sharon -- Morgan, P Jeffrey -- Oozageer, Ravi -- Priestley, John V -- Averill, Sharon -- King, Von R -- Ball, Simon -- Peters, Jo -- Toda, Takashi -- Yamamoto, Ayumu -- Hiraoka, Yasushi -- Augustin, Martin -- Korthaus, Dirk -- Wattler, Sigrid -- Wabnitz, Philipp -- Dickneite, Carmen -- Lampel, Stefan -- Boehme, Florian -- Peraus, Gisela -- Popp, Andreas -- Rudelius, Martina -- Schlegel, Juergen -- Fuchs, Helmut -- Hrabe de Angelis, Martin -- Schiavo, Giampietro -- Shima, David T -- Russ, Andreas P -- Stumm, Gabriele -- Martin, Joanne E -- Fisher, Elizabeth M C -- New York, N.Y. -- Science. 2003 May 2;300(5620):808-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurodegenerative Disease, Institute of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730604" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anterior Horn Cells/pathology ; Apoptosis ; *Axonal Transport ; Cell Differentiation ; Cell Movement ; Central Nervous System/embryology ; Chromosome Mapping ; Dimerization ; Dyneins/chemistry/*genetics/*physiology ; Female ; Ganglia, Spinal/pathology ; Golgi Apparatus/metabolism/ultrastructure ; Heterozygote ; Homozygote ; Lewy Bodies/pathology ; Male ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Motor Neuron Disease/*genetics/pathology/physiopathology ; Motor Neurons/*physiology/ultrastructure ; Mutation ; Mutation, Missense ; *Nerve Degeneration ; Peptide Fragments/metabolism ; Phenotype ; Point Mutation ; Spinal Nerves/growth & development ; Tetanus Toxin/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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  • 9
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    Rapid evolution of egg size in captive salmon (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-15
    Description: Captive breeding and release programs, widely used to supplement populations of declining species, minimize juvenile mortality to achieve rapid population growth. However, raising animals in benign environments may promote traits that are adaptive in captivity but maladaptive in nature. In chinook salmon, hatchery rearing relaxes natural selection favoring large eggs, allowing fecundity selection to drive exceptionally rapid evolution of small eggs. Trends toward small eggs are also evident in natural populations heavily supplemented by hatcheries, but not in minimally supplemented populations. Unintentional selection in captivity can lead to rapid changes in critical life-history traits that may reduce the success of supplementation or reintroduction programs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heath, Daniel D -- Heath, John W -- Bryden, Colleen A -- Johnson, Rachel M -- Fox, Charles W -- New York, N.Y. -- Science. 2003 Mar 14;299(5613):1738-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Great Lakes Institute for Environmental Research and Department of Biological Sciences, University of Windsor, 401 Sunset Avenue, Windsor, Ontario N9B 3P4, Canada. dheath@uwindsor.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12637746" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Body Constitution ; Body Weight ; *Breeding ; Conservation of Natural Resources ; Environment ; Female ; Fertility ; *Fisheries ; Ovum/*physiology ; Salmon/genetics/*physiology ; Selection, 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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  • 10
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    Effects of environment on compensatory mutations to ameliorate costs of antibiotic resistance (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-26
    Description: Most types of antibiotic resistance impose a biological cost on bacterial fitness. These costs can be compensated, usually without loss of resistance, by second-site mutations during the evolution of the resistant bacteria in an experimental host or in a laboratory medium. Different fitness-compensating mutations were selected depending on whether the bacteria evolved through serial passage in mice or in a laboratory medium. This difference in mutation spectra was caused by either a growth condition-specific formation or selection of the compensated mutants. These results suggest that bacterial evolution to reduce the costs of antibiotic resistance can take different trajectories within and outside a host.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bjorkman, J -- Nagaev, I -- Berg, O G -- Hughes, D -- Andersson, D I -- New York, N.Y. -- Science. 2000 Feb 25;287(5457):1479-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bacteriology, Swedish Institute for Infectious Disease Control, S-171 82 Solna, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10688795" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Animals ; Anti-Bacterial Agents/*pharmacology ; *Antiporters ; Carrier Proteins/genetics ; Culture Media ; Drug Resistance, Microbial/*genetics ; Escherichia coli Proteins ; Evolution, Molecular ; Female ; Fusidic Acid/pharmacology ; Membrane Proteins/genetics ; Mice ; Mice, Inbred BALB C ; *Mutation ; Peptide Elongation Factor G/genetics ; Ribosomal Proteins/genetics ; Salmonella typhimurium/*drug effects/*genetics/growth & development/metabolism ; Selection, Genetic ; Serial Passage ; Streptomycin/pharmacology ; Suppression, 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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