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  • Male  (4)
  • American Association for the Advancement of Science (AAAS)  (4)
  • American Geophysical Union (AGU)
  • 2000-2004  (4)
  • 2004  (4)
Collection
Publisher
  • American Association for the Advancement of Science (AAAS)  (4)
  • American Geophysical Union (AGU)
Years
  • 2000-2004  (4)
Year
  • 1
    Publication Date: 2004-07-27
    Description: Psychologists, economists, and advertising moguls have long known that human decision-making is strongly influenced by the behavior of others. A rapidly accumulating body of evidence suggests that the same is true in animals. Individuals can use information arising from cues inadvertently produced by the behavior of other individuals with similar requirements. Many of these cues provide public information about the quality of alternatives. The use of public information is taxonomically widespread and can enhance fitness. Public information can lead to cultural evolution, which we suggest may then affect biological evolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Danchin, Etienne -- Giraldeau, Luc-Alain -- Valone, Thomas J -- Wagner, Richard H -- New York, N.Y. -- Science. 2004 Jul 23;305(5683):487-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉U.P.M.C. CNRS-UMR7625, Bat A-7e etage-Case 237, 7 quai Saint Bernard, 75252 Paris Cedex 05, France. edanchin@snv.jussieu.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15273386" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior, Animal ; Biological Evolution ; Cues ; *Cultural Evolution ; *Decision Making ; Environment ; Feeding Behavior ; Female ; Genes ; Humans ; Male ; Reproduction ; Sexual Behavior, Animal
    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: 2004-05-01
    Description: Receptor tyrosine kinase genes were sequenced in non-small cell lung cancer (NSCLC) and matched normal tissue. Somatic mutations of the epidermal growth factor receptor gene EGFR were found in 15of 58 unselected tumors from Japan and 1 of 61 from the United States. Treatment with the EGFR kinase inhibitor gefitinib (Iressa) causes tumor regression in some patients with NSCLC, more frequently in Japan. EGFR mutations were found in additional lung cancer samples from U.S. patients who responded to gefitinib therapy and in a lung adenocarcinoma cell line that was hypersensitive to growth inhibition by gefitinib, but not in gefitinib-insensitive tumors or cell lines. These results suggest that EGFR mutations may predict sensitivity to gefitinib.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paez, J Guillermo -- Janne, Pasi A -- Lee, Jeffrey C -- Tracy, Sean -- Greulich, Heidi -- Gabriel, Stacey -- Herman, Paula -- Kaye, Frederic J -- Lindeman, Neal -- Boggon, Titus J -- Naoki, Katsuhiko -- Sasaki, Hidefumi -- Fujii, Yoshitaka -- Eck, Michael J -- Sellers, William R -- Johnson, Bruce E -- Meyerson, Matthew -- New York, N.Y. -- Science. 2004 Jun 4;304(5676):1497-500. Epub 2004 Apr 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Medical Oncology and Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15118125" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/drug therapy/genetics/metabolism ; Amino Acid Motifs ; Amino Acid Sequence ; Amino Acid Substitution ; Antineoplastic Agents/pharmacology/therapeutic use ; Carcinoma, Non-Small-Cell Lung/drug therapy/*genetics/metabolism ; Cell Line, Tumor ; Controlled Clinical Trials as Topic ; Enzyme Inhibitors/pharmacology/therapeutic use ; Female ; *Genes, erbB-1 ; Humans ; Japan ; Lung Neoplasms/drug therapy/*genetics/metabolism ; Male ; Molecular Sequence Data ; *Mutation ; Mutation, Missense ; Phosphorylation ; Protein Conformation ; Protein Structure, Tertiary ; Quinazolines/pharmacology/*therapeutic use ; Receptor, Epidermal Growth Factor/*antagonists & ; inhibitors/chemistry/genetics/metabolism ; Sequence Deletion ; Treatment Outcome ; United States
    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: 2004-04-10
    Description: Susceptibility to asthma depends on variation at an unknown number of genetic loci. To identify susceptibility genes on chromosome 7p, we adopted a hierarchical genotyping design, leading to the identification of a 133-kilobase risk-conferring segment containing two genes. One of these coded for an orphan G protein-coupled receptor named GPRA (G protein-coupled receptor for asthma susceptibility), which showed distinct distribution of protein isoforms between bronchial biopsies from healthy and asthmatic individuals. In three cohorts from Finland and Canada, single nucleotide polymorphism-tagged haplotypes associated with high serum immunoglobulin E or asthma. The murine ortholog of GPRA was up-regulated in a mouse model of ovalbumin-induced inflammation. Together, these data implicate GPRA in the pathogenesis of atopy and asthma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Laitinen, Tarja -- Polvi, Anne -- Rydman, Pia -- Vendelin, Johanna -- Pulkkinen, Ville -- Salmikangas, Paula -- Makela, Siru -- Rehn, Marko -- Pirskanen, Asta -- Rautanen, Anna -- Zucchelli, Marco -- Gullsten, Harriet -- Leino, Marina -- Alenius, Harri -- Petays, Tuula -- Haahtela, Tari -- Laitinen, Annika -- Laprise, Catherine -- Hudson, Thomas J -- Laitinen, Lauri A -- Kere, Juha -- New York, N.Y. -- Science. 2004 Apr 9;304(5668):300-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉GeneOS Limited, 00251 Helsinki, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15073379" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Alternative Splicing ; Animals ; Asthma/*genetics/metabolism ; Bronchi/chemistry/cytology ; Chromosomes, Human, Pair 7/*genetics ; Epithelial Cells/chemistry ; Female ; Finland ; Gene Expression ; Genes ; Genetic Linkage ; *Genetic Predisposition to Disease ; Genetic Variation ; Genotype ; *Haplotypes ; Humans ; Hypersensitivity/genetics/metabolism ; Immunoglobulin E/blood ; Inflammation/genetics ; Lung/metabolism ; Male ; Mice ; Myocytes, Smooth Muscle/chemistry ; Polymorphism, Single Nucleotide ; Quebec ; Receptors, G-Protein-Coupled/analysis/*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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  • 4
    Publication Date: 2004-10-23
    Description: The "Down syndrome critical region" (DSCR) is a chromosome 21 segment purported to contain genes responsible for many features of Down syndrome (DS), including craniofacial dysmorphology. We used chromosome engineering to create mice that were trisomic or monosomic for only the mouse chromosome segment orthologous to the DSCR and assessed dysmorphologies of the craniofacial skeleton that show direct parallels with DS in mice with a larger segmental trisomy. The DSCR genes were not sufficient and were largely not necessary to produce the facial phenotype. These results refute specific predictions of the prevailing hypothesis of gene action in DS.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4019810/" 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/PMC4019810/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olson, L E -- Richtsmeier, J T -- Leszl, J -- Reeves, R H -- F33 DE005706/DE/NIDCR NIH HHS/ -- HD24605/HD/NICHD NIH HHS/ -- HD38384/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2004 Oct 22;306(5696):687-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, 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/15499018" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Deletion ; Chromosomes, Human, Pair 21/*genetics ; Chromosomes, Mammalian/*genetics ; Craniofacial Abnormalities/genetics ; Crosses, Genetic ; *Disease Models, Animal ; Down Syndrome/*genetics/pathology ; Female ; Gene Dosage ; Gene Duplication ; Gene Targeting ; Genetic Vectors ; Humans ; Karyotyping ; Male ; Mandible/abnormalities ; Mice ; Mice, Inbred C57BL ; Monosomy ; Phenotype ; Recombination, Genetic ; Skull/abnormalities ; *Trisomy
    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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