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  • Male  (6)
  • Life and Medical Sciences
  • American Association for the Advancement of Science (AAAS)  (6)
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  • 1
    Publication Date: 2003-01-25
    Description: Caloric restriction has been shown to increase longevity in organisms ranging from yeast to mammals. In some organisms, this has been associated with a decreased fat mass and alterations in insulin/insulin-like growth factor 1 (IGF-1) pathways. To further explore these associations with enhanced longevity, we studied mice with a fat-specific insulin receptor knockout (FIRKO). These animals have reduced fat mass and are protected against age-related obesity and its subsequent metabolic abnormalities, although their food intake is normal. Both male and female FIRKO mice were found to have an increase in mean life-span of approximately 134 days (18%), with parallel increases in median and maximum life-spans. Thus, a reduction of fat mass without caloric restriction can be associated with increased longevity in mice, possibly through effects on insulin signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bluher, Matthias -- Kahn, Barbara B -- Kahn, C Ronald -- DK 30136/DK/NIDDK NIH HHS/ -- DK 43051/DK/NIDDK NIH HHS/ -- DK 56116/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2003 Jan 24;299(5606):572-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Joslin Diabetes Center and Department of Medicine, Harvard Medical School, One Joslin Place, Boston, MA, 02215 USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12543978" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/*anatomy & histology/*metabolism ; Aging ; Animals ; Body Constitution ; Body Weight ; Caloric Restriction ; Eating ; Female ; Insulin/metabolism ; Insulin-Like Growth Factor I/metabolism ; *Longevity ; Male ; Mice ; Mice, Knockout ; Receptor, Insulin/*genetics/metabolism ; Signal Transduction ; *Thinness
    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: 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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  • 3
    Publication Date: 2010-01-16
    Description: Over the past two decades, HIV resistance to antiretroviral drugs (ARVs) has risen to high levels in the wealthier countries of the world, which are able to afford widespread treatment. We have gained insights into the evolution and transmission dynamics of ARV resistance by designing a biologically complex multistrain network model. With this model, we traced the evolutionary history of ARV resistance in San Francisco and predict its future dynamics. By using classification and regression trees, we identified the key immunologic, virologic, and treatment factors that increase ARV resistance. Our modeling shows that 60% of the currently circulating ARV-resistant strains in San Francisco are capable of causing self-sustaining epidemics, because each individual infected with one of these strains can cause, on average, more than one new resistant infection. It is possible that a new wave of ARV-resistant strains that pose a substantial threat to global public health is emerging.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, Robert J -- Okano, Justin T -- Kahn, James S -- Bodine, Erin N -- Blower, Sally -- K24RR024369/RR/NCRR NIH HHS/ -- P30-AI27763/AI/NIAID NIH HHS/ -- R01 AI041935/AI/NIAID NIH HHS/ -- R18-HS017784/HS/AHRQ HHS/ -- New York, N.Y. -- Science. 2010 Feb 5;327(5966):697-701. doi: 10.1126/science.1180556. Epub 2010 Jan 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Biomedical Modeling, Semel Institute of Neuroscience & Human Behavior, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA 90024, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20075214" target="_blank"〉PubMed〈/a〉
    Keywords: Anti-HIV Agents/*pharmacology/therapeutic use ; Antiretroviral Therapy, Highly Active ; Computer Simulation ; Disease Outbreaks ; Drug Resistance, Multiple, Viral ; *Drug Resistance, Viral ; Drug Therapy, Combination ; Evolution, Molecular ; Forecasting ; HIV/*drug effects/genetics ; HIV Infections/drug therapy/epidemiology/*transmission/*virology ; HIV Protease Inhibitors/pharmacology/therapeutic use ; Homosexuality, Male ; Humans ; Male ; Models, Statistical ; Monte Carlo Method ; Probability ; Reverse Transcriptase Inhibitors/pharmacology/therapeutic use ; San Francisco/epidemiology
    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: 2005-08-27
    Description: A defect in Klotho gene expression in mice accelerates the degeneration of multiple age-sensitive traits. Here, we show that overexpression of Klotho in mice extends life span. Klotho protein functions as a circulating hormone that binds to a cell-surface receptor and represses intracellular signals of insulin and insulin-like growth factor 1 (IGF1), an evolutionarily conserved mechanism for extending life span. Alleviation of aging-like phenotypes in Klotho-deficient mice was observed by perturbing insulin and IGF1 signaling, suggesting that Klotho-mediated inhibition of insulin and IGF1 signaling contributes to its anti-aging properties. Klotho protein may function as an anti-aging hormone in mammals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2536606/" 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/PMC2536606/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kurosu, Hiroshi -- Yamamoto, Masaya -- Clark, Jeremy D -- Pastor, Johanne V -- Nandi, Animesh -- Gurnani, Prem -- McGuinness, Owen P -- Chikuda, Hirotaka -- Yamaguchi, Masayuki -- Kawaguchi, Hiroshi -- Shimomura, Iichiro -- Takayama, Yoshiharu -- Herz, Joachim -- Kahn, C Ronald -- Rosenblatt, Kevin P -- Kuro-o, Makoto -- R01 AG019712/AG/NIA NIH HHS/ -- R01 AG019712-05/AG/NIA NIH HHS/ -- R01 AG025326/AG/NIA NIH HHS/ -- R01 AG025326-03/AG/NIA NIH HHS/ -- R01AG19712/AG/NIA NIH HHS/ -- R01AG25326/AG/NIA NIH HHS/ -- R37 HL063762/HL/NHLBI NIH HHS/ -- U24 DK059637/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2005 Sep 16;309(5742):1829-33. Epub 2005 Aug 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Texas (UT) Southwestern Medical Center at Dallas, 5323 Harry Hines Bouleuvard, Dallas, TX 75390-9072, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16123266" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/genetics/*physiology ; Animals ; Blood Glucose/analysis ; Cell Line ; Cell Line, Tumor ; Eating ; Female ; Glucuronidase ; Insulin/blood/metabolism ; Insulin Resistance ; Insulin-Like Growth Factor I/metabolism/pharmacology ; Ligands ; Longevity/genetics/*physiology ; Male ; Membrane Proteins/chemistry/*genetics/pharmacology/*physiology ; Mice ; Mice, Transgenic ; Myoblasts/metabolism ; Oxygen Consumption ; Peptide Fragments/chemistry/pharmacology ; Phosphorylation ; Receptor, IGF Type 1/metabolism ; Receptor, Insulin/metabolism ; Receptors, Cell Surface/metabolism ; Recombinant Proteins/chemistry/isolation & purification/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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  • 5
    Publication Date: 2008-05-10
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3501984/" 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/PMC3501984/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Potts, Malcolm -- Halperin, Daniel T -- Kirby, Douglas -- Swidler, Ann -- Marseille, Elliot -- Klausner, Jeffrey D -- Hearst, Norman -- Wamai, Richard G -- Kahn, James G -- Walsh, Julia -- R01 DA015612/DA/NIDA NIH HHS/ -- R01 DA015612-08/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2008 May 9;320(5877):749-50. doi: 10.1126/science.1153843.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Public Health, University of California at Berkeley, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18467575" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/diagnosis/epidemiology/*prevention & control ; Africa/epidemiology ; Circumcision, Male ; Condoms/utilization ; Disease Outbreaks/*prevention & control ; Female ; Humans ; Male ; Public Health ; Sexual Abstinence ; Sexual Partners ; Sexually Transmitted Diseases/prevention & control
    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
    Publication Date: 2015-07-25
    Description: Leslie et al. (Reports, 16 January 2015, p. 262) concluded that "expectations of brilliance" explained the gender makeup of academic disciplines. We reestimated their models after adding measures of disaggregated Graduate Record Examination scores by field. Our results indicated that female representation among Ph.D. recipients is associated with the field's mathematical content and that faculty beliefs about innate ability were irrelevant.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ginther, Donna K -- Kahn, Shulamit -- 1R01AG36820-01/AG/NIA NIH HHS/ -- R01 AG036820/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2015 Jul 24;349(6246):391. doi: 10.1126/science.aaa9632. Epub 2015 Jul 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Economics, Center for Science, Technology and Economic Policy, Institute for Policy and Social Research, University of Kansas, Lawrence, KS 66045, USA. National Bureau of Economic Research, Cambridge, MA 02138, USA. dginther@ku.edu. ; Questrom School of Business, Boston University, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26206926" target="_blank"〉PubMed〈/a〉
    Keywords: *Aptitude ; *Attitude ; Female ; Humans ; *Intelligence ; Male ; Natural Science Disciplines/*manpower ; *Sexism ; Social Sciences/*manpower
    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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