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  • 1
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    Regulation of longevity and stress resistance by Sch9 in yeast (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-04-09
    Description: The protein kinase Akt/protein kinase B (PKB) is implicated in insulin signaling in mammals and functions in a pathway that regulates longevity and stress resistance in Caenorhabditis elegans. We screened for long-lived mutants in nondividing yeast Saccharomyces cerevisiae and identified mutations in adenylate cyclase and SCH9, which is homologous to Akt/PKB, that increase resistance to oxidants and extend life-span by up to threefold. Stress-resistance transcription factors Msn2/Msn4 and protein kinase Rim15 were required for this life-span extension. These results indicate that longevity is associated with increased investment in maintenance and show that highly conserved genes play similar roles in life-span regulation in S. cerevisiae and higher eukaryotes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fabrizio, P -- Pozza, F -- Pletcher, S D -- Gendron, C M -- Longo, V D -- AG 08761-10/AG/NIA NIH HHS/ -- AG09793/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2001 Apr 13;292(5515):288-90. Epub 2001 Apr 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biogerontology, Andrus Gerontology Center, and Department of Biological Sciences, University of Southern California, Los Angeles, CA 90089-0191, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11292860" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/genetics/metabolism ; Amino Acid Sequence ; Animals ; Caenorhabditis elegans/genetics/physiology ; Culture Media ; Cyclic AMP-Dependent Protein Kinases/metabolism ; DNA Transposable Elements ; DNA-Binding Proteins/genetics/metabolism ; Drosophila/genetics/physiology ; Drug Resistance, Microbial ; Gene Deletion ; Hot Temperature ; Longevity ; Molecular Sequence Data ; Mutagenesis, Insertional ; Oxidants/pharmacology ; Paraquat/pharmacology ; Phenotype ; Protein Kinases/chemistry/genetics/*metabolism ; Saccharomyces cerevisiae/enzymology/genetics/*physiology ; *Saccharomyces cerevisiae Proteins ; Signal Transduction ; Transcription Factors/genetics/metabolism ; Transformation, 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)
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  • 2
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    Extending healthy life span--from yeast to humans (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-04-17
    Description: When the food intake of organisms such as yeast and rodents is reduced (dietary restriction), they live longer than organisms fed a normal diet. A similar effect is seen when the activity of nutrient-sensing pathways is reduced by mutations or chemical inhibitors. In rodents, both dietary restriction and decreased nutrient-sensing pathway activity can lower the incidence of age-related loss of function and disease, including tumors and neurodegeneration. Dietary restriction also increases life span and protects against diabetes, cancer, and cardiovascular disease in rhesus monkeys, and in humans it causes changes that protect against these age-related pathologies. Tumors and diabetes are also uncommon in humans with mutations in the growth hormone receptor, and natural genetic variants in nutrient-sensing pathways are associated with increased human life span. Dietary restriction and reduced activity of nutrient-sensing pathways may thus slow aging by similar mechanisms, which have been conserved during evolution. We discuss these findings and their potential application to prevention of age-related disease and promotion of healthy aging in humans, and the challenge of possible negative side effects.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3607354/" 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/PMC3607354/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fontana, Luigi -- Partridge, Linda -- Longo, Valter D -- AG025135/AG/NIA NIH HHS/ -- AG20642/AG/NIA NIH HHS/ -- GM075308/GM/NIGMS NIH HHS/ -- P30 DK056341/DK/NIDDK NIH HHS/ -- P30DK056341/DK/NIDDK NIH HHS/ -- R01 AG020642/AG/NIA NIH HHS/ -- UL1 RR024992/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2010 Apr 16;328(5976):321-6. doi: 10.1126/science.1172539.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Geriatrics and Nutritional Science, Washington University School of Medicine, St. Louis, MO 63110, USA. lfontana@dom.wustl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20395504" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Caenorhabditis elegans/genetics/physiology ; *Caloric Restriction ; Drosophila/genetics/physiology ; Eating ; Haplorhini ; Humans ; *Longevity ; Mice ; Saccharomyces cerevisiae/genetics/physiology ; *Signal Transduction
    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)
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  • 3
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    Biodemographic trajectories of longevity (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-05-23
    Description: Old-age survival has increased substantially since 1950. Death rates decelerate with age for insects, worms, and yeast, as well as humans. This evidence of extended postreproductive survival is puzzling. Three biodemographic insights--concerning the correlation of death rates across age, individual differences in survival chances, and induced alterations in age patterns of fertility and mortality--offer clues and suggest research on the failure of complicated systems, on new demographic equations for evolutionary theory, and on fertility-longevity interactions. Nongenetic changes account for increases in human life-spans to date. Explication of these causes and the genetic license for extended survival, as well as discovery of genes and other survival attributes affecting longevity, will lead to even longer lives.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vaupel, J W -- Carey, J R -- Christensen, K -- Johnson, T E -- Yashin, A I -- Holm, N V -- Iachine, I A -- Kannisto, V -- Khazaeli, A A -- Liedo, P -- Longo, V D -- Zeng, Y -- Manton, K G -- Curtsinger, J W -- AG08761/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1998 May 8;280(5365):855-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute for Demographic Research, Rostock, Germany. jwv@demogr.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9599158" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Animals ; Developed Countries ; Female ; Fertility ; Genes ; Genetic Variation ; Humans ; *Longevity ; Male ; Models, Statistical ; *Mortality
    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)
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  • 4
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    Evolutionary medicine: from dwarf model systems to healthy centenarians? (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-03-01
    Description: Restriction of the number of calories consumed extends longevity in many organisms. In rodents, caloric restriction decreases the levels of plasma glucose and insulin-like growth factor I (IGF-1) and postpones or attenuates cancer, immunosenescence, and inflammation without irreversible side effects. In organisms ranging from yeast to mice, mutations in glucose or IGF-I-like signaling pathways extend life-span but also cause glycogen or fat accumulation and dwarfism. This information suggests a new category of drugs that could prevent or postpone diseases of aging with few adverse effects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Longo, Valter D -- Finch, Caleb E -- AG 01028/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2003 Feb 28;299(5611):1342-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Andrus Gerontology Center, Division of Biogerontology, and Department of Biological Sciences, University of Southern California, 3715 McClintock Avenue, Los Angeles, CA 90089-0191, USA. vlongo@usc.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12610293" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Animals ; Biological Evolution ; Caenorhabditis elegans/genetics/physiology ; Caloric Restriction ; Drosophila/genetics/physiology ; Dwarfism/physiopathology ; Gene Expression Regulation ; Glucose/*metabolism ; Growth Hormone/metabolism ; Human Growth Hormone/metabolism ; Humans ; Insulin-Like Growth Factor I/*metabolism ; *Longevity/genetics ; Mice ; Models, Animal ; Mutation ; Signal Transduction ; Yeasts/genetics/physiology
    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)
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  • 5
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    Medical research: treat ageing (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-07-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fontana, Luigi -- Kennedy, Brian K -- Longo, Valter D -- Seals, Douglas -- Melov, Simon -- England -- Nature. 2014 Jul 24;511(7510):405-7. doi: 10.1038/511405a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Washington University in St. Louis, Missouri, USA, and at Brescia University, Italy. ; Buck Institute for Research on Aging in Novato, California, USA. ; Longevity Institute at the University of Southern California in Los Angeles, USA. ; Department of Integrative Physiology at the University of Colorado Boulder in Boulder, Colorado, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25056047" target="_blank"〉PubMed〈/a〉
    Keywords: Age of Onset ; Aging/*drug effects/genetics/*physiology ; Animals ; Biomarkers ; Biomedical Research/economics/*trends ; Caloric Restriction ; Clinical Trials as Topic ; Diet ; Exercise ; Geriatrics/economics/*trends ; Health ; Humans ; Longevity/*drug effects/genetics/physiology ; Metformin/pharmacology ; Models, Animal ; Precision Medicine/trends ; Preventive Medicine/economics/*trends ; Rejuvenation/*physiology ; Sirolimus/pharmacology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 6
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    Starvation-dependent differential stress resistance protects normal but not cancer cells against high-dose chemotherapy (2008)
    National Academy of Sciences
    Details
    Publication Date: 2008-03-31
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 7
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    Meal frequency and timing in health and disease [Medical Sciences] (2014)
    National Academy of Sciences
    Details
    Publication Date: 2014-11-26
    Description: Although major research efforts have focused on how specific components of foodstuffs affect health, relatively little is known about a more fundamental aspect of diet, the frequency and circadian timing of meals, and potential benefits of intermittent periods with no or very low energy intakes. The most common eating pattern...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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