<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Finch, C. E.</style></author><author><style face="normal" font="default" size="100%">Morgan, T. E.</style></author><author><style face="normal" font="default" size="100%">Longo, V. D.</style></author><author><style face="normal" font="default" size="100%">de Magalhaes, J. P.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Cell resilience in species life spans: a link to inflammation?</style></title><secondary-title><style face="normal" font="default" size="100%">Aging Cell</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Aging cell</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Acute-Phase Reaction/immunology</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Biological</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Death/genetics</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Survival</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA Damage</style></keyword><keyword><style  face="normal" font="default" size="100%">Fibroblasts/pathology</style></keyword><keyword><style  face="normal" font="default" size="100%">Genome/genetics</style></keyword><keyword><style  face="normal" font="default" size="100%">Immunity</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammation/*pathology</style></keyword><keyword><style  face="normal" font="default" size="100%">Innate/immunology</style></keyword><keyword><style  face="normal" font="default" size="100%">Longevity/*physiology</style></keyword><keyword><style  face="normal" font="default" size="100%">Models</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxidative Stress</style></keyword><keyword><style  face="normal" font="default" size="100%">Phylogeny</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Aug</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/20415721</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">4</style></number><edition><style face="normal" font="default" size="100%">2010/04/27</style></edition><volume><style face="normal" font="default" size="100%">9</style></volume><pages><style face="normal" font="default" size="100%">519-26</style></pages><isbn><style face="normal" font="default" size="100%">1474-9726 (Electronic)14</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Species differences in life span have been attributed to cellular survival during various stressors, designated here as &#039;cell resilience&#039;. In primary fibroblast cultures, cell resilience during exposure to free radicals, hypoglycemia, hyperthermia, and various toxins has shown generally consistent correlations with the species characteristic life spans of birds and mammals. However, the mechanistic links of cell resilience in fibroblast cultures to different species life spans are poorly understood. We propose that certain experimental stressors are relevant to somatic damage in vivo during inflammatory responses of innate immunity, particularly, resistance to reactive oxygen species (ROS), low glucose, and hyperthermia. According to this hypothesis, somatic cell resilience determines species differences in longevity during repeated infections and traumatic injuries in the natural environment. Infections and injury expose local fibroblasts and other cells to ROS generated by macrophages and to local temperature elevations. Systemically, acute phase immune reactions cause hypoglycemia and hyperthermia. We propose that cell resilience to somatic stressors incurred in inflammation is important in the evolution of longevity and that longer-lived species are specifically more resistant to immune-related stressors. This hypothesis further specifies Kirkwood&#039;s disposable soma theory. We suggest expanding the battery of stressors and markers used for comparative studies to additional cell types and additional parameters relevant to host defense and to their ecological specificities.&lt;/p&gt;</style></abstract><work-type><style face="normal" font="default" size="100%">Research Support, N.I.H., ExtramuralResearch Support, Non-U.S. Gov&#039;t</style></work-type><notes><style face="normal" font="default" size="100%">&lt;p&gt;&lt;span role=&quot;menubar&quot;&gt;Aging Cell.&lt;/span&gt;&amp;nbsp;2010 Aug;9(4):519-26. doi: 10.1111/j.1474-9726.2010.00578.x. Epub 2010 Apr 23.&amp;nbsp;&lt;/p&gt;</style></notes><custom2><style face="normal" font="default" size="100%">2952360</style></custom2><auth-address><style face="normal" font="default" size="100%">University of Southern California, Los Angeles, CA 90089-0191, USA. cefinch@usc.edu</style></auth-address></record></records></xml>