<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="6.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Leslie B Gordon</style></author><author><style face="normal" font="default" size="100%">Ingrid A Harten</style></author><author><style face="normal" font="default" size="100%">Mary Elizabeth Patti</style></author><author><style face="normal" font="default" size="100%">Alice H Lichtenstein</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Reduced adiponectin and {HDL} cholesterol without elevated C-reactive protein: clues to the biology of premature atherosclerosis in {Hutchinson-Gilford} Progeria Syndrome</style></title><secondary-title><style face="normal" font="default" size="100%">The Journal of Pediatrics</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adiponectin</style></keyword><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Arteriosclerosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Body Mass Index</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Cholesterol</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Intercellular Signaling Peptides and Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">lipids</style></keyword><keyword><style  face="normal" font="default" size="100%">Lipoproteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Progeria</style></keyword><keyword><style  face="normal" font="default" size="100%">Risk Assessment</style></keyword><keyword><style  face="normal" font="default" size="100%">{C-Reactive} Protein</style></keyword><keyword><style  face="normal" font="default" size="100%">{Case-Control} Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">{HDL</style></keyword><keyword><style  face="normal" font="default" size="100%">{LDL</style></keyword><keyword><style  face="normal" font="default" size="100%">} Cholesterol</style></keyword><keyword><style  face="normal" font="default" size="100%">} Collagen</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2005</style></year><pub-dates><date><style  face="normal" font="default" size="100%">mar</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/15756215</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">3</style></number><volume><style face="normal" font="default" size="100%">146</style></volume><pages><style face="normal" font="default" size="100%">336–341</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">{{\textless}AbstractText} {Label=&quot;OBJECTIVES&quot;} {NlmCategory=&quot;OBJECTIVE&quot;{\textgreater}Children} with {Hutchinson-Gilford} Progeria Syndrome {(HGPS)} die of severe premature atherosclerosis at an average age of 13 years. Although the {LMNA} gene defect responsible for this &quot;premature aging syndrome&quot; has been identified, biological mechanisms underlying the accelerated atherosclerosis are unknown. We determined whether children with {HGPS} demonstrate abnormalities in known biomarkers for cardiovascular disease {(CVD)} {risk.{\textless}/AbstractText{\textgreater}} {{\textless}AbstractText} {Label=&quot;STUDY} {DESIGN&quot;} {NlmCategory=&quot;METHODS&quot;{\textgreater}We} quantified serum lipids, lipoproteins, C-reactive protein {(CRP),} and adiponectin in children with {HGPS} and age-matched control {children.{\textless}/AbstractText{\textgreater}} {{\textless}AbstractText} {Label=&quot;RESULTS&quot;} {NlmCategory=&quot;RESULTS&quot;{\textgreater}HDL} cholesterol {(P} &amp;lt; .0001) and adiponectin {(P} &amp;lt; .001) concentrations decreased significantly with increasing age in {HGPS} but not in control children. There was a positive correlation between these variables in {HGPS} ( P &amp;lt; .0001) but not control children. Mean total cholesterol, {LDL} and {HDL} cholesterol, triglyceride, and median {CRP} levels were similar between {HGPS} and control children (all P &amp;gt; {.05).{\textless}/AbstractText{\textgreater}} {{\textless}AbstractText} {Label=&quot;CONCLUSIONS&quot;} {NlmCategory=&quot;CONCLUSIONS&quot;{\textgreater}Declining} {HDL} cholesterol and adiponectin with advancing age may contribute to accelerated atherosclerotic plaque formation in {HGPS.} Several factors frequently associated with {CVD} risk in normal aging (elevated {CRP,} total and {LDL} cholesterol) showed no difference and are unlikely to influence {CVD} risk in {HGPS.} {HDL} and adiponectin may represent significant mediators and potential therapeutic targets for atherosclerosis in {HGPS.{\textless}/AbstractText{\textgreater}}</style></abstract><notes><style face="normal" font="default" size="100%">{PMID:} 15756215</style></notes></record></records></xml>