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<title>The Journals of Gerontology Series A: Biological Sciences and Medical Sciences - recent issues</title>
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<title><![CDATA[Journal of Gerontology: BIOLOGICAL SCIENCES]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/NP?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 13:55:06 PST</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp189</dc:identifier>
<dc:title><![CDATA[Journal of Gerontology: BIOLOGICAL SCIENCES]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>12</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>NP</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>NP</prism:startingPage>
<prism:section>Standing Material</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/NP-a?rss=1">
<title><![CDATA[Biotoc]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/NP-a?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 13:55:06 PST</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp190</dc:identifier>
<dc:title><![CDATA[Biotoc]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>12</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>NP</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>NP</prism:startingPage>
<prism:section>Standing Material</prism:section>
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<title><![CDATA[Cover]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/NP-b?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 13:55:06 PST</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp191</dc:identifier>
<dc:title><![CDATA[Cover]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>12</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>NP</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>NP</prism:startingPage>
<prism:section>Cover</prism:section>
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<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/NP-c?rss=1">
<title><![CDATA[Journal of Gerontology: MEDICAL SCIENCES]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/NP-c?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 13:55:06 PST</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp192</dc:identifier>
<dc:title><![CDATA[Journal of Gerontology: MEDICAL SCIENCES]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>12</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>NP</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>NP</prism:startingPage>
<prism:section>Standing Material</prism:section>
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<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/NP-d?rss=1">
<title><![CDATA[Medtoc]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/NP-d?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 13:55:06 PST</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp193</dc:identifier>
<dc:title><![CDATA[Medtoc]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>12</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>NP</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>NP</prism:startingPage>
<prism:section>Standing Material</prism:section>
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<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1207?rss=1">
<title><![CDATA[Transplantation of Young Ovaries to Old Mice Increased Life Span in Transplant Recipients]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1207?rss=1</link>
<description><![CDATA[
<p>Previously we reported that prepubertally ovariectomized mice that received young transplanted ovaries at a postreproductive age showed a 40% increase in life expectancy. To study this phenomenon in greater detail, 11-month-old ovariectomized and ovary-intact CBA/J mice underwent ovarian transplantation with 60-day-old ovaries or a sham surgery. Results from observations on transplant recipients in the current study extended our previous results. Whereas intact control mice lived an average of 726 days, transplant recipients lived an average of 770 days (i.e., 780 days for intact recipients and 757 days for ovariectomized recipients). If intact recipients had ceased reproductive cycling by the time of transplant, we observed a further increase in mean life span to 811 days. These results demonstrate that young ovaries enhanced longevity when transplanted to old mice and that ovarian status, examined by means of ovariectomy and ovarian transplantation, clearly influenced the potential of young transplanted ovaries to positively impact longevity.</p>
]]></description>
<dc:creator><![CDATA[Mason, J. B., Cargill, S. L., Anderson, G. B., Carey, J. R.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 13:55:06 PST</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp134</dc:identifier>
<dc:title><![CDATA[Transplantation of Young Ovaries to Old Mice Increased Life Span in Transplant Recipients]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>12</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1211</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1207</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1212?rss=1">
<title><![CDATA[Mice Deficient in Both Mn Superoxide Dismutase and Glutathione Peroxidase-1 Have Increased Oxidative Damage and a Greater Incidence of Pathology but No Reduction in Longevity]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1212?rss=1</link>
<description><![CDATA[
<p>To test the impact of increased mitochondrial oxidative stress as a mechanism underlying aging and age-related pathologies, we generated mice with a combined deficiency in two mitochondrial-localized antioxidant enzymes, Mn superoxide dismutase (MnSOD) and glutathione peroxidase-1 (Gpx-1). We compared life span, pathology, and oxidative damage in <I>Gpx1<sup>&ndash;</sup></I><sup>/<I>&ndash;</I></sup>, <I>Sod2</I><sup>+/<I>&ndash;</I></sup><I>Gpx1</I><sup>+/<I>&ndash;</I></sup>, <I>Sod2</I><sup>+/<I>&ndash;</I></sup><I>Gpx1<sup>&ndash;</sup></I><sup>/<I>&ndash;</I></sup>, and wild-type control mice. Oxidative damage was elevated in <I>Sod2</I><sup>+/<I>&ndash;</I></sup><I>Gpx1<sup>&ndash;</sup></I><sup>/<I>&ndash;</I></sup> mice, as shown by increased DNA oxidation in liver and skeletal muscle and increased protein oxidation in brain. Surprisingly, <I>Sod2</I><sup>+/<I>&ndash;</I></sup><I>Gpx1<sup>&ndash;</sup></I><sup>/<I>&ndash;</I></sup> mice showed no reduction in life span, despite increased levels of oxidative damage. Consistent with the important role for oxidative stress in tumorigenesis during aging, the incidence of neoplasms was significantly increased in the older <I>Sod2</I><sup>+/<I>&ndash;</I></sup><I>Gpx1<sup>&ndash;</sup></I><sup>/<I>&ndash;</I></sup> mice (28&ndash;30 months). Thus, these data do not support a significant role for increased oxidative stress as a result of compromised mitochondrial antioxidant defenses in modulating life span in mice and do not support the oxidative stress theory of aging.</p>
]]></description>
<dc:creator><![CDATA[Zhang, Y., Ikeno, Y., Qi, W., Chaudhuri, A., Li, Y., Bokov, A., Thorpe, S. R., Baynes, J. W., Epstein, C., Richardson, A., Van Remmen, H.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 13:55:06 PST</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp132</dc:identifier>
<dc:title><![CDATA[Mice Deficient in Both Mn Superoxide Dismutase and Glutathione Peroxidase-1 Have Increased Oxidative Damage and a Greater Incidence of Pathology but No Reduction in Longevity]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>12</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1220</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1212</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1221?rss=1">
<title><![CDATA[Attenuation of Age-Related Metabolic Dysfunction in Mice With a Targeted Disruption of the C{beta} Subunit of Protein Kinase A]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1221?rss=1</link>
<description><![CDATA[
<p>The cyclic adenosine monophosphate&ndash;dependent protein kinase A (PKA) pathway helps regulate both cell growth and division, and triglyceride storage and metabolism in response to nutrient status. Studies in yeast show that disruption of this pathway promotes longevity in a manner similar to caloric restriction. Because PKA is highly conserved, it can be studied in mammalian systems. This report describes the metabolic phenotype of mice lacking the PKA catalytic subunit C&beta;. We confirmed that C&beta; has high levels of expression in the brain but also showed moderate levels in liver. C&beta;-null animals had reduced basal PKA activity while appearing overtly normal when fed standard rodent chow. However, the absence of C&beta; protected mice from diet-induced obesity, steatosis, dyslipoproteinemia, and insulin resistance, without any differences in caloric intake or locomotor activity. These findings have relevant pharmacological implications because aging in mammals is characterized by metabolic decline associated with obesity, altered body fat distribution, and insulin resistance.</p>
]]></description>
<dc:creator><![CDATA[Enns, L. C., Morton, J. F., Mangalindan, R. S., McKnight, G. S., Schwartz, M. W., Kaeberlein, M. R., Kennedy, B. K., Rabinovitch, P. S., Ladiges, W. C.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 13:55:06 PST</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp133</dc:identifier>
<dc:title><![CDATA[Attenuation of Age-Related Metabolic Dysfunction in Mice With a Targeted Disruption of the C{beta} Subunit of Protein Kinase A]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>12</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1231</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1221</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1232?rss=1">
<title><![CDATA[Effects of Chronic Overload on Muscle Hypertrophy and mTOR Signaling in Young Adult and Aged Rats]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1232?rss=1</link>
<description><![CDATA[
<p>We examined the effect of 28 days of overload on mammalian target of rapamycin (mTOR) and extracellular signal&ndash;regulated kinase (ERK) signaling in young adult (Y; 6-month old) and aged (O; 30-month old) Fischer 344 <FONT FACE="arial,helvetica">x</FONT> Brown Norway rats subjected to bilateral synergist ablation (SA) of two thirds of the gastrocnemius muscle or sham surgery (CON). Although plantaris (PLA) muscle hypertrophy was attenuated by aging, mTOR phosphorylation was 44% and 35% greater in Y SA and O SA compared with CON (<I>p</I> = .038). Ribosomal protein S6 phosphorylation was 114% and 24% higher in Y SA and O SA compared with CON (<I>p</I> = .009). Eukaryotic initiation factor 2B phosphorylation was 33% and 9% higher in Y SA and O SA compared with CON (<I>p</I> = .04). Translational signaling in young adult and aged plantaris muscle is equally responsive to chronic overload.</p>
]]></description>
<dc:creator><![CDATA[Chale-Rush, A., Morris, E. P., Kendall, T. L., Brooks, N. E., Fielding, R. A.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 13:55:06 PST</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp146</dc:identifier>
<dc:title><![CDATA[Effects of Chronic Overload on Muscle Hypertrophy and mTOR Signaling in Young Adult and Aged Rats]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>12</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1239</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1232</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1243?rss=1">
<title><![CDATA[Brain Volumes, Cognitive Impairment, and Conjugated Equine Estrogens]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1243?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>Postmenopausal conjugated equine estrogens (CEE) therapies increase the risk of cognitive impairment in women aged 65 years or older and are associated with smaller regional brain volumes; however, the link between these two phenomena has not been established.</p>
</sec>
<sec><st>Methods</st>
<p>Standardized magnetic resonance imaging was performed on 1,403 women, 1&ndash;4 years after they had participated in randomized placebo-controlled clinical trials of CEE-based therapies. Women included in this report were aged 65&ndash;80 years and free of dementia and mild cognitive impairment (MCI) when originally enrolled in the trials, which lasted an average of 4&ndash;6 years and were conducted at 14 academic U.S. medical centers. The associations that regional brain volumes and ischemic lesion volumes had with the development of cognitive impairment (i.e., dementia or MCI) were contrasted between treatment groups using analyses of covariance.</p>
</sec>
<sec><st>Results</st>
<p>Fifty-three women developed MCI or probable dementia during follow-up. Among women who had been prescribed CEE-based therapies, cognitive impairment was associated with relatively smaller hippocampal (<I>p</I> = .0002) and total brain volumes (<I>p</I> = .03). Qualitatively, these associations appeared to be independent of their level of pretreatment cognitive function. Among women who had been prescribed placebo, these relationships were not evident; instead, cognitive impairment was associated with greater ischemic lesion volume in the frontal lobe (<I>p</I> = .007) and overall (<I>p</I> = .02).</p>
</sec>
<sec><st>Conclusion</st>
<p>A mechanism by which CEE-based postmenopausal hormone therapy induces cognitive impairment appears to be through increased brain atrophy.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Espeland, M. A., Tindle, H. A., Bushnell, C. A., Jaramillo, S. A., Kuller, L. H., Margolis, K. L., Mysiw, W. J., Maldjian, J. A., Melhem, E. R., Resnick, S. M., for the Women's Health Initiative Memory Study]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 13:55:06 PST</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp128</dc:identifier>
<dc:title><![CDATA[Brain Volumes, Cognitive Impairment, and Conjugated Equine Estrogens]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>12</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1250</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1243</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1251?rss=1">
<title><![CDATA[Total and Cause-Specific Mortality in the Cardiovascular Health Study]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1251?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>Few cohort studies have adequate numbers of carefully reviewed deaths to allow an analysis of unique and shared risk factors for cause-specific mortality. Shared risk factors could be targeted for prevention of premature death and the study of longevity.</p>
</sec>
<sec><st>Methods</st>
<p>A total of 5,888 community-dwelling persons aged 65 years or older living in four communities in the United States participated in the Cardiovascular Health Study cohort. Participants were initially recruited from 1989 to 1990; an additional 687 black participants were recruited in 1992&ndash;1993. The average length of follow-up was 16 years. Total and cause-specific mortality, including cardiovascular disease, stroke, cancer, dementia, pulmonary disease, infection, and other cause, were examined as outcomes. Variables previously associated with total mortality were examined for each cause of death using Cox proportional hazard models.</p>
</sec>
<sec><st>Results</st>
<p>Multiple risk factors were related to total mortality. When examining specific causes, many factors were related to cardiovascular death, whereas fewer were related to other causes. For most causes, risk factors were specific for that cause. For example, <I>apolipoprotein E 4</I> was strongly associated for dementia death and forced vital capacity with pulmonary death. Age, male sex, markers of inflammation, and cognitive function were related to multiple causes of death.</p>
</sec>
<sec><st>Conclusions</st>
<p>In these older adults, associations of risk factors with a given cause of death were related to specific deficits in that same organ system. Inflammation may represent a common pathway to all causes of death.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Newman, A. B., Sachs, M. C., Arnold, A. M., Fried, L. P., Kronmal, R., Cushman, M., Psaty, B. M., Harris, T. B., Robbins, J. A., Burke, G. L., Kuller, L. H., Lumley, T.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 13:55:06 PST</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp127</dc:identifier>
<dc:title><![CDATA[Total and Cause-Specific Mortality in the Cardiovascular Health Study]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>12</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1261</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1251</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1262?rss=1">
<title><![CDATA[Cognitive Speed of Processing Training Delays Driving Cessation]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1262?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>As our population ages, interventions that can prolong safe driving for older adults will be increasingly important.</p>
</sec>
<sec><st>Methods</st>
<p>Data from two studies were combined in order to investigate the effectiveness of cognitive training in delaying driving cessation. Stratified Cox hazard regressions were used to examine risk of driving cessation as a function of training participation, baseline driving, and visual acuity.</p>
</sec>
<sec><st>Results</st>
<p>Older drivers with cognitive speed of processing difficulties who completed speed of processing training were 40% less likely to cease driving over the subsequent 3 years (hazard ratio = 0.596, 95% confidence interval 0.356&ndash;0.995, <I>p</I> = .048). Whereas 14% of older drivers who did not receive speed of processing training ceased driving, only 9% of those who completed eight or more sessions of speed of processing training ceased driving.</p>
</sec>
<sec><st>Conclusion</st>
<p>Speed of processing training may delay driving cessation among older drivers with speed of processing difficulty.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Edwards, J. D., Delahunt, P. B., Mahncke, H. W.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 13:55:06 PST</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp131</dc:identifier>
<dc:title><![CDATA[Cognitive Speed of Processing Training Delays Driving Cessation]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>12</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1267</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1262</prism:startingPage>
<prism:section>Brief Report</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1268?rss=1">
<title><![CDATA[Trajectories of Dehydroepiandrosterone Sulfate Predict Mortality in Older Adults: The Cardiovascular Health Study]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1268?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>Dehydroepiandrosterone sulfate (DHEAS) has been proposed as an antiaging hormone, but its importance is unclear. Assessment of an individual&rsquo;s ability to maintain a DHEAS set point, through examination of multiple DHEAS levels over time, may provide insight into biologic aging.</p>
</sec>
<sec><st>Methods</st>
<p>Using Cox proportional hazard models, we examined the relationship between DHEAS trajectory patterns and all-cause death in 950 individuals aged &ge;65 years who were enrolled in the Cardiovascular Health Study and had DHEAS levels measured at three to six time points.</p>
</sec>
<sec><st>Results</st>
<p>Overall, there was a slight decline in DHEAS levels over time (&ndash;0.013 &micro;g/mL/y). Three trajectory components were examined: slope, variability, and baseline DHEAS. When examined individually, a steep decline or extreme variability in DHEAS levels was associated with higher mortality (<I>p</I> &lt; .001 for each), whereas baseline DHEAS level was not. In adjusted models including all three components, steep decline (hazard ratio [HR] 1.75, confidence interval [CI] 1.32&ndash;2.33) and extreme variability (HR 1.89, CI 1.47&ndash;2.43) remained significant predictors of mortality, whereas baseline DHEAS level remained unpredictive of mortality (HR 0.97 per standard deviation, CI 0.88&ndash;1.07). The effect of trajectory pattern was more pronounced in men than in women. Individuals with both a steep decline and extreme variability in DHEAS levels had a significantly higher death rate than those with neither pattern (141 <I>vs</I> 48 deaths per 1,000 person-years, <I>p</I> &lt; .001).</p>
</sec>
<sec><st>Conclusions</st>
<p>Our data show significant heterogeneity in the individual trajectories of DHEAS levels and suggest that these trajectories provide important biologic information about the rate of aging, whereas the DHEAS level itself does not.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Cappola, A. R., O'Meara, E. S., Guo, W., Bartz, T. M., Fried, L. P., Newman, A. B.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 13:55:06 PST</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp129</dc:identifier>
<dc:title><![CDATA[Trajectories of Dehydroepiandrosterone Sulfate Predict Mortality in Older Adults: The Cardiovascular Health Study]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>12</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1274</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1268</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1275?rss=1">
<title><![CDATA[Evidence for Neurocognitive Plasticity in At-Risk Older Adults: The Experience Corps Program]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1275?rss=1</link>
<description><![CDATA[
<sec><st>Objective</st>
<p>To determine whether Experience Corps (EC), a social service program, would improve age-vulnerable executive functions and increase activity in brain regions in a high-risk group through increased cognitive and physical activity.</p>
</sec>
<sec><st>Methods</st>
<p>Eight community-dwelling, older female volunteers and nine matched wait-list controls were recruited to serve in the ongoing EC: Baltimore program in three elementary schools. We employed functional magnetic resonance imaging (fMRI) preintervention and postintervention to examine whether EC volunteers improved executive function and showed increased activity in the prefrontal cortex relative to controls. fMRI volunteers were trained and placed with other volunteers 15 h/wk for 6 months during the academic year to assist teachers in kindergarten through third grade to promote children&rsquo;s literacy and academic achievement.</p>
</sec>
<sec><st>Results</st>
<p>Participants were African American and had low education, low income, and low Mini-Mental State Examination scores (<I>M</I> = 24), indicative of elevated risk for cognitive impairment. Volunteers exhibited intervention-specific increases in brain activity in the left prefrontal cortex and anterior cingulate cortex over the 6-month interval relative to matched controls. Neural gains were matched by behavioral improvements in executive inhibitory ability.</p>
</sec>
<sec><st>Conclusions</st>
<p>Using fMRI, we demonstrated intervention-specific short-term gains in executive function and in the activity of prefrontal cortical regions in older adults at elevated risk for cognitive impairment. These pilot results provide proof of concept for use-dependent brain plasticity in later life, and, that interventions designed to promote health and function through everyday activity may enhance plasticity in key regions that support executive function.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Carlson, M. C., Erickson, K. I., Kramer, A. F., Voss, M. W., Bolea, N., Mielke, M., McGill, S., Rebok, G. W., Seeman, T., Fried, L. P.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 13:55:06 PST</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp117</dc:identifier>
<dc:title><![CDATA[Evidence for Neurocognitive Plasticity in At-Risk Older Adults: The Experience Corps Program]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>12</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1282</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1275</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1283?rss=1">
<title><![CDATA[Religious Attendance Reduces Cognitive Decline Among Older Women With High Levels of Depressive Symptoms]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1283?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>There is growing evidence that regular attendance at religious functions is associated with less cognitive decline (CD). However, little research has investigated factors that may moderate the religious attendance&ndash;CD relationship. The present study examined the effects of gender and depressive symptoms on the relationship between religious attendance and CD.</p>
</sec>
<sec><st>Methods</st>
<p>Data were drawn from waves 1 and 2 of the Duke Established Populations for Epidemiologic Studies of the Elderly, which were 3 years apart. Participants consisted of a sample of community-dwelling older adults aged 65 years and older (<I>N</I> = 2,938). Linear regression analyses were conducted controlling for important demographic-, socioeconomic-, and health-related variables. Cognitive functioning was assessed at both waves to examine change in errors over time.</p>
</sec>
<sec><st>Results</st>
<p>Greater religious attendance was related to less CD. In addition, there was a three-way interaction between religious attendance, gender, and depressive symptoms in predicting CD. Among women with higher levels of depressive symptoms, those who less frequently attended religious services experienced greater CD than those who more frequently attended religious services. The interaction between attendance and depressive symptoms in men did not reach significance.</p>
</sec>
<sec><st>Conclusions</st>
<p>Religious attendance may offer mental stimulation that helps to maintain cognitive functioning in later life, particularly among older depressed women. Given the possible benefits religious attendance may have on cognitive functioning, it may be appropriate in certain instances for clinicians to recommend that clients reengage in religious activities they may have given up as a result of their depression.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Corsentino, E. A., Collins, N., Sachs-Ericsson, N., Blazer, D. G.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 13:55:06 PST</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp116</dc:identifier>
<dc:title><![CDATA[Religious Attendance Reduces Cognitive Decline Among Older Women With High Levels of Depressive Symptoms]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>12</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1289</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1283</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1290?rss=1">
<title><![CDATA[Driving Cessation and Health Trajectories in Older Adults]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1290?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>Older adults who cease driving have poorer health than those who continue to drive. However, it is unclear whether the transition to driving cessation itself results in health declines or whether driving cessation subsequently exacerbates health declines over time.</p>
</sec>
<sec><st>Methods</st>
<p>The current study addresses these questions using multilevel modeling among 690 older adults from the Advanced Cognitive Training for Independent and Vital Elderly study. Driving status and health, as indicated by the SF-36 questionnaire, self-rated health, physical performance (Turn 360&deg; Test), and depressive symptoms were assessed at baseline and at 1-, 2-, 3-, and 5-year follow-up visits.</p>
</sec>
<sec><st>Results</st>
<p>The transition to driving cessation was accompanied by significant declines in physical and social functioning, physical performance, and physical role (<I>ps</I> &lt; .05). Health declines after driving cessation were steeper for general health.</p>
</sec>
<sec><st>Conclusions</st>
<p>The transition to driving cessation is associated with health declines for older adults as measured by several indicators. Additionally, general health declines more sharply following driving cessation. These findings highlight the importance of interventions to sustain driving mobility among older adults.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Edwards, J. D., Lunsman, M., Perkins, M., Rebok, G. W., Roth, D. L.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 13:55:07 PST</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp114</dc:identifier>
<dc:title><![CDATA[Driving Cessation and Health Trajectories in Older Adults]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>12</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1295</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1290</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1296?rss=1">
<title><![CDATA[Factors Associated With Recovery of Prehospital Function Among Older Persons Admitted to a Nursing Home With Disability After an Acute Hospitalization]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1296?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>The objective of this study was to identify the factors associated with recovery of prehospital function among older persons admitted to a nursing home with disability after an acute hospitalization.</p>
</sec>
<sec><st>Methods</st>
<p>The analytic sample included 292 participants of an ongoing cohort study who had one or more admissions to a nursing home with disability after an acute hospitalization during nearly 10 years of follow-up, yielding a total of 364 "index" nursing home admissions. Information on nursing home admissions, hospitalizations, and disability in essential activities of daily living was ascertained during monthly telephone interviews. Data on potential predictors of functional recovery were collected during comprehensive assessments, which were completed every 18 months for 90 months. Participants were considered to have recovered if they were discharged home within 6 months of their nursing home admission at (or above) their prehospital level of function.</p>
</sec>
<sec><st>Results</st>
<p>Recovery of prehospital function was observed for 115 (31.6%) of the 364 index nursing home admissions. In the multivariate analysis, the strongest associations were observed for the best category of performance, relative to the poorest category, for gross motor coordination (hazard ratio [HR] 13.5, 95% confidence interval [CI] 4.02&ndash;45.0) and manual dexterity (HR 10.0, 95% CI 2.94&ndash;34.3). Only two other factors were independently associated with recovery of prehospital function: not cognitively impaired (HR 3.0, 95% CI 1.46&ndash;6.14) and no significant weight loss (HR 1.96, 95% CI 1.06&ndash;3.63).</p>
</sec>
<sec><st>Conclusions</st>
<p>In the setting of an acute hospitalization leading to a nursing home admission with disability, the likelihood of recovering prehospital function is low. The factors associated with recovery include faster performance on tests of gross motor coordination and manual dexterity and the absence of cognitive impairment and significant weight loss.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Gill, T. M., Gahbauer, E. A., Han, L., Allore, H. G.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 13:55:07 PST</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp115</dc:identifier>
<dc:title><![CDATA[Factors Associated With Recovery of Prehospital Function Among Older Persons Admitted to a Nursing Home With Disability After an Acute Hospitalization]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>12</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1303</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1296</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1304?rss=1">
<title><![CDATA[Frailty and the Degradation of Complex Balance Dynamics During a Dual-Task Protocol]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1304?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>Balance during quiet stance involves the complex interactions of multiple postural control systems, which may degrade with frailty. The complexity of center of pressure (COP) dynamics, as quantified using multiscale entropy (MSE), during quiet standing is lower in older adults, especially those with falls. We hypothesized that COP dynamics from frail elderly individuals demonstrate less complexity than those from nonfrail elderly controls; complexity decreases when performing a dual task; and postural complexity during quiet standing is independent of other conventional correlates of balance control, such as age and vision.</p>
</sec>
<sec><st>Methods</st>
<p>We analyzed data from a population-based study of community-dwelling older adults. Frailty phenotype (nonfrail, prefrail, or frail) was determined for 550 participants (age 77.9 &plusmn; 5.5 years). COP excursions were quantified for 10 trials of 30 seconds each. Participants concurrently performed a serial subtraction task in half of the trials. Complexity of balance dynamics was quantified using MSE. Root-mean-square sway amplitude was also computed.</p>
</sec>
<sec><st>Results</st>
<p>Of the 550, 38% were prefrail and 9% were frail. Complexity of the COP dynamics in the anteroposterior direction was lower in prefrail (8.78 &plusmn; 1.91 [mean &plusmn; <I>SD</I>]) and frail (8.38 &plusmn; 2.13) versus nonfrail (9.20 &plusmn; 1.74) groups (<I>p</I> &lt; .001). Complexity reduced by a comparable amount in all three groups while performing the subtraction task (<I>p</I> &lt; .001). Quiet standing complexity was independently associated with frailty after adjusting for covariates related to balance while sway amplitude was not.</p>
</sec>
<sec><st>Conclusion</st>
<p>Cognitive distractions during standing may further compromise balance control in frail individuals, leading to an increased risk of falls.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Kang, H. G., Costa, M. D., Priplata, A. A., Starobinets, O. V., Goldberger, A. L., Peng, C.-K., Kiely, D. K., Cupples, L. A., Lipsitz, L. A.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 13:55:07 PST</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp113</dc:identifier>
<dc:title><![CDATA[Frailty and the Degradation of Complex Balance Dynamics During a Dual-Task Protocol]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>12</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1311</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1304</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1312?rss=1">
<title><![CDATA[Cardiac Autonomic Dysfunction Is Associated With White Matter Lesions in Patients With Mild Cognitive Impairment]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1312?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>Cardiac autonomic dysfunction has been associated with cognitive impairment, but the underlying pathogenesis is complex and cerebral white matter lesions (WMLs) might be implicated.</p>
</sec>
<sec><st>Methods</st>
<p>Time and frequency heart rate variability (HRV) and visual rating of WMLs were carried out in 42 patients with mild cognitive impairment.</p>
</sec>
<sec><st>Results</st>
<p>After adjustment for relevant demographic and clinical characteristics, including left ventricular mass, reduced HRV indices of parasympathetic (root mean square of successive difference of RR intervals, RMSSD) and sympathetic modulation (low-frequency [LF] power) were associated with increased WML score (RMSSD: <I>B</I> &ndash;0.30, 95% CI &ndash;0.52 to &ndash;0.08, <I>p</I> = .01; LF: <I>B</I> &ndash;0.24, 95% CI &ndash;0.46 to &ndash;0.02, <I>p</I> = .05). In a multiple-adjusted model, RMSSD was the major independent predictor of WMLs (<I>B</I> &ndash;0.35, 95% CI &ndash;0.57 to &ndash;0.13, <I>p</I> = .002).</p>
</sec>
<sec><st>Conclusion</st>
<p>The evidence for an independent association of cardiac autonomic dysfunction with WMLs might suggest its role in the pathogenesis of WMLs.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Galluzzi, S., Nicosia, F., Geroldi, C., Alicandri, A., Bonetti, M., Romanelli, G., Zulli, R., Frisoni, G. B.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 13:55:07 PST</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp105</dc:identifier>
<dc:title><![CDATA[Cardiac Autonomic Dysfunction Is Associated With White Matter Lesions in Patients With Mild Cognitive Impairment]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>12</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1315</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1312</prism:startingPage>
<prism:section>Rapid Communication</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1316?rss=1">
<title><![CDATA[Measures of Physical Performance Capture the Excess Disability Associated With Hip Pain or Knee Pain in Older Persons]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1316?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>Hip pain (HP) and knee pain (KP) may specifically affect function and performance; few studies investigate the functional impact of HP or KP in the same population.</p>
</sec>
<sec><st>Methods</st>
<p>Population-based sample of older individuals living in the Chianti area (Tuscany, Italy) (1998&ndash;2000); 1006 persons (564 women and 442 men) were included in this analysis; 11.9% reported HP and 22.4% reported KP in the past 4 weeks. Self-reported disability and lower extremity performance, measured by 400-m walk test and by the short physical performance battery (SPPB, including standing balance, chair raising, and 4-m walk test), were compared in participants reporting HP or KP versus those free of these conditions; the relationship of HP or KP with performance and self-reported disability was studied, adjusting for age, sex, hip or knee flexibility, muscle strength, multiple joint pain, major medical conditions, and depression.</p>
</sec>
<sec><st>Results</st>
<p>Participants reporting HP were more likely to report disability in shopping, cutting toenails, carrying a shopping bag, and using public transportation; those with KP reported more disability in cutting toenails and carrying a shopping bag. Participants reporting HP or KP had significantly lower SPPB scores. Adjusting by SPPB, pain no longer predicted self-reported disability, except for "HP&mdash;carrying a shopping bag."</p>
</sec>
<sec><st>Conclusions</st>
<p>In our cohort of older persons, those with HP reported disability in a wider range of activities than those with KP. Physical performance measured by SPPB was impaired in both conditions. Reduced lower extremity performance captures the excess disability associated with either HP or KP.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Cecchi, F., Molino-Lova, R., Di Iorio, A., Conti, A. A., Mannoni, A., Lauretani, F., Benvenuti, E., Bandinelli, S., Macchi, C., Ferrucci, L.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 13:55:07 PST</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp125</dc:identifier>
<dc:title><![CDATA[Measures of Physical Performance Capture the Excess Disability Associated With Hip Pain or Knee Pain in Older Persons]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>12</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1324</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1316</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1325?rss=1">
<title><![CDATA[Longitudinal Association Between Depressive Symptoms and Disability Burden Among Older Persons]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1325?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>Although depressive symptoms in older persons are common, their association with disability burden is not well understood. The authors evaluated the association between level of depressive symptoms and severity of subsequent disability over time and determined whether this relationship differed by sex.</p>
</sec>
<sec><st>Methods</st>
<p>Participants included 754 community-living persons aged 70 years or older who underwent monthly assessments of disability in four essential activities of daily living for up to 117 months. Disability was categorized each month as none, mild, and severe. Depressive symptoms, assessed every 18 months, were categorized as low (referent group), moderate, and high. Multinomial logit models invoking <I>Generalized Estimating Equation</I> were used to calculate odds ratios and 95% confidence intervals.</p>
</sec>
<sec><st>Results</st>
<p>Moderate (odds ratio = 1.30; 95% confidence interval: 1.18&ndash;1.43) and high (odds ratio = 1.68; 95% confidence interval: 1.50&ndash;1.88) depressive symptoms were associated with mild disability, whereas only high depressive symptoms were associated with severe disability (odds ratio = 2.05; 95% confidence interval: 1.76&ndash;2.39). Depressive symptoms were associated with disability burden in both men and women, with modest differences by sex; men had an increased likelihood of experiencing severe disability at both moderate and high levels of depressive symptoms, whereas only high depressive symptoms were associated with severe disability in women.</p>
</sec>
<sec><st>Conclusions</st>
<p>Levels of depressive symptoms below the threshold for subsyndromal depression are associated with increased disability burden in older persons. Identifying and treating varying levels of depressive symptoms in older persons may ultimately help to reduce the burden of disability in this population.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Barry, L. C., Allore, H. G., Bruce, M. L., Gill, T. M.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 13:55:07 PST</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp135</dc:identifier>
<dc:title><![CDATA[Longitudinal Association Between Depressive Symptoms and Disability Burden Among Older Persons]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>12</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1332</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1325</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1333?rss=1">
<title><![CDATA[Basic ADL Disability and Functional Limitation Rates Among Older Americans From 2000-2005: The End of the Decline?]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/12/1333?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>This study sought to determine whether the rates of basic activities of daily living (ADL) disabilities and functional limitations declined, remained the same, or increased between 2000 and 2005 when (a) only community-dwelling Americans aged 65 and older were examined and (b) when institutionalized older adults were included.</p>
</sec>
<sec><st>Method</st>
<p>Using data from the American Community Survey and the National Nursing Home Survey, we calculated annual prevalence rates of basic ADL disabilities and functional limitations and fitted regression lines to examine trends over time.</p>
</sec>
<sec><st>Results</st>
<p>The rates of basic ADL disabilities among community-dwelling adults aged 65 and older increased 9% between 2000 and 2005. When institutionalized elders were included, basic ADL disability rates were stable among men but increased among women. Functional limitation rates did not significantly change between 2000 and 2005.</p>
</sec>
<sec><st>Conclusion</st>
<p>These findings suggest an end of the decline in disability rates among older Americans, which, if confirmed, could have important implications for health care.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Fuller-Thomson, E., Yu, B., Nuru-Jeter, A., Guralnik, J. M., Minkler, M.]]></dc:creator>
<dc:date>Thu, 05 Nov 2009 13:55:07 PST</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp130</dc:identifier>
<dc:title><![CDATA[Basic ADL Disability and Functional Limitation Rates Among Older Americans From 2000-2005: The End of the Decline?]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>12</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1336</prism:endingPage>
<prism:publicationDate>2009-12-01</prism:publicationDate>
<prism:startingPage>1333</prism:startingPage>
<prism:section>Brief Report</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/NP?rss=1">
<title><![CDATA[Journal of Gerontology: BIOLOGICAL SCIENCES]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/NP?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Thu, 08 Oct 2009 23:43:25 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp167</dc:identifier>
<dc:title><![CDATA[Journal of Gerontology: BIOLOGICAL SCIENCES]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>NP</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>NP</prism:startingPage>
<prism:section>Standing Material</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/NP-a?rss=1">
<title><![CDATA[Medtoc]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/NP-a?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Thu, 08 Oct 2009 23:43:25 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp168</dc:identifier>
<dc:title><![CDATA[Medtoc]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>NP</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>NP</prism:startingPage>
<prism:section>Standing Material</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/NP-b?rss=1">
<title><![CDATA[Journal of Gerontology: MEDICAL SCIENCES]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/NP-b?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Thu, 08 Oct 2009 23:43:25 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp169</dc:identifier>
<dc:title><![CDATA[Journal of Gerontology: MEDICAL SCIENCES]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>NP</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>NP</prism:startingPage>
<prism:section>Standing Material</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/NP-c?rss=1">
<title><![CDATA[Cover]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/NP-c?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Thu, 08 Oct 2009 23:43:25 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp170</dc:identifier>
<dc:title><![CDATA[Cover]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>NP</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>NP</prism:startingPage>
<prism:section>Cover</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/NP-d?rss=1">
<title><![CDATA[Biotoc]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/NP-d?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Thu, 08 Oct 2009 23:43:25 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp171</dc:identifier>
<dc:title><![CDATA[Biotoc]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>NP</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>NP</prism:startingPage>
<prism:section>Standing Material</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1103?rss=1">
<title><![CDATA[Insulin-Like Growth Factors and Leukocyte Telomere Length: The Cardiovascular Health Study]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1103?rss=1</link>
<description><![CDATA[
<p>The insulin-like growth factor (IGF) axis may affect immune cell replicative potential and telomere dynamics. Among 551 adults 65 years and older, leukocyte telomere length (LTL), insulin-like growth factor-1 (IGF-1), and insulin-like growth factor&ndash;binding proteins 1 and 3 (IGFBP-1, IGFBP-3) were measured. Multivariate linear regression was used to model the association of LTL with IGF-1 and IGFBPs, while controlling for confounding and increasing precision by adjusting for covariates. We observed a significant association between higher IGF-1 and longer LTL after adjustment for age, sex, race, smoking status, body mass index, hypertension, diabetes, and serum lipids. The results suggested an increase of .08 kb in LTL for each standard deviation increase of IGF-1 (<I>p</I> = .04). IGFBP-1 and IGFBP-3 were not significantly associated with LTL. High IGF-1 may be an independent predictor of longer LTL, consistent with prior evidence suggesting a role for IGF-1 in mechanisms relating to telomere maintenance.</p>
]]></description>
<dc:creator><![CDATA[Kaplan, R. C., Fitzpatrick, A. L., Pollak, M. N., Gardner, J. P., Jenny, N. S., McGinn, A. P., Kuller, L. H., Strickler, H. D., Kimura, M., Psaty, B. M., Aviv, A.]]></dc:creator>
<dc:date>Thu, 08 Oct 2009 23:43:25 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp036</dc:identifier>
<dc:title><![CDATA[Insulin-Like Growth Factors and Leukocyte Telomere Length: The Cardiovascular Health Study]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1106</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1103</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1107?rss=1">
<title><![CDATA[Calorie Restriction Enhances T-Cell-Mediated Immune Response in Adult Overweight Men and Women]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1107?rss=1</link>
<description><![CDATA[
<p>Calorie restriction (CR) enhances immune response and prolongs life span in animals. However, information on the applicability of these results to humans is limited. T-cell function declines with age. We examined effects of CR on T-cell function in humans. Forty-six overweight, nonobese participants aged 20&ndash;42 years were randomly assigned to 30% or 10% CR group for 6 months. Delayed-type hypersensitivity (DTH), T-cell proliferation (TP), and prostaglandin E<SUB>2</SUB> (PGE<SUB>2</SUB>) productions were determined before and after CR. DTH and TP to T-cell mitogens were increased in both groups over baseline (<I>p</I> &le; .019). However, number of positive responses to DTH antigens (<I>p</I> = .016) and TP to anti-CD3 reached statistical significance only after 30% CR (<I>p</I> = .001). Lipopolysaccharide-stimulated PGE<SUB>2</SUB> was reduced in both groups but reached statistical significance after 30% CR (<I>p</I> &le; .029). These results, for the first time, show that 6-month CR in humans improves T-cell function.</p>
]]></description>
<dc:creator><![CDATA[Ahmed, T., Das, S. K., Golden, J. K., Saltzman, E., Roberts, S. B., Meydani, S. N.]]></dc:creator>
<dc:date>Thu, 08 Oct 2009 23:43:25 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp101</dc:identifier>
<dc:title><![CDATA[Calorie Restriction Enhances T-Cell-Mediated Immune Response in Adult Overweight Men and Women]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1113</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1107</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1114?rss=1">
<title><![CDATA[Overexpression of Mn Superoxide Dismutase Does Not Increase Life Span in Mice]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1114?rss=1</link>
<description><![CDATA[
<p>Genetic manipulations of Mn superoxide dismutase (MnSOD), SOD2 expression have demonstrated that altering the level of MnSOD activity is critical for cellular function and life span in invertebrates. In mammals, <I>Sod2</I> homozygous knockout mice die shortly after birth, and alterations of MnSOD levels are correlated with changes in oxidative damage and in the generation of mitochondrial reactive oxygen species. In this study, we directly tested the effects of overexpressing MnSOD in young (4&ndash;6 months) and old (26&ndash;28 months) mice on mitochondrial function, levels of oxidative damage or stress, life span, and end-of-life pathology. Our data show that an approximately twofold overexpression of MnSOD throughout life in mice resulted in decreased lipid peroxidation, increased resistance against paraquat-induced oxidative stress, and decreased age-related decline in mitochondrial ATP production. However, this change in MnSOD expression did not alter either life span or age-related pathology.</p>
]]></description>
<dc:creator><![CDATA[Jang, Y. C., Perez, V. I., Song, W., Lustgarten, M. S., Salmon, A. B., Mele, J., Qi, W., Liu, Y., Liang, H., Chaudhuri, A., Ikeno, Y., Epstein, C. J., Van Remmen, H., Richardson, A.]]></dc:creator>
<dc:date>Thu, 08 Oct 2009 23:43:26 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp100</dc:identifier>
<dc:title><![CDATA[Overexpression of Mn Superoxide Dismutase Does Not Increase Life Span in Mice]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1125</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1114</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1126?rss=1">
<title><![CDATA[Is Altered Expression of Hepatic Insulin-Related Genes in Growth Hormone Receptor Knockout Mice Due to GH Resistance or a Difference in Biological Life Spans?]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1126?rss=1</link>
<description><![CDATA[
<p>Growth hormone receptor knockout (GHRKO) mice live about 40%&ndash;55% longer than their normal (N) littermates. Previous studies of 21-month-old GHRKO and N mice showed major alterations of the hepatic expression of genes involved in insulin signaling. Differences detected at this age may have been caused by the knockout of the growth hormone receptor (GHR) or by differences in biological age between GHRKO and N mice. To address this question, we compared GHRKO and N mice at ages corresponding to the same percentage of median life span to see if the differences of gene expression persisted. Comparison of GHRKO and N mice at ~50% of biological life span showed significant differences in hepatic expression of all 14 analyzed genes. We conclude that these changes are due to disruption of GHR gene and the consequent suppression of growth hormone signaling rather than to differences in "biological age" between mutant and normal animals sampled at the same chronological age.</p>
]]></description>
<dc:creator><![CDATA[Panici, J. A., Wang, F., Bonkowski, M. S., Spong, A., Bartke, A., Pawlikowska, L., Kwok, P.-Y., Masternak, M. M.]]></dc:creator>
<dc:date>Thu, 08 Oct 2009 23:43:26 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp111</dc:identifier>
<dc:title><![CDATA[Is Altered Expression of Hepatic Insulin-Related Genes in Growth Hormone Receptor Knockout Mice Due to GH Resistance or a Difference in Biological Life Spans?]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1133</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1126</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1134?rss=1">
<title><![CDATA[Genetic (Co)Variation for Life Span in Rhabditid Nematodes: Role of Mutation, Selection, and History]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1134?rss=1</link>
<description><![CDATA[
<p>The evolutionary mechanisms maintaining genetic variation in life span, particularly post-reproductive life span, are poorly understood. We characterized the effects of spontaneous mutations on life span in the rhabditid nematodes <I>Caenorhabditis elegans</I> and <I>C. briggsae</I> and standing genetic variance for life span and correlation of life span with fitness in <I>C. briggsae</I>. Mutations decreased mean life span, a signature of directional selection. Mutational correlations between life span and fitness were consistently positive. The average selection coefficient against new mutations in <I>C. briggsae</I> was approximately 2% when homozygous. The pattern of phylogeographic variation in life span is inconsistent with global mutation&ndash;selection balance (MSB), but MSB appears to hold at the local level. Standing genetic correlations in <I>C. briggsae</I> reflect mutational correlations at a local scale but not at a broad phylogeographic level. At the local scale, results are broadly consistent with predictions of the "mutation accumulation" hypothesis for the evolution of aging.</p>
]]></description>
<dc:creator><![CDATA[Joyner-Matos, J., Upadhyay, A., Salomon, M. P., Grigaltchik, V., Baer, C. F.]]></dc:creator>
<dc:date>Thu, 08 Oct 2009 23:43:26 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp112</dc:identifier>
<dc:title><![CDATA[Genetic (Co)Variation for Life Span in Rhabditid Nematodes: Role of Mutation, Selection, and History]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1145</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1134</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1146?rss=1">
<title><![CDATA[Age-Related Changes of Claudin Expression in Mouse Liver, Kidney, and Pancreas]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1146?rss=1</link>
<description><![CDATA[
<p>Tight junctions (TJs) play crucial roles in tissue homeostasis and inflammation through their roles in the control of paracellular transport and barrier function. There is evidence that these functions are compromised in older organisms, but the exact mechanisms leading to TJ deterioration are not well understood. Claudin proteins are a family of membrane proteins that constitute the structural barrier elements of TJs and therefore play a major role in their formation and function. Using immunohistochemistry and immunoblotting, we have studied the expression of six different claudin proteins (claudin-1, -2, -3, -4, -5, and -7) in three tissues (liver, kidney, and pancreas) of aging male and female mice. In general, we find an age-dependent decrease in the expression of several claudin proteins in all three tissues observed, although the exact changes are tissue specific. Our findings provide a possible basis for the decrease in tissue barrier function in older organisms.</p>
]]></description>
<dc:creator><![CDATA[D'Souza, T., Sherman-Baust, C. A., Poosala, S., Mullin, J. M., Morin, P. J.]]></dc:creator>
<dc:date>Thu, 08 Oct 2009 23:43:26 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp118</dc:identifier>
<dc:title><![CDATA[Age-Related Changes of Claudin Expression in Mouse Liver, Kidney, and Pancreas]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1153</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1146</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1154?rss=1">
<title><![CDATA[Age-Associated Increase in Cleaved Caspase 3 Despite Phosphorylation of IGF-1 Receptor in the Rat Retina]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1154?rss=1</link>
<description><![CDATA[
<p>Diseases of aging produce many alterations in the retina, but changes in growth factor signaling in normal aging are less characterized. This study investigated modifications in insulin-like growth factor-1 (IGF-1) receptor (IGF-1R) signaling in the retina of Brown Norway <FONT FACE="arial,helvetica">x</FONT> Fischer 344 F1 hybrid rats at 8, 22, and 32 months. Immunoblotting for proteins involved in IGF-1R signal transduction and electroretinograms were done to evaluate changes with aging. Aging produced a significant decrease in b-wave and oscillatory potential amplitudes in the retina. Aging produced increased phosphorylation of IGF-1R. Despite the increase in IGF-1R activity, insulin receptor substrate-1 (IRS-1) phosphorylation was significantly decreased with increasing age. Akt activity was significantly decreased at 22 and 32 months of age, resulting in increased cleaved caspase 3 levels. The results suggest that regulation of IRS-1 phosphorylation may modulate apoptotic rates in the aging retina, potentially preventing activation of vascular endothelial cell growth factor.</p>
]]></description>
<dc:creator><![CDATA[Jiang, Y., Walker, R. J., Steinle, J. J.]]></dc:creator>
<dc:date>Thu, 08 Oct 2009 23:43:26 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp102</dc:identifier>
<dc:title><![CDATA[Age-Associated Increase in Cleaved Caspase 3 Despite Phosphorylation of IGF-1 Receptor in the Rat Retina]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1159</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1154</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1163?rss=1">
<title><![CDATA[Call for Papers: Aging Versus Disease]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1163?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Newman, A. B., Ferrucci, L.]]></dc:creator>
<dc:date>Thu, 08 Oct 2009 23:43:26 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp039</dc:identifier>
<dc:title><![CDATA[Call for Papers: Aging Versus Disease]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1164</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1163</prism:startingPage>
<prism:section>Editorial</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1165?rss=1">
<title><![CDATA[Toward a Common Language of Disablement]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1165?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Jette, A. M.]]></dc:creator>
<dc:date>Thu, 08 Oct 2009 23:43:26 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp093</dc:identifier>
<dc:title><![CDATA[Toward a Common Language of Disablement]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1168</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1165</prism:startingPage>
<prism:section>Guest Editorial</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1169?rss=1">
<title><![CDATA[The Challenge of Understanding the Disablement Process in Older Persons: Commentary Responding to Jette AM. Toward a Common Language of Disablement]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1169?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Guralnik, J. M., Ferrucci, L.]]></dc:creator>
<dc:date>Thu, 08 Oct 2009 23:43:26 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp094</dc:identifier>
<dc:title><![CDATA[The Challenge of Understanding the Disablement Process in Older Persons: Commentary Responding to Jette AM. Toward a Common Language of Disablement]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1171</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1169</prism:startingPage>
<prism:section>Guest Editorial</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1172?rss=1">
<title><![CDATA[Adopting the ICF Language for Studying Late-life Disability: A Field of Dreams?]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1172?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Freedman, V. A.]]></dc:creator>
<dc:date>Thu, 08 Oct 2009 23:43:26 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp095</dc:identifier>
<dc:title><![CDATA[Adopting the ICF Language for Studying Late-life Disability: A Field of Dreams?]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1174</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1172</prism:startingPage>
<prism:section>Guest Editorial</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1175?rss=1">
<title><![CDATA[Beyond Dueling Models: Commentary Responding to: Guralnik JM, Ferrucci L. The Challenge of Understanding the Disablement Process in Older Persons and Freedman V. Adopting the ICF Language for Studying Late-life Disability: A Field of Dreams?]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1175?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Jette, A. M.]]></dc:creator>
<dc:date>Thu, 08 Oct 2009 23:43:26 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp096</dc:identifier>
<dc:title><![CDATA[Beyond Dueling Models: Commentary Responding to: Guralnik JM, Ferrucci L. The Challenge of Understanding the Disablement Process in Older Persons and Freedman V. Adopting the ICF Language for Studying Late-life Disability: A Field of Dreams?]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1176</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1175</prism:startingPage>
<prism:section>Invited Response to Letter to the Editor</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1177?rss=1">
<title><![CDATA[Interleukin-18 Polymorphism and Physical Functioning in Older People: A Replication Study and Meta-Analysis]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1177?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>Levels of the proinflammatory cytokine interleukin-18 (IL-18) are raised in old age and are associated with reduced physical functioning. Previous studies have indicated that the C allele of the rs5744256 polymorphism in the IL-18 gene is strongly associated with reduced circulating IL-18 levels. This variant has previously been associated with improved locomotor performance in old age, but the finding requires independent replication.</p>
</sec>
<sec><st>Methods</st>
<p>We examined the association between the IL-18 polymorphism rs5744256 and physical functioning in three cohorts with a total of 4,107 participants aged 60&ndash;85 years: the English Longitudinal Study of Ageing, Caerphilly, and Boyd Orr. We meta-analyzed (<I>N</I> = 6,141) the results with data from the original paper reporting this association: Iowa-Established Populations for Epidemiological Study of the Elderly and InCHIANTI cohorts. Physical functioning was assessed by timed walks or the get up and go test. As locomotor performance tests differed between the cohorts and the distributions of times to complete the test (in seconds) were positively skewed, we used the reciprocal transformation and computed study-specific <I>z</I> scores.</p>
</sec>
<sec><st>Results</st>
<p>Based on the three new studies, the estimated linear regression coefficient per C allele was 0.011 (95% confidence interval [95% CI]: &ndash;0.04 to 0.06). A meta-analysis that pooled the data from all studies showed weak evidence of an effect, with a regression coefficient of 0.047 (95% CI: 0.010 to 0.083).</p>
</sec>
<sec><st>Conclusions</st>
<p>We did not replicate an association between the IL-18 rs5744256 polymorphism and the physical function in people aged 60&ndash;85 years. However, pooling data from all studies suggested a weak association of the C allele of the rs5744256 single nucleotide polymorphism on improving walking times in old age.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Thomas, K., Rafiq, S., Frayling, T. M., Ebrahim, S., Kumari, M., Gallacher, J., Ferrucci, L., Bandinelli, S., Wallace, R. B., Melzer, D., Martin, R. M., Ben-Shlomo, Y.]]></dc:creator>
<dc:date>Thu, 08 Oct 2009 23:43:26 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp092</dc:identifier>
<dc:title><![CDATA[Interleukin-18 Polymorphism and Physical Functioning in Older People: A Replication Study and Meta-Analysis]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1182</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1177</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1183?rss=1">
<title><![CDATA[Higher Inflammatory Marker Levels in Older Persons: Associations With 5-Year Change in Muscle Mass and Muscle Strength]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1183?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>There is growing evidence that higher levels of inflammatory markers are associated with physical decline in older persons, possibly through the catabolic effects of inflammatory markers on muscle. The aim of this study was to investigate the association between serum levels of inflammatory markers and loss of muscle mass and strength in older persons.</p>
</sec>
<sec><st>Methods</st>
<p>Using data on 2,177 men and women in the Health, Aging, and Body Composition Study, we examined 5-year change in thigh muscle area estimated by computed tomography and grip and knee extensor strength in relation to serum levels of interleukin-6 (IL-6), C-reactive protein, tumor necrosis factor-alpha (TNF-), and soluble receptors (measured in a subsample) at baseline.</p>
</sec>
<sec><st>Results</st>
<p>Higher levels of inflammatory markers were generally associated with greater 5-year decline in thigh muscle area. Most associations, with the exception of soluble receptors, were attenuated by adjustment for 5-year change in weight. Higher TNF- and interleukin-6 soluble receptor levels remained associated with greater decline in grip strength in men. Analyses in a subgroup of weight-stable persons showed that higher levels of TNF- and its soluble receptors were associated with 5-year decline in thigh muscle area and that higher levels of TNF- were associated with decline in grip strength.</p>
</sec>
<sec><st>Conclusions</st>
<p>TNF- and its soluble receptors showed the most consistent associations with decline in muscle mass and strength. The results suggest a weight-associated pathway for inflammation in sarcopenia.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Schaap, L. A., Pluijm, S. M. F., Deeg, D. J. H., Harris, T. B., Kritchevsky, S. B., Newman, A. B., Colbert, L. H., Pahor, M., Rubin, S. M., Tylavsky, F. A., Visser, M., for the Health ABC Study]]></dc:creator>
<dc:date>Thu, 08 Oct 2009 23:43:26 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp097</dc:identifier>
<dc:title><![CDATA[Higher Inflammatory Marker Levels in Older Persons: Associations With 5-Year Change in Muscle Mass and Muscle Strength]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1189</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1183</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1190?rss=1">
<title><![CDATA[A Randomized Trial of Two Forms of Therapeutic Activity to Improve Walking: Effect on the Energy Cost of Walking]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1190?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>Therapeutic activities to improve mobility often include walking practice and exercises to improve deficits in endurance, strength, and balance. Because walking may also be energy inefficient in people with decreased mobility, another approach is to reduce energy cost by improving timing and coordination (TC) of movement.</p>
</sec>
<sec><st>Methods</st>
<p>This pilot randomized trial of older adults with slow and variable gait offered two types of therapeutic activity over 12 weeks. One addressed Walking, Endurance, Balance, and Strength (WEBS) and the other focused on TC. Outcomes were energy cost of walking and measures of mobility.</p>
</sec>
<sec><st>Results</st>
<p>Of 50 participants (mean age, 77.2 &plusmn; 5.5 years, 65% women), 47 completed the study. Baseline gait speed was 0.85 &plusmn; 0.13 m/s and energy cost of walking was 0.30 &plusmn; 0.10 mL/kg/m, nearly twice normal. Both interventions increased gait speed (TC by 0.21 m/s and WEBS by 0.14 m/s, <I>p</I> &lt; .001). TC reduced the energy cost of walking 0.10 &plusmn; 0.03 mL/kg/m more than WEBS (<I>p</I> &lt; .001) and reduced the modified Gait Abnormalities Rating Scale 1.5 &plusmn; 0.6 more points than WEBS (<I>p</I> &lt; .05). TC had a 9.8 &plusmn; 3.5 points greater gain than WEBS in self-reported confidence in walking (<I>p</I> &lt; .01).</p>
</sec>
<sec><st>Conclusions</st>
<p>In older adults with slow and variable gait, activity focused on TC reduced the energy cost of walking and improved confidence in walking more than WEBS while generating at least equivalent gains in mobility. To optimize mobility, future larger studies should assess various combinations of TC and WEBS over longer periods of time.</p>
</sec>
]]></description>
<dc:creator><![CDATA[VanSwearingen, J. M., Perera, S., Brach, J. S., Cham, R., Rosano, C., Studenski, S. A.]]></dc:creator>
<dc:date>Thu, 08 Oct 2009 23:43:26 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp098</dc:identifier>
<dc:title><![CDATA[A Randomized Trial of Two Forms of Therapeutic Activity to Improve Walking: Effect on the Energy Cost of Walking]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1198</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1190</prism:startingPage>
<prism:section>Brief Report</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1199?rss=1">
<title><![CDATA[FALL-RELATED HIP FRACTURES]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/11/1199?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Stolee, P., Poss, J., Cook, R. J., Byrne, K., Hirdes, J. P.]]></dc:creator>
<dc:date>Thu, 08 Oct 2009 23:43:26 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp072</dc:identifier>
<dc:title><![CDATA[FALL-RELATED HIP FRACTURES]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1199</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1199</prism:startingPage>
<prism:section>Authors' Response to Letter to the Editor</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/NP?rss=1">
<title><![CDATA[Journal of Gerontology: BIOLOGICAL SCIENCES]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/NP?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 16:34:09 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp138</dc:identifier>
<dc:title><![CDATA[Journal of Gerontology: BIOLOGICAL SCIENCES]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>NP</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>NP</prism:startingPage>
<prism:section>Standing Material</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/NP-a?rss=1">
<title><![CDATA[Biotoc]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/NP-a?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 16:34:09 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp139</dc:identifier>
<dc:title><![CDATA[Biotoc]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>NP</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>NP</prism:startingPage>
<prism:section>Standing Material</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/NP-b?rss=1">
<title><![CDATA[Cover]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/NP-b?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 16:34:09 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp140</dc:identifier>
<dc:title><![CDATA[Cover]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>NP</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>NP</prism:startingPage>
<prism:section>Cover</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/NP-c?rss=1">
<title><![CDATA[Journal of Gerontology: MEDICAL SCIENCES]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/NP-c?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 16:34:09 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp141</dc:identifier>
<dc:title><![CDATA[Journal of Gerontology: MEDICAL SCIENCES]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>NP</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>NP</prism:startingPage>
<prism:section>Standing Material</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/NP-d?rss=1">
<title><![CDATA[Medtoc]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/NP-d?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 16:34:09 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp142</dc:identifier>
<dc:title><![CDATA[Medtoc]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>NP</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>NP</prism:startingPage>
<prism:section>Standing Material</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/1015?rss=1">
<title><![CDATA[Accelerated Features of Age-Related Bone Loss in Zmpste24 Metalloproteinase-Deficient Mice]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/1015?rss=1</link>
<description><![CDATA[
<p>Age-related bone loss is associated with changes in bone cellularity, which include marrow fat infiltration and decreasing levels of osteoblastogenesis. The mechanisms that explain these changes remain unclear. Although nuclear lamina alterations occur in premature aging syndromes that include changes in body fat and severe osteoporosis, the role of proteins of the nuclear lamina in age-related bone loss remains unknown. Using the Zmpste24-null progeroid mice (Zmpste24<sup>&ndash;/&ndash;</sup>), which exhibit nuclear lamina defects and accumulate unprocessed prelamin A, we identified several alterations in bone cellularity in vivo. We found that defective prelamin A processing induced accelerated features of age-related bone loss including lower osteoblast and osteocyte numbers and higher levels of marrow adipogenesis. In summary, processing of prelamin A could become a new approach to regulate osteoblastogenesis and bone turnover and thus for the prevention and treatment of senile osteoporosis.</p>
]]></description>
<dc:creator><![CDATA[Rivas, D., Li, W., Akter, R., Henderson, J. E., Duque, G.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 16:34:09 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp089</dc:identifier>
<dc:title><![CDATA[Accelerated Features of Age-Related Bone Loss in Zmpste24 Metalloproteinase-Deficient Mice]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1024</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1015</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/1025?rss=1">
<title><![CDATA[Nitric Oxide Activity and Isoenzyme Expression in the Senescence-Accelerated Mouse P8 Model of Alzheimer's Disease: Effects of Anti-Amyloid Antibody and Antisense Treatments]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/1025?rss=1</link>
<description><![CDATA[
<p>Amyloid beta protein (A&beta;) in Alzheimer&rsquo;s disease induces oxidative stress through several mechanisms, including stimulation of nitric oxide synthase (NOS) activity. We examined NOS activity and expression in the senescence-accelerated mouse P8 (SAMP8) line. The SAMP8 strain develops with aging cognitive impairments, increases in A&beta;, and oxidative stress, all reversed by amyloid precursor protein antisense or A&beta; antibody treatment. We found here that hippocampal NOS activity in 12-month-old SAMP8 mice was nearly double that of 2-month-old SAMP8 or CD-1 mice, but with no change in NOS isoenzyme mRNA and protein levels. Antisense or antibody treatment further increased NOS activity in aged SAMP8 mice. Antisense treatment increased inducible NOS (iNOS) mRNA levels, decreased neuronal NOS mRNA and protein levels, but did not affect endothelial NOS (eNOS) or iNOS protein or eNOS mRNA levels. These results suggest a complex relation between A&beta; and NOS in the SAMP8 that is largely mediated through posttranslational mechanisms.</p>
]]></description>
<dc:creator><![CDATA[Ali, A. K., Banks, W. A., Kumar, V. B., Shah, G. N., Lynch, J. L., Farr, S. A., Fleegal-DeMotta, M. A., Morley, J. E.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 16:34:09 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp074</dc:identifier>
<dc:title><![CDATA[Nitric Oxide Activity and Isoenzyme Expression in the Senescence-Accelerated Mouse P8 Model of Alzheimer's Disease: Effects of Anti-Amyloid Antibody and Antisense Treatments]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1030</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1025</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/1031?rss=1">
<title><![CDATA[Deceleration of Senescence in Normal Human Fibroblasts by Withanone Extracted From Ashwagandha Leaves]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/1031?rss=1</link>
<description><![CDATA[
<p>Ashwagandha is an Ayurvedic shrub that forms a common ingredient of health supplements, tonics, and Indian home remedies designed to promote health and quality of life. Though sustained through experience and history, there are only a limited laboratory studies and experimental evidence to its effects. In our efforts to characterize Ashwagandha activities and their molecular mechanisms, we initially prepared leaf extract of Ashwagandha (i-Extract) that showed tumor-inhibitory activity. In the present study, we demonstrate that a major component of i-Extract and withanone (i-Factor) protected the normal human fibroblasts against the toxicity caused by withaferin A. It increased the in vitro division potential of normal human cells that appeared to be mediated by decreased accumulation of molecular damage, downregulation of the senescence-specific &beta;-galactosidase activity and the senescence marker protein, p21<sup>WAF-1</sup>, protection against oxidative damage, and induction of proteasomal activity. To the best of our knowledge, we provide the first example of phytochemical(s) (i-Extract and withanone) that have both anticancer and antiaging activities and point to the molecular link between aging and cancer.</p>
]]></description>
<dc:creator><![CDATA[Widodo, N., Shah, N., Priyandoko, D., Ishii, T., Kaul, S. C., Wadhwa, R.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 16:34:09 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp088</dc:identifier>
<dc:title><![CDATA[Deceleration of Senescence in Normal Human Fibroblasts by Withanone Extracted From Ashwagandha Leaves]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1038</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1031</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/1039?rss=1">
<title><![CDATA[Statement by the Growth Hormone Research Society on the GH/IGF-I Axis in Extending Health Span]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/1039?rss=1</link>
<description><![CDATA[
<p>Despite the fact that growth hormone (GH) has not been approved for antiaging purposes, its use for this indication is widespread and increasing. The Growth Hormone Research Society (GRS) convened an international workshop to critically review and debate the available evidence related to the use of GH in the older adults and the relationship between the GH/insulin-like growth factor I (IGF-I) axis and the aging process. This statement presents the conclusions reached and gives recommendations for future studies in this research field regarding the use of GH and growth hormone secretagogues (GHS) for promoting health span. The participants concluded that, until future clinical research in this area is conducted, in particular carefully designed, long-term studies, using validated outcome parameters, the clinical use of GH or GHS in older adults, alone or in combination with testosterone, cannot be recommended. In addition, future basic studies in model systems, to continue to unravel GH/IGF-I effects related to human life span and health span, were advocated.</p>
]]></description>
<dc:creator><![CDATA[Thorner, M. O.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 16:34:09 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp091</dc:identifier>
<dc:title><![CDATA[Statement by the Growth Hormone Research Society on the GH/IGF-I Axis in Extending Health Span]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1044</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1039</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/1045?rss=1">
<title><![CDATA[The NIA Interventions Testing Program Announces the 2009 Solicitation of Proposals]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/1045?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 16:34:09 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp124</dc:identifier>
<dc:title><![CDATA[The NIA Interventions Testing Program Announces the 2009 Solicitation of Proposals]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1045</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1045</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/1049?rss=1">
<title><![CDATA[Nonlinear Multisystem Physiological Dysregulation Associated With Frailty in Older Women: Implications for Etiology and Treatment]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/1049?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>Frailty in older adults, defined as a constellation of signs and symptoms, is associated with abnormal levels in individual physiological systems. We tested the hypothesis that it is the critical mass of physiological systems abnormal that is associated with frailty, over and above the status of each individual system, and that the relationship is nonlinear.</p>
</sec>
<sec><st>Methods</st>
<p>Using data on women aged 70&ndash;79 years from the Women&rsquo;s Health and Aging Studies I and II, multiple analytic approaches assessed the cross-sectional association of frailty with eight physiological measures.</p>
</sec>
<sec><st>Results</st>
<p>Abnormality in each system (anemia, inflammation, insulin-like growth factor-1, dehydroepiandrosterone-sulfate, hemoglobin A1c, micronutrients, adiposity, and fine motor speed) was significantly associated with frailty status. However, adjusting for the level of each system measure, the mean number of systems impaired significantly and nonlinearly predicted frailty. Those with three or more systems impaired were most likely to be frail, with odds of frailty increasing with number of systems at abnormal level, from odds ratios (ORs) of 4.8 to 11 to 26 for those with one to two, three to four, and five or more systems abnormal (<I>p</I> &lt; .05 for all). Finally, two subgroups were identified, one with isolated or no systems abnormal and a second (in 30%) with multiple systems abnormal. The latter group was independently associated with being frail (OR = 2.6, <I>p</I> &lt; .05), adjusting for confounders and chronic diseases and then controlling for individual systems.</p>
</sec>
<sec><st>Conclusions</st>
<p>Overall, these findings indicate that the likelihood of frailty increases nonlinearly in relationship to the number of physiological systems abnormal, and the number of abnormal systems is more predictive than the individual abnormal system. These findings support theories that aggregate loss of complexity, with aging, in physiological systems is an important cause of frailty. Implications are that a threshold loss of complexity, as indicated by number of systems abnormal, may undermine homeostatic adaptive capacity, leading to the development of frailty and its associated risk for subsequent adverse outcomes. It further suggests that replacement of any one deficient system may not be sufficient to prevent or ameliorate frailty.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Fried, L. P., Xue, Q.-L., Cappola, A. R., Ferrucci, L., Chaves, P., Varadhan, R., Guralnik, J. M., Leng, S. X., Semba, R. D., Walston, J. D., Blaum, C. S., Bandeen-Roche, K.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 16:34:09 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp076</dc:identifier>
<dc:title><![CDATA[Nonlinear Multisystem Physiological Dysregulation Associated With Frailty in Older Women: Implications for Etiology and Treatment]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1057</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1049</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/1058?rss=1">
<title><![CDATA[A Cross-Sectional and Longitudinal Study of the Relationship Between Walking Speed and Cognitive Function in Community-Dwelling Elderly People]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/1058?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>Previous reports have shown links between cognitive function and physical performance in the elderly people, but it is unclear whether some specific cognitive domains are more strongly associated with measures of physical function such as walking speed. We investigated cross-sectional and longitudinal relationships between performance in five cognitive tests and walking speed among community-dwelling elderly people in the Dijon center (France) of the Three-City Study.</p>
</sec>
<sec><st>Methods</st>
<p>At baseline, 3,769 participants aged 65&ndash;85 years had measurements of 6-m walking speed, global cognition (Mini-Mental State Examination), verbal fluency (Isaacs Set Test [IST]), psychomotor speed (Trail Making Test part A [TMT-A]), executive function (TMT part B), and memory (Benton Visual Retention Test). After a mean follow-up of 7 years, walking speed was again measured in 1,732 of these participants.</p>
</sec>
<sec><st>Results</st>
<p>In cross-sectional analyses, slower maximum walking speed (MWS) at baseline was significantly associated with poorer performance in each cognitive test. The association was stronger with TMT-A (&beta; [<I>SE</I>] = &ndash;.127 [0.014], <I>p</I> &lt; .0001) and IST (&beta; [<I>SE</I>] = .120 [0.014], <I>p</I> &lt; .0001) than with the other tests. Only TMT-A (&beta; [<I>SE</I>] = &ndash;.053 [0.021], <I>p</I> = .01) and IST (&beta; [<I>SE</I>] = .063 [0.022], <I>p</I> = .004) were associated with the degree of MWS decline over time.</p>
</sec>
<sec><st>Conclusions</st>
<p>This study shows both cross-sectional and longitudinal associations between cognition and walking speed among community-dwelling elderly people. Poorer verbal fluency and slower psychomotor speed were more specifically associated with slower baseline MWS and with a stronger decline in MWS over time.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Soumare, A., Tavernier, B., Alperovitch, A., Tzourio, C., Elbaz, A.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 16:34:09 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp077</dc:identifier>
<dc:title><![CDATA[A Cross-Sectional and Longitudinal Study of the Relationship Between Walking Speed and Cognitive Function in Community-Dwelling Elderly People]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1065</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1058</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/1066?rss=1">
<title><![CDATA[Associations of the Limb Fat to Trunk Fat Ratio With Markers of Cardiometabolic Risk in Elderly Men and Women]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/1066?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>The ratio of limb fat to trunk fat (LF/TF) is associated with markers of cardiometabolic risk in elderly men and women. It is unknown if LF/TF is associated with cardiometabolic risk beyond that explained by LF and TF independently.</p>
</sec>
<sec><st>Methods</st>
<p>Participants included abdominally obese men (<I>n</I> = 58) and women (<I>n</I> = 78) between 60 and 80 years of age. Regional adiposity was quantified using magnetic resonance imaging. Insulin resistance, fasting glucose, high-density lipoprotein (HDL) cholesterol, plasma triglycerides, and adiponectin were determined using standard procedures.</p>
</sec>
<sec><st>Results</st>
<p>After control for potential confounders, TF was positively associated with fasting glucose, insulin resistance, and plasma triglycerides and negatively associated with HDL cholesterol and adiponectin (<I>p</I> &le; .05). These associations were strengthened after further control for LF (<I>p</I> &lt; .05), with the exception of adiponectin in men (<I>p</I> &gt; .05). After control for potential confounders, LF was negatively associated with adiponectin in men (<I>p</I> &lt; .05) but not with any other marker of cardiometabolic risk (<I>p</I> &gt; .05). After further control for TF, LF was negatively associated with plasma triglycerides and positively associated with HDL cholesterol in both genders combined (<I>p</I> &lt; .05) and with adiponectin in women (<I>p</I> &lt; .05) but not in men (<I>p</I> &gt; .05). LF/TF was not associated with any marker of cardiometabolic risk after control for LF and TF.</p>
</sec>
<sec><st>Conclusion</st>
<p>These results suggest that it is the absolute, rather than relative, amounts of LF and TF that have the greatest influence on cardiometabolic risk in elderly men and women.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Saunders, T. J., Davidson, L. E., Janiszewski, P. M., Despres, J.-P., Hudson, R., Ross, R.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 16:34:10 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp079</dc:identifier>
<dc:title><![CDATA[Associations of the Limb Fat to Trunk Fat Ratio With Markers of Cardiometabolic Risk in Elderly Men and Women]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1070</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1066</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/1071?rss=1">
<title><![CDATA[Hormone Therapy and Skeletal Muscle Strength: A Meta-Analysis]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/1071?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>Our objective was to perform a systematic review and meta-analysis of the research literature that compared muscle strength in postmenopausal women who were and were not on estrogen-based hormone therapy (HT).</p>
</sec>
<sec><st>Methods</st>
<p>Twenty-three relevant studies were found. Effect sizes (ESs) were calculated as the standardized mean difference, and meta-analyses were completed using a random effects model.</p>
</sec>
<sec><st>Results</st>
<p>HT was found to result in a small beneficial effect on muscle strength in postmenopausal women (overall ES = 0.23; <I>p</I> = .003) that equated to an ~5% greater strength for women on HT. Among the 23 studies, various muscle groups were assessed for strength, and those that benefitted the most were the thumb adductors (ES = 1.14; <I>p</I> &lt; .001). Ten studies that compared muscle strength in rodents that were and were not estradiol deficient were also analyzed. The ES for absolute strength was moderate but not statistically significant (ES = 0.44; <I>p</I> = .12), whereas estradiol had a large effect on strength normalized to muscle size (ES = 0.66; <I>p</I> = .03).</p>
</sec>
<sec><st>Conclusion</st>
<p>Overall, estrogen-based treatments were found to beneficially affect strength.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Greising, S. M., Baltgalvis, K. A., Lowe, D. A., Warren, G. L.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 16:34:10 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp082</dc:identifier>
<dc:title><![CDATA[Hormone Therapy and Skeletal Muscle Strength: A Meta-Analysis]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1081</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1071</prism:startingPage>
<prism:section>Review Article</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/1082?rss=1">
<title><![CDATA[Social Inequality in Walking Speed in Early Old Age in the Whitehall II Study]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/1082?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>We investigated social inequalities in walking speed in early old age.</p>
</sec>
<sec><st>Methods</st>
<p>Walking speed was measured by timed 8-ft (2.44 m) test in 6,345 individuals, with mean age of 61.1 (<I>SD</I> 6.0) years. Current or last known civil service employment grade defined socioeconomic position.</p>
</sec>
<sec><st>Results</st>
<p>Mean walking speed was 1.36 (<I>SD</I> 0.29) m/s in men and 1.21 (<I>SD</I> 0.30) in women. Average age- and ethnicity-adjusted walking speed was approximately 13% higher in the highest employment grade compared with the lowest. Based on the relative index of inequality (RII), the difference in walking speed across the social hierarchy was 0.15 m/s (95% confidence interval [CI] 0.12&ndash;0.18) in men and 0.17 m/s (0.12&ndash;0.22) in women, corresponding to an age-related difference of 18.7 (13.6&ndash;23.8) years in men and 14.9 (9.9&ndash;19.9) years in women. The RII for slow walking speed (logistic model for lowest sex-specific quartile vs others) adjusted for age, sex, and ethnicity was 3.40 (2.64&ndash;4.36). Explanatory factors for the social gradient in walking speed included Short-Form 36 physical functioning, labor market status, financial insecurity, height, and body mass index. Demographic, psychosocial, behavioral, biologic, and health factors in combination accounted for 40% of social inequality in walking speed.</p>
</sec>
<sec><st>Conclusion</st>
<p>Social inequality in walking speed is substantial in early old age and reflects many factors beyond the direct effects of physical health.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Brunner, E., Shipley, M., Spencer, V., Kivimaki, M., Chandola, T., Gimeno, D., Singh-Manoux, A., Guralnik, J., Marmot, M.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 16:34:10 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp078</dc:identifier>
<dc:title><![CDATA[Social Inequality in Walking Speed in Early Old Age in the Whitehall II Study]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1089</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1082</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/1090?rss=1">
<title><![CDATA[Previous Hepatitis A Virus Infection Is Related to Slower Psychomotor Speed in Elderly Adults]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/1090?rss=1</link>
<description><![CDATA[
<sec><st>Background</st>
<p>Patients with chronic viral hepatitis are at a higher risk for cognitive dysfunction. Little is known about the association between hepatitis A virus (HAV) infection and cognitive function.</p>
</sec>
<sec><st>Methods</st>
<p>From the National Health and Nutrition Examination Survey, 1999&ndash;2002, we selected study participants (&ge;60 years, <I>n</I> = 1,529) without hepatitis B, C, or D virus infection; without previous hepatitis A vaccination; and without abnormal liver function. HAV-seropositive participants represented people with previous HAV infection. Psychomotor speed and executive functioning domain of cognitive function were measured by the Digit Symbol Substitution Test (DSST).</p>
</sec>
<sec><st>Results</st>
<p>HAV-seropositive participants had lower DSST scores than HAV-seronegative participants (weighted mean, 44.4 vs 53.9, <I>p</I> &lt; .001). We designated HAV-seronegative participants as the reference group. Univariate analysis demonstrated that the weighted &beta; coefficient of DSST score was &ndash;9.55 (95% confidence interval [CI] &ndash;9.57 to &ndash;9.54, <I>p</I> &lt; .001) for the HAV-seropositive participants. In a multivariable model, the weighted adjusted &beta; coefficient of DSST score was &ndash;2.48 (95% CI &ndash;2.49 to &ndash;2.46, <I>p</I> &lt; .001) for the HAV-seropositive participants.</p>
</sec>
<sec><st>Conclusion</st>
<p>HAV seropositivity is associated with slower psychomotor speed among the U.S. community-dwelling elders.</p>
</sec>
]]></description>
<dc:creator><![CDATA[Hsieh, C.-F., Liu, C.-K., Fang, T.-J., Yu, Y.-H., Lai, C.-L., Kuo, H.-K.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 16:34:10 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp081</dc:identifier>
<dc:title><![CDATA[Previous Hepatitis A Virus Infection Is Related to Slower Psychomotor Speed in Elderly Adults]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1096</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1090</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/1097?rss=1">
<title><![CDATA[Definition of Hypertension for the "Old-Old"]]></title>
<link>http://biomedgerontology.oxfordjournals.org/cgi/content/short/64A/10/1097?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Finestone, A.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 16:34:10 PDT</dc:date>
<dc:identifier>info:doi/10.1093/gerona/glp080</dc:identifier>
<dc:title><![CDATA[Definition of Hypertension for the "Old-Old"]]></dc:title>
<dc:publisher>The Gerontological Society of America</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>64A</prism:volume>
<prism:endingPage>1097</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1097</prism:startingPage>
<prism:section>LETTER TO THE EDITOR</prism:section>
</item>

</rdf:RDF>