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<title>Publications - Biobehavioral Health Science</title>
<link>http://hdl.handle.net/10027/8249</link>
<description/>
<pubDate>Sun, 26 May 2013 06:28:28 GMT</pubDate>
<dc:date>2013-05-26T06:28:28Z</dc:date>
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<title>Functional Performance in Chronic Obstructive Pulmonary Disease Declines with Time</title>
<link>http://hdl.handle.net/10027/8556</link>
<description>Functional Performance in Chronic Obstructive Pulmonary Disease Declines with Time
Kapella, Mary C.; Larson, Janet L.; Covey, Margaret K.; Alex, Charles G.
Purpose. It is well known that people with chronic obstructive pulmonary disease (COPD)&#13;
experience declines in functional  erformance, but little is known about the rate of decline. The purpose of this research was to describe the rate of decline in functional performance and to examine the contribution of disease severity, body composition, symptoms and functional&#13;
capacity. Functional performance was defined as the activities that people choose to engage in on a day-to-day basis.&#13;
Methods. People (N=108) with COPD were enrolled and followed yearly for three years with: self-reported functional performance (Functional Performance Inventory), spirometry, lung volumes, diffusion capacity, body composition (dual energy x-ray absorptiometry), dyspnea and&#13;
fatigue (Chronic Respiratory Disease Questionnaire) and functional capacity (six-minute walk distance (6MWD), isokinetic strength of knee flexors and extensors, handgrip strength and maximal inspiratory pressure). A total of 88 subjects completed a (mean ± SD) of 2.7 + 0.9 years of follow-up.&#13;
Results. Significant negative slopes were observed for functional performance (P=0.001), spirometry (the ratio of forced expiratory volume in one second to forced vital capacity ((FEV1/FVC), P&lt;0.0001), diffusion capacity (P&lt;0.0001) and muscle strength (P&lt;0.0001). The slopes for dyspnea, fatigue and functional capacity were not significantly different from zero, but&#13;
there was wide individual variation. Hierarchical regression demonstrated that 31% of the variance in the slope of functional performance was accounted for by the hierarchical model and the primary predictors were the slopes of the FEV1/FVC, 6MWD and muscle strength (knee flexors/extensor and handgrip).&#13;
Conclusions. Subjects experienced a slow decline in functional performance, associated with declines in functional capacity and increases in body fat. Symptoms were relatively stable and not associated with declines in functional performance.
This is a non-final version of an article published in final form in American College of Sports Medicine at&#13;
DOI:10.1249/MSS.0b013e3181eb6024
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<pubDate>Tue, 01 Feb 2011 06:00:00 GMT</pubDate>
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<dc:date>2011-02-01T06:00:00Z</dc:date>
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<title>Modulation of Ischemia-Induced NMDAR1 Activation by Environmental Enrichment Decreases Oxidative Damage</title>
<link>http://hdl.handle.net/10027/8297</link>
<description>Modulation of Ischemia-Induced NMDAR1 Activation by Environmental Enrichment Decreases Oxidative Damage
Briones, Teresita L.; Rogozinska, Magdalena; Woods, Julie
In this study, we examined whether enriched environment (EE) housing has direct neuroprotective effects on oxidative damage following transient global cerebral ischemia. Fifty-two adult maleWistar rats were included in the study and received either ischemia or sham surgery. Once fully awake, rats in each group were randomly assigned to either: EE housing or socially paired housing (CON). Animals remained in their assigned environment for 7 days, and then were killed. Our data showed that glutamate receptor expression was significantly&#13;
higher in the hippocampus of the ischemia CON group than in the ischemia EE group. Furthermore, the oxidative DNA damage, protein oxidation, and neurodegeneration in the hippocampus of the ischemia CON&#13;
group were significantly increased compared to the ischemia EE group. These results suggest that EE housing possibly modulated the ischemia-induced glutamate excitotoxicity, which then attenuated the oxidative damage and neurodegeneration in the ischemia EE rats.
This is a copy of an article published in the Journal of Neurotrauma © 2011 copyright Mary Ann Liebert, Inc; Journal of Neurotrauma is available online at: http://www.liebertonline.com.&#13;
DOI: 10.1089/neu.2011.1842
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<pubDate>Thu, 01 Dec 2011 06:00:00 GMT</pubDate>
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<dc:date>2011-12-01T06:00:00Z</dc:date>
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