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	<title>The Longevity Project &#187; Abstracts</title>
	<atom:link href="http://thelongevityproject.com/category/abstracts/feed/" rel="self" type="application/rss+xml" />
	<link>http://thelongevityproject.com</link>
	<description>Information center for prevention, cognition and sustainable aging</description>
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		<title>Effects of low habitual cocoa intake on blood pressure and bioactive nitric oxide: a randomized controlled trial</title>
		<link>http://thelongevityproject.com/effects-of-low-habitual-cocoa-intake-on-blood-pressure-and-bioactive-nitric-oxide-a-randomized-controlled-trial/</link>
		<comments>http://thelongevityproject.com/effects-of-low-habitual-cocoa-intake-on-blood-pressure-and-bioactive-nitric-oxide-a-randomized-controlled-trial/#comments</comments>
		<pubDate>Thu, 12 Nov 2009 17:16:19 +0000</pubDate>
		<dc:creator>TLP</dc:creator>
				<category><![CDATA[Abstracts]]></category>
		<category><![CDATA[bioactive nitric oxide]]></category>
		<category><![CDATA[blood pressure]]></category>
		<category><![CDATA[cocoa]]></category>
		<category><![CDATA[dark chocolate]]></category>
		<category><![CDATA[polyphenols]]></category>

		<guid isPermaLink="false">http://thelongevityproject.com/?p=516</guid>
		<description><![CDATA[CONTEXT: Regular intake of cocoa-containing foods is linked to lower cardiovascular mortality in observational studies. Short-term interventions of at most 2 weeks indicate that high doses of cocoa can improve endothelial function and reduce blood pressure (BP) due to the action of the cocoa polyphenols, but the clinical effect of low habitual cocoa intake on [...]]]></description>
			<content:encoded><![CDATA[<p>CONTEXT: <strong>Regular intake of cocoa-containing foods</strong> is linked to lower cardiovascular mortality in observational studies. Short-term interventions of at most 2 weeks indicate that high doses of cocoa can improve endothelial function and <strong>reduce blood pressure</strong> (BP) due to the action of the <strong>cocoa polyphenols</strong>, but the clinical effect of low habitual cocoa intake on BP and the underlying BP-lowering mechanisms are unclear. OBJECTIVE: To determine effects of low doses of polyphenol-rich dark chocolate on BP. DESIGN, SETTING, AND PARTICIPANTS: Randomized, controlled, investigator-blinded, parallel-group trial involving 44 adults aged 56 through 73 years (24 women, 20 men) with untreated upper-range prehypertension or stage 1 hypertension without concomitant risk factors. The trial was conducted at a primary care clinic in Germany between January 2005 and December 2006. INTERVENTION: Participants were randomly assigned to receive for 18 weeks either 6.3 g (30 kcal) per day of dark chocolate containing 30 mg of polyphenols or matching polyphenol-free white chocolate. MAIN OUTCOME MEASURES: Primary outcome measure was the change in <strong>BP</strong> after 18 weeks. Secondary outcome measures were changes in plasma markers of <strong>vasodilative nitric oxide</strong> (S-nitrosoglutathione) and <strong>oxidative stress</strong> (8-isoprostane), and bioavailability of <strong>cocoa polyphenols</strong>. RESULTS: From baseline to 18 weeks, dark chocolate intake reduced mean (SD) systolic BP by -2.9 (1.6) mm Hg (P &lt; .001) and diastolic BP by -1.9 (1.0) mm Hg (P &lt; .001) without changes in body weight, plasma levels of lipids, glucose, and 8-isoprostane. Hypertension prevalence declined from 86% to 68%. The BP decrease was accompanied by a sustained increase of S-nitrosoglutathione by 0.23 (0.12) nmol/L (P &lt; .001), and a dark chocolate dose resulted in the appearance of cocoa phenols in plasma. White chocolate intake caused no changes in BP or plasma biomarkers. CONCLUSIONS: Data in this relatively small sample of otherwise healthy individuals with above-optimal BP indicate that inclusion of small amounts of polyphenol-rich dark chocolate as part of a usual diet efficiently reduced BP and improved formation of vasodilative nitric oxide.</p>
<p class="citation"><a title="JAMA : the journal of the American Medical Association." href="javascript:AL_get(this,%20'jour',%20'JAMA.');">JAMA.</a> 2007 Jul 4;298(1):49-60.</p>
<p class="auth_list"><a href="http://www.ncbi.nlm.nih.gov/pubmed?term=%22Taubert%20D%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract">Taubert D</a>, <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=%22Roesen%20R%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract">Roesen R</a>, <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=%22Lehmann%20C%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract">Lehmann C</a>, <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=%22Jung%20N%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract">Jung N</a>, <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=%22Sch%C3%B6mig%20E%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract">SchÃ¶mig E</a>.</p>
<p class="aff">Department of Pharmacology, University Hospital of Cologne, Cologne, Germany. dirk.taubert@medizin.uni-koeln.de</p>
<p>Comment in:</p>
<ul class="comm_corr">
<li><a href="http://www.ncbi.nlm.nih.gov/pubmed/17954536?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract">JAMA. 2007 Oct 24;298(16):1862-3; author reply 1863-4. </a></li>
<li><a href="http://www.ncbi.nlm.nih.gov/pubmed/18580726?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstract">South Med J. 2008 Jul;101(7):670.</a></li>
</ul>
<div class="icons"><a href="http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?PrId=3051&amp;itool=Abstract-def&amp;uid=17609490&amp;nlmid=7501160&amp;db=pubmed&amp;url=http://jama.ama-assn.org/cgi/pmidlookup?view=long&amp;pmid=17609490" target="_blank"><img id="linkout-icon-def-jama_full_free" src="http://www.ncbi.nlm.nih.gov/corehtml/query/egifs/http:--highwire.stanford.edu-icons-externalservices-pubmed-custom-jama_full_free.gif" border="0" alt="Click here to read" /></a></div>
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		</item>
		<item>
		<title>Dietary pattern and depressive symptoms in middle age</title>
		<link>http://thelongevityproject.com/dietary-pattern-and-depressive-symptoms-in-middle-age/</link>
		<comments>http://thelongevityproject.com/dietary-pattern-and-depressive-symptoms-in-middle-age/#comments</comments>
		<pubDate>Thu, 05 Nov 2009 15:12:36 +0000</pubDate>
		<dc:creator>TLP</dc:creator>
				<category><![CDATA[Abstracts]]></category>
		<category><![CDATA[depression]]></category>
		<category><![CDATA[diet]]></category>
		<category><![CDATA[dietary pattern]]></category>
		<category><![CDATA[fish]]></category>
		<category><![CDATA[fruits]]></category>
		<category><![CDATA[vegetable]]></category>

		<guid isPermaLink="false">http://thelongevityproject.com/?p=512</guid>
		<description><![CDATA[BACKGROUND: Studies of diet and depression have focused primarily on individual nutrients. AIMS: To examine the association between dietary patterns and depression using an overall diet approach. METHOD: Analyses were carried on data from 3486 participants (26.2% women, mean age 55.6 years) from the Whitehall II prospective cohort, in which two dietary patterns were identified: [...]]]></description>
			<content:encoded><![CDATA[<p>BACKGROUND: Studies of diet and depression have focused primarily on individual nutrients. AIMS: To examine the association between dietary patterns and depression using an overall diet approach. METHOD: Analyses were carried on data from 3486 participants (26.2% women, mean age 55.6 years) from the Whitehall II prospective cohort, in which two dietary patterns were identified: &#8216;whole food&#8217; (heavily loaded by vegetables, fruits and fish) and &#8216;processed food&#8217; (heavily loaded by sweetened desserts, fried food, processed meat, refined grains and high-fat dairy products). Self-reported depression was assessed 5 years later using the Center for Epidemiologic Studies &#8211; Depression (CES-D) scale. RESULTS: After adjusting for potential confounders, participants in the highest tertile of the whole food pattern had lower odds of CES-D depression (OR = 0.74, 95% CI 0.56-0.99) than those in the lowest tertile. In contrast, high consumption of processed food was associated with an increased odds of CES-D depression (OR = 1.58, 95% CI 1.11-2.23). CONCLUSIONS: In middle-aged participants, a processed food dietary pattern is a risk factor for CES-D depression 5 years later, whereas a whole food pattern is protective.</p>
<p class="citation">Br J Psychiatry. 2009 Nov;195(5):408-13.</p>
<p class="auth_list">Akbaraly TN, Brunner EJ, Ferrie JE, Marmot MG, Kivimaki M, Singh-Manoux A.</p>
<p class="aff">Department of Epidemiology and Public Health, University College London, London WC1E 6BT, UK. tasnime.akbaraly@inserm.fr</p>
<div class="icons"><a href="http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?PrId=3051&amp;itool=Abstract-def&amp;uid=19880930&amp;nlmid=0342367&amp;db=pubmed&amp;url=http://bjp.rcpsych.org/cgi/pmidlookup?view=long&amp;pmid=19880930" target="_blank"><img id="linkout-icon-def-entrez" src="http://www.ncbi.nlm.nih.gov/corehtml/query/egifs/http:--highwire.stanford.edu-icons-externalservices-pubmed-notfree-bjprcpsych-entrez.gif" border="0" alt="Click here to read" /></a></div>
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		</item>
		<item>
		<title>Circadian Timing of Food Intake Contributes to Weight Gain</title>
		<link>http://thelongevityproject.com/circadian-timing-of-food-intake-contributes-to-weight-gain/</link>
		<comments>http://thelongevityproject.com/circadian-timing-of-food-intake-contributes-to-weight-gain/#comments</comments>
		<pubDate>Fri, 04 Sep 2009 19:15:15 +0000</pubDate>
		<dc:creator>CL</dc:creator>
				<category><![CDATA[Abstracts]]></category>
		<category><![CDATA[circadian clock]]></category>
		<category><![CDATA[weight gain]]></category>

		<guid isPermaLink="false">http://thelongevityproject.com/?p=510</guid>
		<description><![CDATA[Studies of body weight regulation have focused almost entirely on caloric intake and energy expenditure. However, a number of recent studies in animals linking energy regulation and the circadian clock at the molecular, physiological, and behavioral levels raise the possibility that the timing of food intake itself may play a significant role in weight gain. [...]]]></description>
			<content:encoded><![CDATA[<p class="caff">Studies of body weight regulation have focused almost entirely on caloric intake and energy expenditure. However, a number of recent studies in animals linking energy regulation and the circadian clock at the molecular, physiological, and behavioral levels raise the possibility that the timing of food intake itself may play a significant role in weight gain. The present study focused on the role of the circadian phase of food consumption in weight gain. We provide evidence that nocturnal mice fed a high-fat diet only during the 12-h light phase gain significantly more weight than mice fed only during the 12-h dark phase. A better understanding of the role of the circadian system for weight gain could have important implications for developing new therapeutic strategies for combating the obesity epidemic facing the human population today.</p>
<p id="aug">Deanna M.Â Arble<sup>1</sup>, JosephÂ Bass<sup>1,2</sup>, Aaron D.Â Laposky<sup>1</sup>, Martha H.Â Vitaterna<sup>1</sup> and Fred W.Â Turek<sup>1</sup></p>
<ol>
<li id="aff1"><sup>1</sup>Center for Sleep and Circadian Biology, Northwestern University, Evanston, Illinois, USA</li>
<li id="aff2"><sup>2</sup>Department of Medicine, Feinberg School of Medicine, Northwestern University, Evanston, Illinois, USA</li>
</ol>
<p class="caff">Correspondence: Fred W. Turek (fturek@northwestern.edu)</p>
<p class="caff"><em>Obesity</em> (2009) doi:10.1038/oby.2009.264</p>
]]></content:encoded>
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		<item>
		<title>Dairy augmentation of total and central fat loss in obese subjects</title>
		<link>http://thelongevityproject.com/dairy-augmentation-of-total-and-central-fat-loss-in-obese-subjects/</link>
		<comments>http://thelongevityproject.com/dairy-augmentation-of-total-and-central-fat-loss-in-obese-subjects/#comments</comments>
		<pubDate>Mon, 04 May 2009 13:29:24 +0000</pubDate>
		<dc:creator>TLP</dc:creator>
				<category><![CDATA[Abstracts]]></category>
		<category><![CDATA[dairy]]></category>
		<category><![CDATA[fat loss]]></category>
		<category><![CDATA[obesity]]></category>
		<category><![CDATA[yoghurt]]></category>

		<guid isPermaLink="false">http://thelongevityproject.com/?p=508</guid>
		<description><![CDATA[BACKGROUND AND OBJECTIVE: We have previously demonstrated an antiobesity effect of dietary Ca; this is largely mediated by Ca suppression of calcitriol levels, resulting in reduced adipocyte intracellular Ca2+ and, consequently, a coordinated increase in lipid utilization and decrease in lipogenesis. Notably, dairy Ca is markedly more effective than other Ca sources. DESIGN: Obese subjects [...]]]></description>
			<content:encoded><![CDATA[<p class="abstract">BACKGROUND AND OBJECTIVE: We have previously demonstrated an antiobesity effect of dietary Ca; this is largely mediated by Ca suppression of calcitriol levels, resulting in reduced adipocyte intracellular Ca2+ and, consequently, a coordinated increase in lipid utilization and decrease in lipogenesis. Notably, dairy Ca is markedly more effective than other Ca sources. DESIGN: Obese subjects were placed on balanced deficit (-500 kcal/day) diets and randomized to control (400-500 mg Ca/day; n = 16) or yogurt (1100 mg Ca/day; n = 18) treatments for 12 weeks. Dietary macronutrients and fiber were held constant at the US average. MEASUREMENTS: Body weight, body fat and fat distribution (by dual-energy X-ray absorptiometry), blood pressure and circulating lipids were measured at baseline and after 12 weeks of intervention. RESULTS: Fat loss was markedly increased on the yogurt diet (-4.43+/-0.47 vs -2.75+/-0.73 kg in yogurt and control groups; P&lt;0.005) while lean tissue loss was reduced by 31% on the yogurt diet. Trunk fat loss was augmented by 81% on the yogurt vs control diet (P&lt;0.001), and this was reflected in a markedly greater reduction in waist circumference (-3.99+/-0.48 vs -0.58+/-1.04 cm, P&lt;0.001). Further, the fraction of fat lost from the trunk was higher on the yogurt diet vs control (P&lt;0.005). CONCLUSION: Isocaloric substitution of yogurt for other foods significantly augments fat loss and reduces central adiposity during energy restriction.</p>
<p class="abstract"><a href="http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Zemel%20MB%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Zemel MB</strong></a>, <a href="http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Richards%20J%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Richards J</strong></a>, <a href="http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Mathis%20S%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Mathis S</strong></a>, <a href="http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Milstead%20A%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Milstead A</strong></a>, <a href="http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Gebhardt%20L%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Gebhardt L</strong></a>, <a href="http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&amp;Cmd=Search&amp;Term=%22Silva%20E%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus"><strong>Silva E</strong></a>.</p>
<p class="affiliation">Department of Nutrition, The University of Tennessee, Knoxville, TN 37996-1920, USA. mzemel@utk.edu</p>
<p class="abstract"><span class="ti"><strong> </strong><span title="International journal of obesity (2005)."><a href="javascript:AL_get(this,%20'jour',%20'Int%20J%20Obes%20(Lond).');">Int J Obes (Lond).</a></span> 2005 Apr;29(4):391-7.</span><span class="featured_linkouts"><a href="http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?PrId=3094&amp;itool=AbstractPlus-def&amp;uid=15672113&amp;db=pubmed&amp;url=http://dx.doi.org/10.1038/sj.ijo.0802880" target="_blank"><img id="linkout-icon-def-lo_npg" src="http://www.ncbi.nlm.nih.gov/corehtml/query/egifs/http:--www.nature.com-images-lo_npg.gif" border="0" alt="Click here to read" /></a> </span><span class="linkbar"><script>&lt;!-- 
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		<title>Effects of cardiorespiratory fitness and cerebral blood flow on cognitive outcomes in older women</title>
		<link>http://thelongevityproject.com/effects-of-cardiorespiratory-fitness-and-cerebral-blood-flow-on-cognitive-outcomes-in-older-women/</link>
		<comments>http://thelongevityproject.com/effects-of-cardiorespiratory-fitness-and-cerebral-blood-flow-on-cognitive-outcomes-in-older-women/#comments</comments>
		<pubDate>Fri, 23 Jan 2009 19:00:57 +0000</pubDate>
		<dc:creator>TLP</dc:creator>
				<category><![CDATA[Abstracts]]></category>
		<category><![CDATA[aging]]></category>
		<category><![CDATA[cerebrovascular circulation]]></category>
		<category><![CDATA[cognitive function]]></category>
		<category><![CDATA[exercise]]></category>
		<category><![CDATA[hypertension]]></category>
		<category><![CDATA[transcranial Doppler ultrasound]]></category>
		<category><![CDATA[women]]></category>

		<guid isPermaLink="false">http://thelongevityproject.com/?p=105</guid>
		<description><![CDATA[The mechanisms by which aerobic fitness confers beneficial effects on cognition with aging are unclear but may involve cerebrovascular adaptations. In a cross-sectional study of women from the community (n = 42; age range = 50â€“90 years), we sought to determine whether physical fitness is associated with higher cerebrovascular function, and its relationship to cognition. [...]]]></description>
			<content:encoded><![CDATA[<p>The mechanisms by which aerobic fitness confers beneficial effects on cognition with aging are unclear but may involve cerebrovascular adaptations. In a cross-sectional study of women from the community (n = 42; age range = 50â€“90 years), we sought to determine whether physical fitness is associated with higher cerebrovascular function, and its relationship to cognition. Main outcome measures included resting cerebral blood flow, cerebrovascular reserve, physical fitness (i.e., View the MathML source) and cognition. Physically fit women had lower resting mean arterial pressure (MAP) and higher cerebrovascular conductance (CVC) than sedentary women. Overall cognition was negatively correlated with age and positively correlated with View the MathML source. View the MathML source was a predictor of resting CVC and MAP, and CVC and MAP when end-tidal gases were held constant at near-resting values. MAP and CVC were predictors of cognition. This study identified strong associations between physical fitness, vascular function and cognition, and provides new understanding regarding the mechanisms by which fitness positively impacts cognition with aging. The implications of this research are considerable and warrant future investigation.</p>
<p>Allison D. Brown, Carly A. McMorris, R. Stewart Longman, Richard Leigh, Michael D. Hill, Christine M. Friedenreich and Marc J. Poulina</p>
<p><a href="http://www.sciencedirect.com/science?_ob=ArticleURL&amp;_udi=B6T09-4V7KBNY-1&amp;_user=10&amp;_rdoc=1&amp;_fmt=&amp;_orig=search&amp;_sort=d&amp;view=c&amp;_acct=C000050221&amp;_version=1&amp;_urlVersion=0&amp;_userid=10&amp;md5=67e8f4254fcf42e953454e433db3c213">full-text article</a></p>
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		<title>A randomized placebo-controlled trial of Ginkgo biloba for the prevention of cognitive decline</title>
		<link>http://thelongevityproject.com/a-randomized-placebo-controlled-trial-of-ginkgo-biloba-for-the-prevention-of-cognitive-decline/</link>
		<comments>http://thelongevityproject.com/a-randomized-placebo-controlled-trial-of-ginkgo-biloba-for-the-prevention-of-cognitive-decline/#comments</comments>
		<pubDate>Tue, 08 Jul 2008 09:05:47 +0000</pubDate>
		<dc:creator>TLP</dc:creator>
				<category><![CDATA[Abstracts]]></category>
		<category><![CDATA[cognitive decline]]></category>
		<category><![CDATA[Ginkgo biloba]]></category>
		<category><![CDATA[stroke]]></category>
		<category><![CDATA[transient ischemic attack]]></category>

		<guid isPermaLink="false">http://thelongevityproject.com/a-randomized-placebo-controlled-trial-of-ginkgo-biloba-for-the-prevention-of-cognitive-decline/</guid>
		<description><![CDATA[

OBJECTIVE: To assess the feasibility, safety, and efficacy of Ginkgo biloba extract (GBE) on delaying the progression to cognitive impairment in normal elderly aged 85 and older. METHODS: Randomized, placebo-controlled, double-blind, 42-month pilot study with 118 cognitively intact subjects randomized to standardized GBE or placebo. Kaplan-Meier estimation, Cox proportional hazard, and random-effects models were used [...]]]></description>
			<content:encoded><![CDATA[<dl class="AbstractPlusReport">
<dd class="abstract">
<p class="abstract">OBJECTIVE: To assess the feasibility, safety, and efficacy of Ginkgo biloba extract (GBE) on delaying the progression to cognitive impairment in normal elderly aged 85 and older. METHODS: Randomized, placebo-controlled, double-blind, 42-month pilot study with 118 cognitively intact subjects randomized to standardized GBE or placebo. Kaplan-Meier estimation, Cox proportional hazard, and random-effects models were used to compare the risk of progression from Clinical Dementia Rating (CDR) = 0 to CDR = 0.5 and decline in episodic memory function between GBE and placebo groups. RESULTS: In the intention-to-treat analysis, there was no reduced risk of progression to CDR = 0.5 (log-rank test, p = 0.06) among the GBE group. There was no less of a decline in memory function among the GBE group (p = 0.05). In the secondary analysis, where we controlled the medication adherence level, the GBE group had a lower risk of progression from CDR = 0 to CDR = 0.5 (HR = 0.33, p = 0.02), and a smaller decline in memory scores (p = 0.04). There were more ischemic strokes and TIAs in the GBE group (p = 0.01). CONCLUSIONS: In unadjusted analyses, Ginkgo biloba extract (GBE) neither altered the risk of progression from normal to Clinical Dementia Rating (CDR) = 0.5, nor protected against a decline in memory function. Secondary analysis taking into account medication adherence showed a protective effect of GBE on the progression to CDR = 0.5 and memory decline. Results of larger prevention trials taking into account medication adherence may clarify the effectiveness of GBE. More stroke and TIA cases observed among the GBE group requires further study to confirm.</p>
<dl class="AbstractPlusReport">
<dt class="head">
<p class="abstitle"><span class="ti"><strong>1: </strong><span title="Neurology.">Neurology.</span> 2008 May 6;70(19 Pt 2):1809-17. Epub  2008 Feb 27.</span></p>
<p class="abstitle"><span class="ti"></span><span class="featured_linkouts"><a href="http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?PrId=3051&amp;itool=AbstractPlus-def&amp;uid=18305231&amp;db=pubmed&amp;url=http://www.neurology.org/cgi/pmidlookup?view=long&amp;pmid=18305231" target="_blank"><img src="http://www.ncbi.nlm.nih.gov/corehtml/query/egifs/http:--highwire.stanford.edu-icons-externalservices-pubmed-notfree-neurology-entrez.gif" alt="Click here to read" border="0" /></a> </span><span class="linkbar"><script language="JavaScript1.2"><!--  var Menu18305231 = [    ["UseLocalConfig", "jsmenu3Config", "", ""],   ["LinkOut", "window.top.location='/sites/entrez?Cmd=ShowLinkOut&#038;Db=pubmed&#038;TermToSearch=18305231&#038;ordinalpos=1&#038;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus' ", "", ""] 				 ] 				 --></script><a href="javascript:PopUpMenu2_Set(Menu18305231);" class="dblinks" onmouseout="PopUpMenu2_Hide();" target="_self">Links</a></span></p>
</dt>
<dd class="abstract">
<dl class="commcorr">
<dt>Comment in:</dt>
<dd>       Neurology. 2008 May 6;70(19 Pt 2):1730-1.      </dd>
</dl>
</dd>
<dd class="abstract">
<p class="authors">&nbsp;</p>
<p class="authors"><strong>Dodge HH</strong>, <strong>Zitzelberger T</strong>, <strong>Oken BS</strong>, <strong>Howieson D</strong>, <strong>Kaye J</strong>.</p>
<p class="affiliation">Department of Public Health, Oregon State University, Corvallis, OR 97401, USA. Hiroko.Dodge@oregonstate.edu</p>
</dd>
</dl>
<p class="abstract">&nbsp;</p>
</dd>
</dl>
]]></content:encoded>
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		</item>
		<item>
		<title>Public computer surfaces are reservoirs for methicillin-resistant staphylococci</title>
		<link>http://thelongevityproject.com/public-computer-surfaces-are-reservoirs-for-methicillin-resistant-staphylococci/</link>
		<comments>http://thelongevityproject.com/public-computer-surfaces-are-reservoirs-for-methicillin-resistant-staphylococci/#comments</comments>
		<pubDate>Wed, 14 May 2008 14:06:09 +0000</pubDate>
		<dc:creator>TLP</dc:creator>
				<category><![CDATA[Abstracts]]></category>
		<category><![CDATA[Germs]]></category>
		<category><![CDATA[computer keyboard]]></category>
		<category><![CDATA[fomite]]></category>

		<guid isPermaLink="false">http://thelongevityproject.com/public-computer-surfaces-are-reservoirs-for-methicillin-resistant-staphylococci/</guid>
		<description><![CDATA[

The role of computer keyboards used by students of a metropolitan university as reservoirs of antibiotic-resistant staphylococci was determined. Putative methicillin (oxacillin)-resistant staphylococci isolates were identified from keyboard swabs following a combination of biochemical and genetic analyses. Of 24 keyboards surveyed, 17 were contaminated with staphylococci that grew in the presence of oxacillin (2 mg [...]]]></description>
			<content:encoded><![CDATA[<dl class="AbstractPlusReport">
<dd class="abstract">
<p class="abstract">The role of computer keyboards used by students of a metropolitan university as reservoirs of antibiotic-resistant staphylococci was determined. Putative methicillin (oxacillin)-resistant staphylococci isolates were identified from keyboard swabs following a combination of biochemical and genetic analyses. Of 24 keyboards surveyed, 17 were contaminated with staphylococci that grew in the presence of oxacillin (2 mg l(-1)). Methicillin (oxacillin)-resistant Staphylococcus aureus (MRSA), -S. epidermidis (MRSE) and -S. hominis (MRSH) were present on two, five and two keyboards, respectively, while all three staphylococci co-contaminated one keyboard. Furthermore, these were found to be part of a greater community of oxacillin-resistant bacteria. Combined with the broad user base common to public computers, the presence of antibiotic-resistant staphylococci on keyboard surfaces might impact the transmission and prevalence of pathogens throughout the community.</p>
<dl class="AbstractPlusReport">
<dt class="head">
<p class="abstitle"><span class="ti"><strong>1: </strong><span title="The ISME journal."><a href="javascript:AL_get(this, 'jour', 'ISME J.');">ISME J.</a></span> 2007 Jul;1(3):265-8. Epub  2007 May 31.</span><span class="featured_linkouts"><a href="http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?PrId=3094&amp;itool=AbstractPlus-def&amp;uid=18043636&amp;db=pubmed&amp;url=http://dx.doi.org/10.1038/ismej.2007.36" target="_blank"><img src="http://www.ncbi.nlm.nih.gov/corehtml/query/egifs/http:--www.nature.com-images-lo_npg.gif" alt="Click here to read" border="0" /></a> </span><span class="linkbar"><script language="JavaScript1.2"><!--  var Menu18043636 = [    ["UseLocalConfig", "jsmenu3Config", "", ""],   ["Compound (MeSH Keyword)" , "window.top.location=\\\'/sites/entrez?Db=pccompound&#038;DbFrom=pubmed&#038;Cmd=Link&#038;LinkName=pubmed_pccompound_mesh&#038;LinkReadableName=Compound%20(MeSH%20Keyword)&#038;IdsFromResult=18043636&#038;ordinalpos=1&#038;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus\\\' ", "", ""],   ["Nucleotide" , "window.top.location=\\\'/sites/entrez?Db=nuccore&#038;DbFrom=pubmed&#038;Cmd=Link&#038;LinkName=pubmed_nuccore&#038;LinkReadableName=Nucleotide&#038;IdsFromResult=18043636&#038;ordinalpos=1&#038;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus\\\' ", "", ""],   ["Substance (MeSH Keyword)" , "window.top.location=\\\'/sites/entrez?Db=pcsubstance&#038;DbFrom=pubmed&#038;Cmd=Link&#038;LinkName=pubmed_pcsubstance_mesh&#038;LinkReadableName=Substance%20(MeSH%20Keyword)&#038;IdsFromResult=18043636&#038;ordinalpos=1&#038;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus\\\' ", "", ""],   ["PopSet" , "window.top.location=\\\'/sites/entrez?Db=popset&#038;DbFrom=pubmed&#038;Cmd=Link&#038;LinkName=pubmed_popset&#038;LinkReadableName=PopSet&#038;IdsFromResult=18043636&#038;ordinalpos=1&#038;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus\\\' ", "", ""],   ["LinkOut", "window.top.location=\\\'/sites/entrez?Cmd=ShowLinkOut&#038;Db=pubmed&#038;TermToSearch=18043636&#038;ordinalpos=1&#038;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus\\\' ", "", ""] 				 ] 				 --></script><a href="javascript:PopUpMenu2_Set(Menu18043636);" onmouseout="PopUpMenu2_Hide();" class="dblinks" target="_self">Links</a></span></p>
</dt>
<dd class="abstract">
<h2></h2>
<p class="authors"><!--AuthorList--><strong>Kassem II</strong>, <strong>Sigler V</strong>, <strong>Esseili MA</strong>.</p>
<p class="affiliation">Laboratory for Microbial Ecology, Department of Environmental Sciences, University of Toledo, Toledo, OH 43606, USA.</p>
</dd>
</dl>
<p class="abstract">&nbsp;</p>
</dd>
</dl>
]]></content:encoded>
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		<slash:comments>0</slash:comments>
		</item>
		<item>
		<title>Computer keyboard and mouse as a reservoir of pathogens in an intensive care unit</title>
		<link>http://thelongevityproject.com/computer-keyboard-and-mouse-as-a-reservoir-of-pathogens-in-an-intensive-care-unit/</link>
		<comments>http://thelongevityproject.com/computer-keyboard-and-mouse-as-a-reservoir-of-pathogens-in-an-intensive-care-unit/#comments</comments>
		<pubDate>Wed, 14 May 2008 14:04:45 +0000</pubDate>
		<dc:creator>TLP</dc:creator>
				<category><![CDATA[Abstracts]]></category>
		<category><![CDATA[Germs]]></category>
		<category><![CDATA[computer keyboard]]></category>
		<category><![CDATA[fomite]]></category>
		<category><![CDATA[fomites]]></category>
		<category><![CDATA[intensive care unit]]></category>
		<category><![CDATA[reservoir]]></category>

		<guid isPermaLink="false">http://thelongevityproject.com/computer-keyboard-and-mouse-as-a-reservoir-of-pathogens-in-an-intensive-care-unit/</guid>
		<description><![CDATA[

OBJECTIVE: User interfaces of patient data management systems (PDMS) in intensive care units (ICU), like computer keyboard and mouse, may serve as reservoirs for the transmission of microorganisms. Pathogens may be transferred via the hands of personnel to the patient causing nosocomial infections. The purpose of this study was to examine the microbial contamination of [...]]]></description>
			<content:encoded><![CDATA[<dl class="AbstractPlusReport">
<dd class="abstract">
<p class="abstract">OBJECTIVE: User interfaces of patient data management systems (PDMS) in intensive care units (ICU), like computer keyboard and mouse, may serve as reservoirs for the transmission of microorganisms. Pathogens may be transferred via the hands of personnel to the patient causing nosocomial infections. The purpose of this study was to examine the microbial contamination of computer user interfaces with potentially pathogenic microorganisms, compared with other fomites in a surgical intensive care unit of a tertiary teaching hospital. METHODS: Sterile swab samples were received from patient&#8217;s bedside computer keyboard and mouse, and three other sites (infusion pumps, ventilator, ward round trolley) in the patient&#8217;s room in a 14 bed surgical intensive care unit at a university hospital. At the central ward samples from keyboard and mouse of the physician&#8217;s workstation, and control buttons of the ward&#8217;s intercom and telephone receiver were obtained. Quantitative and qualitative bacteriological sampling occurred during two periods of three months each on eight nonconsecutive days. RESULTS: In all 14 patients&#8217; rooms we collected a total of 1118 samples: 222 samples from keyboards and mice, 214 from infusion pumps and 174 from the ward&#8217;s trolley. From the central ward 16 samples per formites were obtained (computer keyboard and mouse at the physician&#8217;s workstation and the ward&#8217;s intercom and telephone receiver). Microbacterial analysis from samples in patients&#8217; rooms yielded 26 contaminated samples from keyboard and mouse (5.9%) compared with 18 positive results from other fomites within patients&#8217; rooms (3.0%; p &lt; 0.02). At the physician&#8217;s computer terminal two samples obtained from the mouse (6.3%) showed positive microbial testing whereas the ward&#8217;s intercom and telephone receiver were not contaminated (p = 0.15). CONCLUSIONS: The colonization rate for computer keyboard and mouse of a PDMS with potentially pathogenic microorganisms is greater than that of other user interfaces in a surgical ICU. These fomites may be additional reservoirs for the transmision of microorganisms and become vectors for cross-transmission of nosocomial infections in the ICU setting.</p>
<dl class="AbstractPlusReport">
<dt class="head">
<p class="abstitle"><span class="ti"><strong>1: </strong><span title="Journal of clinical monitoring and computing."><a href="javascript:AL_get(this, 'jour', 'J Clin Monit Comput.');">J Clin Monit Comput.</a></span> 2004 Feb;18(1):7-12.</span><span class="featured_linkouts"><a href="http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?PrId=3055&amp;itool=AbstractPlus-def&amp;uid=15139578&amp;db=pubmed&amp;url=http://www.kluweronline.com/art.pdf?issn=1387-1307&amp;volume=18&amp;page=7" target="_blank"><img src="http://www.ncbi.nlm.nih.gov/corehtml/query/egifs/http:--production.springer.de-OnlineResources-Logos-springerlink.gif" alt="Click here to read" border="0" /></a> </span><span class="linkbar"><script language="JavaScript1.2"><!--  var Menu15139578 = [    ["UseLocalConfig", "jsmenu3Config", "", ""],   ["LinkOut", "window.top.location=\\\'/sites/entrez?Cmd=ShowLinkOut&#038;Db=pubmed&#038;TermToSearch=15139578&#038;ordinalpos=1&#038;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstractPlus\\\' ", "", ""] 				 ] 				 --></script><a href="javascript:PopUpMenu2_Set(Menu15139578);" onmouseout="PopUpMenu2_Hide();" class="dblinks" target="_self">Links</a></span></p>
</dt>
<dd class="abstract">
<h2></h2>
<p class="authors"><!--AuthorList--><strong>Hartmann B</strong>, <strong>Benson M</strong>, <strong>Junger A</strong>, <strong>Quinzio L</strong>, <strong>Röhrig R</strong>, <strong>Fengler B</strong>, <strong>Färber UW</strong>, <strong>Wille B</strong>, <strong>Hempelmann G</strong>.</p>
<p class="affiliation">Department of Anesthesiology, Intensive Care Medicine, and Pain Therapy, University Hospital, Giessen.</p>
</dd>
</dl>
<p class="abstract">&nbsp;</p>
</dd>
</dl>
]]></content:encoded>
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		</item>
		<item>
		<title>Dietary patterns and risk of dementia: the Three-City cohort study</title>
		<link>http://thelongevityproject.com/dietary-patterns-and-risk-of-dementia-the-three-city-cohort-study/</link>
		<comments>http://thelongevityproject.com/dietary-patterns-and-risk-of-dementia-the-three-city-cohort-study/#comments</comments>
		<pubDate>Thu, 17 Jan 2008 18:20:11 +0000</pubDate>
		<dc:creator>TLP</dc:creator>
				<category><![CDATA[Abstracts]]></category>
		<category><![CDATA[Alzheimer]]></category>
		<category><![CDATA[dementia]]></category>
		<category><![CDATA[fish]]></category>
		<category><![CDATA[fruits]]></category>
		<category><![CDATA[omega-3]]></category>
		<category><![CDATA[vegetables]]></category>

		<guid isPermaLink="false">http://thelongevityproject.com/dietary-patterns-and-risk-of-dementia-the-three-city-cohort-study/</guid>
		<description><![CDATA[

BACKGROUND: Dietary fatty acids and antioxidants may contribute to decrease dementia risk, but epidemiologic data remain controversial. The aim of our study was to analyze the relationship between dietary patterns and risk of dementia or Alzheimer disease (AD), adjusting for sociodemographic and vascular risk factors, and taking into account the ApoE genotype. METHODS: A total [...]]]></description>
			<content:encoded><![CDATA[<dl class="PubmedArticle">
<dd class="abstract">
<p class="abstract">BACKGROUND: Dietary fatty acids and antioxidants may contribute to decrease dementia risk, but epidemiologic data remain controversial. The aim of our study was to analyze the relationship between dietary patterns and risk of dementia or Alzheimer disease (AD), adjusting for sociodemographic and vascular risk factors, and taking into account the ApoE genotype. METHODS: A total of 8,085 nondemented participants aged 65 and over were included in the Three-City cohort study in Bordeaux, Dijon, and Montpellier (France) in 1999-2000 and had at least one re-examination over 4 years (rate of follow-up 89.1%). An independent committee of neurologists validated 281 incident cases of dementia (including 183 AD). RESULTS: Daily consumption of fruits and vegetables was associated with a decreased risk of all cause dementia (hazard ratio [HR] 0.72, 95% CI 0.53 to 0.97) in fully adjusted models. Weekly consumption of fish was associated with a reduced risk of AD (HR 0.65, 95% CI 0.43 to 0.994) and all cause dementia but only among ApoE epsilon 4 noncarriers (HR 0.60, 95% CI 0.40 to 0.90). Regular use of omega-3 rich oils was associated with a decreased risk of borderline significance for all cause dementia (HR 0.46, 95% CI 0.19 to 1.11). Regular consumption of omega-6 rich oils not compensated by consumption of omega-3 rich oils or fish was associated with an increased risk of dementia (HR 2.12, 95% CI 1.30 to 3.46) among ApoE epsilon 4 noncarriers. CONCLUSION: Frequent consumption of fruits and vegetables, fish, and omega-3 rich oils may decrease the risk of dementia and Alzheimer disease, especially among ApoE epsilon 4 noncarriers.</p>
<p class="abstract">&nbsp;</p>
<dl class="PubmedArticle">
<dt class="head">
<p class="abstitle"><span class="ti"><strong>1: </strong><span title="Neurology.">Neurology.</span> 2007 Nov 13;69(20):1921-30.</span><span class="featured_linkouts"><a href="http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?PrId=3051&amp;itool=AbstractPlus-def&amp;uid=17998483&amp;db=pubmed&amp;url=http://www.neurology.org/cgi/pmidlookup?view=long&amp;pmid=17998483" target="_blank"><img src="http://www.ncbi.nlm.nih.gov/corehtml/query/egifs/http:--highwire.stanford.edu-icons-externalservices-pubmed-notfree-neurology-entrez.gif" alt="Click here to read" border="0" /></a> </span><span class="linkbar"><script language="JavaScript1.2"><!--  var Menu17998483 = [    ["UseLocalConfig", "jsmenu3Config", "", ""],   ["LinkOut", "window.top.location='/sites/entrez?Cmd=ShowLinkOut&#038;Db=pubmed&#038;TermToSearch=17998483&#038;ordinalpos=1&#038;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus' ", "", ""] 				 ] 				 --></script></span></p>
</dt>
<dd class="abstract">
<h2></h2>
<p class="authors"><!--AuthorList--><strong>Barberger-Gateau P</strong>, <strong>Raffaitin C</strong>, <strong>Letenneur L</strong>, <strong>Berr C</strong>, <strong>Tzourio C</strong>, <strong>Dartigues JF</strong>, <strong>AlpÃ©rovitch A</strong>.</p>
<p class="affiliation">INSERM, U593, University Victor Segalen Bordeaux 2, case 11, 146 rue LÃ©o-Saignat, F-33076 Bordeaux cedex, France. Pascale.Barberger-Gateau@isped.u-bordeaux2.fr</p>
</dd>
</dl>
<p class="abstract">&nbsp;</p>
</dd>
</dl>
]]></content:encoded>
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		</item>
		<item>
		<title>Mediterranean diet and risk for Alzheimer&#8217;s disease</title>
		<link>http://thelongevityproject.com/mediterranean-diet-and-risk-for-alzheimers-disease/</link>
		<comments>http://thelongevityproject.com/mediterranean-diet-and-risk-for-alzheimers-disease/#comments</comments>
		<pubDate>Mon, 07 Jan 2008 09:35:12 +0000</pubDate>
		<dc:creator>TLP</dc:creator>
				<category><![CDATA[Abstracts]]></category>
		<category><![CDATA[Alzheimer-s disease]]></category>
		<category><![CDATA[Mediterranean diet]]></category>

		<guid isPermaLink="false">http://thelongevityproject.com/mediterranean-diet-and-risk-for-alzheimers-disease/</guid>
		<description><![CDATA[

OBJECTIVE: Previous research in Alzheimer&#8217;s disease (AD) has focused on individual dietary components. There is converging evidence that composite dietary patterns such as the Mediterranean diet (MeDi) is related to lower risk for cardiovascular disease, several forms of cancer, and overall mortality. We sought to investigate the association between MeDi and risk for AD. METHODS: [...]]]></description>
			<content:encoded><![CDATA[<dl class="PubmedArticle">
<dt class="head">
<p class="abstitle"><span class="ti"></span>OBJECTIVE: Previous research in Alzheimer&#8217;s disease (AD) has focused on individual dietary components. There is converging evidence that composite dietary patterns such as the Mediterranean diet (MeDi) is related to lower risk for cardiovascular disease, several forms of cancer, and overall mortality. We sought to investigate the association between MeDi and risk for AD. METHODS: A total of 2,258 community-based nondemented individuals in New York were prospectively evaluated every 1.5 years. Adherence to the MeDi (zero- to nine-point scale with higher scores indicating higher adherence) was the main predictor in models that were adjusted for cohort, age, sex, ethnicity, education, apolipoprotein E genotype, caloric intake, smoking, medical comorbidity index, and body mass index. RESULTS: There were 262 incident AD cases during the course of 4 (+/-3.0; range, 0.2-13.9) years of follow-up. Higher adherence to the MeDi was associated with lower risk for AD (hazard ratio, 0.91; 95% confidence interval, 0.83-0.98; p=0.015). Compared with subjects in the lowest MeDi tertile, subjects in the middle MeDi tertile had a hazard ratio of 0.85 (95% confidence interval, 0.63-1.16) and those at the highest tertile had a hazard ratio of 0.60 (95% confidence interval, 0.42-0.87) for AD (p for trend=0.007). INTERPRETATION: We conclude that higher adherence to the MeDi is associated with a reduction in risk for AD. Ann Neurol 2006.</p>
<p class="abstitle">&nbsp;</p>
</dt>
<dl class="PubmedArticle">
<dd class="abstract">
<p class="authors"><!--AuthorList--><strong>Scarmeas N</strong>, <strong>Stern Y</strong>, <strong>Tang MX</strong>, <strong>Mayeux R</strong>, <strong>Luchsinger JA</strong>.</p>
<p class="affiliation">Taub Institute for Research in Alzheimer&#8217;s Disease and the Aging Brain, New York, NY 10032, USA. ns257@columbia.edu</p>
</dd>
</dl>
<p class="abstitle"><span class="ti"><span title="Annals of neurology.">Ann Neurol.</span> 2006 Jun;59(6):912-21.</span><span class="featured_linkouts"><a href="http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?PrId=3058&amp;itool=AbstractPlus-def&amp;uid=16622828&amp;db=pubmed&amp;url=http://dx.doi.org/10.1002/ana.20854" target="_blank"><img src="http://www.ncbi.nlm.nih.gov/corehtml/query/egifs/http:--www3.interscience.wiley.com-images-wiley_interscience_134x30.gif" alt="Click here to read" border="0" /></a> </span><span class="linkbar"><br />
<script language="JavaScript1.2"><!--  var Menu16622828 = [    ["UseLocalConfig", "jsmenu3Config", "", ""],   ["LinkOut", "window.top.location=\'/sites/entrez?Cmd=ShowLinkOut&#038;Db=pubmed&#038;TermToSearch=16622828&#038;ordinalpos=1&#038;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus\' ", "", ""] 				 ] 				 --</script><br />
</span></p>
</dl>
]]></content:encoded>
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		</item>
	</channel>
</rss>
