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    <channel rdf:about="http://www.biomedcentral.com/feeds/latestarticles/portal?portalId=9001&amp;quantity=&amp;format=rss&amp;version=">
        <title>BioMed Central - Latest Articles</title>
        <link>http://www.biomedcentral.com/</link>
        <description>The latest research articles published by BioMed Central</description>
        <dc:date>2013-05-21T00:00:00Z</dc:date>
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                    This is an RSS newsfeed from BioMed Central
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                    It is intended to be used with an RSS reader. For more information about RSS newsfeeds from BioMed Central, visit
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        <item rdf:about="http://www.biomedcentral.com/1741-7007/11/60">
        <title>In pursuit of an HIV vaccine: an interview with Andrew McMichael</title>
        <description>No description available</description>
        <link>http://www.biomedcentral.com/1741-7007/11/60</link>
                <dc:creator>Andrew J McMichael</dc:creator>
                <dc:source>BMC Biology 2013, 11:60</dc:source>
        <dc:date>2013-05-21T00:00:00Z</dc:date>
        <dc:identifier>${item.identifier}</dc:identifier>
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                <prism:publicationName>BMC Biology</prism:publicationName>
        <prism:issn>1741-7007</prism:issn>
        <prism:volume>11</prism:volume>
        <prism:startingPage>60</prism:startingPage>
        <prism:publicationDate>2013-05-21T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.biomedcentral.com/1741-7007/11/57">
        <title>Thirty years on: HIV receptor gymnastics and the prevention of infection</title>
        <description>During 30 years of research on human immunodeficiency virus (HIV), our knowledge of its cellular receptors - CD4, CCR5 and CXCR4 - has illuminated aspects of the pathogenesis of the acquired immune deficiency syndrome (AIDS). Studying how the HIV envelope glycoproteins interact with the receptors led to anti-retroviral drugs based on blocking the docking or fusion of virus to the host cell. Genetic polymorphisms of CCR5 determine resistance to HIV infection and the rate of progression to AIDS. Eliciting neutralizing antibodies to the sites of receptor interaction on HIV glycoproteins is a promising approach to HIV vaccine development.</description>
        <link>http://www.biomedcentral.com/1741-7007/11/57</link>
                <dc:creator>Robin A Weiss</dc:creator>
                <dc:source>BMC Biology 2013, 11:57</dc:source>
        <dc:date>2013-05-21T00:00:00Z</dc:date>
        <dc:identifier>${item.identifier}</dc:identifier>
                            <dc:title>HIV receptor gymnastics</dc:title>
                            <dc:description>&lt;p&gt;Robin Weiss, in an article to mark the 30&lt;sup&gt;th&lt;/sup&gt; anniversary of the discovery of the human immunodeficiency virus (HIV), reviews the complex interactions of the virus with the specialized surface molecules by which it gains entry into cells, and how this has led to drugs that block it.&lt;/p&gt;</dc:description>
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                <prism:publicationName>BMC Biology</prism:publicationName>
        <prism:issn>1741-7007</prism:issn>
        <prism:volume>11</prism:volume>
        <prism:startingPage>57</prism:startingPage>
        <prism:publicationDate>2013-05-21T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://alzres.com/content/5/3/24">
        <title>Alzheimer&apos;s disease risk alleles in &lt;it&gt;TREM2 &lt;/it&gt;illuminate innate immunity in Alzheimer&apos;s disease</title>
        <description>Genetic studies have provided the best evidence for cause and effect relationships in Alzheimer&apos;s disease (AD). Indeed, the identification of deterministic mutations in the APP, PSEN1 and PSEN2 genes and subsequent preclinical studies linking these mutations to alterations in A&#946; production and aggregation have provided pivotal support for the amyloid cascade hypothesis. In addition, genetic, pathologic and biological studies of APOE have also indicated that the genetic risk for AD associated with APOE4 can be attributed, at least in part, to its pro-amyloidogenic effect on A&#946;. In recent years a number of SNPs that show unequivocal genome-wide association with AD risk have implicated novel genetic loci as modifiers of AD risk. However, the functional implications of these genetic associations are largely unknown. For almost all of these associations, the functional variants have not been identified. Very recently, two large consortiums demonstrated that rare variants in the triggering receptor expressed on myeloid cells 2 (TREM2) gene confer significant risk for AD. TREM2 is a type 1 membrane receptor protein primarily expressed on microglia in the central nervous system that has been shown to regulate phagocytosis and activation of monocytes. Previously it had been shown that homozygous loss of function mutations in TREM2 cause polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL, Nasu Hakola disease) and also a pure form of early-onset dementia. The association of TREM2 variants with AD brings innate immune signaling into the light, affirming innate immunity&apos;s role as a significant factor in AD pathogenesis.</description>
        <link>http://alzres.com/content/5/3/24</link>
                <dc:creator>Todd E Golde</dc:creator>
                <dc:creator>Wolfgang J Streit</dc:creator>
                <dc:creator>Paramita Chakrabarty</dc:creator>
                <dc:source>Alzheimer&apos;s Research &amp; Therapy 2013, 5:24</dc:source>
        <dc:date>2013-05-21T00:00:00Z</dc:date>
        <dc:identifier>${item.identifier}</dc:identifier>
                            <dc:title>TREM2 variants and AD risk</dc:title>
                            <dc:description>&lt;p&gt;Golde and colleagues review the function of innate immune signalling in Alzheimer&apos;s disease (AD) following recent studies showing variants of TREM2, a triggering receptor on myeloid cells, is significantly associated with AD risk.&lt;/p&gt;</dc:description>
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                <prism:publicationName>Alzheimer&apos;s Research &amp; Therapy</prism:publicationName>
        <prism:issn>1758-9193</prism:issn>
        <prism:volume>5</prism:volume>
        <prism:startingPage>24</prism:startingPage>
        <prism:publicationDate>2013-05-21T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.aoemj.com/content/25/1/7">
        <title>Association of Diabetes Mellitus with a Combination of Vitamin D Deficiency and Arsenic Exposure in the Korean General Population: Analysis of 2008&amp;#8211;2009 Korean National Health and Nutrition Examination Survey Data</title>
        <description>ObjectivesWe present data from the Korean National Health and Nutritional Examination Survey (KNHANES) 2008&#8211;2009 on the combination of vitamin D deficiency and arsenic exposure on diabetes mellitus (DM) in a representative sample of the adult Korean population.
Methods:
This study was based on data obtained from the KNHANES 2008&#8211;2009, which was conducted for 3 years (2007&#8211;2009) using a rolling sampling design that involved a complex, stratified, multistage, probability-cluster survey of a representative sample of the non-institutionalized civilian population in South Korea.
Results:
Data analysis revealed that subjects who showed both vitamin D levels in the 1st quartile (Q) and urinary arsenic levels in the 4th Q, had a 302% increased risk of having DM, as compared with those whose vitamin D and urinary arsenic levels were in the 4th Q and 1st Q, respectively.
Conclusion:
The present study reconfirmed an association of DM with low vitamin D levels and arsenic exposure, and further showed a combination of vitamin D deficiency and arsenic exposure on DM in the general Korean population. To the best of our knowledge, this is the first report describing a combination of vitamin D deficiency and arsenic exposure on DM. The present findings have important public health implications.</description>
        <link>http://www.aoemj.com/content/25/1/7</link>
                <dc:creator>Byung-Kook Lee</dc:creator>
                <dc:creator>Yangho Kim</dc:creator>
                <dc:source>Annals of Occupational and Environmental Medicine 2013, 25:7</dc:source>
        <dc:date>2013-05-21T00:00:00Z</dc:date>
        <dc:identifier>${item.identifier}</dc:identifier>
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                <prism:publicationName>Annals of Occupational and Environmental Medicine</prism:publicationName>
        <prism:issn>2052-4374</prism:issn>
        <prism:volume>25</prism:volume>
        <prism:startingPage>7</prism:startingPage>
        <prism:publicationDate>2013-05-21T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.aoemj.com/content/25/1/6">
        <title>Posttraumatic Growth and Related Factors of Child Protective Service Workers</title>
        <description>ObjectivesThe aim of the study is to measure the level of vicarious trauma, posttraumatic growth (PTG), and other factors affecting PTG among child protective service workers.
Methods:
We include posttraumatic stress, social support, stress coping, and demographic data as independent variables. Data was collected from 255 full-time social workers from 43 child protective agencies as acomplete enumeration and 204 included in the final analysis.
Results:
The major findings of the study were as follows: The mean score of PTG was 44.09 (SD:21.73). Hierarchical multiple regression was adopted and &quot;pursuing social support as a way of coping with stress&quot; was the strongest predictive factor (&#946;=0.319, p&lt;0.001) of PTG.
Conclusion:
We suggest that child protective workers are vulnerable to posttraumatic stress and mental health services are indicated. We also recommend various types of training for stress coping program, especially strengthening the social support system of the child protective service workers in South Korea.</description>
        <link>http://www.aoemj.com/content/25/1/6</link>
                <dc:creator>Young Rhee</dc:creator>
                <dc:creator>Young Ko</dc:creator>
                <dc:creator>In Han</dc:creator>
                <dc:source>Annals of Occupational and Environmental Medicine 2013, 25:6</dc:source>
        <dc:date>2013-05-21T00:00:00Z</dc:date>
        <dc:identifier>${item.identifier}</dc:identifier>
                                <prism:require>/content/figures/2052-4374-25-6-toc.gif</prism:require>
                <prism:publicationName>Annals of Occupational and Environmental Medicine</prism:publicationName>
        <prism:issn>2052-4374</prism:issn>
        <prism:volume>25</prism:volume>
        <prism:startingPage>6</prism:startingPage>
        <prism:publicationDate>2013-05-21T00:00:00Z</prism:publicationDate>
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        <item rdf:about="${item.url}">
        <title>The Relationship of Liver Function Tests to Mixed Exposure to Lead and Organic Solvents</title>
        <description>ObjectiveThis study aims to compare liver function indices (aspartate aminotransferase [AST], alanine aminotransferase [ALT], and gamma glutamyl transferase [GGT]) among males who work with lead, organic solvents, or both lead and organic solvents, under the permissible exposure limit (PEL).
Methods:
A total of 593 (out of 2,218) male workers who agreed to share their personal health information for medical research were selected for this study. Those excluded were hepatitis B carriers, individuals exposed to occupational risk factors other than lead and organic solvents, and individuals without liver function results. The 593 were divided into five groups: a lead-exposed group, an organic solvent-exposed group exposed to trichloroethylene (TCE co-exposed solvent group), an organic solvent-exposed group not exposed to trichloroethylene (TCE non-exposed solvent group), a lead and organic solvent-exposed group (mixed exposure group), and a non-exposed group (control group).We performed a one way-analysis of variance (one way-ANOVA) test to compare the geometric means of liver function indices among the groups, using a general linear model (GLM) to adjust for age, work duration, body mass index (BMI), smoking, and alcohol intake. In addition, we performed a binary logistic regression analysis to compare the odds ratios among groups with an abnormal liver function index, according to a cut-off value.
Results:
The ALT and AST of the mixed exposure group were higher than those of the other groups. The GGT of the mixed exposure group was higher than the TCE co-exposed solvent group, but there was no difference among the control group, TCE non-exposed solvent group, lead-exposed group, and mixed exposure group. The same result was evident after adjusting by GLM for age, work duration, BMI, smoking, and alcohol intake, except that ALT from the mixed exposure group showed no difference from the TCE co-exposed solvent group.When the cut-off values of the AST, ALT, and GGT were 40 IU/L, 42 IU/L, and 63 IU/L, respectively, a logistic regression analysis showed no differences in the odds ratios of those who had an abnormal liver function index among the groups. However, if the cut-off values of the AST, ALT, and GGT were 30 IU/L, 30 IU/L, and 40 IU/L, respectively, the odds ratio of the AST in the mixed exposure group was 4.39 (95% CI 1.86-10.40) times higher than the control.
Conclusion:
This study indicates that a mixed exposure to lead and organic solvents is dangerous, even if each single exposure is safe under the permissible exposure limit. Therefore, to ensure occupational health and safety in industry, a continuous efforts to study the effects from exposure to mixed chemicals is needed.</description>
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                <dc:creator>Won-Joon Chang</dc:creator>
                <dc:creator>Kyu-Tak Joe</dc:creator>
                <dc:creator>Hye-Young Park</dc:creator>
                <dc:creator>Jong-Do Jeong</dc:creator>
                <dc:creator>Duk-Hee Lee</dc:creator>
                <dc:source>Annals of Occupational and Environmental Medicine 2013, 25:5</dc:source>
        <dc:date>2013-05-21T00:00:00Z</dc:date>
        <dc:identifier>${item.identifier}</dc:identifier>
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                <prism:publicationName>Annals of Occupational and Environmental Medicine</prism:publicationName>
        <prism:issn>2052-4374</prism:issn>
        <prism:volume>25</prism:volume>
        <prism:startingPage>5</prism:startingPage>
        <prism:publicationDate>2013-05-21T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.aoemj.com/content/25/1/4">
        <title>Manganese Neurotoxicity: a Focus on Glutamate Transporters</title>
        <description>Manganese (Mn) is an essential element that is required in trace amount for normal growth, development as well maintenance of proper function and regulation of numerous cellular and biochemical reactions. Yet, excessive Mn brain accumulation upon chronic exposure to occupational or environmental sources of this metal may lead to a neurodegenerative disorder known as manganism, which shares similar symptoms with idiopathic Parkinson&#8217;s disease (PD). In recent years, Mn exposure has gained public health interest for two primary reasons: continuous increased usage of Mn in various industries, and experimental findings on its toxicity, linking it to a number of neurological disorders. Since the first report on manganism nearly two centuries ago, there have been substantial advances in the understanding of mechanisms associated with Mn-induced neurotoxicity. This review will briefly highlight various aspects of Mn neurotoxicity with a focus on the role of astrocytic glutamate transporters in triggering its pathophysiology.</description>
        <link>http://www.aoemj.com/content/25/1/4</link>
                <dc:creator>Pratap Karki</dc:creator>
                <dc:creator>Eunsook Lee</dc:creator>
                <dc:creator>Michael Aschner</dc:creator>
                <dc:source>Annals of Occupational and Environmental Medicine 2013, 25:4</dc:source>
        <dc:date>2013-05-21T00:00:00Z</dc:date>
        <dc:identifier>${item.identifier}</dc:identifier>
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                <prism:publicationName>Annals of Occupational and Environmental Medicine</prism:publicationName>
        <prism:issn>2052-4374</prism:issn>
        <prism:volume>25</prism:volume>
        <prism:startingPage>4</prism:startingPage>
        <prism:publicationDate>2013-05-21T00:00:00Z</prism:publicationDate>
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        <title>Congratulatory Message for the New International Journal, Annals of Occupational and Environmental Medicine</title>
        <description>No description available</description>
        <link>http://www.aoemj.com/content/25/1/3</link>
                <dc:creator>Yangho Kim</dc:creator>
                <dc:source>Annals of Occupational and Environmental Medicine 2013, 25:3</dc:source>
        <dc:date>2013-05-21T00:00:00Z</dc:date>
        <dc:identifier>${item.identifier}</dc:identifier>
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        <prism:issn>2052-4374</prism:issn>
        <prism:volume>25</prism:volume>
        <prism:startingPage>3</prism:startingPage>
        <prism:publicationDate>2013-05-21T00:00:00Z</prism:publicationDate>
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        <title>Congratulatory Message from the President of International Commission on Occupational Health</title>
        <description>No description available</description>
        <link>http://www.aoemj.com/content/25/1/2</link>
                <dc:creator>Kazutaka Kogi</dc:creator>
                <dc:source>Annals of Occupational and Environmental Medicine 2013, 25:2</dc:source>
        <dc:date>2013-05-21T00:00:00Z</dc:date>
        <dc:identifier>${item.identifier}</dc:identifier>
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                <prism:publicationName>Annals of Occupational and Environmental Medicine</prism:publicationName>
        <prism:issn>2052-4374</prism:issn>
        <prism:volume>25</prism:volume>
        <prism:startingPage>2</prism:startingPage>
        <prism:publicationDate>2013-05-21T00:00:00Z</prism:publicationDate>
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        <title>The Launch of Annals of Occupational and Environmental Medicine</title>
        <description>No description available</description>
        <link>http://www.aoemj.com/content/25/1/1</link>
                <dc:creator>Sang Baek Ko</dc:creator>
                <dc:source>Annals of Occupational and Environmental Medicine 2013, 25:1</dc:source>
        <dc:date>2013-05-21T00:00:00Z</dc:date>
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        <prism:issn>2052-4374</prism:issn>
        <prism:volume>25</prism:volume>
        <prism:startingPage>1</prism:startingPage>
        <prism:publicationDate>2013-05-21T00:00:00Z</prism:publicationDate>
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