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<title>Nature Reviews Rheumatology - Issue - nature.com science feeds</title>
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<title>Nature Reviews Rheumatology</title>
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                     <title>Rheumatoid arthritis: MRI points to inflammation as source of cartilage damage</title>
<link>http://feeds.nature.com/~r/nrrheum/rss/current/~3/Xa0gNuM-EqY/nrrheum.2013.76</link>
<description>Bone erosion, cartilage damage and inflammation—three aspects of the clinical manifestations of rheumatoid arthritis (RA)—interact at a molecular level in the underlying pathology of the disease. Characterizing the sequence of microscopic pathogenic events in RA and relating them chronologically to macroscopic morphological changes is the </description>
<content:encoded><![CDATA[

<p>Nature Reviews Rheumatology 9, 319 (2013).  
            <a href="http://dx.doi.org/10.1038/nrrheum.2013.76">doi:10.1038/nrrheum.2013.76</a>
</p>
<p>Author: Emma Leah</p>
<p>Bone erosion, cartilage damage and inflammation&#8212;three aspects of the clinical manifestations of rheumatoid arthritis (RA)&#8212;interact at a molecular level in the underlying pathology of the disease. Characterizing the sequence of microscopic pathogenic events in RA and relating them chronologically to macroscopic morphological changes is the </p>
<img src="http://feeds.feedburner.com/~r/nrrheum/rss/current/~4/Xa0gNuM-EqY" height="1" width="1"/>]]></content:encoded>
<dc:title>Rheumatoid arthritis: MRI points to inflammation as source of cartilage damage</dc:title>
<dc:creator>Emma Leah</dc:creator>
<dc:identifier>doi:10.1038/nrrheum.2013.76</dc:identifier>
<dc:source>Nature Reviews Rheumatology 9, 319 (2013)</dc:source>
<dc:date>2013-05-21</dc:date>
<prism:publicationName>Nature Reviews Rheumatology</prism:publicationName>
<prism:publicationDate>2013-05-21</prism:publicationDate>
<prism:doi>10.1038/nrrheum.2013.76</prism:doi>
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<prism:volume>9</prism:volume>
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                     <title>Imaging: Colour Doppler ultrasonography in inflammatory disease</title>
<link>http://feeds.nature.com/~r/nrrheum/rss/current/~3/SU9onB_zzHw/nrrheum.2013.65</link>
<description>The knees of patients with inflammatory arthritis (n = 39) or severe osteoarthritis (n = 72) were examined using colour Doppler ultrasonography (CDUS), and synovial fluid white blood cell count was used to confirm inflammatory status. Patients with inflammatory arthritis had </description>
<content:encoded><![CDATA[

<p>Nature Reviews Rheumatology 9, 320 (2013).  
            <a href="http://dx.doi.org/10.1038/nrrheum.2013.65">doi:10.1038/nrrheum.2013.65</a>
</p>
<p>The knees of patients with inflammatory arthritis (n = 39) or severe osteoarthritis (n = 72) were examined using colour Doppler ultrasonography (CDUS), and synovial fluid white blood cell count was used to confirm inflammatory status. Patients with inflammatory arthritis had </p>
<img src="http://feeds.feedburner.com/~r/nrrheum/rss/current/~4/SU9onB_zzHw" height="1" width="1"/>]]></content:encoded>
<dc:title>Imaging: Colour Doppler ultrasonography in inflammatory disease</dc:title>
<dc:identifier>doi:10.1038/nrrheum.2013.65</dc:identifier>
<dc:source>Nature Reviews Rheumatology 9, 320 (2013)</dc:source>
<dc:date>2013-04-30</dc:date>
<prism:publicationName>Nature Reviews Rheumatology</prism:publicationName>
<prism:publicationDate>2013-04-30</prism:publicationDate>
<prism:doi>10.1038/nrrheum.2013.65</prism:doi>
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<prism:volume>9</prism:volume>
<prism:number>6</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>320</prism:startingPage>
<prism:endingPage>320</prism:endingPage>
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<item rdf:about="http://dx.doi.org/10.1038/nrrheum.2013.66">
                     <title>Rheumatoid arthritis: Air pollution does not correlate with autoantibodies</title>
<link>http://feeds.nature.com/~r/nrrheum/rss/current/~3/Nf9JBvv9yOc/nrrheum.2013.66</link>
<description>Previous studies have suggested correlations between the development of rheumatoid arthritis (RA) and exposures to smoking and air pollution. To investigate the latter potential link, RA-related autoantibodies and swollen or tender joints were assessed in people without RA who are first-degree relatives of patients with </description>
<content:encoded><![CDATA[

<p>Nature Reviews Rheumatology 9, 320 (2013).  
            <a href="http://dx.doi.org/10.1038/nrrheum.2013.66">doi:10.1038/nrrheum.2013.66</a>
</p>
<p>Previous studies have suggested correlations between the development of rheumatoid arthritis (RA) and exposures to smoking and air pollution. To investigate the latter potential link, RA-related autoantibodies and swollen or tender joints were assessed in people without RA who are first-degree relatives of patients with </p>
<img src="http://feeds.feedburner.com/~r/nrrheum/rss/current/~4/Nf9JBvv9yOc" height="1" width="1"/>]]></content:encoded>
<dc:title>Rheumatoid arthritis: Air pollution does not correlate with autoantibodies</dc:title>
<dc:identifier>doi:10.1038/nrrheum.2013.66</dc:identifier>
<dc:source>Nature Reviews Rheumatology 9, 320 (2013)</dc:source>
<dc:date>2013-04-30</dc:date>
<prism:publicationName>Nature Reviews Rheumatology</prism:publicationName>
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<prism:doi>10.1038/nrrheum.2013.66</prism:doi>
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<prism:startingPage>320</prism:startingPage>
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                     <title>Inflammatory myopathies: Pulmonary function correlates with clinical parameters</title>
<link>http://feeds.nature.com/~r/nrrheum/rss/current/~3/EeoluUfyQnI/nrrheum.2013.67</link>
<description>Pulmonary function tests were performed in 38 children (aged 6–23 years) with definite or probable idiopathic inflammatory myopathy. A total of 37% (14/38) of patients had impaired lung function, defined as a total lung capacity or diffusing capacity </description>
<content:encoded><![CDATA[

<p>Nature Reviews Rheumatology 9, 320 (2013).  
            <a href="http://dx.doi.org/10.1038/nrrheum.2013.67">doi:10.1038/nrrheum.2013.67</a>
</p>
<p>Pulmonary function tests were performed in 38 children (aged 6&#8211;23 years) with definite or probable idiopathic inflammatory myopathy. A total of 37% (14/38) of patients had impaired lung function, defined as a total lung capacity or diffusing capacity </p>
<img src="http://feeds.feedburner.com/~r/nrrheum/rss/current/~4/EeoluUfyQnI" height="1" width="1"/>]]></content:encoded>
<dc:title>Inflammatory myopathies: Pulmonary function correlates with clinical parameters</dc:title>
<dc:identifier>doi:10.1038/nrrheum.2013.67</dc:identifier>
<dc:source>Nature Reviews Rheumatology 9, 320 (2013)</dc:source>
<dc:date>2013-04-30</dc:date>
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                     <title>Osteoarthritis: Specialized footwear improves knee loading</title>
<link>http://feeds.nature.com/~r/nrrheum/rss/current/~3/zDXOYFbC-kQ/nrrheum.2013.68</link>
<description>Wearing a flat, flexible 'mobility shoe' for ≥6 h per day, 6 days per week for 24 weeks reduced knee adduction movements in patients with osteoarthritis of the knee, whether the patient was wearing the mobility shoe (18% reduction, P</description>
<content:encoded><![CDATA[

<p>Nature Reviews Rheumatology 9, 320 (2013).  
            <a href="http://dx.doi.org/10.1038/nrrheum.2013.68">doi:10.1038/nrrheum.2013.68</a>
</p>
<p>Wearing a flat, flexible 'mobility shoe' for &#8805;6 h per day, 6 days per week for 24 weeks reduced knee adduction movements in patients with osteoarthritis of the knee, whether the patient was wearing the mobility shoe (18% reduction, P</p>
<img src="http://feeds.feedburner.com/~r/nrrheum/rss/current/~4/zDXOYFbC-kQ" height="1" width="1"/>]]></content:encoded>
<dc:title>Osteoarthritis: Specialized footwear improves knee loading</dc:title>
<dc:identifier>doi:10.1038/nrrheum.2013.68</dc:identifier>
<dc:source>Nature Reviews Rheumatology 9, 320 (2013)</dc:source>
<dc:date>2013-04-30</dc:date>
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<prism:publicationDate>2013-04-30</prism:publicationDate>
<prism:doi>10.1038/nrrheum.2013.68</prism:doi>
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<prism:startingPage>320</prism:startingPage>
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                     <title>Paediatric rheumatology: New risk loci for JIA identified</title>
<link>http://feeds.nature.com/~r/nrrheum/rss/current/~3/OXWm-LN0_Dw/nrrheum.2013.69</link>
<description>A study by the international Juvenile Arthritis Consortium for Immunochip (JACI) has revealed many new risk loci associated with juvenile idiopathic arthritis (JIA). The findings increase understanding of the genetic basis of susceptibility to this disease and the mechanisms underlying its pathogenesis.The study utilized </description>
<content:encoded><![CDATA[

<p>Nature Reviews Rheumatology 9, 320 (2013).  
            <a href="http://dx.doi.org/10.1038/nrrheum.2013.69">doi:10.1038/nrrheum.2013.69</a>
</p>
<p>Author: David Killock</p>
<p>A study by the international Juvenile Arthritis Consortium for Immunochip (JACI) has revealed many new risk loci associated with juvenile idiopathic arthritis (JIA). The findings increase understanding of the genetic basis of susceptibility to this disease and the mechanisms underlying its pathogenesis.The study utilized </p>
<img src="http://feeds.feedburner.com/~r/nrrheum/rss/current/~4/OXWm-LN0_Dw" height="1" width="1"/>]]></content:encoded>
<dc:title>Paediatric rheumatology: New risk loci for JIA identified</dc:title>
<dc:creator>David Killock</dc:creator>
<dc:identifier>doi:10.1038/nrrheum.2013.69</dc:identifier>
<dc:source>Nature Reviews Rheumatology 9, 320 (2013)</dc:source>
<dc:date>2013-05-07</dc:date>
<prism:publicationName>Nature Reviews Rheumatology</prism:publicationName>
<prism:publicationDate>2013-05-07</prism:publicationDate>
<prism:doi>10.1038/nrrheum.2013.69</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrrheum.2013.69</prism:url>
<prism:volume>9</prism:volume>
<prism:number>6</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>320</prism:startingPage>
<prism:endingPage>320</prism:endingPage>
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<item rdf:about="http://dx.doi.org/10.1038/nrrheum.2013.63">
                     <title>Osteoarthritis: Chondroprotection by histone deacetylase inhibition</title>
<link>http://feeds.nature.com/~r/nrrheum/rss/current/~3/jG641guDBMI/nrrheum.2013.63</link>
<description>Histone deacetylases (HDACs) regulate transcription, including that of genes encoding matrix metalloproteinases (MMPs). The possibility of using HDAC inhibitors (HDACi) to treat osteoarthritis (OA) via repression of cartilage-degrading MMP expression has now been advanced by work published in Arthritis &amp; Rheumatism by Ian Clark </description>
<content:encoded><![CDATA[

<p>Nature Reviews Rheumatology 9, 321 (2013).  
            <a href="http://dx.doi.org/10.1038/nrrheum.2013.63">doi:10.1038/nrrheum.2013.63</a>
</p>
<p>Author: Emma Leah</p>
<p>Histone deacetylases (HDACs) regulate transcription, including that of genes encoding matrix metalloproteinases (MMPs). The possibility of using HDAC inhibitors (HDACi) to treat osteoarthritis (OA) via repression of cartilage-degrading MMP expression has now been advanced by work published in Arthritis &amp; Rheumatism by Ian Clark </p>
<img src="http://feeds.feedburner.com/~r/nrrheum/rss/current/~4/jG641guDBMI" height="1" width="1"/>]]></content:encoded>
<dc:title>Osteoarthritis: Chondroprotection by histone deacetylase inhibition</dc:title>
<dc:creator>Emma Leah</dc:creator>
<dc:identifier>doi:10.1038/nrrheum.2013.63</dc:identifier>
<dc:source>Nature Reviews Rheumatology 9, 321 (2013)</dc:source>
<dc:date>2013-04-30</dc:date>
<prism:publicationName>Nature Reviews Rheumatology</prism:publicationName>
<prism:publicationDate>2013-04-30</prism:publicationDate>
<prism:doi>10.1038/nrrheum.2013.63</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrrheum.2013.63</prism:url>
<prism:volume>9</prism:volume>
<prism:number>6</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>321</prism:startingPage>
<prism:endingPage>321</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrrheum.2013.63</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nrrheum.2013.75">
                     <title>Connective tissue diseases: HMGB1 helps elicit anti-dsDNA antibody production in SLE</title>
<link>http://feeds.nature.com/~r/nrrheum/rss/current/~3/fvcOybL3KvE/nrrheum.2013.75</link>
<description>Antibodies against double-stranded DNA (dsDNA) are found in patients with systemic lupus erythematosus (SLE), and are implicated in the development of SLE-related nephritis. An article now published in The Journal of Immunology reports that HMGB1, a chromatin-associated protein, is required in the DNA-containing immune </description>
<content:encoded><![CDATA[

<p>Nature Reviews Rheumatology 9, 321 (2013).  
            <a href="http://dx.doi.org/10.1038/nrrheum.2013.75">doi:10.1038/nrrheum.2013.75</a>
</p>
<p>Author: Megan Cully</p>
<p>Antibodies against double-stranded DNA (dsDNA) are found in patients with systemic lupus erythematosus (SLE), and are implicated in the development of SLE-related nephritis. An article now published in The Journal of Immunology reports that HMGB1, a chromatin-associated protein, is required in the DNA-containing immune </p>
<img src="http://feeds.feedburner.com/~r/nrrheum/rss/current/~4/fvcOybL3KvE" height="1" width="1"/>]]></content:encoded>
<dc:title>Connective tissue diseases: HMGB1 helps elicit anti-dsDNA antibody production in SLE</dc:title>
<dc:creator>Megan Cully</dc:creator>
<dc:identifier>doi:10.1038/nrrheum.2013.75</dc:identifier>
<dc:source>Nature Reviews Rheumatology 9, 321 (2013)</dc:source>
<dc:date>2013-05-14</dc:date>
<prism:publicationName>Nature Reviews Rheumatology</prism:publicationName>
<prism:publicationDate>2013-05-14</prism:publicationDate>
<prism:doi>10.1038/nrrheum.2013.75</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrrheum.2013.75</prism:url>
<prism:volume>9</prism:volume>
<prism:number>6</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>321</prism:startingPage>
<prism:endingPage>321</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrrheum.2013.75</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nrrheum.2013.64">
                     <title>Connective tissue diseases: Disease severity directly affected by diet in a mouse model of SLE</title>
<link>http://feeds.nature.com/~r/nrrheum/rss/current/~3/kO8wmb_2IcY/nrrheum.2013.64</link>
<description>Systemic lupus erythematosus (SLE) aetiology, although incompletely understood, is known to have a genetic element and to be influenced by hormones and environmental factors, such as diet. Research from Bruce Richardson and colleagues, published in Arthritis &amp; Rheumatism, now shows that modification of dietary </description>
<content:encoded><![CDATA[

<p>Nature Reviews Rheumatology 9, 322 (2013).  
            <a href="http://dx.doi.org/10.1038/nrrheum.2013.64">doi:10.1038/nrrheum.2013.64</a>
</p>
<p>Author: Jenny Buckland</p>
<p>Systemic lupus erythematosus (SLE) aetiology, although incompletely understood, is known to have a genetic element and to be influenced by hormones and environmental factors, such as diet. Research from Bruce Richardson and colleagues, published in Arthritis &amp; Rheumatism, now shows that modification of dietary </p>
<img src="http://feeds.feedburner.com/~r/nrrheum/rss/current/~4/kO8wmb_2IcY" height="1" width="1"/>]]></content:encoded>
<dc:title>Connective tissue diseases: Disease severity directly affected by diet in a mouse model of SLE</dc:title>
<dc:creator>Jenny Buckland</dc:creator>
<dc:identifier>doi:10.1038/nrrheum.2013.64</dc:identifier>
<dc:source>Nature Reviews Rheumatology 9, 322 (2013)</dc:source>
<dc:date>2013-04-30</dc:date>
<prism:publicationName>Nature Reviews Rheumatology</prism:publicationName>
<prism:publicationDate>2013-04-30</prism:publicationDate>
<prism:doi>10.1038/nrrheum.2013.64</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrrheum.2013.64</prism:url>
<prism:volume>9</prism:volume>
<prism:number>6</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>322</prism:startingPage>
<prism:endingPage>322</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrrheum.2013.64</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nrrheum.2013.70">
                     <title>Paediatric rheumatology: uPA–uPAR at the heart of cardiac neonatal lupus</title>
<link>http://feeds.nature.com/~r/nrrheum/rss/current/~3/FHBnqpQKKU0/nrrheum.2013.70</link>
<description>Neonatal lupus, the most severe manifestation of which is congenital heart block, is caused by the transfer of specific maternal autoantibodies to the fetus. The mechanisms by which these antibodies result in cardiac injury have not been fully elucidated, but a new study highlights a </description>
<content:encoded><![CDATA[

<p>Nature Reviews Rheumatology 9, 322 (2013).  
            <a href="http://dx.doi.org/10.1038/nrrheum.2013.70">doi:10.1038/nrrheum.2013.70</a>
</p>
<p>Author: Isabel Woodman</p>
<p>Neonatal lupus, the most severe manifestation of which is congenital heart block, is caused by the transfer of specific maternal autoantibodies to the fetus. The mechanisms by which these antibodies result in cardiac injury have not been fully elucidated, but a new study highlights a </p>
<img src="http://feeds.feedburner.com/~r/nrrheum/rss/current/~4/FHBnqpQKKU0" height="1" width="1"/>]]></content:encoded>
<dc:title>Paediatric rheumatology: uPA–uPAR at the heart of cardiac neonatal lupus</dc:title>
<dc:creator>Isabel Woodman</dc:creator>
<dc:identifier>doi:10.1038/nrrheum.2013.70</dc:identifier>
<dc:source>Nature Reviews Rheumatology 9, 322 (2013)</dc:source>
<dc:date>2013-05-07</dc:date>
<prism:publicationName>Nature Reviews Rheumatology</prism:publicationName>
<prism:publicationDate>2013-05-07</prism:publicationDate>
<prism:doi>10.1038/nrrheum.2013.70</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrrheum.2013.70</prism:url>
<prism:volume>9</prism:volume>
<prism:number>6</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>322</prism:startingPage>
<prism:endingPage>322</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrrheum.2013.70</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nrrheum.2013.60">
                     <title>Rheumatoid arthritis: Erosion defined: back to basics</title>
<link>http://feeds.nature.com/~r/nrrheum/rss/current/~3/qGxkuBxoJ88/nrrheum.2013.60</link>
<description>Current classification criteria for rheumatoid arthritis allow its classification on the basis of the presence of erosions, in the absence of other indicators. Nevertheless, definition or quantitation of erosions was lacking. A European task force has now addressed this issue by analysing radiographic erosions in two cohorts of patients with early disease.</description>
<content:encoded><![CDATA[

<p>Nature Reviews Rheumatology 9, 323 (2013).  
            <a href="http://dx.doi.org/10.1038/nrrheum.2013.60">doi:10.1038/nrrheum.2013.60</a>
</p>
<p>Authors: Jonathan Kay &amp; Ellen M. Gravallese</p>
<p>Current classification criteria for rheumatoid arthritis allow its classification on the basis of the presence of erosions, in the absence of other indicators. Nevertheless, definition or quantitation of erosions was lacking. A European task force has now addressed this issue by analysing radiographic erosions in two cohorts of patients with early disease.</p>
<img src="http://feeds.feedburner.com/~r/nrrheum/rss/current/~4/qGxkuBxoJ88" height="1" width="1"/>]]></content:encoded>
<dc:title>Rheumatoid arthritis: Erosion defined: back to basics</dc:title>
<dc:creator>Jonathan Kay</dc:creator>
<dc:creator>Ellen M. Gravallese</dc:creator>
<dc:identifier>doi:10.1038/nrrheum.2013.60</dc:identifier>
<dc:source>Nature Reviews Rheumatology 9, 323 (2013)</dc:source>
<dc:date>2013-04-23</dc:date>
<prism:publicationName>Nature Reviews Rheumatology</prism:publicationName>
<prism:publicationDate>2013-04-23</prism:publicationDate>
<prism:doi>10.1038/nrrheum.2013.60</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrrheum.2013.60</prism:url>
<prism:volume>9</prism:volume>
<prism:number>6</prism:number>
<prism:section>News and Views</prism:section>
<prism:startingPage>323</prism:startingPage>
<prism:endingPage>324</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrrheum.2013.60</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nrrheum.2013.62">
                     <title>Clinical guidelines: Can wise choices solve the health-care crisis?</title>
<link>http://feeds.nature.com/~r/nrrheum/rss/current/~3/VbxvmrjaCNw/nrrheum.2013.62</link>
<description>The American College of Rheumatology recently published a list of five strategies (comprising four diagnostic procedures and one therapeutic approach) that they consider to be often unnecessary and thus potentially wasteful. By itself this list is useful, but finding a way to reduce wasteful strategies will be a challenge.</description>
<content:encoded><![CDATA[

<p>Nature Reviews Rheumatology 9, 324 (2013).  
            <a href="http://dx.doi.org/10.1038/nrrheum.2013.62">doi:10.1038/nrrheum.2013.62</a>
</p>
<p>Author: Maarten Boers</p>
<p>The American College of Rheumatology recently published a list of five strategies (comprising four diagnostic procedures and one therapeutic approach) that they consider to be often unnecessary and thus potentially wasteful. By itself this list is useful, but finding a way to reduce wasteful strategies will be a challenge.</p>
<img src="http://feeds.feedburner.com/~r/nrrheum/rss/current/~4/VbxvmrjaCNw" height="1" width="1"/>]]></content:encoded>
<dc:title>Clinical guidelines: Can wise choices solve the health-care crisis?</dc:title>
<dc:creator>Maarten Boers</dc:creator>
<dc:identifier>doi:10.1038/nrrheum.2013.62</dc:identifier>
<dc:source>Nature Reviews Rheumatology 9, 324 (2013)</dc:source>
<dc:date>2013-05-07</dc:date>
<prism:publicationName>Nature Reviews Rheumatology</prism:publicationName>
<prism:publicationDate>2013-05-07</prism:publicationDate>
<prism:doi>10.1038/nrrheum.2013.62</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrrheum.2013.62</prism:url>
<prism:volume>9</prism:volume>
<prism:number>6</prism:number>
<prism:section>News and Views</prism:section>
<prism:startingPage>324</prism:startingPage>
<prism:endingPage>326</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrrheum.2013.62</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nrrheum.2013.74">
                     <title>Paediatric rheumatology: Where are the innovations in paediatric rheumatology?</title>
<link>http://feeds.nature.com/~r/nrrheum/rss/current/~3/1wZFcK7o73E/nrrheum.2013.74</link>
<description>Rapid progress is being made in the field of rheumatology. Nevertheless, disappointingly, the limited resources of the paediatric rheumatology community are being expended on the publication of consensus guidelines that represent fossilization of old ideas rather than real innovation that leads to the improved care of children.</description>
<content:encoded><![CDATA[

<p>Nature Reviews Rheumatology 9, 326 (2013).  
            <a href="http://dx.doi.org/10.1038/nrrheum.2013.74">doi:10.1038/nrrheum.2013.74</a>
</p>
<p>Author: Thomas J. A. Lehman</p>
<p>Rapid progress is being made in the field of rheumatology. Nevertheless, disappointingly, the limited resources of the paediatric rheumatology community are being expended on the publication of consensus guidelines that represent fossilization of old ideas rather than real innovation that leads to the improved care of children.</p>
<img src="http://feeds.feedburner.com/~r/nrrheum/rss/current/~4/1wZFcK7o73E" height="1" width="1"/>]]></content:encoded>
<dc:title>Paediatric rheumatology: Where are the innovations in paediatric rheumatology?</dc:title>
<dc:creator>Thomas J. A. Lehman</dc:creator>
<dc:identifier>doi:10.1038/nrrheum.2013.74</dc:identifier>
<dc:source>Nature Reviews Rheumatology 9, 326 (2013)</dc:source>
<dc:date>2013-05-14</dc:date>
<prism:publicationName>Nature Reviews Rheumatology</prism:publicationName>
<prism:publicationDate>2013-05-14</prism:publicationDate>
<prism:doi>10.1038/nrrheum.2013.74</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrrheum.2013.74</prism:url>
<prism:volume>9</prism:volume>
<prism:number>6</prism:number>
<prism:section>News and Views</prism:section>
<prism:startingPage>326</prism:startingPage>
<prism:endingPage>327</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrrheum.2013.74</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nrrheum.2013.25">
                     <title>To Wnt or not to Wnt: the bone and joint health dilemma</title>
<link>http://feeds.nature.com/~r/nrrheum/rss/current/~3/dKpfpI5j1m4/nrrheum.2013.25</link>
<description>The Wnt signalling cascades have essential roles in development, growth and homeostasis of joints and the skeleton. Progress in basic research, particularly relating to our understanding of intracellular signalling cascades and fine regulation of receptor activation in the extracellular space, has provided novel insights into </description>
<content:encoded><![CDATA[

<p>Nature Reviews Rheumatology 9, 328 (2013).  
            <a href="http://dx.doi.org/10.1038/nrrheum.2013.25">doi:10.1038/nrrheum.2013.25</a>
</p>
<p>Authors: Rik J. Lories, Maripat Corr &amp; Nancy E. Lane</p>
<p>The Wnt signalling cascades have essential roles in development, growth and homeostasis of joints and the skeleton. Progress in basic research, particularly relating to our understanding of intracellular signalling cascades and fine regulation of receptor activation in the extracellular space, has provided novel insights into </p>
<img src="http://feeds.feedburner.com/~r/nrrheum/rss/current/~4/dKpfpI5j1m4" height="1" width="1"/>]]></content:encoded>
<dc:title>To Wnt or not to Wnt: the bone and joint health dilemma</dc:title>
<dc:creator>Rik J. Lories</dc:creator>
<dc:creator>Maripat Corr</dc:creator>
<dc:creator>Nancy E. Lane</dc:creator>
<dc:identifier>doi:10.1038/nrrheum.2013.25</dc:identifier>
<dc:source>Nature Reviews Rheumatology 9, 328 (2013)</dc:source>
<dc:date>2013-03-05</dc:date>
<prism:publicationName>Nature Reviews Rheumatology</prism:publicationName>
<prism:publicationDate>2013-03-05</prism:publicationDate>
<prism:doi>10.1038/nrrheum.2013.25</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrrheum.2013.25</prism:url>
<prism:volume>9</prism:volume>
<prism:number>6</prism:number>
<prism:section>Review</prism:section>
<prism:startingPage>328</prism:startingPage>
<prism:endingPage>339</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrrheum.2013.25</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nrrheum.2013.43">
                     <title>The phenotypic and genetic signatures of common musculoskeletal pain conditions</title>
<link>http://feeds.nature.com/~r/nrrheum/rss/current/~3/b6DBFBlxVvc/nrrheum.2013.43</link>
<description>Musculoskeletal pain conditions, such as fibromyalgia and low back pain, tend to coexist in affected individuals and are characterized by a report of pain greater than expected based on the results of a standard physical evaluation. The pathophysiology of these conditions is largely unknown, we </description>
<content:encoded><![CDATA[

<p>Nature Reviews Rheumatology 9, 340 (2013).  
            <a href="http://dx.doi.org/10.1038/nrrheum.2013.43">doi:10.1038/nrrheum.2013.43</a>
</p>
<p>Authors: Luda Diatchenko, Roger B. Fillingim, Shad B. Smith &amp; William Maixner</p>
<p>Musculoskeletal pain conditions, such as fibromyalgia and low back pain, tend to coexist in affected individuals and are characterized by a report of pain greater than expected based on the results of a standard physical evaluation. The pathophysiology of these conditions is largely unknown, we </p>
<img src="http://feeds.feedburner.com/~r/nrrheum/rss/current/~4/b6DBFBlxVvc" height="1" width="1"/>]]></content:encoded>
<dc:title>The phenotypic and genetic signatures of common musculoskeletal pain conditions</dc:title>
<dc:creator>Luda Diatchenko</dc:creator>
<dc:creator>Roger B. Fillingim</dc:creator>
<dc:creator>Shad B. Smith</dc:creator>
<dc:creator>William Maixner</dc:creator>
<dc:identifier>doi:10.1038/nrrheum.2013.43</dc:identifier>
<dc:source>Nature Reviews Rheumatology 9, 340 (2013)</dc:source>
<dc:date>2013-04-02</dc:date>
<prism:publicationName>Nature Reviews Rheumatology</prism:publicationName>
<prism:publicationDate>2013-04-02</prism:publicationDate>
<prism:doi>10.1038/nrrheum.2013.43</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrrheum.2013.43</prism:url>
<prism:volume>9</prism:volume>
<prism:number>6</prism:number>
<prism:section>Review</prism:section>
<prism:startingPage>340</prism:startingPage>
<prism:endingPage>350</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrrheum.2013.43</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nrrheum.2013.27">
                     <title>Determining who should be referred for total hip and knee replacements</title>
<link>http://feeds.nature.com/~r/nrrheum/rss/current/~3/6B1jjnjBWmM/nrrheum.2013.27</link>
<description>Total hip and total knee replacements (THR and TKR respectively), the definitive treatments for end-stage arthritis, are both safe and extremely successful in relieving pain and improving function. However, physicians who care for patients with chronic hip and knee arthritis are often the 'gatekeepers' to </description>
<content:encoded><![CDATA[

<p>Nature Reviews Rheumatology 9, 351 (2013).  
            <a href="http://dx.doi.org/10.1038/nrrheum.2013.27">doi:10.1038/nrrheum.2013.27</a>
</p>
<p>Author: Lisa A. Mandl</p>
<p>Total hip and total knee replacements (THR and TKR respectively), the definitive treatments for end-stage arthritis, are both safe and extremely successful in relieving pain and improving function. However, physicians who care for patients with chronic hip and knee arthritis are often the 'gatekeepers' to </p>
<img src="http://feeds.feedburner.com/~r/nrrheum/rss/current/~4/6B1jjnjBWmM" height="1" width="1"/>]]></content:encoded>
<dc:title>Determining who should be referred for total hip and knee replacements</dc:title>
<dc:creator>Lisa A. Mandl</dc:creator>
<dc:identifier>doi:10.1038/nrrheum.2013.27</dc:identifier>
<dc:source>Nature Reviews Rheumatology 9, 351 (2013)</dc:source>
<dc:date>2013-03-12</dc:date>
<prism:publicationName>Nature Reviews Rheumatology</prism:publicationName>
<prism:publicationDate>2013-03-12</prism:publicationDate>
<prism:doi>10.1038/nrrheum.2013.27</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrrheum.2013.27</prism:url>
<prism:volume>9</prism:volume>
<prism:number>6</prism:number>
<prism:section>Review</prism:section>
<prism:startingPage>351</prism:startingPage>
<prism:endingPage>357</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrrheum.2013.27</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nrrheum.2013.24">
                     <title>Arachnodactyly—a key to diagnosing heritable disorders of connective tissue</title>
<link>http://feeds.nature.com/~r/nrrheum/rss/current/~3/nZrzwiOI8BM/nrrheum.2013.24</link>
<description>Arachnodactyly literally means spidery fingers, and describes the long, slender fingers typical of patients with Marfan syndrome (MFS). Many clinicians regard arachnodactyly as pathognomonic of MFS; however, this view is misleading as arachnodactyly is a key element of the marfanoid habitus, which is present in </description>
<content:encoded><![CDATA[

<p>Nature Reviews Rheumatology 9, 358 (2013).  
            <a href="http://dx.doi.org/10.1038/nrrheum.2013.24">doi:10.1038/nrrheum.2013.24</a>
</p>
<p>Authors: Rodney Grahame &amp; Alan J. Hakim</p>
<p>Arachnodactyly literally means spidery fingers, and describes the long, slender fingers typical of patients with Marfan syndrome (MFS). Many clinicians regard arachnodactyly as pathognomonic of MFS; however, this view is misleading as arachnodactyly is a key element of the marfanoid habitus, which is present in </p>
<img src="http://feeds.feedburner.com/~r/nrrheum/rss/current/~4/nZrzwiOI8BM" height="1" width="1"/>]]></content:encoded>
<dc:title>Arachnodactyly—a key to diagnosing heritable disorders of connective tissue</dc:title>
<dc:creator>Rodney Grahame</dc:creator>
<dc:creator>Alan J. Hakim</dc:creator>
<dc:identifier>doi:10.1038/nrrheum.2013.24</dc:identifier>
<dc:source>Nature Reviews Rheumatology 9, 358 (2013)</dc:source>
<dc:date>2013-03-12</dc:date>
<prism:publicationName>Nature Reviews Rheumatology</prism:publicationName>
<prism:publicationDate>2013-03-12</prism:publicationDate>
<prism:doi>10.1038/nrrheum.2013.24</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrrheum.2013.24</prism:url>
<prism:volume>9</prism:volume>
<prism:number>6</prism:number>
<prism:section>Review</prism:section>
<prism:startingPage>358</prism:startingPage>
<prism:endingPage>364</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrrheum.2013.24</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nrrheum.2013.36">
                     <title>Management of cancer treatment-induced bone loss</title>
<link>http://feeds.nature.com/~r/nrrheum/rss/current/~3/2nQ6znqsecs/nrrheum.2013.36</link>
<description>The survival prospects for many patients with cancer are steadily improving. As a result, survivorship issues are of increasing importance as attempts are made to minimize the long-term adverse effects of cancer treatments. Cancer therapies can adversely affect bone health, particularly in women with breast </description>
<content:encoded><![CDATA[

<p>Nature Reviews Rheumatology 9, 365 (2013).  
            <a href="http://dx.doi.org/10.1038/nrrheum.2013.36">doi:10.1038/nrrheum.2013.36</a>
</p>
<p>Authors: Robert E. Coleman, Emma Rathbone &amp; Janet E. Brown</p>
<p>The survival prospects for many patients with cancer are steadily improving. As a result, survivorship issues are of increasing importance as attempts are made to minimize the long-term adverse effects of cancer treatments. Cancer therapies can adversely affect bone health, particularly in women with breast </p>
<img src="http://feeds.feedburner.com/~r/nrrheum/rss/current/~4/2nQ6znqsecs" height="1" width="1"/>]]></content:encoded>
<dc:title>Management of cancer treatment-induced bone loss</dc:title>
<dc:creator>Robert E. Coleman</dc:creator>
<dc:creator>Emma Rathbone</dc:creator>
<dc:creator>Janet E. Brown</dc:creator>
<dc:identifier>doi:10.1038/nrrheum.2013.36</dc:identifier>
<dc:source>Nature Reviews Rheumatology 9, 365 (2013)</dc:source>
<dc:date>2013-03-19</dc:date>
<prism:publicationName>Nature Reviews Rheumatology</prism:publicationName>
<prism:publicationDate>2013-03-19</prism:publicationDate>
<prism:doi>10.1038/nrrheum.2013.36</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrrheum.2013.36</prism:url>
<prism:volume>9</prism:volume>
<prism:number>6</prism:number>
<prism:section>Review</prism:section>
<prism:startingPage>365</prism:startingPage>
<prism:endingPage>374</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrrheum.2013.36</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nrrheum.2012.205">
                     <title>The role of IL-17-secreting mast cells in inflammatory joint disease</title>
<link>http://feeds.nature.com/~r/nrrheum/rss/current/~3/xUPfxlLkV9E/nrrheum.2012.205</link>
<description>The proinflammatory cytokine IL-17 has an important role in pathogenesis of several inflammatory diseases. In immune-mediated joint diseases, IL-17 can induce secretion of other proinflammatory cytokines such as IL-1, IL-6 and TNF, as well as matrix metalloproteinase enzymes, leading to inflammation, cartilage breakdown, osteoclastogenesis and </description>
<content:encoded><![CDATA[

<p>Nature Reviews Rheumatology 9, 375 (2013).  
            <a href="http://dx.doi.org/10.1038/nrrheum.2012.205">doi:10.1038/nrrheum.2012.205</a>
</p>
<p>Authors: Tony J. Kenna &amp; Matthew A. Brown</p>
<p>The proinflammatory cytokine IL-17 has an important role in pathogenesis of several inflammatory diseases. In immune-mediated joint diseases, IL-17 can induce secretion of other proinflammatory cytokines such as IL-1, IL-6 and TNF, as well as matrix metalloproteinase enzymes, leading to inflammation, cartilage breakdown, osteoclastogenesis and </p>
<img src="http://feeds.feedburner.com/~r/nrrheum/rss/current/~4/xUPfxlLkV9E" height="1" width="1"/>]]></content:encoded>
<dc:title>The role of IL-17-secreting mast cells in inflammatory joint disease</dc:title>
<dc:creator>Tony J. Kenna</dc:creator>
<dc:creator>Matthew A. Brown</dc:creator>
<dc:identifier>doi:10.1038/nrrheum.2012.205</dc:identifier>
<dc:source>Nature Reviews Rheumatology 9, 375 (2013)</dc:source>
<dc:date>2012-12-11</dc:date>
<prism:publicationName>Nature Reviews Rheumatology</prism:publicationName>
<prism:publicationDate>2012-12-11</prism:publicationDate>
<prism:doi>10.1038/nrrheum.2012.205</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrrheum.2012.205</prism:url>
<prism:volume>9</prism:volume>
<prism:number>6</prism:number>
<prism:section>Perspectives</prism:section>
<prism:startingPage>375</prism:startingPage>
<prism:endingPage>379</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrrheum.2012.205</feedburner:origLink></item>
</rdf:RDF>
