some of which may not fit in an atom feed.
looking at the existing RSS tool, it looks like the only thing we're missing from the RSS feed that exists in the generic XML feed are the subject categories.
we are currently supplying google scholar with subject categories, but it's not required so we could live without this for a bit.
if there's a way to handle subject categories in an atom feed that would be ideal.
we do need a way to grab a generic xml feed for articles and their metadata (and the current RSS tool does provide this), so if this is impossible for 0.7, please put it on the schedule for the next release.
current RSS output example:
[plos@plosweb01 ~]$ /usr/local/topaz/bin/rss -baseURL http://plostopaz01.localdomain -rss
...
<channel>
<title>PLoS ONE Alerts</title>
<link>http://www.plosone.org</link>
<image>
<url>http://www.plosone.org/images/pone_favicon.ico</url>
<title>PLoS ONE Alerts</title>
<link>http://www.plosone.org</link>
</image>
<description>PLoS ONE Journal</description>
<item>
<title>Mutants in the Mouse NuRD/Mi2 Component P66α Are Embryonic Lethal</title>
<pubDate>Wed, 13 Jun 2007 00:00:00 GMT</pubDate>
<link>http://www.plosone.org/article/fetchArticle.action?articleURI=info:doi/10.1371/journal.pone.0000519</link>
<description>BackgroundThe NuRD/Mi2 chromatin complex is involved in histone modifications and contains a large number of subunits, including the p66 protein. There are two mouse and human p66 paralogs, p66α and p66β.
The functions of these genes are not clear, in part because there are no mutants available, except in invertebrate model systems.MethodologyWe made loss of function mutants in the mouse p66α gene (mp66α, official name Gatad2a,
MGI:2384585). We found that mp66α is essential for development, as mutant embryos die around day 10 of embryogenesis. The gene is not required for normal blastocyst development or for implantation. The phenotype of mutant embry
os and the pattern of gene expression in mutants are consistent with a role of mp66α in gene silencing.Conclusionmp66α is an essential gene, required for early mouse development. The lethal phenotype supports a role in executio
n of methylated DNA silencing.</description>
<author>Susan Marino, Roel Nusse</author>
</item>
generic XML example:
[plos@plosweb01 ~]$ /usr/local/topaz/bin/rss -baseURL http://plostopaz01.localdomain
<articles>
<article>
<uri>info:doi/10.1371/journal.pone.0000519</uri>
<title>Mutants in the Mouse NuRD/Mi2 Component P66α Are Embryonic Lethal</title>
<description><sec><title>Background</title><p>The NuRD/Mi2 chromatin complex is involved in histone modifications and contains a large number of subunits, including the p66 protein. There are two mouse and human p66 paralog
s, p66α and p66β. The functions of these genes are not clear, in part because there are no mutants available, except in invertebrate model systems.</p></sec><sec><title>Methodology</title><p>We made loss of function mutants in
the mouse p66α gene (mp66α, official name Gatad2a, MGI:2384585). We found that mp66α is essential for development, as mutant embryos die around day 10 of embryogenesis. The gene is not required for normal blastocyst development
or for implantation. The phenotype of mutant embryos and the pattern of gene expression in mutants are consistent with a role of mp66α in gene silencing.</p></sec><sec><title>Conclusion</title><p>mp66α is an essential gene, re
quired for early mouse development. The lethal phenotype supports a role in execution of methylated DNA silencing.</p></sec></description>
<date>2007-06-13</date>
<authors>
<author>Susan Marino</author>
<author>Roel Nusse</author>
</authors>
<categories>
<category>Developmental Biology</category>
<category>Genetics and Genomics</category>
</categories>
<subjects>
<subject>Developmental Biology</subject>
<subject>Developmental Biology/Embryology</subject>
<subject>Genetics and Genomics/Epigenetics</subject>
</subjects>
</article>
}}}
