<?xml version="1.0" encoding="UTF-8"?>

<rdf:RDF
 xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#"
 xmlns="http://purl.org/rss/1.0/"
 xmlns:content="http://purl.org/rss/1.0/modules/content/"
 xmlns:taxo="http://purl.org/rss/1.0/modules/taxonomy/"
 xmlns:dc="http://purl.org/dc/elements/1.1/"
 xmlns:syn="http://purl.org/rss/1.0/modules/syndication/"
 xmlns:admin="http://webns.net/mvcb/"
>

<channel rdf:about="http://www.gourt.com/Health/Medicine/Medical-Specialties/Gastroenterology.html">
<title>Gastroenterology RSS : Gourt</title>
<link>http://www.gourt.com/Health/Medicine/Medical-Specialties/Gastroenterology.html</link>
<description></description>
<dc:language>en-us</dc:language>
<dc:rights>Copyright 2007, Gourt.com</dc:rights>
<dc:date>2009-11-07T21:06+13:00
</dc:date>
<dc:publisher>rtruog@gourt.com</dc:publisher>
<dc:creator>rtruog@gourt.com</dc:creator>
<dc:subject>Gastroenterology RSS : Gourt</dc:subject>
<syn:updatePeriod>hourly</syn:updatePeriod>
<syn:updateFrequency>1</syn:updateFrequency>
<syn:updateBase>1901-01-01T00:00+00:00</syn:updateBase>
<items>
 <rdf:Seq>
  <rdf:li rdf:resource="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_kentucky/page_2.html" />
  <rdf:li rdf:resource="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_georgia/page_1.html" />
  <rdf:li rdf:resource="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_florida/page_8.html" />
  <rdf:li rdf:resource="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_virginia/page_2.html" />
  <rdf:li rdf:resource="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_virginia/page_3.html" />
  <rdf:li rdf:resource="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_texas/page_3.html" />
  <rdf:li rdf:resource="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_florida/page_3.html" />
  <rdf:li rdf:resource="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_montana/page_2.html" />
  <rdf:li rdf:resource="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_iowa/page_5.html" />
  <rdf:li rdf:resource="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_montana/page_5.html" />
  <rdf:li rdf:resource="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_maryland/page_2.html" />
  <rdf:li rdf:resource="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_texas/page_2.html" />
  <rdf:li rdf:resource="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_massachusetts/page_8.html" />
  <rdf:li rdf:resource="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_new_york/page_13.html" />
  <rdf:li rdf:resource="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_georgia/page_7.html" />
  <rdf:li rdf:resource="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_arizona/page_2.html" />
  <rdf:li rdf:resource="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_north_carolina/page_11.html" />
  <rdf:li rdf:resource="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_new_york/page_1.html" />
  <rdf:li rdf:resource="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_north_carolina/page_8.html" />
  <rdf:li rdf:resource="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_south_carolina/page_8.html" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1569199309001283&#x26;_version=1&#x26;md5=3eed4f18c49519f55beea779a0c00580" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1590865809003946&#x26;_version=1&#x26;md5=c1950b5beb06bc5dfcc59e762342cf92" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1590865809003958&#x26;_version=1&#x26;md5=32041a6f8991e5dce3d85805dace57fc" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0399832009003790&#x26;_version=1&#x26;md5=8c3c40461a3ff7226d87a890323535b1" />
  <rdf:li rdf:resource="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=19894117&#x26;dopt=Abstract" />
  <rdf:li rdf:resource="http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215279" />
  <rdf:li rdf:resource="http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215269" />
  <rdf:li rdf:resource="http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215231" />
  <rdf:li rdf:resource="http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215268" />
  <rdf:li rdf:resource="http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215215" />
  <rdf:li rdf:resource="http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215241" />
  <rdf:li rdf:resource="http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215294" />
  <rdf:li rdf:resource="http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215238" />
  <rdf:li rdf:resource="http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215176" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0016508509019428&#x26;_version=1&#x26;md5=0da22f762aa08f1615e3419514d733a4" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0016508509019416&#x26;_version=1&#x26;md5=71f12c3d7021e35b66df7ea0cb0f920b" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S001650850901943X&#x26;_version=1&#x26;md5=82d2293c4da19dc7c9b3588ee1514fe0" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0399832009003820&#x26;_version=1&#x26;md5=8ee240a2912559a066933da1b2e5f93a" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0399832009003819&#x26;_version=1&#x26;md5=97035973f8b46399347c8666f4c79686" />
  <rdf:li rdf:resource="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0399832009003807&#x26;_version=1&#x26;md5=47fe532851489a328347fccc9a018a31" />
  <rdf:li rdf:resource="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=19892037&#x26;dopt=Abstract" />
  <rdf:li rdf:resource="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=19892036&#x26;dopt=Abstract" />
  <rdf:li rdf:resource="http://feeds.nature.com/~r/nrgastro/rss/current/~3/6EczFqDXt0w/nrgastro.2009.183" />
  <rdf:li rdf:resource="http://feeds.nature.com/~r/nrgastro/rss/current/~3/n0xUDblhqGA/nrgastro.2009.174" />
  <rdf:li rdf:resource="http://feeds.nature.com/~r/nrgastro/rss/current/~3/NS1JmP5cMwU/nrgastro.2009.170" />
  <rdf:li rdf:resource="http://feeds.nature.com/~r/nrgastro/rss/current/~3/YbQ1ULJo4rs/nrgastro.2009.173" />
  <rdf:li rdf:resource="http://feeds.nature.com/~r/nrgastro/rss/current/~3/Bjl19zYzhP0/nrgastro.2009.171" />
  <rdf:li rdf:resource="http://feeds.nature.com/~r/nrgastro/rss/current/~3/9ttiaNi-7Js/nrgastro.2009.172" />
  <rdf:li rdf:resource="http://feeds.nature.com/~r/nrgastro/rss/current/~3/CH4NKYVNgeY/nrgastro.2009.175" />
  <rdf:li rdf:resource="http://feeds.nature.com/~r/nrgastro/rss/current/~3/qP2jjSPKn4g/nrgastro.2009.169" />
  <rdf:li rdf:resource="http://feeds.nature.com/~r/nrgastro/rss/current/~3/Wc29tismNOE/nrgastro.2009.176" />
  <rdf:li rdf:resource="http://feeds.nature.com/~r/nrgastro/rss/current/~3/991aJVVOjkc/nrgastro.2009.179" />
  <rdf:li rdf:resource="http://feeds.nature.com/~r/nrgastro/rss/current/~3/HYuLl6XQVmM/nrgastro.2009.180" />
  <rdf:li rdf:resource="http://feeds.nature.com/~r/nrgastro/rss/current/~3/VMJonn04k7o/nrgastro.2009.178" />
  <rdf:li rdf:resource="http://feeds.nature.com/~r/nrgastro/rss/current/~3/DXLezKbUTyo/nrgastro.2009.168" />
  <rdf:li rdf:resource="http://feeds.nature.com/~r/nrgastro/rss/current/~3/rwyzkOd3BbA/nrgastro.2009.167" />
  <rdf:li rdf:resource="http://feeds.nature.com/~r/nrgastro/rss/current/~3/42z8GGz4z4Q/nrgastro.2009.163" />
  <rdf:li rdf:resource="http://feeds.nature.com/~r/nrgastro/rss/current/~3/yZJHLX1v3uc/nrgastro.2009.166" />
  <rdf:li rdf:resource="http://feeds.nature.com/~r/nrgastro/rss/current/~3/YshNmdWBReY/nrgastro.2009.162" />
  <rdf:li rdf:resource="http://feeds.nature.com/~r/nrgastro/rss/current/~3/jgHtCJpH7Zc/nrgastro.2009.165" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21161" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21158" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21157" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21154" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21153" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21147" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21149" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21148" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21146" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21144" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21138" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21114" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21124" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21152" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21151" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21145" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21142" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21141" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21139" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21137" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21136" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21093" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21123" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21140" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21143" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21119" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21113" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21052" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21126" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21125" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21121" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21117" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21112" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21110" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21120" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21118" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21107" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21111" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21109" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21108" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21106" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21098" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21097" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21086" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20995" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21116" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21105" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21104" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21103" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21102" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21100" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21099" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21096" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21080" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21115" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21082" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21101" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21068" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21066" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21063" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21059" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21055" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21053" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21016" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21094" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21092" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21091" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21090" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21089" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21087" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21084" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21077" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21070" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21081" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21074" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21073" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21071" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21058" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21057" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21088" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21085" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21083" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21056" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21045" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20983" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21095" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21079" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21062" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21061" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21078" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21069" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21065" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21064" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21046" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21075" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21050" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21048" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21043" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21067" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21054" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21051" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21042" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21038" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21037" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21035" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21032" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21027" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21025" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20997" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21060" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21049" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21047" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21044" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21040" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21033" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21024" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21005" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21021" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21072" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21009" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21010" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21041" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20998" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21031" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21029" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21028" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21020" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21017" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21011" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21008" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21007" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20996" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21015" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21006" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21002" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21000" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20994" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20992" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20991" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20982" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21014" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.21003" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20985" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20970" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20928" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20989" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20981" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20968" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20964" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20954" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20987" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20988" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20971" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20958" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20955" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20953" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20980" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20929" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20911" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20913" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20912" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20905" />
  <rdf:li rdf:resource="http://dx.doi.org/10.1002%2Fibd.20779" />
 </rdf:Seq>
</items>
</channel>

<item rdf:about="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_kentucky/page_2.html">
<title>University City :: Kentucky :: Medical Search Consultants</title>
<link>http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_kentucky/page_2.html</link>
<description><![CDATA[ Join Group of 2  This is an excellent opportunity for a BE/BC Gastroenterologist to join 2 others as an expansion to this very busy practice.  The group has a very loyal referral base that is sending ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_georgia/page_1.html">
<title>Coastal Georgia :: Georgia :: Medical Search Consultants</title>
<link>http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_georgia/page_1.html</link>
<description><![CDATA[ HOSPITAL EMPLOYEE OR INCOME GUARANTEE  This is an excellent opportunity for a BE/BC Gastroenterologist to join 2 others in a very busy regional medical center practice setting.  This is a high-volume ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_florida/page_8.html">
<title>Great Location :: Florida :: Intelligent Placement Solutions, Inc</title>
<link>http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_florida/page_8.html</link>
<description><![CDATA[Join a 2 person single specialty practice.  The surgical center is ownd by multiple physicians.  Buy in is an option.  Call is 1:4  Less that 10% of  patients come from the hospitals.  This is a two year ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_virginia/page_2.html">
<title>Great Location :: Virginia :: Intelligent Placement Solutions, Inc</title>
<link>http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_virginia/page_2.html</link>
<description><![CDATA[Currently recruiting for a BE/BC Gastroenterologist Physician. Option to begin new practice or work with existing group in town. This is a Hospital Employed Position.  Generous Sign-On Bonus and Relocation ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_virginia/page_3.html">
<title>Great Location :: Virginia :: Intelligent Placement Solutions, Inc</title>
<link>http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_virginia/page_3.html</link>
<description><![CDATA[Join a single specialty practice with a great group of GI's.  They are looking for a energetic, aggressive physician.  Good communication skills needed.  Little managed care.  Partnership track available. ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_texas/page_3.html">
<title>Great Location :: Texas :: Intelligent Placement Solutions, Inc</title>
<link>http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_texas/page_3.html</link>
<description><![CDATA[Multi specialty group of 18 primary care providers and 1 surgeon is looking for a GI to join their group.  The group employment salary will be around the low $400,000 vicinity on a net income guarantee ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_florida/page_3.html">
<title>Not Disclosed :: Florida :: Locum Medical Group</title>
<link>http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_florida/page_3.html</link>
<description><![CDATA[A busy practice in southern Florida is seeking a Board Certified or Board Eligible Gastroenterologist for a permanent, employed position. You can expect to see approximately 20 patients per day and call ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_montana/page_2.html">
<title>Not Disclosed :: Montana :: Locum Medical Group</title>
<link>http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_montana/page_2.html</link>
<description><![CDATA[A facility in the largest metropolitan area of Montana seeks to hire a Board Certified or Board Eligible Gastroenterologist. Candidates need not to be licensed to practice medicine in Montana to be considered ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_iowa/page_5.html">
<title>Not Disclosed :: Iowa :: Locum Medical Group</title>
<link>http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_iowa/page_5.html</link>
<description><![CDATA[A group located in north central Iowa is looking to expand by adding a Board Certified or Board Eligible Gastroenterologist as the 3rd physician within the department. The group services a family oriented ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_montana/page_5.html">
<title>Not Disclosed :: Montana :: Locum Medical Group</title>
<link>http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_montana/page_5.html</link>
<description><![CDATA[A permanent Gastroenterologist is needed for an opportunity in central Montana. This health group is one of the largest in the state with brand new facilities to practice at throughout the area. The candidate ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_maryland/page_2.html">
<title>Not Disclosed :: Maryland :: Locum Medical Group</title>
<link>http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_maryland/page_2.html</link>
<description><![CDATA[A large multi-specialty group, only 35 minutes from D.C. in the state of Maryland, is seeking a permanent Gastroenterologist to join their group. There is currently one other gastroenterologist in the ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_texas/page_2.html">
<title>Not Disclosed :: Texas :: Locum Medical Group</title>
<link>http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_texas/page_2.html</link>
<description><![CDATA[If you are looking for a permanent, employed position with an established three-person group for 2009, this is the opportunity for you. You will be required to see 20-25 patients per if scheduled for ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_massachusetts/page_8.html">
<title>Southeastern :: Massachusetts :: New England Physician Recruitment Center</title>
<link>http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_massachusetts/page_8.html</link>
<description><![CDATA[  Gastroenterology-Coastal Massachusetts-Cape Cod   Gastroenterology-Coastal Massachusetts, hospital employed, with ERCP;   call 1/4, high 300; quaterly bonus, stellar group practice on the water  Lorileo@neprc.com ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_new_york/page_13.html">
<title>Middletown :: New York :: New England Physician Recruitment Center</title>
<link>http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_new_york/page_13.html</link>
<description><![CDATA[ Gastroenterology-NY-- TOP Salaries and Incentives- New Yorks finest group  top money-interviewing early ORANGE COUNTY AREA  We are looking for  a  Gastroenterologist   to join large group of 6 in very ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_georgia/page_7.html">
<title>NorthWest :: Georgia :: Intelligent Placement Solutions, Inc</title>
<link>http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_georgia/page_7.html</link>
<description><![CDATA[Looking for 2009 candidates.  Join a well-established, single specialty; GI practice with steady growth for over 25 years. There is a strong referral base.  The Endoscopy Center is physician owned and ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_arizona/page_2.html">
<title>NorthWest :: Arizona :: Intelligent Placement Solutions, Inc</title>
<link>http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_arizona/page_2.html</link>
<description><![CDATA[Seeking BC/BE Gastroenterologist to be solo/assoicate with exsiting GI or be employed.  Need to have ERCP. Currently 100% of procedures are being performed at Ambulatory Surgery Center (except for inpatient ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_north_carolina/page_11.html">
<title>SouthEast :: North Carolina :: Intelligent Placement Solutions, Inc</title>
<link>http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_north_carolina/page_11.html</link>
<description><![CDATA[Join solo Gastroenterologist.  Hospital offering income gaurentee.  Practice owns their endoscopy center but also do endoscopies at hospital.  Looking for a general GI.      Hospital provides area residents ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_new_york/page_1.html">
<title>Eastern :: New York :: New England Physician Recruitment Center</title>
<link>http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_new_york/page_1.html</link>
<description><![CDATA[ Gastroenterology  need 60 minutes from NY City     Medical facility 60 minutes from NY City seeks .Gastroenterology  ,  New facility opened last year, allows them to serve community with more physicians ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_north_carolina/page_8.html">
<title>North :: North Carolina :: Intelligent Placement Solutions, Inc</title>
<link>http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_north_carolina/page_8.html</link>
<description><![CDATA[Solo opportunity with income guarentee in the beautiful foothills of the Blue Ridge Mountaitns..  There is another GI in town.  No shared call at this time. State of the art hospital- GI equipment  Not ]]></description>
</item>

<item rdf:about="http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_south_carolina/page_8.html">
<title>South :: South Carolina :: Intelligent Placement Solutions, Inc</title>
<link>http://www.physemp.com/physician_jobs/all_gastroenterology_jobs_in_south_carolina/page_8.html</link>
<description><![CDATA[Two physicians to start a practice with full support of the hospital. Great opportunity with the support of the medical community to work with hospital in building an inpatient/outpatient practice.  We ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1569199309001283&#x26;_version=1&#x26;md5=3eed4f18c49519f55beea779a0c00580">
<title>A 10-year large-scale cystic fibrosis carrier screening in the Italian population</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1569199309001283&#x26;_version=1&#x26;md5=3eed4f18c49519f55beea779a0c00580</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1590865809003946&#x26;_version=1&#x26;md5=c1950b5beb06bc5dfcc59e762342cf92">
<title>Polycystins play a key role in the modulation of cholangiocyte proliferation?</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1590865809003946&#x26;_version=1&#x26;md5=c1950b5beb06bc5dfcc59e762342cf92</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1590865809003958&#x26;_version=1&#x26;md5=32041a6f8991e5dce3d85805dace57fc">
<title>Endoscopic Ultrasound-guided cholangiopancreatography and rendezvous techniques</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S1590865809003958&#x26;_version=1&#x26;md5=32041a6f8991e5dce3d85805dace57fc</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0399832009003790&#x26;_version=1&#x26;md5=8c3c40461a3ff7226d87a890323535b1">
<title>Marqueurs non invasifs de fibrose dans la maladie alcoolique du foie</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0399832009003790&#x26;_version=1&#x26;md5=8c3c40461a3ff7226d87a890323535b1</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=19894117&#x26;dopt=Abstract">
<title>Effects of the Gastrin-Releasing Peptide Antagonist RC-3095 in a Rat Model of Ulcerative Colitis.</title>
<link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=19894117&#x26;dopt=Abstract</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215279">
<title>The London OMED position statement for credentialing and quality assurance in digestive endoscopy</title>
<link>http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215279</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215269">
<title>Review of endoscopic devices for weight reduction: old and new balloons and implantable prostheses</title>
<link>http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215269</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215231">
<title>Novel over-the-scope-clip system for gastrotomy closure in natural orifice transluminal endoscopic surgery (NOTES): an ex vivo comparison study</title>
<link>http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215231</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215268">
<title>Value of magnifying endoscopy in classifying colorectal polyps based on vascular pattern</title>
<link>http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215268</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215215">
<title>Pneumomediastinum is a frequent but minor complication during esophageal endoscopic submucosal dissection</title>
<link>http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215215</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215241">
<title>Randomized controlled trial comparing endoscopic clips and over-the-scope clips for closure of natural orifice transluminal endoscopic surgery gastrotomies</title>
<link>http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215241</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215294">
<title>The suction pseudopolyp technique: a novel method for the removal of small flat nonpolypoid lesions of the colon and rectum</title>
<link>http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215294</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215238">
<title>Small-bowel endoscopy</title>
<link>http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215238</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215176">
<title>Biliary endoscopic retrograde cholangiopancreatography</title>
<link>http://www.thieme-connect.com/DOI/DOI10.1055/s-0029-1215176</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0016508509019428&#x26;_version=1&#x26;md5=0da22f762aa08f1615e3419514d733a4">
<title>NFAT-Induced Histone Acetylation Relay Switch Promotes c-Myc-Dependent Growth in Pancreatic Cancer Cells</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0016508509019428&#x26;_version=1&#x26;md5=0da22f762aa08f1615e3419514d733a4</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0016508509019416&#x26;_version=1&#x26;md5=71f12c3d7021e35b66df7ea0cb0f920b">
<title>The mitochondrial protein hTID-1 partners with the caspase-cleaved APC tumor suppressor to facilitate apoptosis</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0016508509019416&#x26;_version=1&#x26;md5=71f12c3d7021e35b66df7ea0cb0f920b</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S001650850901943X&#x26;_version=1&#x26;md5=82d2293c4da19dc7c9b3588ee1514fe0">
<title>Cell-type specific gene expression signature in liver underlies response to interferon therapy in chronic hepatitis C infection</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S001650850901943X&#x26;_version=1&#x26;md5=82d2293c4da19dc7c9b3588ee1514fe0</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0399832009003820&#x26;_version=1&#x26;md5=8ee240a2912559a066933da1b2e5f93a">
<title>Comorbidit&#xE9; et h&#xE9;patotoxicit&#xE9; du tabac et des substances r&#xE9;cr&#xE9;atives</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0399832009003820&#x26;_version=1&#x26;md5=8ee240a2912559a066933da1b2e5f93a</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0399832009003819&#x26;_version=1&#x26;md5=97035973f8b46399347c8666f4c79686">
<title>Questions de pr&#xE9;-test</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0399832009003819&#x26;_version=1&#x26;md5=97035973f8b46399347c8666f4c79686</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0399832009003807&#x26;_version=1&#x26;md5=47fe532851489a328347fccc9a018a31">
<title>R&#xE9;ponses au pr&#xE9;-test</title>
<link>http://www.sciencedirect.com/science?_ob=GatewayURL&#x26;_origin=IRSSCONTENT&#x26;_method=citationSearch&#x26;_piikey=S0399832009003807&#x26;_version=1&#x26;md5=47fe532851489a328347fccc9a018a31</link>
<description><![CDATA[ ]]></description>
</item>

<item rdf:about="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=19892037&#x26;dopt=Abstract">
<title>Response to Letter to the Editor Re: A Very Low-carbohydrate Diet Improves Symptoms and Quality of Life in Diarrhea-Predominant Irritable Bowel Syndrome.</title>
<link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=19892037&#x26;dopt=Abstract</link>
<description><![CDATA[
	Related Articles
        Response to Letter to the Editor Re: A Very Low-carbohydrate Diet Improves Symptoms and Quality of Life in Diarrhea-Predominant Irritable Bowel Syndrome.
        Clin Gastroenterol Hepatol. 2009 Nov 2;
        Authors:  Austin GL, Dalton CB, Hu Y, Morris CB, Hankins J, Weinland SR, Westman EC, Yancy WS, Drossman DA
        
        PMID: 19892037 [PubMed - as supplied by publisher]
    ]]></description>
</item>

<item rdf:about="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=19892036&#x26;dopt=Abstract">
<title>Reply Letter: Thank you for your interest in our work.</title>
<link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&#x26;db=PubMed&#x26;cmd=Retrieve&#x26;list_uids=19892036&#x26;dopt=Abstract</link>
<description><![CDATA[
	Related Articles
        Reply Letter: Thank you for your interest in our work.
        Clin Gastroenterol Hepatol. 2009 Nov 2;
        Authors:  Kallwitz ER
        
        PMID: 19892036 [PubMed - as supplied by publisher]
    ]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/6EczFqDXt0w/nrgastro.2009.183">
<title>Great (cultural) expectations</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/6EczFqDXt0w/nrgastro.2009.183</link>
<description><![CDATA[I consider myself to be quite fortunate. I enjoy being able to travel and observe different cultures. This has been the case since early in my professional career and doesn't apply to international travel alone. I recall excursions to various locations within the US—rural and ]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/n0xUDblhqGA/nrgastro.2009.174">
<title>Celiac disease: Progress towards noninvasive diagnosis and follow-up</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/n0xUDblhqGA/nrgastro.2009.174</link>
<description><![CDATA[


Celiac disease: Progress towards noninvasive diagnosis and follow-up

Nature Reviews Gastroenterology &amp; Hepatology 6, 625 (2009). doi:10.1038/nrgastro.2009.174

Author: Natalie J. Wood

]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/NS1JmP5cMwU/nrgastro.2009.170">
<title>IBS: Soluble fiber benefits patients with IBS</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/NS1JmP5cMwU/nrgastro.2009.170</link>
<description><![CDATA[


IBS: Soluble fiber benefits patients with IBS

Nature Reviews Gastroenterology &amp; Hepatology 6, 626 (2009). doi:10.1038/nrgastro.2009.170

Author: Rachel Jones

]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/YbQ1ULJo4rs/nrgastro.2009.173">
<title>Colorectal cancer: Increased folate intake could reduce risk of colorectal cancer</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/YbQ1ULJo4rs/nrgastro.2009.173</link>
<description><![CDATA[


Colorectal cancer: Increased folate intake could reduce risk of colorectal cancer

Nature Reviews Gastroenterology &amp; Hepatology 6, 626 (2009). doi:10.1038/nrgastro.2009.173

Author: Isobel Franks

]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/Bjl19zYzhP0/nrgastro.2009.171">
<title>Liver: Genetic risk factor identified for cystic fibrosis liver disease</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/Bjl19zYzhP0/nrgastro.2009.171</link>
<description><![CDATA[


Liver: Genetic risk factor identified for cystic fibrosis liver disease

Nature Reviews Gastroenterology &amp; Hepatology 6, 627 (2009). doi:10.1038/nrgastro.2009.171

Author: Rachel Jones

]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/9ttiaNi-7Js/nrgastro.2009.172">
<title>GERD: Novel approach to treatment</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/9ttiaNi-7Js/nrgastro.2009.172</link>
<description><![CDATA[


GERD: Novel approach to treatment

Nature Reviews Gastroenterology &amp; Hepatology 6, 627 (2009). doi:10.1038/nrgastro.2009.172

Author: Ezzie Hutchinson

]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/CH4NKYVNgeY/nrgastro.2009.175">
<title>Mast cell stabilization and POI</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/CH4NKYVNgeY/nrgastro.2009.175</link>
<description><![CDATA[


Mast cell stabilization and POI

Nature Reviews Gastroenterology &amp; Hepatology 6, 627 (2009). doi:10.1038/nrgastro.2009.175

Author: Isobel Franks

]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/qP2jjSPKn4g/nrgastro.2009.169">
<title>In brief</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/qP2jjSPKn4g/nrgastro.2009.169</link>
<description><![CDATA[Ulcerative colitisIn this open-label study, 20 patients with ulcerative colitis were given adalimumab, a fully human monoclonal antibody to tumor necrosis factor (TNF). 13 patients were intolerant or unresponsive to the chimeric anti-TNF antibody infliximab. Adalimumab was well tolerated and seemed to be beneficial ]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/Wc29tismNOE/nrgastro.2009.176">
<title>Pancreatic cancer: A new triple combination therapy?</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/Wc29tismNOE/nrgastro.2009.176</link>
<description><![CDATA[


Pancreatic cancer: A new triple combination therapy?

Nature Reviews Gastroenterology &amp; Hepatology 6, 628 (2009). doi:10.1038/nrgastro.2009.176

Author: Isobel Franks

]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/991aJVVOjkc/nrgastro.2009.179">
<title>Hepatitis: New hope for difficult cases of autoimmune hepatitis</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/991aJVVOjkc/nrgastro.2009.179</link>
<description><![CDATA[Autoimmune hepatitis is an inflammatory liver disease of unknown etiology that predominantly affects females, and requires immunosuppressive treatment. A new study investigates the role of mycophenolate mofetil as a rescue treatment for children with the disease.]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/HYuLl6XQVmM/nrgastro.2009.180">
<title>GERD: Persistent symptoms on therapy&#x2014;test on therapy</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/HYuLl6XQVmM/nrgastro.2009.180</link>
<description><![CDATA[When all state-of-the-art reflux monitoring technologies are available, which should be used for patients who have persistent reflux symptoms despite acid suppressive therapy? A single-center study has investigated this clinical dilemma and provides guidance on the best diagnostic strategy.]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/VMJonn04k7o/nrgastro.2009.178">
<title>Gastrointestinal bleeding: Trends in gastrointestinal bleeding: top down and bottom up!</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/VMJonn04k7o/nrgastro.2009.178</link>
<description><![CDATA[Advances in gastroenterology, including the introduction of PPIs, effective therapies for Helicobacter pylori infection, and endoscopic intervention, have promised to improve the incidence and outcomes of gastrointestinal bleeding and perforation. However, have these improvements been borne out in clinical practice?]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/DXLezKbUTyo/nrgastro.2009.168">
<title>Hepatitis C: Thyroid dysfunction in patients with hepatitis C on IFN-&#x3B1; therapy</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/DXLezKbUTyo/nrgastro.2009.168</link>
<description><![CDATA[IFN-α therapy for hepatitis C is associated with a high prevalence of thyroid dysfunction, which is often irreversible. Two studies have recently investigated the role of HCV, PEG-IFN-α and ribavirin in the development of autoimmune thyroid disorders in patients with hepatitis C on antiviral treatment.]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/rwyzkOd3BbA/nrgastro.2009.167">
<title>Diagnosis and management of lower gastrointestinal bleeding</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/rwyzkOd3BbA/nrgastro.2009.167</link>
<description><![CDATA[Lower gastrointestinal bleeding (LGIB) can present as an acute and life-threatening event or as chronic bleeding, which might manifest as iron-deficiency anemia, fecal occult blood or intermittent scant hematochezia. Bleeding from the small bowel has been shown to be a distinct entity, and LGIB is ]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/42z8GGz4z4Q/nrgastro.2009.163">
<title>The management of patients awaiting liver transplantation</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/42z8GGz4z4Q/nrgastro.2009.163</link>
<description><![CDATA[Since it was first performed in 1963, liver transplantation has become the only effective curative treatment in patients with liver failure. During the interval between being added to the waiting list and receiving a graft, the patient's condition may deteriorate as a result of disease ]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/yZJHLX1v3uc/nrgastro.2009.166">
<title>Current understanding of osteoporosis associated with liver disease</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/yZJHLX1v3uc/nrgastro.2009.166</link>
<description><![CDATA[Osteoporosis is a common complication of many types of liver disease. Research into the pathogenesis of osteoporosis has revealed that the mechanisms of bone loss differ between different types of liver disease. This Review summarizes our current understanding of osteoporosis associated with liver disease and ]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/YshNmdWBReY/nrgastro.2009.162">
<title>Endoscopic and pathological aspects of colitis-associated dysplasia</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/YshNmdWBReY/nrgastro.2009.162</link>
<description><![CDATA[The risk of developing colorectal cancer in patients with colitis-associated dysplasia is considerable. Surveillance programs in patients with ulcerative colitis and Crohn's disease aim to detect dysplastic lesions early and rely heavily on taking random biopsy samples along the length of the colon. Diagnosing dysplasia ]]></description>
</item>

<item rdf:about="http://feeds.nature.com/~r/nrgastro/rss/current/~3/jgHtCJpH7Zc/nrgastro.2009.165">
<title>Liver transplantation after radioembolization in a patient with unresectable HCC</title>
<link>http://feeds.nature.com/~r/nrgastro/rss/current/~3/jgHtCJpH7Zc/nrgastro.2009.165</link>
<description><![CDATA[Background. A 58-year-old white man who was being followed by his hepatologist for nonalcoholic steatohepatitis-related liver cirrhosis and portal hypertension and who had been found to have a biopsy-proven hepatocellular carcinoma (HCC) on routine screening, self-referred to our center for a second opinion on ]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21161">
<title>Exogenous alkaline phosphatase for the treatment of patients with moderate to severe ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21161</link>
<description><![CDATA[Increased activity of intestinal alkaline phosphatase (AP) occurs locally in patients with ulcerative colitis (UC), aimed at repairing inflammatory tissue damage. We evaluated the safety and preliminary efficacy of exogenous AP administered to patients with UC in an open-label, first-in-patient exploratory trial, conducted in the Internal Medicine and Gastroenterology hospital departments in the Czech Republic and Italy.Twenty-one patients were enrolled (13 females), age 23-54 years, with steroid- and/or immunosuppressant-refractory, moderate/severe UC (Mayo score 6-11). Oral AP enzyme 30,000 U was administered daily for 7 days, intraduodenally. Efficacy outcomes were changes in Mayo score at Day 21 posttreatment; changes in Modified Truelove-Witts Severity index (MTWSI) at Days 21, 63; C-reactive protein and stool calprotectin levels at Days 7, 21, 63. Safety evaluations were adverse events and laboratory abnormalities reported up to Day 63 posttreatment.No clinically relevant adverse events causing withdrawal or considered serious, or laboratory abnormalities or antibody formation against AP were observed. Mayo scores were significantly decreased at Day 21, and MTWSI at Days 21 and 63. C-reactive protein and stool calprotectin levels were decreased at Days 21 and 63. Clinical response on the Mayo score after a single 7-day AP course was 48% at Day 21.In this uncontrolled trial, administration of exogenous AP enzyme daily over a 7-day course to patients with UC was associated with short-term improvement in disease activity scores, with clinical effects being observed within 21 days and associated with reductions in C-reactive protein and stool calprotectin. AP enzyme treatment was well tolerated and nonimmunogenic. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21158">
<title>Babesiosis in a patient on infliximab for Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21158</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21157">
<title>Campylobacter concisus and other Campylobacter species in children with newly diagnosed Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21157</link>
<description><![CDATA[Campylobacter concisus and other members of the Campylobacter genus have recently been suggested as possible etiological agents of Crohn's disease (CD). To further investigate this issue we determined the prevalence of these organisms in pediatric patients newly diagnosed with CD.DNA was extracted from fecal specimens collected from 54 children with CD, 27 noninflammatory bowel disease (non-IBD), and 33 healthy controls and subjected to polymerase chain reaction (PCR) sequencing.Detection of C. concisus DNA using a newly developed PCR assay targeting the 16S rRNA gene of C. concisus showed that 65% (35/54) of fecal samples from CD children were positive, a prevalence significantly higher than that in the healthy (33%, 11/33, P = 0.008) and non-IBD controls (37%, 10/27, P = 0.03). The prevalence of all Campylobacter DNA using genus-specific primers in children with CD was 72% (39/54), which was significantly higher than the 30% (10/33, P = 0.0002) and 30% (8/27, P = 0.0003) observed in healthy and non-IBD controls, respectively.Given the strengthening evidence for a significantly higher prevalence of C. concisus and other non-jejuni Campylobacter species in pediatric CD, investigation into the role of these non-jejuni Campylobacter species in the initiation of human IBD is clearly a priority. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21154">
<title>Safety of immunomodulators and biologics for the treatment of inflammatory bowel disease during pregnancy and breast-feeding</title>
<link>http://dx.doi.org/10.1002%2Fibd.21154</link>
<description><![CDATA[The aim of this article is to critically review available data regarding the safety of immunomodulators and biological therapies during pregnancy and breast-feeding in women with inflammatory bowel disease. Methotrexate and thalidomide can cause congenital anomalies and are contraindicated during pregnancy (and breast-feeding). Although thiopurines have a Food and Drug Administration (FDA) rating D, available data suggest that these drugs are safe and well tolerated during pregnancy. Although traditionally women receiving azathioprine or mercaptopurine have been discouraged from breast-feeding because of theoretical potential risks, it seems that these drugs may be safe in this scenario. Treatment with cyclosporine for steroid-refractory ulcerative colitis (UC) during pregnancy can be considered safe and effective, and the use of this drug should be considered in cases of severe UC as a means of avoiding urgent surgery. Breast-feeding is contraindicated for patients receiving cyclosporine. Biological therapies appear to be safe in pregnancy, as no increased risk of malformations has been demonstrated. Therefore, the limited clinical results available suggest that the benefits of infliximab and adalimumab in attaining response and maintaining remission in pregnant patients might outweigh the theoretical risks of drug exposure to the fetus. Stopping therapy in the third trimester may be considered, as it seems that transplacental transfer of infliximab is low prior to this. Certolizumab differs from infliximab and adalimumab in that it is a Fab fragment of an antitumor necrosis factor alpha monoclonal antibody, and therefore it may not be necessary to stop certolizumab in the third trimester. The use of infliximab is probably compatible with breast-feeding. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21153">
<title>Diagnostic value of noninvasive combined fluorine-18 labeled fluoro-2-deoxy-D-glucose positron emission tomography and computed tomography enterography in active Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21153</link>
<description><![CDATA[The role of combined localized positron emission tomography (lPET) and computed tomography enterography (CTe) in Crohn's disease is unclear. We examined if this imaging modality using fluorine-18 labeled-fluoro-2-deoxy-D-glucose (FDG) could more effectively identify disease activity.52 lPET-CTe scans were analyzed in this retrospective study. CTe scores and FDG uptake were quantified. Correlations of CTe scores and standard uptake value (SUV) with C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), short Inflammatory Bowel Disease Questionnaire (sIBDq), and Harvey-Bradshaw index (HBI) were estimated using Pearson analysis. Imaging scores were compared to medical outcome by logistics regression model.CTe scores correlated with SUV, but additional abnormal segments of small bowel were not identified. In all, 38 (79%) abnormal CTe segments demonstrated increased FDG uptake with mean SUVmax 4.77; 10 (21%) abnormal CTe segments lacked FDG accumulation, with mean SUVmax 1.27. There was no correlation between SUVmax and CRP, ESR, sIBDq, or HBI. There were no significant differences in clinical indices, biochemical parameters, and presence of multiple abnormal segments between medical responders and uptake were associated with failed medical therapy (P = 0.001).PET scanning added to CTe did not identify additional abnormal segments when compared to CTe alone. Abnormal segments with mucosal enhancement on CTe that did not accumulate FDG were significantly associated with failure of medical therapy. A larger trial is warranted to confirm if combined lPET-CTe has an important role in the clinical management of stricturing Crohn's disease. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21147">
<title>Prevalence of hepatitis B and C and risk factors for nonvaccination in inflammatory bowel disease patients in Northeast France</title>
<link>http://dx.doi.org/10.1002%2Fibd.21147</link>
<description><![CDATA[Data regarding the prevalence of hepatitis C (HCV) and hepatitis B (HBV) in inflammatory bowel disease (IBD) patients are conflicting.In all, 315 IBD (252 Crohn's disease [CD] and 63 ulcerative colitis [UC]) patients were consecutively recruited between June 2005 and May 2009.The median age was 33 years (interquartile range [IQR]: 24-43) and median disease duration was 5 years (IQR: 2-11). Present and/or past HBV and HCV infection was found in 2.86% of 315 patients (CD: HBsAg 0.79%, anti-HBc 2.78%, anti-HCV 0.79%; UC: HBsAg 1.59%, anti-HBc 1.59%, anti-HCV 1.59%). Effective vaccination (anti-HBs without anti-HBc) was present in 48.9% of 315 patients. In multivariate analysis, age at diagnosis over 31 years (odds ratio [OR] 0.29; 95% confidence interval [CI] 0.15-0.58; P = 0.005), disease duration over 7 years (OR 0.43; 95% CI 0.23-0.83; P = 0.005), age at inclusion over 33 years (OR 0.44; 95% CI 0.20-0.94; P = 0.005), and CD (OR 0.29; 95% CI 0.15-0.58; P = 0.005) were associated with the lack of effective vaccination. Two HBsAg-positive patients, including 1 under curative nucleoside/nucleotide analog treatment, had received 6 and 7 infliximab infusions, and 1 HCV RNA-positive subject had been receiving corticosteroid and azathioprine therapies for 12 and 33 months, respectively. No viral reactivation occurred in these patients.The prevalence of HBV and HCV infection in French IBD patients is similar to that of the general population. While the ECCO recommends an effective HBV vaccination in IBD, half of the patients were not vaccinated. The nonvaccination risk factors identified in our study may allow targeted vaccination coverage. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21149">
<title>Tissue factor -1208D&#x3E;I polymorphism is associated with D-dimer levels in patients with inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21149</link>
<description><![CDATA[No abstract]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21148">
<title>Novel model of TH2-polarized chronic ileitis: The SAMP1 mouse</title>
<link>http://dx.doi.org/10.1002%2Fibd.21148</link>
<description><![CDATA[SAMP1/Yit mice develop spontaneous, segmental, transmural ileitis recapitulating many features of Crohn's disease (CD). The ileitic phenotype may have arisen during crosses of SAMP1 mice selected for the presence of skin lesions. We hereby describe that the original SAMP1 strain similarly develops ileitis. Our aim was to characterize the histopathological and immunological features of this model and assess its responsiveness to standard inflammatory bowel disease (IBD) therapy.The time course of histopathological features of ileitis was assessed. Immune compartments were characterized by flow cytometry. Ileal cytokine profiles and transcription factors were determined by real-time reverse-transcription polymerase chain reaction (RT-PCR). Finally, response to corticosteroid therapy and its effect on immune compartments and cellularity was evaluated.Histological features and time course of disease were conserved, compared to those reported in SAMP1/Yit strains, with similar expansion of CD19+, CD4+, and CD8+ effector (CD44high CD62Llow), and central memory lymphocytes (CD44highCD62Lhigh). However, different from SAMP1/YitFc mice, analysis of ileal cytokine profiles revealed initial TH1 polarization followed by TH2-polarized profile accompanied by prominent eosinophilia during late disease. Lastly, corticosteroids attenuated ileitis, resulting in decreased lymphocyte subsets and cellularity of compartments.Here we report that the ileitic phenotype of SAMP1-related strains was already present in the original SAMP1 strain. By contrast, the cytokine profile within the terminal ilea of SAMP1 is distinct from the mixed TH1/TH2 profile of SAMP1/YitFc mice during late disease, as it shows predominant TH2 polarization. Dissemination of these strains may advance our understanding of CD pathogenesis, which in 60% of patients involves the terminal ileum. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21146">
<title>Cdcs1 a major colitis susceptibility locus in mice; Subcongenic analysis reveals genetic complexity</title>
<link>http://dx.doi.org/10.1002%2Fibd.21146</link>
<description><![CDATA[The cytokine-deficiency-induced colitis susceptibility (Cdcs)1 locus is a major modifier of murine inflammatory bowel disease (IBD) and was originally identified in experimental crosses of interleukin-10-deficient (Il10-/-) mice. Congenic mice, in which this locus was reciprocally transferred between IBD-susceptible C3H/HeJBir-Il10-/- and resistant C57BL/6J-Il10-/- mice, revealed that this locus likely acts by inducing innate hypo- and adaptive hyperresponsiveness, associated with impaired NF-[kappa]B responses of macrophages. The aim of the present study was to dissect the complexity of Cdcs1 by further development and characterization of reciprocal Cdcs1 congenic strains and to identify potential candidate genes in the congenic interval.In total, 15 reciprocal congenic strains were generated from Il10-/- mice of either C3H/HeJBir or C57BL/6J genetic backgrounds by 10 cycles of backcrossing. Colitis activity was monitored by histological grading. Candidate genes were identified by fine mapping of congenic intervals, sequencing, microarray analysis, and a high-throughput real-time reverse-transcription polymerase chain reaction (RT-PCR) approach using bone marrow-derived macrophages.Within the originally identified Cdcs1-interval, 3 independent regions were detected that likely contain susceptibility-determining genetic factors (Cdcs1.1, Cdcs1.2, and Cdcs1.3). Combining results of candidate gene approaches revealed Fcgr1, Cnn3, Larp7, and Alpk1 as highly attractive candidate genes with polymorphisms in coding or regulatory regions and expression differences between susceptible and resistant mouse strains.Subcongenic analysis of the major susceptibility locus Cdcs1 on mouse chromosome 3 revealed a complex genetic structure. Candidate gene approaches revealed attractive genes within the identified regions. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21144">
<title>MDP-NOD2 stimulation induces HNP-1 secretion, which contributes to NOD2 antibacterial function</title>
<link>http://dx.doi.org/10.1002%2Fibd.21144</link>
<description><![CDATA[Human neutrophil peptide 1 (HNP-1) is a defensin with antibacterial activity secreted by various cells as a component of the innate immune host defense. NOD2 is a cytoplasmic protein that recognizes bacterial derived muramyl dipeptide, and is involved in bacterial clearance. The aim of the present study was to investigate the relationship between antibacterial activity of NOD2 and HNP-1 expression in epithelial cell lines.Gentamicin protection assay using Salmonella typhimurium was performed in Caco-2 cells. The mRNA level was determined by quantitative reverse-transcription polymerase chain reaction (RT-PCR) and defensin expression was assessed by Western blot and enzyme-linked immunosorbent assay (ELISA). Nuclear factor-[kappa]B activation was assessed using pIV luciferase and Renilla plasmids. A NOD2 mutant was generated by site-directed mutagenesis.Among the defensins tested, only HNP-1 expression is induced in colonic epithelial model HCT116 cells after MDP-LD stimulation. HNP-1 secretion is significantly increased after MDP-LD stimulation in the cell supernatant of intestinal epithelial cells expressing endogenous NOD2, but not in cells that lack endogenous NOD2 expression. HNP-1 is required for NOD2-dependent NF-[kappa]B activation after MDP-LD stimulation since hnp-1 siRNA transfection abrogated the response to MDP-LD stimulation. The antibacterial function of NOD2 against S. typhimurium was impaired when expression of HNP-1 was blocked by siRNA.HNP-1 secretion depends on NOD2 stimulation by MDP-LD and contributes to antibacterial activity in intestinal epithelial cells expressing endogenous NOD2, but not NOD2 3020insC mutant associated with increased susceptibility to Crohn's disease. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21138">
<title>Surgery for low-grade colorectal dysplasia in ulcerative colitis: Decisions, decisions</title>
<link>http://dx.doi.org/10.1002%2Fibd.21138</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21114">
<title>A33 antigen-deficient mice have defective colonic mucosal repair</title>
<link>http://dx.doi.org/10.1002%2Fibd.21114</link>
<description><![CDATA[A33 antigen is a transmembrane protein expressed predominantly in normal intestinal epithelium and most colon cancers and cell lines. The function of A33 antigen is unclear, but indirect evidence indicates a role in cell adhesion, trafficking, and the gut immune response. The aim of this study was to determine the contribution made by A33 antigen in mediating colonic repair following colitis induction in the A33 antigen-deficient mutant mouse.Colitis was induced by treatment with TNBS/ethanol. A33 antigen-deficient or wildtype mice were sacrificed at 0, 3, 7, and 14 days after colitis induction and morphological damage, mucosal proliferation, and inflammatory cell infiltration were quantified. In a subsequent study, following the induction of colitis mice were monitored for 22 days and morbidity and mortality determined.Mice lacking A33 antigen expression were compromised in their ability to resolve TNBS-induced damage and exhibited distinct crypt pathology. In A33 antigen-deficient mice morphological damage remained unresolved at 14 days postcolitis induction. Increases in colonic cell proliferation were delayed in A33 antigen-deficient mice, and the rate of crypt fission was increased after TNBS treatment. Commensurate with these observations, polymorphonuclear cell infiltration was suppressed in the absence of A33 antigen. Mortality following colitis induction was 20% higher in A33 antigen-deficient mice than in wildtype controls.Mice deficient in A33 antigen expression show impaired resolution of hapten-induced mucosal damage, leading to increased mortality, associated with impaired epithelial cell proliferation and a suppressed adaptive immune response. This study suggests a contribution for A33 antigen in the colonic healing response following mucosal damage. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21124">
<title>TL1A produced by lamina propria macrophages induces Th1 and Th17 immune responses in cooperation with IL-23 in patients with Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21124</link>
<description><![CDATA[Tumor necrosis factor (TNF)-like protein 1A (TL1A) is a member of the TNF superfamily and contributes to the pathogenesis of Crohn's disease (CD) by stimulating T-helper (Th) 1 cells. In addition to Th1, recent studies have focused on the role of Th17 cells in the pathogenesis of CD. Here we tried to clarify the role of TL1A in Th1 and Th17 immunity in CD.TL1A expression was assessed by quantitative reverse-transcription polymerase chain reaction (RT-PCR) in lamina propria (LP) macrophages (LP-M[phis]s) from normal controls (NC) and patients with CD or ulcerative colitis (UC). Purified LP CD4+ T cells were stimulated with TL1A and/or IL-23 and interferon gamma (IFN-[gamma]) and interleukin (IL)-17 levels were analyzed. We also examined the effect of TL1A on naïve CD4+ T-cell differentiation.We found that LP-M[phis]s are a major producer of TL1A. TL1A expression was markedly enhanced in LP-M[phis]s from CD patients compared with NC or UC patients. IL-23, in addition to TL1A, was induced in LP-M[phis]s by commensal bacteria stimulation. TL1A and IL-23 synergistically promoted the production of IFN-[gamma] and IL-17 by LP T cells, while TL1A alone did not induce cytokine production. Furthermore, TL1A promoted Th17 differentiation from naïve T cells by LP-M[phis]s; however, IL-23 did not show any synergistic effects on Th17 differentiation.TL1A expressed in LP-M[phis]s might play an important role in the pathogenesis of CD by inducing Th1 and Th17 immunity. IL-23 differentially regulated these functions of TL1A on memory and naïve T cells. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21152">
<title>Natural history of Crohn&#x27;s disease: Comparison between childhood- and adult-onset disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21152</link>
<description><![CDATA[Childhood-onset Crohn's disease (CD) might reflect a more severe form of disease. To test this hypothesis we analyzed the long-term natural history of CD in an adult cohort of patients with childhood-onset compared to adult-onset CD.We selected 206 childhood-onset CD patients among 2992 adult patients with a diagnosis of CD established before December 31, 2000. Disease characteristics were prospectively assessed during follow-up until December 2007 and compared to adult-onset CD patients matched 2 to 1 on gender, year of CD diagnosis, and disease location.Compared to adult-onset CD, patients with childhood-onset CD were more likely to have a severe disease, with an increased year-by-year disease activity index (37% of patient-years in childhood-onset group versus 31% in the adult-onset group, P < 0.001). Immunosuppressant requirement was also increased with a 10-year cumulative risk of 54 ± 3% in childhood-onset CD group versus 45 ± 2%, in the adult-onset CD group (P < 0.001). Cumulative risks of stricturing and penetrating complications and surgical resections were not statistically different between groups. Accordingly, these events occurred at a younger age in the childhood-onset CD group. At the age of 30 years the actuarial risk of having undergone an extensive intestinal resection was 48 ± 5% in the childhood-onset group versus 14 ± 2% in the adult-onset group (P < 0.001).Patients with childhood-onset CD exhibit a more active disease and require more immunosuppressive therapy. This feature is observed irrespective of the disease location, suggesting an intrinsic more severe phenotype. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21151">
<title>Interleukin-19 protects mice from innate-mediated colonic inflammation</title>
<link>http://dx.doi.org/10.1002%2Fibd.21151</link>
<description><![CDATA[Inflammatory bowel disease (IBD) results from the chronic dysregulation of the mucosal immune system and the aberrant activation of both the innate and the adaptive immune responses. We used two complementary models of colonic inflammation to examine the roles of interleukin (IL)-19 in colonic inflammation and thus its possible role in IBD.Using gene-targeting, we generated IL-19-deficient mice. To study the activation of the innate immune response during colonic inflammation we characterized an innate immune-mediated model of colitis induced by dextran sulfate sodium (DSS). DSS can induce not only acute colitis but also chronic colitis. In addition to the acute DSS-induced colitis model, we used a chronic DSS-induced colitis model that is associated with the activation of both Th1 and Th2 cytokines as well as innate immune response in the colon.We show that IL-19-deficient mice are more susceptible to experimental acute colitis induced by DSS, and this increased susceptibility is correlated with the accumulation of macrophages and the increased production of IFN-[gamma], IL-1[beta], IL-6, IL-12, TNF-[alpha], and KC. Additionally, cytokine production in IL-19-deficient macrophages was enhanced on stimulation of lipopolysaccharide (LPS) through reduced phosphorylation of STAT1 and STAT3. Moreover, our results clearly demonstrate that IL-19 is required for B-cell infiltration during chronic DSS-induced colitis, which may be mediated by IL-13 and IL-6.The finding that IL-19 drives pathogenic innate immune responses in the colon suggests that the selective targeting of IL-19 may be an effective therapeutic approach in the treatment of human IBD. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21145">
<title>Inflammatory bowel disease in young people: The case for transitional clinics</title>
<link>http://dx.doi.org/10.1002%2Fibd.21145</link>
<description><![CDATA[The incidence of inflammatory bowel disease (IBD) is increasing among adolescents. In all, 25% of patients are diagnosed before the age of 16, when they are traditionally transferred from the pediatric to the adult service.We conducted a retrospective case-controlled study to characterize patients treated in a novel transitional adolescent-young adult IBD clinic. This compared disease extent, radiation exposure, therapeutic strategy, and requirement for surgery in 100 adolescents with controls from our adult IBD clinic matched for disease duration.The median (range) ages for the adolescent and adult population was 19 (16-28) and 43 (24-84), with a median age at diagnosis of 15 (3-26) and 39 (13-82) respectively (P < 0.001). Crohn's disease was significantly more common in the adolescents. Disease distribution was ileocolonic in 69% of adolescents and 28% of adults, restricted to the ileum in 20% of adolescents and 47% of adults, and colonic only in 11% and 22%, respectively. Upper gastrointestinal involvement occurred in 23% of adolescents, but was not seen in adults (P < 0.01). Total ulcerative colitis was seen in 67% of adolescents and 44% of adults (P < 0.01). Contrary to previous data adolescents did not receive more ionizing radiation than adults. Requirement for immunosuppressive therapy was higher in the adolescent group (53% versus 31%, respectively, P < 0.01). Likewise, 20% of adolescents had required biological therapy compared to only 8% in the adult cohort (P < 0.05).Gastroenterologists should recognize that IBD is more complex when presenting in adolescence and our data support the creation of specific adolescent transitional clinics. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21142">
<title>Genome-wide gene expression analysis of mucosal colonic biopsies and isolated colonocytes suggests a continuous inflammatory state in the lamina propria of patients with quiescent ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21142</link>
<description><![CDATA[Genome-wide gene expression (GWGE) profiles of mucosal colonic biopsies have suggested the existence of a continuous inflammatory state in quiescent ulcerative colitis (UC). The aim of this study was to use DNA microarray-based GWGE profiling of mucosal colonic biopsies and isolated colonocytes from UC patients and controls in order to identify the cell types responsible for the continuous inflammatory state.Adjacent mucosal colonic biopsies were obtained endoscopically from the descending colon in patients with active UC (n = 8), quiescent UC (n = 9), and with irritable bowel syndrome (controls, n = 10). After isolation of colonocytes and subsequent extraction of total RNA, GWGE data were acquired using Human Genome U133 Plus 2.0 GeneChip Array (Affymetrix, Santa Clara, CA). Data analysis was carried out by principal component analysis and projection to latent structure-discriminant analysis using the SIMCA-P 11 software (Umetrics, Umeå, Sweden).A clear separation between active UC, quiescent UC, and control biopsies were found, whereas the model for the colonocytes was unable to distinguish between quiescent UC and controls. The differentiation between quiescent UC and control biopsies was governed by unique profiles containing gene expressions with significant fold changes. These primarily belonged to the family of homeostatic chemokines, revealing a plausible explanation for the abnormal regulated innate immune response seen in patients with UC.This study has demonstrated the presence of a continuous inflammatory state in quiescent UC, which seems to reflect an altered gene expression profile of lamina propria cells. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21141">
<title>Magnetic resonance imaging for Crohn&#x27;s disease: Is this really the end of colonoscopy?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21141</link>
<description><![CDATA[No abstract]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21139">
<title>The good, the bad, and the ugly: Adverse events and Crohn&#x27;s therapies</title>
<link>http://dx.doi.org/10.1002%2Fibd.21139</link>
<description><![CDATA[No abstract]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21137">
<title>Perianal fistulae in Crohn&#x27;s Disease: Current and future approaches to treatment</title>
<link>http://dx.doi.org/10.1002%2Fibd.21137</link>
<description><![CDATA[Perianal fistulae are common in Crohn's disease but rarely heal without treatment. The main aim of treatment is to effectively close the fistula without affecting sphincter integrity and continence. Traditional surgical and medical approaches are not without their limitations and may result in either comorbidity, such as fecal incontinence, or incomplete healing of the fistulae. Over the last 2 decades these limitations have led to a paradigm shift toward the use of biomaterials, and more recently cell-based therapies, which have met with variable degrees of success. This review discusses the traditional and current methods of treatment, as well as emerging and possible alternative approaches that may improve fistula healing. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21136">
<title>Fecal calprotectin variability in Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21136</link>
<description><![CDATA[No abstract]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21093">
<title>A further cause of secondary restless legs syndrome: Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21093</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21123">
<title>Colocolic intussusception in a patient with ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21123</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21140">
<title>Clostridium difficile and inflammatory bowel disease: More questions than answers?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21140</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21143">
<title>Crohn&#x27;s disease patient with right lower quadrant abdominal pain for 20 years due to an appendiceal neuroma (Fibrous obliteration of the appendix)</title>
<link>http://dx.doi.org/10.1002%2Fibd.21143</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21119">
<title>Ulcerative colitis in a Southern European country: A national perspective</title>
<link>http://dx.doi.org/10.1002%2Fibd.21119</link>
<description><![CDATA[The incidence, prevalence, and even the clinical behavior of ulcerative colitis (UC) are highly variable in different world regions. In previous studies, Portugal was reported as having a milder clinical behavior. The aim of this study was to apply the Montreal Classification in a large group of UC Portuguese patients in order to describe their clinical characteristics and evaluate variables potentially useful for outcome prediction.A cross-sectional study based on data collected from a nationwide online registry was undertaken.In all, 2863 patients with UC were included. Twenty-one percent had ulcerative proctitis, 52% left-sided colitis, and 28% extensive colitis. Sixty percent of patients had taken steroids, 14% immunosuppressors, 1% biologicals, and 4.5% were submitted to surgery. Patients with extensive colitis had more severe activity, needing more steroids, immunosuppressors, and surgery. At the time of diagnosis 61% were less than 40 years old and 5% less than 16. Younger patients also had a more aggressive initial course. Thirty-eight percent of patients had only taken salicylates during the disease course and were characterized by a lower incidence of systemic symptoms at presentation (3.8% versus 8.8%, P < 0.001), fewer extraintestinal manifestations (7.7% versus 24.0%, P < 0.001), and a higher prevalence of proctitis (32.1% versus 10.0%).A more aggressive phenotype was found in extensive colitis and in the initial course of younger patients, with an increased need for steroids and immunosuppressors. In addition, a significant percentage of patients, particularly with proctitis, showed a milder clinical evolution and were maintained in remission only with salicylates. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21113">
<title>Cerebral thromboembolic events in pediatric patients with inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21113</link>
<description><![CDATA[There is a recognized association between pediatric inflammatory bowel disease (IBD) and cerebral thromboembolic events (CTEs). Historical reporting had described the association as strongest between ulcerative colitis (UC), rather than Crohn's disease (CD). We describe the incidence and outcome of CTE in pediatric IBD patients from a single center over 5 years and the relative proportion of stroke reported in the literature in patients with UC and CD before and after January 2000.Demographic data were extracted on all newly diagnosed cases of IBD in our center from January 2003 to January 2008 to ascertain patient characteristics, disease type, risk factors for CTE, modality of neuroimaging, and outcome. A literature search was performed to identify all articles describing stroke in pediatric IBD. All identified studies were stratified into those published before and after January 1 2000.In all, 154 new patients diagnosed with IBD (male 56%) (UC 30%, CD 64%, IBD unclassified [IBDU] 6%) were reviewed. Four cases of CTE occurred in our population over 5 years (2.6%). All patients had a risk factor for CTE. Fifteen case series were identified with 32 patients. There was a significant increase in the proportion strokes affecting patients with CD reported after January 2000 (P = 0.02).CTE affects a proportion of pediatric IBD patients. Although resolution of physical impairment is the norm, significant morbidity exists. Our study suggests a secular trend toward CTE in CD. Primary prevention with the identification and amelioration of identifiable risk factors should be the clinical objective in future studies. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21052">
<title>Mycobacterium avium subsp. Paratuberculosis (MAP) as a modifying factor in Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21052</link>
<description><![CDATA[Crohn's disease (CD) is a multifactorial syndrome with genetic and environmental contributions. Mycobacterium avium subspecies paratuberculosis (MAP) has been frequently isolated from mucosal tissues of patients with CD but the cellular immune response to this bacterium has been poorly described. Our aim was to examine the influence of MAP on T-cell proliferation and cytokine responses in patients with inflammatory bowel disease (IBD).Peripheral blood mononuclear cells (PBMCs) and mesenteric lymph node cells (MLNCs) were obtained from IBD patients and non-IBD controls. PBMC T-cell proliferation in response to MAP was determined using CFSE labeling and flow cytometry. The specificity of cytokine responses to MAP was controlled by parallel exposure to Listeria monocytogenes (LM) or Salmonella typhimurium (ST).Coincubation of PBMCs with MAP induced significantly more T-cell proliferation (P < 0.0001) in PBMCs isolated from CD patients compared to PBMCs obtained from ulcerative colitis (UC) patients or healthy volunteers. In addition, PBMCs from CD patients secreted significantly higher (P < 0.05) levels of tumor necrosis factor-alpha (TNF-[alpha]; 2302 ± 230 pg/mL) and interleukin (IL)-10 (299 ± 48 pg/mL) in response to MAP compared to UC patients (TNF-[alpha]: 1219 ± 411 pg/mL; IL-10: 125 ± 19 pg/mL) and controls (TNF-[alpha]: 1447 ± 173 pg/mL; IL-10: 127 ± 12 pg/mL). No difference in cytokine responses was observed in response to LM or ST. MLNCs from both CD and UC patients secreted significantly more TNF-[alpha] and IL-8 in response to MAP compared to MLNCs from non-IBD control patients.Increased proliferation of T cells and an altered cytokine response suggest that prior exposure to MAP and engagement of the immune system is common in patients with CD. This does not imply causation but does support further examination of this bacterium as an environmental modifying factor. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21126">
<title>Association between blood flow and inflammatory state in a T-cell transfer model of inflammatory bowel disease in mice</title>
<link>http://dx.doi.org/10.1002%2Fibd.21126</link>
<description><![CDATA[Adoptive transfer of naive T-lymphocyte subsets into lymphopenic mice initiates chronic gut inflammation that mimics several aspects of inflammatory bowel disease (IBD). Patients with IBD can have profound alterations in intestinal blood flow, but whether the same is true in the T-cell transfer model has yet to be determined.In the current study, chronic intestinal inflammation was induced in recombinase-activating gene-1-deficient (RAG-/-) mice by adoptive transfer of CD4+ T-lymphocytes obtained from interleukin-10 deficient (IL-10-/-) mice.Four weeks later, widespread colonic inflammation was observed in the reconstituted recipients, in contrast to 2 control sets of mice injected with a different subset of lymphocytes or with vehicle alone. We observed that the resulting pathology induced in the reconstituted RAG-/- mice was divided distinctly into 2 subsets: 1 with blood flow near normal with very high inflammation scores, and the other with severely attenuated blood flow but with much lower signs of inflammation. Colonic and ileal blood flow rates in the latter subset of CD4+ mice averaged only [ap]30% compared to the mice with higher inflammation scores. The lower blood flow rates were associated with greatly reduced red blood cell concentrations in the tissue, suggesting a possible loss of vascular density.In this model of chronic intestinal inflammation, mild inflammation was associated with significant decreases in blood flow. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21125">
<title>Turner&#x27;s syndrome, autoimmune thyroiditis, and Crohn&#x27;s disease in the same patient: A combination emphasizing the role of X-chromosome in inflammatory bowel disease patients</title>
<link>http://dx.doi.org/10.1002%2Fibd.21125</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21121">
<title>Recurrent cytomegalovirus infection in ileal pouch-anal anastomosis for ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21121</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21117">
<title>Teduglutide, a novel mucosally active analog of glucagon-like peptide-2 (GLP-2) for the treatment of moderate to severe Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21117</link>
<description><![CDATA[Teduglutide, an analog of glucagon-like peptide-2 (GLP-2), is associated with trophic effects on gut mucosa. Its role in the treatment of active Crohn's disease (CD) was assessed in a pilot, randomized, placebo-controlled, double-blinded, dose-ranging study.Subjects with moderate-to-severe CD were randomized 1:1:1:1 to placebo or 1 of 3 doses of teduglutide (0.05, 0.10, or 0.20 mg/kg daily) delivered as a daily subcutaneous injection for 8 weeks. The primary outcome measure was the percentage of subjects in each group that responded to treatment, defined as a decrease in Crohn's Disease Activity Index (CDAI) score to  100 points. At week 8 there was an optional 12-week open-label period of treatment with teduglutide 0.10 mg/kg/d.One hundred subjects were enrolled and 71 completed the study. The mean baseline CDAI score was 290.8 ± 57.6 and was similar across groups. There were numerically higher response and remission rates in all teduglutide-treated groups as compared with placebo, although the percentage of subjects who achieved a clinical response or remission was more substantial, and seen as early as week 2 of treatment in the highest dose (0.2 mg/kg/d) group (44% response and 32% remission versus 32% response and 20% remission in the placebo group). Of subjects who had not achieved remission during the 8-week placebo-controlled phase in the higher-dose group, 50% achieved remission during the more prolonged, open-label treatment phase. Plasma citrulline was similar across groups at baseline, but increased substantially over time in all teduglutide groups when compared with placebo at week 8. Adverse events were not different between placebo and active treatment groups.Teduglutide is a novel and potentially effective therapy for inducing remission and mucosal healing in patients with active moderate-to-severe CD. Further clinical investigation of this growth factor is warranted. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21112">
<title>The position of the amino group on the benzene ring is critical for mesalamine&#x27;s improvement of replication fidelity</title>
<link>http://dx.doi.org/10.1002%2Fibd.21112</link>
<description><![CDATA[Individuals with ulcerative colitis are at high risk of developing colitis-associated cancer. 5-Aminosalicylate (5-ASA) protects from cancer by its antiinflammatory activity as well as by altering cell growth, inducing apoptosis, and reducing replication errors. So far neither 5-ASA's structural specificity nor its pharmacophore group have been identified. Here we compared 5-ASA with its analogs (4-ASA and 3-ASA) and its metabolite N-acetyl-5-ASA (NAc-5-ASA).Superoxide scavenging was analyzed by lucigenin-amplified chemiluminescence. Cell growth, cell cycle distribution, and replication fidelity at a (CA)13 microsatellite were measured in HCT116 and HT29 colon epithelial cells by MTT and flow cytometry. Nuclear protein extracts were blotted for replication protein A (RPA), claspin, p53, and p53Ser15.All compounds inhibited the growth of colon epithelial cells at a similar level and displayed potent scavenging properties, with 3-ASA being the most active, followed by 5-ASA, 4-ASA, and NAc-5-ASA. Besides 5-ASA, only 4-ASA caused an increase in the S-phase population (56%-69% and 49%-62% in HCT116 and HT29 cells, respectively). This was accompanied by nuclear recruitment of replication proteins RPA and claspin as well as phosphorylation of p53Ser15, both of which were weaker or absent with 3-ASA or NAc-5-ASA. 5-ASA was the only compound that lowered mutations at a (CA)13 microsatellite.5-ASA shares its growth inhibitory and superoxide scavenging properties with its structural analogs and metabolite, but the position of the amino group is critical for reducing replication errors. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21110">
<title>Pityriasis lichenoides chronica induced by adalimumab therapy for Crohn&#x27;s disease: Report of 2 cases successfully treated with methotrexate</title>
<link>http://dx.doi.org/10.1002%2Fibd.21110</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21120">
<title>Relationships between inflammatory bowel disease and perinatal factors: Both maternal and paternal disease are related to preterm birth of offspring</title>
<link>http://dx.doi.org/10.1002%2Fibd.21120</link>
<description><![CDATA[The aims of this study were to explore the influences of familial, maternal, and paternal inflammatory disease (IBD) on perinatal outcomes in the offspring and the risk for development of IBD related to perinatal factors.Eighty-five patients with Crohn's disease (CD) and 86 with ulcerative colitis (UC) were included from a population-based incidence study enrolled 1990-1994. Family and birth records of these patients, as well as of their 207 infants, were drawn from the Norwegian Medical Birth Registry, established in 1967, and compared with the national birth cohort from the same period.Maternal (odds ratio [OR] = 2.15, 95% confidence interval [CI]: 1.36, 3.39) and paternal IBD (OR = 3.02, 95% CI: 1.82, 5.01) influenced the risk of preterm birth (<37 weeks), which further increased if the affected parents had a first-degree relative with IBD (OR = 4.29, 95% CI: 1.59, 11.63). Maternal CD was associated with lower birth weight in the offspring (crude difference: 271.79 g, 95% CI: 87.83, 455.77, versus controls). Maternal UC increased the risk of perinatal bacterial infection in the offspring (OR = 6.03, 95% CI: 2.03, 17.91). IBD patients (2.3%) were less likely to be delivered by cesarean section than controls (8.1%) (OR = 0.27, CI: 95%: 0.10, 0.73).Familial, maternal, and paternal IBD were linked to preterm birth, which might be explained by genetic mechanisms. The present protective effect of cesarean sections needs further clarification in future studies. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21118">
<title>Small bowel resection rates in Crohn&#x27;s disease and the indication for surgery over time: Experience from a large tertiary care center</title>
<link>http://dx.doi.org/10.1002%2Fibd.21118</link>
<description><![CDATA[Our primary aim was to determine if the rate of small bowel resection (SBR) has declined over time among Crohn's disease (CD) patients seen at a single academic institution. A secondary aim was to establish whether the indication for surgery has changed.Patients with a primary or secondary ICD-9 code for CD (555.0-555.9) who underwent SBR at the University of Pittsburgh were included. Patients were divided into 4 separate time periods based on when they had surgery: 1995-1998 (Period 1), 1999-2001 (Period 2), 2002-2004 (Period 3), and 2005-2007 (Period 4). Medical records were reviewed for the 6 months preceding surgery. Use of 5-ASAs, immunomodulators (IMs), tumor necrosis factor (TNF) antagonists, and corticosteroids were noted. Disease behavior was defined as nonstricturing, nonpenetrating (B1), stricturing (B2), and penetrating (B3). Proportions of patients undergoing SBR were calculated according to calendar cohort and these rates were examined for time trends.In all, 227 unique patients were analyzed for a total of 236 surgeries. The rates of 5-ASA, IM, and corticosteroid use were similar across the 4 time periods. By contrast, TNF antagonist usage progressively increased over time (0%, 18%, 34%, 35%; P = 0.0002). The annual rate of SBR per period did not change (1.6%, 1.9%, 1.6%, 1.9%; P = 0.93). Similarly, the disease behavior did not change over time.While the frequency of TNF antagonist use in CD at the University of Pittsburgh has increased over time, the rate of SBR and indication for surgery has remained unchanged. These findings may be explained by long-standing, complicated disease refractory to medical therapy. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21107">
<title>Perforin deficiency attenuates inflammation and tumor growth in colitis-associated cancer</title>
<link>http://dx.doi.org/10.1002%2Fibd.21107</link>
<description><![CDATA[Patients with inflammatory bowel disease (IBD) have a markedly increased risk to develop colon cancer, but there are only limited data about the host antitumor response in such colitis-associated cancer. In the present study we aimed at assessing the role of perforin-dependent effector mechanisms in the immune response in a murine model of colitis-associated colon cancer.Wildtype and perforin-deficient mice were analyzed in a mouse model of colitis-associated colon cancer using azoxymethane (AOM) and dextran sodium sulfate (DSS).Tumors of wildtype mice showed infiltration of CD4+, CD8+ T cells, natural killer (NK) cells, high numbers of apoptotic cells, and expression of the transcription factor eomesodermin and cytotoxic effector proteins, suggesting a potential role of the antitumor immune response in AOM/DSS tumorigenesis. Furthermore, perforin deficiency resulted in reduced apoptosis of epithelial cells as compared to wildtype mice, whereas tumor infiltration by NK cells, CD8+, and CD4+ T cells was unchanged. However, perforin-deficient mice surprisingly developed significantly fewer tumors than wildtype mice. Subsequent studies identified an important role of perforin in regulating colitis activity, as perforin deficiency caused a significant reduction of DSS colitis activity and proinflammatory cytokine production as compared to wildtype controls.Perforin is involved in both the antitumor immune response and the regulation of activity of mucosal inflammation in colitis-associated cancer. Our data emphasize the possible consequences for therapeutic strategies targeting colitis-associated colon cancer. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21111">
<title>Mapping of inflammatory bowel disease in northern France: Spatial variations and relation to affluence</title>
<link>http://dx.doi.org/10.1002%2Fibd.21111</link>
<description><![CDATA[Geographic variations in the incidence of inflammatory bowel disease (IBD) may reflect variations in the distribution of environmental etiologic factors. We assessed spatial variation in the incidence of IBD in northern France and analyzed its association with a deprivation index.All cases of IBD included in the EPIMAD registry between 1990 and 2003 were extracted. The standardized incidence ratio (SIR) was calculated for each canton in the region. The association between incidence and deprivation was assessed using the Townsend deprivation index.The mean annual incidence rates of Crohn's disease (CD) and ulcerative colitis (UC) were 6.2 × 10-5 and 3.8 × 10-5, respectively. The mean cumulative numbers of cases by canton were 18.4 (1-183) for CD and 11.3 (0-148) for UC. For both CD and UC, mapping depicted spatial heterogeneity in the SIR with spatial autocorrelation. A high relative risk (RR) of CD was observed in mainly rural and periurban cantons of the region. For UC, a high RR was found in cantons of the south and the center of Pas-de-Calais. No significant correlation was observed between spatial variations in IBD and deprivation.The incidence of IBD is associated with spatial heterogeneity in northern France. The noteworthy predominance of CD in agricultural areas warrants further investigations. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21109">
<title>Transmission ratio distortion of DLG5 R30Q: Evidence for prenatal selection?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21109</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21108">
<title>Butyrate utilization by the colonic mucosa in inflammatory bowel diseases: A transport deficiency</title>
<link>http://dx.doi.org/10.1002%2Fibd.21108</link>
<description><![CDATA[The short-chain fatty acid butyrate, which is mainly produced in the lumen of the large intestine by the fermentation of dietary fibers, plays a major role in the physiology of the colonic mucosa. It is also the major energy source for the colonocyte. Numerous studies have reported that butyrate metabolism is impaired in intestinal inflamed mucosa of patients with inflammatory bowel disease (IBD). The data of butyrate oxidation in normal and inflamed colonic tissues depend on several factors, such as the methodology or the models used or the intensity of inflammation. The putative mechanisms involved in butyrate oxidation impairment may include a defect in beta oxidation, luminal compounds interfering with butyrate metabolism, changes in luminal butyrate concentrations or pH, and a defect in butyrate transport. Recent data show that butyrate deficiency results from the reduction of butyrate uptake by the inflamed mucosa through downregulation of the monocarboxylate transporter MCT1. The concomitant induction of the glucose transporter GLUT1 suggests that inflammation could induce a metabolic switch from butyrate to glucose oxidation. Butyrate transport deficiency is expected to have clinical consequences. Particularly, the reduction of the intracellular availability of butyrate in colonocytes may decrease its protective effects toward cancer in IBD patients. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21106">
<title>CXCL12 Is a constitutive and inflammatory chemokine in the intestinal immune system</title>
<link>http://dx.doi.org/10.1002%2Fibd.21106</link>
<description><![CDATA[Inflammatory bowel disease (IBD) is characterized by increased lymphocytic infiltrate to the lamina propria (LP) and upregulation of inflammatory chemokines and receptors. CXCL12 is a constitutive chemokine involved in lung, brain, and joint inflammation. We hypothesized that CXCL12 and its receptor, CXCR4, would have a constitutive and inflammatory role in the gut.Intestinal epithelial cells (IECs) and T lymphocytes were isolated from intestinal mucosa of IBD and control patients undergoing bowel resection. Autologous T cells were isolated from peripheral blood (PB). CXCL12 and CXCR4 expression by IECs was assessed by polymerase chain reaction and immunohistochemistry, lymphocyte phenotype by flow cytometry, and migration by Transwells.IECs expressed CXCL12 and expression was increased and more diffuse in IBD compared to normal crypts (ulcerative colitis [UC] > Crohn's disease [CD], inflamed > noninflamed). CXCR4 was expressed by IECs, LP T cells (LPTs), and PB T cells (PBTs), and CXCR4+ cells were increased in IBD LP in situ. PBTs and LPTs from all patients had a high and comparable migration toward CXCL12 (P < 0.0001 and P < 0.05 vs. medium, respectively). Migration toward IBD-IEC-derived supernatant was significantly higher compared to normal. Antibodies against CXCR4 and CXCL12 blocked migration.CXCL12 is expressed by normal IECs and upregulated and differentially distributed in IBD IECs. CXCR4 is expressed by IECs and LPTs, and CXCR4+ cells are significantly increased in IBD LP. CXCL12 is chemotactic for both PBTs and LPTs. Thus, CXCL12 and CXCR4 have a constitutive and inflammatory role in the intestinal mucosa and their selective therapeutic manipulation may be considered in IBD management. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21098">
<title>Does psychological counseling alter the natural history of inflammatory bowel disease?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21098</link>
<description><![CDATA[There is increasing evidence that psychological stress can increase mucosal inflammation and worsen the course of inflammatory bowel disease (IBD). We have now assessed whether psychotherapy by a counselor specially trained in the management of IBD can influence the course of disease.Using retrospective case note review, we compared the course of IBD in 24 patients (13 ulcerative colitis; 11 Crohn's disease), during the year before (year 1) and the year after referral (year 2) for supportive outpatient psychotherapy to an IBD counselor, to that of 24 IBD controls who were matched to individual cases for age, sex, disease, duration of disease, medication at baseline, and for relapse rate in year 1. Counselor assessments were made using a visual analog scale 0-6 (0 denotes poor, 6 excellent response to counseling). The results are shown as median (range).Patients were referred for counseling because of disease-related stress (14 patients), work problems (3), concerns about surgery (5), and bereavement (2); they received 6 (1-13) 1-hour sessions in year 2. In the year after starting counseling (year 2), patients had fewer relapses (0 [0-2]) and outpatient attendances (3.5 [1-10]) than in the year before referral (year 1) (2 [0-5], P = 0.0008; and 6.5 [1-17], P = 0.0006, respectively; furthermore, steroid usage (1 course [0-4] before, 0 [0-2] after, P = 0.005) and relapse-related use of other IBD medications declined during psychotherapy (1 drug [0-5] before, 0 [0-2] after, P = 0.002). There were no differences in any of these measures between years 1 and 2 in the control group. Numbers of hospital admissions did not change between year 1 and 2 in either group. In the 20 patients who attended >1 session counseling helped solve stress-related difficulties (counselor's score 4 [3-5]), the counselor scored them 4 (3-6) overall in psychological well-being after the counseling sessions.IBD-focused counseling may improve not only psychological well-being, but also the course of IBD in individuals with psychosocial stress. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21097">
<title>TLR5 is not required for flagellin-mediated exacerbation of DSS colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21097</link>
<description><![CDATA[The two forms of human inflammatory bowel disease, Crohn's disease (CD) and ulcerative colitis (UC), are both associated with loss of tolerance to gut microbial antigens. The dominant antigen recognized by antibody and T-cell responses in patients with CD is bacterial flagellin. Flagellin is also the only known ligand for Toll-like receptor 5 (TLR5), a key protein in innate immunity. Although flagellin activates TLR5 to produce inflammatory responses in many cell types in the gut, there is conflicting evidence as to whether TLR5 is harmful or protective in CD and murine colitis models. A recent study found that administration of flagellin enemas to mice along with dextran sodium sulfate (DSS) made their colitis worse.We sought to determine whether this exacerbation was due to TLR5 ligation, or to TLR5-independent adaptive immune responses to flagellin as an antigen, by using a transposon insertional mutant of the Escherichia coli H18 flagellin, 2H3, which lacks TLR5 stimulatory activity.We found that flagellin enemas produced only a mild exacerbation of DSS colitis, and that 2H3 was equivalent to or worse than wildtype flagellin. Moreover, we found that DSS colitis was more severe in TLR5-/- mice than wildtype C57BL/6 mice.Together, these results suggest that flagellin-mediated exacerbation of colitis is independent of TLR5. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21086">
<title>5-aminosalicylic acid interferes in the cell cycle of colorectal cancer cells and induces cell death modes</title>
<link>http://dx.doi.org/10.1002%2Fibd.21086</link>
<description><![CDATA[Epidemiological data suggests that 5-aminosalicylic acid (5-ASA), a nonsteroidal antiinflammatory drug used in the treatment of inflammatory bowel diseases, prevents colorectal cancer development in these patients, although the mechanisms remain incompletely understood.Here we report that 5-ASA prevents growth of several colorectal cancer cell lines by interfering in the cell cycle, i.e., an S-phase and G2/M phase arrest, dependent on 5-ASA dosage and concentration, together with an increased mitotic index. In addition, prolonged cell cycle arrest by repeated 5-ASA treatment induced apoptosis and caused abnormal spindle organization leading to mitotic catastrophe, another form of cell death.These observations illustrate that 5-ASA has chemopreventive and chemotherapeutic properties. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20995">
<title>Localization of the lipopolysaccharide recognition complex in the human healthy and inflamed premature and adult gut</title>
<link>http://dx.doi.org/10.1002%2Fibd.20995</link>
<description><![CDATA[Microbiota in the intestinal lumen provide an abundant source of potentially detrimental antigens, including lipopolysaccharide (LPS), a potent immunostimulatory product of Gram-negative bacteria recognized by the host via TLR-4 and MD-2. An aberrant immune response to LPS or other bacterial antigens has been linked to inflammatory bowel disease (IBD) and necrotizing enterocolitis (NEC).We investigated which cells express MD-2 in the normal and inflamed ileum from neonates and adults by immunohistochemistry. Moreover, MD-2 and TLR4 mRNA expression in normal adult ileum was studied by reverse-transcription polymerase chain reaction (RT-PCR) on cells isolated by laser capture microdissection.Premature infants did not show MD-2 expression either in epithelial cells or in the lamina propria. Similarly, MD-2 was absent in epithelial cells and lamina propria inflammatory cells in preterm infants with NEC. MD-2 protein in the healthy term neonatal and adult ileum was predominantly expressed by Paneth cells and some resident inflammatory cells in the lamina propria. MD-2 and TLR-4 mRNA expression was restricted to crypt cells. Also in IBD, Paneth cells were still the sole MD-2-expressing epithelial cells, whereas inflammatory cells (mainly plasma cells) were responsible for the vast majority of the MD-2 expression.The absence of MD-2 in the immature neonatal gut suggests impaired LPS sensing, which could predispose neonates to NEC upon microbial colonization of the immature intestine. The apparent expression of MD-2 by Paneth cells supports the critical concept that these cells respond to luminal bacterial products in order to maintain homeostasis with the intestinal microbiota in vivo. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21116">
<title>Association between Helicobacter pylori infection and inflammatory bowel disease: A meta-analysis and systematic review of the literature</title>
<link>http://dx.doi.org/10.1002%2Fibd.21116</link>
<description><![CDATA[Epidemiologic data suggest a protective effect of Helicobacter pylori infection against the development of autoimmune disease. Laboratory data illustrate H. pylori's ability to induce immune tolerance and limit inflammatory responses. Numerous observational studies have investigated the association between H. pylori infection and inflammatory bowel disease (IBD). Our aim was to perform a systematic review and meta-analysis of this association.Medline, EMBASE, bibliographies, and meeting abstracts were searched by 2 independent reviewers. Of 369 abstracts reviewed, 30 promising articles were reviewed in detail. Twenty-three studies met our inclusion criteria (subject N = 5903). Meta-analysis was performed with the metan command in Stata 10.1.Overall, 27.1% of IBD patients had evidence of infection with H. pylori compared to 40.9% of patients in the control group. The estimated relative risk of H. pylori infection in IBD patients was 0.64 (95% confidence interval [CI]: 0.54-0.75). There was significant heterogeneity in the included studies that could not be accounted for by the method of IBD and H. pylori diagnosis, study location, or study population age.These results suggest a protective benefit of H. pylori infection against the development of IBD. Heterogeneity among studies and the possibility of publication bias limit the certainty of this finding. Further studies investigating the effect of eradication of H. pylori on the development of IBD are warranted. Because environmental hygiene and intestinal microbiota may be strong confounders, further mechanistic studies in H. pylori mouse models are also necessary to further define the mechanism of this negative association. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21105">
<title>Analysis of 39 Crohn&#x27;s disease risk loci in Swedish inflammatory bowel disease patients</title>
<link>http://dx.doi.org/10.1002%2Fibd.21105</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21104">
<title>Epstein-Barr virus and parvovirus B19 coinfection in a Crohn&#x27;s disease patient under azathioprine</title>
<link>http://dx.doi.org/10.1002%2Fibd.21104</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21103">
<title>Ileal pouch for everyone, even when we are not sure of the diagnosis before or at colectomy?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21103</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21102">
<title>Body mass index and disease activity at treatment initiation: Potential new predictors of response to azathioprine therapy in IBD</title>
<link>http://dx.doi.org/10.1002%2Fibd.21102</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21100">
<title>Current thinking on recurrence: Does anastomotic surgical technique affect recurrence rates in Crohn&#x27;s patients?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21100</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21099">
<title>Incidence of stricturing and penetrating complications of Crohn&#x27;s disease diagnosed in pediatric patients</title>
<link>http://dx.doi.org/10.1002%2Fibd.21099</link>
<description><![CDATA[The development of disease complications is poorly characterized in pediatric patients with Crohn's disease (CD).We retrospectively determined the cumulative incidence of stricturing and penetrating complications of CD prior to first surgery utilizing data from 989 consecutively enrolled CD patients (age 0-17 years at diagnosis) collected between January 2000 and November 2003 and stored in the Pediatric IBD Consortium Registry.Mean age at diagnosis was 11.5 ± 3.8 (standard deviation) years. Median follow-up time was 2.8 years. Prior to first surgery, the cumulative incidence of stricturing or penetrating complications was 27% at 5 years and 38% at 10 years from the diagnosis of inflammatory bowel disease. The cumulative incidence of complicated disease was lowest in isolated colonic disease (P = 0.009). Penetrating complications that followed stricturing complications prior to first surgery occurred within 2 years of stricturing complications (cumulative incidence was 13% at 2 years from diagnosis of stricturing disease). Stricturing complications that followed penetrating complications prior to first surgery occurred within 8 years of penetrating complications (cumulative incidence was 26% at 8 years from diagnosis of penetrating complications).Strictures, abscesses, and fistulas are common in pediatric CD. Earlier aggressive management may be indicated. Prospective study is required to identify genetic and serologic markers that predict a patient's risk for the development of complicated disease and to determine optimal treatment regimens. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21096">
<title>Plasma chromogranin A in patients with inflammatory bowel disease: A possible explanation</title>
<link>http://dx.doi.org/10.1002%2Fibd.21096</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21080">
<title>Effect of EP4 agonist (ONO-4819CD) for patients with mild to moderate ulcerative colitis refractory to 5-aminosalicylates: A randomized phase II, placebo-controlled trial</title>
<link>http://dx.doi.org/10.1002%2Fibd.21080</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21115">
<title>Lessons from geographic mapping of IBD in France</title>
<link>http://dx.doi.org/10.1002%2Fibd.21115</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21082">
<title>Adalimumab for cutaneous metastatic Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21082</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21101">
<title>Getting the steak without the sizzle: Is MR enterography as good as CT enterography?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21101</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21068">
<title>Antigen-presenting cells exposed to Lactobacillus acidophilus NCFM, Bifidobacterium bifidum BI-98, and BI-504 reduce regulatory T cell activity</title>
<link>http://dx.doi.org/10.1002%2Fibd.21068</link>
<description><![CDATA[The effect in vitro of six different probiotic strains including Lactobacillus acidophilus NCFMTM, Lactobacillus salivarius Ls-33, Lactobacillus paracasei subsp. paracasei YS8866441, Lactobacillus plantarum Lp-115, Bifidobacterium bifidum BI-504 and BI-98 was studied on splenic enteroantigen-presenting cells (APC) and CD4+CD25+ T-regulatory cells (Tregs) in splenocyte-T cell proliferation assays.Splenocytes exposed to enteroantigen +/- probiotics were used to stimulate cultured CD4+CD25- T cells to which titrated numbers of Tregs were added. Cytokine assays were performed by use of neutralizing antibodies and ELISA.Exposure of APCs to enteroantigens and the series of probiotic strains mentioned above did not influence the stimulatory capacity of APCs on proliferative enteroantigen-specific T cells. However, exposure to B. bifidum BI-98, BI-504 and L. acidophilus NCFMTM consistently reduced the suppressive activity of Tregs. The suppressive activity was analyzed using fractionated components of the probiotics, and showed that a component of the cell wall is responsible for the decreased Treg activity in the system. The probiotic-induced suppression of Treg function is not mediated by changes in APC-secretion of the inflammatory cytokines IL-6 or IL-1b.We conclude that certain probiotic strains can modify APCs to cause reduced Treg activity. This effect apparently depends on a direct APC-to-Treg cell contact. The APC-mediated suppressive effect on Treg function of certain probiotic strains may constrain the anti-inflammatory activity, which is often desired from probiotic therapy. This unexpected function of certain probiotic strains should be taken into consideration when designing adjuvant therapies with these bacteria, or when probiotic strains are selected for improvement of gut-associated inflammation like IBD. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21066">
<title>Ablation of gly96/immediate early gene-X1 (gly96/iex-1) aggravates DSS-induced colitis in mice: Role for gly96/iex-1 in the regulation of NF-[kappa]B</title>
<link>http://dx.doi.org/10.1002%2Fibd.21066</link>
<description><![CDATA[Inflammatory bowel diseases (IBDs) result from environmental and genetic factors and are characterized by an imbalanced immune response in the gut and deregulated activation of the transcription factor NF-[kappa]B. Addressing the potential role of gly96/iex-1 in the regulation of NF-[kappa]B in IBD, we used the dextran sodium sulfate (DSS) colitis model in mice in which the gly96/iex-1 gene had been deleted.C57BL/6 mice of gly96/iex-1-/- or gly96/iex-1+/+ genotype were treated continuously with 4% DSS (5 days) and repeatedly with 2% DSS (28 days) for inducing acute and chronic colitis, respectively. In addition to clinical and histological exploration, colon organ culture and bone marrow-derived cells (BMCs) were analyzed for chemo/cytokine expression and NF-[kappa]B activation.Compared to wildtype littermates, gly96/iex-1-/- mice exhibited an aggravated phenotype of both acute and chronic colitis, along with a greater loss of body weight and colon length. Colonic endoscopy revealed a higher degree of hyperemia, edema, and bleeding in gly96/iex-1-/- mice, and immunohistochemistry detected massive mucosal infiltration of leukocytes and marked histological changes. The expression of proinflammatory chemo- and cytokines was higher in the colon of DSS-treated gly96/iex-1-/- mice, and the NF-[kappa]B activation was enhanced particularly in the distal colon. In cultured BMCs from gly96/iex-1-/- mice, Pam3Cys4 treatment induced expression of proinflammatory mediators to a higher degree than in gly96/iex-1+/+ BMCs, along with greater NF-[kappa]B activation.Based on the observation that genetic ablation of gly96/iex-1 triggers intestinal inflammation in mice, we demonstrate for the first time that gly96/iex-1 exerts strong antiinflammatory activity via its NF-[kappa]B-counterregulatory effect. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21063">
<title>Going with the flow of autophagy in Crohn&#x27;s disease: IRGM risk polymorphism found upstream</title>
<link>http://dx.doi.org/10.1002%2Fibd.21063</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21059">
<title>Distribution of peroxisome proliferator-activated receptor-gamma polymorphisms in Chinese and Dutch patients with inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21059</link>
<description><![CDATA[As peroxisome proliferator-activated receptor-gamma (PPAR-[gamma]) is frequently expressed in colon, its genetic polymorphism may play a role in the etiology of inflammatory bowel disease (IBD). The aims of the present study were to determine the distribution of PPAR-[gamma] polymorphisms Pro12Ala and C161T and to explore the association between the PPAR-[gamma] genotypes and phenotypes of IBD patients.A total of 244 IBD patients [212 ulcerative colitis (UC) and 32 Crohn's disease (CD)] and 220 controls in the Chinese population and 603 IBD patients (302 UC and 301 CD) and 180 controls in the white Dutch population were enrolled in the study. The phenotypes of Chinese IBD patients were grouped according to disease location. The PPAR-[gamma] polymorphisms Pro12Ala and C161T were genotyped by PCR-based methods.In the Chinese population, T carriers of the PPAR-[gamma] C161T polymorphism were more common in UC patients than in the controls [37.7% vs. 25.5%, odds ratio 1.77, 95% confidence interval 1.18-2.68, P = 0.007], whereas Ala carriers of the Pro12Ala polymorphism showed no significant association in UC patients, but there was a significant association of Ala carriers with more extensive disease among the UC patients (P = 0.002); Pro12Ala and C161T genotypes did not show any associations with CD patients. No associations were found for the PPAR-[gamma] C161T SNP studied in the Dutch IBD population.Our study showed the potential association between the PPAR-[gamma] C161T polymorphism and UC patients in the central Chinese population. This finding was not replicated in the Dutch population. Further studies are necessary to explore the functional implication of the PPAR-[gamma] C161T polymorphism in Chinese UC patients. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21055">
<title>Age distribution of IBD hospitalization</title>
<link>http://dx.doi.org/10.1002%2Fibd.21055</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21053">
<title>Widespread but not localized neoplasia in inflammatory bowel disease worsens the prognosis of colorectal cancer</title>
<link>http://dx.doi.org/10.1002%2Fibd.21053</link>
<description><![CDATA[Patients with inflammatory bowel disease (IBD) are at increased risk of colorectal cancer (CRC). Recently, new phenotypes of CRC in IBD have been suggested. Studies of the prognosis of CRC in IBD have shown conflicting results. The aim of the study was to analyze factors for prognosis in CRC-IBD, including the impact of the new phenotypes.By using the nationwide, population-based Cancer Registry of Norway, we compared survival of a CRC-IBD cohort with CRC in the background population (all-CRC), adjusting for the topographical distribution of dysplasia at cancer diagnosis (widespread versus localized neoplasia in IBD) and other factors. We also analyzed prognostic factors within CRC-IBD.The mean age at CRC diagnosis was 43 years in widespread, 52 years in localized neoplasia IBD, and 70 years in all-CRC (P < 0.05). Adjusted for cofactors, prognosis of CRC-IBD was poorer compared to all-CRC (mortality rate ratio [MRR] 3.71, 95% confidence interval [CI]: 2.54-5.42, P < 0.001). Prognosis of widespread neoplasia IBD was poorer compared to all-CRC (MRR 4.27, 95% CI: 2.83-6.44, P < 0.001) and compared to localized neoplasia IBD (MRR 3.58, 95% CI: 0.87-14.72, P = 0.076). Survival was not significantly different between localized neoplasia IBD and all-CRC (P = 0.132).The results demonstrate lower age and poorer survival of CRC in IBD compared to CRC in the background population. The unfavorable effect of IBD on prognosis of CRC was pronounced in widespread neoplasia IBD. The diagnosis of this phenotype seems to be an important prognostic sign in patients with CRC in IBD. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21016">
<title>High gene expression of MDR1 (ABCB1) is associated with medical treatment response and long-term remission in patients with ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21016</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21094">
<title>A new tool to measure the burden of Crohn&#x27;s disease and its treatment: Do patient and physician perceptions match?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21094</link>
<description><![CDATA[Health-related quality of life (HRQOL) is difficult to efficiently measure in the clinic setting. Our aim was to develop and test a simple tool to measure the burden of Crohn's disease (CD) and its treatment and to compare how patients and their physicians perceive the impact of CD on HRQOL.A cross-sectional, self-administered questionnaire was distributed to patients with CD. The questionnaire included a feeling thermometer to measure disease and treatment burden, which was compared to the Short Inflammatory Bowel Disease Questionnaire (SIBDQ). At that visit, the patient's physician completed a questionnaire containing the feeling thermometer and the Harvey Bradshaw index (HBI). Nonparametric tests were use to report results.In all, 113 surveys were completed. The median age of respondents was 40 years and 68% were female. Using the feeling thermometer (scale 0-100), patients reported their current health as a median of 70 (interquartile range [IQR] 50-80) and their disease specific burden as 20 (IQR 10-40). Treatment-specific burden was 6.9 (IQR 1.3-20). Physicians perceived their patients' current health as a median of 71.3 (IQR 57.5-90) with a disease burden of 12.5 (IQR 5-30). Spearman's rho between the burden of symptoms measured by the feeling thermometer and the SIBDQ was -0.71. The correlation between patient and physician perception of current health was 0.73.Two questions using the feeling thermometer provide a quick and accurate assessment of the burden of CD on patients. Physicians' perception of the burden of disease was similar to their patients. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21092">
<title>Platelet-activating factor-induced NF-[kappa]B activation and IL-8 production in intestinal epithelial cells are Bcl10-dependent</title>
<link>http://dx.doi.org/10.1002%2Fibd.21092</link>
<description><![CDATA[Platelet-activating factor (PAF), a potent proinflammatory phospholipid mediator, has been implicated in inducing intestinal inflammation in diseases such as inflammatory bowel disease (IBD) and necrotizing enterocolitis (NEC). However, its mechanisms of inducing inflammatory responses are not fully understood. Therefore, studies were designed to explore the mechanisms of PAF-induced inflammatory cascade in intestinal epithelial cells.Nuclear factor kappa B (NF-[kappa]B) activation was measured by luciferase assay and enzyme-linked immunosorbent assay (ELISA), and interleukin 8 (IL-8) production was determined by ELISA. B-cell lymphoma 10 (Bcl10), caspase recruitment domain-containing membrane-associated guanylate kinase protein 3 (CARMA3), and mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1) mRNA and protein levels were assessed by real-time reverse-transcription polymerase chain reaction (RT-PCR) and Western blot, respectively. siRNA silencing of Bcl10 was used to examine its role in PAF-induced NF-[kappa]B activation and IL-8 production. The promoter region of the Bcl10 gene was cloned with the PCR method and promoter activity measured by luciferase assay.The adaptor protein Bcl10 appeared to play an important role in the PAF-induced inflammatory pathway in human intestinal epithelial cells. Bcl10 was required for PAF-induced I[kappa]B[alpha] phosphorylation, NF-[kappa]B activation, and IL-8 production in NCM460, a cell line derived from normal human colon, and Caco-2, a transformed human intestinal cell line. PAF also stimulated Bcl10 interactions with CARMA3 and MALT1, and upregulated Bcl10 expression in these cells via transcriptional regulation.These findings highlight a novel PAF-induced inflammatory pathway in intestinal epithelial cells, requiring Bcl10 as a critical mediator and involving CARMA3/Bcl10/MALT1 interactions. The proinflammatory effects of PAF play prominent roles in the pathogenesis of IBD and this pathway may present important targets for intervention in chronic inflammatory diseases of the intestine. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21091">
<title>Circulating levels of chemerin and adiponectin are higher in ulcerative colitis and chemerin is elevated in Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21091</link>
<description><![CDATA[Chemerin is an adipokine that stimulates chemotaxis of cells of the innate immune system. Inflammatory bowel disease (IBD) is linked to an impaired immune response and, therefore, we hypothesized that systemic chemerin may be altered in IBD patients.Serum was collected from patients with Crohn's disease (CD, 230 patients), ulcerative colitis (UC, 80 patients), and healthy controls (HC, 80 probands). Chemerin and adiponectin, which has already been measured in the serum of similar cohorts by others, were determined by enzyme-linked immunosorbent assay (ELISA).Chemerin was elevated in IBD compared to HC and was higher in male CD than UC patients. Female and male CD patients had lower adiponectin levels compared to UC, and adiponectin was lower in female CD patients compared to female HC. Adiponectin tended to be higher in female and male UC patients compared to HC and this difference became significant in the whole study group. Correlations with disease activity were only found in males. Here, chemerin was higher in CD patients on remission but was reduced in UC with nonactive disease. Adiponectin was higher in UC with inactive disease. Treatment with corticosteroids was linked to elevated adiponectin in male CD patients and higher chemerin in female UC patients. Unlike adiponectin, which was elevated in female serum in all cohorts, chemerin was only higher in female UC patients.These findings further indicate potential regulatory functions of adipokines in intestinal inflammation that are partly gender-dependent and that may even be associated with the distinct immunopathogenesis of UC and CD. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21090">
<title>Female gender and surgery impair relationships, body image, and sexuality in inflammatory bowel disease: Patient perceptions</title>
<link>http://dx.doi.org/10.1002%2Fibd.21090</link>
<description><![CDATA[There is a paucity of literature on the impact of inflammatory bowel disease (IBD) on relationships, body image, and sexual function from a patient perspective. This study sought to describe patients' perceptions of these issues.In all, 347 patients, age 18-50 years, from a hospital-based IBD database were surveyed by post. Quantitative and qualitative data were obtained on demographics, relationships, quality of life (QoL), body image, and sexual function. Comparisons were made by diagnosis, gender, and operative status. Univariate and multivariable analyses and logistic regressions were performed; P < 0.05 was regarded as significant.The response rate was 62.5%. Overall, 88.5% reported impaired QoL; 50.2% a negative effect on relationship status; and 66.8% impaired body image (females 74.8% versus males 51.4%, P = 0.0007; operated 81.4% versus nonoperated 51.3%, P = 0.0003). A greater proportion of women reported decreased frequency of sexual activity, as did operated subjects (female 66.3% versus male 40.5%, P < 0.0001; operated 68.5% versus nonoperated 50.4%, P = 0.0113). Women and operated subjects also more often reported decreased libido (female 67.1% versus male 41.9% P = 0.0005; operated 67.4% versus nonoperated 52.6%, P = 0.035). 9.7% omitted medication because of perceived negative effect(s) on sexual function. Logistic regression revealed that female gender negatively affected body image, libido, and sexual activity, while limited resection surgery negatively affected body image (all P < 0.005).A large proportion of patients perceive IBD to negatively affect many aspects of sexuality. Females and operated subjects more frequently perceived these negative effects. These findings are important in overall clinical care of patients with IBD and should be addressed. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21089">
<title>Crohn&#x27;s proctitis: A distinct entity</title>
<link>http://dx.doi.org/10.1002%2Fibd.21089</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21087">
<title>Mesalamine (pentasa)-induced painful skin lesions</title>
<link>http://dx.doi.org/10.1002%2Fibd.21087</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21084">
<title>Prospective randomized open-label multicenter phase I/II dose escalation trial of visilizumab (HuM291) in severe steroid-refractory ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21084</link>
<description><![CDATA[Visilizumab is a humanized IgG2 monoclonal anti-CD3 antibody. We evaluated its safety and dose response in severe intravenous steroid-refractory ulcerative colitis (UC).In all, 104 patients were treated. In Stage I, 73 patients were randomly assigned to receive intravenous visilizumab 5, 7.5, 10, or 12.5 [mu]g/kg/day for 2 consecutive days. In Stage II, 33 patients received visilizumab at the optimal clinical dose (OCD) of 5 [mu]g/kg/day for 2 days. Symptomatic response and remission were defined by the modified Truelove-Witts severity index. Clinical response and remission were defined by the Mayo score.The rates of symptomatic response at day 15 in the 5, 7.5, 10, or 12.5 [mu]g/kg dose groups were 71%, 70%, 50%, and 61%, respectively, in Stage I and in 54% in Stage II. The symptomatic remission rates were 35%, 5%, 22%, and 11% in Stage I and 18% in Stage II. The rates of clinical response at day 30 in the 5, 7.5, 10, or 12.5 [mu]g/kg dose groups were 71%, 65%, 50%, and 67%, respectively, in Stage I and 55% in Stage II. The clinical remission rates were 6%, 5%, 0%, and 11% in Stage I and 6% in Stage II. All patients experienced adverse events. Serious adverse events included abdominal abscess, cytomegalovirus infection, atrial fibrillation, herpes zoster, and esophageal candidiasis.Treatment with visilizumab induced symptomatic response and clinical response. Results with 5 [mu]g/kg/day were similar to those observed with higher doses (NCT00267306 at ). (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21077">
<title>Course of inflammatory bowel disease in patients infected with human immunodeficiency virus</title>
<link>http://dx.doi.org/10.1002%2Fibd.21077</link>
<description><![CDATA[Human immunodeficiency virus (HIV) infection depletes CD4+ lymphocytes, which may benefit patients with inflammatory bowel disease (IBD). The aim was to compare the course of IBD in HIV patients with a matched group of IBD seronegative patients.A total of 20 IBD (14 Crohn's disease, 6 ulcerative colitis) HIV infected patients and 40 matched control seronegative IBD patients (2 controls per case) were compared regarding relapse of their disease. The CD4+ count was followed every 6 months and a value of [le]500 cells/[mu]L was used to define patients with immunosuppression. Relapse rates per year of follow-up were compared among the 2 groups and survival curves for cumulative remission rates were compared with a log-rank test. Multivariate analysis was used to discriminate among the impact of different variables on the risk of IBD relapse.The median duration of follow-up was 8.4 years (range 0.6-18 years). The mean relapse rate for the HIV+IBD group was 0.016/year of follow-up as compared to 0.053/year of follow-up for the IBD-matched control group (P = 0.032). Regarding the HIV-positive/IBD group, 14 patients were immunosuppressed at any given time during the follow-up period. None of these patients experienced an IBD relapse, whereas 3 out of the 6 without immunosuppression relapsed (P = 0.017). According to the multivariate analysis, HIV status was the only risk factor independently associated with a lower probability of IBD relapse.HIV infection reduces the relapse rates in IBD patients and this may be attributed to the lower CD4+ counts seen in these patients. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21070">
<title>Glucocorticoid bioactivity does not predict response to steroid therapy in severe pediatric ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21070</link>
<description><![CDATA[The pathophysiological basis for corticosteroid (CS) failure in ulcerative colitis (UC) is unknown. A transactivation glucocorticoid bioassay (GBA) was developed to measure the biological activity of CS by quantifying glucocorticoid response elements. This approach eliminates differences in bioavailability, chemistry, affinity, and other potential differences between the various steroids regarding their ability to activate the glucocorticoid receptor. In this multicenter prospective study, we aimed to evaluate whether CS bioavailability plays a role in CS refractoriness in severe pediatric UC.GBA (using COS-1 transfected cells) was measured in the serum of 50 children (52% males, age 13.4 ± 3.5 years) admitted for acute severe UC on the third day of CS treatment. Demographic, clinical, and laboratory data were prospectively recorded.Of the children enrolled, 16 (32%) failed CS therapy and required infliximab (n = 14) or colectomy (n = 2) within a median of 10 days (interquartile range [IQR] 6.5-14.5). Reflecting internal validity of the assay, GBA was highly correlated with the last CS dose and the time interval to bloodletting (r = -0.41 and r = -0.54, respectively; P < 0.001). There was no statistically significant difference in the GBA levels between responders and nonresponders (249 nM versus 200 nM cortisol equivalent, P = 0.18). In a multivariate regression model adjusted for time elapsed from CS and the administered dose, GBA did not predict response to CS (P = 0.34).The lack of correlation of GBA level and treatment outcome lends support to the hypothesis that the bioavailability, type, and dosing of intravenous CS are not associated with response or failure to the drug. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21081">
<title>Oral valganciclovir for colonic dilatation in ulcerative colitis associated with human cytomegalovirus infection</title>
<link>http://dx.doi.org/10.1002%2Fibd.21081</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21074">
<title>Detailed haplotype-tagging study of germline variation of MUC19 in inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21074</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21073">
<title>T-cell regulation of neutrophil infiltrate at the early stages of a murine colitis model</title>
<link>http://dx.doi.org/10.1002%2Fibd.21073</link>
<description><![CDATA[T-cells are a main target for antiinflammatory drugs in inflammatory bowel disease. As the innate immune system is also implicated in the pathogenesis of these diseases, T-cell suppressors may not only inhibit T-cell-dependent production of proinflammatory mediators but also affect innate immune cell function. Specifically, these drugs may impair innate immune cell recruitment and activation through inhibition of T-cells or act independent of T-cell modulation. We explored the extent of immune modulation by the T-cell inhibitor tacrolimus in a murine colitis model.We assessed the effects of tacrolimus on trinitro-benzene sulphonic acid (TNBS) colitis in wildtype and Rag2-deficient mice. The severity of colitis was assessed by means of histological scores and weight loss. We further characterized the inflammation using immunohistochemistry and by analysis of isolated intestinal leukocytes at various stages of disease.Tacrolimus-treated wildtype mice were less sensitive to colitis and had fewer activated T-cells. Inhibition of T-cell function was associated with strongly diminished recruitment of infiltrating neutrophils in the colon at the early stages of this model. In agreement, immunohistochemistry demonstrated that tacrolimus inhibited production of the neutrophil chemoattractants CXCL1 and CXCL2. Rag2-deficient mice displayed an enhanced baseline level of lamina propria neutrophils that was moderately increased in TNBS colitis and remained unaffected by tacrolimus.Both the innate and the adaptive mucosal immune system contribute to TNBS colitis. Tacrolimus suppresses colitis directly through inhibition of T-cell activation and by suppression of T-cell-mediated recruitment of neutrophils. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21071">
<title>Guillain-Barr&#xE9; syndrome during a relapse of ulcerative colitis: A case report</title>
<link>http://dx.doi.org/10.1002%2Fibd.21071</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21058">
<title>Age distribution of IBD hospitalization</title>
<link>http://dx.doi.org/10.1002%2Fibd.21058</link>
<description><![CDATA[The ages of patients with Crohn's disease (CD) and ulcerative colitis (UC) are characterized by a bimodal distribution. The present study used hospital statistics to compare the age distribution of inflammatory bowel disease (IBD) among different countries.Hospital statistics from the period 1994 to 2007 were obtained through special requests to the national statistical offices of 9 European countries. Hospitalization was expressed as age- and sex-specific rates per 10,000 living people.Hospitalization rates of different countries varied between 1.2 and 4.3 discharges per 10,000 for CD and between 0.7 and 4.7 discharges per 10,000 for UC. Countries with high CD rates were associated with similarly high UC rates (r = 0.955, P < 0.0001). In all countries alike, the age-distribution of CD hospitalization was characterized by a large peak in younger patients followed by a small peak in older patients. UC hospitalization was characterized by a small peak in younger patients followed by a large peak in older patients.The bimodal age distribution of IBD hospitalization can be explained in terms of varying exposure to 2 separate environmental risk factors that affected consecutive age groups differently over the course of the 20th century. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21057">
<title>Effect of natural commensal-origin DNA on toll-like receptor 9 (TLR9) signaling cascade, chemokine IL-8 expression, and barrier integritiy of polarized intestinal epithelial cells</title>
<link>http://dx.doi.org/10.1002%2Fibd.21057</link>
<description><![CDATA[The intestinal epithelium is constantly exposed to high levels of genetic material like bacterial DNA. Under normal physiological conditions, the intestinal epithelial monolayer as a formidable dynamic barrier with a high-polarity structure facilitates only a controlled and selective flux on components between the lumen and the underlining mucosa and even is able to facilitate structure-based macromolecules movement. The aim of this study was to test the effect of natural commensal-origin DNA on the TLR9 signaling cascade and the barrier integrity of polarized intestinal epithelial cells (IECs).Polarized HT-29 and T84 cells were treated with TNF-[alpha] in the presence or absence of DNA from Lactobacillus rhamnosus GG (LGG) and Bifidobacterium longum. TLR9 and interleukin-8 (IL-8) mRNA expression was assessed by semiquantitative and TaqMan real-time reverse-transcription polymerase chain reaction. Expression of TLR9 protein, degradation of inhibitor of kappa B alpha (I[kappa]B[alpha]), and p38 mitogen-activated protein kinase (p38 MAP) phosphorylation were assessed by Western blotting. To further reveal the role of TLR9 signaling, the TLR9 gene was silenced by siRNA. IL-8 secretion was measured by an enzyme-linked immunosorbent assay. Nuclear factor-kappa B (NF-[kappa]B) activity was assessed by the electrophoretic mobility shift assay (EMSA) and NF-[kappa]B-dependent luciferase reporter gene assays. As an indicator of tight junction formation and monolayer integrity of epithelial cell monolayers, transepithelial electrical resistance (TER) was repetitively monitored. Transmonolayer movement of natural commensal-origin DNA across monolayers was monitored using qRT-PCR and nested PCR based on bacterial 16S rRNA genes.In response to apically applied natural commensal-origin DNA, polarized HT-29 and T84 cells enhanced expression of TLR9 in a specific manner, which was subsequently associated with attenuation of TNF-[alpha]-induced NF-[kappa]B activation and NF-[kappa]B-mediated IL-8 expression. TLR9 silencing abolished this inhibitory effect. Apically applied LGG DNA attenuated TNF-[alpha]-enhanced NF-[kappa]B activity by reducing I[kappa]B[alpha] degradation and p38 phosphorylation. LGG DNA did not decrease the TER but rather diminished the TNF-[alpha]-induced TER reduction. Translocation of natural commensal-origin DNA into basolateral compartments did not occur under tested conditions.Our study indicates that TLR9 signaling mediates, at least in part, the anti-inflammatory effects of natural commensal-origin DNA on the gut because TLR9 silencing abolished the inhibitory effect of natural commensal-origin DNA on TNF-[alpha]-induced IL-8 secretion in polarized IECs. The nature of the TLR9 agonist, the polarity of cells, and the tight junction integrity of IECs has to be taken into account in order to predict the outcome of TLR9 signaling. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21088">
<title>Assessing disease activity in ulcerative colitis: Patients or their physicians?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21088</link>
<description><![CDATA[We aimed to determine the optimal approach to assess disease activity (i.e., biological inflammation) in ulcerative colitis (UC) by comparing patients' and physicians' rating of the disease.This was a prospective, multicenter, double-cohort study. The first cohort was composed of 94 children with UC (parent proxy when required) and their physicians who provided independent clinical report and global assessment of disease, rated on a 100 mm visual analog scale. Constructs of disease activity (including mucosal inflammation, laboratory tests, Mayo score, and the Pediatric UC Activity Index), were scored by an independent blinded physician and used to compare validity of the assessment. Of the 94 children, 43 were seen at a follow-up visit and provided a global rating of change in disease activity. To ascertain whether age influences assessment accuracy, a second cohort of 86 adult UC patients were analyzed in a similar way.In both cohorts the physician global assessment had higher correlations with all constructs of disease activity than did the patient' global assessment (for colonoscopic score r = 0.76 vs. r = 0.29, P = 0.002). Even with abdominal pain, a subjective item, the physician's rating had higher correlation than the patient's rating. Similarly, the physician rating of change better reflected change in disease activity than that of the patient rating.For indirect measurement of biological activity on the basis of symptoms and signs, clinician assessments are superior to those of patients. Patient assessments, physician assessments, and direct measurement of disease activity provide complementary information in clinical research. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21085">
<title>Value of fractional exhaled nitric oxide (FENO) for the diagnosis of pulmonary involvement due to inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21085</link>
<description><![CDATA[Pulmonary involvement due to inflammatory bowel disease (IBD) is frequent when evaluating a patient with IBD and pulmonary involvement remains complicated. Most of the patients are asymptomatic and the methods used are mostly invasive or expensive procedures. The aim of this prospective study is to evaluate the value of the fractional exhaled nitric oxide (FENO) level for the diagnosis of pulmonary involvement due to IBD and to investigate any correlation between FENO level and disease activity.Thirty-three nonsmoker patients with IBD (25 ulcerative colitis [UC] and 8 Crohn's Disease [CD]) who were free of corticosteroid treatment and 25 healthy subjects as a control group were enrolled in this study. All patients with IBD were investigated for pulmonary involvement with medical history, physical examination, chest roentgenogram, oxygen saturation, blood eosinophil levels, pulmonary function tests (PFTs), high-resolution computed tomography (HRCT), and FENO level.Pulmonary involvement was established in 15 patients (45.5%) with IBD. The FENO level was higher in patients with pulmonary involvement than without pulmonary involvement and healthy controls independent from the pulmonary symptoms, eosinophil count, duration of disease, activity of disease, and surgery history (FENO: 32 ± 20; 24 ± 8; 14 ± 8 ppb, respectively) (P < 0.05). In addition, diffusion capacity (DLCO) was found to be significantly lower in patients with CD compared with UC (P < 0.05).This study showed that an increased FENO level may be used for identifying patients with IBD who need further pulmonary evaluation. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21083">
<title>Azathioprine maintains long-term steroid-free remission through 3 years in patients with steroid-dependent ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21083</link>
<description><![CDATA[Studies assessing the efficacy of azathioprine (AZA) in steroid-dependent ulcerative colitis (SD-UC) are scarce. The purpose of this trial was to explore the efficacy of AZA in maintaining steroid-free remission in SD-UC patients and the factors associated with sustained response.In this observational cohort study, 42 subjects with SD-UC were recruited for AZA therapy during a 3-year period. AZA was adjusted for a target dose of 2-3 mg/kg/day. Steroid therapy was tapered off following a standardized regimen. The primary endpoint was the annual rate of steroid-free response to AZA. Secondary endpoints included clinical recurrence, yearly steroid dose, and safety of treatment.On an intention-to-treat basis, the proportion of patients remaining in steroid-free remission at 12, 24, and 36 months was 0.55, 0.52, and 0.45, respectively. A significant decrease in the flare-ups rate and in requirement for steroids were observed during 3 years on AZA compared with the previous year (P = 0.000 for both). Patients with and without sustained response were comparable according to demographics, extent of disease, dose of AZA, steroids, and 5-aminosalicylate (5-ASA) use. Only disease duration <36 months was associated with off-steroids remission (P = 0.02, odds ratio [OR] 3.12, 95% confidence interval [CI] 1.89-7.64). The AZA benefit-risk profile was favorable.In this open-label observational trial AZA showed sustained efficacy for maintenance of clinical remission off steroids and steroid sparing through 3 years of therapy in SD-UC. Patients with earlier UC are those who most probably will have sustained steroid-free remission at the end of 12 months while on AZA. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21056">
<title>Prevalence of Clostridium difficile infection in Polish pediatric patients with inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21056</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21045">
<title>Mind-body complementary alternative medicine use and quality of life in adolescents with inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21045</link>
<description><![CDATA[Mind-body complementary and alternative medicine (CAM) modalities (e.g., relaxation or meditation) for symptom management have not been well studied in adolescents with inflammatory bowel disease (IBD). The purposes of this study were to: 1) determine the prevalence of 5 types of mind-body CAM use, and consideration of use for symptom management; 2) assess characteristics associated with regular mind-body CAM use; and 3) examine whether regular and/or considered mind-body CAM use are associated with health-related quality of life (HRQOL).Sixty-seven adolescents with IBD ages 12-19 recruited from a children's hospital completed a questionnaire on CAM use and the Pediatric Quality of Life Inventory. Logistic regression models were estimated for regular and considered CAM use.Participants mean (SD) age was 15.5 (2.1) years; 37 (55%) were female; 53 (79%) were white; and 20 (30%) had moderate disease severity. Adolescents used prayer (62%), relaxation (40%), and imagery (21%) once/day to once/week for symptom management. In multivariate analyses, females were more likely to use relaxation (odds ratio [OR] = 4.38, 95% confidence interval [CI] = 1.25-15.29, c statistic = 0.73). Younger adolescents were more likely to regularly use (OR = 0.63, 95% CI = 0.42-0.95, c statistic = 0.72) or consider using (OR = 0.77, 95% CI = 0.59-1.00, c statistic = 0.64) meditation. Adolescents with more severe disease (OR = 4.17, 95% CI = 1.07-16.29, c statistic = 0.83) were more willing to consider using relaxation in the future. Adolescents with worse HRQOL were more willing to consider using prayer and meditation for future symptom management (P < 0.05).Many adolescents with IBD either currently use or would consider using mind-body CAM for symptom management. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20983">
<title>Looking in the mouth for Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20983</link>
<description><![CDATA[It is widely acknowledged among gastroenterologists that the oral cavity may be involved in Crohn's disease (CD). However, the specific manifestations are poorly appreciated. Although oral aphthous ulceration is probably not diagnostically useful in patients with suspected CD, disease-specific manifestations do occur and are particularly common in children presenting with CD. These manifestations can be subtle, often are subclinical, yet commonly harbor diagnostically useful material (granulomas). Orofacial granulomatosis (OFG) is conventionally used to describe patients with overt oral disease without obvious involvement of the gastrointestinal tract. However, many patients with OFG have subclinical intestinal CD or will progress to develop overt intestinal CD with time. The management of severe oral disease is challenging and lacks a clear evidence base. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21095">
<title>Significant association of appendiceal neoplasms and ulcerative colitis rather than Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21095</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21079">
<title>Exposure of mouse colon to dietary bile acid supplement induces sessile adenomas</title>
<link>http://dx.doi.org/10.1002%2Fibd.21079</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21062">
<title>Probiotic for new onset ulcerative colitis in children: Baby&#x27;s got bac(teria)</title>
<link>http://dx.doi.org/10.1002%2Fibd.21062</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21061">
<title>On the role of ischemia in the pathogenesis of IBD: A review</title>
<link>http://dx.doi.org/10.1002%2Fibd.21061</link>
<description><![CDATA[Inflammatory bowel disease (IBD) is a chronic intestinal disorder comprising 2 distinct but often overlapping diseases: Crohn's disease and ulcerative colitis. Although much research to identify the etiology of IBD has focused on genetic constitution, infectious causes, and immune dysregulation, its exact cause and pathogenesis remain incompletely understood. Mesenteric blood flow, the intestinal microcirculation, and intestinal ischemia also have been proposed as etiologic, although they remain less-explored themes despite evidence suggesting a contributory role in IBD pathogenesis. The anatomy, architecture, and function of the splanchnic microcirculation will be reviewed here with regard to the development of intestinal microvascular ischemia, a pathologic process that appears to precede the classic changes that characterize IBD. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21078">
<title>Veto on vedolizumab (MLN0002) for Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21078</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21069">
<title>Fecal calprotectin mirrors inflammation of the distal ileum and bowel function after restorative proctocolectomy for pediatric-onset ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21069</link>
<description><![CDATA[The goal was to cross-sectionally assess fecal calprotectin after restorative proctocolectomy for pediatric-onset ulcerative colitis (UC).Fecal calprotectin, histology of the distal ileum, inflammation biochemistry, episodes of pouchitis, and bowel function were cross-sectionally determined at early adulthood in 32 patients who had undergone proctocolectomy with ileoanal anastomosis for UC at a mean (SD) age of 12.0 ± 4.1 years.A total of 15 (47%) patients showed increased (>100 [mu]g/g) fecal calprotectin (669 ± 866 [mu]g/g), although their serum C-reactive protein (5.2 ± 3.8 mg/L), erythrocyte sedimentation rate (13 ± 13 mm/h), and white blood cell count (6.7 ± 1.7 E9/L) were normal or slightly elevated. Calprotectin correlated positively with the histological neutrophil count of the distal ileum (r = 0.715; P < 0.001), the frequency of pouchitis (r = 0.468; P < 0.01), and with the maximum daily frequency of bowel actions (r = 0.610; P < 0.001). Mean fecal calprotectin was 71 ± 50 [mu]g/g among patients with no history of pouchitis (n = 10), 290 ± 131 [mu]g/g among patients with a single episode of pouchitis (n = 15), and 832 ± 422 [mu]g/g among those with recurrent pouchitis (P = 0.019 between recurrent pouchitis and no pouchitis). Sensitivity, specificity, positive predictive value, and negative predictive value for fecal calprotectin concentration over 300 [mu]g/g to detect recurrent pouchitis were 57%, 92%, 67%, and 89%, respectively.Neutrophilic inflammation of the distal ileum, as reflected by fecal calprotectin, is common after restorative proctocolectomy for pediatric-onset UC. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21065">
<title>Do 5-ASAs prevent colorectal neoplasia in patients with ulcerative colitis? Still no answers</title>
<link>http://dx.doi.org/10.1002%2Fibd.21065</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21064">
<title>Appendicitis, not appendectomy, is protective against ulcerative colitis, both in the general population and first-degree relatives of patients with IBD</title>
<link>http://dx.doi.org/10.1002%2Fibd.21064</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21046">
<title>Association of the novel serologic anti-glycan antibodies anti-laminarin and anti-chitin with complicated Crohn&#x27;s disease behavior</title>
<link>http://dx.doi.org/10.1002%2Fibd.21046</link>
<description><![CDATA[We tested a panel of novel serological anti-glycan antibodies including the previously unpublished anti-laminarin IgA (Anti-L) and anti-chitin IgA (Anti-C) carbohydrate antibodies for the presence in Crohn's disease (CD) patients, diagnosis and differentiation of CD, association with complicated disease behavior, and marker stability over time.The presence of Anti-L, Anti-C, anti-chitobioside IgA (ACCA), anti-laminaribioside IgG (ALCA), anti-mannobioside IgG (AMCA), and anti-Saccaromyces cervisiae IgG (gASCA) carbohydrate antibodies were tested in serum samples from 824 participants (363 CD, 130 ulcerative colitis [UC], 74 other gastrointestinal diseases, and 257 noninflammatory bowel/gastrointestinal disease controls) of the German IBD-network by enzyme-linked immunosorbent assay (ELISA; Glycominds, Lod, Israel) and for perinuclear antineutrophil cytoplasmic antibody (pANCA) by immunofluorescence.In all, 77.4% of the CD patients were positive for at least 1 of the anti-glycan antibodies. gASCA or the combination of gASCA/pANCA remained most accurate for the diagnosis of CD, but the combined use of the antibodies improved differentiation of CD from UC. Several single markers as well as an increasing antibody response were independently linked to a severe disease phenotype, as shown for the occurrence of complications, CD-related surgery, early disease onset, and ileal disease location. This was observed for both quantitative and qualitative antibody responses. The antibody status remained stable over time in most IBD patients.A panel of anti-glycan antibodies including the novel Anti-L and Anti-C may aid in differentiation of CD from UC, is associated with complicated CD behavior and IBD-related surgery, and is stable over time in a large patient cohort. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21075">
<title>Cytokine mRNA expression in steroid-na&#xEF;ve patients with ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21075</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21050">
<title>Identification of a novel staining pattern of bile duct epithelial cells in primary sclerosing cholangitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21050</link>
<description><![CDATA[Primary sclerosing cholangitis (PSC) is an inflammatory disease of the bile ducts with an unknown etiology. A number of autoantigens have been proposed, but an early diagnostic marker is still lacking. Our aim was to identify such an autoantigen.Immunostaining was performed on normal human bile duct with sera from patients with PSC and controls. To identify an autoantigen a cDNA library from normal human choledochus was constructed and immunoscreened with patient sera. Using in vitro transcription and translation and immunoprecipitation we examined the immunoreactivity against PDZ domain containing 1 (PDZK1) in 35 patients with PSC, 198 control patients, and 94 healthy controls.We observed a previously unpublished staining pattern in which cytoplasmatic granules and apical cell membranes of biliary epithelial cells were stained by PSC sera. Strong immunoreactivity to these structures was obtained with 12 out of 35 PSC sera (34%) but not with sera from healthy controls. By screening the cDNA library we identified PDZK1 as a candidate antigen. Immunoreactivity against PDZK1 was detected in 9% of PSC patients, 2% of inflammatory bowel disease (IBD) patients, 8% of autoimmune pancreatitis patients, 18% of Grave's disease patients, and 1% of healthy controls.Previously unpublished, specific, and strong autoantibodies against epithelial cells of the bile duct in PSC sera were identified. Furthermore, PDZK1 is suggested as a potential new autoantigen. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21048">
<title>World Gastroenterology Organisation Practice Guidelines for the Diagnosis and Management of IBD in 2010</title>
<link>http://dx.doi.org/10.1002%2Fibd.21048</link>
<description><![CDATA[Inflammatory bowel disease (IBD) represents a group of idiopathic, chronic, inflammatory intestinal conditions. Its two main disease categories are: Crohn's disease (CD) and ulcerative colitis (UC), which feature both overlapping and distinct clinical and pathological features. While these diseases have, in the past, been most evident in the developed world, their prevalence in the developing world has been gradually increasing in recent decades. This poses unique issues in diagnosis and management which have been scarcely addressed in the literature or in extant guidelines. Depending on the nature of the complaints, investigations to diagnose either form of IBD or to assess disease activity will vary and will also be influenced by geographic variations in other conditions that might mimic IBD. Similarly, therapy varies depending on the phenotype of the disease being treated and available resources. The World Gastroenterology Organization has, accordingly, developed guidelines for diagnosing and treating IBD using a cascade approach to account for variability in resources in countries around the world. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21043">
<title>Characterization of single-nucleotide polymorphisms relevant to inflammatory bowel disease in commonly used gastrointestinal cell lines</title>
<link>http://dx.doi.org/10.1002%2Fibd.21043</link>
<description><![CDATA[The era of genome-wide association studies (GWAS) has led to the identification of many inflammatory bowel disease (IBD)-associated single-nucleotide polymorphisms (SNPs) with unknown function. The next step would be to identify the functional consequences of these polymorphisms in order to target them efficiently for therapeutic purposes. One way to study this type of genetic variation is the use of cell line models. However, to characterize the functional effect of a SNP, it is important to know if the selected cell line model itself carries the studied genetic variation. Here, we genotyped 50 IBD markers across 32 susceptibility genes in 9 commonly used gastrointestinal cell lines.We used Sequenom, TaqMan, and DNA sequencing for the genotyping. To determine the expression profile of the selected genes, we conducted real-time RT-PCR.We found variant SNPs in all analyzed cell lines. Almost every minor allele was carried by at least one of the tested cell lines. We analyzed the effect of 4 SNPs in more detail using quantitative real-time RT-PCR (qRT-PCR) comprising genes ATG16L1, CD14, MDR1, and OCTN2. According to our data, only 2 of the commonly studied SNPs in MDR1 and CD14 have an impact on gene expression.We have identified genotype variants in all analyzed cell lines. Some of them are functional and alter the response to drugs (MDR1) or affect bacterial recognition (TLR4, NOD2). Our results highlight that the genotype should not be neglected in experimental design when using model cell lines. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21067">
<title>Endoscopic ultrasound to guide the combined medical and surgical management of pediatric perianal Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21067</link>
<description><![CDATA[Perianal fistulas are a debilitating manifestation of Crohn's disease (CD) in the pediatric population and present a management challenge. The aims of this study were to describe our experience using endoscopic ultrasound (EUS) to guide management of perianal CD (PCD) in a pediatric population, and determine whether using EUS to monitor healing after seton placement improves outcomes.We conducted a retrospective study of 2 cohorts: pediatric subjects with PCD who underwent EUS and pediatric subjects who underwent seton placement between 2002 and 2007.In all, 25 children underwent a total of 42 EUS procedures. Of 28 EUSs performed to evaluate suspected perianal disease, complex fistulizing disease was identified in 15 (54%). Setons were placed after most EUSs demonstrating complex fistulizing disease and after none demonstrating superficial or no fistulizing disease. Of 14 EUSs performed to monitor healing around a seton, 7 (50%) demonstrated persistent peri-seton inflammation. Setons were more often left in place after an EUS revealing persistent inflammation (86% versus 0%), and the patients were more likely to have a biologic initiated or changed (57% versus 0%). Among all subjects who underwent seton placement, time from seton removal to recurrence was longer for those followed by EUS compared to those followed by physical exam only; however, we were not powered to test for statistical significance.EUS to guide the combined medical and surgical management of PCD is feasible in the pediatric population. Larger prospective studies are needed to determine if EUS-directed management improves outcomes in pediatric patients with PCD. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21054">
<title>Similar geographic variations of mortality and hospitalization associated with IBD and Clostridium difficile colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21054</link>
<description><![CDATA[Superinfection with Clostridium difficile can aggravate the symptoms of preexisting inflammatory bowel disease (IBD). The study served to assess whether the geographic variation of IBD within the United States might be influenced by C. difficile infection.Hospitalization data of the Healthcare Cost and Utilization Project (HCUP) from 2001-2006 and mortality data from 1979-2005 of the US were analyzed by individual states. Hospitalization and mortality associated with Crohn's disease (CD), ulcerative colitis (UC), and C. difficile colitis were correlated with each other, using weighted least square linear regression with the population size of individual states as weight.Among the hospitalization rates, there were strong correlations between both types of IBD, as well as each type of IBD with C. difficile colitis. Similarly, among the mortality rates there were strong correlations between both types of IBD, as well as each type of IBD with C. difficile colitis. Lastly, each type of hospitalization rate was also strongly correlated with each type of mortality rate. In general, hospitalization and mortality associated with IBD tended to be frequent in many of the northern states and infrequent in the Southwest and several southern states.The similarity in the geographic distribution of the 3 diseases could indicate the influence of C. difficile colitis in shaping the geographic patterns of IBD. It could also indicate that shared environmental risk factors influence the occurrence of IBD, as well as C. difficile colitis. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21051">
<title>Does primary sclerosing cholangitis impact quality of life in patients with inflammatory bowel disease?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21051</link>
<description><![CDATA[Impairment of health-related quality of life (HRQoL) is an important concern in inflammatory bowel disease (IBD; ulcerative colitis [UC], Crohn's disease [CD]). Between 2%-10% of patients with IBD have primary sclerosing cholangitis (PSC). There has been limited examination of the disease-specific HRQoL in this population compared to non-PSC IBD controls.This was a retrospective, case-control study performed at a tertiary referral center. Cases comprised 26 patients with a known diagnosis of PSC and IBD (17 UC, 9 CD). Three random controls were selected for each case after matching for IBD type, gender, age, and duration of disease. Disease-specific HRQoL was measured using the Short Inflammatory Bowel Disease Questionnaire (SIBDQ). Disease activity for CD was measured using the Harvey-Bradshaw index (HB) and using the UC activity index for UC. Independent predictors of HRQoL were identified.There was no significant difference in the age, gender distribution, or disease duration between PSC-IBD and controls. There was no difference in use of immunomodulators or biologics between the 2 groups. Mean SIBDQ score was comparable between PSC-IBD patients (54.5) and controls (54.1), both for UC and CD. Likewise, the disease activity scores were also similar (2.8 versus 3.1, P = 0.35). On multivariate analysis, higher disease activity score (-1.33, 95% confidence interval [CI] 95% CI -1.85 to -0.82) and shorter disease duration were predictive of lower HRQoL. Coexisting PSC did not influence IBD-related HRQoL. There was a higher proportion of permanent work disability in PSC-IBD (7.7%) compared to controls (0%).PSC does not seem to influence disease-specific HRQoL in our patients with IBD but is associated with a higher rate of work disability. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21042">
<title>Survival of the probiotic Escherichia coli Nissle 1917 (EcN) in the gastrointestinal tract given in combination with oral mesalamine to healthy volunteers</title>
<link>http://dx.doi.org/10.1002%2Fibd.21042</link>
<description><![CDATA[Mesalamine and the probiotic E. coli Nissle 1917 (EcN) are both effective agents for the treatment of ulcerative colitis. A combined therapy may have more than additive efficacy. However, mesalamine may have antimicrobial effects on EcN.In this prospective, randomized, double-blind, placebo-controlled study, 48 healthy volunteers took EcN in a run-in phase for 17 days (5-50 × 109 viable bacteria od). If stool samples became positive for EcN, volunteers received combination treatment with EcN plus either mesalamine (1500 mg twice a day) or placebo for 1 week. Fecal samples were further tested for EcN in 2- to 3-day intervals until a maximum of 48 weeks after treatment. Patient diaries, blood, and urine were checked to assess safety, compliance, and tolerance.During run-in, viable EcN were detected in 45 of the 48 volunteers (94%); 2 volunteers were positive before taking EcN. From days 1 to 7 of combination treatment (n = 40), the number of EcN-positive volunteers varied between 70% and 80% in the mesalamine group and between 85% and 95% in the placebo group. Differences between the groups were not significant (normal approximation: day 3, P > 0.15; day 5, P > 0.25; day 7, P > 0.076). At treatment discontinuation, 16 of 20 volunteers in the mesalamine group and 15 of 20 volunteers in the placebo group were EcN positive, whereas this figure dropped continuously up to week 12 after discontinuation (mesalamine, 7 of 20; placebo, 4 of 20). No differences between the groups were seen with regard to tolerance and safety.The combination of EcN and mesalamine has no significant effect on the survival of EcN in healthy volunteers. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21038">
<title>Fontolizumab in moderate to severe Crohn&#x27;s disease: A phase 2, randomized, double-blind, placebo-controlled, multiple-dose study</title>
<link>http://dx.doi.org/10.1002%2Fibd.21038</link>
<description><![CDATA[The safety and efficacy of fontolizumab, a humanized anti-interferon gamma antibody, was investigated in patients with Crohn's disease (CD). Elevated gut mucosal levels of interferon gamma, a key cytokine involved in the inflammatory process of CD, are associated with disease symptoms.A total of 201 patients with Crohn's Disease Activity Index (CDAI) scores between 250 and 450 were randomized to receive an initial intravenous dose of 1.0 or 4.0 mg/kg fontolizumab or placebo, followed by up to 3 subcutaneous doses of 0.1 or 1.0 mg/kg fontolizumab or placebo every 4 weeks. Clinical response at day 29, the primary efficacy endpoint, was defined as a decrease in the CDAI of at least 100 points from baseline levels.Of 201 patients, 135 (67%) completed the study. Day 29 response rates were similar in all treatment groups (31%-38%). At subsequent timepoints a significantly greater proportion of patients in the 1.0 mg/kg intravenous / 1.0 mg/kg subcutaneous fontolizumab group had clinical response and significantly greater improvement in the CDAI score compared with patients who received placebo. All fontolizumab groups had significant improvement in C-reactive protein levels. The overall frequency of adverse events was similar in all groups (58%-75%); most events were related to exacerbation of CD. There was a low frequency (5.2%) of neutralizing antibodies to fontolizumab.Although a strong clinical response to fontolizumab was not observed, significant decreases in C-reactive protein levels suggest a biological effect. Fontolizumab was well tolerated, and further studies to assess its efficacy are warranted. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21037">
<title>Efficacy of infliximab in refractory pouchitis and Crohn&#x27;s disease-related complications of the pouch: A Belgian case series</title>
<link>http://dx.doi.org/10.1002%2Fibd.21037</link>
<description><![CDATA[Up to 25% of inflammatory bowel disease (IBD) patients undergoing surgery with an ileal pouch-anal anastomosis (IPAA) will develop chronic pouchitis not responding to antibiotics. In case reports, thiopurine analogs and infliximab (IFX) have been proposed as effective therapy in this setting. We analyzed the long-term efficacy of IFX in Belgian patients with refractory pouch complications.We identified 28 IPAA patients who received IFX for refractory luminal inflammation (pouchitis and/or pre-pouch ileitis, n = 25) and/or pouch fistula (n = 7). Patients with elements of Crohn's disease after review of the colectomy specimen were excluded. Clinical response was defined as complete in case of cessation of diarrhea, blood loss, and abdominal pain, and as partial in case of marked clinical improvement. Fistula response was defined as complete in case of cessation and as partial in case of reduction of fistula drainage.Eighty-two percent of patients were concomitantly treated with immunomodulatory agents. At week 10 following start of IFX, 88% of patients with refractory luminal inflammation showed clinical response (14 partial, 8 complete), while 6 patients (86%) showed fistula response (3 partial, 3 complete). The mPDAI dropped significantly from 9.0 (interquartile range [IQR] 8.0-10.0) to 4.5 (3.0-7.0) points (P < 0.001). After a median follow-up of 20 (7-36) months, 56% showed sustained clinical response while 3 out of 7 fistula patients showed sustained fistula response. Five patients needed permanent ileostomy.In this series, IFX was effective long-term in IPAA patients with refractory luminal inflammation and pouch fistula. These results warrant a prospective multicenter randomized controlled trial. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21035">
<title>Increased serum levels of L-arginine in ulcerative colitis and correlation with disease severity</title>
<link>http://dx.doi.org/10.1002%2Fibd.21035</link>
<description><![CDATA[L-arginine (L-Arg) is a semi-essential amino acid that is the substrate for both nitric oxide and polyamine synthesis. Cellular uptake of L-Arg is an active transport process that is subject to competitive inhibition by L-ornithine (L-Orn) and L-lysine (L-Lys). We investigated L-Arg utilization in patients with ulcerative colitis (UC).Serum was collected from 14 normal controls and 22 UC patients with pancolitis of moderate or severe activity by histopathology score. The Mayo Disease Activity Index (DAI) and endoscopy subscore were assessed. Serum amino acid levels were measured by high-performance liquid chromatography. Arginine availability index (AAI) was defined as [L-Arg]/([L-Orn] + [L-Lys]).Serum L-Arg levels were significantly associated with histopathologic grade (P = 0.001). L-Arg levels were increased in subjects with severe colitis when compared to those with moderate colitis or normal mucosa. L-Orn + L-Lys levels were also increased in severe colitis, so that AAI was not significantly increased. L-Arg levels were also strongly associated with the endoscopy subscore (P < 0.001). There was a strong correlation between DAI and L-Arg levels (r = 0.656, P < 0.001).Serum L-Arg levels correlate with UC disease severity but availability is not increased due to competitive inhibition by L-Orn and L-Lys. Our findings suggest that L-Arg uptake by cells in the inflamed colon is defective, which may contribute to the pathogenesis of UC. Studies delineating the mechanism of uptake inhibition could enhance our understanding of UC or lead to novel treatment options. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21032">
<title>Need for standardization in population-based quality of life studies: A review of the current literature</title>
<link>http://dx.doi.org/10.1002%2Fibd.21032</link>
<description><![CDATA[In this systematic review we focus on the current use of and knowledge on health related quality of life in unselected, population-based IBD cohorts. We made a systematic literature search and included for comprehensive review papers that described a population-based cohort and that used validated HRQoL instruments. We show that even studies defined by the authors as population-based do not always meet the criteria set for being population-based. The heterogeneity of the study populations we have reviewed emphasizes that "population-based" must be defined very meticulously and that study populations need to be scrutinized with regard to all characteristics of the cohort before one can compare their results. Different definitions of study populations as population-based affect outcomes. We also show that use of the same HRQoL questionnaires does not guarantee comparable results as there are several different versions of the questionnaires, the different translations are not always comparable and at last there are several methods of computing and presenting the data. Detailed accumulation of knowledge and thorough meta analyses is therefore difficult hence we find it necessary to raise a discussion on the need of standardization in this field of research and we make some simple recommendations on factors we find important. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21027">
<title>Mitochondrial dysfunction, persistent oxidative damage, and catalase inhibition in immune cells of na&#xEF;ve and treated Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21027</link>
<description><![CDATA[Oxidative stress is considered a potential etiological factor for Crohn's disease (CD). We characterized the reactive oxygen species (ROS) generated in immune peripheral cells of CD patients, as well as their antioxidant enzyme status and the presence of oxidative damage. In addition, mitochondrial function ([Delta][Psi]m) was analyzed to detect the possible origin of ROS.Cells were obtained from patients at the onset of disease, prior to any treatment. Experiments were repeated when patients were in clinical remission. A set of experiments was carried out in a group of CD patients in persistent morphological remission. Controls were healthy volunteers who were not receiving any treatment at the time. The generation of superoxide, hydrogen peroxide (H2O2) and nitric oxide, [Delta][Psi]m, superoxide dismutase (SOD) and catalase (CAT) activities, and concentrations of malondyaldehyde (MDA) and 8-oxo-deoxyguanosine (8-oxo-dG) were measured.SOD activity and H2O2 production were significantly higher during active CD but returned to control levels in remission. [Delta][Psi]m was inhibited during active CD and, although it returned to control levels, its recovery took longer than clinical remission. CAT activity was permanently inhibited during CD, independent of the disease activity. MDA and 8-oxo-dG were permanently elevated.Oxidative stress during active CD depends on H2O2 production. The inhibition of [Delta][Psi]m suggests that this organelle is a source of ROS. CAT is permanently inhibited in CD, the biological significance of which is under study. The persistent oxidative damage detected may have implications for the evolution of the disease. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21025">
<title>Assessment of appropriateness of indications for CT enterography in younger patients</title>
<link>http://dx.doi.org/10.1002%2Fibd.21025</link>
<description><![CDATA[The small potential risk of radiation-induced cancer is increased in younger patients undergoing serial imaging with computed tomography enterography (CTE). We sought to determine the appropriateness of CTEs based on clinical indication in patients [le]35 years old, and the potential impact of evolution of practice to alternative magnetic resonance enterography (MRE).Over a 7-year period, the medical records of all patients [le]35 years old undergoing CTE were reviewed to determine the clinical indications for each CTE exam. An interdisciplinary consensus panel evaluated the appropriateness of all CTE exams based on American College of Radiology appropriateness criteria and peer-reviewed literature, classifying indications into "appropriate" or "inappropriate." For repeat CTEs, an "alternative MRE suggested" pathway was created. Criteria for evolution of practice to "alternative MRE" were suspicion of obstruction and evaluation of disease activity/therapeutic response in the absence of new symptoms.In all, 2022 patients [le]35 years old underwent 2295 CTEs. Ninety-nine percent (2008/2022) of first-time CTE exams were "appropriate" by the defined criteria. A total of 197 patients (9.7%) underwent multiple exams, with 73% of these patients having Crohn's disease. Repeat exams occurred in 9% (18/197) with obstructive symptoms and evaluation of disease activity/therapeutic response in the absence of new symptoms in 41% (80/197).A multidisciplinary expert panel concluded that the vast majority of young patients underwent clinically appropriate first-time CTE exams. However, a shift in clinical practice to MRE appears warranted for approximately half of young patients undergoing repeat CTE examinations. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20997">
<title>Importance of mucosal healing in ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.20997</link>
<description><![CDATA[Treatment of patients with ulcerative colitis (UC) has traditionally focused on improving symptoms, with the main objective of inducing and maintaining symptomatic remission. However, new evidence suggests that concentrating exclusively on clinical outcome measures may not be adequate to achieve long-term treatment success. Indeed, physicians should also be assessing the reduction of endoscopic activity, with the intention of achieving complete mucosal healing (defined as the absence of all mucosal ulceration, both microscopic and macroscopic, providing a sigmoidoscopy score of 0, as assessed on the Ulcerative Colitis Disease Activity Index). As a consequence of the customary reliance on symptomatic outcome measures, relatively few clinical trials have used mucosal healing or a composite including mucosal healing as a primary endpoint. This situation may soon change as new guidelines recommend the incorporation of mucosal healing into the primary endpoint of all new clinical trials in patients with UC. These recommendations are derived, in part, from data that have illustrated a correlation between mucosal healing and several important factors including long-term remission rates, disease-related complications (e.g., risk of colorectal cancer), healthcare utilization (e.g., need for colectomy), and patient quality of life. We already have drugs available to us that can effectively induce and maintain complete mucosal healing over long periods of time. This review evaluates the effect of medical therapy on mucosal healing in patients with UC and explores the importance of this outcome measure, both from the patient's perspective and clinical trial experience. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21060">
<title>Book Review - G.I. Joe: The Life and Career of Joseph B. Kirsner</title>
<link>http://dx.doi.org/10.1002%2Fibd.21060</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21049">
<title>Sulfasalazine-induced nephrotic syndrome in a patient with ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21049</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21047">
<title>TNF-[alpha] is an important pathogenic factor contributing to reactivation of cytomegalovirus in inflamed mucosa of colon in patients with ulcerative colitis: Lesson from clinical experience</title>
<link>http://dx.doi.org/10.1002%2Fibd.21047</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21044">
<title>Development of glomerulonephritis early in the course of Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21044</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21040">
<title>Gastrointestinal manifestations in primary immune disorders</title>
<link>http://dx.doi.org/10.1002%2Fibd.21040</link>
<description><![CDATA[The gastrointestinal tract is the largest lymphoid organ in the body containing T and B lymphocytes, macrophages, and dendritic cells. Despite the fact that these cells are constantly confronted with antigen primarily in the form of food and bacteria, immune responses in the gut are tightly regulated to maintain homeostasis. Without this balance of active immunity and tolerance, mucosal inflammation may ensue, and manifest as Crohn's disease, ulcerative colitis, pernicious anemia, or celiac sprue. Therefore, it is not unreasonable that inflammatory diseases of the gut are commonly encountered in patients with primary immune deficiencies. The exact pathogenesis of gastrointestinal diseases in the setting of primary immunodeficiency remains unknown, however, both humoral and cell-mediated immunity appear to play a role in preventing intestinal inflammation. Patients presenting with atypical gastrointestinal disease and/or failure to respond to conventional therapy should be evaluated for an underlying primary immune disorder in order to initiate appropriate treatment, such as immunoglobulin or in more severe cases bone marrow transplantation, to prevent long term complications. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21033">
<title>Salmonella septic arthritis in a patient with Crohn&#x27;s disease on infliximab</title>
<link>http://dx.doi.org/10.1002%2Fibd.21033</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21024">
<title>Improving quality of care in IBD: A STEEEP challenge</title>
<link>http://dx.doi.org/10.1002%2Fibd.21024</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21005">
<title>Acute lymphoid leukemia in a Crohn&#x27;s disease patient during treatment with adalimumab after a prolonged treatment with azathioprine and steroids</title>
<link>http://dx.doi.org/10.1002%2Fibd.21005</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21021">
<title>Reduced muscle mass and bone size in pediatric patients with inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21021</link>
<description><![CDATA[Decreased bone mineral density has been reported in children with inflammatory bowel disease (IBD). We used peripheral quantitative computed tomography (pQCT) to assess bone mineralization, geometry, and muscle cross-sectional area (CSA) in pediatric IBD.In a cross-sectional study, pQCT of the forearm was applied in 143 IBD patients (mean age 13.9 ± 3.5 years); 29% were newly diagnosed, 98 had Crohn's disease, and 45 had ulcerative colitis. Auxological data, cumulative glucocorticoid dose, disease activity indices, laboratory markers for inflammation, and bone metabolism were related to the results of pQCT.Patients were compromised in height (-0.82 ± 1.1 SD), weight (-0.77 ± 1.0 SD), muscle mass (-1.12 ± 1.0 SD), and total bone cross-sectional area (-0.79 ± 1.0 SD) compared to age- and sex-matched healthy controls (z-scores). In newly diagnosed patients, the ratio of bone mineral mass per muscle CSA was higher than in those with longer disease duration (1.00 versus 0.30, P = 0.007). Serum albumin level and disease activity correlated with muscle mass, accounting for 41.0% of variability in muscle mass (P < 0.01). The trabecular bone mineral density z-score was on average at the lower normal level (-0.40 ± 1.3 SD, P < 0.05).Reduced bone geometry was explained only in part by reduced height. Bone disease in children with IBD seems to be secondary to muscle wasting, which is already present at diagnosis. With longer disease duration, bone adapts to the lower muscle CSA. Serum albumin concentration is a good marker for muscle wasting and abnormal bone development. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21072">
<title>Granulocyte-macrophage colony-stimulating factor elicits bone marrow-derived cells that promote efficient colonic mucosal healing</title>
<link>http://dx.doi.org/10.1002%2Fibd.21072</link>
<description><![CDATA[Granulocyte-macrophage colony-stimulating factor (GM-CSF) therapy is effective in treating some Crohn's disease (CD) patients and protects mice from colitis induced by dextran sulfate sodium (DSS) administration. However, its mechanisms of action remain elusive. We hypothesized that GM-CSF affects intestinal mucosal repair.DSS colitic mice were treated with daily pegylated GM-CSF or saline and clinical, histological, and inflammatory parameters were kinetically evaluated. Further, the role of bone marrow-derived cells in the impact of GM-CSF therapy on DSS colitis was addressed using cell transfers.GM-CSF therapy reduced clinical signs of colitis and the release of inflammatory mediators. GM-CSF therapy improved mucosal repair, with faster ulcer reepithelialization, accelerated hyperproliferative response of epithelial cells in ulcer-adjacent crypts, and lower colonoscopic ulceration scores in GM-CSF-administered mice relative to untreated mice. We observed that GM-CSF-induced promotion of mucosal repair is timely associated with a reduction in neutrophil numbers and increased accumulation of CD11b+ monocytic cells in colon tissues. Importantly, transfer of splenic GM-CSF-induced CD11b+ myeloid cells into DSS-exposed mice improved colitis, and lethally irradiated GM-CSF receptor-deficient mice reconstituted with wildtype bone marrow cells were protected from DSS-induced colitis upon GM-CSF therapy. Lastly, GM-CSF-induced CD11b+ myeloid cells were shown to promote in vitro wound repair.Our study shows that GM-CSF-dependent stimulation of bone marrow-derived cells during DSS-induced colitis accelerates colonic tissue repair. These data provide a putative mechanism for the observed beneficial effects of GM-CSF therapy in Crohn's disease. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21009">
<title>Severe sporotrichoid fishtank granuloma following infliximab therapy for Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21009</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21010">
<title>Disability in inflammatory bowel diseases: Developing ICF core sets for patients with inflammatory bowel diseases based on the international classification of functioning, disability, and health</title>
<link>http://dx.doi.org/10.1002%2Fibd.21010</link>
<description><![CDATA[The inflammatory bowel diseases (IBDs) are associated with a reduced quality of life. The impact of IBD on disability remains largely unknown. With the International Classification of Functioning, Disability, and Health (ICF) of the World Health Organization (WHO), we can now rely on a globally agreed-upon framework and system for classifying the typical spectrum of problems in the functioning of persons with a specific disease given the environmental context in which they live. The aim of this article is to outline the methods to be utilized to develop ICF Core Sets for IBD. The project is a cooperation between the ICF Research Branch of the WHO, the IPNIC group, the International Society of Physical Rehabilitation Medicine (ISPRM), and the International Organization on Inflammatory Bowel Disease (IOIBD). Four worldwide studies will be conducted from 2009 to 2010. ICF categories relevant for IBD will be identified by systematic literature review of outcomes and measures used in IBD research, semistructured patient interviews, Internet-based expert survey, and cross-sectional study for clinical applicability. The final definition of ICF Core Sets for IBD will be determined at a Consensus Conference. Field testing will then be used to validate the ICF Core Sets. ICF Core Sets are being designed to provide useful standards for research and clinical practice. This tool will enable research that improves understanding of functioning, disability, and health in IBD, and may lead to interventions to improve and maintain functioning and minimize disability among IBD patients throughout the world. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21041">
<title>Osteoporosis in patients over 50 years of age following restorative proctocolectomy for ulcerative colitis: Is DXA screening warranted?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21041</link>
<description><![CDATA[Ulcerative colitis (UC) and increasing age are associated with an increased risk of osteoporosis. Screening of postmenopausal women and men older than 50 years with ulcerative colitis for osteoporosis is recommended. The prevalence of osteoporosis in restorative proctocolectomy (RPC) patients more than 50 years old is not known.Fifty-three consecutive patients older than age 50 who had undergone RPC for UC underwent a bone density scan (DXA). Sex, smoking status, age at diagnosis of UC, duration of UC, age at RPC, years since RPC, age at DXA, and pouch histological inflammatory score were recorded. The Kruskal-Wallis test and Spearman's correlation coefficient were used to analyze the data.Fifty-three patients were studied; their median age was 58 years, and the median age at RPC was 45. The prevalence of osteopenia and osteoporosis was 43.4% and 13.2%, respectively. Age at RPC was negatively correlated with bone density (P = 0.041, r = 0.281), and there was a negative correlation approaching significance with age at the time of DXA (P = 0.071, r = -0.250). No other factor studied correlated with bone density.The prevalence of osteoporosis and osteopenia found in this study is similar to that reported for UC patients who have not undergone RPC. Patients having RPC should be screened in line with current UC guidelines, targeting those older than 50 years. (Inflamm Bowel Dis 2009)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20998">
<title>Splenic tuberculosis in a patient with Crohn&#x27;s disease on infliximab: Case report</title>
<link>http://dx.doi.org/10.1002%2Fibd.20998</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21031">
<title>Epithelial vanin-1 controls inflammation-driven carcinogenesis in the colitis-associated colon cancer model</title>
<link>http://dx.doi.org/10.1002%2Fibd.21031</link>
<description><![CDATA[Vanin-1 is an epithelial pantetheinase that provides cysteamine to tissue and regulates response to stress. Vanin-1 is expressed by enterocytes, and its absence limits intestinal epithelial cell production of proinflammatory signals. A link between chronic active inflammation and cancer is illustrated in patients with ulcerative colitis, who have an augmented risk of developing colorectal cancer. Indeed, sustained inflammation provides advantageous growth conditions to tumors. We examined whether epithelial cells affect tumorigenesis through vanin-1-dependent modulation of colonic inflammation.To vanin-1-/- mice, we applied the colitis-associated cancer (CAC) protocol, which combines injection of azoxymethane (AOM) with repeated administrations of dextran sodium sulfate (DSS). We numbered tumors and quantified macrophage infiltration and molecular markers of cell death and proliferation. We also tested DSS-induced colitis. We scored survival, tissue damages, proinflammatory cytokine production, and tissue regeneration. Finally, we explored activation pathways by biochemical analysis on purified colonic epithelial cells (CECs) and in situ immunofluorescence.Vanin-1-/- mice displayed a drastically reduced incidence of colorectal cancer in the CAC protocol and manifested mild clinical signs of DSS-induced colitis. The early impact of vanin-1 deficiency on tumor induction was directly correlated to the amount of inflammation and subsequent epithelial proliferation rather than cell death rate; all this was linked to the modulation of NF-[kappa]B pathway activation in CECs.These results emphasize the importance of the intestinal epithelium in the control of mucosal inflammation acting as a cofactor in carcinogenesis. This might lead to novel anti-inflammatory strategies useful in cancer therapy. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21029">
<title>Resolvin E1, an endogenous lipid mediator derived from eicosapentaenoic acid, prevents dextran sulfate sodium-induced colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21029</link>
<description><![CDATA[Resolvin E1 (RvE1), an endogenous lipid mediator derived from eicosapentaenoic acid, has been identified in local inflammation during the healing stage. RvE1 reduces inflammation in several types of animal models including peritonitis and retinopathy and blocks human neutrophil transendothelial cell migration. The RvE1 receptor ChemR23 is expressed on myeloid cells such as macrophages and dendritic cells. The aim of this study was to determine whether RvE1 regulates colonic inflammation when the innate immune response of macrophages plays a key role in pathogenesis and tissue damage.The RvE1 receptor ChemR23 was expressed in mouse peritoneal macrophages as defined by flow cytometry. Peritoneal macrophages were pretreated with RvE1, followed by lipopolysaccharide stimulation, whereupon transcriptional levels of proinflammatory cytokines were analyzed.RvE1 treatment led to inhibition of proinflammatory cytokines including TNF-[alpha] and IL-12p40. In HEK293 cells, pretreatment with RvE1 inhibited TNF-[alpha]-induced nuclear translocation of NF-[kappa]B in a ChemR23-dependent manner. These results suggested that RvE1 could regulate proinflammatory responses of macrophages expressing ChemR23. Therefore, we investigated the beneficial effects of RvE1 in dextran sulfate sodium-induced colitis. RvE1 treatment led to amelioration of colonic inflammation.These results indicate that RvE1 suppresses proinflammatory responses of macrophages. RvE1 and its receptor may therefore be useful as therapeutic targets in the treatment of human inflammatory bowel disease and other inflammatory disorders. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21028">
<title>Quality of care in inflammatory bowel disease: A review and discussion</title>
<link>http://dx.doi.org/10.1002%2Fibd.21028</link>
<description><![CDATA[The Institute of Medicine's publications To Err Is Human and Crossing the Quality Chasm publicized the widespread deficits in U.S. health care quality. Emerging studies continue to reveal deficits in the quality of adult and pediatric care, including subspecialty care. The inflammatory bowel diseases (IBD) Crohn's disease and ulcerative colitis require diligent, long-term management and attention to their impact on intestinal and extraintestinal organ systems. Although the quality of IBD care has not been prospectively or comprehensively evaluated in the United States, several small studies have demonstrated significant variation in care. As variation may indicate underuse, overuse, or misuse of medical services, such variation suggests a clear need for translating evidence-based practices into the actual practice and follow-up provided for patients. This article reviews the history, rationale, and methods of quality measurement and improvement and identifies the unique challenges in adapting these general strategies to the care of the inflammatory bowel diseases. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21020">
<title>Sterile seroma after surgical drainage of purulent psoas abscess in Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.21020</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21017">
<title>Potential for amino acids supplementation during inflammatory bowel diseases</title>
<link>http://dx.doi.org/10.1002%2Fibd.21017</link>
<description><![CDATA[The pathophysiology of inflammatory bowel diseases (IBDs) is multifactorial and involves interactions of gut luminal content with mucosal barrier and especially immune cells. Malnutrition is a frequent issue during IBD flares, especially in Crohn's disease (CD) patients, and nutritional support is frequently used to treat malnutrition but also in an attempt to modulate intestinal inflammation. The use of oral or enteral nutrition intervention in IBDs may be effective, alone or in combination with drugs, to achieve and maintain remission. However, standard diets are less effective than new-generation biotherapies and could be improved by supplementation with specific immunomodulatory amino acids. Experimental studies evaluating glutamine, the preferential substrate for enterocytes, are promising. Some clinical studies with oral glutamine in CD are until now disappointing, but new formulations and targeting could enhance glutamine efficacy at the site of mucosal lesions. The role of arginine, involved in nitric oxide and polyamines synthesis, still remains debated. However, the effects of these amino acids in IBD have been poorly documented in humans. Other candidates like glycine, cysteine, histidine, or taurine should also be evaluated in the future. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21011">
<title>Circulating midkine in Crohn&#x27;s disease: Clinical implications</title>
<link>http://dx.doi.org/10.1002%2Fibd.21011</link>
<description><![CDATA[A noninvasive marker facilitating differential diagnosis in Crohn's disease (CD) is sought after. Midkine is a heparin-binding growth factor of angiogenic and chemotactic properties, positively evaluated as a tumor marker, and a possible association with CD has not yet been investigated.Circulating midkine was measured in 91 CD patients and 108 controls and related to disease clinical and biochemical activity, inflammation severity, and angiogenesis. Midkine diagnostic value in comparison with C-reactive protein (CRP) was evaluated by receiver operating characteristic (ROC) analysis.Circulating midkine was elevated both in quiescent and active disease compared to controls (147, 506, and 93 pg/mL, respectively), and corresponded well with disease activity (r = 0.49, P < 0.001). Midkine significantly correlated with inflammatory indices: CRP (r = 0.49), erythrocyte sedimentation rate (r = 0.31), leukocytes (r = 0.48), platelets (r = 0.52), albumin (r = -0.49), transferrin (r = -0.47), and IL-6 (r = 0.54); hematological variables: hemoglobin (r = -0.38), hematocrit (r = -0.43), and iron (r = -0.58); angiogenic factors: vascular endothelial growth factor-A (r = 0.42), fibroblast growth factor-2 (r = 0.54), and platelet-derived growth factor-BB (r = 0.57). Midkine elevation corresponded well (r = -0.41) with the drop in paraoxonase-1 activity - a quorum-quenching factor. Midkine as a marker of active CD had sensitivity and specificity of 86% and 97%, respectively, whereas CRP was 83% and 92%.CD is associated with an elevation of midkine, which corresponds well with disease activity and reflects the severity of inflammatory response and exacerbation of pathological angiogenesis. Midkine performance as a disease marker was slightly better than that of CRP. Its high specificity and likelihood ratios for positive test results might recommend midkine as a possible "ruling in" marker in CD. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21008">
<title>Hospitalizations are increasing among minority patients with Crohn&#x27;s disease and ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.21008</link>
<description><![CDATA[Rates of inflammatory bowel disease (IBD) appear to be increasing among nonwhite populations outside the United States, but national data describing the incidence and prevalence of IBD are not available for minority patients. The aim of this study was to examine time trends of hospital discharge among minority patients with IBD.Nationally representative data describing hospital discharges were obtained from the National Hospital Discharge Survey for the years 1994 to 2006. Race-specific annual proportions of hospitalizations including a discharge diagnosis of ulcerative colitis and Crohn's disease were calculated. Trends in proportions were assessed for statistical significance using the extended Mantel-Haenszel [chi]-square test for trend.The proportion of hospitalizations including a discharge diagnosis of IBD increased significantly from 1994 to 2006 among the total population and among Asian, black, and white patients separately. Increases were statistically significant when analysis was performed for Crohn's disease and ulcerative colitis combined and separately. Marked increases were seen among Asians.The proportion of hospitalizations including a discharge diagnosis of IBD increased significantly among minority and nonminority patients from 1994 through 2006. The causes underlying these changes are not certain and should be further investigated. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21007">
<title>Overall and cause-specific mortality in Crohn&#x27;s disease: A meta-analysis of population-based studies</title>
<link>http://dx.doi.org/10.1002%2Fibd.21007</link>
<description><![CDATA[An overview of mortality risk among unselected patients with Crohn's disease (CD) is lacking. We therefore performed a systematic review and meta-analysis of population-based studies on overall and cause-specific mortality in CD.MEDLINE (January 1965 to February 2008), abstracts from international conferences and reference lists of selected articles were searched systematically. All articles fulfilling the predefined inclusion criteria were scrutinized for data on population size, time of follow-up, gender, age, and observed to expected deaths. STATA meta-analysis software was used to calculate overall and cause-specific pooled standardized mortality ratios (SMR, observed/expected).Nine studies were included with overall SMRs ranging from 0.72-3.2, resulting in a significantly increased pooled SMR of 1.39 (95% confidence interval [CI]: 1.30-1.49). Regarding cause-specific mortality, a significantly increased risk of death from cancer (SMR 1.50, 95% CI: 1.18-1.92), in particular of pulmonary cancer (SMR 2.72, 95% CI: 1.35-5.45), as well as chronic obstructive pulmonary disease (SMR 2.55, 95% CI: 1.19-5.47), gastrointestinal diseases (SMR 6.76, 95% CI: 4.37-10.45), and genitourinary diseases (SMR 3.28, 95% CI: 1.69-6.35) was observed.Among unselected patients with CD, overall mortality was slightly but significantly higher than in the general population - primarily explained by deaths from gastrointestinal, respiratory, and genitourinary diseases. Notably, mortality from colorectal cancer was not increased. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20996">
<title>Cerebral venous thrombosis in inflammatory bowel diseases</title>
<link>http://dx.doi.org/10.1002%2Fibd.20996</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21015">
<title>Does methotrexate induce mucosal healing in Crohn&#x27;s disease?</title>
<link>http://dx.doi.org/10.1002%2Fibd.21015</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21006">
<title>Atrioventricular block associated with Crohn&#x27;s relapsing colitis in a 12-year-old child</title>
<link>http://dx.doi.org/10.1002%2Fibd.21006</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21002">
<title>Psychosocial symptoms and competence among adolescents with inflammatory bowel disease and their peers</title>
<link>http://dx.doi.org/10.1002%2Fibd.21002</link>
<description><![CDATA[The aim was to evaluate psychosocial symptoms and competence as reported by the parents and the adolescents themselves among patients with inflammatory bowel disease (IBD) in relation to population-based controls.Standardized Achenbach questionnaires - Child Behavior Checklist (CBCL) for the parents and Youth Self-Report (YSR) for the adolescents - were sent to Finnish families of adolescents with IBD (age 10-18 years), and their controls matched for age, gender, and place of residence. The final study group comprised 160 adolescents with IBD and 236 controls with their parents, respectively.According to parent reports, adolescents with IBD had more symptoms of anxious/depressed mood (P < 0.001), withdrawn/depressed mood (P < 0.05), social problems (P < 0.05), thought problems (P < 0.001), somatic complaints (P < 0.001), and lower competence (P < 0.05) than population-based controls. Unexpectedly, there was no group difference in the amount of self-reported psychosocial symptoms, somatic complaints, or competence between adolescents with IBD and their peers. However, adolescents with severe IBD reported significantly more emotional problems (P < 0.001) than those with mild symptoms or controls.According to parents, adolescents with IBD have more emotional problems, social problems, thought problems, and lower competence than their population-based peers. Self-perceived severity of the IBD symptoms is associated with a larger amount of parent and self-reported emotional symptoms. Complementary methods should be used while assessing the psychosocial well-being of adolescents with IBD as questionnaires alone may be insufficient. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21000">
<title>Comparison of several activity indices for the evaluation of endoscopic activity in UC: Inter- and intraobserver consistency</title>
<link>http://dx.doi.org/10.1002%2Fibd.21000</link>
<description><![CDATA[This study evaluated inter- and intraobserver agreement in the assessment of ulcerative colitis (UC) activity using 4 established indices and a newly designed Modified 6-point Activity Index.In all, 279 endoscopic pictures of inflammatory lesions from 93 UC patients were displayed twice to 4 expert and 4 trainee endoscopists, at an interval of 1 month. Each picture was assessed for inflammatory changes using established indices (Matts, Schroeder [a.k.a. Mayo Score], Baron, and Blackstone) and our new Modified 6-point Activity Index. Weighted kappa statistics were used to estimate intra- and interobserver variation.The Matts and Schroeder indices gave a "good" degree of concordance for expert endoscopists in terms of inter- and intraobserver agreements (0.74-0.78); this was not so evident with the Baron and Blackstone indices (0.61-0.73). For trainee endoscopists, all scores for inter- and intraobserver weighted kappa values using established indices (0.41-0.51) were lower than for the experts. The degree of concordance using the Modified 6-point Activity Index was rated as "good" for inter- and intraobserver agreements for expert endoscopists (0.65 and 0.79), and as "moderate" for trainee endoscopists (0.54 and 0.64).Accurate assessment of UC disease activity from endoscopic findings benefited from experience. For expert endoscopists, the Matts and Schroeder indices proved the most reliable of the 4 established indices. Current endoscopic technologies may be adequate for assessing UC activity, particularly if modified to permit a finer classification of disease severity based on 6 grades, as with our newly developed Modified 6-point Activity Index. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20994">
<title>Asymmetric dimethylarginine (ADMA), symmetric dimethylarginine (SDMA), arginine, and 8-iso-prostaglandin F2[alpha] (8-iso-PGF2[alpha]) level in patients with inflammatory bowel diseases</title>
<link>http://dx.doi.org/10.1002%2Fibd.20994</link>
<description><![CDATA[Intestinal microvessels of patients with inflammatory bowel disease (IBD) show microvascular endothelial dysfunction. It may contribute to reduced perfusion, poor ulcer healing, and sustained chronic inflammation. The aim of the study was to assess endothelial dysfunction and oxidative stress markers in patients with IBD.Serum levels of asymmetric dimethylarginine (ADMA), symmetric dimethylarginine (SDMA), arginine, and 8-iso-prostaglandin F2[alpha] (8-iso-PGF2[alpha]) were measured in 31 consecutive patients with ulcerative colitis (UC) and 32 with Crohn's disease (CD). Apparently healthy subjects served as age- and sex-matched controls. Associations between these markers and the disease activity and laboratory variables were evaluated.ADMA, SDMA, and 8-iso-PGF2[alpha] levels were increased in the IBD group as compared to the control group and higher in patients with CD than UC (P < 0.05 for all comparisons). Arginine levels were similar in all the groups. In the CD and UC groups ADMA and SDMA showed positive correlation with 8-iso-PGF2[alpha] (r from 0.47-0.67; P < 0.01 for all comparisons). ADMA and SDMA correlated positively with the CD activity (r = 0.4, P = 0.025; r = 0.4, P = 0.024, respectively) and the 8-iso-PGF2[alpha] level correlated positively with the UC activity (r = 0.4, P = 0.026).This is the first study to show that in patients with IBD there is enhanced ADMA generation that might be associated with oxidative stress, and these effects are more pronounced in the CD group. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20992">
<title>Crohn&#x27;s disease is associated with restless legs syndrome</title>
<link>http://dx.doi.org/10.1002%2Fibd.20992</link>
<description><![CDATA[Extraintestinal manifestations of Crohn's disease (CD) have not previously included the central nervous system (CNS). Restless legs syndrome (RLS) is a CNS disorder that is either idiopathic or secondary to a number of diseases. The aim of this study was to determine if RLS was associated with CD because both are associated with iron deficiency, inflammation, and bacterial overgrowth.Consecutive CD outpatients (N = 272) were prospectively surveyed at 4 centers for criteria for RLS. Incidence (having RLS at any point in time), prevalence (having RLS at time of survey), clinical characteristics, risk factors, and potential qualitative relationship between RLS and gastrointestinal symptoms were queried.The incidence of RLS in patients with CD was 42.7%. Prevalence was 30.2% compared with 9% of spouses. CD patients with and without RLS had a mean age of 46.8 versus 42.6 years, small intestine involvement in 77.9% versus 66.7%, colon involvement in 39.7% versus 63.2%, and prior iron deficiency anemia in 49.3% versus 33.1%. There was no difference between the CD groups with respect to current iron deficiency, RLS family history, or rare prevalence of concomitant RLS disorders. In 91.8% of patients with RLS and CD, RLS started during or after the onset of CD diagnosis. Among 73 patients with RLS, 67 (44.5%) stated there was a relationship between qualitative RLS symptom improvement with overall CD symptom improvement.These results demonstrate that RLS occurs frequently in CD and appears to be a possible extraintestinal manifestation. The potential relationship of RLS with CD activity warrants further investigation. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20991">
<title>Autophagy at the gut interface: Mucosal responses to stress and the consequences for inflammatory bowel diseases</title>
<link>http://dx.doi.org/10.1002%2Fibd.20991</link>
<description><![CDATA[Autophagy is a conserved homeostatic process by which cells degrade and recycle cytoplasmic contents and organelles. Recently, autophagy has come to prominence as a factor in many disease states, including inflammatory bowel diseases. In this review we explore the recent discoveries in autophagy and how these relate to the special conditions experienced by the gut mucosa. We will pay particular attention to autophagy as an innate immune process and its role in the development and education of the adaptive immune system. (Inflamm Bowel Dis 2009;)]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20982">
<title>Elevated serum chromogranin A in irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD): A shared model for pathogenesis?</title>
<link>http://dx.doi.org/10.1002%2Fibd.20982</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21014">
<title>Disability in IBD: The devil is in the details</title>
<link>http://dx.doi.org/10.1002%2Fibd.21014</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.21003">
<title>Endoscopy and MR enteroclysis: Equivalent tools in predicting clinical recurrence in patients with Crohn&#x27;s disease after ileocolic resection</title>
<link>http://dx.doi.org/10.1002%2Fibd.21003</link>
<description><![CDATA[Ileocolonoscopy poses the gold standard in the evaluation of postoperative recurrence of Crohn's disease (CD) at the site of ileocolonic anastomosis. Magnetic resonance enteroclysis (MRE) on the other hand is a promising technique for small bowel imaging. The aim was to compare MRE and ileocolonoscopy for predicting clinical recurrence in CD patients who have undergone ileocolonic resection.We included 29 patients in the study. The median time since index operation was 35 months and between ileocolonoscopy and MRE was 3 days. Patients were followed up for a maximum of 2 years unless clinical recurrence occurred earlier. Endoscopic findings were evaluated on a 5-grade scale (i0-i4), whereas MRE findings on the neoterminal ileum and anastomosis were assessed according to a previously validated 4-grade scale MR score (MR0-MR3).By classifying patients into subgroups of endoscopic severity of postoperative recurrence using as a threshold an endoscopic score of i3, we found that 10% of patients in the i0 to i2 group had a clinical recurrence during the 2-year follow-up period as compared to 52.6% of subjects with i3 to i4 (P = 0.043). The corresponding clinical exacerbation rates in the subgroups based on MRE severity assessment were 12.5% for MR0 to MR1 and 50% for MR2 to MR3 (P = 0.09).Our data suggest that colonoscopy and MR enteroclysis are of similar value to predict the risk of clinical recurrence in postoperative patients with Crohn's disease. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20985">
<title>Familial aggregation and antimicrobial response dose-dependently affect the risk for Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20985</link>
<description><![CDATA[An increased risk of Crohn's disease (CD) has been reported consistently in first-degree relatives of patients. Our aim was to test whether a combination of CD-associated genes involved in innate immunity and/or antibody responses to microbial antigens may be valuable in identifying healthy relatives at risk.We investigated 86 families from Belgium and northern France, 45 with at least 3 first-degree relatives with CD, 24 with a single case, and 17 control families without inflammatory bowel disease (IBD). The cohort consisted of 186 CD patients, 290 healthy relatives, and 142 controls (total 618). Genetic (NOD2, NOD1, TLR4, CARD8) and serologic markers (ASCA, ACMA, ALCA, ACCA, A[Sigma]MA, OmpC, CBir1, I2) were determined in all subjects. All Belgian families were prospectively followed up for 54 months.In multiple-affected families, an increment of affected first-degree relatives and of positive antibodies were additive risks factors for CD (P < 0.0001), independent of NOD2 mutations. When comparing subjects from multiple-affected families, having 3 additional first-degree relatives with CD and 1 additional positive antibody increased the odds for CD to 9.19 (95% confidence interval [CI]: 4.07-20.80). After a follow-up of 54 months among all Belgian families, a total of 4 new diagnoses of IBD were confirmed in the multiple-affected families only, resulting in a 57-fold increase in incidence within multiple-affected families compared to the known incidence of IBD in our region.We found an additive risk increment for CD in subjects from multicase families per additional affected relative and per additional positive antibody, independent of NOD2. Furthermore, a very high disease incidence was observed in these multiple-affected families. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20970">
<title>Efficacy of oral tacrolimus on intestinal Behcet&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20970</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20928">
<title>Pityrosporum folliculitis in a Crohn&#x27;s disease patient receiving infliximab</title>
<link>http://dx.doi.org/10.1002%2Fibd.20928</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20989">
<title>Validity, reliability, and responsiveness of the EQ-5D in inflammatory bowel disease in Germany</title>
<link>http://dx.doi.org/10.1002%2Fibd.20989</link>
<description><![CDATA[The EuroQol (EQ)-5D questionnaire is a generic instrument measuring health-related quality of life. Its validity, reliability, and responsiveness were assessed in a large sample of Crohn's disease (CD) and ulcerative colitis (UC) patients.The EQ-5D was completed initially (270 CD and 232 UC subjects) and after 4 weeks (447 subjects) with a transition question rating health change. Responsiveness of EQ visual analog scale (EQ-VAS) and the United Kingdom (UK-index) and German EQ-5D index (EQ-index) scores to reported changes in health was evaluated by standardized response means (SRM) and meaningful differences (MDs).EQ-VAS and EQ-index scores correlated well with disease activity indices and differed significantly between active disease and remission groups. All scores were reliable in test-retest (ICC: EQ-VAS: 0.89; UK-index: 0.76; German EQ-index: 0.72). According to SRM, EQ-VAS was more responsive for deterioration in health than for improvement in health and was more responsive than index scores. Index scores were most responsive for deterioration in health in subjects in remission and for improved health in subjects with active disease. MDs for improved health (EQ-VAS: 10.9; UK EQ-index: 0.076; German EQ-index: 0.050) and deteriorated health (EQ-VAS: -14.4; UK EQ-index: -0.109; German EQ-index: -0.067) were significant, but MD of EQ-VAS also differed significantly according to disease activity.The EQ-5D generates valid, reliable, and responsive preference-based valuations of health in CD and UC. EQ-VAS scores were more responsive than EQ-5D index scores. Thus, small health differences that are important from the patient's perspective may not be reflected in the EQ-index. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20981">
<title>Current smoking, not duration of remission, delays Crohn&#x27;s disease relapse following azathioprine withdrawal</title>
<link>http://dx.doi.org/10.1002%2Fibd.20981</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20968">
<title>Role of diet in the development of inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20968</link>
<description><![CDATA[The inflammatory bowel diseases (IBDs) are a group of heterogeneous disorders characterized by acute and chronic inflammatory changes in the small or large bowel, or in both. Increasing incidence and prevalence figures for IBD both in the developed and developing world indicate that environmental factors are at least as significant in IBD as genetic susceptibility. Of these, diet and the host microbiota are likely to play important but as yet poorly defined roles. The major constituents of a standard "Western" diet may contribute to, or protect against, intestinal inflammation via several mechanisms. These include the effects of insulin resistance and short-chain fatty acids such as butyrate, modification of intestinal permeability, the antiinflammatory role of polyunsaturated fatty acids, and the effect of sulfur compounds from protein on host microbiota. This detailed review critically assesses the evidence for the role of diet in the development of IBD and examines the evidence for obesity as a contributing factor to IBD pathogenesis. Particular attention is focused on methodological issues including suitability of cases and controls, confounders such as smoking, and total energy expenditure. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20964">
<title>Thyroid disorders and inflammatory bowel diseases: Retrospective evaluation of 909 patients from an Italian Referral Center</title>
<link>http://dx.doi.org/10.1002%2Fibd.20964</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20954">
<title>Adalimumab-induced psoriasis of the scalp with diffuse alopecia: A severe potentially irreversible cutaneous side effect of TNF-alpha blockers</title>
<link>http://dx.doi.org/10.1002%2Fibd.20954</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20987">
<title>Is it time for increased pap performance? Cervical cancer and pap testing in women with inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20987</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20988">
<title>Barriers to adherence among adolescents with inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20988</link>
<description><![CDATA[The purpose of this study was to describe barriers to adherence among adolescents with inflammatory bowel disease (IBD) and to examine demographic, disease-related, and treatment regimen-related correlates of adherence barriers using a multimethod reporting strategy. A final goal was to examine relationships between the frequencies of barriers and levels of nonadherence.In all, 64 adolescents (ages 11-18) participated, along with 61 mothers and 25 fathers. Barriers to adherence and ratings of medication adherence were assessed via patient and parent reports. Disease activity ratings were provided by pediatric gastroenterologists.Lack of time and medication side effects were commonly reported barriers across adolescent, mother, and father reports. Other adolescent-reported barriers included missing medication due to feeling well or discontinuing medication based on the belief that the medication was not working. The prevalence of adherence barriers was not consistently associated with adolescent age, sex, time since diagnosis, or disease activity. Adolescents whose regimen involved more than 1 daily medication administration had more adherence barriers based on adolescent and maternal report than did those whose regimen involved 1 or less than 1 daily medication administration. Finally, adherence barriers were significantly higher among families reporting imperfect adherence as compared to those reporting perfect adherence.Barriers to medication adherence do exist among adolescents with IBD and may have negative implications for medication adherence. Systematic assessment of barriers during routine medical appointments may help to identify and modify these barriers and ultimately improve adherence. Inflamm Bowel Dis 2009]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20971">
<title>Solitary rectal ulcer syndrome in association with ulcerative colitis: A case report</title>
<link>http://dx.doi.org/10.1002%2Fibd.20971</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20958">
<title>Adalimumab as therapy for fistulizing orofacial Crohn&#x27;s disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20958</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20955">
<title>Physicians may inadequately address Sexuality in women with inflammatory bowel disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20955</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20953">
<title>Clostridium difficile-associated diarrhea in Crohn&#x27;s disease patients with Ostomy</title>
<link>http://dx.doi.org/10.1002%2Fibd.20953</link>
<description><![CDATA[No Abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20980">
<title>Varicella pneumonia in an immunocompromised inflammatory bowel disease patient</title>
<link>http://dx.doi.org/10.1002%2Fibd.20980</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20929">
<title>Prepouch ileitis, myth or reality? The first case with acute abdomen</title>
<link>http://dx.doi.org/10.1002%2Fibd.20929</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20911">
<title>Volvulus of an ileal J-pouch</title>
<link>http://dx.doi.org/10.1002%2Fibd.20911</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20913">
<title>Ulcerative colitis and primary sclerosing cholangitis as part of autoimmune polyglandular syndrome type III</title>
<link>http://dx.doi.org/10.1002%2Fibd.20913</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20912">
<title>Chronic granulomatous disease</title>
<link>http://dx.doi.org/10.1002%2Fibd.20912</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20905">
<title>Likelihood ratio for Crohn&#x27;s disease as a function of Anti-Saccharomyces cerevisiae antibody concentration</title>
<link>http://dx.doi.org/10.1002%2Fibd.20905</link>
<description><![CDATA[No abstract.]]></description>
</item>

<item rdf:about="http://dx.doi.org/10.1002%2Fibd.20779">
<title>Endoscopic healing should be a goal for everyone with ulcerative colitis</title>
<link>http://dx.doi.org/10.1002%2Fibd.20779</link>
<description><![CDATA[No abstract.]]></description>
</item>

</rdf:RDF>