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        <title>Gut via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Gut' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Gut&t=Gut&s=Search&f=source]]></link>
        <lastBuildDate>Wed, 08 Feb 2012 16:28:18 +0100</lastBuildDate>
        <item>
            <title>Correction</title>
            <link>http://www.medworm.com/index.php?rid=5660506&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F472-b%3Frss%3D1</link>
            <description>Benamouzig R, Uzzan B, Deyra J, et al. Prevention by daily soluble aspirin of colorectal adenoma recurrence: 4-year results of the APACC randomised trial. Gut 2012;61:255&amp;ndash;61.
There are two numerical errors in the last sentence of the &quot;Results&quot; paragraph of the Abstract of this paper. This sentence should be read as follows: &quot;Also, the proportion of patients with at least one advanced adenoma did not differ (10/102 (10 %) in the aspirin group vs 7/83 (8.4 %) in the placebo group; NS).&quot; (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660506</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>The need for standardised outcome reporting in colorectal surgery</title>
            <link>http://www.medworm.com/index.php?rid=5660505&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F472-a%3Frss%3D1</link>
            <description>We were interested to read the paper by Morris et al demonstrating significant variation in 30-day postoperative mortality following major colorectal cancer surgery in National Health Service hospitals in England.1 While we agree that understanding the underlying causes of this variation will be invaluable to inform best practice, we think that it is necessary to choose a definition of postoperative mortality that provides information relevant to patients as well as clinicians. In cardiothoracic surgery, this issue has been debated for some years, resulting in a measure of &amp;lsquo;operative mortality&amp;rsquo; which encompasses any death occurring (a) within 30&amp;nbsp;days after surgery, in or out of hospital, and (b) any death occurring after 30&amp;nbsp;days during the same hospitalisation subsequ...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660505</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Authors' response</title>
            <link>http://www.medworm.com/index.php?rid=5660504&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F471%3Frss%3D1</link>
            <description>Patients with hyperplastic polyposis syndrome (HPS) harbour multiple colorectal hyperplastic polyps and are at risk of developing colorectal cancer (CRC).1 2 In two recent studies from our study group, we described the risk of CRC in patients with HPS during follow-up and the RR of CRC/polyps in first-degree relatives (FDRs) of patients with HPS compared to the general population.1 2 In reaction to our manuscripts, Orlowska3 recommends that a distinction be made between sessile serrated adenomas and traditional serrated adenomas. We agree with this remark, considering that these serrated polyp subtypes differ in histological and geographical characteristics and in molecular profiles.4 Considering that both studies from our group involved retrospective data of which a large part was derived...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660504</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5660504</guid>        </item>
        <item>
            <title>Hyperplastic polyposis syndrome and the risk of colorectal cancer</title>
            <link>http://www.medworm.com/index.php?rid=5660503&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F470-b%3Frss%3D1</link>
            <description>I read with great interest the two reports by Boparai and coworkers in Gut on the increased risk of colorectal carcinoma (CRC) in 77 hyperplastic/serrated polyposis syndrome (HPS) patients during follow-up1 and in 347 HPS first-degree relatives (FDRs).2 To date, follow-ups have been performed in only 43/308 (14.0%) HPS patients and HPS coexistence with CRC in FDRs has been analysed in only 29/308 (9.4%) HPS patients described up to the end of 2009 (table 1). Nevertheless, there are some points to be explained:The term &amp;lsquo;(sessile) serrated adenoma&amp;rsquo; should be abbreviated as SSA, instead of SA (serrated adenoma). SSA, characterised by abnormal proliferation, is included in the non-dysplastic group contrary to SA, which belongs to the dysplastic serrated polyp category because of th...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660503</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5660503</guid>        </item>
        <item>
            <title>Authors' response</title>
            <link>http://www.medworm.com/index.php?rid=5660502&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F470-a%3Frss%3D1</link>
            <description>We thank Dr Ben-Horin for his comments published in the February 2012 issue of Gut1 in respect of our small, first in man, trial of rituximab for ulcerative colitis.2 We sympathise with his concern that potentially useful treatments should not be ignored on the basis of underpowered trials, however the p value of 1.0 for the primary endpoint comparison between rituximab and placebo seems adequate justification for our negative conclusion regarding efficacy and is quite different from the p=0.22 that Ben-Horin cites for his hypothetical discussion of ACT1. The use of remission rather than response for the primary endpoint is now widely encouraged for trials in UC where a partial response, particularly in the patient groups included in this trial with resistant disease, is of limited benefit...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660502</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5660502</guid>        </item>
        <item>
            <title>Virulence factors or ancestral origin of Helicobacter pylori: which is a better predictor of gastric cancer risk?</title>
            <link>http://www.medworm.com/index.php?rid=5660501&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F469%3Frss%3D1</link>
            <description>We examined the association between virulence factors, including cag pathogenicity island, vacA, babA, iceA and OipA, of H pylori strains isolated from Columbian subjects and clinical outcomes.2 We found that although OipA and cag pathogenicity island are linked with each other, only... (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660501</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5660501</guid>        </item>
        <item>
            <title>Allogeneic mesenchymal stem cell transplantation in seven patients with refractory inflammatory bowel disease</title>
            <link>http://www.medworm.com/index.php?rid=5660500&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F468%3Frss%3D1</link>
            <description>We refer to two articles by Duijvestein et al and Ciccocioppo et al1 2 in which the authors suggest that administration of autologous bone marrow-derived mesenchymal stem cells (MSCs) is safe and feasible in the treatment of refractory Crohn's disease (CD). However, to date there are few data about allogeneic MSC transplantation (MSCT) for patients with inflammatory bowel disease (IBD). We wish to report our experience of allogeneic MSCT in seven patients with IBD. Infused allogeneic MSCs were obtained from the bone marrow or umbilical cord. Bone marrow was aspirated from healthy relatives of three patients. Umbilical cords were obtained from local maternity hospitals after normal deliveries. The isolated MSCs were given by intravenous infusions as 1x106 cells per kilogram of body weight. ...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660500</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5660500</guid>        </item>
        <item>
            <title>GI highlights from the literature</title>
            <link>http://www.medworm.com/index.php?rid=5660499&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F466%3Frss%3D1</link>
            <description>Basic sciencePreservation of immune quiescence in inflammatory bowel disease: the role of dendritic cell A20 expression &amp;nbsp;Hammer GE, Turer EE, Taylor KE, et al. Expression of A20 by dendritic cells preserves immune homeostasis and prevents colitis and spondyloarthritis. Nat Immunol 2011;12:1184&amp;ndash;93. doi:10.1038/ni.2135 Dendritic cells (DCs) are known to play a key role in innate immune activation, but may also regulate immune homeostasis. This recent paper from Averil Ma and colleagues at the University of California, San Francisco, examined the role of the ubiquitin-editing protein A20 within DCs to identify how A20-dependent DC functions are implicated in intestinal homeostasis. A20 is a potent anti-inflammatory protein that negatively regulates the transcription factor nuclear ...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660499</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5660499</guid>        </item>
        <item>
            <title>Shared decision making in inflammatory bowel disease: helping patients understand the tradeoffs between treatment options</title>
            <link>http://www.medworm.com/index.php?rid=5660498&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F459%3Frss%3D1</link>
            <description>The treatment of inflammatory bowel disease is becoming more complicated with new medications and new treatment paradigms. Although data are accumulating that the earlier use of immunomodulators and anti-tumor necrosis factor agents are more effective than the standard &quot;step-up&quot; pyramidal treatment algorithm, patients may not be comfortable with this more intensive therapeutic approach. The process of shared decision making engages patients in treatment decisions to optimize the chance that a chosen therapy matches their personal preferences for care. Decision aids are standard shared decision making tools, which are used to present evidence-based data in a patient-friendly manner to help patients with preference- sensitive decisions. Not all care decisions are preference-sensitive, and no...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660498</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5660498</guid>        </item>
        <item>
            <title>Pancreatic ductal adenocarcinoma and acinar cells: a matter of differentiation and development?</title>
            <link>http://www.medworm.com/index.php?rid=5660497&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F449%3Frss%3D1</link>
            <description>Pancreatic ductal adenocarcinoma (PDAC) has long been considered to arise from pancreatic ducts on the basis of its morphology, the occurrence of dysplasia in putative preneoplastic ductal lesions, and the absence of acinar dysplasia in the pancreas of patients with PDAC. However, evidence gathered through both in vitro studies and&amp;mdash;more importantly&amp;mdash;genetic mouse models of PDAC shows that ductal-type tumours can arise from acinar cells. These findings raise new important questions related to PDAC pathophysiology and call for in-depth studies of acinar cell differentiation in order to better understand PDAC biology. The authors review these issues and discuss how the novel findings should impact on future work aiming at early diagnosis and improved outcome of patients with PDAC. ...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660497</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5660497</guid>        </item>
        <item>
            <title>Recruitment of histone deacetylases HDAC1 and HDAC2 by the transcriptional repressor ZEB1 downregulates E-cadherin expression in pancreatic cancer</title>
            <link>http://www.medworm.com/index.php?rid=5660496&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F439%3Frss%3D1</link>
            <description>Conclusions
These findings imply an important role for histone deacetylation in the downregulation of E-cadherin in human pancreatic cancer. Recruitment of HDACs to the CDH1 promoter is regulated by the transcription factor ZEB1, and inhibition of HDACs may be a promising antitumour therapy for pancreatic cancer. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660496</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5660496</guid>        </item>
        <item>
            <title>Chemokine-driven lymphocyte infiltration: an early intratumoural event determining long-term survival in resectable hepatocellular carcinoma</title>
            <link>http://www.medworm.com/index.php?rid=5660495&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F427%3Frss%3D1</link>
            <description>Conclusion
A 14 immune-gene signature, which identifies molecular cues driving tumour infiltration by lymphocytes, accurately predicts survival of patients with HCC especially in early disease. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660495</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5660495</guid>        </item>
        <item>
            <title>Pharmacological inhibition of the chemokine CCL2 (MCP-1) diminishes liver macrophage infiltration and steatohepatitis in chronic hepatic injury</title>
            <link>http://www.medworm.com/index.php?rid=5660494&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F416%3Frss%3D1</link>
            <description>Conclusions
These results demonstrate the successful pharmacological inhibition of hepatic monocyte/macrophage infiltration by blocking MCP-1 during chronic liver damage in two in vivo models. The associated ameliorated steatosis development suggests that inhibition of MCP-1 is an interesting novel approach for pharmacological treatment in liver inflammation and steatohepatitis. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660494</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5660494</guid>        </item>
        <item>
            <title>Prevalence of non-alcoholic fatty liver disease and advanced fibrosis in Hong Kong Chinese: a population study using proton-magnetic resonance spectroscopy and transient elastography</title>
            <link>http://www.medworm.com/index.php?rid=5660493&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F409%3Frss%3D1</link>
            <description>Conclusion
NAFLD is found in over a quarter of the general adult Chinese population, but the proportion of patients with advanced fibrosis is low. Modest alcohol consumption does not increase the risk of fatty liver or liver fibrosis. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660493</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5660493</guid>        </item>
        <item>
            <title>Higher adenoma detection rates with cap-assisted colonoscopy: a randomised controlled trial</title>
            <link>http://www.medworm.com/index.php?rid=5660492&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F402%3Frss%3D1</link>
            <description>Conclusions
CAC detected a 13% higher number of subjects with at least one adenoma and 59% higher adenomas per subject. CAC is a safe, effective and practical means to improve adenoma detection rates.

Clinical Trial Registration
NCT 01211132. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660492</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5660492</guid>        </item>
        <item>
            <title>A rare gastrointestinal presentation of a common malignancy</title>
            <link>http://www.medworm.com/index.php?rid=5660491&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F401%3Frss%3D1</link>
            <description>Clinical presentation A 61-year-old man presented with a 4-week history of rectal bleeding, constipation, bloating, abdominal distension and low back pain. His bowels had not opened for 4&amp;nbsp;days prior to admission. Physical examination revealed a distended, tympanic abdomen. Routine laboratory tests confirmed renal failure (urea 13&amp;nbsp;mmol/l, creatinine 200&amp;nbsp;&amp;mu;mol/l), hypercalcaemia (3.7&amp;nbsp;mmol/l), albumin 32&amp;nbsp;g/l and C-reactive protein (CRP) 25&amp;nbsp;mg/l. Parathormone was suppressed (7&amp;nbsp;pg/l (15&amp;ndash;65)). Abdominal x-ray suggested an ileus. CT abdomen revealed mural thickening of the left hemi-colon along with collapse of the third lumbar vertebra. An isotope bone scan was unremarkable, while MRI of the spine confirmed the presence of multiple lytic lesions. Immuno...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660491</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5660491</guid>        </item>
        <item>
            <title>Aberrant DNA methylation associated with aggressiveness of gastrointestinal stromal tumour</title>
            <link>http://www.medworm.com/index.php?rid=5660490&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F392%3Frss%3D1</link>
            <description>Conclusion
Our results suggest that GIST is not, in epigenetic terms, a uniform disease and that DNA methylation in a set of genes is associated with aggressive clinical behavior and unfavorable prognosis. The genes identified may potentially serve as biomarkers for predicting aggressive GISTs with poor survivability. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660490</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5660490</guid>        </item>
        <item>
            <title>Serological response to the 2009 H1N1 influenza vaccination in patients with inflammatory bowel disease</title>
            <link>http://www.medworm.com/index.php?rid=5660489&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F385%3Frss%3D1</link>
            <description>Conclusions
Patients with IBD vaccinated with the 2009 H1N1 influenza vaccine had a low rate of seroprotection, particularly among those who were immunosuppressed. Although there is a need for studies of the clinical benefit of vaccines in this population, patients with IBD need to be aware of this reduced immunogenicity. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660489</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5660489</guid>        </item>
        <item>
            <title>Interleukin-1{beta} (IL-1{beta}) promotes susceptibility of Toll-like receptor 5 (TLR5) deficient mice to colitis</title>
            <link>http://www.medworm.com/index.php?rid=5660488&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F373%3Frss%3D1</link>
            <description>Conclusion
Regardless of whether they harbour a colitogenic microbiota, loss of TLR5 predisposes mice to colitis triggered by immune dysregulation via an IL-1&amp;beta;-dependent pathway. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660488</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5660488</guid>        </item>
        <item>
            <title>Visceral hypersensitivity in endometriosis: a new target for treatment?</title>
            <link>http://www.medworm.com/index.php?rid=5660487&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F367%3Frss%3D1</link>
            <description>Conclusion
Visceral hypersensitivity is extremely common in endometriosis and could be intensifying the pain. This finding might explain why mildly affected individuals often complain of severe symptoms out of proportion to the extent of their disease. This study has introduced a completely new concept into the understanding of pain in endometriosis and could open up new opportunities for treatment. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660487</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5660487</guid>        </item>
        <item>
            <title>Bifidobacterium infantis 35624 administration induces Foxp3 T regulatory cells in human peripheral blood: potential role for myeloid and plasmacytoid dendritic cells</title>
            <link>http://www.medworm.com/index.php?rid=5660486&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F354%3Frss%3D1</link>
            <description>Conclusions
B infantis administration to humans selectively promotes immunoregulatory responses, suggesting that this microbe may have therapeutic utility in patients with inflammatory disease. Cross-talk between multiple pattern-recognition receptors and metabolic pathways determines the innate and subsequent T regulatory cell response to B infantis. These findings link nutrition, microbiota and the induction of tolerance within the gastrointestinal mucosa. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660486</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5660486</guid>        </item>
        <item>
            <title>Synergistic tumour suppressor activity of E-cadherin and p53 in a conditional mouse model for metastatic diffuse-type gastric cancer</title>
            <link>http://www.medworm.com/index.php?rid=5660485&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F344%3Frss%3D1</link>
            <description>Conclusion
This mouse line is the first genetically engineered mouse model of DGC and is very useful for clarifying the mechanism underlying gastric carcinogenesis, and provides a new approach to the treatment and prevention of DGC. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660485</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5660485</guid>        </item>
        <item>
            <title>Mechanism of association between BMI and dysfunction of the gastro-oesophageal barrier in patients with normal endoscopy</title>
            <link>http://www.medworm.com/index.php?rid=5660484&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F337%3Frss%3D1</link>
            <description>Conclusion
The association between reflux and BMI may be largely explained by effects of increased intra-abdominal pressure. However, the reduced LOS pressure associated with BMI may be mediated by another mechanism or effects of chronic rather than acute elevation of intra-abdominal pressure. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660484</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Reasons to consider earlier treatment of chronic HBV infections</title>
            <link>http://www.medworm.com/index.php?rid=5660483&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F333%3Frss%3D1</link>
            <description>Introduction Chronic hepatitis B virus (HBV) infection is a serious public health problem, leading to cirrhosis, hepatocellular carcinoma (HCC) and liver failure. In highly endemic areas and among immigrants from these areas, most cases of chronic hepatitis B are due to HBV infection at birth or during the first year of life. Cirrhosis and HCC may occur at any age, but infections early in life are typically asymptomatic for the first few decades. Sharp rises in the incidence of fibrosis, cirrhosis and HCC generally do not appear until after the age of 30, the incidence of HCC showing a sharp rise after the age of 40. Approximately 50% of deaths in HBV carriers may be due to either chronic liver disease or HCC. Cirrhosis is a consequence of hepatocyte death and chronic inflammation in the l...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660483</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5660483</guid>        </item>
        <item>
            <title>Bifidobacteria and subsets of dendritic cells: friendly players in immune regulation!</title>
            <link>http://www.medworm.com/index.php?rid=5660482&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F331%3Frss%3D1</link>
            <description>The mammalian gastrointestinal tract harbours a vast number of bacterial residents, recently referred to as the microbiota, which are instrumental in supporting energy metabolism and immune function of the host. A large number of studies have highlighted the fact that certain (pathogenic) micro-organisms can be harmful to the health of their host, while more recently an increasing number of papers have attributed direct beneficial health effects to the gut microbial community. As these bacteria encode 100 times more genes than present in the human genome, the partnership of the host with its microbiota constitute a &amp;lsquo;superorganism&amp;rsquo;.1 Homoeostasis in this superorganism is sustained through an optimal cohabitation of the host with this microbiota, keeping the balance between comme...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660482</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5660482</guid>        </item>
        <item>
            <title>A ZEB1-HDAC pathway enters the epithelial to mesenchymal transition world in pancreatic cancer</title>
            <link>http://www.medworm.com/index.php?rid=5660481&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2F329%3Frss%3D1</link>
            <description>Epithelial to mesenchymal transition (EMT) correlates with high-grade malignancy including the competence to form metastases. In addition, EMT has recently been linked to cellular self-renewal programmes of cancer stem cells and apoptosis/anoikis resistance, which are all features of therapeutic resistance. The EMT programme is driven by several transcription factors (TFs), such as the transcriptional regulators SNAIL, SLUG, ZEB1 and ZEB2 and the basic helix&amp;ndash;loop&amp;ndash;helix factors E47 and TWIST. These proteins target and repress the CDH1 gene, which encodes for E-cadherin, an important caretaker of the epithelial state. Expression studies in human pancreatic cancer showed expression of SNAIL in 78% and of SLUG in 50% of cases.1 Although no or low levels of TWIST are expressed in pa...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660481</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5660481</guid>        </item>
        <item>
            <title>Highlights from this issue</title>
            <link>http://www.medworm.com/index.php?rid=5660480&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F3%2Fi%3Frss%3D1</link>
            <description>Luminal GIH1N1 influenza vaccination and IBD The global pandemic of novel influenza A (H1N1) affected 70 countries in 2009. There was particular concern for infection in immunocompromised patients, including those with IBD. The 2009 H1N1 influenza vaccine produced seroprotection rates of &amp;gt;85% in the general population but there are no data on the immunogenicity of the vaccine in patients with IBD. In this issue of Gut, Cullen et al report their observational prospective open-label study which examined the immunogenicity of the 2009 H1N1 influenza vaccine in IBD patients. Patients with IBD vaccinated with the 2009 H1N1 influenza vaccine had a low rate of seroprotection, particularly those who were immunosuppressed or received combination immunosuppression (see table 1). An assay of T lym...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5660480</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5660480</guid>        </item>
        <item>
            <title>Correction</title>
            <link>http://www.medworm.com/index.php?rid=5538529&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F327-b%3Frss%3D1</link>
            <description>After the publication of their letter in 2006 (Dom&amp;iacute;nguez-Mu&amp;ntilde;oz JE, Iglesias-Garc&amp;iacute;a J, Iglesias-Rey M, et al. Optimising the therapy of exocrine pancreatic insufficiency by the association of a proton pump inhibitor to enteric coated pancreatic extracts. Gut 2006;55:1056&amp;ndash;7; doi: 10.1136/gut.2006.094912), the authors discovered that the software used to calculate the 13CO2-cumulative recovery rate erroneously multiplied the results by two. Since all groups were affected equally, the interpretation of data and the conclusion remain the same. For further reference, all 13CO2-cumulative recovery rate values need to be divided by two. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538529</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538529</guid>        </item>
        <item>
            <title>Randomised placebo-controlled trial of rituximab (anti-CD20) in active ulcerative colitis</title>
            <link>http://www.medworm.com/index.php?rid=5538528&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F327-a%3Frss%3D1</link>
            <description>I read with interest the study by Leiper and colleagues,1 and the authors should be commended for initiating this investigator-driven study. However, I beg to differ with the conclusion that reads &amp;lsquo;Rituximab has no significant effect on inducing remission in moderately active UC [ulcerative colitis] not responding to oral steroids.&amp;rsquo; The authors state that the sample-size calculations were based on 80% power for excluding, at p&amp;lt;0.05, an 80% remission rate with active treatment compared with a predicted 25% placebo remission rate with 2:1 randomisation of rituximab compared with placebo. It is unclear why remission rather than response, as in most studies, was chosen to be the primary outcome, especially given that postfactum response rate was better in the active drug arm com...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538528</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538528</guid>        </item>
        <item>
            <title>Transjugular intrahepatic portosystemic shunt for portal vein thrombosis in cirrhosis</title>
            <link>http://www.medworm.com/index.php?rid=5538527&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F326-b%3Frss%3D1</link>
            <description>We read with interest the recent study by Luca et al demonstrating excellent short- and long-term outcomes of transjugular intrahepatic portosystemic shunt (TIPS) for the management of portal vein thrombosis (PVT) in patients with liver cirrhosis.1 More notably, the TIPS success rate can reach 100%. Additionally, the independent predictors for complete portal vein recanalisation have been proposed, including thrombosis of a single vein at inclusion, PVT severity of grade I (&amp;lt;25% of lumen occupancy), de novo diagnosis of PVT and absence of gastro-oesophageal varices. In spite of these important findings, several points of this study are worthy of further discussion. First, even though this study was the largest case series consisting of 70 PVT-TIPS patients, only two presented with caver...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538527</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538527</guid>        </item>
        <item>
            <title>The relevance of symptom association analysis in GORD patients undergoing anti-reflux surgery</title>
            <link>http://www.medworm.com/index.php?rid=5538526&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F326-a%3Frss%3D1</link>
            <description>We read with great interest the article by Broeders et al1 on the effects of anti-reflux surgery on weakly acidic reflux and belching. The authors evaluated 31 gastro-oesophageal reflux disease (GORD) patients, refractory to proton pump inhibitors, by means of upper gastrointestinal endoscopy, validated symptoms questionnaires, stationary oesophageal manometry and 24-hour impedance&amp;ndash;pH monitoring off antisecretory therapy before and 6&amp;nbsp;months after laparoscopic Nissen fundoplication (LNF). They observed that LNF reduced oesophageal acid exposure time (AET) and proximal migration of reflux events and similarly controlled both acidic and weakly acidic reflux, while gas reflux was diminished to a lesser extent. Moreover, they found that out of 15 patients with persisting symptoms aft...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538526</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538526</guid>        </item>
        <item>
            <title>NK receptors: it's all in the name</title>
            <link>http://www.medworm.com/index.php?rid=5538525&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F325%3Frss%3D1</link>
            <description>We read with interest the paper by Muhanna et al on natural killer cells, their role in ameliorating liver fibrosis and in particular the role of inhibitory receptors for major histocompatibility complex (MHC) class I.1 We would like to clarify the often confusing terminology of inhibitory receptors for natural killer cells. In the article by Muhanna et al, they refer to KIR as &amp;lsquo;killer immunoglobulin-related receptors&amp;rsquo;. This is not correct. The terminology &amp;lsquo;KIR&amp;rsquo; correctly applies to the &amp;lsquo;killer cell immunoglobulin-like receptors&amp;rsquo; as defined by an international panel of natural killer cell experts2 and subsequently adopted by the nomenclature committee of the Human Genome Organisation (http://www.genenames.org/). For clarification purposes, the human KIR ...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538525</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538525</guid>        </item>
        <item>
            <title>Crohn's disease patients treated with adalimumab benefit from co-treatment with immunomodulators</title>
            <link>http://www.medworm.com/index.php?rid=5538524&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F324-b%3Frss%3D1</link>
            <description>We read with interest the study by Sokol et al in Gut, emphasising the need for co-treatment with immunomodulators in patients receiving infliximab maintenance therapy. Concomitant use of immunosuppressives was associated with reduced disease activity and infliximab dose escalation, presumably through a lowered frequency of antibody formation.1 Although adalimumab is a 100% human anti-tumour necrosis factor monoclonal antibody, it is not devoid of immunogenicity. Antibodies against adalimumab have been reported in 2.6&amp;ndash;38% of patients treated for Crohn's disease or rheumatoid arthritis.2 However, the long-term efficacy of the combination of adalimumab plus immunosuppressives in this setting is not known. One observational study from Karmiris et al performed at a single tertiary care c...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538524</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538524</guid>        </item>
        <item>
            <title>Author's response</title>
            <link>http://www.medworm.com/index.php?rid=5538523&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F324-a%3Frss%3D1</link>
            <description>We have shown that a diet that is deprived of iron prevents ileitis in a mouse model of Crohn's disease (TNFdeltaARE mice).1 In his comment, Buchman2 was concerned that we misinterpreted our findings, as he supposed that sulphate may be more important than iron in the development of colitis in our rodent experiments. Most importantly, according to the composition of the experimental diets used in our studies (diet C1000 and C1038, Altromin GmbH, Lage, Germany), the total amount of sulphate salts (magnesium sulphate, iron sulphate, manganese sulphate and copper sulphate) in the control diet is comparable with the amount added to the low iron-sulphate diet (6586 vs 6520&amp;nbsp;mg/kg). The total sulphur content is 2792 and 2696&amp;nbsp;mg/kg, respectively. Thus, we can exclude that the observation...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538523</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538523</guid>        </item>
        <item>
            <title>Is iron over-rated? Sulphates may be the more important compound in development of colitis in rodent models, and perhaps humans</title>
            <link>http://www.medworm.com/index.php?rid=5538522&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F323%3Frss%3D1</link>
            <description>Werner et al showed that oral iron sulphate supplementation resulted in the development of ileitis in a rodent model, while parenteral administration of the same compound did not.1 I submit that these observations, although valid, may be true and unrelated. The colono-toxic effects of the sulphur component of iron sulphate were first observed following the development of acute colitis in rodents treated with dextran sodium sulphate.2 3 Sulphide compounds appear to be the most toxic to isolated colonocytes.4 Sulphate-reducing bacteria found in the colon and terminal ileum produce hydrogen sulphide,5 which in turn is converted to anionic sulphide by colonic bicarbonate.6 Hydrogen sulphide itself impairs colonocyte butyrate utilisation,4 and in vitro studies of rat and human colonic tissue ha...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538522</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538522</guid>        </item>
        <item>
            <title>Authors' response</title>
            <link>http://www.medworm.com/index.php?rid=5538521&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F322-c%3Frss%3D1</link>
            <description>We appreciate the comments by Riegert-Johnson et al1 on our manuscript concerning cancer risk and mortality in patients with Peutz&amp;ndash;Jeghers syndrome (PJS).2 We fully agree that it is of major importance for the clinical management and surveillance of PJS patients to establish whether their gastrointestinal malignancies are from hamartomas, coexisting adenomas or otherwise normal-appearing mucosa. This is indeed, as Dr Riegert-Johnson and colleagues mention, an issue of debate. Although several studies have reported a hamartoma&amp;ndash;adenoma&amp;ndash;carcinoma sequence,3&amp;ndash;5 other data contradict this hypothesis. This includes the fact that the location of gastrointestinal cancers does not always correlate with the location of the hamartomas2 6 and the predominant persistent non-invas...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538521</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538521</guid>        </item>
        <item>
            <title>High cancer risk and increased mortality in patients with Peutz-Jeghers syndrome</title>
            <link>http://www.medworm.com/index.php?rid=5538520&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F322-b%3Frss%3D1</link>
            <description>We read with interest the informative, and needed, update on the Dutch Peutz&amp;ndash;Jeghers syndrome (PJS) cohort by van Lier et al.1 Our group has translated Peutz's original paper from Dutch,2 and the findings are germane to the report of van Lier et al (translation archived on the National Institutes of Health PubMed website http://www.ncbi.nlm.nih.gov/books/NBK7027/). A critical and controversial topic in the care of PJS patients is the pathogenesis of PJS-associated gastrointestinal carcinomas. One paradigm holds that the carcinomas develop in sequence from PJS hamartomatous polyps and the other paradigm is that they develop independently of polyps. The question is not trivial; if the carcinomas do develop from polyps, then endoscopic polypectomy will decrease cancer risk. One of the P...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538520</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538520</guid>        </item>
        <item>
            <title>Authors' response</title>
            <link>http://www.medworm.com/index.php?rid=5538519&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F322-a%3Frss%3D1</link>
            <description>We thank Dr Vande Casteele and colleagues for their interest in our work and commend them for their interesting case.1 2 As written in our manuscript, we have had several, and in some cases serial, measurements of infliximab and antidrug antibody (ADA) levels in the patients reported. However, we limited the results to the last sample available before loss of response occurred to better meet the aim of the study, which was to investigate the immunogenic fragment of infliximab and its possible diagnostic role in patients having inflammatory bowel disease with loss of response. We absolutely agree that serial measurements may allow early detection of pharmacodynamic changes which possibly herald the later onset of clinical events such as loss of response or infusion reactions. The case repor...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538519</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538519</guid>        </item>
        <item>
            <title>Early serial trough and antidrug antibody level measurements predict clinical outcome of infliximab and adalimumab treatment</title>
            <link>http://www.medworm.com/index.php?rid=5538518&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F321%3Frss%3D1</link>
            <description>We read with great interest the recent article by Ben-Horin et al which concludes that the measurement of trough levels of infliximab (TLI) combined with the measurement of antibodies to infliximab (ATI) is highly correlated with the clinical response to the therapeutic.1 Infliximab (Remicade) and adalimumab (Humira), both monoclonal antibodies towards TNF-&amp;alpha;, are widely used in the treatment of Crohn's disease and ulcerative colitis. Loss of efficacy, infusion and injection-site reactions and hypersensitivity reactions have been described due to the development of antibodies towards these agents.2 We agree with Ben-Horin et al that the interpretation of ATI with TLI is important to document the clinical response of a patient to infliximab. However, we urge that these measurements are...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538518</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538518</guid>        </item>
        <item>
            <title>GI highlights from the literature</title>
            <link>http://www.medworm.com/index.php?rid=5538517&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F319%3Frss%3D1</link>
            <description>Basic science&amp;beta;-catenin and hepatocyte regeneration&amp;mdash;a role in hepatocellular carcinoma? &amp;nbsp;Wang EY, Yeh SH, Tsai TF, et al. Depletion of &amp;beta;-catenin from mature hepatocytes of mice promotes expansion of hepatic progenitor cells and tumor development. Proc Natl Acad Sci U S A 2011;108:18384&amp;ndash;9. Mature hepatocytes turn over relatively slowly. The long-term effects of hepatocyte &amp;beta;-catenin deficiency have not been fully addressed. Previous conditional &amp;beta;-catenin knockout (KO) mice studies demonstrated only modest reduction in liver mass. Wang and colleagues followed conditional KO mice (Alb-Cre;Ctnnb1flx/flx) until 20&amp;nbsp;months of age. Selective depletion of &amp;beta;-catenin in hepatocytes was confirmed in mice at 2&amp;nbsp;months of age. Surprisingly, after 7&amp;nbsp;m...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538517</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538517</guid>        </item>
        <item>
            <title>Family studies in Crohn's disease: new horizons in understanding disease pathogenesis, risk and prevention</title>
            <link>http://www.medworm.com/index.php?rid=5538516&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F311%3Frss%3D1</link>
            <description>This article reviews current knowledge of the at-risk phenotype in relatives of patients with CD and focuses on the implications for the design of future studies. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538516</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538516</guid>        </item>
        <item>
            <title>Spontaneous bacterial peritonitis: recent guidelines and beyond</title>
            <link>http://www.medworm.com/index.php?rid=5538515&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F297%3Frss%3D1</link>
            <description>Introduction Spontaneous bacterial peritonitis (SBP) is the most frequent and life-threatening infection in patients with liver cirrhosis requiring prompt recognition and treatment. It is defined by the presence of &amp;gt;250 polymorphonuclear cells (PMN)/mm3 in ascites in the absence of an intra-abdominal source of infection or malignancy. In this review we discuss the current opinions reflected by recent guidelines (American Association for the Study of Liver Diseases, European Association for the Study of the Liver, Deutsche Gesellschaft f&amp;uuml;r Verdauungs- und Stoffwechselkrankheiten),1&amp;ndash;4 with particular focus on controversial issues as well as open questions that need to be addressed in the future. First, diagnostic criteria and tools available for rapid and accurate diagnosis are...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538515</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538515</guid>        </item>
        <item>
            <title>Impact of hepatitis C triple therapy availability upon the number of patients to be treated and associated costs in France: a model-based analysis</title>
            <link>http://www.medworm.com/index.php?rid=5538514&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F290%3Frss%3D1</link>
            <description>Conclusion
These model-based estimates indicate that new anti-HCV treatments may result in a three- to fourfold increase in the number of G1 patients to be treated in France in 2012. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538514</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538514</guid>        </item>
        <item>
            <title>The putative tumour suppressor microRNA-124 modulates hepatocellular carcinoma cell aggressiveness by repressing ROCK2 and EZH2</title>
            <link>http://www.medworm.com/index.php?rid=5538513&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F278%3Frss%3D1</link>
            <description>Conclusion
These data highlight an important role for miR-124 in the regulation of invasion and metastasis in the molecular aetiology of HCC, and suggest a potential application of miR-124 in prognosis prediction and cancer treatment. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538513</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538513</guid>        </item>
        <item>
            <title>Persistent severe gastrointestinal bleeding in a man with metastatic somatostatinoma</title>
            <link>http://www.medworm.com/index.php?rid=5538512&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F277%3Frss%3D1</link>
            <description>Clinical presentation A 50-year-old man with known metastatic pancreatic somatostatinoma was admitted with a 1-day history of haematemesis, melaena and haematochezia. Following an initial diagnosis 14&amp;nbsp;years earlier, he underwent distal pancreatectomy and splenectomy, followed by lateral hepatectomy a year later for residual hepatic disease, as well as biliary stenting for malignant obstructive jaundice. He was subsequently started on sunitinib, and his disease had remained stable before this presentation. At admission, he was haemodynamically stable, with haemoglobin concentration of 6.2&amp;nbsp;g/dl and platelet count of 126x109/l. Other blood tests were unremarkable. Oesophagogastroduodenoscopy revealed a large amount of blood in the stomach, portal hypertensive gastropathy and multipl...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538512</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538512</guid>        </item>
        <item>
            <title>Interleukin-6-driven progranulin expression increases cholangiocarcinoma growth by an Akt-dependent mechanism</title>
            <link>http://www.medworm.com/index.php?rid=5538511&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F268%3Frss%3D1</link>
            <description>Conclusions
Evidence is presented for a role for progranulin as a novel growth factor regulating cholangiocarcinoma growth. Specific targeting of progranulin may represent an alternative for the development of therapeutic strategies. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538511</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538511</guid>        </item>
        <item>
            <title>Cigarette smoking, smoking cessation and acute pancreatitis: a prospective population-based study</title>
            <link>http://www.medworm.com/index.php?rid=5538510&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F262%3Frss%3D1</link>
            <description>Conclusion
Smoking is an important risk factor for non-gallstone-related acute pancreatitis. Early smoking cessation should be recommended as a part of the clinical management of patients with acute pancreatitis. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538510</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538510</guid>        </item>
        <item>
            <title>Prevention by daily soluble aspirin of colorectal adenoma recurrence: 4-year results of the APACC randomised trial</title>
            <link>http://www.medworm.com/index.php?rid=5538509&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F255%3Frss%3D1</link>
            <description>Conclusion
Daily low-dose aspirin decreased adenoma recurrence significantly at 1&amp;nbsp;year but not at year 4. This discrepancy might be explained by a differential effect of aspirin according to the natural history of the polyp.

Trial Registration Number
NCT 00224679. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538509</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538509</guid>        </item>
        <item>
            <title>TERC polymorphisms are associated both with susceptibility to colorectal cancer and with longer telomeres</title>
            <link>http://www.medworm.com/index.php?rid=5538508&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F248%3Frss%3D1</link>
            <description>Conclusions
Common genetic variation at TERC is associated with both longer telomeres and an increased risk of CRC, a potential mechanism being reduced levels of cell senescence or death. This finding is somewhat paradoxical, given retrospective studies reporting that CRC cases have shorter telomeres than controls. One possibility is that that association actually results from poorer survival in patients with longer telomeres. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538508</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538508</guid>        </item>
        <item>
            <title>Development of the first disability index for inflammatory bowel disease based on the international classification of functioning, disability and health</title>
            <link>http://www.medworm.com/index.php?rid=5538507&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F241%3Frss%3D1</link>
            <description>Conclusions
The IBD disability index is now available. It will be used in studies to evaluate the long-term effect of IBD on patient functional status and will serve as a new endpoint in disease-modification trials. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538507</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538507</guid>        </item>
        <item>
            <title>Thiopurines prevent advanced colorectal neoplasia in patients with inflammatory bowel disease</title>
            <link>http://www.medworm.com/index.php?rid=5538506&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F235%3Frss%3D1</link>
            <description>Conclusion
Thiopurine use protects IBD patients against the development of AN. The effect of 5-ASA appeared to be less pronounced. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538506</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538506</guid>        </item>
        <item>
            <title>Switch to adalimumab in patients with Crohn's disease controlled by maintenance infliximab: prospective randomised SWITCH trial</title>
            <link>http://www.medworm.com/index.php?rid=5538505&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F229%3Frss%3D1</link>
            <description>Conclusion
Elective switching from infliximab to adalimumab is associated with loss of tolerance and loss of efficacy within 1&amp;nbsp;year. Adherence to the first anti-TNF agent is recommended. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538505</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538505</guid>        </item>
        <item>
            <title>Cell polarity-determining proteins Par-3 and PP-1 are involved in epithelial tight junction defects in coeliac disease</title>
            <link>http://www.medworm.com/index.php?rid=5538504&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F220%3Frss%3D1</link>
            <description>Conclusions
Changes in cell polarity proteins Par-3 and PP-1 are associated with altered expression and assembly of TJ proteins claudin-2, -3, -5 and -7 and ZO-1, causing paracellular leakage in active coeliac disease. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538504</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538504</guid>        </item>
        <item>
            <title>Irritable bowel syndrome and chronic fatigue 3 years after acute giardiasis: historic cohort study</title>
            <link>http://www.medworm.com/index.php?rid=5538503&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F214%3Frss%3D1</link>
            <description>Conclusions
Infection with Giardia lamblia in a non-endemic area was associated with a high prevalence of IBS and chronic fatigue 3&amp;nbsp;years after acute illness, and the risk was significantly higher than in the control group. This shows that the potential consequences of giardiasis are more serious than previously known. Further studies are needed, especially in areas where giardiasis is endemic. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538503</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538503</guid>        </item>
        <item>
            <title>Intestinal renin-angiotensin system is stimulated after deletion of Lkb1</title>
            <link>http://www.medworm.com/index.php?rid=5538502&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F202%3Frss%3D1</link>
            <description>Conclusions
Taken together, these data reveal a novel role for Lkb1 in regulation of the gastrointestinal renin&amp;ndash;angiotensin system. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538502</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538502</guid>        </item>
        <item>
            <title>Hepcidin is localised in gastric parietal cells, regulates acid secretion and is induced by Helicobacter pylori infection</title>
            <link>http://www.medworm.com/index.php?rid=5538501&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F193%3Frss%3D1</link>
            <description>Conclusions
Hepcidin is a product of parietal cells regulating gastric acid production and may contribute to development of gastric ulcers under stress conditions. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538501</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538501</guid>        </item>
        <item>
            <title>Practice guidance on the management of acute and chronic gastrointestinal problems arising as a result of treatment for cancer</title>
            <link>http://www.medworm.com/index.php?rid=5538500&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F179%3Frss%3D1</link>
            <description>Conclusions
All cancer units must develop simple methods to identify the many patients who need help and establish routine referral pathways to specialist gastroenterologists where patients can receive safe and effective treatment. Early contact with oncologists and/or specialist surgeons with input from the patient's family and friends often helps the gastroenterologist to refine management strategies. Increased training in the late effects of cancer treatment is required. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538500</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538500</guid>        </item>
        <item>
            <title>StellaTUM: current consensus and discussion on pancreatic stellate cell research</title>
            <link>http://www.medworm.com/index.php?rid=5538499&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F172%3Frss%3D1</link>
            <description>This article is not a review article on the functions of PSC. Instead, members of the Pancreatic Star Alliance... (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538499</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538499</guid>        </item>
        <item>
            <title>Progranulin and cholangiocarcinoma: another bad boy on the block!</title>
            <link>http://www.medworm.com/index.php?rid=5538498&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F170%3Frss%3D1</link>
            <description>Cholangiocarcinoma (CCA) is a cancer that may develop in any portion of the biliary tree and is characterised by a bad prognosis and virtually no response to chemotherapy.1 2 In Western countries the incidence of intrahepatic CCA is progressively growing while that of extrahepatic CCA is stable or slightly decreasing.3 A number of recent studies have investigated the agents and mechanisms modulating the proliferation of CCA cells including growth factors, cytokines, neuropeptides and hormones.4 In their paper published in this issue of Gut, Frampton et al5 provide compelling evidence that progranulin (PGRN) represents a new growth factor for CCA. The expression and secretion of PGRN is upregulated in CCA cell lines and human CCA biopsies, and this is in part occurs via interleukin 6 (IL-6)...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538498</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538498</guid>        </item>
        <item>
            <title>Anti-TNF antibody therapy in Crohn's disease: the risk of a switch</title>
            <link>http://www.medworm.com/index.php?rid=5538497&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2F169%3Frss%3D1</link>
            <description>The efficacy of infliximab and adalimumab for the treatment of Crohn's disease has been shown in randomised controlled trials and corroborated in observational studies. However, one of the most worrying aspects of biological therapies for patients and clinicians is the variable but relevant proportion of patients on long-term treatment in whom there is a loss of response. From studies evaluating the incidence of loss of response to infliximab in patients with Crohn's disease (including more than 2000 patients and more than 6000 patient-years of follow-up), it is estimated that approximately 40% will lose response to infliximab, and the annual risk for loss of response to infliximab is calculated to be about 13% per patient-year of treatment.1 Similarly, data from a systematic review on the...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538497</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538497</guid>        </item>
        <item>
            <title>Highlights from this issue</title>
            <link>http://www.medworm.com/index.php?rid=5538496&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F2%2Fi%3Frss%3D1</link>
            <description>Practice guidance on managing GI problems resulting from cancer treatment The last 3&amp;nbsp;decades have seen a threefold increase in the numbers of survivors of cancer. Chronic gastrointestinal side effects are a common cause of morbidity and reduced quality of life. Side effects of treatment are frequently missed or overlooked because the current priority of cancer follow-up is to perform surveillance for recurrent cancer. Individual GPs are unlikely to have many patients with complex problems after cancer therapy and so will require guidance if these patients are to be optimally managed. Symptoms can often be alleviated or cured. In view of the urgent need for guidance on how to manage such patients, the President of the British Society of Gastroenterology commissioned this landmark docum...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5538496</comments>
            <pubDate>Sat, 24 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5538496</guid>        </item>
        <item>
            <title>The Authors' reply</title>
            <link>http://www.medworm.com/index.php?rid=5469571&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F167%3Frss%3D1</link>
            <description>We thank Abu-Elmagd and Mazariegos1 for their comments and are pleased to have the opportunity to explain our work further. Our study2 aimed to determine which indications for intestinal transplantation (ITx) were most closely associated with an increased risk of death on home parenteral nutrition (HPN), and whether deaths were due to causes that could be avoided by ITx. The indications for ITx we considered were those described by Medicare, USA, and the American Society of Transplantation; they include objective parameters which allow clear patient identification. Our results confirm that our baseline patient categorisation was appropriate. Ninety-five per cent of patients who were weaned off HPN belonged to the non-candidate group, and 95% of patients who underwent ITx belonged to the c...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469571</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469571</guid>        </item>
        <item>
            <title>Intestinal transplantation and the European implication: impact of experience and study design</title>
            <link>http://www.medworm.com/index.php?rid=5469570&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F166%3Frss%3D1</link>
            <description>Pironi et al recently published an article challenging current indications for intestinal transplantation (IT).1 The European home parenteral nutrition (HPN) database of 41 centres in nine countries was utilised and a 5-year prospective cross-sectional survey was conducted focusing on transplant candidacy with survival and causes of death as end points. With appreciation of the authors' scientific contribution, we felt obligated to highlight major flaws in the study design. Identification of HPN patients who are candidates for transplant was the Achilles' heel of the study. Unfortunately, such determination, without formal listing, was based upon broad definitions and questionnaire data short of documented objective testing that is crucial to transplant candidacy.2 Another major concern is...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469570</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469570</guid>        </item>
        <item>
            <title>The Author's reply</title>
            <link>http://www.medworm.com/index.php?rid=5469569&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F165-b%3Frss%3D1</link>
            <description>I appreciate the comments by Drs Johnson and Fitzsimmons.1 In my opinion, three separate issues need to be emphasised when trying to understand the long-term time trends of gastric cancer, gastric ulcer and duodenal ulcer as evidenced by their mortality data in my recent article in Gut.2 First, the time trends depicted in the article are not a fluke of the birth-cohort analysis or solely related to the use of mortality data, but truly reflective of changes in the underlying epidemiology of these three diseases. The vital statistics serve as a means to accumulate large populations with gastric cancer or peptic ulcer from different countries and group such patients by their age or time of birth. The fact that the patients died from these diagnoses is only of marginal relevance to the outcom...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469569</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469569</guid>        </item>
        <item>
            <title>Comment on 'differences in the birth-cohort patterns of gastric cancer and peptic ulcer'</title>
            <link>http://www.medworm.com/index.php?rid=5469568&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F165-a%3Frss%3D1</link>
            <description>We examined mortality data for England from 1950, and reported the downward slope of cohort incidence of gastric cancer from 1870. The international comparisons made by Sonnenberg are fascinating, and suggest a possible link with industrialisation. We are not social historians, but we read in Wikipedia3 that in Britain, the first Industrial Revolution, which began in the 18th century, merged into the Second Industrial Revolution around 1850, when technological and economic progress gained momentum with the development of steam-powered ships and railways. Similar changes occurred in other European nations at this time. In Japan, industrialisation began in the late 19th century. In the 1870s, the Meiji... (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469568</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469568</guid>        </item>
        <item>
            <title>The Authors' reply</title>
            <link>http://www.medworm.com/index.php?rid=5469567&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F164%3Frss%3D1</link>
            <description>We would like to thank Op De Be&amp;eacute;ck et al1 for their interest in the evaluation of antibodies to the zymogen granule membrane glycoprotein 2 (GP2) in patients with inflammatory bowel disease (IBD). Their meticulous investigation of a large, well-characterised cohort of patients and controls revealed good reproducibility, linearity and robustness of the anti-GP2 assays, confirming the assay performance reported in a recent study by our group.2 Both studies found a comparable, high specificity of anti-GP2 for Crohn's disease (CD). On testing 100 patients with ulcerative colitis (UC) and 162 blood donors (BDs) as controls in our study, the specificity reached a value of 94.3% (95% CI 90.7% to 96.8%). This value is similar to the specificity of 93.9% reported by Op De Be&amp;eacute;ck et al...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469567</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469567</guid>        </item>
        <item>
            <title>Antibodies to GP2, the major zymogen granule membrane glycoprotein, in inflammatory bowel diseases</title>
            <link>http://www.medworm.com/index.php?rid=5469566&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F162-c%3Frss%3D1</link>
            <description>It was with interest that we read the paper by Roggenbuck et al1 in a recent issue of Gut, where GP2, the major zymogen granule membrane glycoprotein, is demonstrated to be the autoantigen of pancreatic antibodies in Crohn's disease. The authors concluded that quantification of this novel Crohn's disease-specific marker could significantly improve the serological diagnosis of inflammatory bowel disease. A commercial assay for the detection of anti-GP2 antibodies has recently become available (Generic Assays, Dahlewitz/Berlin). In the present paper, we evaluated this assay on a large well-characterised study population. The patient cohort has been previously described2 and consisted of 164 patients with Crohn's disease, 118 patients with ulcerative colitis, and 75 control patients with othe...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469566</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469566</guid>        </item>
        <item>
            <title>The Authors' reply</title>
            <link>http://www.medworm.com/index.php?rid=5469565&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F162-b%3Frss%3D1</link>
            <description>The new data presented in Dr Zorzi's letter1 2 are a valuable contribution to the evolving evidence that colorectal cancer screening programmes that use an immunochemical faecal occult blood test (iFOBT) should expect a difference in clinical effectiveness between periods of hot and cold weather. The stark winter&amp;ndash;summer difference in the year-1 proportional incidence is larger than might have been expected, but both year-1 and year-2 data illustrate how effective iFOBT is during the winter. Dr Zorzi's data not only provide a further incentive to adopt iFOBT for screening but also demonstrate to kit manufacturers how much more effective their products could be if more potent inhibitors of haemoglobin denaturation were adopted for use in iFOBT kits. The relative merits of iFOBT recogn...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469565</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469565</guid>        </item>
        <item>
            <title>Limited effect of summer warming on the sensitivity of colorectal cancer screening</title>
            <link>http://www.medworm.com/index.php?rid=5469564&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F162-a%3Frss%3D1</link>
            <description>In their recent paper, Grazzini and colleagues1 reported a decrease in the positivity of the immunochemical faecal occult blood test (iFOBT) for colorectal cancer screening during the summer period. Their results predict a higher rate of false-negative iFOBT results during the hot season. This effect is likely to be higher for patients with minor neoplastic lesions, where the haemoglobin concentration in faeces is usually lower2 than in patients with larger adenomas or invasive cancers. Evaluating the seasonal proportional incidence of interval cancers (ICs) and hence the sensitivity of iFOBT-based screening programmes may help to clarify this point. We are soon going to publish the sensitivity estimates of five Italian iFOBT-based screening programmes according to the proportional method....</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469564</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469564</guid>        </item>
        <item>
            <title>GI highlights from the literature</title>
            <link>http://www.medworm.com/index.php?rid=5469563&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F160%3Frss%3D1</link>
            <description>Basic scienceDietary influences on the gut microbiome &amp;nbsp;Wu GD, Chen J, Hoffman C, et al. Linking long-term dietary patterns with gut microbial enterotypes. Science 2011;334:105&amp;ndash;8. Mounting evidence suggests that the gut microbiota may influence the development of human diseases such as autoimmunity, obesity, and inflammatory bowel disease. Diet may serve as a modifiable factor that can influence the composition of the host microbiome. Wu et al recently reported findings of a cross sectional study of 98 healthy volunteers investigating dietary influences on the gut microbiota. Short-term and long-term dietary intake was assessed by the use of food frequency questionnaires. Massively parallel sequencing of 16S ribosomal bacterial DNA sequences was performed on DNA isolated from sto...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469563</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469563</guid>        </item>
        <item>
            <title>Genetic determinants of alcoholic liver disease</title>
            <link>http://www.medworm.com/index.php?rid=5469562&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F150%3Frss%3D1</link>
            <description>Alcoholic liver disease (ALD) accounts for the majority of chronic liver disease in Western countries. The spectrum of ALD includes steatosis with or without fibrosis in virtually all individuals with an alcohol consumption of &amp;gt;80&amp;nbsp;g/day, alcoholic steatohepatitis of variable severity in 10&amp;ndash;35% and liver cirrhosis in approximately 15% of patients. Once cirrhosis is established, there is an annual risk for hepatocellular carcinoma of 1&amp;ndash;2%. Environmental factors such as drinking patterns, coexisting liver disease, obesity, diet composition and comedication may modify the natural course of ALD. Twin studies have revealed a substantial contribution of genetic factors to the evolution of ALD, as demonstrated by a threefold higher disease concordance between monozygotic twins ...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469562</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469562</guid>        </item>
        <item>
            <title>Omega-3 polyunsaturated fatty acids for the treatment and prevention of colorectal cancer</title>
            <link>http://www.medworm.com/index.php?rid=5469561&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F135%3Frss%3D1</link>
            <description>Omega ()-3 polyunsaturated fatty acids (PUFAs) are naturally occurring substances that are well tolerated and have been used extensively for the prevention of cardiovascular disease. More recently, -3 PUFAs have been recognised to have anticancer activity. There is also evidence suggesting improved efficacy and/or tolerability of conventional cancer chemotherapy when administered with -3 PUFAs. The purpose of this review is to (i) describe the mechanisms by which -3 PUFAs are thought to have antineoplastic activity, (ii) review published preclinical and clinical studies that support anti-colorectal cancer activity and (iii) summarise current clinical trials investigating the potential therapeutic role(s) of -3 PUFAs at different stages of colorectal carcinogenesis, from adenoma (polyp) pre...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469561</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469561</guid>        </item>
        <item>
            <title>Viral clearance is associated with improved insulin resistance in genotype 1 chronic hepatitis C but not genotype 2/3</title>
            <link>http://www.medworm.com/index.php?rid=5469560&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F128%3Frss%3D1</link>
            <description>Conclusions
SVR is associated with a reduction in HOMA-IR in patients with HCV genotype 1 but not in those with genotype 2/3. Genotype 1 may have a direct effect on the development of IR, independent of host metabolic factors, and may be partially reversed by viral eradication. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469560</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469560</guid>        </item>
        <item>
            <title>MRI: the new reference standard in quantifying hepatic steatosis?</title>
            <link>http://www.medworm.com/index.php?rid=5469559&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F117%3Frss%3D1</link>
            <description>Conclusions
With the use of a well-defined set of biological standards, MRI can predict intrahepatic fat with high accuracy. In contrast to biopsies, this method is non-invasive, giving a representative assessment of the whole liver. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469559</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469559</guid>        </item>
        <item>
            <title>Satavaptan for the management of ascites in cirrhosis: efficacy and safety across the spectrum of ascites severity</title>
            <link>http://www.medworm.com/index.php?rid=5469558&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F108%3Frss%3D1</link>
            <description>Conclusion
Satavaptan, alone or in combination with diuretics, is not clinically beneficial in the long-term management of ascites in cirrhosis. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469558</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469558</guid>        </item>
        <item>
            <title>Performance measures in three rounds of the English bowel cancer screening pilot</title>
            <link>http://www.medworm.com/index.php?rid=5469557&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F101%3Frss%3D1</link>
            <description>Conclusions
Performance measures are commensurate with expectations in a screening programme reaching its third round of screening, but a substantial ongoing effort is needed, particularly to address the effects of deprivation and ethnicity in relation to uptake. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469557</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469557</guid>        </item>
        <item>
            <title>Role of acute diverticulitis in the development of complicated colonic diverticular disease and 1-year mortality after diagnosis in the UK: population-based cohort study</title>
            <link>http://www.medworm.com/index.php?rid=5469556&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F95%3Frss%3D1</link>
            <description>Conclusions
Although most patients have experienced no prior episodes of acute diverticulitis, fistula formation is preceded by bouts of inflammation. Excess 1-year mortality across the spectrum of CCDD compared with the general population is substantial. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469556</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469556</guid>        </item>
        <item>
            <title>A rare cause of bloody diarrhoea</title>
            <link>http://www.medworm.com/index.php?rid=5469555&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F94%3Frss%3D1</link>
            <description>Clinical presentation A 67-year-old woman presented with a 6-week history of progressive abdominal distension. Her clinical examination revealed a palpable pelvic mass. She underwent total abdominal hysterectomy, salpingo-oophorectomy and removal of a 3&amp;nbsp;kg ovarian cystadenoma. Postoperatively she had renal impairment; urine microscopy revealed red cell casts and renal biopsy demonstrated a segmental crescentic necrotising glomerulonephritis. This was successfully treated with pulsed steroids and cyclophosphamide. Three weeks later, she developed breathlessness, with fleeting pulmonary infiltrates on chest radiography, and was treated with plasmaphaeresis with resolution of symptoms. She was referred to the gastroenterology department with a 2-week history of lower abdominal pain and b...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469555</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469555</guid>        </item>
        <item>
            <title>Visceral adipocytes: old actors in obesity and new protagonists in Crohn's disease?</title>
            <link>http://www.medworm.com/index.php?rid=5469554&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F86%3Frss%3D1</link>
            <description>Conclusion
In patients with CD, VAT distant from uhMES is affected by inflammation and displays features similar to those of VAT of patients with severe OB. The small diameter of VAT adipocytes of CD, together with their high expression of anti-inflammatory genes, suggests a potentially protective role for this tissue. VAT adipocytes may play an important role in the pathophysiology and/or activity of CD. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469554</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469554</guid>        </item>
        <item>
            <title>Mesenteric fat as a source of C reactive protein and as a target for bacterial translocation in Crohn's disease</title>
            <link>http://www.medworm.com/index.php?rid=5469553&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F78%3Frss%3D1</link>
            <description>Conclusion
Mesenteric fat is an important source of CRP in CD. CRP production by mesenteric adipocytes may be triggered by local inflammation and bacterial translocation to mesenteric fat, providing a mechanism whereby mesenteric fat hyperplasia may contribute to inflammatory response in CD. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469553</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469553</guid>        </item>
        <item>
            <title>Longitudinal study of infectious intestinal disease in the UK (IID2 study): incidence in the community and presenting to general practice</title>
            <link>http://www.medworm.com/index.php?rid=5469552&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F69%3Frss%3D1</link>
            <description>Conclusions
IID poses a substantial community and healthcare burden in the UK. Control efforts must focus particularly on reducing the burden due to Campylobacter and enteric viruses. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469552</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469552</guid>        </item>
        <item>
            <title>Increased risk of end-stage renal disease in individuals with coeliac disease</title>
            <link>http://www.medworm.com/index.php?rid=5469551&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F64%3Frss%3D1</link>
            <description>Conclusion
This study indicates that individuals with biopsy-verified CD suffer increased risk of subsequent ESRD. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469551</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469551</guid>        </item>
        <item>
            <title>Copper and liver disease</title>
            <link>http://www.medworm.com/index.php?rid=5469550&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F63%3Frss%3D1</link>
            <description>This is an introduction to the Gut tutorial &amp;lsquo;Copper and liver disease&amp;rsquo; hosted on BMJ Learning&amp;mdash;the best available learning website for medical professionals from the BMJ Group. Astute clinical examination may suggest the diagnosis of Wilson's disease in a patient with typical clinical features. However, often, the confirmation of this diagnosis is difficult. Copper overload can present as a variety of liver and neurological disorders. Not suspecting the diagnosis of Wilson's disease and delay in confirming the suspected diagnosis remain a problem with this disease. The diagnosis and treatment of Wilson's disease as well as the newer developments in the understanding of copper metabolism are discussed in this tutorial. To access the tutorial (Interactive Case History), clic...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469550</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469550</guid>        </item>
        <item>
            <title>Vitamin D3 upregulated protein 1 deficiency promotes N-methyl-N-nitrosourea and Helicobacter pylori-induced gastric carcinogenesis in mice</title>
            <link>http://www.medworm.com/index.php?rid=5469549&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F53%3Frss%3D1</link>
            <description>Conclusion
Our data show that VDUP1 negatively regulates H pylori-associated gastric carcinogenesis, in part by disrupting cell growth and inhibiting the induction of TNF&amp;alpha;, NF-B and COX-2. These findings provide important insights into the role of VDUP1 in H pylori-associated tumourigenesis. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469549</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469549</guid>        </item>
        <item>
            <title>Gastrokine 1 induces senescence through p16/Rb pathway activation in gastric cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=5469548&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F43%3Frss%3D1</link>
            <description>Conclusion
These results provide comprehensive molecular evidence of GKN1 in inducing senescence of gastric cancer cells, and indicate that GKN1 might be a potential novel target for gastric cancer therapeutics. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469548</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469548</guid>        </item>
        <item>
            <title>Constipation and recurrent abdominal distension in a 39-year-old woman with irritable bowel syndrome</title>
            <link>http://www.medworm.com/index.php?rid=5469547&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F42%3Frss%3D1</link>
            <description>Clinical presentation A 39-year-old woman with a previous diagnosis of irritable bowel syndrome presented with progressively worsening episodes of marked abdominal distension and difficulties with defecation. She had a long history of constipation and had tried a variety of laxatives with an unsatisfactory response. Recent colonoscopy was unremarkable. Physical exam revealed a protuberant abdomen with tympany and high-pitched bowel sounds. Inspection of the anus showed no perianal lesions and absent perineal descent with straining at defecation. A digital rectal examination revealed high anal sphincter tone and absence of puborectalis relaxation with simulated defecation. There was no palpable stool in the rectum. Computed tomographic enterography with scout film showed a markedly dilated ...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469547</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469547</guid>        </item>
        <item>
            <title>MicroRNA-375 inhibits tumour growth and metastasis in oesophageal squamous cell carcinoma through repressing insulin-like growth factor 1 receptor</title>
            <link>http://www.medworm.com/index.php?rid=5469546&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F33%3Frss%3D1</link>
            <description>Conclusions
This study demonstrates that miR-375 has a strong tumour-suppressive effect through inhibiting the expression of IGF1R. The downregulation of miR-375, which is mainly caused by promoter methylation, is one of the molecular mechanisms involved in the development and progression of ESCC. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469546</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469546</guid>        </item>
        <item>
            <title>Guidelines for the management of gastroenteropancreatic neuroendocrine (including carcinoid) tumours (NETs)</title>
            <link>http://www.medworm.com/index.php?rid=5469545&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F6%3Frss%3D1</link>
            <description>These guidelines update previous guidance published in 2005. They have been revised by a group who are members of the UK and Ireland Neuroendocrine Tumour Society with endorsement from the clinical committees of the British Society of Gastroenterology, the Society for Endocrinology, the Association of Surgeons of Great Britain and Ireland (and its Surgical Specialty Associations), the British Society of Gastrointestinal and Abdominal Radiology and others. The authorship represents leaders of the various groups in the UK and Ireland Neuroendocrine Tumour Society, but a large amount of work has been carried out by other specialists, many of whom attended a guidelines conference in May 2009. We have attempted to represent this work in the acknowledgements section. Over the past few years, the...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469545</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469545</guid>        </item>
        <item>
            <title>Mesenteric fat in Crohn's disease: the hot spot of inflammation?</title>
            <link>http://www.medworm.com/index.php?rid=5469544&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F3%3Frss%3D1</link>
            <description>The phenomenon of creeping fat in Crohn's disease (CD), characterised by a hypertrophy of the mesenteric fat surrounding inflamed intestinal segments, was first described by Burrill B Crohn himself at the beginning of the past century.1 An MRI study confirmed this specific finding only a decade ago.2 Nonetheless, the functional impact remained to be elucidated. The fat tissue was solely considered as a storage and endocrine organ for a long time; two parallel developments triggered a paradigm shift: First, in vitro and in vivo studies provided evidence that adipokines released by adipocytes are critical in the regulation of the immune system.3 Furthermore, preadipocytes and adipocytes were found to express functional receptors of the innate immune system. Second, obesity, and in particular...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469544</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469544</guid>        </item>
        <item>
            <title>Gained in translation: the importance of biologically relevant models of Helicobacter pylori-induced gastric cancer</title>
            <link>http://www.medworm.com/index.php?rid=5469543&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F2%3Frss%3D1</link>
            <description>The attributable risk of gastric cancer conferred by Helicobacter pylori ranges from 75% to more than 90% depending on H pylori prevalence; however, only a fraction of colonised persons ever develop neoplasia.1 2 Disease risk involves well-choreographed interactions between pathogen and host, which are dependent upon strain-specific bacterial factors as well as host genotypic traits, each of which can be amplified by the environment. In their paper published in Gut, Kwon et al provide fresh insights into the role of a tumour suppressor, vitamin D3 upregulated protein 1 (VDUP1), in H pylori-associated gastric carcinogenesis (see page 53).3 Importantly, these investigators used multiple model systems to demonstrate that VDUP1 negatively regulates carcinogenesis induced by the combination of ...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469543</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469543</guid>        </item>
        <item>
            <title>Gut goes from strength to strength</title>
            <link>http://www.medworm.com/index.php?rid=5469542&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2F1%3Frss%3D1</link>
            <description>2011 was an excellent year for the Gut family. Our team of dedicated associate editors, editorial staff, publishers and reviewers ensured that the journal continues to deliver the highest quality clinical science from all corners of the globe. Our impact factor climbed from 9.3 to 10.6, which is a major achievement for our journal. In 2011, we have received a record number of manuscripts allowing us the luxury of selecting the very best for publication. We instituted a maximal drive towards efficiency and boast arguably the most favourable editorial handling times for any major journal. The most crucial marker is the average time to reach decision for reviewed manuscripts, which now stands at 19&amp;nbsp;days. This means that the overwhelming number of reviewed manuscripts receive a decision i...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469542</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469542</guid>        </item>
        <item>
            <title>Highlights from this issue</title>
            <link>http://www.medworm.com/index.php?rid=5469541&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F61%2F1%2Fi%3Frss%3D1</link>
            <description>Luminal GIPromising new approach to treatment of oesophageal cancer MicroRNA's are a relatively recently discovered form of small RNA's that suppress the expression of target genes. There are over 700 identified microRNAs in humans and each microRNA regulates the expression of multiple target genes. They are often over or under expressed in cancer and they appear to play an important role in the behaviour of many cancers. One of these microRNA's, miR-375, has been shown to be involved in glucose regulation and &amp;beta;-cell growth and is down-regulated in gastric and liver cancer. Kong and colleagues now show that miR-375 is also strongly down-regulated in oesophageal squamous cell carcinoma secondary to DNA methylation and that the decreased expression associates with advanced stage, distan...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5469541</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5469541</guid>        </item>
        <item>
            <title>Electronic nose versus canine nose: clash of the titans</title>
            <link>http://www.medworm.com/index.php?rid=5388345&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1768%3Frss%3D1</link>
            <description>We read with great interest the article by Sonoda et al1 on canine scent detection in those with colorectal cancer. The concept of using a dog to detect diseases is not new; there are many reported incidents of dogs barking at their owners (or even trying to bite the leg off of an owner with melanoma!) who are later shown to have the disease. Several studies have shown that dogs are able to detect, among others, breath, lung, bladder, ovary, prostate and skin cancers. In these reports, the dog is trained to recognise the disease state (in fact, the dog is reminded of these different groups usually the morning of the experiment). It is also important to recognise that the dog achieves this separation even within the &amp;lsquo;multi-odour&amp;rsquo; hospital environment, unlike modern sophisticated...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388345</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
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        <item>
            <title>The Authors' reply</title>
            <link>http://www.medworm.com/index.php?rid=5388344&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1767-b%3Frss%3D1</link>
            <description>We thank Dr Hutchinson and Dr Davies for their comments1 regarding the use of alternative options in patients with cirrhosis and refractory ascites. The use of other potential therapies for patients with refractory ascites is attractive and should perhaps be considered in selected cases. Therapies such as clonidine, a centrally acting &amp;alpha;2-agonist and sympatholytic agent, and the use of vasoconstrictors such as midodrine have been studied as treatment options for refractory ascites.2&amp;ndash;4 These agents improve renal function, urinary sodium excretion and serum sodium levels and decrease the levels of vasoactive/antinatriuretic systems in patients with advanced cirrhosis. In the case of clonidine, data stem from studies that evaluated the diuretic effects of this medication in patient...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388344</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388344</guid>        </item>
        <item>
            <title>The use of clonidine with diuretic therapy in the treatment of refractory ascites in patients with cirrhosis awaiting liver transplantation</title>
            <link>http://www.medworm.com/index.php?rid=5388343&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1767-a%3Frss%3D1</link>
            <description>We have read the comprehensive review article by C&amp;aacute;rdenas and Gin&amp;egrave;s that details the management of ascites, hyponatraemia, hepatorenal syndrome, bacterial infections, hepatic encephalopathy and variceal bleeding in patients with decompensated chronic liver disease.1 It is well recognised that such conditions alter pre-, peri- and post-orthotopic liver transplant (OLT) outcomes. However, there is one important issue around the management of refractory ascites that the authors have failed to address. While the role of maintaining a low-sodium diet, diuretic therapy and paracentesis are discussed, the authors suggest only repeated paracentesis and transjugular intrahepatic portosystemic shunt as treatment options for refractory ascites. It has been known for over 20&amp;nbsp;years t...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388343</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388343</guid>        </item>
        <item>
            <title>The Authors' reply</title>
            <link>http://www.medworm.com/index.php?rid=5388342&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1766-b%3Frss%3D1</link>
            <description>We read with interest the comments raised by Gleeson et al.1 We thank the authors for their valuable remarks. The aim of our prospective study was not to investigate the natural history of alcoholic steatohepatitis (ASH). Therefore, patients were not selected based on the presence or absence of ASH. The primary aim of the study was to elucidate whether acute-on-chronic liver failure (ACLF), as defined in the literature,2&amp;ndash;4 really exists as a clinical identity and more specifically as a complication of cirrhosis. We could demonstrate that among those with symptomatic cirrhosis (70/250 patients with alcoholic cirrhosis), there is a subgroup of patients which is characterised by rapid progressive jaundice with evolution to multiorgan failure. Alcoholic hepatitis indeed plays a role in t...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388342</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388342</guid>        </item>
        <item>
            <title>Comments on 'Early features of acute-on-chronic liver failure: a prospective cohort study'</title>
            <link>http://www.medworm.com/index.php?rid=5388341&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1766-a%3Frss%3D1</link>
            <description>We read with interest the study by Katoonizadeh et al1 of acute-on-chronic (alcoholic) liver failure (ACLF) and the accompanying Editorial 2 which cites our report3 of liver histology in decompensated alcoholic liver disease (ALD). We found features of alcoholic hepatitis (intralobular neutrophils, Mallory bodies and ballooning) to be more frequent and more severe in patients biopsied within a month of first onset of decompensation, compared with those biopsied before decompensation or later, and argued for a causal relationship. We acknowledge the strengths of the prospective study of Katoonizadeh et al1 but would interpret their results differently. Their definition of ACLF1 excludes patients with no prior liver disease and also those without cirrhosis on biopsy. It thus excludes many pa...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388341</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388341</guid>        </item>
        <item>
            <title>GI highlights from the literature</title>
            <link>http://www.medworm.com/index.php?rid=5388340&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1764%3Frss%3D1</link>
            <description>Post-ERCP mortality and provider volume &amp;nbsp;Bodger K, Bowering K, Sarkar S, et al. All-cause mortality after first ERCP in England: clinically guided analysis of hospital episode statistics with linkage to registry of death. Gastrointest Endosc 2011;74:825&amp;ndash;33. A large body of published evidence in a variety of surgical disciplines supports the notion that doing more is better&amp;mdash;that high procedural volume centres and, indeed, high-volume operators have superior outcomes. Intuitively, a volume&amp;ndash;outcome relationship might be expected to apply to the practice of endoscopic retrograde cholangipancreatography (ERCP) from the well-recognised complexity of this procedure, which has relatively high attendant risks and requirements for a dedicated highly skilled multidisciplinary t...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388340</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388340</guid>        </item>
        <item>
            <title>Early use of immunosuppressives or TNF antagonists for the treatment of Crohn's disease: time for a change</title>
            <link>http://www.medworm.com/index.php?rid=5388339&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1754%3Frss%3D1</link>
            <description>Crohn's disease is a chronic inflammatory disorder that follows a progressive and destructive course. Ultimately, uncontrolled inflammation leads to bowel damage from disease-related complications such as strictures, fistulas and abscesses and surgical resection. Conventional &amp;lsquo;step-care&amp;rsquo;, whereby corticosteroids and immunosuppressives are prescribed sequentially, is an incremental approach to treatment that does not prevent disease progression and conveys an important risk of adverse events from repeated courses of corticosteroids. Although the immunosuppressives azathioprine, 6-mercaptopurine and methotrexate are corticosteroid-sparing, they are not highly effective for inducing mucosal healing or preventing disease progression. Tumour necrosis factor antagonists induce and ma...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388339</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388339</guid>        </item>
        <item>
            <title>New IBD genetics: common pathways with other diseases</title>
            <link>http://www.medworm.com/index.php?rid=5388338&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1739%3Frss%3D1</link>
            <description>Complex disease genetics has been revolutionised in recent years by the advent of genome-wide association (GWA) studies. The chronic inflammatory bowel diseases (IBDs), Crohn's disease and ulcerative colitis have seen notable successes culminating in the discovery of 99 published susceptibility loci/genes (71 Crohn's disease; 47 ulcerative colitis) to date. Approximately one-third of loci described confer susceptibility to both Crohn's disease and ulcerative colitis. Amongst these are multiple genes involved in IL23/Th17 signalling (IL23R, IL12B, JAK2, TYK2 and STAT3), IL10, IL1R2, REL, CARD9, NKX2.3, ICOSLG, PRDM1, SMAD3 and ORMDL3. The evolving genetic architecture of IBD has furthered our understanding of disease pathogenesis. For Crohn's disease, defective processing of intracellular b...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388338</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388338</guid>        </item>
        <item>
            <title>Vitamin D inhibits proliferation and profibrotic marker expression in hepatic stellate cells and decreases thioacetamide-induced liver fibrosis in rats</title>
            <link>http://www.medworm.com/index.php?rid=5388337&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1728%3Frss%3D1</link>
            <description>Conclusion
1,25(OH)2D3 has antiproliferative and antifibrotic effects on liver fibrosis in in vitro and in vivo models and may be considered as having potential therapeutic value. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388337</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388337</guid>        </item>
        <item>
            <title>Coronary artery disease and cardiovascular outcomes in patients with non-alcoholic fatty liver disease</title>
            <link>http://www.medworm.com/index.php?rid=5388336&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1721%3Frss%3D1</link>
            <description>Conclusions
In patients with clinical indications for coronary angiogram, fatty liver is associated with coronary artery disease independently of other metabolic factors. However, fatty liver cannot predict cardiovascular mortality and morbidity in patients with established coronary artery disease. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388336</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388336</guid>        </item>
        <item>
            <title>Prognosis of invasive intraductal papillary mucinous neoplasm depends on histological and precursor epithelial subtypes</title>
            <link>http://www.medworm.com/index.php?rid=5388335&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1712%3Frss%3D1</link>
            <description>Conclusions
Tubular, colloid and oncocytic invasive IPMNs have varying prognosis, and arise from different epithelial subtypes. Colloid and oncocytic types have markedly improved biology, whereas the tubular type has a course that resembles PDAC. Analysis of these subtypes indicates that the background epithelium plays an equally, if not more, important role in defining the biology and prognosis of invasive IPMNs. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388335</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388335</guid>        </item>
        <item>
            <title>Keeping abdominal pain in the family</title>
            <link>http://www.medworm.com/index.php?rid=5388334&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1711%3Frss%3D1</link>
            <description>Clinical presentation A previously fit 30-year old software technician was admitted with a 2-week history of severe abdominal pain, associated with nausea and bloody diarrhoea. He had no medical or surgical history, was a non-smoker and took no medication or recreational drugs. His mother, brother and maternal grandmother had had deep vein thromboses or pulmonary emboli. On examination he was afebrile, with central abdominal tenderness but no evidence of peritonism. His white cell count (16.1x109/litre) and C-reactive protein (CRP, 138&amp;nbsp;mg/litre) were elevated. Serum amylase and lactate were normal. Chest and plain abdominal x-radiographs were unremarkable, but an abdominal CT scan (figure 1), performed because of a clinical suspicion of gut ischaemia, showed characteristic features of...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388334</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388334</guid>        </item>
        <item>
            <title>Type 2 diabetes risk variants and colorectal cancer risk: the Multiethnic Cohort and PAGE studies</title>
            <link>http://www.medworm.com/index.php?rid=5388333&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1703%3Frss%3D1</link>
            <description>Conclusion
The findings suggest that diabetes risk variants also influence colorectal cancer susceptibility, possibly through mechanisms different from those for diabetes. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388333</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388333</guid>        </item>
        <item>
            <title>Maternal B vitamin supplementation from preconception through weaning suppresses intestinal tumorigenesis in Apc1638N mouse offspring</title>
            <link>http://www.medworm.com/index.php?rid=5388332&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1695%3Frss%3D1</link>
            <description>Conclusions
These changes indicate a de-repression of the Wnt pathway in pups of deficient dams and form a plausible mechanism by which maternal B vitamin intake modulates tumorigenesis in offspring. These data indicate that maternal B vitamin supplementation suppresses, while deficiency promotes, intestinal tumorigenesis in Apc1638N offspring. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388332</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388332</guid>        </item>
        <item>
            <title>Effect of maternal and postweaning folic acid supplementation on colorectal cancer risk in the offspring</title>
            <link>http://www.medworm.com/index.php?rid=5388331&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1687%3Frss%3D1</link>
            <description>Conclusions
The data suggest for the first time that maternal folic acid supplementation at the level equivalent to the average postfortification total folate intake in North America and to that recommended to women at reproductive age protects against the development of colorectal cancer in the offspring. This protective effect may be mediated in part by increased global DNA methylation and decreased epithelial proliferation and DNA damage in the colorectum. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388331</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388331</guid>        </item>
        <item>
            <title>Interleukin 21 controls tumour growth and tumour immunosurveillance in colitis-associated tumorigenesis in mice</title>
            <link>http://www.medworm.com/index.php?rid=5388330&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1678%3Frss%3D1</link>
            <description>Conclusion
These results indicate that IL-21 orchestrates colitis-associated tumorigenesis, leading to the hypothesis that high IFN and low IL-17A expression reduces tumour cell proliferation and increases tumour immunosurveillance. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388330</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388330</guid>        </item>
        <item>
            <title>Association of TNFSF15 polymorphism with irritable bowel syndrome</title>
            <link>http://www.medworm.com/index.php?rid=5388329&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1671%3Frss%3D1</link>
            <description>Conclusions
TNFSF15 is a susceptibility gene for IBS and IBS constipation. As TL1A, the protein encoded by TNFSF15, contributes to the modulation of inflammatory responses, the results support a role of immune activation in IBS. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388329</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388329</guid>        </item>
        <item>
            <title>The MUC13 cell-surface mucin protects against intestinal inflammation by inhibiting epithelial cell apoptosis</title>
            <link>http://www.medworm.com/index.php?rid=5388328&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1661%3Frss%3D1</link>
            <description>Conclusions
These novel findings indicate a protective role for Muc13 in the colonic epithelium by inhibiting toxin-induced apoptosis and have important implications for intestinal infections, inflammatory diseases and the development of intestinal cancer. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388328</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388328</guid>        </item>
        <item>
            <title>Duodenal mass in a patient with weight loss and liver dysfunction</title>
            <link>http://www.medworm.com/index.php?rid=5388327&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1659%3Frss%3D1</link>
            <description>Clinical presentation A 59-year-old Japanese man presented to our hospital with loss of appetite and 7&amp;nbsp;kg decrease in weight over 6&amp;nbsp;months. His medical history was unremarkable, except for hearing difficulty. He took medication for hypertension. His vital signs and physical examination were normal. Laboratory data at presentation were as follows: total bilirubin 0.4&amp;nbsp;mg/dl (reference 0.2&amp;ndash;1.0); alanine aminotransferase 58&amp;nbsp;IU/l (reference 10&amp;ndash;40); aspartate aminotransferase 68&amp;nbsp;IU/l (reference 5&amp;ndash;40); alkaline phosphatase 697&amp;nbsp;IU/l (reference 104&amp;ndash;338); gamma-glutamyl transpeptidase 178&amp;nbsp;IU/l (reference 0&amp;ndash;79); white blood cells 4300/microlitre (reference 3700&amp;ndash;9300); haemoglobin 12.1&amp;nbsp;g/dl (reference 13.0&amp;ndash;16.5); blood u...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388327</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388327</guid>        </item>
        <item>
            <title>Suboptimal gastroprotective coverage of NSAID use and the risk of upper gastrointestinal bleeding and ulcers: an observational study using three European databases</title>
            <link>http://www.medworm.com/index.php?rid=5388326&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1650%3Frss%3D1</link>
            <description>Conclusions
The risk of UGI events was significantly higher in nsNSAID users with GPA non-adherence. This underlines the importance of strategies to improve GPA adherence. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388326</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388326</guid>        </item>
        <item>
            <title>Divergent trends for gastric cancer incidence by anatomical subsite in US adults</title>
            <link>http://www.medworm.com/index.php?rid=5388325&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1644%3Frss%3D1</link>
            <description>Conclusions
Long- and short-term incidence trends for gastric cancers indicate a shifting distribution by anatomical subsite. Corpus cancer may have distinctive aetiology and changing risk factor exposures, warranting further investigation. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388325</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388325</guid>        </item>
        <item>
            <title>Wnt2 secreted by tumour fibroblasts promotes tumour progression in oesophageal cancer by activation of the Wnt/{beta}-catenin signalling pathway</title>
            <link>http://www.medworm.com/index.php?rid=5388324&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1635%3Frss%3D1</link>
            <description>Conclusions
TF-secreted Wnt2 acts as a growth and invasion-promoting factor through activating the canonical Wnt/&amp;beta;-catenin signalling pathway in oesophageal cancer cells. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388324</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388324</guid>        </item>
        <item>
            <title>Gastrointestinal and liver diseases: genetic and epigenetic markers</title>
            <link>http://www.medworm.com/index.php?rid=5388323&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1630%3Frss%3D1</link>
            <description>Molecular analyses The basic aspects of molecular, cell and stem cell biology are central to biomedical research and are increasingly becoming part of patient care in clinical practice (&amp;lsquo;translational medicine&amp;rsquo;). The genetic material of humans is made up of DNA that in its entirety makes up an individual's genome that is structurally organised into 46 chromosomes (44 autosomes and two sex chromosomes XX or XY, defining the female or male phenotype). A seminal scientific achievement was deciphering the complete nucleotide sequence of the human genome by the concerted effort of the international human genome organisation project 10&amp;nbsp;years ago.1 2 This was followed by the era of &amp;lsquo;genomics&amp;rsquo; that aim at unravelling the complete genetic information of an individual.3 ...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388323</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388323</guid>        </item>
        <item>
            <title>British Society of Gastroenterology (BSG) guidelines for management of autoimmune hepatitis</title>
            <link>http://www.medworm.com/index.php?rid=5388322&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1611%3Frss%3D1</link>
            <description>Autoimmune hepatitis (AIH) is a chronic inflammatory liver disease which, if untreated, often leads to cirrhosis, liver failure and death. Major advances were made in its management based on controlled trials performed in England and the USA in the 1970s and 1980s. Unfortunately, in recent decades there has been a dearth of controlled clinical trials and, thus, many questions regarding the optimal management of this disease remain unanswered. Many promising newer immunosuppressive therapies await formal comparison with standard therapies and also many important details in relation to the application of standard therapies remain unclear. These guidelines describe the optimal management strategies in adults based on available published evidence, including the American Association for the Stu...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388322</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388322</guid>        </item>
        <item>
            <title>Colitis-associated cancer: the dark side of inflammatory bowel disease</title>
            <link>http://www.medworm.com/index.php?rid=5388321&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2F1609%3Frss%3D1</link>
            <description>The intrinsic connection between inflammation and cancer promotion is well established and is especially strong in patients with colorectal cancer (CRC), the second most common cause of cancer-related death in Western countries.1 2 The administration of non-steroidal anti-inflammatory drugs in controlled studies reduces the incidence of colon cancer in patients with familial adenoma polyposis, confirming the link between inflammation and colon cancer.3 Several lines of evidence indicate that chronic inflammation predisposes the tissue to cancer by inducing gene mutation, inhibiting apoptosis or stimulating angiogenesis and cell proliferation. Patients with inflammatory bowel disease (IBD) are at increased risk of developing CRC and, in particular, an association between IBD and the develop...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388321</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388321</guid>        </item>
        <item>
            <title>Highlights from this issue</title>
            <link>http://www.medworm.com/index.php?rid=5388320&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F12%2Fi%3Frss%3D1</link>
            <description>Host genetics and IBS Irritable bowel syndrome (IBS) is the most common gastrointestinal disorder but its aetiology remains poorly understood. A genetic link in IBS is supported by familial clustering and a higher incidence in monozygotic twins. In this issue of Gut, Zucchelli et al examined the hypothesis that genes contributing to epithelial barrier integrity, control of mucosal immune responses and interactions with bacteria in the gut are associated with IBS. They tested 30 known susceptibility loci for Crohn's disease in 1992 individuals from two independent case-control cohorts from Sweden and the USA. The Crohn's disease risk allele rs4263839 G in the TNFSF15 gene was significantly associated with an increased risk of both IBS (p=2.2310&amp;ndash;5; OR 1.37) and more markedly, constipat...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5388320</comments>
            <pubDate>Fri, 04 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5388320</guid>        </item>
        <item>
            <title>TGF{alpha}-associated MUC2 and MUC3 expression of the gastric epithelium in Menetrier's disease during remission of ulcerative colitis</title>
            <link>http://www.medworm.com/index.php?rid=5274638&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1607-b%3Frss%3D1</link>
            <description>The broad clinical heterogeneity of M&amp;eacute;n&amp;eacute;trier's disease (MD) has been recently described by Rich et al.1 There are few reports on MD patients with a history of ulcerative colitis (UC). Overexpression of the transforming growth factor &amp;alpha; (TGF&amp;alpha;) leads to gastric epithelium abnormalities similar to those of MD.2 A significant increase in TGF&amp;alpha; levels has been observed in inactive UC compared with healthy controls. TGF&amp;alpha; could be the link between both inactive UC and the development of MD. TGF&amp;alpha; stimulates gastric cell proliferation as well as mucin biosynthesis. Normal gastric mucosa expresses MUC1 and MUC5Ac in foveolar epithelium and MUC6 in the glands, while MUC2 and MUC3 are predominantly expressed in goblet cells and enterocytes, respectively, of t...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274638</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274638</guid>        </item>
        <item>
            <title>The Authors' reply</title>
            <link>http://www.medworm.com/index.php?rid=5274637&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1607-a%3Frss%3D1</link>
            <description>We would like to thank Mr Adrian Jubb and his colleagues for sharing their interesting findings.1 In our opinion their data provide additional support for our study2 but fall short of sufficiently addressing the question of the correlation between 11p15.5 DNA copy number gain and ASCL2 expression in liver metastases of colorectal cancer. Consistent with our findings, Jubb et al did not detect copy number aberrations on chromosome band 11p15.5 in two additional sets of primary colorectal cancers (pCRC). Nevertheless, over-expression of ASCL2 RNA was demonstrated by Jubb et al as well as in our study (pCRC vs. normal colon, p&amp;lt;0.001). This is not surprising since ASCL2 has been shown to be a direct target of the Wnt pathway3 which is upregulated in the majority of colorectal cancers. There...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274637</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274637</guid>        </item>
        <item>
            <title>Ascl2 and 11p15.5 amplification in colorectal cancer</title>
            <link>http://www.medworm.com/index.php?rid=5274636&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1606%3Frss%3D1</link>
            <description>We read with interest the recent article by Stange et al1 describing gain of 11p or 11p15.5 in approximately one-quarter of colorectal cancer liver metastases compared with matched primary adenocarcinomas. Stange et al speculated that this event may be targeting several putative oncogenes and focused on achaete scute-like (Ascl)2 in particular.1 However, on examining our own published2 3 and unpublished data, we reached different conclusions regarding the role of Ascl2 in colorectal cancer. We queried two series of primary colorectal cancers with both expression microarray and array comparative genomic hybridisation data. The first dataset relates to 37 cases (experiments conducted at Genentech; 100&amp;nbsp;k single nucleotide polymorphism array and HG-U133B GeneChip expression microarray (Af...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274636</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274636</guid>        </item>
        <item>
            <title>The Authors' reply</title>
            <link>http://www.medworm.com/index.php?rid=5274635&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1605-a%3Frss%3D1</link>
            <description>We thank Drs Molina-Infante and Gisbert1 for their letter and for their appreciation of our study.2 We completely agree that the discrepancy between their study and our study as to the efficacy of levofloxacin-containing sequential treatment in Helicobacter pylori eradication might be at least in part due to the very low (ie, 3%) prevalence of H pylori strains resistant to this antimicrobial in our region compared with their geographical area. We also agree that clarithromycin-containing sequential treatment is achieving disappointing results in areas with a high prevalence of clarithromycin and/or dual (ie, metronidazole + clarithromycin) resistance and that, therefore, its role in this setting should be critically reconsidered. Recently, a study by Hsu et al has demonstrated high efficac...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274635</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274635</guid>        </item>
        <item>
            <title>Levofloxacin in first-line eradication regimens for Helicobacter pylori: better test antibiotic susceptibility before treating</title>
            <link>http://www.medworm.com/index.php?rid=5274634&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1605%3Frss%3D1</link>
            <description>We sincerely congratulate Romano et al1 for their recent manuscript in Gut showing that levofloxacin-containing sequential therapy can overcome suboptimal cure rates of clarithromycin-containing sequential therapy (&amp;le;80% in the intention-to-treat analysis), in a setting with a high clarithromycin resistance rate (20%) but a low levofloxacin resistance rate (3%). Interestingly, we failed to replicate their results in a prior trial with quite a similar design,2 even though the fluoroquinolone resistance rate in Spain has been reported to be as low as 6%.3 In our trial, intention-to-treat eradication rates for clarithromycin-containing (76%) and levofloxacin-containing (82%) 10-day sequential therapies were suboptimal. These poor results are likely related to a higher prevalence of levoflox...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274634</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274634</guid>        </item>
        <item>
            <title>Sequential therapy for Helicobacter pylori eradication: is levofloxacin better?</title>
            <link>http://www.medworm.com/index.php?rid=5274633&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1604%3Frss%3D1</link>
            <description>We read with great interest the study by Romano et al on a modified sequential therapy regimen for Helicobacter pylori eradication.1 Basically, the trial showed that a novel levofloxacin-based regimen was more effective than the standard, clarithromycin-based sequential regimen, irrespective of levofloxacin dose used (250&amp;nbsp;mg or 500&amp;nbsp;mg twice daily). We thank the authors for seeking to improve the efficacy of sequential therapy. However, a note of caution is probably required when the authors suggest that &amp;lsquo;the levofloxacin-based regimen might be used as first-line therapy in those geographical areas where primary clarithromycin resistance is &amp;gt;15%&amp;rsquo;.1 Indeed, the high efficacy of such a therapy could depend on the very low prevalence (3.7%) of primary levofloxacin resi...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274633</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274633</guid>        </item>
        <item>
            <title>The Authors' reply</title>
            <link>http://www.medworm.com/index.php?rid=5274632&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1603%3Frss%3D1</link>
            <description>We appreciate Dr Targher and colleagues' comments1 about our study.2 The authors raise two important questions: how exactly the cohort of individuals with chronic liver disease (CLD) was selected and why cardiovascular mortality (CVM) was not independently associated with CLDs. We would like to provide additional clarification. First, regarding the inclusion criteria for alcoholic liver disease (ALD), we included data from both self-reported excessive alcohol consumption and abnormal liver enzymes. Individuals with excessive alcohol consumption accompanied by normal liver enzymes were not excluded from the entire study. Nevertheless, they were not considered as having ALD or CLD and were not included in the &amp;lsquo;healthy control&amp;rsquo; group. Given the relatively low threshold selected fo...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274632</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274632</guid>        </item>
        <item>
            <title>Risk of all-cause and cardiovascular mortality in patients with chronic liver disease</title>
            <link>http://www.medworm.com/index.php?rid=5274631&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1602%3Frss%3D1</link>
            <description>We read with interest the article by Stepanova et al in a recent issue of Gut. These authors used death certificate data from the third National Health and Nutrition Examination survey (NHANES-III 1988&amp;ndash;1994) in order to assess the impact of metabolic syndrome components on all-cause and cause-specific mortality in patients with chronic liver disease (CLD).1 They concluded that components of the metabolic syndrome are independently associated with overall and liver-related mortality in patients with CLD (principally among those with viral hepatitis C, alcohol-related liver disease (ALD) or non-alcoholic fatty liver disease (NAFLD)).1 Overall, the article is well written and the authors have discussed their results cautiously and in a balanced way, given the well-recognised limitations...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274631</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274631</guid>        </item>
        <item>
            <title>Immune reactivity to {beta}-tubulin isotype 5 and vesicular integral-membrane protein 36 in patients with autoimmune gastrointestinal disorders</title>
            <link>http://www.medworm.com/index.php?rid=5274630&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1601%3Frss%3D1</link>
            <description>It was with interest that we read the paper by Terjung et al1, in a recent issue of Gut, where human myeloid cell-specific &amp;beta;-tubulin isotype 5 was identified as the target antigen of atypical p-ANCA in autoimmune liver disorders. The authors suggest cross-reactivity with the bacterial protein FtsZ, probably reflecting an abnormal immune response to intestinal microorganisms.1 In attempts to identify novel anti-nuclear and anti-neutrophil antibodies in autoimmune hepatitis, we performed 2D gel electrophoresis and western blotting starting from nuclear HeLa cell extracts or enriched nuclear envelope extracts from HL60 cells or neutrophils. The blots were incubated with serum samples from patients with autoimmune hepatitis and controls. Spots to which there was reactivity with serum from...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274630</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274630</guid>        </item>
        <item>
            <title>GI highlights from the literature</title>
            <link>http://www.medworm.com/index.php?rid=5274629&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1600%3Frss%3D1</link>
            <description>Linaclotide for the treatment of chronic idiopathic constipation &amp;nbsp;Lembo AJ, Schneier HA, Shiff SJ, et al. Two randomized trials of linaclotide for chronic constipation. N Engl J Med 2011;365:527&amp;ndash;36. Chronic idiopathic constipation (CIC) is common in the community, with a population prevalence of between 5% and 20%. The condition is difficult to treat, with a significant proportion of individuals with CIC either non-responsive to or dissatisfied with the efficacy of laxatives. New pharmaceutical agents of proven benefit are therefore required. Linaclotide is a guanylate cyclase C receptor agonist that has shown promise in previous phase II randomised controlled trials for CIC. Lembo et al report the results of two large multicentre phase III randomised controlled trials, studying...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274629</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274629</guid>        </item>
        <item>
            <title>The balancing act: endogenous modulation of pain in functional gastrointestinal disorders</title>
            <link>http://www.medworm.com/index.php?rid=5274628&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1589%3Frss%3D1</link>
            <description>Functional gastrointestinal disorders (FGIDs) are characterised by visceral pain or discomfort with an unknown cause. There is increasing evidence for abnormal processing of sensory input in FGIDs. Modulation of sensory input occurs at all levels of the nervous system, with a dynamic balance between facilitation and inhibition and close integration with the body's wider homoeostatic control. Cognitive, emotional, autonomic and spinal reflex pathways effectively orchestrate supraspinal and spinal pain modulation, as demonstrated in neurophysiological and brain imaging studies. Endogenous pain modulation has been studied in visceral pain conditions and abnormal regulation has been shown in irritable bowel syndrome (IBS) and functional dyspepsia, as well as other chronic pain syndromes. A maj...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274628</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274628</guid>        </item>
        <item>
            <title>Crohn's disease: NOD2, autophagy and ER stress converge</title>
            <link>http://www.medworm.com/index.php?rid=5274627&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1580%3Frss%3D1</link>
            <description>Polymorphisms in NOD2, encoding an intracellular pattern recognition receptor, contribute the largest fraction of genetic risk for Crohn's disease among the &amp;gt;40 risk loci identified so far. Autophagy plays a prominent role in the innate immune response towards intracellular bacteria. The discovery of the autophagy genes ATG16L1 and IRGM as risk factors for Crohn's disease turned autophagy into the spotlight in inflammatory bowel disease (IBD). Remarkably, NOD2 has recently been identified as a potent autophagy inducer. A physical interaction of NOD2 and ATG16L1 appears to be required for autophagic clearance of intracellular pathogens. Moreover, Crohn's disease-associated NOD2 and ATG16L1 variants exhibit a defect in the induction of an autophagic response and hence predict autophagy as...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274627</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274627</guid>        </item>
        <item>
            <title>p38 MAP kinase is a therapeutic target for hepatic encephalopathy in rats with portacaval shunts</title>
            <link>http://www.medworm.com/index.php?rid=5274626&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1572%3Frss%3D1</link>
            <description>Conclusion
These findings suggest that reducing neuroinflammation by using inhibitors of p38 would improve the neurological status in HE without inducing secondary effects in the kidney. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274626</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274626</guid>        </item>
        <item>
            <title>Molecular footprints reveal the impact of the protective HLA-A*03 allele in hepatitis C virus infection</title>
            <link>http://www.medworm.com/index.php?rid=5274625&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1563%3Frss%3D1</link>
            <description>Conclusions
It is proposed that at least part of the protective effect of HLA-A*03 results from targeting of this key epitope in a functional site: the requirement for two mutations to balance fitness and escape provides an initial host advantage. This study highlights the potential protective impact of common HLA-A alleles against persistent viruses, with important implications for HCV vaccine studies. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274625</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274625</guid>        </item>
        <item>
            <title>Altered brain microstructure assessed by diffusion tensor imaging in patients with chronic pancreatitis</title>
            <link>http://www.medworm.com/index.php?rid=5274624&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1554%3Frss%3D1</link>
            <description>Conclusion
The findings suggest that microstructural changes of the brain accompany pain in CP. The changes are likely to be a consequence of ongoing pain and structural reorganisation of the neuromatrix as also seen in other diseases characterised by chronic pain. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274624</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274624</guid>        </item>
        <item>
            <title>Statins augment the chemosensitivity of colorectal cancer cells inducing epigenetic reprogramming and reducing colorectal cancer cell 'stemness' via the bone morphogenetic protein pathway</title>
            <link>http://www.medworm.com/index.php?rid=5274623&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1544%3Frss%3D1</link>
            <description>Conclusions
Statins act as DNMT inhibitors, demethylating the BMP2 promoter, activating BMP signalling, inducing differentiation of CRC cells, and reducing &amp;lsquo;stemness&amp;rsquo;. This study indicates that statins may be able to be used as differentiating agents in combined or adjuvant therapy in CRC with the CpG island methylator phenotype. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274623</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274623</guid>        </item>
        <item>
            <title>Five-year risk for advanced colorectal neoplasia after initial colonoscopy according to the baseline risk stratification: a prospective study in 2452 asymptomatic Koreans</title>
            <link>http://www.medworm.com/index.php?rid=5274622&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1537%3Frss%3D1</link>
            <description>Conclusions
The surveillance interval for low-risk patients could be extended beyond 5&amp;nbsp;years. Colonoscopic surveillance should be targeted to high-risk patients, and 3-year follow-up after initial polypectomy may be appropriate. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274622</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274622</guid>        </item>
        <item>
            <title>Genetic polymorphisms of IL-23R and IL-17A and novel insights into their associations with inflammatory bowel disease</title>
            <link>http://www.medworm.com/index.php?rid=5274621&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1527%3Frss%3D1</link>
            <description>Conclusions
The results provide insights into the genetic and epigenetic interactions in the IL-23R/IL-17 axis that are associated with elevated expression of IL-17 and IBD pathogenesis. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274621</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274621</guid>        </item>
        <item>
            <title>Randomised placebo-controlled trial of rituximab (anti-CD20) in active ulcerative colitis</title>
            <link>http://www.medworm.com/index.php?rid=5274620&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1520%3Frss%3D1</link>
            <description>Conclusions
Rituximab has no significant effect on inducing remission in moderately active UC not responding to oral steroids. There was a possible short-term response that was not sustained. Rituximab is well tolerated in UC.

Clinical trial number
NCT00261118. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274620</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
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        <item>
            <title>Systemic antibody responses to gut commensal bacteria during chronic HIV-1 infection</title>
            <link>http://www.medworm.com/index.php?rid=5274619&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1506%3Frss%3D1</link>
            <description>Conclusion
Neither HIV-associated enteropathy nor B cell dysfunction impact on the high-affinity systemic antibody responses to gut commensal bacteria. HIV-associated hypergammaglobulinaemia is therefore unlikely to be driven by induction of antimicrobiota antibodies. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274619</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274619</guid>        </item>
        <item>
            <title>Left lower quadrant abdominal pain caused by an IUCD</title>
            <link>http://www.medworm.com/index.php?rid=5274618&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1505%3Frss%3D1</link>
            <description>Clinical presentation A previously healthy 42-year-old woman presented with mild left lower quadrant abdominal pain. There was no relevant medical or family history except she had a T-shaped copper intrauterine contraceptive device (IUCD) inserted 10&amp;nbsp;years previously. The remainder of her obstetric history was non-specific and included one normal vaginal delivery. Physical examination and laboratory findings at the time of presentation were unremarkable. Plain radiographs of the abdomen identified the IUCD in the pelvic cavity (figure 1); however, the IUCD was not detected during gynaecological ultrasonography. Further abdominal CT scanning did not reveal any definite focal lesions and the IUCD was not identified (figure 2). Question What is your diagnosis? What additional tests are i...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274618</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274618</guid>        </item>
        <item>
            <title>SR-PSOX/CXCL16 plays a critical role in the progression of colonic inflammation</title>
            <link>http://www.medworm.com/index.php?rid=5274617&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1494%3Frss%3D1</link>
            <description>Conclusions
SR-PSOX/CXCL16 plays a critical role in colonic inflammation and could be a potential therapeutic target for patients with IBD. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274617</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274617</guid>        </item>
        <item>
            <title>Cryptic genetic gluten intolerance revealed by intestinal antitransglutaminase antibodies and response to gluten-free diet</title>
            <link>http://www.medworm.com/index.php?rid=5274616&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1487%3Frss%3D1</link>
            <description>Conclusions
A new form of genetic-dependent gluten intolerance has been described in which none of the usual diagnostic markers is present. Symptoms and intestinal anti-TG2 antibodies respond to a gluten free-diet. The detection of intestinal anti-TG2 antibodies by the phage-antibody libraries has an important diagnostic and therapeutic impact for the subjects with gluten-dependent intestinal or extraintestinal symptoms.

Clinical trial number
NCT00677495. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274616</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274616</guid>        </item>
        <item>
            <title>Diarrhoea and massive duodenal round cell infiltration in a 27-year-old HIV positive female</title>
            <link>http://www.medworm.com/index.php?rid=5274615&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1486%3Frss%3D1</link>
            <description>Clinical presentation A 27-year-old black female with recently diagnosed HIV infection (CD4+ T cells 9/&amp;micro;l; viral load &amp;gt;106&amp;nbsp;copies/ml) was admitted to the hospital with diarrhoea, malaise, weight loss and &amp;lsquo;heavy legs&amp;rsquo;. On clinical examination, the emaciated patient (body mass index 15.8) was in a compromised clinical condition with bilateral ankle oedema. Laboratory tests revealed several pathological values including low albumen 15&amp;nbsp;g/l (reference level: 34&amp;ndash;48) and severe pancytopenia (haemoglobin 4.5&amp;nbsp;g/dl, reference 12&amp;ndash;16; white blood cell count (WBC) 3.6/nl, reference 4&amp;ndash;10, platelet count (PLT, 61/nl, reference 140&amp;ndash;400). Mean corpuscular volume (MCV, 80.2 fl) was at the lower limit of the reference level (80&amp;ndash;99). Upper gast...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274615</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274615</guid>        </item>
        <item>
            <title>Helicobacter pylori DNA decreases pro-inflammatory cytokine production by dendritic cells and attenuates dextran sodium sulphate-induced colitis</title>
            <link>http://www.medworm.com/index.php?rid=5274614&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1479%3Frss%3D1</link>
            <description>Conclusions
This study indicates that H pylori DNA has the ability to downregulate pro-inflammatory responses from DC and this may partly explain the inverse association between H pylori and IBD. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274614</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274614</guid>        </item>
        <item>
            <title>Response of unexplained chest pain to proton pump inhibitor treatment in patients with and without objective evidence of gastro-oesophageal reflux disease</title>
            <link>http://www.medworm.com/index.php?rid=5274613&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1473%3Frss%3D1</link>
            <description>Conclusions
Unexplained chest pain in patients with endoscopic or pH-monitoring evidence of GORD tends to improve, but not resolve, with PPI therapy, whereas GORD-negative patients have little or no response. Heartburn was a poor predictor of whether patients with chest pain were GORD-positive or GORD-negative by objective testing. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274613</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274613</guid>        </item>
        <item>
            <title>Guidelines for the management of oesophageal and gastric cancer</title>
            <link>http://www.medworm.com/index.php?rid=5274612&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1449%3Frss%3D1</link>
            <description>Introduction Over the past decade the Improving Outcomes Guidance (IOG) document has led to service re-configuration in the NHS and there are now 41 specialist centres providing oesophageal and gastric cancer care in England and Wales. The National Oesophago-Gastric Cancer Audit, which was supported by the British Society of Gastroenterology, the Association of Upper Gastrointestinal Surgeons (AUGIS) and the Royal College of Surgeons of England Clinical Effectiveness Unit, and sponsored by the Department of Health, has been completed and has established benchmarks for the service as well as identifying areas for future improvements.1&amp;ndash;3 The past decade has also seen changes in the epidemiology of oesophageal and gastric cancer. The incidence of lower third and oesophago-gastric juncti...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274612</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274612</guid>        </item>
        <item>
            <title>Exploring the hidden heritability of inflammatory bowel disease</title>
            <link>http://www.medworm.com/index.php?rid=5274611&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1447%3Frss%3D1</link>
            <description>In recent years the inflammatory bowel diseases (IBD)&amp;mdash;Crohn's disease and ulcerative colitis&amp;mdash;have emerged as a model for all complex traits in the successful dissection of the molecular basis of inherited susceptibility by non-parametric linkage analysis1 2 and genome-wide association studies (GWAS).3&amp;ndash;5 The recent meta-analyses of GWAS carried out by the International Inflammatory Bowel Disease Genetics Consortium have now reported the identification of 99 susceptibility loci involved in the pathogenesis of Crohn's disease and ulcerative colitis.4 5 These successes in candidate gene discovery have provided new insights into the pathogenetic mechanisms involved in the chronic intestinal inflammation associated with IBD. These data provide strong evidence that Crohn's disea...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274611</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274611</guid>        </item>
        <item>
            <title>Abnormal brain microstructure in patients with chronic pancreatitis</title>
            <link>http://www.medworm.com/index.php?rid=5274610&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2F1445%3Frss%3D1</link>
            <description>The emergence of brain imaging studies has allowed a better knowledge of pain processing in the central nervous system in both normal and pathological conditions. In particular, abnormal loci of activation have been demonstrated in areas of the &amp;lsquo;pain matrix&amp;rsquo; involved in sensory-discriminative (primary sensory and insular cortices), affective (anterior cingulate cortex), cognitive (prefrontal cortex) and limbic (amygdala) components in patients with chronic abdominal pain as observed in irritable bowel syndrome (IBS).1 A widespread aberrant central processing of pain (central sensitisation) is observed in these patients.2 In addition, abnormal structural grey matter integrity in IBS that correlates with individual disease symptoms, duration of IBS or the personality characterist...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274610</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274610</guid>        </item>
        <item>
            <title>Highlights from this issue</title>
            <link>http://www.medworm.com/index.php?rid=5274609&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F11%2Fi%3Frss%3D1</link>
            <description>Helicobacter pylori DNA may attenuate experimental colitis IBD patients have a lower prevalence of H pylori infection compared with the rest of the population but the clinical relevance of this finding has always been intriguing. In this issue of Gut, Kao et al shed some light on this puzzle. Their work shows that H pylori DNA, which is shed into the distal intestinal track, is capable of unique immunoregulatory properties. In-vitro experiments revealed the inability of H pylori DNA to stimulate type I IFN or interleukin-12 production from mouse or human dendritic cells. H pylori DNA was also able to suppress Escherichia coli DNA production of type I IFN and IL-12. Most fascinatingly, the administration of H pylori DNA before the induction of DSS colitis significantly ameliorated the sever...</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5274609</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5274609</guid>        </item>
        <item>
            <title>Correction</title>
            <link>http://www.medworm.com/index.php?rid=5196927&amp;cid=s_30381_17_f&amp;fid=30381&amp;url=http%3A%2F%2Fgut.bmj.com%2Fcgi%2Fcontent%2Fshort%2F60%2F10%2F1444-c%3Frss%3D1</link>
            <description>Sung JJY, Chan FKL, Chen M, et al. Asia-Pacific Working Group consensus on non-variceal upper gastrointestinal bleeding. Gut 2011;60:1170&amp;ndash;7. Dr Chun Ying Wu's affiliation should be Asia-Pacific Working Group, Taiwan. (Source: Gut)</description>
            <author>Gut</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5196927</comments>
            <pubDate>Sun, 04 Sep 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5196927</guid>        </item>
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