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            type="text/xsl"?><rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#"><channel rdf:about="http://onlinelibrary.wiley.com/rss/journal/10.1111/(ISSN)1751-2980" xmlns="http://purl.org/rss/1.0/"><title>Journal of Digestive Diseases</title><description> Wiley Online Library : Journal of Digestive Diseases</description><link>http://dx.doi.org/10.1111%2F%28ISSN%291751-2980</link><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc</dc:publisher><dc:language xmlns:dc="http://purl.org/dc/elements/1.1/">en</dc:language><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/">© Chinese Medical Association Shanghai Branch; Chinese Society of Gastroenterology; Renji Hospital, Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</dc:rights><prism:issn xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">1751-2972</prism:issn><prism:eIssn xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">1751-2980</prism:eIssn><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><prism:coverDisplayDate xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">March 2012</prism:coverDisplayDate><prism:volume xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">13</prism:volume><prism:number xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">3</prism:number><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">123</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">194</prism:endingPage><image rdf:resource="http://onlinelibrary.wiley.com/store/10.1111/cdd.2012.13.issue-3/asset/cover.gif?v=1&amp;s=bc2d8a67a37ab004f1e25754f85860dc391a88ee"/><items><rdf:Seq><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00587.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00586.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00585.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00584.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00583.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00582.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00564.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00581.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00580.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00579.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00578.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00577.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00575.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00576.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00574.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00573.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00497.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00567.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00569.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00563.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00571.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00570.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00566.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00568.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00572.x"/><rdf:li rdf:resource="http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00565.x"/></rdf:Seq></items></channel><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00587.x" xmlns="http://purl.org/rss/1.0/"><title>Is obesity a risk factor for severe acute pancreatitis, occurring of complication and increasing of mortality: An update meta-analysis and systemic review</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00587.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Is obesity a risk factor for severe acute pancreatitis, occurring of complication and increasing of mortality: An update meta-analysis and systemic review</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Su Mei CHEN</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Guang Su XIONG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Shu Ming WU</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-02-14T06:35:00.40863-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2012.00587.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2012.00587.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00587.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Objective: </b> To systematically evaluate whether obesity could be a prognostic indicator for the severity, development of complication and mortality of acute pancreatitis by meta-analysis and systemic review.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Methods: </b> Eligible articles were retrieved by searching electronic databases. Clinical studies that evaluated the association between obesity and disease course of patients with acute pancreatitis were taken for meta-analysis. RevMan 4.2.8 was used for statistical analysis. Main endpoints were incidence of severe acute pancreatitis, local complication, systemic complication, and in-hospital mortality.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Results: </b> Twelve clinical studies with a total of 1483 cases were included in the analysis. Obese patients had significantly increased risk of severe acute pancreatitis (RR = 2.20, 95% CI 1.82 ∼ 2.66, <em>P</em>&lt;0.05), local complication (RR = 2.68, 95% CI 2.09∼3.43, <em>P</em>&lt;0.05), systemic complication (RR = 2.14, 95% CI 1.42∼3.21, <em>P</em>&lt;0.05) and in-hospital mortality (RR = 2.59, 95% CI 1.66∼4.03, <em>P</em>&lt;0.05) when compared with non-obese patients.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Conclusions: </b> Obesity is a definitive risk factor of morbidity and in-hospital mortality for acute pancreatitis and may be served as a prognostic indicator of acute pancreatitis.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>© 2012 The Authors. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd</p></div>]]></content:encoded><description>Objective:  To systematically evaluate whether obesity could be a prognostic indicator for the severity, development of complication and mortality of acute pancreatitis by meta-analysis and systemic review.Methods:  Eligible articles were retrieved by searching electronic databases. Clinical studies that evaluated the association between obesity and disease course of patients with acute pancreatitis were taken for meta-analysis. RevMan 4.2.8 was used for statistical analysis. Main endpoints were incidence of severe acute pancreatitis, local complication, systemic complication, and in-hospital mortality.Results:  Twelve clinical studies with a total of 1483 cases were included in the analysis. Obese patients had significantly increased risk of severe acute pancreatitis (RR = 2.20, 95% CI 1.82 ∼ 2.66, P&lt;0.05), local complication (RR = 2.68, 95% CI 2.09∼3.43, P&lt;0.05), systemic complication (RR = 2.14, 95% CI 1.42∼3.21, P&lt;0.05) and in-hospital mortality (RR = 2.59, 95% CI 1.66∼4.03, P&lt;0.05) when compared with non-obese patients.Conclusions:  Obesity is a definitive risk factor of morbidity and in-hospital mortality for acute pancreatitis and may be served as a prognostic indicator of acute pancreatitis.© 2012 The Authors. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd</description></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00586.x" xmlns="http://purl.org/rss/1.0/"><title>Autoimmune pancreatitis – A novel disease?</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00586.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Autoimmune pancreatitis – A novel disease?</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Guido NJ TYTGAT</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-02-10T01:24:28.029348-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2012.00586.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2012.00586.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00586.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00585.x" xmlns="http://purl.org/rss/1.0/"><title>IgG4-related sclerosing cholangitis with autoimmune pancreatitis and periaortitis: A case report and review of the literature</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00585.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">IgG4-related sclerosing cholangitis with autoimmune pancreatitis and periaortitis: A case report and review of the literature</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Hui Jun SHU</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Bei TAN</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Hua Dan XUE</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ai Ming YANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jia Ming QIAN</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-02-09T11:18:31.041748-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2012.00585.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2012.00585.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00585.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>© 2012 The Authors. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</p></div>]]></content:encoded><description>© 2012 The Authors. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</description></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00584.x" xmlns="http://purl.org/rss/1.0/"><title>A case of pancreatic carcinoma mimicking diffuse-type autoimmune pancreatitis: Important diagnostic role of pancreatic juice cytology using endoscopic naso-pancreatic drainage</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00584.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">A case of pancreatic carcinoma mimicking diffuse-type autoimmune pancreatitis: Important diagnostic role of pancreatic juice cytology using endoscopic naso-pancreatic drainage</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Hiroyuki MATSUBAYASHI</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Keiko SASAKI</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Kaori NAGATA</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Hideyuki KANEMOTO</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-02-09T11:15:28.960892-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2012.00584.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2012.00584.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00584.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>© 2012 The Authors. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</p></div>]]></content:encoded><description>© 2012 The Authors. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</description></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00583.x" xmlns="http://purl.org/rss/1.0/"><title>Relationship between pancreatic/extrapancreatic lesions and serum levels of IgG/IgG4 in IgG4-related diseases</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00583.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Relationship between pancreatic/extrapancreatic lesions and serum levels of IgG/IgG4 in IgG4-related diseases</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Hisato IGARASHI</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Tetsuhide ITO</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Takamasa OONO</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Taichi NAKAMURA</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Nao FUJIMORI</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Yusuke NIINA</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Masayuki HIJIOKA</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Masahiko UCHIDA</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ringaku LEE</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Risa IWAO</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Kazuhiko Nakamura</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Kazuhiro Kotoh</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ryoichi TAKAYANAGI</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-02-06T14:47:35.547322-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2012.00583.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2012.00583.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00583.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Objective:</b> The concept of immunoglobulin (Ig) G4-related diseases has recently been proposed. Some researchers have suggested that serum IgG4 level is an indicator for diagnosis and disease activity. We investigated the relationship between the number of involved organ/region and serum IgG/IgG4 levels.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Methods:</b> Numbers of pancreatic/extrapancreatic lesions and serum IgG and IgG4 levels were examined in 46 patients with IgG4-related diseases at diagnosis prior to the initiation of steroid treatment. The relationship between serum IgG and IgG4 levels and the number of regions involved were examined by groups: group A (1 region involved, <em>n</em>= 7), group B (2 regions, <em>n</em>= 11), group C (3 regions, <em>n</em>= 12), group D (4 regions, <em>n</em>= 9), and group E (5–7 regions, <em>n</em>= 7).</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Results:</b> Both serum IgG and IgG4 levels increased with inflamed region numbers. Mean serum IgG were 1511, 1865, 2092, 2329 and 3259 mg/dL in group A, B, C, D and E, while mean IgG4 levels were 399, 470, 470, 986 and 1649 mg/dL, respectively. Regression analysis also suggested that serum IgG4 was correlated with the number of regions involved. Additionally, serum IgG4 was higher in patients with multiple lesions when accompanied by sclerosing sialadenitis.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Conclusion:</b> Patients with IgG4-related disease of high serum IgG and IgG4 levels should be systematically examined for involved lesions.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>© 2012 The Authors. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</p></div>]]></content:encoded><description>Objective: The concept of immunoglobulin (Ig) G4-related diseases has recently been proposed. Some researchers have suggested that serum IgG4 level is an indicator for diagnosis and disease activity. We investigated the relationship between the number of involved organ/region and serum IgG/IgG4 levels.Methods: Numbers of pancreatic/extrapancreatic lesions and serum IgG and IgG4 levels were examined in 46 patients with IgG4-related diseases at diagnosis prior to the initiation of steroid treatment. The relationship between serum IgG and IgG4 levels and the number of regions involved were examined by groups: group A (1 region involved, n= 7), group B (2 regions, n= 11), group C (3 regions, n= 12), group D (4 regions, n= 9), and group E (5–7 regions, n= 7).Results: Both serum IgG and IgG4 levels increased with inflamed region numbers. Mean serum IgG were 1511, 1865, 2092, 2329 and 3259 mg/dL in group A, B, C, D and E, while mean IgG4 levels were 399, 470, 470, 986 and 1649 mg/dL, respectively. Regression analysis also suggested that serum IgG4 was correlated with the number of regions involved. Additionally, serum IgG4 was higher in patients with multiple lesions when accompanied by sclerosing sialadenitis.Conclusion: Patients with IgG4-related disease of high serum IgG and IgG4 levels should be systematically examined for involved lesions.© 2012 The Authors. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</description></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00582.x" xmlns="http://purl.org/rss/1.0/"><title>Differentiation of autoimmune pancreatitis with pancreatic carcinoma remains a challenge to physicians</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00582.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Differentiation of autoimmune pancreatitis with pancreatic carcinoma remains a challenge to physicians</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Pei Li GONG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Tao Tao LIU</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Xi Zhong SHEN</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-02-06T14:47:21.004775-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2012.00582.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2012.00582.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00582.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Objective:</b> The aim of this study was to summarize the clinical features of autoimmune pancreatitis (AIP) and review the advances in the differential diagnosis with pancreatic carcinoma, thus helping to make a correct diagnosis and avoiding unnecessary surgery in clinical practice.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Methods:</b> Five patients diagnosed as AIP in accordance with HISORt criteria in Zhongshan Hospital, Fudan University from 2008 to 2010 were enrolled in the study. Clinical features were analyzed and related literatures were reviewed.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Results:</b> Four of the 5 patients had obstructive jaundice, abdominal pain and weight loss, together with serological changes such as elevation of alkaline phosphatase (ALP), γ-glutamyltranspeptidase (γ-GT) and serum bilirubin. Two of them showed high serum IgG4 levels. Both focal and diffuse changes were found on computed tomography (CT) and magnetic resonance imaging (MRI). Three of our patients had operation performed because of a high suspicion of malignant tumor, and steroid therapy was administered to the other two patients diagnosed initially as AIP. No relapse was observed during follow-up.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Conclusion:</b> Although some recent advances have been made in helping the diagnosis of AIP, the differentiation of AIP with pancreatic carcinoma is still a challenge. In clinical practice, it must be reminded to exclude AIP before making the diagnosis of pancreatic carcinoma.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>© 2012 The Authors. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</p></div>]]></content:encoded><description>Objective: The aim of this study was to summarize the clinical features of autoimmune pancreatitis (AIP) and review the advances in the differential diagnosis with pancreatic carcinoma, thus helping to make a correct diagnosis and avoiding unnecessary surgery in clinical practice.Methods: Five patients diagnosed as AIP in accordance with HISORt criteria in Zhongshan Hospital, Fudan University from 2008 to 2010 were enrolled in the study. Clinical features were analyzed and related literatures were reviewed.Results: Four of the 5 patients had obstructive jaundice, abdominal pain and weight loss, together with serological changes such as elevation of alkaline phosphatase (ALP), γ-glutamyltranspeptidase (γ-GT) and serum bilirubin. Two of them showed high serum IgG4 levels. Both focal and diffuse changes were found on computed tomography (CT) and magnetic resonance imaging (MRI). Three of our patients had operation performed because of a high suspicion of malignant tumor, and steroid therapy was administered to the other two patients diagnosed initially as AIP. No relapse was observed during follow-up.Conclusion: Although some recent advances have been made in helping the diagnosis of AIP, the differentiation of AIP with pancreatic carcinoma is still a challenge. In clinical practice, it must be reminded to exclude AIP before making the diagnosis of pancreatic carcinoma.© 2012 The Authors. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</description></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00564.x" xmlns="http://purl.org/rss/1.0/"><title>Clinical outcomes of palliative self-expanding metallic stents in patients with malignant colorectal obstruction</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00564.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Clinical outcomes of palliative self-expanding metallic stents in patients with malignant colorectal obstruction</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Byung Chang KIM</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Kyung Su HAN</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Chang Won HONG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Dae Kyung SOHN</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ji Won PARK</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Sung Chan PARK</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Sun Young KIM</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ji-Yeon BAEK</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Hyo Seong CHOI</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Hee Jin CHANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Dae Yong KIM</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jae Hwan OH</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-02-06T14:44:46.526591-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2012.00564.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2012.00564.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00564.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Objective:</b> Self-expanding metallic stents (SEMS) are useful palliative options in unresectable obstructive tumors and as bridge to surgery in malignant colorectal obstruction. The aim of this study was to evaluate the clinical outcomes of SEMS in palliation for colorectal malignant obstruction.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Methods:</b> Data of 104 malignant colorectal obstructive patients who underwent SEMS insertions at the National Cancer Center (NCC), Korea from January 2004 to June 2008 were analyzed retrospectively. Clinical outcomes and complications for palliative SEMS insertion (<em>n </em>= 54) were analyzed. Covered stents were used in 9 insertions and uncovered stents in 45.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Results:</b> SEMS were placed in the right colon in two patients, and in the left colon and rectum in all other patients. For primary SEMS insertion, technical success (TS) rate was 87.0% and clinical success (CS) rate 89.4%, while there were early complications in 24.0% insertions and late complications in 23.4%. There was no procedure-related mortality. Stent migration was greater in the case of small stent diameter and the covered type of SEMS. Median time to obstruction and migration were 85 and 101 days, respectively. TS and CS for SEMS reinsertion were comparable with those for primary SEMS insertion.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Conclusions:</b> Palliative SEMS are effective and favorable procedures for malignant colorectal obstruction but have some complications. Stent migration is associated with covered type and small diameter stent and other factors do not affect the stent complication in the present study and adverse events that occurred are manageable.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>© 2012 The Authors. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</p></div>]]></content:encoded><description>Objective: Self-expanding metallic stents (SEMS) are useful palliative options in unresectable obstructive tumors and as bridge to surgery in malignant colorectal obstruction. The aim of this study was to evaluate the clinical outcomes of SEMS in palliation for colorectal malignant obstruction.Methods: Data of 104 malignant colorectal obstructive patients who underwent SEMS insertions at the National Cancer Center (NCC), Korea from January 2004 to June 2008 were analyzed retrospectively. Clinical outcomes and complications for palliative SEMS insertion (n = 54) were analyzed. Covered stents were used in 9 insertions and uncovered stents in 45.Results: SEMS were placed in the right colon in two patients, and in the left colon and rectum in all other patients. For primary SEMS insertion, technical success (TS) rate was 87.0% and clinical success (CS) rate 89.4%, while there were early complications in 24.0% insertions and late complications in 23.4%. There was no procedure-related mortality. Stent migration was greater in the case of small stent diameter and the covered type of SEMS. Median time to obstruction and migration were 85 and 101 days, respectively. TS and CS for SEMS reinsertion were comparable with those for primary SEMS insertion.Conclusions: Palliative SEMS are effective and favorable procedures for malignant colorectal obstruction but have some complications. Stent migration is associated with covered type and small diameter stent and other factors do not affect the stent complication in the present study and adverse events that occurred are manageable.© 2012 The Authors. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</description></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00581.x" xmlns="http://purl.org/rss/1.0/"><title>Anxiety and depression in various functional gastrointestinal disorders: Do differences exist?</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00581.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Anxiety and depression in various functional gastrointestinal disorders: Do differences exist?</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Juanda Leo HARTONO</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Sanjiv MAHADEVA</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Khean-Lee GOH</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-02-06T14:44:37.35242-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2012.00581.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2012.00581.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00581.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Objective:</b> To examine the differences in the prevalence of anxiety and depression in patients with functional dyspepsia (FD), nonerosive reflux disease (NERD), irritable bowel syndrome (IBS) and healthy controls.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Methods:</b> Consecutive patients attending the Endoscopy Unit of Faculty of Medicine, University of Malaya were interviewed. All FGIDs were diagnosed according to the Rome criteria. Anxiety and depression were diagnosed using a locally validated version of the Hospital Anxiety and Depression Scale.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Results:</b> A total of 248 subjects were recruited (62 in FD, NERD, IBS and control groups, respectively) with no differences in basic demography. There was a higher prevalence of anxiety and depression in FD, NERD and IBS groups compared with the control group (43.5%, 45.2% and 67.7% <em>vs</em> 14.5%, <em>P</em> &lt; 0.001; and 22.6%, 33.9% and 38.7% <em>vs</em> 6.5%, <em>P</em> &lt; 0.0001). IBS patients had a higher rate of anxiety than FD (67.7% vs 43.5%, <em>P</em>= 0.01) and NERD (67.7% vs 45.2%, <em>P</em>= 0.02), while no significant differences in depression rates were observed among all three groups.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Conclusion:</b> Anxiety is more common in IBS compared to FD and NERD, indicating a possible causal link in the former.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>© 2012 The Authors. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</p></div>]]></content:encoded><description>Objective: To examine the differences in the prevalence of anxiety and depression in patients with functional dyspepsia (FD), nonerosive reflux disease (NERD), irritable bowel syndrome (IBS) and healthy controls.Methods: Consecutive patients attending the Endoscopy Unit of Faculty of Medicine, University of Malaya were interviewed. All FGIDs were diagnosed according to the Rome criteria. Anxiety and depression were diagnosed using a locally validated version of the Hospital Anxiety and Depression Scale.Results: A total of 248 subjects were recruited (62 in FD, NERD, IBS and control groups, respectively) with no differences in basic demography. There was a higher prevalence of anxiety and depression in FD, NERD and IBS groups compared with the control group (43.5%, 45.2% and 67.7% vs 14.5%, P &lt; 0.001; and 22.6%, 33.9% and 38.7% vs 6.5%, P &lt; 0.0001). IBS patients had a higher rate of anxiety than FD (67.7% vs 43.5%, P= 0.01) and NERD (67.7% vs 45.2%, P= 0.02), while no significant differences in depression rates were observed among all three groups.Conclusion: Anxiety is more common in IBS compared to FD and NERD, indicating a possible causal link in the former.© 2012 The Authors. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</description></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00580.x" xmlns="http://purl.org/rss/1.0/"><title>Fractalkine as a marker for assessment of severe acute pancreatitis</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00580.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Fractalkine as a marker for assessment of severe acute pancreatitis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Li Ya HUANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ping CHEN</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ling Xiao XU</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Yu Fen ZHOU</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Wei Guang LI</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Yao Zong YUAN</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-01-16T19:02:46.564779-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2012.00580.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2012.00580.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00580.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Objective:</b> Chemokine fractalkine (FKN) plays an important role in the development of inflammatory diseases. The aim of this study was to study the role of FKN in the development of severe acute pancreatitis (SAP).</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Methods:</b> Serum FKN level in SAP rat model was determined by enzyme linked immunosorbent assay (ELISA). The FKN mRNA and protein levels in pancreas tissue were measured by reverse transcriptase polymerase chain reaction (RT-PCR), Western blot, and immunohistochemistry.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Results:</b> Serum FKN level in SAP rat increased significantly (<em>P</em> &lt; 0.05). FKN mRNA and protein levels in pancreas tissue also increased significantly (<em>P</em> &lt; 0.05) reaching the peak at 16 h. FKN mRNA and protein in lung tissue increased and reached the peak at 16 h (<em>P</em> &lt; 0.05). Meanwhile, FKN in kidney tissue increased and reached the peak at 48 h (<em>P</em> &lt; 0.05). Immunohistochemistry showed the overexpression of FKN in pancreas, lung and kidney tissues.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Conclusion:</b> FKN was involved in the progression of SAP and might be a valuable marker for the assessment of SAP.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>© 2012 The Authors. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</p></div>]]></content:encoded><description>Objective: Chemokine fractalkine (FKN) plays an important role in the development of inflammatory diseases. The aim of this study was to study the role of FKN in the development of severe acute pancreatitis (SAP).Methods: Serum FKN level in SAP rat model was determined by enzyme linked immunosorbent assay (ELISA). The FKN mRNA and protein levels in pancreas tissue were measured by reverse transcriptase polymerase chain reaction (RT-PCR), Western blot, and immunohistochemistry.Results: Serum FKN level in SAP rat increased significantly (P &lt; 0.05). FKN mRNA and protein levels in pancreas tissue also increased significantly (P &lt; 0.05) reaching the peak at 16 h. FKN mRNA and protein in lung tissue increased and reached the peak at 16 h (P &lt; 0.05). Meanwhile, FKN in kidney tissue increased and reached the peak at 48 h (P &lt; 0.05). Immunohistochemistry showed the overexpression of FKN in pancreas, lung and kidney tissues.Conclusion: FKN was involved in the progression of SAP and might be a valuable marker for the assessment of SAP.© 2012 The Authors. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</description></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00579.x" xmlns="http://purl.org/rss/1.0/"><title>Inflammatory bowel disease since the 21st Century in China–Turning challenges into opportunities</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00579.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Inflammatory bowel disease since the 21st Century in China–Turning challenges into opportunities</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Qin OUYANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Lin Yun XUE</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-01-09T13:04:53.010705-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2012.00579.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2012.00579.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00579.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>© 2012 The Authors. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</p></div>]]></content:encoded><description>© 2012 The Authors. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</description></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00578.x" xmlns="http://purl.org/rss/1.0/"><title>Promoter Methylation Regulates Cigarette Smoke-Stimulated Cyclooxygenase-2 Expression in Esophageal Squamous Carcinoma Cells</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00578.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Promoter Methylation Regulates Cigarette Smoke-Stimulated Cyclooxygenase-2 Expression in Esophageal Squamous Carcinoma Cells</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Xin Ying MENG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Sheng Tao ZHU</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Qiao Zhi ZHOU</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Peng LI</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Yong Jun WANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Shu Tian ZHANG</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-01-09T13:04:14.583591-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2012.00578.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2012.00578.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00578.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">ABSTRACT</h3><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Objective: </b> Cigarette smoke extracts (CSE) could promote esophageal squamous cell carcinoma (ESCC) through up regulating cyclooxygenase-2(COX-2) expression. Promoter methylation mediates transcriptional modulation of COX-2 gene. We tried to explore whether COX-2 promoter methylation regulates COX-2 expression and functional activity in ESCC cells exposed to CSE.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Methods </b> The methylation status of the COX-2 promoter in two human ESCC cell lines, EC109 and TE-1, was examined using bisulfite sequencing analysis. COX-2 mRNA and protein expression were detected by RT-PCR and Western blot. Prostaglandin (PG) E<sub>2</sub> was examined by ELISA.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Results </b> The promoter was densely methylated in TE-1 which had low level of COX-2 expression and less methylated in EC109 with relatively high level of COX-2 expression. Stimulation by cigarette smoke ethanol extract (EE) resulted in increased COX-2 expression in EC109, but not in TE-1. Treatment with 5-aza-deoxycytidine (5-aza-DC) demethylated the promoter and up-regulated COX-2 expression as well as PGE<sub>2</sub> production in TE-1, especially followed by stimulation with EE. No significant effect was observed in EC109.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Conclusion </b> These findings suggest that the promoter methylation may be one of the mechanisms regulating COX-2 expression in ESCC in response to stimulation of CSE.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>© 2012 The Author. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</p></div>]]></content:encoded><description>Objective:  Cigarette smoke extracts (CSE) could promote esophageal squamous cell carcinoma (ESCC) through up regulating cyclooxygenase-2(COX-2) expression. Promoter methylation mediates transcriptional modulation of COX-2 gene. We tried to explore whether COX-2 promoter methylation regulates COX-2 expression and functional activity in ESCC cells exposed to CSE.Methods  The methylation status of the COX-2 promoter in two human ESCC cell lines, EC109 and TE-1, was examined using bisulfite sequencing analysis. COX-2 mRNA and protein expression were detected by RT-PCR and Western blot. Prostaglandin (PG) E2 was examined by ELISA.Results  The promoter was densely methylated in TE-1 which had low level of COX-2 expression and less methylated in EC109 with relatively high level of COX-2 expression. Stimulation by cigarette smoke ethanol extract (EE) resulted in increased COX-2 expression in EC109, but not in TE-1. Treatment with 5-aza-deoxycytidine (5-aza-DC) demethylated the promoter and up-regulated COX-2 expression as well as PGE2 production in TE-1, especially followed by stimulation with EE. No significant effect was observed in EC109.Conclusion  These findings suggest that the promoter methylation may be one of the mechanisms regulating COX-2 expression in ESCC in response to stimulation of CSE.© 2012 The Author. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</description></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00577.x" xmlns="http://purl.org/rss/1.0/"><title>Clinical prognostic variables in young patients (under 40 years) with hepatitis B virus-associated hepatocellular carcinoma</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00577.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Clinical prognostic variables in young patients (under 40 years) with hepatitis B virus-associated hepatocellular carcinoma</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Fotini Manizate</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Wei Luan</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Gerald A. Villanueva</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Nuh N. Rahbari</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Herman T. Yee</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Daniel M Labow</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Qin Wang</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Spiros P. Hiotis</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-01-09T13:03:50.780653-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2012.00577.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2012.00577.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00577.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Objectiove: </b> Hepatocellular carcinoma <b>(</b>HCC) patients diagnosed early (within Milan criteria) have the best chance for long-term survival. However, many Hepatitis B virus (HBV)-associated HCC develop outside of current practice guidelines for HCC screening. The purpose of this study is to determine the impact of withholding cancer screening in chronic HBV patients who do not meet current screening recommendations.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Methods: </b> Patients who presented to a single New York public hospital with HCC were assessed for HCC risk factors, cirrhosis, and tumor-specific factors. Eligibility for liver transplantation or resection with favorable outcome was determined by applying Milan criteria.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Results: </b> 93 patients developed HCC in association with HBV; and 18/93 (19%) developed cancer at a young age (under age 40). Cirrhosis was infrequently associated with HCC in this group, with the majority of cancers occurring in non-cirrhotic patients (12/18, 67%). Patients who developed HCC outside of American Association for the Study of Liver Diseases (AASLD) cancer screening recommendations (young age, non-cirrhotic) were eligible for liver transplantation or resection with favorable outcome in 0/12 (0%) cases (by application of Milan criteria). This compared unfavorably to the remaining patients diagnosed within AASLD screening recommendations, who did meet Milan criteria upon initial diagnosis in 14/81 (17%) cases.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Conclusions: </b> Current guidelines for HCC screening in patients with HBV may lead to delay in diagnosis in non-cirrhotic patients under age 40. Consideration should be given to modifying current recommendations to advocate entering HBV patients into a cancer-screening program at a younger age.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>© 2012 The Author. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</p></div>]]></content:encoded><description>Objectiove:  Hepatocellular carcinoma (HCC) patients diagnosed early (within Milan criteria) have the best chance for long-term survival. However, many Hepatitis B virus (HBV)-associated HCC develop outside of current practice guidelines for HCC screening. The purpose of this study is to determine the impact of withholding cancer screening in chronic HBV patients who do not meet current screening recommendations.Methods:  Patients who presented to a single New York public hospital with HCC were assessed for HCC risk factors, cirrhosis, and tumor-specific factors. Eligibility for liver transplantation or resection with favorable outcome was determined by applying Milan criteria.Results:  93 patients developed HCC in association with HBV; and 18/93 (19%) developed cancer at a young age (under age 40). Cirrhosis was infrequently associated with HCC in this group, with the majority of cancers occurring in non-cirrhotic patients (12/18, 67%). Patients who developed HCC outside of American Association for the Study of Liver Diseases (AASLD) cancer screening recommendations (young age, non-cirrhotic) were eligible for liver transplantation or resection with favorable outcome in 0/12 (0%) cases (by application of Milan criteria). This compared unfavorably to the remaining patients diagnosed within AASLD screening recommendations, who did meet Milan criteria upon initial diagnosis in 14/81 (17%) cases.Conclusions:  Current guidelines for HCC screening in patients with HBV may lead to delay in diagnosis in non-cirrhotic patients under age 40. Consideration should be given to modifying current recommendations to advocate entering HBV patients into a cancer-screening program at a younger age.© 2012 The Author. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</description></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00575.x" xmlns="http://purl.org/rss/1.0/"><title>Lansoprazole-based sequential and concomitant therapy for the first-line Helicobacter pylori eradication</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00575.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Lansoprazole-based sequential and concomitant therapy for the first-line Helicobacter pylori eradication</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Yao-Kang HUANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Meng-Chieh WU</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Sophie S.W. WANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Chao-Hung KUO</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Yi-Chern LEE</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ling-Li CHANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Chung-Shi WANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Yen-Hsu CHEN</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Wen-Ming WANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Deng-Chyang WU</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Fu-Chen KUO</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-01-09T13:03:44.698829-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2012.00575.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2012.00575.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00575.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">ABSTRACT</h3><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>AIM: </b> Growing evidences have suggested that the sequential and concomitant quadruple therapies for <em>Helicobacter pylori</em> (<em>H. pylori</em>) eradication are more efficacious than original triple therapy. The aim of this prospective study was to compare the efficacy of the first-line lansoprazole-based sequential therapy and concomitant therapy (lansoprazole, amoxicillin, clarithromycin and metronidazole) for <em>H. pylori</em> eradication.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>METHODS: </b> A total of 169 patients with <em>H. pylori</em> infection were randomly assigned to either sequential therapy group (<em>n</em>= 85) or concomitant therapy group (<em>n</em>= 84). Follow-up endoscopy or urea breath test was examined at least 12 weeks after eradication.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>RESULTS: </b> Comparable <em>H. pylori</em> eradication rate was observed in both sequential therapy and concomitant therapy groups by either intention-to-treat analysis [sequential, 80.0% (68/85) <em>vs.</em> concomitant, 88.1% (74/84); <em>P</em>= 0.27] or per protocol analysis [sequential, 85.3% (64/75) <em>vs</em> concomitant, 94.6% (70/74); <em>P</em>= 0.60]. Adverse effects were reported and good compliance was observed in both groups (<em>P</em>= 0.72). Although dual antibiotics resistance affected the therapeutic efficacy of sequential therapy (<em>P</em>= 0.03), not concomitant therapy (<em>P</em>= 0.74), it was not an independent factor to predict the treatment outcome.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>CONCLUSION: </b> The first-line lansoprazole-based sequential therapy and concomitant therapy were well-tolerated and comparable in terms of <em>H. pylori</em> eradication rate.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>© 2012 The Author. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</p></div>]]></content:encoded><description>AIM:  Growing evidences have suggested that the sequential and concomitant quadruple therapies for Helicobacter pylori (H. pylori) eradication are more efficacious than original triple therapy. The aim of this prospective study was to compare the efficacy of the first-line lansoprazole-based sequential therapy and concomitant therapy (lansoprazole, amoxicillin, clarithromycin and metronidazole) for H. pylori eradication.METHODS:  A total of 169 patients with H. pylori infection were randomly assigned to either sequential therapy group (n= 85) or concomitant therapy group (n= 84). Follow-up endoscopy or urea breath test was examined at least 12 weeks after eradication.RESULTS:  Comparable H. pylori eradication rate was observed in both sequential therapy and concomitant therapy groups by either intention-to-treat analysis [sequential, 80.0% (68/85) vs. concomitant, 88.1% (74/84); P= 0.27] or per protocol analysis [sequential, 85.3% (64/75) vs concomitant, 94.6% (70/74); P= 0.60]. Adverse effects were reported and good compliance was observed in both groups (P= 0.72). Although dual antibiotics resistance affected the therapeutic efficacy of sequential therapy (P= 0.03), not concomitant therapy (P= 0.74), it was not an independent factor to predict the treatment outcome.CONCLUSION:  The first-line lansoprazole-based sequential therapy and concomitant therapy were well-tolerated and comparable in terms of H. pylori eradication rate.© 2012 The Author. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</description></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00576.x" xmlns="http://purl.org/rss/1.0/"><title>Once-daily versus multiple-daily mesalamine for patients with ulcerative colitis: a meta-analysis</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00576.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Once-daily versus multiple-daily mesalamine for patients with ulcerative colitis: a meta-analysis</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jin Lu TONG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Chen Peng ZHANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Mei Lan HUANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Xi Tao XU</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Yu Qi QIAO</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Zhi Hua RAN</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-01-09T13:03:41.097466-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2012.00576.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2012.00576.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00576.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">ABSTRACT</h3><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Objective: </b> To systematically review the efficacy and safety of <b>once-daily</b> (OD) for the treatment of <b>ulcerative colitis</b> (UC) compared with <b>multiple-daily</b> (MD).</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Methods: </b> We searched electronic database up to July, 2011 for related studies evaluating the efficacy of OD versus MD for the treatment of UC. Only randomized controlled trials (RCTs) were considered eligible. The primary outcome was remission rates or relapse rates using an intention-to-treat (ITT) analysis and a per-protocol (PP) analysis. Pooled relative risk (RR) and 95% confidence intervals (95% CI) were calculated. Publication bias was assessed with funnel plot.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Results: </b> We identified 10 randomized trials, including nine full-text manuscripts and one abstract. Once-daily dosing mesalamine was shown to be as effective as MD dosing for maintenance of clinical remission in patients with quiescent UC (RR = 1.00, 95 % CI 0.89 – 1.12) by ITT analysis. For active UC, there was mild significant benefit achieved by once-daily dosing mesalamine compared with MD dosing (RR = 0.80, 95 % CI 0.64 – 0.99). Total adverse events were similar with OD <em>vs.</em> MD mesalamine in quiescent UC (RR = 1.06, 95 % CI 0.93 – 1.20). Compliance with OD was slightly better than MD (RR = 0.92, 95 % CI 0.82 – 1.03).</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Conclusions: </b> Once-daily mesalamine is similarly effective with a comparable safety profile to multiple-daily regimens for the maintenance treatment of ulcerative colitis, even more effective for inducing remission in active UC.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>© 2012 The Author. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</p></div>]]></content:encoded><description>Objective:  To systematically review the efficacy and safety of once-daily (OD) for the treatment of ulcerative colitis (UC) compared with multiple-daily (MD).Methods:  We searched electronic database up to July, 2011 for related studies evaluating the efficacy of OD versus MD for the treatment of UC. Only randomized controlled trials (RCTs) were considered eligible. The primary outcome was remission rates or relapse rates using an intention-to-treat (ITT) analysis and a per-protocol (PP) analysis. Pooled relative risk (RR) and 95% confidence intervals (95% CI) were calculated. Publication bias was assessed with funnel plot.Results:  We identified 10 randomized trials, including nine full-text manuscripts and one abstract. Once-daily dosing mesalamine was shown to be as effective as MD dosing for maintenance of clinical remission in patients with quiescent UC (RR = 1.00, 95 % CI 0.89 – 1.12) by ITT analysis. For active UC, there was mild significant benefit achieved by once-daily dosing mesalamine compared with MD dosing (RR = 0.80, 95 % CI 0.64 – 0.99). Total adverse events were similar with OD vs. MD mesalamine in quiescent UC (RR = 1.06, 95 % CI 0.93 – 1.20). Compliance with OD was slightly better than MD (RR = 0.92, 95 % CI 0.82 – 1.03).Conclusions:  Once-daily mesalamine is similarly effective with a comparable safety profile to multiple-daily regimens for the maintenance treatment of ulcerative colitis, even more effective for inducing remission in active UC.© 2012 The Author. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</description></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00574.x" xmlns="http://purl.org/rss/1.0/"><title>The efficacy of fenofibrate in Chinese patients with primary biliary cirrhosis partially responding to ursodeoxycholic acid therapy</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00574.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">The efficacy of fenofibrate in Chinese patients with primary biliary cirrhosis partially responding to ursodeoxycholic acid therapy</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Xiao Feng Han</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Qi Xia Wang</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Yuan Liu</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Zheng Rui You</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Zhao Lian Bian</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">De Kai Qiu</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Xiong Ma</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-01-09T13:00:44.027539-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2012.00574.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2012.00574.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00574.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Objective: </b> The aim of the study was to investigate the efficacy of fenofibrate combination therapy in Chinese patients with primary biliary cirrhosis (PBC) who had partial response to standard doses of ursodeoxycholic acid (UDCA) for at least one year</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Methods: </b> PBC patients were treated with UDCA (13–15mg/kg/d) for more than one year. The biochemical response to UDCA treatment was evaluated after treatment. Fenofibrate (200 mg/d) was added to 22 patients with partial response to UDCA.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Results: </b> In patients with partial response to UDCA, serum alkaline phosphatase (ALP) and γ-glutamyltranspeptidase (γ-GT) levels significantly decreased after 3-month combination therapy of UDCA and fenofibrate, 68% of these patients even had normal value of serum ALP level after 3-month treatment. Serum triglycercide (TG) and cholesterol (TC) levels were improved, alanine transaminase (ALT) and aspartate transaminase (AST) were also decreased during the combination therapy. However, fenofibrate had no significant effects on serum bilirubin levels. The improvement of liver biochemical tests was maintained in some patients with long-term therapy (at least 6 months). No obvious side effects were observed in patients taking fenofibrate</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Conclusions: </b> Fenofibrate is effective for improving liver biochemical tests in the patients who have partial response to UDCA monotherapy. It is worthy to explore the efficacy of fenofibrate on histological changes in PBC patients</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p>© 2012 The Authors. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd</p></div>]]></content:encoded><description>Objective:  The aim of the study was to investigate the efficacy of fenofibrate combination therapy in Chinese patients with primary biliary cirrhosis (PBC) who had partial response to standard doses of ursodeoxycholic acid (UDCA) for at least one yearMethods:  PBC patients were treated with UDCA (13–15mg/kg/d) for more than one year. The biochemical response to UDCA treatment was evaluated after treatment. Fenofibrate (200 mg/d) was added to 22 patients with partial response to UDCA.Results:  In patients with partial response to UDCA, serum alkaline phosphatase (ALP) and γ-glutamyltranspeptidase (γ-GT) levels significantly decreased after 3-month combination therapy of UDCA and fenofibrate, 68% of these patients even had normal value of serum ALP level after 3-month treatment. Serum triglycercide (TG) and cholesterol (TC) levels were improved, alanine transaminase (ALT) and aspartate transaminase (AST) were also decreased during the combination therapy. However, fenofibrate had no significant effects on serum bilirubin levels. The improvement of liver biochemical tests was maintained in some patients with long-term therapy (at least 6 months). No obvious side effects were observed in patients taking fenofibrateConclusions:  Fenofibrate is effective for improving liver biochemical tests in the patients who have partial response to UDCA monotherapy. It is worthy to explore the efficacy of fenofibrate on histological changes in PBC patients© 2012 The Authors. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd</description></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00573.x" xmlns="http://purl.org/rss/1.0/"><title>Endoscopic removal of a long sharp metallic foreign body by a snared magnet: An attractive solution</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00573.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Endoscopic removal of a long sharp metallic foreign body by a snared magnet: An attractive solution</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Marcy Coash </dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">George Y. Wu</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-01-09T12:59:13.606673-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2012.00573.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2012.00573.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2012.00573.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>© 2012 The Authors. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</p></div>]]></content:encoded><description>© 2012 The Authors. Journal of Digestive Diseases © 2012 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.</description></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00497.x" xmlns="http://purl.org/rss/1.0/"><title>Low-dose hepatic computed tomography (CT) perfusion imaging and its preliminary application</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00497.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Low-dose hepatic computed tomography (CT) perfusion imaging and its preliminary application</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Wen Jing WANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Liang ZHONG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Xiao Lan HUA</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Yu FAN</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Lan LI</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jian Rong XU</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2011-03-22T06:43:45.339093-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2011.00497.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2011.00497.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00497.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">no</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<h3 xhtml="http://www.w3.org/1999/xhtml" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib">Abstract</h3><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>OBJECTIVE:</b> Computed tomography perfusion imaging (CTPI) is a rapid and non-invasive functional imaging method that reflects hemodynamic changes of liver diseases. However, large radiation dosage limits its clinical applications. We aimed to evaluate the feasibility of low-dose CTPI in normal liver and its preliminary application in hepatocellular carcinoma (HCC).</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Methods:</b> CTPI was performed in 34 healthy volunteers randomly divided into three groups with applications of different tube currents, including conventional-dose group, medium-dose group, and low-dose group. The perfusion parameters of each group were compared and low-dose CTPI was performed in 13 patients with HCC.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Results:</b> Relatively satisfactory images and perfusion parameters of liver CTPI were acquired with different tube currents. There were no significant differences between the parameters of the three groups (<em>P </em>&gt; 0.05). The effective dosage of conventional, medium, and low-dose liver CTPI were 19.62 mSv, 12.61 mSv, and 7.01 mSv, respectively. The radiation dosage of low-dose liver CTPI was reduced to 64.27% compared with that of the conventional group. HBF, HPI, and HAP of HCC were higher than the background liver parenchyma and normal liver.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>Conclusion:</b> Low-dose liver CTPI achieved the result of perfusion parameters similar to that of the conventional-dose, whereas the radiation dosage was reduced by 2/3. Low-dose liver CTPI can reflect the hemodynamic changes of HCC, and has potential clinical value in diagnosis and differential diagnosis of liver diseases.</p></div>]]></content:encoded><description>OBJECTIVE: Computed tomography perfusion imaging (CTPI) is a rapid and non-invasive functional imaging method that reflects hemodynamic changes of liver diseases. However, large radiation dosage limits its clinical applications. We aimed to evaluate the feasibility of low-dose CTPI in normal liver and its preliminary application in hepatocellular carcinoma (HCC).Methods: CTPI was performed in 34 healthy volunteers randomly divided into three groups with applications of different tube currents, including conventional-dose group, medium-dose group, and low-dose group. The perfusion parameters of each group were compared and low-dose CTPI was performed in 13 patients with HCC.Results: Relatively satisfactory images and perfusion parameters of liver CTPI were acquired with different tube currents. There were no significant differences between the parameters of the three groups (P &gt; 0.05). The effective dosage of conventional, medium, and low-dose liver CTPI were 19.62 mSv, 12.61 mSv, and 7.01 mSv, respectively. The radiation dosage of low-dose liver CTPI was reduced to 64.27% compared with that of the conventional group. HBF, HPI, and HAP of HCC were higher than the background liver parenchyma and normal liver.Conclusion: Low-dose liver CTPI achieved the result of perfusion parameters similar to that of the conventional-dose, whereas the radiation dosage was reduced by 2/3. Low-dose liver CTPI can reflect the hemodynamic changes of HCC, and has potential clinical value in diagnosis and differential diagnosis of liver diseases.</description></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00567.x" xmlns="http://purl.org/rss/1.0/"><title>How to diagnose and manage patients with Barrett's esophagus in China</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00567.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">How to diagnose and manage patients with Barrett's esophagus in China</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Qin HUANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Dian Chun FANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jing Yuan FANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Min Hu CHEN</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jun ZHANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Lin LIN</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ning DAI</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Cheng Gong YU</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Hong Jie ZHANG</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2011.00567.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2011.00567.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00567.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">123</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">132</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>In order to prevent the development of Barrett's esophagus (BE)-related esophageal cancer in China and facilitate the communication of research results among different centers, we propose using standardized diagnostic criteria and taking a conservative approach to diagnose and manage BE patients. BE patients without dysplasia need to be treated medically. For low-grade dysplasia, an annual endoscopy with biopsies is recommended, along with medical therapy. For high-grade dysplasia and intramucosal carcinoma, an endoscopic or surgical intervention is suggested. All BE patients should be followed up closely.</p></div>]]></content:encoded><description>In order to prevent the development of Barrett's esophagus (BE)-related esophageal cancer in China and facilitate the communication of research results among different centers, we propose using standardized diagnostic criteria and taking a conservative approach to diagnose and manage BE patients. BE patients without dysplasia need to be treated medically. For low-grade dysplasia, an annual endoscopy with biopsies is recommended, along with medical therapy. For high-grade dysplasia and intramucosal carcinoma, an endoscopic or surgical intervention is suggested. All BE patients should be followed up closely.</description></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00569.x" xmlns="http://purl.org/rss/1.0/"><title>Oxidative stress and redox signaling mechanisms of alcoholic liver disease: Updated experimental and clinical evidence</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00569.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Oxidative stress and redox signaling mechanisms of alcoholic liver disease: Updated experimental and clinical evidence</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Hong ZHU</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Zhenquan JIA</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Hara MISRA</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Y Robert LI</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2011.00569.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2011.00569.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00569.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">133</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">142</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p>Alcoholic liver disease (ALD) is a major cause of morbidity and mortality in the United States and Europe. The spectrum of ALD ranges from fatty liver to alcoholic hepatitis and cirrhosis, which may eventually lead to hepatocellular carcinoma. In developed countries as well as developing nations, ALD is a major cause of end-stage liver disease that requires liver transplantation. The most effective therapy for ALD is alcohol abstinence; however, for individuals with severe ALD and those in whom alcohol abstinence is not achievable, targeted therapies are absolutely necessary. In this context, advances of our understanding of the pathophysiology of ALD over the past two decades have contributed to the development of therapeutic modalities (e.g., pentoxifylline and corticosteroids) for the disease although the efficacy of the available treatments remains limited. This article is intended to succinctly review the recent experimental and clinical findings of the involvement of oxidative stress and redox signaling in the pathophysiology of ALD and the development of mechanistically based antioxidant modalities targeting oxidative stress and redox signaling mechanisms. The biochemical and cellular sources of reactive oxygen and nitrogen species (ROS/RNS) and dysregulated redox signaling pathways associated with alcohol consumption are particularly discussed to provide insight into the molecular basis of hepatic cell dysfunction and destruction as well as tissue remodeling underlying ALD.</p></div>]]></content:encoded><description>Alcoholic liver disease (ALD) is a major cause of morbidity and mortality in the United States and Europe. The spectrum of ALD ranges from fatty liver to alcoholic hepatitis and cirrhosis, which may eventually lead to hepatocellular carcinoma. In developed countries as well as developing nations, ALD is a major cause of end-stage liver disease that requires liver transplantation. The most effective therapy for ALD is alcohol abstinence; however, for individuals with severe ALD and those in whom alcohol abstinence is not achievable, targeted therapies are absolutely necessary. In this context, advances of our understanding of the pathophysiology of ALD over the past two decades have contributed to the development of therapeutic modalities (e.g., pentoxifylline and corticosteroids) for the disease although the efficacy of the available treatments remains limited. This article is intended to succinctly review the recent experimental and clinical findings of the involvement of oxidative stress and redox signaling in the pathophysiology of ALD and the development of mechanistically based antioxidant modalities targeting oxidative stress and redox signaling mechanisms. The biochemical and cellular sources of reactive oxygen and nitrogen species (ROS/RNS) and dysregulated redox signaling pathways associated with alcohol consumption are particularly discussed to provide insight into the molecular basis of hepatic cell dysfunction and destruction as well as tissue remodeling underlying ALD.</description></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00563.x" xmlns="http://purl.org/rss/1.0/"><title>Octarepeat peptides of prion are essential for multidrug resistance in gastric cancer cells</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00563.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Octarepeat peptides of prion are essential for multidrug resistance in gastric cancer cells</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ji Heng WANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jing Ping DU</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Shu Jun LI</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Li Ping ZHAI</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Xin Yan YANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Zhi Hong WANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Zi Tao WU</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ying HAN</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2011.00563.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2011.00563.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00563.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">143</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">152</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p><b>OBJECTIVE: </b> In previous studies cellular prion protein (PrPc) is confirmed to be involved in multidrug resistance (MDR) of gastric cancer. Although octarepeat peptides are important functional domains of PrPc and are closely related to the transport of Cu<sup>2+</sup>/Zn<sup>2+</sup> and antioxidative function, the significance in MDR remains unknown. We aimed to investigate the role of octarepeat peptides in gastric cancer MDR.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>METHODS: </b> Small interfering RNA (siRNA) against PrPc were transfected into adriamycin-resistant gastric cancer cell lines to inhibit the expression of wild type PrPc, and then constructs encoding PrPc without octarepeat peptides and PrPc without the fifth repeat peptide were transfected, respectively, to establish the cell models. <em>In vitro</em> drug sensitivity, cell apoptosis, measurement of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione (GSH), as well as changes in glutathione S-transferase (GST) were detected.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>RESULTS: </b><em>In vitro</em> drug sensitivity test showed that octarepeat peptides could modulate the drug resistance of gastric cancer cells, but the deletion of the fifth repeat peptide had no effect. Specifically, the anti-apoptotic capacity of gastric cancer cells decreased significantly when the octarepeat peptides of PrPc was absent. Moreover, the activities of total SOD, Cu<sup>2+</sup>/Zn<sup>2+</sup>-SOD, GSH-Px, GSH, and GST detected in different stressing periods revealed that cells lacking octarepeat peptides of PrPc exhibited weakened responses to stress. However, absence of the fifth repeat peptide did not exert any effect on stress response.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>CONCLUSION: </b> The octarepeat peptides of prion is responsible for MDR in gastric cancer cells while the fifth repeat peptide is not.</p></div>]]></content:encoded><description>OBJECTIVE:  In previous studies cellular prion protein (PrPc) is confirmed to be involved in multidrug resistance (MDR) of gastric cancer. Although octarepeat peptides are important functional domains of PrPc and are closely related to the transport of Cu2+/Zn2+ and antioxidative function, the significance in MDR remains unknown. We aimed to investigate the role of octarepeat peptides in gastric cancer MDR.METHODS:  Small interfering RNA (siRNA) against PrPc were transfected into adriamycin-resistant gastric cancer cell lines to inhibit the expression of wild type PrPc, and then constructs encoding PrPc without octarepeat peptides and PrPc without the fifth repeat peptide were transfected, respectively, to establish the cell models. In vitro drug sensitivity, cell apoptosis, measurement of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione (GSH), as well as changes in glutathione S-transferase (GST) were detected.RESULTS: In vitro drug sensitivity test showed that octarepeat peptides could modulate the drug resistance of gastric cancer cells, but the deletion of the fifth repeat peptide had no effect. Specifically, the anti-apoptotic capacity of gastric cancer cells decreased significantly when the octarepeat peptides of PrPc was absent. Moreover, the activities of total SOD, Cu2+/Zn2+-SOD, GSH-Px, GSH, and GST detected in different stressing periods revealed that cells lacking octarepeat peptides of PrPc exhibited weakened responses to stress. However, absence of the fifth repeat peptide did not exert any effect on stress response.CONCLUSION:  The octarepeat peptides of prion is responsible for MDR in gastric cancer cells while the fifth repeat peptide is not.</description></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00571.x" xmlns="http://purl.org/rss/1.0/"><title>Natural course of nonalcoholic fatty liver disease in southern China: A prospective cohort study</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00571.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Natural course of nonalcoholic fatty liver disease in southern China: A prospective cohort study</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Yong Jian ZHOU</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Yu Yuan LI</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Yu Qiang NIE</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Chun Ming HUANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Chuang Yu CAO</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2011.00571.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2011.00571.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00571.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">153</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">160</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p><b>OBJECTIVE: </b> Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease, the natural course of which has not been well documented. This study aimed to perform a prospective cohort study to investigate NAFLD in a Chinese population.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>METHODS: </b> Using our previous epidemiological survey, 3543 patients were followed-up for a median of 4 years (range 3.6–4.8 years). Of these patients, 624 participated in a new survey. Interviews, physical examinations, biochemical tests and abdominal ultrasonography were repeated for these patient.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>RESULTS: </b> The annual incidence of NAFLD was 9.1% (male 7.3% <em>vs</em> female 9.7%, <em>P</em> = 0.047). Among 117 NAFLD patients at baseline, 51 (43.6%) remained unchanged, 26 (22.2%) became worse, and 40 (34.2%) improved. Patients with simultaneous metabolic syndrome (MS) showed accelerated progression (<em>P</em> = 0.026). For the NAFLD patients, both general annual mortality rates and cardiovascular disease deaths (both 0.54%) were significantly higher than those of patients without NAFLD (0.19% and 0.17%, <em>P</em> = 0.005). Age and several variables related to MS were risk factors for NAFLD progression.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>CONCLUSIONS: </b> The incidence of NAFLD in southern China is relatively lower in comparison with that of the developed countries. Patients with NAFLD have a benign prognosis. Variables related to MS are risk factors for NAFLD occurrence and progression.</p></div>]]></content:encoded><description>OBJECTIVE:  Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease, the natural course of which has not been well documented. This study aimed to perform a prospective cohort study to investigate NAFLD in a Chinese population.METHODS:  Using our previous epidemiological survey, 3543 patients were followed-up for a median of 4 years (range 3.6–4.8 years). Of these patients, 624 participated in a new survey. Interviews, physical examinations, biochemical tests and abdominal ultrasonography were repeated for these patient.RESULTS:  The annual incidence of NAFLD was 9.1% (male 7.3% vs female 9.7%, P = 0.047). Among 117 NAFLD patients at baseline, 51 (43.6%) remained unchanged, 26 (22.2%) became worse, and 40 (34.2%) improved. Patients with simultaneous metabolic syndrome (MS) showed accelerated progression (P = 0.026). For the NAFLD patients, both general annual mortality rates and cardiovascular disease deaths (both 0.54%) were significantly higher than those of patients without NAFLD (0.19% and 0.17%, P = 0.005). Age and several variables related to MS were risk factors for NAFLD progression.CONCLUSIONS:  The incidence of NAFLD in southern China is relatively lower in comparison with that of the developed countries. Patients with NAFLD have a benign prognosis. Variables related to MS are risk factors for NAFLD occurrence and progression.</description></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00570.x" xmlns="http://purl.org/rss/1.0/"><title>Risk factors and outcomes of massive red blood cell transfusion following living donor liver transplantation</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00570.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Risk factors and outcomes of massive red blood cell transfusion following living donor liver transplantation</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Chuan LI</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Kai MI</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Tian Fu WEN</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Lu Nan YAN</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Bo LI</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Yong Gang WEI</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jia Ying YANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ming Qing XU</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Wen Tao WANG</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2011.00570.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2011.00570.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00570.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">161</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">167</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p><b>OBJECTIVES: </b> To identify the factors influencing blood loss and secondary blood transfusion and to investigate the outcomes of patients who underwent a massive blood transfusion (MBT) following living donor liver transplantation (LDLT).</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>METHODS: </b> Patients who underwent primary adult-to-adult right hepatic lobe LDLT were included in the study, and were divided into the MBT group [≥ 6 red blood cell (RBC) units in 24 h] and the non-massive blood transfusion (NMBT) group (&lt; 6 RBC units in 24 h). All potential risk factors, length of intensive care unit (ICU) stay and long-term survival rate of the patients in the two groups were analyzed.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>RESULTS: </b> The data of 181 eligible patients were retrospectively analyzed. A decreased long-term survival rate, a higher incidence of postoperative infection and prolonged ICU stay were observed in the MBT group. No significant difference was observed in survival rate between patients having platelet transfusion &gt; 2 units and ≤ 2 units. Hemoglobin &lt; 100 g/L, platelet counts &lt; 70 × 10<sup>9</sup>/L, fibrinogen level &lt; 1.5 g/L and history of upper abdominal surgery were found to be independent risk factors.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>CONCLUSIONS: </b> Blood transfusion during LDLT can be predicted using preoperative variables. Massive RBC transfusion may lead to poor long-term survival, higher postoperative infection rate and prolonged ICU stay. Platelet transfusion may not be a risk factor for long-term survival.</p></div>]]></content:encoded><description>OBJECTIVES:  To identify the factors influencing blood loss and secondary blood transfusion and to investigate the outcomes of patients who underwent a massive blood transfusion (MBT) following living donor liver transplantation (LDLT).METHODS:  Patients who underwent primary adult-to-adult right hepatic lobe LDLT were included in the study, and were divided into the MBT group [≥ 6 red blood cell (RBC) units in 24 h] and the non-massive blood transfusion (NMBT) group (&lt; 6 RBC units in 24 h). All potential risk factors, length of intensive care unit (ICU) stay and long-term survival rate of the patients in the two groups were analyzed.RESULTS:  The data of 181 eligible patients were retrospectively analyzed. A decreased long-term survival rate, a higher incidence of postoperative infection and prolonged ICU stay were observed in the MBT group. No significant difference was observed in survival rate between patients having platelet transfusion &gt; 2 units and ≤ 2 units. Hemoglobin &lt; 100 g/L, platelet counts &lt; 70 × 109/L, fibrinogen level &lt; 1.5 g/L and history of upper abdominal surgery were found to be independent risk factors.CONCLUSIONS:  Blood transfusion during LDLT can be predicted using preoperative variables. Massive RBC transfusion may lead to poor long-term survival, higher postoperative infection rate and prolonged ICU stay. Platelet transfusion may not be a risk factor for long-term survival.</description></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00566.x" xmlns="http://purl.org/rss/1.0/"><title>In vitro and in vivo characterization of silk fibroin/gelatin composite scaffolds for liver tissue engineering</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00566.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">In vitro and in vivo characterization of silk fibroin/gelatin composite scaffolds for liver tissue engineering</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Zhao YANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Li Sha XU</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Fang YIN</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Yong Quan SHI</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Ying HAN</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Lin ZHANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Hai Feng JIN</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Yong Zhan NIE</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jing Bo WANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Xing HAO</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Dai Ming FAN</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Xin Min ZHOU</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2011.00566.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2011.00566.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00566.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">168</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">178</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p><b>OBJECTIVE: </b> To investigate the cytotoxicity of silk fibroin/gelatin (SF/G) composite scaffolds <em>in vitro</em> as well as their biocompatibility and degradation <em>in vivo.</em></p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>METHODS: </b> The proliferation and relative growth rate of human hepatic QZG cells grown on different blends of two-dimensional (2-D) SF/G scaffolds were assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Flow cytometry was used to evaluate apoptotic rate of QZG cells on different blends of 2-D SF/G scaffolds. The effect of silk protein materials on cell growth was observed by scanning electron microscopy. Three-dimensional (3-D) SF/G scaffolds of three different ratios (diameter 10 mm, thickness 1 mm) were implanted into subcutaneous pockets on male Sprague–Dawley (SD) rats. On the 7th, 14th and 30th day post-implantation, the rats were sacrificed. The scaffold area including the surrounding tissues was retrieved. Hematoxylin and eosin staining was performed for observation under a light microscope.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>RESULTS: </b> Significant cell attachment and proliferation on the SF/G scaffolds were observed. As the increased gelatin concentration, SF/G scaffolds became more amenable to cell adhesion. After the subcutaneous implantation of the SF/G scaffolds in SD rats, immunological rejection tests showed only slight inflammation, measured by the presence of inflamed cells on day 7 and 14. By day 30, each scaffold had been completely infiltrated and organized by fibroblasts and inflamed cells. The greater the gelatin concentration in the scaffold, the faster the degradation rate.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>CONCLUSION: </b> Composite SF/G scaffolds are a promising candidate matrix for implantable bio-artificial livers.</p></div>]]></content:encoded><description>OBJECTIVE:  To investigate the cytotoxicity of silk fibroin/gelatin (SF/G) composite scaffolds in vitro as well as their biocompatibility and degradation in vivo.METHODS:  The proliferation and relative growth rate of human hepatic QZG cells grown on different blends of two-dimensional (2-D) SF/G scaffolds were assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Flow cytometry was used to evaluate apoptotic rate of QZG cells on different blends of 2-D SF/G scaffolds. The effect of silk protein materials on cell growth was observed by scanning electron microscopy. Three-dimensional (3-D) SF/G scaffolds of three different ratios (diameter 10 mm, thickness 1 mm) were implanted into subcutaneous pockets on male Sprague–Dawley (SD) rats. On the 7th, 14th and 30th day post-implantation, the rats were sacrificed. The scaffold area including the surrounding tissues was retrieved. Hematoxylin and eosin staining was performed for observation under a light microscope.RESULTS:  Significant cell attachment and proliferation on the SF/G scaffolds were observed. As the increased gelatin concentration, SF/G scaffolds became more amenable to cell adhesion. After the subcutaneous implantation of the SF/G scaffolds in SD rats, immunological rejection tests showed only slight inflammation, measured by the presence of inflamed cells on day 7 and 14. By day 30, each scaffold had been completely infiltrated and organized by fibroblasts and inflamed cells. The greater the gelatin concentration in the scaffold, the faster the degradation rate.CONCLUSION:  Composite SF/G scaffolds are a promising candidate matrix for implantable bio-artificial livers.</description></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00568.x" xmlns="http://purl.org/rss/1.0/"><title>Experimental pancreatitis results in increased blood-brain barrier permeability in rats: A potential role of MCP-1</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00568.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Experimental pancreatitis results in increased blood-brain barrier permeability in rats: A potential role of MCP-1</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Zhen DING</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jun LIU</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Rong LIN</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Xiao Hua HOU</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2011.00568.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2011.00568.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00568.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">179</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">185</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[<div class="para" xmlns:ol="http://www.wiley.com/namespaces/ol/xsl-lib" xmlns="http://www.w3.org/1999/xhtml"><p><b>OBJECTIVE: </b> To measure the changes of blood-brain barrier (BBB) permeability in rats with acute pancreatitis (AP) and to investigate the role of monocyte chemoattractant protein (MCP)-1 expression in this alteration.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>METHODS: </b> Rat model of severe acute pancreatitis (SAP) and mild acute pancreatitis (MAP) was induced by pancreatic duct infusion of 5% and 0.5% sodium choleate, respectively, and a saline infusion was used in the control. The severity of AP was evaluated by a pathological score system. BBB permeability was detected by Evan's blue tracer and BBB tight junction was assessed by brain occludin expression. Immunohistochemistry and real-time polymerase chain reaction were used to detect MCP-1 expression in the brain. Nifedipine was used as the antagonist of MCP-1.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>RESULTS: </b> Compared to the control group, change of BBB permeability was more significant in SAP groups, but not in MAP groups. Occludin level decreased 12 h after SAP induction. Pathological score of SAP group was higher than that in MAP group. BBB opening was associated with pancreatic injury. Brain MCP-1 expression was detected in all the SAP groups, which was correlated with increased BBB permeability, but was not found in the control group or the MAP group. After treatment with nifedipine, brain MCP-1 level decreased and BBB function improved synchronously in SAP groups.</p></div><div class="para" xmlns="http://www.w3.org/1999/xhtml"><p><b>CONCLUSIONS: </b> BBB permeability increased in SAP significantly and time-dependently, and was correlated with brain MCP-1 expression. Nifedipine may improve BBB function by inhibiting MCP-1 expression.</p></div>]]></content:encoded><description>OBJECTIVE:  To measure the changes of blood-brain barrier (BBB) permeability in rats with acute pancreatitis (AP) and to investigate the role of monocyte chemoattractant protein (MCP)-1 expression in this alteration.METHODS:  Rat model of severe acute pancreatitis (SAP) and mild acute pancreatitis (MAP) was induced by pancreatic duct infusion of 5% and 0.5% sodium choleate, respectively, and a saline infusion was used in the control. The severity of AP was evaluated by a pathological score system. BBB permeability was detected by Evan's blue tracer and BBB tight junction was assessed by brain occludin expression. Immunohistochemistry and real-time polymerase chain reaction were used to detect MCP-1 expression in the brain. Nifedipine was used as the antagonist of MCP-1.RESULTS:  Compared to the control group, change of BBB permeability was more significant in SAP groups, but not in MAP groups. Occludin level decreased 12 h after SAP induction. Pathological score of SAP group was higher than that in MAP group. BBB opening was associated with pancreatic injury. Brain MCP-1 expression was detected in all the SAP groups, which was correlated with increased BBB permeability, but was not found in the control group or the MAP group. After treatment with nifedipine, brain MCP-1 level decreased and BBB function improved synchronously in SAP groups.CONCLUSIONS:  BBB permeability increased in SAP significantly and time-dependently, and was correlated with brain MCP-1 expression. Nifedipine may improve BBB function by inhibiting MCP-1 expression.</description></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00572.x" xmlns="http://purl.org/rss/1.0/"><title>Consecutive extrapulmonary paragonimiasis involving liver and colon</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00572.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Consecutive extrapulmonary paragonimiasis involving liver and colon</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Chang Wook PARK</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Woo Jin CHUNG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Young Lan KWON</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Yong Jin KIM</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Eun Soo KIM</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Byung Kuk JANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Kyung Sik PARK</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Kwang Bum CHO</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jae Seok HWANG</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Jung Hyuk KWON</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2011.00572.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2011.00572.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00572.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">186</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">189</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item><item rdf:about="http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00565.x" xmlns="http://purl.org/rss/1.0/"><title>Metastatic malignant melanoma of the gallbladder diagnosed by cytology of endoscopic naso-gallbladder drainage fluid</title><link>http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00565.x</link><dc:title xmlns:dc="http://purl.org/dc/elements/1.1/">Metastatic malignant melanoma of the gallbladder diagnosed by cytology of endoscopic naso-gallbladder drainage fluid</dc:title><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Hiroyuki MATSUBAYASHI</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Yoshio KIYOHARA</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Keiko SASAKI</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Hideyuki KANEMOTO</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Kumiko URIKURA</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Noboru KAWATA</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Hirokazu KIMURA</dc:creator><dc:creator xmlns:dc="http://purl.org/dc/elements/1.1/">Hiroyuki ONO</dc:creator><dc:date xmlns:dc="http://purl.org/dc/elements/1.1/">2012-03-01T00:00:00-05:00</dc:date><dc:identifier xmlns:dc="http://purl.org/dc/elements/1.1/">doi:10.1111/j.1751-2980.2011.00565.x</dc:identifier><dc:rights xmlns:dc="http://purl.org/dc/elements/1.1/"/><dc:publisher xmlns:dc="http://purl.org/dc/elements/1.1/">John Wiley &amp; Sons, Inc.</dc:publisher><prism:doi xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">10.1111/j.1751-2980.2011.00565.x</prism:doi><prism:url xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">http://dx.doi.org/10.1111%2Fj.1751-2980.2011.00565.x</prism:url><prism:startingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">190</prism:startingPage><prism:endingPage xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/">194</prism:endingPage><content:encoded xmlns:content="http://purl.org/rss/1.0/modules/content/"><![CDATA[]]></content:encoded><description/></item></rdf:RDF>
