The hepatocyte-specific contrast agent gadolinium ethoxybenzyl diethylenetriamine pentaacetic acid (Gd-EOB-DTPA) was developed to improve the detection and characterization of focal liver lesions at magnetic resonance (MR) imaging. Approximately 50% of the injected dose is taken up into the functional hepatocyte and is excreted via the biliary system. Because of this property, Gd-EOB-DTPA has the potential to be a biliary contrast agent. When combined with T2-weighted MR cholangiography, Gd-EOB-DTPA-enhanced MR imaging can allow morphologic and functional assessment of the biliary system. Gd-EOB-DTPA-enhanced MR cholangiography could be effective in evaluation of biliary anatomy, differentiation of biliary from extrabiliary lesions, diagnosis of cholecystitis, assessment of bile duct obstruction, detection of bile duct injury including leakage and stricture, evaluation of biliary-enteric anastomoses, postprocedure evaluation, differentiation of biloma from other pathologic conditions, and evaluation of sphincter of Oddi dysfunction. However, the clinical applications of this imaging technique have not yet been fully explored, and further investigations are needed to determine the utility of Gd-EOB-DTPA-enhanced MR cholangiography in a clinical setting.
A nomogram predicting malignancy in patients with BD-IPMN was constructed using a logistic regression model. This nomogram may be useful in identifying patients at risk of malignancy and for selecting optimal treatment methods. The nomogram is freely available at http://statgen.snu.ac.kr/software/nomogramIPMN.
Up-regulation of IFN-stimulated genes (ISGs) is sustained in hepatitis C virus (HCV)-infected livers. Here, we investigated the mechanism of prolonged ISG expression and its role in IFN responsiveness during HCV infection in relation to unphosphorylated IFN-stimulated gene factor 3 (U-ISGF3), recently identified as a tripartite transcription factor formed by high levels of IFN response factor 9 (IRF9), STAT1, and STAT2 without tyrosine phosphorylation of the STATs. The level of U-ISGF3, but not tyrosine phosphorylated STAT1, is significantly elevated in response to IFN-λ and IFN-β during chronic HCV infection. U-ISGF3 prolongs the expression of a subset of ISGs and restricts HCV chronic replication. However, paradoxically, high levels of U-ISGF3 also confer unresponsiveness to IFN-α therapy. As a mechanism of U-ISGF3-induced resistance to IFN-α, we found that ISG15, a U-ISGF3-induced protein, sustains the abundance of ubiquitin-specific protease 18 (USP18), a negative regulator of IFN signaling. Our data demonstrate that U-ISGF3 induced by IFN-λs and -β drives prolonged expression of a set of ISGs, leading to chronic activation of innate responses and conferring a lack of response to IFN-α in HCVinfected liver.hepatitis C virus | U-ISGF3 | interferon | interferon-stimulated genes
There is a wide variety of congenital anomalies that may affect the gastrointestinal tract. Most symptomatic congenital anomalies are found in newborns and infants. Such anomalies are relatively rare in adolescents and adults, and they may be difficult to identify because clinical symptoms often are nonspecific and insidious, causing them to be mistaken for other common abdominal conditions. Multimodality imaging is useful in evaluating congenital anomalies of the gastrointestinal tract in adults. The imaging features at radiography, fluoroscopy, ultrasonography, computed tomography, and magnetic resonance imaging may help identify congenital gastrointestinal anomalies such as congenital esophageal stenosis, gastric volvulus, duodenal web, annular pancreas, heterotopic pancreas, cecal volvulus, anomalies of the omphalomesenteric duct, Hirschsprung disease, and gastrointestinal duplication cyst. Familiarity with the imaging features of the various congenital anomalies of the gastrointestinal tract and their complications is important to establish the correct diagnosis and determine appropriate treatment, which is critical to avoid life-threatening complications.
Background
The prevalent location and incidence of intraductal papillary neoplasm of the bile duct (IPNB) and invasive carcinoma associated with them have varied markedly among studies due to differences in diagnostic criteria and tumor location.
Methods
IPNBs were classified into two types: Type 1 IPNB, being histologically similar to intraductal papillary mucinous neoplasm of the pancreas, and Type 2 IPNB, having a more complex histological architecture with irregular papillary branching or foci of solid‐tubular components. Medical data were evaluated.
Results
Among 694 IPNB patients, 520 and 174 had Type 1 and Type 2, respectively. The levels of AST, ALT, ALP, T. Bil, and CEA were significantly higher in patients with Type 2 than in those with Type 1. Type 1 IPNB was more frequently located in the intrahepatic bile duct than Type 2, whereas Type 2 was more frequently located in the distal bile duct than Type 1 IPNB (P < 0.001). There were significant differences in 5‐year cumulative survival rates (75.2% vs 50.9%; P < 0.0001) and 5‐year cumulative disease‐free survival rates (64.1% vs 35.3%; P < 0.0001) between the two groups.
Conclusion
Type 1 and Type 2 IPNBs differ in their clinicopathological features and prognosis. This classification may help to further understand IPNB.
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