Selective biliary cannulation is an essential prerequisite for therapeutic endoscopic retrograde cholangiopancreatography (ERCP). The cap-fitted forward-viewing endoscope has been used for ERCP in patients with surgically altered anatomy. In this case series, 12 patients with periampullary diverticulum underwent ERCP using the cap-assisted forward-viewing endoscope due to failure of biliary cannulation using the standard technique. Successful ERCP was achieved in all patients with no serious complications.

BackgroundBlack tea has been shown to elicit anti-oxidant, anti-carcinogenic, anti-inflammatory and anti-mutagenic properties. In this study, we investigated the impact of black tea extract (BTE) on lipopolysaccharide (LPS)-induced NF-κB signaling in bone marrow derived-macrophages (BMM) and determined the therapeutic efficacy of this extract on colon inflammation.MethodsThe effect of BTE on LPS-induced NF-κB signaling and pro-inflammatory gene expression was evaluated by RT-PCR, Western blotting, immunofluorescence and electrophoretic mobility shift assay (EMSA). The in vivo efficacy of BTE was assessed in mice with 3% dextran sulfate sodium (DSS)-induced colitis. The severity of colitis was measured by weight loss, colon length and histologic scores.ResultsLPS-induced IL-12p40, IL-23p19, IL-6 and IL-1β mRNA expressions were inhibited by BTE. LPS-induced IκBα phosphorylation/degradation and nuclear translocation of NF-κB/p65 were blocked by BTE. BTE treatment blocked LPS-induced DNA-binding activity of NF-κB. BTE-fed, DSS-exposed mice showed the less weight loss, longer colon length and lower histologic score compared to control diet-fed, DSS-exposed mice. DSS-induced IκBα phosphorylation/degradation and phosphorylation of NF-κB/p65 were blocked by BTE. An increase of cleaved caspase-3 and poly (ADP-ribose) polymerase (PARP) in DSS-exposed mice was blocked by BTE.ConclusionsThese results indicate that BTE attenuates colon inflammation through the blockage of NF-κB signaling and apoptosis in DSS-induced experimental colitis model.

These results indicate that knockdown of RON inhibits AP-1 activity and induces apoptosis and cell cycle arrest through the modulation of Akt/FoxO signaling in human colorectal cancer cells.

IntroductionCholecystokinin (CCK) belongs to a group of endogenous molecules known as brain-gut neuropeptides and functions as a neuropeptide as well as a gut hormone. It remains unclear whether genetic variation of the CCK receptor plays a role in irritable bowel syndrome (IBS). The aim of this study was to determine and compare the allele and genotype frequencies of the CCK1 receptor polymorphisms between healthy controls and patients with IBS.MethodsGenotyping of 80 patients with IBS (who met the Rome III criteria) and 76 healthy controls was performed. We performed PCR amplification for the CCK1 receptor intron 1 779 T > C and Exon 1 G > A. We confirmed polymorphisms by direct sequencing method.ResultsThere was a significantly different trend for genotypic distributions of the CCK1 receptor polymorphism between patients with IBS and healthy controls (p for trend = 0.048). The CCK1 receptor intron 1 779 T >C polymorphic type was more common in patients with 'IBS-constipation predominant (IBS-C) and IBS-mixed (IBS-M) forms' (19/31, 61.3%) than healthy controls 32/76, 42.1% adjusted odd ratio 2.43, 95% Confidence interval 1.01-5.86). The genotypic distributions of the CCK1 receptor exon 1 polymorphism were not significantly different between the two groups (p for trend = 0.223).ConclusionsCCK1 receptor polymorphisms were associated with IBS. In particular, the CCK1 receptor intron 1 779 T > C polymorphic type was associated with 'IBS-C and IBS-M'. Further studies are needed in larger number of patients with an even distribution of IBS subtypes.

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