PurposeBile duct dilatation after cholecystectomy continues to be a matter of controversy. We aimed determine the magnitude of common bile duct (CBD) dilatation after cholecystectomy followed up to 1 year.MethodsSixty-four cases (age, 47.3 ± 11.7 years; men, 28; women, 36) enrolled in this study. They received laparoscopic cholecystectomy in Chungbuk National University Hospital for symptomatic cholelithiasis or gallbladder polyps with normal bile duct, less than 7 mm. The CBD diameter was measured by one radiologist using ultrasonography at the maximum point after full length evaluation of extrahepatic bile duct. Forty-five and thirty-one cases were followed at 6 months and 1 year, respectively.ResultsThe CBD was dilated slightly from 4.1 mm at baseline to 5.1 mm at 6 months and 6.1 mm at 12 months after cholecystectomy. The number of cases of CBD dilatation of more than 7 mm at 6 months and at 12 months after cholecystectomy were 11 (24.4%) and 9 (29.0%), respectively. Seven cases at 6 months and 5 cases at 12 months showed bile duct dilation of more than 3 mm compared to baseline. There were no cases having bile duct dilation of more than 10 mm.ConclusionPostcholecystectomy dilatation of the bile duct occured slightly in most cases. But some cases showed more than 3 mm dilatation over baseline. Asymptomatic bile duct dilatation of up to 10 mm can be considered as normal range in patients after cholecystectomy.

Local delivery of paclitaxel suppressed PC in a rat model by the inhibition of epithelial-glandular proliferation and may offer an effective therapeutic option for biliary stricture.

The tumor suppressor gene p16 INK4A is a cyclin-dependent kinase inhibitor (CDKI) and an important cell cycle regulator. We have previously constructed a recombinant adenovirus which expresses p16 (Adp16) and shown that infection in a variety of human tumor cell lines with this recombinant virus results in high levels of p16 INK4A protein expression resulting in cell cycle arrest and loss of cyclin-cdk activity. Furthermore, adenoviral-mediated overexpression of wild-type p16 INK4A is more toxic in cancer cells which express mutant forms of p16 INK4A compared to cancer cell lines containing endogenous wild-type p16. TUNEL assay and DAPI staining following infection of MDA-MB 231 breast cancer cells with Adp16 indicate that p16 INK4A -mediated cytotoxicity was associated with apoptosis. This is supported by studies demonstrating a decrease in cpp32 and cyclinB1 protein levels and induction of poly (ADP-ribose) polymerase (PARP) cleavage following infection of MDA-MB-231 cells with Adp16. These results suggest that gene therapy using Adp16 may be a promising treatment option for human cancers containing alterations in p16 expression. Cell Death and Differentiation (2000) 7, 706 ± 711.

The lateral approach liver hanging maneuver is a simple, safe, and reproducible approach as dissection of the anterior surface of the inferior vena cava and between the three major hepatic veins is not required. This technique may be useful in laparoscopic anatomical liver resections.

The thorns of Gleditsia sinensis are a traditional Oriental medicine used for the treatment of swelling, suppuration, carbuncle and skin diseases. In the present study, we identified a novel molecular mechanism by which an ethanol extract of Gleditsia sinensis thorns (EEGS) inhibits the growth of the SNU-5 human gastric cancer cell line. EEGS treatment inhibited cell growth and was associated with G1 phase cell cycle arrest at a concentration of 400 µg/ml (IC50) in SNU-5 cells. Treatment with EEGS also stimulated p21WAF1 expression, which significantly decreased the expression of cyclins and cyclin-dependent kinases (CDKs). Further study suggested that p38 MAP kinase pathways may be involved in the inhibition of cell proliferation through p21WAF1‑dependent G1 phase cell cycle arrest in EEGS-treated cells. In addition, NF-κB and AP-1 transcription factor binding sites were identified as the cis-elements for tumor necrosis factor-α (TNF-α)-induced matrix metalloproteinase-9 (MMP-9) expression in SNU-5 cells, as determined by gel-shift assay. Treatment of cells with EEGS suppressed MMP-9 expression induced by TNF-α via a decrease in the binding activity of both NF-κB and AP-1 motifs. These data demonstrate that EEGS-mediated inhibition of cell growth appears to involve the activation of p38 MAP kinase, subsequently leading to the induction of p21WAF1 and the downregulation of cyclin D1/CDK4 and cyclin E/CDK2 complexes. Moreover, EEGS strongly inhibited TNF-α-induced MMP-9 expression by impeding the DNA binding activity of NF-κB and AP-1. Overall, these results provide a potential mechanism for EEGS in the treatment of gastric cancer.