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Background/aims: Surgical site infection (SSI) is still a source of major complications in digestive tract surgery, especially in hepatobiliary region. To decrease the incidence of SSI, we have investigated whether methods of intradermal suture in benign hepatobiliary patients are in fact useful., Methodology: Cohort study was carried out to compare the intradermal suture group (ISG) and the metallic stapler group (MSG) for laparotomy of benign biliary tract disease. The surgical technique employed for SSI prevention was always the same, excluding the method of skin sutures. Wounds with pus were defined as infected if pus were observed after the surgery. All patients were followed for at least 3 months after their respective operations., Results: The incidence of SSI in ISG was lower than in MSG (p < 0.05). However, the risk factors and the incidence of wound infection did not correlate with each other statistically., Conclusion: In cases of benign biliary tract disease, intradermal suture seemed to be quite appropriate for prevention of SSI, even though operation time was a little longer than with use of a metallic stapler.

The mechanism by which breast cancers progress to hormone independence does not always require the loss of estrogen receptor(ER) expression or function. Cellular alterations that disturb the normal pathway of estrogen-regulated growth may contribute to a state of hormone independence. We and others have described an inverse relationship between estrogen stimulation of ER(+) breast cancer cell lines and their expression of neu. Amplification and overexpression of neu are known to enhance cellular transformation and increase the metastatic potential of cancer cells. Clinically, they are also correlated with more aggressive tumor phenotypes. Therefore, expression of neu may represent a key regulatory point in estrogenic control of cellular growth and transformation. In this communication we demonstrate that the presence of E2/ER can repress transformation of NIH/3T3 cells by the neu oncogene. Furthermore, we have investigated the effects of E2/ER on growth and transformation of an ER(+), neu-overexpressing breast cancer cell line. We report that the presence of E2/ER in these cells leads to repression of the transformed phenotype (as measured by anchorage-independent growth) while stimulating cellular proliferation (in monolayer culture) and propose a model for the role of neu in progression to hormone independence based on these results.