KCS score may be clinically simple and useful for assessing advanced neoplasia risk in Korea. However, racial disparity should be considered in risk stratification-based screening in each country.

We report a rare case of giant mesenteric lipoma presenting with colicky abdominal pain. A 29-yr-old woman underwent laparoscopic resection for a giant mesenteric lipoma causing compression of the ileal loop. The resected ileal segment was encased by a giant fatty tissue, and normal mucosal fold patterns of the resected ileum were effaced by the mass. Microscopically, the mass was characterized by homogenous mature adipose tissue without cellular atypia, which was compatible with the diagnosis of a mesenteric lipoma. Despite the benign nature of this tumor, total excision with or without the affected intestinal loop should be considered if intestinal symptoms such as abdominal pain are present.

Polydeoxyribonucleotide (PDRN) interacts with the adenosine A 2A -receptor and stimulates vascular endothelial growth factor (VEGF) expression. While it has been indicated that PDRN might accelerate wound healing, its impact on gastric ulcers (GU) is still unknown. We investigated the effects of PDRN on VEGF expression in relation to inflammation and apoptosis in GU by using Mongolian gerbils. GU was induced by injection of acetic acid into the subserosal surface of the stomach. The gerbils in the PDRN-treated groups received daily intraperitoneal injections of PDRN over 2 weeks. Reverse transcriptase-polymerase chain reaction (RT-PCR) for tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, and IL-6, as well as terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling (TUNEL) assay, immunohistochemistry for caspase-3, and western blot for VEGF, Bax, and Bcl-2 were conducted. Acetic acid injection induced GU, and VEGF expression in the gastric mucosa was enhanced by GU. PDRN treatment decreased ulcer size and led to overexpression of VEGF in GU. Expression of TNF-α, IL-1β, and IL-6 was increased in GU, and PDRN treatment decreased the expression of these cytokines. The numbers of TUNEL-positive and caspase-3-positive cells were increased by GU, while PDRN reduced these numbers. Induction of GU enhanced the ratio of Bax to Bcl-2, while PDRN diminished this ratio. Overexpression of VEGF and inhibition of inflammation and apoptosis by PDRN may be the underlying mechanisms of PDRN action on GU healing.

In patients with early LC, the risk of postpolypectomy bleeding was acceptably low and there was no case with DPPB. Therefore, polypectomy can be performed with caution. IPPB was associated with the size and the gross morphology of the polyps. However, LC-related variables in patients with early LC did not impact IPPB.

The rat hepatocytes were immortalized using a temperature-sensitive mutant of SV40 large T antigen (tsT) to develop as a possible substitute for primary hepatocytes. Four rat hepatocyte lines that have been developed and maintained more than passage 50, were characterized for their cellular morphology, T antigen and p53 expression, chromosomes, liverspecific differentiation, telomerase activity and anchorage independent growth. All of four cell lines showed a typical epithelial cell morphology, but the population-doubling time became short with passage: 18 to 60%. T antigen expression was increased with passage about 3 to 65 times at permissive temperature but decreased significantly at non-permissive temperature. The expression level of p53 unchanged during passages was also decreased at non-permissive temperature. The distribution of chromosome number changed somewhat with passage. The production levels of albumin and urea in four cell lines were 2.4 to 13.0% and 7.5 to 19.9% of those produced in primary hepatocytes, respectively and were decreased to an undetectable level with passage. Telomerase activity was increased 10 fold following immortalization of cells, but anchorage independent growth of cells did not develop. These results indicate that conditionally immortalized hepatocytes become dedifferentiated with in vitro passage, which may be caused by marked chromosomal damages that occur with compulsive and continuous replications by the increment of T antigen content with passage and its sequential inhibition of p53 function.