Severity of mucosal inflammation was evaluated using the Mayo score of endoscopic index at each location (rectum, sigmoid colon, descending colon, and the oral side of the splenic flexure) in each patient. The colonic PD0325901 clinical trial site with maximum inflammation was determined for each patient. Results: Of 545 patients, 319 (59%) had maximum inflammation in the rectum, 79 (14%)
in the sigmoid colon, 70 (13%) in the descending colon, and 77 (14%) on the oral side of the splenic flexure. Severe inflammatory activity (Mayo 3) was observed more frequently in patients who had maximum activity in the descending colon or the more proximal portion than those who had this in the rectum or sigmoid colon (42% vs 25%, P < 0.0001). The first-attack patients were significantly more frequently found in patients with maximum severity in the descending colon or the oral side of splenic flexure than those with maximum severity in the rectum or sigmoid colon (P = 0.016). Moreover, among 134 patients with no inflammation in the rectum and sigmoid colon, 54 (40%) had inflamed mucosa in the descending colon or the more proximal portion. Conclusions:
Sigmoidoscopy is not sufficient for evaluating inflammation in UC patients. In particular, colonoscopy is necessary for first-attack patients and patients who have a discrepancy between rectosigmoid observation and symptoms. “
“The identification of resident stem cells in the mouse gallbladder is, to date, unexplored. In addition, the relationship between adult gallbladder stem cells and intrahepatic bile duct (IHBD) cells is not well understood. The aim of this study was to isolate stem cells selleck chemicals from an adult mouse gallbladder and determine whether they were unique, compared to IHBD cells. By limiting dilution analyses and index sorts, we found that an EpCAM+CD49fhi epithelial cell subpopulation from primary gallbladder is enriched in colony-forming cells, compared to EpCAM+CD49flo
cells. EpCAM+CD49fhi cells expressed cluster of differentiation (CD)29, CD133, and stem cell antigen-1, but were negative for lineage markers CD31, CD45, and F4/80. Using a novel feeder cell-culture system, we observed long-term (>passage 20) and clonal expansion of the EpCAM+CD49fhi cells in vitro. In a matrigel differentiation assay, EpCAM+CD49f+ cells expanding in Alanine-glyoxylate transaminase vitro underwent organotypic morphogenesis forming ductular structures and cysts. These structures are similar to, and recapitulate a transport function of, primary gallbladder. EpCAM+CD49f+ cells also engraft into the subcutaneous space of recipient mice. We compared primary gallbladder and IHBD cells by flow cytometry and found phenotypic differences in the expression of CD49f, CD49e, CD81, CD26, CD54, and CD166. In addition, oligonucleotide microarrays showed that the expanded EpCAM+CD49f+ gallbladder cells and IHBD cells exhibit differences related to lipid and drug metabolism.