Does smad3 loss confer resistance to the development of trinitrobenzene sulfonic acid-induced colorectal fibrosis?
These results indicate that Smad3 loss confers resistance to the development of TNBS-induced colonic fibrosis. The reduced fibrotic response appears to be due to a reduction in fibrogenic mesenchymal cell activation and ECM production and accumulation. Smad3 could be a novel target for potential treatment of intestinal fibrosis, especially in inflammatory bowel disease.
Differences in knowledge, attitudes, and intentions to comply with UP between students with and without clinical experience may have important implications for the timing and content of interventions designed to improve compliance with UP.