This paper presents the research process and methods used to evaluate and improve a web-based health information resource intended for the public. The resource is called Community Connect to Research (CC2R) (www.connecttoresearch.org). The research process was an iterative one that involved collaboration with many partners. Two formal evaluations were conducted in 2009 and 2010 using key informant interviews, usability interviews, focus groups, an online survey, and readability and suitability assessment tools. These methods provided us with users’ perspective on the overall design, content, and literacy demands of the web site as well as valuable feedback on their interaction with the web site. We subsequently redesigned CC2R, making significant improvements based on what we learned from the evaluation. The second evaluation revealed that the redesign addressed many issues found in the first evaluation and identified additional areas of possible improvement. Overall, both evaluations suggested that participants believed that the web site was useful and valuable, indicating that CC2R is indeed a health information resource that provides patients and families with accessible, relevant, and high-quality information. Our experience suggests that regular formal evaluation is an essential tool for effective ongoing enhancement of health information resources meant for the public.

Background & Aims: RET receptor tyrosine kinase is necessary for enteric nervous system (ENS) development. Loss-of-function RET mutations cause Hirschsprung disease (HSCR), in which infants are born with aganglionic bowel. Despite surgical correction, HSCR patients often experience chronic defecatory dysfunction and enterocolitis, suggesting that RET is important after development. To test this hypothesis, we determined the location of postnatal RET and its significance in gastrointestinal (GI) motility. Methods: RetCFP/+ mice and human transcriptional profiling data were studied to identify the enteric neuronal and epithelial cells that express RET. To determine whether RET signaling in these cells regulates adult gut motility in vivo, genetic and pharmacologic approaches were used to disrupt RET in either all RET-expressing cells, a major subset of enteric neurons, or intestinal epithelial cells. Results: Distinct subsets of enteric neurons and enteroendocrine cells expressed RET in the adult intestine. RET disruption in the intestinal epithelium, rather than in enteric neurons, slowed GI motility selectively in adult male mice. This effect was phenocopied by RET kinase inhibition. Most RET+ epithelial cells were either enterochromaffin cells that release serotonin (5-HT) or L-cells that release peptide YY (PYY), both of which can alter motility. RET kinase inhibition exaggerated PYY release in a nutrient-dependent manner without altering 5-HT secretion. PYY receptor blockade fully rescued dysmotility in mice lacking epithelial RET. Conclusion: RET signaling normally limits nutrient-dependent PYY release from L-cells and this activity is necessary for normal intestinal motility in male mice. These effects could contribute to post-operative dysmotility in HSCR, which predominantly affects males, and uncovers a mechanism that could be targeted to treat post-prandial GI dysfunction.