Background: Idiosyncratic terminology and frameworks in the study of patient safety have been tolerated but are increasingly problematic. Agreement on standard language and frameworks is needed for optimal improvement and dissemination of knowledge about patient safety. Methods: Patient safety events were assessed using critical incident analysis, a method used to classify risks that has been more recently applied to medicine. Clinician interviews and clinician reports to a web based reporting system were used for analysis of hospital based and ambulatory care events, respectively. Events were classified independently by three investigators. Results: A pediatric patient safety taxonomy, relevant to both hospital based and ambulatory pediatric care, was developed from the analysis of 122 hospital based and 144 ambulatory care events. It is composed of four main categories: (1) problem type; (2) domain of medicine; (3) contributing factors in the patient (child-specific), environment (latent conditions) and care providers (human factors); and (4) outcome or result of the event and level of harm. A classification of preventive mechanisms was also developed. Inter-rater reliability of classifications ranged from 72% to 86% for sub-categories of the taxonomy.Conclusions: This patient safety taxonomy reflects the nature of events that occur in both pediatric hospital based and ambulatory care settings. It is flexible in its construction, permits analysis to begin at any point, and depicts the relationships and interactions of elements of an event.
We have described a novel macrophage-derived mucin secretagogue (MMS-68) that mediates mucin secretion in colon cancer cell lines and explants of normal and inflammatory bowel disease (IBD) mucosa. We compared MMS-68 induced mucin release with other known intestinal mucin secretagogues in normal colon explants and in the HT-29 colon cancer cell line, and to study the effects of MMS-68 on mucin release from inflamed and uninflamed ulcerative colitis (UC) and Crohn's disease (CD) mucosa. In normal colonic explants and HT-29 cells, each of the secretagogues including, MMS-68-induced mucin release two- to fivefold more than culture medium alone. In HT-29 cells, MMS-68 plus leukotriene C4 (LTC4) induced a 50% increase in mucin release over either secretagogue alone, and MMS-68 plus platelet-activating factor (PAF) markedly enhanced mucin release by eightfold over either secretagogue. In colonic explants from patients with UC and CD, the mucin release in response to MMS-68 was similar to that of normal colonic explants. Likewise, in isolated epithelial cells from CD and UC (whether involved or uninvolved), MMS-68-induced release was similar to that of epithelial cells isolated from normal colonic mucosa. The number of MMS-68-producing macrophages was lower in uninflamed UC mucosa compared with inflamed UC mucosa and CD mucosa. The mucin secretagogue activity of MMS-68 is comparable to that of other known secretagogues, and PAF can have a synergistic effect on this activity. Whole tissue explants and isolated colonic epithelial cells from patients with IBD respond at least as well as their normal counterparts to MMS-68. MMS-68 may play a role in mucin secretion in normal and inflamed colonic tissue.
We have described a novel macrophage-derived tnucin secretagogue (MMS-68) that mediates mucin secretion in colon cancer cell lines and explants of normal and inflammatory bowel disease (IBD) mucosa. we compared MMS-68 induced mucin release with other known intestinal mucin secretagogues in normal colon explants and in the HT-29 colon cancer cell line, and to study the effects of MMS-68 on mucin release from inflamed and uninflamed ulcerative colitis (UC) and Crohn's disease (CD) mucosa. In normal colonic explants and HT-29 cells, each of the secretagogues including MMS-68-induced mucin release two-to fivefold more than culture medium alone. I n HT-29 cells, MMS-68 plus leukotriene C, (LTC,) induced ;I 50% increase in mucin release over either secretagoguc alone, and MMS-68 plus platelet-activating factor (PAF) markedly enhanced mucin release by eightfold over either secretagogue. In colonic explants from patients with UC
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