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We hypothesized that an interested medical student group would be helpful in reviewing tutorial cases and giving relevant feedback on the curricular integration of cross-cultural content using case triggers in a preclinical gastrointestinal pathophysiology course. Self-selected student leaders (n = 9) reviewed pre-existing problem-based learning tutorial cases (n = 3) with cross-cultural triggers, and provided narrative feedback to course faculty. The cases were modified and used for the entire class in the following 2 years. Participating course students' comments and teaching faculty feedback were also noted. Outcomes were a change in case content, student global evaluations of the course, and self-reported faculty comfort with teaching the cases. All three tutorial cases were reviewed by a separate group of 2–3 students. Major and minor revisions were made to each case based on the student feedback. These cases were used in 2007 and 2008 and were the major change to the course during that time. Overall course evaluation scores improved significantly from 2006 to 2008 (p = 0.000). Tutors (n = 22 in 2007; n = 23 in 2008) expressed relief during tutor meetings that students had reviewed the cases. A general framework for eliciting student feedback on problem-based cases was developed. Student feedback, consisting of self-selected students' case reviews and solicited course and tutor comments, added value to a curricular reform to improve the integration of cross-cultural content into a problem-based learning curriculum. Our study underscores the fundamental link between teachers and students as partners in curricular development.

BACKGROUND:: Fatty acid ethyl esters (FAEE) are nonoxidative ethanol metabolites shown to produce toxic effects in the liver and pancreas in vivo and in vitro. Because alcohol-induced chronic pancreatitis is associated with mutations in the gene responsible for cystic fibrosis (CFTR), we hypothesized that CFTR dysfunction leads to increased levels of these toxic nonoxidative ethanol metabolites following alcohol administration.METHODS:: Cystic fibrosis (CF) and wild-type (WT) mice were injected intraperitoneally with 1, 2, or 3 g/kg of 50% ethanol. Mice were sacrificed and the liver and pancreas removed for FAEE analysis.RESULTS:: The mean FAEE concentration (pmol/g) detected in the liver of cftr mice following injection with 2 g/kg of ethanol was significantly greater than the amount detected in WT (p < 0.005). A similar trend in FAEE concentration was seen in the pancreas, but the difference was not statistically different. In both the liver and pancreas, analysis of individual FAEE species demonstrated a selective increase in ethyl oleate.CONCLUSION:: These data show an association between CFTR dysfunction and qualitative and quantitative changes in FAEE in liver and pancreas upon ethanol exposure. [ABSTRACT FROM AUTHOR]

Some of the pathological manifestations of cystic fibrosis are in accordance with an impaired expression and/or activity of PPARγ. We hypothesized that PPARγ expression is altered in tissues lacking the normal cystic fibrosis transmembrane regulator protein (CFTR). PPARγ mRNA levels were measured in colonic mucosa, ileal mucosa, adipose tissue, lung, and liver from wild-type and cftr-/- mice by quantitative RT-PCR. PPARγ expression was decreased twofold in CFTR-regulated tissues (colon, ileum, and lung) from cftr-/- mice compared to wild-type littermates. In contrast, no differences were found in fat and liver. Immunohistochemical analysis of PPARγ in ileum and colon revealed a predominantly nuclear localization in wild-type mucosal epithelial cells while tissues from cftr-/- mice showed a more diffuse, lower intensity labeling. A significant decrease in PPARγ expression was confirmed in nuclear extracts of colon mucosa by Western blot analysis. In addition, binding of the PPARγ/RXR heterodimer to an oligonucletotide containing a peroxisome proliferator responsive element (PPRE) was also decreased in colonic mucosa extracts from cftr-/- mice. Treatment of cftr-/- mice with the PPARγ ligand rosiglitazone restored both the nuclear localization and binding to DNA, but did not increase RNA levels. We conclude that PPARγ expression in cftr-/- mice is downregulated at the RNA and protein levels and its function diminished. These changes may be related to the loss of function of CFTR and may be relevant to the pathogenesis of metabolic abnormalities associated with cystic fibrosis in humans. © 2004 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]