Revitalizing pathology laboratories in a gastrointestinal pathophysiology course using multimedia and team-based learning techniques.

In 2008, we changed the gastrointestinal pathology laboratories in a gastrointestinal pathophysiology course to a more interactive format using modified team-based learning techniques and multimedia presentations. The results were remarkably positive and can be used as a model for pathology laboratory improvement in any organ system. Over a two-year period, engaging and interactive pathology laboratories were designed.

Persistent psychological or physical symptoms following endoscopic procedures: an unrecognized post-endoscopy adverse event.

Background: Depression and post-traumatic stress disorder have been described after surgical procedures, but not after gastrointestinal endoscopy.

Aims: The aim of our retrospective survey was to determine if new-onset, persistent (>1 month) psychological and/or physical symptoms develop after gastrointestinal endoscopy. We also sought to assess how endoscopy teams respond to patient discomfort during the procedure.

Using medical students to enhance curricular integration of cross-cultural content.

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.

Integration of racial, cultural, ethnic, and socioeconomic factors into a gastrointestinal pathophysiology course.

Background & Aims: Our study describes a faculty development program to encourage the integration of racial, cultural, ethnic, and socioeconomic factors such as obesity, inability to pay for essential medications, the use of alternative medicine, dietary preferences, and alcoholism in a gastrointestinal pathophysiology course.

Methods: We designed a 1-hour faculty development session with longitudinal reinforcement of concepts. The session focused on showing the relevance of racial, ethnic, cultural, and socioeconomic factors to gastrointestinal diseases, and encouraged tutors to take an active and pivotal role in discussion of these factors.

Evidence of increased flux to n-6 docosapentaenoic acid in phospholipids of pancreas from cftr-/- knockout mice.

An association has been reported between alterations in fatty acid metabolism and cystic fibrosis (CF). We hypothesized that these alterations are specific for a particular lipid component(s) and are the result of a specific metabolic defect. The different lipid classes were examined for fatty acid changes by using pancreatic homogenates and primary cultures of pancreatic acini from cftr(-/-) (CF) and wild-type mice.

Liver and skeletal muscle lipids have differing fatty acid profiles in short-gut rats fed via parenteral nutrition.

Background: In short-gut rats, we showed marked abnormalities in plasma lipid fatty acids using parenteral nutrition (PN) with lipid vs sham surgery rats. This suggests that either sensing or metabolism of parenteral lipid is abnormal in malabsorption. The goal of this study was to determine fatty acid profiles in skeletal muscle and liver in short-gut rats treated with PN compared with sham rats.

Ethanol administration to cystic fibrosis knockout mice results in increased fatty acid ethyl ester production.

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.

Decreased expression of peroxisome proliferator activated receptor gamma in cftr-/- mice.

Some of the pathological manifestations of cystic fibrosis are in accordance with an impaired expression and/or activity of PPARgamma. We hypothesized that PPARgamma expression is altered in tissues lacking the normal cystic fibrosis transmembrane regulator protein (CFTR). PPARgamma mRNA levels were measured in colonic mucosa, ileal mucosa, adipose tissue, lung, and liver from wild-type and cftr-/- mice by quantitative RT-PCR.

Oral docosahexaenoic acid given to pregnant mice increases the amount of surfactant in lung and amniotic fluid in preterm fetuses.

Objective: Our purpose was to determine whether docosahexaenoic acid increased surfactant production, as reflected by increased dipalmitoyl phosphatidylcholine, in mouse fetal lung and amniotic fluid.

Study Design: On day 9.5 of gestation, pregnant mice were given docosahexaenoic acid orally at 0, 5, 10, or 20 mg per day and were killed at day 16.

Induction of colitis in cftr-/- mice results in bile duct injury.

It is unknown why some patients with inflammatory bowel disease develop primary sclerosing cholangitis. We have recently shown that patients with primary sclerosing cholangitis have an increased prevalence of mutations in the gene responsible for cystic fibrosis (CFTR) compared with individuals with inflammatory bowel disease alone. Our aim was to examine whether induction of colitis by oral dextran leads to bile duct injury in mice heterozygous or homozygous for mutations in CFTR.

Abnormal regulation of serum lipid fatty acid profiles in short gut rats fed parenteral nutrition with lipid.

Despite absence of essential fatty acid deficiency (EFAD), increases in arachidonic acid to linoleic acid ratios occur in serum phospholipid of patients treated with chronic total parenteral nutrition (TPN). The parenteral lipid component of TPN contains abundant linoleate; thus low phospholipid linoleate may reflect increased conversion to arachidonate. Arachidonic acid excess has been associated with a proinflammatory milieu through increased eicosanoid production and might contribute to the increases in inflammatory markers seen in home TPN patients.

Association of cystic fibrosis with abnormalities in fatty acid metabolism.

Background: Patients with cystic fibrosis have altered levels of plasma fatty acids. We previously demonstrated that arachidonic acid levels are increased and docosahexaenoic acid levels are decreased in affected tissues from cystic fibrosis-knockout mice. In this study we determined whether humans with mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene have a similar fatty acid defect in tissues expressing CFTR.

Characterization of LPS-induced lung inflammation in cftr-/- mice and the effect of docosahexaenoic acid.

The mechanism by which Pseudomonas causes excessive inflammation in the cystic fibrosis lung is unclear. We have reported that arachidonic acid is increased and docosahexaenoic acid (DHA) decreased in lung, pancreas, and ileum from cftr-/- mice. Oral DHA corrected this defect and reversed the pathology.