Predicting and enhancing American Board of Surgery In-Training Examination performance: does writing questions really help?

BACKGROUND: The generative learning model posits that individuals remember content they have generated better than materials created by others. The goals of this study were to evaluate question generation as a study method for the American Board of Surgery In-Training Examination (ABSITE) and determine whether practice test scores and other data predict ABSITE performance. METHODS: Residents (n = 206) from 6 general surgery programs were randomly assigned to one of the two study conditions. One group wrote questions for practice examinations. All residents took 2 practice examinations. RESULTS: There was not a significant effect of writing questions on ABSITE score. Practice test scores, United States Medical Licensing Examination Step 1 scores, and previous ABSITE scores were significantly correlated with ABSITE performance. CONCLUSIONS: The generative learning model was not supported. Performance on practice tests and other data can be used for early identification of residents at risk of performing poorly on the ABSITE.

Computed tomography to diagnose blunt diaphragm injuries: not ready for prime time.

Diaphragm injuries after blunt trauma are uncommon but require early diagnosis to expedite repair. The advancing technology of computed tomography (CT) scanners has improved the detection of almost all traumatic injuries; however, the literature regarding the diagnostic accuracy of CT scan for blunt diaphragm injuries is lacking. The purpose of this study was to determine the CT scan findings in the setting of known blunt diaphragm injury. We performed a retrospective review of all blunt trauma patients with a known diaphragm injury confirmed at laparotomy who also had a preoperative CT scan of the torso. Every CT scan was retrospectively reviewed by a board-certified radiologist for evidence of diaphragm injury as well as associated abdominal and thoracic injuries. Forty-two patients sustaining blunt trauma had preoperative CT scans of the torso and a diaphragm injury confirmed at laparotomy. Only 57 per cent of CT scans showed evidence of diaphragmatic injury. The most common thoracic injury identified was a pulmonary contusion (79%). Although the advancement of imaging technology has markedly improved the diagnosis and management of blunt traumatic injuries, the detection of diaphragm injuries using CT continues to be low and reconstructions do not help in finding diaphragm injuries.

Glutamine activates peroxisome proliferator-activated receptor-γ in intestinal epithelial cells via 15-S-HETE and 13-OXO-ODE: a novel mechanism.

Glutamine possesses gut-protective effects both clinically and in the laboratory. We have shown in a rodent model of mesenteric ischemia-reperfusion that enteral glutamine increased peroxisome proliferator-activated receptor-γ (PPAR-γ) and was associated with a reduction in mucosal injury and inflammation. The mechanism by which glutamine activates PPAR-γ is unknown, and we hypothesized that it was via a ligand-dependent mechanism. Intestinal epithelial cells, IEC-6, were co-transfected with PPAR-γ response element-luciferase promoter/reporter construct. Cells were pretreated with increasing concentrations of glutamine ± GW9662 (a specific antagonist of PPAR-γ) and analyzed for PPAR-γ response element luciferase activity as an indicator of PPAR-γ activation. PPAR-γ nuclear activity was assessed by electrophoretic mobility shift assay. Cell lysates were subjected to tandem mass spectroscopy for measurement of prostaglandin and lipoxygenase metabolites. A time- and concentration-dependent increase in PPAR-γ transcriptional activity, but not mRNA or protein, was demonstrated. Activity was abrogated by the PPAR-γ inhibitor, GW9662, and changes in activity correlated with PPAR-γ nuclear binding. Glutamine, via degradation to glutamate, activated the metabolic by-products of the lipoxygenase and linoleic acid pathways, 15-S-hydroxyeicosatetraenoic acid and dehydrogenated 13-hydroxyoctaolecadienoic acid, known endogenous PPAR-γ ligands in the small bowel. This novel mechanism may explain the gut-protective effects of enteral glutamine.