How to Teach Laboratory Stewardship in the Undergraduate Medical Curriculum?

OBJECTIVES: Promotion of high-quality care at a lower cost requires educational initiatives across the continuum of medical education. A needs assessment was performed to inform the design of an educational tool with the goal of teaching laboratory stewardship to medical students. METHODS: The needs assessment consisted of semistructured interviews with core clerkship directors and residency program directors at our institution, a national survey to the Undergraduate Medical Educators Section (UMEDS) of the Association of Pathology Chairs, and a review of existing online resources that teach high-value care. RESULTS: Two major themes emerged regarding opportunities to enhance laboratory stewardship education: appropriate ordering (knowledge of test indications, pretest/posttest probability, appropriateness criteria, recognition of unnecessary testing) and correct interpretation (understanding test specifications, factors that affect the test result, recognizing inaccurate results). CONCLUSIONS: The online educational tool will focus on the curricular needs identified, using a multidisciplinary approach for development and implementation.

More than a camera holder: teaching surgical skills to medical students.

BACKGROUND: Students often experience passive learning in their surgical rotations as they are delegated to holding the camera during laparoscopic cases. We introduced a laparoscopic skills course to medical students to provide hands-on experience. We hypothesized that the course will improve basic laparoscopic skills and increase interest in a surgical career. MATERIALS AND METHODS: All students on the core surgery rotation attended two sessions in the surgical simulation laboratory lead by Department of Surgery faculty members. Surveys were used before and after the course to assess video game (VG) use and interest in a surgical career. Course effectiveness was assessed with a laparoscopic peg transfer exercise. RESULTS: One hundred one students participated with 82 students documenting preinstruction and postinstruction peg transfer times. There was an overall improvement in median transfer times after instruction (before 63 s [interquartile range {IQR} 46-84.5] versus after 50.5 s [IQR 39-65.2], P < 0.001). When stratified by gender, men (n = 40) had faster median preintervention peg transfer times than women (n = 61; 65 s [IQR 51-88]) versus 81 s [IQR 65-98] (P = 0.030). However, both genders had equivalent postinstruction transfer times (men 48 s [IQR 36-61] versus women 51.3 s [IQR 43.2-68.3], P = 0.478). A similar trend was observed between students with and without prior VG use. Of the 50 students who completed both surveys, there was no significant increase (pre-24% versus post-34%, P = 0.29) or decrease (pre-32% versus post-22%, P = 0.13) in interest in a surgical career after the course. CONCLUSIONS: A laparoscopic course for medical students is effective in improving laparoscopic skills. Although male gender and VG use may be associated with better intrinsic skills, instruction and practice allow female students and non-VG users to "catch up." A longer follow-up study is warranted to determine true interest in a surgical career.

Cyclosporine A prevents vascular hyperpermeability after hemorrhagic shock by inhibiting apoptotic signaling.

BACKGROUND: Hemorrhagic shock (HS) is associated with the activation of caspase-dependent or -independent apoptotic signaling pathways, disruption of endothelial cell adherens junctions, and vascular hyperpermeability. Recent studies have suggested that the vascular hyperpermeability observed after HS is associated with activation of the intrinsic apoptotic signaling cascade resulting in caspase-mediated cleavage of endothelial cell adherens proteins and subsequent cell-cell detachment. We hypothesized that cyclosporine A (CsA) would attenuate vascular hyperpermeability after HS by protecting mitochondrial transition pores and thereby preventing the activation of caspase-mediated apoptotic signaling. The objective of this study was to determine the effect of CsA on, HS-induced hyperpermeability, mitochondrial membrane depolarization, mitochondrial release of cytochrome c, and caspase 3 activation. METHODS: HS was induced in Sprague-Dawley rats by withdrawing blood to reduce the mean arterial pressure to 40 mm Hg for 60 minutes. CsA (10 microL/mL) was given 10 minutes before the shock period. The mesenteric postcapillary venules of the proximal ileum were monitored for permeability changes using intravital microscopy. The changes in mitochondrial transmembrane potential were determined using the cationic dye JC-1. Mitochondrial release of cytochrome c in to the cytosol was detected using ELISA. Caspase-3 activity was measured using a fluorometric assay. RESULTS: HS induced vascular hyperpermeability, release of cytochrome c, and activation of caspase-3 (p < 0.05). CsA (10 microL/mL) attenuated HS-induced hyperpermeability (p < 0.05) and prevented HS-induced decrease in mitochondrial transmembrane potential. CsA treatment decreased the HS-induced rise in cytosolic cytochrome c levels and caspase-3 activity (p < 0.05). CONCLUSIONS: These findings demonstrate that CsA protects mitochondrial permeability transition pores to prevent HS-induced release of cytochrome c and caspase-3 activation.

Alpha lipoic acid attenuates microvascular endothelial cell hyperpermeability by inhibiting the intrinsic apoptotic signaling.

BACKGROUND: This study examined whether alpha lipoic acid (ALA), an antioxidant with anti-apoptotic properties, synthesized in mitochondria of endothelial cells, would inhibit intrinsic apoptotic signaling and microvascular endothelial cell hyperpermeability. METHODS: Rat lung microvascular endothelial cells were transfected with BAK (BH3) peptide (5 microg/mL) or active caspase-3 (5 microg/mL) and were pretreated with ALA (10 and 100 micromol/L). Hyperpermeability was determined using fluorescein isothiocyanate albumin-flux across the cells grown as monolayer. Reactive oxygen species (ROS) formation was determined using 123 dihydrorhodamine and mitochondrial membrane potential using JC-1. Cytochrome c levels and caspase-3 activity were determined using an enzyme-linked immunosorbent assay and a fluorometric assay, respectively. RESULTS: ALA (100 micromol/L) pretreatment attenuated BAK (BH3)-induced hyperpermeability and ROS formation. ALA restored BAK (BH3)-induced collapse in mitochondrial membrane potential and decreased BAK (BH3)-induced cytochrome c release and caspase-3 activity. CONCLUSIONS: These findings suggest that ALA attenuates BAK-induced monolayer hyperpermeability through the inhibition of ROS formation and intrinsic apoptotic signaling.