Development of a 3D printed simulator for closed reduction of distal radius fractures.

BACKGROUND: The use of simulators in medical education is critical for developing procedural competence prior to treating patients. Current training of emergency physicians to perform distal radius fracture reduction is inconsistent and inadequate. APPROACH: We developed a 3D printed distal radius fracture simulation training model that is easy to assemble and relatively inexpensive. We present step-by-step instructions to reproduce the model. EVALUATION: The model was found to have high fidelity for training by both instructors and participants in a simulation-based mastery learning course. REFLECTION: We successfully designed a low cost, easy to reproduce, high fidelity model for use in a simulation-based mastery learning course to teach distal radius fracture reduction.

Simulation-Based Mastery Learning to Teach Distal Radius Fracture Reduction.

INTRODUCTION: Distal radius fractures are common orthopedic injuries managed in emergency departments. Simulation-based mastery learning is widely recognized to improve provider competence for bedside procedures but has not been studied to teach fracture management. This study evaluated the effectiveness of a simulation-based mastery learning curriculum to teach distal radius fracture reduction to novice orthopedic surgery and emergency medicine residents. METHODS: We created a novel mastery learning checklist using the Mastery Angoff method of standard setting, paired with a new simulation model designed for this project, to teach orthopedic surgery and emergency medicine interns (N = 22) at the study site. Orthopedic surgery and emergency medicine faculty members participated in checklist development, curriculum design, and implementation. Training included just-in-time asynchronous education with a readiness assessment test, in-classroom expert demonstration, and deliberate practice with feedback. Residents completed a pretest/posttest skills examination and a presurvey/postsurvey assessing procedural confidence. RESULTS: Standard setting resulted in a 41-item checklist with minimum passing score of 37/41 items. All participants met or surpassed the minimum passing score on postexamination. Postsurvey confidence levels were significantly higher than presurvey in all aspects of the distal radius fracture procedure (P < 0.05). CONCLUSIONS: This study demonstrated that a simulation-based mastery learning curriculum improved skills and confidence performing distal radius fracture reductions for orthopedic surgery and emergency medicine interns. Future planned studies include curriculum testing across additional institutions, examination of clinical impact, and application of mastery learning for other orthopedic procedures.

The MYC Oncogene Cooperates with Sterol-Regulated Element-Binding Protein to Regulate Lipogenesis Essential for Neoplastic Growth.

Lipid metabolism is frequently perturbed in cancers, but the underlying mechanism is unclear. We present comprehensive evidence that oncogene MYC, in collaboration with transcription factor sterol-regulated element-binding protein (SREBP1), regulates lipogenesis to promote tumorigenesis. We used human and mouse tumor-derived cell lines, tumor xenografts, and four conditional transgenic mouse models of MYC-induced tumors to show that MYC regulates lipogenesis genes, enzymes, and metabolites. We found that MYC induces SREBP1, and they collaborate to activate fatty acid (FA) synthesis and drive FA chain elongation from glucose and glutamine. Further, by employing desorption electrospray ionization mass spectrometry imaging (DESI-MSI), we observed in vivo lipidomic changes upon MYC induction across different cancers, for example, a global increase in glycerophosphoglycerols. After inhibition of FA synthesis, tumorigenesis was blocked, and tumors regressed in both xenograft and primary transgenic mouse models, revealing the vulnerability of MYC-induced tumors to the inhibition of lipogenesis.

Oncogene KRAS activates fatty acid synthase, resulting in specific ERK and lipid signatures associated with lung adenocarcinoma.

KRAS gene mutation causes lung adenocarcinoma. KRAS activation has been associated with altered glucose and glutamine metabolism. Here, we show that KRAS activates lipogenesis, and this activation results in distinct proteomic and lipid signatures. By gene expression analysis, KRAS is shown to be associated with a lipogenesis gene signature and specific induction of fatty acid synthase (FASN). Through desorption electrospray ionization MS imaging (DESI-MSI), specific changes in lipogenesis and specific lipids are identified. By the nanoimmunoassay (NIA), KRAS is found to activate the protein ERK2, whereas ERK1 activation is found in non-KRAS-associated human lung tumors. The inhibition of FASN by cerulenin, a small molecule antibiotic, blocked cellular proliferation of KRAS-associated lung cancer cells. Hence, KRAS is associated with activation of ERK2, induction of FASN, and promotion of lipogenesis. FASN may be a unique target for KRAS-associated lung adenocarcinoma remediation.