Establishing a process to translate and adapt health education materials for natives and immigrants: The case of Mandarin adaptations of cardiac rehabilitation education

Background: Cardiac rehabilitation (CR) is a proven model of secondary prevention in which patient education is a core component. Objectives: to translate and culturally-adapt CR patient education for Mandarin-speaking patients living in China as well as immigrants, and offer recommendation for best practices in adaptation for both. Methods: these steps were undertaken in China and Canada: (1) preparation; (2) translation and adaptation; (3) review by healthcare providers based on PEMAT-P; (4) think-aloud review by patients; and (5) finalization. Results: Two independent Mandarin translations were undertaken using best practices: one domestic (China) and one international (immigrants). Input by 23 experts instigated revisions. Experts rated the language and content as culturally-appropriate, and perceived the materials would benefit their patients. A revised version was then administered to 36 patients, based on which a few edits were made to optimize understandability. Conclusions: some important differences emerged between translations adapted for native versus immigrant settings.This project has received funds from Toronto Rehab Foundation for the translation of materials (international version)

MYC regulates fatty acid metabolism through a multigenic program in claudin-low triple negative breast cancer

Background: Recent studies have suggested that fatty acid oxidation (FAO) is a key metabolic pathway for the growth of triple negative breast cancers (TNBCs), particularly those that have high expression of MYC. However, the underlying mechanism by which MYC promotes FAO remains poorly understood. Methods: We used a combination of metabolomics, transcriptomics, bioinformatics, and microscopy to elucidate a potential mechanism by which MYC regulates FAO in TNBC. Results: We propose that MYC induces a multigenic program that involves changes in intracellular calcium signalling and fatty acid metabolism. We determined key roles for fatty acid transporters (CD36), lipases (LPL), and kinases (PDGFRB, CAMKK2, and AMPK) that each contribute to promoting FAO in human mammary epithelial cells that express oncogenic levels of MYC. Bioinformatic analysis further showed that this multigenic program is highly expressed and predicts poor survival in the claudin-low molecular subtype of TNBC, but not other subtypes of TNBCs, suggesting that efforts to target FAO in the clinic may best serve claudin-low TNBC patients. Conclusion: We identified critical pieces of the FAO machinery that have the potential to be targeted for improved treatment of patients with TNBC, especially the claudin-low molecular subtype