Preparing healthcare leaders of the digital age with an integrative artificial intelligence curriculum: a pilot study.

Artificial intelligence (AI) is rapidly being introduced into the clinical workflow of many specialties. Despite the need to train physicians who understand the utility and implications of AI and mitigate a growing skills gap, no established consensus exists on how to best introduce AI concepts to medical students during preclinical training. This study examined the effectiveness of a pilot Digital Health Scholars (DHS) non-credit enrichment elective that paralleled the Dartmouth Geisel School of Medicine's first-year preclinical curriculum with a focus on introducing AI algorithms and their applications in the concurrently occurring systems-blocks. From September 2022 to March 2023, ten self-selected first-year students enrolled in the elective curriculum run in parallel with four existing curricular blocks (Immunology, Hematology, Cardiology, and Pulmonology). Each DHS block consisted of a journal club, a live-coding demonstration, and an integration session led by a researcher in that field. Students' confidence in explaining the content objectives (high-level knowledge, implications, and limitations of AI) was measured before and after each block and compared using Mann-Whitney U tests. Students reported significant increases in confidence in describing the content objectives after all four blocks (Immunology: U = 4.5, p = 0.030; Hematology: U = 1.0, p = 0.009; Cardiology: U = 4.0, p = 0.019; Pulmonology: U = 4.0, p = 0.030) as well as an average overall satisfaction level of 4.29/5 in rating the curriculum content. Our study demonstrates that a digital health enrichment elective that runs in parallel to an institution's preclinical curriculum and embeds AI concepts into relevant clinical topics can enhance students' confidence in describing the content objectives that pertain to high-level algorithmic understanding, implications, and limitations of the studied models. Building on this elective curricular design, further studies with a larger enrollment can help determine the most effective approach in preparing future physicians for the AI-enhanced clinical workflow.

Acute Genetic Ablation of Cardiac Sodium/Calcium Exchange in Adult Mice: Implications for Cardiomyocyte Calcium Regulation, Cardioprotection, and Arrhythmia.

Background Sodium-calcium (Ca2+) exchanger isoform 1 (NCX1) is the dominant Ca2+ efflux mechanism in cardiomyocytes and is critical to maintaining Ca2+ homeostasis during excitation-contraction coupling. NCX1 activity has been implicated in the pathogenesis of cardiovascular diseases, but a lack of specific NCX1 blockers complicates experimental interpretation. Our aim was to develop a tamoxifen-inducible NCX1 knockout (KO) mouse to investigate compensatory adaptations of acute ablation of NCX1 on excitation-contraction coupling and intracellular Ca2+ regulation, and to examine whether acute KO of NCX1 confers resistance to triggered arrhythmia and ischemia/reperfusion injury. Methods and Results We used the α-myosin heavy chain promoter (Myh6)-MerCreMer promoter to create a tamoxifen-inducible cardiac-specific NCX1 KO mouse. Within 1 week of tamoxifen injection, NCX1 protein expression and current were dramatically reduced. Diastolic Ca2+ increased despite adaptive reductions in Ca2+ current and action potential duration and compensatory increases in excitation-contraction coupling gain, sarcoplasmic reticulum Ca2+ ATPase 2 and plasma membrane Ca2+ ATPase. As these adaptations progressed over 4 weeks, diastolic Ca2+ normalized and SR Ca2+ load increased. Left ventricular function remained normal, but mild fibrosis and hypertrophy developed. Transcriptomics revealed modification of cardiovascular-related gene networks including cell growth and fibrosis. NCX1 KO reduced spontaneous action potentials triggered by delayed afterdepolarizations and reduced scar size in response to ischemia/reperfusion. Conclusions Tamoxifen-inducible NCX1 KO mice adapt to acute genetic ablation of NCX1 by reducing Ca2+ influx, increasing alternative Ca2+ efflux pathways, and increasing excitation-contraction coupling gain to maintain contractility at the cost of mild Ca2+-activated hypertrophy and fibrosis and decreased survival. Nevertheless, KO myocytes are protected against spontaneous action potentials and ischemia/reperfusion injury.