BackgroundThe purpose of this study was to develop a preclerkship elective and assess its effectiveness in supplementing medical students’ education.MethodsA group of medical students under the guidance of two faculty advisors developed an elective consisting of six sessions covering a variety of practical aspects of diabetes care/education taught by an interprofessional team. Following the course completion, a survey was emailed to the enrollees who attended at least one session. The results were analyzed using Wilcoxon signed-rank and descriptive analyses.ResultsA total of 14 medical students were enrolled (nine first year and five second year). An average of 4.4 sessions/student was attended. Thirteen students attended at least one session and were surveyed. The survey response rate was ~62% (8/13). All eight students indicated that the course was valuable and would recommend it to their colleagues. A Wilcoxon signed-rank test revealed a statistically significant increase in students’ confidence in all five areas assessed following participation in the course, P<0.05 with a large effect (r>0.5).ConclusionThis study suggests the feasibility of developing disease state-specific preclerkship elective courses and that such courses can be beneficial in supplementing medical student education with practical knowledge.

Background/purposeThe purpose of this study was to evaluate the effectiveness of supplemental diabetes-related training modalities and volunteer activities in increasing first-year medical students’ knowledge/comfort in providing diabetes self-management education and support (DSMES) to patients.MethodsA group of medical students developed supplemental diabetes-related training/volunteer programs. The training modalities included an optional 7-session interprofessionally taught Diabetes Enrichment Elective and a 3-hour endocrinologist-led training session intended to prepare students for involvement in an inpatient DSMES volunteer program. The volunteer program provided the students with the opportunity to provide DSMES to patients with diabetes admitted to an academic medical center. Those participating in any of the stated programs were compared to those with no such training regarding confidence in providing DSMES using an optional online survey. The results were analyzed by using Mann–Whitney U test and descriptive analyses.ResultsA total of 18 first-year medical students responded to the optional survey with a response rate of ~30% (10 of 33) among participants in any training/volunteer program. First-year medical students who attended any of the offered optional programs had statistically significant higher comfort level in 4 of the 6 areas assessed regarding providing DSMES compared with those with no such training (p<0.05), with medium to large effect size (r=0.48–0.59).ConclusionThis study suggests that the supplemental preclerkship diabetes-specific training modalities/volunteer programs can provide benefit in providing medical students with practical knowledge while improving their confidence in providing DSMES to patients with diabetes.

Approximately 5-10% of all Hypertrophic Cardiomyopathy (HCM) mutations reside within cardiac troponin T (cTnT). Residue Arg92 of cTnT represents a mutational hotspot, including Arg92Leu (R92L) and Arg92Trp (R92W). Interestingly, patients expressing these substitutions that differ by only a single amino acid present with distinct phenotypes and disease severity. Studying the differential effects of the R92 mutations on Ca 2+ homeostasis revealed an age-dependent increase in phospholamban (PLB) phosphorylation at Thr17 (targeted by CaMKII) only in R92W mice. Thus, we hypothesized a mutation-specific role of CaMKII in cTnT-linked HCM progression and tested this hypothesis via genetic partial inhibition of CaMKII (AC3I peptide) in both R92W and R92L transgenic mice. A progressive increase in PKA-mediated PLB-Ser16 phosphorylation was observed in the AC3I/RW mice, leading to an increase in SERCA2 activity. This improved Ca 2+ re-uptake activity was coupled with a decrease in atrial mass, indicative of a decrease in diastolic filling pressure. Thus, the R92W mutation initiates downstream pathophysiologic activation of CaMKII, leading to progressive cardiomyopathic remodeling. Partial inhibition of CaMKII in R92W mice resulted in the alteration of the natural history of HCM, indicating a potential therapeutic target for patients expressing the mutation. In contrast, AC3I/RL mice showed no change in SERCA2 activity or atrial morphology, suggesting a CaMKII-independent progression to disease for R92L-linked HCM. Finally, R92L and R92W mice were treated with diltiazem hydrochloride, an L-type Ca 2+ channel blocker, and diastolic function monitored over time. R92W mice showed improvement in diastolic function with treatment while R92L mice showed a progressive decrease in diastolic function. These findings suggest that closely related mutations, even at the same residue, can have discrete molecular effects that result in mutation-specific ventricular remodeling and these observations can be incorporated in targeted disease management.