Introduction
Teaching is an important competency in graduate medical education (GME). Many residency programs have implemented curricula to develop residents’ teaching skills and observed structured ...teaching experiences (OSTEs) have been used to assess these skills. There is an increasing focus on building teaching skills earlier in the medical education continuum, however, there is limited literature on assessing medical students’ teaching skills. The authors developed an OSTE for medical students enrolled in a students-as-teachers course to address this gap and provide formative feedback on teaching skills.
Materials and Methods
OSTEs were conducted for fourth-year medical students (M4s) enrolled in a Students as Teachers Advanced Elective at a US medical school. An M4 observed a first-year medical student (M1) during a simulated encounter with a standardized patient. The M4 gave feedback and a chalk talk. A physician observer assessed the M4’s teaching using the modified Stanford Faculty Development Program (SFDP) questionnaire. The M1s and M4s also completed the SFDP. The M4 completed pre- and post-OSTE self-efficacy surveys (score range 6-30) and a post-OSTE acceptability survey.
Results
All (30/30) M4s completed the OSTE. The SFDP identified common teaching strengths and areas for growth. ANOVA tests demonstrated significant differences between the mean (SD) scores from physician assessors, M1s, and M4s 4.56 (0.63) vs. 4.87 (0.35) vs. 4.08 (0.74), p<0.001. There was a statistically significant difference in mean (SD) self-efficacy scores pre- and post-OSTE 18.72 (3.39) vs. 23.83 (3.26), p<0.001. All M4s (30/30) somewhat or strongly agreed with all three OSTE acceptability questions.
Lessons Learned
The authors successfully conducted an OSTE in an M4 advanced elective. The OSTE was highly acceptable to participants, and M4s demonstrated improved teaching self-efficacy. Further research should explore the validity of the OSTE to measure medical students’ teaching skills and the long-term impact of developing teaching skills in medical school.
Abstract
Disclosure: N.A. Belsky: None. J. Tamaroff: None. A.H. Shoemaker: None.
Background: Pediatric type 2 diabetes (T2D) is increasing in prevalence, yet the pathophysiology and disease ...progression is less understood than in adults. It is unclear what definition of pediatric prediabetes predicts progression to T2D or long-term morbidity. Strategies are needed to better identify at risk individuals who could benefit from close follow up and early intervention. This study utilized a Pediatric Prediabetes Clinic to assess what factors may be associated with increased risk of progression to T2D in children over time. Methods: We conducted a retrospective chart review of the initial visit for all children referred to the clinic over 7 years. Inclusion criteria included hemoglobin A1c and ≥1 glucose result from an oral glucose tolerance test. Children with type 1 diabetes, MODY, or T2D on initial visit were excluded. Patients were assigned to either the T2D progression or non-progression group for further analysis based on 2022 ADA criteria. Additional information was manually charted for the T2D progression group from each visit from initial presentation through diagnosis of T2D. Results: 552 patients were included, 6.5% (n= 36) progressed to T2D over 2.4 ± 1.5 years. At the initial visit, T2D progressors had a higher BMI (mean difference 4.4 kg/m2, p = 0.002) and weight (mean difference 14.2 kg, p = 0.004). Initial visit HbA1c (5.7± 0.3 vs. 6.0±0.3%, p <0.001), 2h glucose (141±28 vs. 114±2mg/dL, p <0.001) and fasting c-peptide (4.8±2.1 vs. 3.6±2.0 ng/mL, p = 0.001) were also higher in the T2D progression group. On a fasting lipid panel, triglycerides (138±64 vs. 109±59 mg/dL, p = 0.015) were higher and HDL was lower (38±5 vs. 41±9 mg/dL, p = 0.003) in T2D progressors. Fasting plasma glucose was not significantly different between groups. Mean age at T2D diagnosis was 14.9 years (range 9.9 – 18.3 years). In a multivariable model, male sex (HR 2.4, p = 0.012), initial visit HbA1c (HR 1.3 per 0.1% increase, p <0.001), and 2-hour glucose level (HR 1.2 per 10 mg/dL increase, p = 0.014) were all predictive of increased likelihood of progression over time, while age did not reach significance (HR 0.9, p = 0.05). On average, patients who progressed to T2D had an increase in BMI of 4.2 kg/m2 from initial visit to time of T2D diagnosis and children consistently taking metformin took longer to progress (43 ± 21 vs. 26 ± 16 months, p= 0.016). Discussion: Overall, few patients with prediabetes developed T2D over the 7-year period, highlighting the importance of identifying which patients should receive early intervention and close follow-up. Initial visit laboratory values (particularly HbA1c and non-fasting glucose) and weight trajectory may allow for risk stratification, while fasting plasma glucose is less helpful. Preventing further worsening of obesity and metformin therapy could be important interventions for diabetes prevention in children.
Presentation: Friday, June 16, 2023
Abstract
Background
Pediatric type 2 diabetes (T2D) is increasing in prevalence, yet it is unclear what definition of pediatric prediabetes predicts progression to T2D. Strategies are needed to ...better identify at risk individuals who could benefit from early intervention.
Methods
Retrospective chart review of a pediatric prediabetes clinic over 7 years. Inclusion criteria include hemoglobin A1c (HbA1C) and ≥1 glucose from oral glucose tolerance test. Exclusion criteria include type 1 diabetes, maturity onset diabetes of the young, or T2D on initial visit.
Results
A total of 552 patients were included, 6.5% (n = 36) progressed to T2D over 2.4 ± 1.5 years. At initial visit, T2D progressors had a higher body mass index (38.6 ± 6.5 vs 34.2 ± 8.4 kg/m2, P = .002), HbA1C (6.0 ± 0.3%, vs 5.7± 0.3, P < .001), 2-hour glucose (141 ± 28 vs 114 ± 29 mg/dL, P < .001), and C-peptide (4.8 vs 3.6 ng/mL, P = .001). Fasting glucose was not significantly different. In a multivariable model, male sex (hazard ratio HR, 2.4; P = .012), initial visit HbA1C (HR, 1.3 per 0.1% increase; P < .001), and 2-hour glucose level (HR, 1.2 per 10 mg/dL increase; P = .014) were all predictive of T2D progression. Patients who progressed to T2D had an increase in body mass index of 4.2 kg/m2 and children consistently taking metformin took longer to progress (43 ± 21 vs 26 ± 16 months; P = .016).
Discussion
A total of 6.5% of patients with prediabetes developed T2D over a 7-year period. Initial visit laboratory values and weight trajectory may allow for risk stratification, whereas fasting plasma glucose is less helpful. Weight stabilization and metformin therapy could be important interventions for diabetes prevention in children.
Introduction: While the outcome for children with acute lymphoblastic leukemia (ALL) has improved dramatically, the prognosis for those who relapse remains poor. One of the most common alterations ...found at relapse is the p.E1099K missense change within the SET domain of NSD2, a histone methyltransferase that di-methylates histone 3 lysine 36 (H3K36). NSD2 has 3 isoforms, two of which, Type II (canonical) and REIIBP (C-terminal), contain the SET domain, and another, Type I (N-terminal), that does not. The p.E1099K mutation leads to increased enzymatic activity, but pathways leading to a clonal advantage are unknown in ALL.
Methods: We used short hairpin RNAs (shRNAs) to target knockdown of two combinations of NSD2 isoforms: shI/II targets Types I and II, shII/RE targets Type II and REIIBP. Three different B-cell lines (Reh, 697, and KOPN-8) with 2 wildtype (WT) copies of NSD2 were stably transduced with shII/RE. Two B-Cell lines, RS4;11 and RCH-ACV, heterozygous for the NSD2 p.E1099K mutation, were transduced with shI/II and shII/RE. As a control, each B-cell line was stably transduced with a scrambled non-targeting (NT) shRNA. NSD2 knockdown was confirmed by Western Blots.
Cell lines were treated for 5 days with chemotherapy agents commonly used in pediatric ALL treatments (mercaptopurine (MP), cytarabine, methotrexate, prednisone, and doxorubicin). Cytotoxicity was assessed by CellTiter- Glo® and significance between IC50s was determined by ANOVA and post hoc Tukey test. Cell proliferation was measured by cell counting with trypan blue. Cell cycle progression in RS4;11 lines was monitored with Edu staining and flow cytometry with and without exposure to MP.
Results: Similar to previously reported results, knockdown of NSD2 in the 3 WT B-cell lines had no effect on cell proliferation. However, shI/II reduced growth by 40% in RS4;11 and 20% in RCH-ACV, while shII/RE decreased proliferation by 45% in RS4;11 and 55% in RCH-ACV when compared to their NT control. In RS4;11, both shI/II and shII/RE led to a similar 10% decrease in cells progressing through S phase compared to NT, which could be due to either a slower progression through cell cycle or less cells entering the cell cycle.
Knockdown of NSD2 resulted in sensitivity to 6MP compared to NT in both RS4;11 and RCH-ACV lines. RS4;11 shII/RE had an IC50 3.2-fold more sensitive ( p<.01) and the RS4;11 shI/II IC50 was 1.25-fold more sensitive (NS) versus the NT control. Similarly, RCH-ACV shII/RE had an IC50 3.4-fold more sensitive (p<.01) and the RCH-ACV shI/II IC50 was 2.6-fold more sensitive (p<.01) compared to the NT control. No significant changes in drug sensitivity were noted for the 3 WT NSD2 knockdown B-cell lines compared to their NT controls.
During a 120 hour exposure to MP, 34% more RS4;11 shII/RE cells were arrested in the G phase than NT controls, while 26% more RS4;11 shI/II cells were arrested in G phase relative to NT controls. This result indicates MP exposure leads to a reduced percentage of knockdown cells able to progress through the cell cycle. Overall, simultaneously reduced expression of Type II and REIIBP had a greater effect of on cell proliferation and MP response compared to the co-reduction of Types I and II NSD2 in the p.E1099K heterozygous cell lines.
Conclusion: The p.E1099K mutation confers a growth advantage and resistance to MP, a cornerstone of ALL therapy. Concurrent reduction of Type II and REIIBP expression by shII/RE resulted in the largest impact on proliferation and MP sensitivity. Both of these isoforms include the SET domain containing the p.E1099K mutation, which indicates one or both isoforms could be responsible for changes in the chromatin state and other possible alterations that lead to a clonal advantage. Based on our findings, determining the mechanism of resistance to MP imparted by NSD2 p.E1099K is now a top priority.
No relevant conflicts of interest to declare.
Favorable histology (FH) Wilms tumor (WT) is one of the most curable of all human cancers, yet a small minority of patients fail treatment. The underlying biological pathways that lead to therapy ...resistance are unknown. We report a case of initially unresectable, FH WT which revealed limited necrosis and persistent blastemal predominant histology following neoadjuvant chemotherapy. Despite intensification of therapy and whole abdominal radiation, the patient relapsed and succumbed to her disease. In an effort to discover candidate drivers of drug resistance, whole exome sequencing and copy number analysis were performed on samples from all 3 tumor specimens. Sequencing results revealed outgrowth of clones with a dramatically different genetic landscape including dominant mutations that could explain therapy evasion, some of which have not been previously reported in WT. Our results implicate PPM1D, previously shown to be associated with drug resistance in other tumors, as the major driver of treatment failure.
Although teaching is an essential part of Graduate Medical Education and the practice of medicine, it is not often formally taught in Undergraduate Medical Education. Vanderbilt University School of ...Medicine (VUSM) has addressed this gap by creating a year-long Students-as-Teachers elective for post-clerkship medical students. The elective utilizes diverse activities to emphasize core tenets of medical education theory while simultaneously providing authentic teaching opportunities. The success of the elective is primarily attributable to its structure and design, the collaborative and supportive medical education environment, and student initiative and engagement. This manuscript describes the implementation and outcomes of the Students-as-Teachers elective.
PDF
