Fellows as teachers: a model to enhance pediatric resident education

Pressures on academic faculty to perform beyond their role as educators has stimulated interest in complementary approaches in resident medical education. While fellows are often believed to detract from resident learning and experience, we describe our preliminary investigations utilizing clinical fellows as a positive force in pediatric resident education. Our objectives were to implement a practical approach to engage fellows in resident education, evaluate the impact of a fellow-led education program on pediatric resident and fellow experience, and investigate if growth of a fellowship program detracts from resident procedural experience.This study was conducted in a neonatal intensive care unit (NICU) where fellows designed and implemented an education program consisting of daily didactic teaching sessions before morning clinical rounds. The impact of a fellow-led education program on resident satisfaction with their NICU experience was assessed via anonymous student evaluations. The potential value of the program for participating fellows was also evaluated using an anonymous survey.The online evaluation was completed by 105 residents. Scores were markedly higher after the program was implemented in areas of teaching excellence (4.44 out of 5 versus 4.67, p<0.05) and overall resident learning (3.60 out of 5 versus 4.61, p<0.001). Fellows rated the acquisition of teaching skills and enhanced knowledge of neonatal pathophysiology as the most valuable aspects of their participation in the education program. The anonymous survey revealed that 87.5% of participating residents believed that NICU fellows were very important to their overall training and education.While fellows are often believed to be a detracting factor to residency training, we found that pediatric resident attitudes toward the fellows were generally positive. In our experience, in the specialty of neonatology a fellow-led education program can positively contribute to both resident and fellow learning and satisfaction. Further investigation into the value of utilizing fellows as a positive force in resident education in other medical specialties appears warranted

Igf2 ligand dependency of Pten(+/-) developmental and tumour phenotypes in the mouse.

The tumour suppressor PTEN is a key negative regulator of the PI3K-Akt pathway, and is frequently either reduced or lost in human tumours. Murine genetic studies have confirmed that reduction of Pten promotes tumourigenesis in multiple organs, and demonstrated dependency of tumour development on the activation of downstream components such as Akt. Insulin-like growth factors (IGFs) act via IGF1R to activate the PI3K-Akt pathway, and are commonly upregulated in cancer. A context-dependent interplay between IGFs and PTEN exists in normal tissue and tumours; increased IGF2 ligand supply induces Pten expression creating an autoregulatory negative feedback loop, whereas complete loss of PTEN may either cooperate with IGF overexpression in tumour promotion, or result in desensitisation to IGF ligand. However, it remains unknown whether neoplasia associated with Pten loss is dependent on upstream IGF ligand supply in vivo. We evaluated this by generation of Pten(+/-) mice with differing allelic dosage of Igf2, an imprinted gene encoding the potent embryonic and tumour growth factor Igf2. We show that biallelic Igf2 supply potentiates a previously unreported Pten(+/-) placental phenotype and results in strain-dependent cardiac hyperplasia and neonatal lethality. Importantly, we also show that the effects of Pten loss in vivo are modified by Igf2 supply, as lack of Igf2 results in extended survival and delayed tumour development while biallelic supply is associated with reduced lifespan and accelerated neoplasia in females. Furthermore, we demonstrate that reduction of PTEN protein to heterozygote levels in human MCF7 cells is associated with increased proliferation in response to IGF2, and does not result in desensitisation to IGF2 signalling. These data indicate that the effects of Pten loss at heterozygote levels commonly observed in human tumours are modified by Igf2 ligand, and emphasise the importance of the evaluation of upstream pathways in tumours with Pten loss