RESUMO
The complexity of the material being taught in clinical neuroscience within the medical school curriculum requires creative pedagogies to teach medical students effectively. Many clinical teaching strategies have been developed and are well described to address these challenges. However, only a few have been evaluated to determine their impact on the performance of students studying clinical neuroscience. Interactive, 2-hour, self-directed small-group interactive clinical case-based learning sessions were conducted weekly for 4 weeks to integrate concepts learned in the corresponding didactic lectures. Students in the small groups analyzed cases of patients suffering from neurological disease that were based on eight learning objectives that allowed them to evaluate neuroanatomical data and clinical findings before presenting their case analysis to the larger group. Students' performances on the formative quizzes and summative tests were compared to those of first-year medical students in the previous year for whom the self-directed, small-group interactive clinical sessions were not available. There was a significant improvement in the summative performance of first-year medical students with self-directed clinical case learning in the second year (Y2) of teaching clinical neuroscience (P < 0.05) when compared with first-year students in the first year (Y1) for whom the self-directed learning approach was not available. Student performance in the formative assessments between Y1 and Y2 was not significantly different (P = 0.803). A target of ≥70% student scoring above 80% in the final summative examination was met. The current study revealed evidence for the impact and educational outcomes of a self-directed, clinical teaching strategy in a clinical neuroscience curriculum for first-year medical students. Anat Sci Educ 11: 478-487. © 2017 American Association of Anatomists.
Assuntos
Desempenho Acadêmico/estatística & dados numéricos , Educação de Graduação em Medicina/métodos , Neuroanatomia/educação , Estudantes de Medicina/estatística & dados numéricos , Ensino , Adulto , Encéfalo/anatomia & histologia , Encéfalo/diagnóstico por imagem , Currículo , Educação de Graduação em Medicina/estatística & dados numéricos , Feminino , Humanos , Masculino , Avaliação de Programas e Projetos de Saúde , Faculdades de Medicina/organização & administração , Faculdades de Medicina/estatística & dados numéricos , Adulto JovemRESUMO
IGF-1 receptor (IGF-1R) signaling is associated with increased tumorigenesis of epithelial cancers. In light of recent epidemiological studies correlating high circulating levels of IGF-1 with increased risk of second primary tumors (SPTs) of the head and neck, we examined IGF system and epidermal growth factor receptor (EGFR) expression in human head and neck squamous cell carcinoma (HNSCC) matched pairs and a cross-section of HNSCC cell lines. Employing the latter, we demonstrated that IGF-1 stimulated S-phase transition in a PI 3-K/Akt and Erk-dependent manner in 5 of 8 cell lines, with Erk activation being dependent upon EGFR kinase activity. IGF-1 stimulated thymidine incorporation was inhibited by treatment with IGFBP-3, the IGF-1R tyrosine kinase inhibitor NVP-AEW541, or the EGFR tyrosine kinase inhibitor AG1478. Combining IGFBP-3 with NVP-AEW541 or AG1478 abrogated IGF-1 responses at 10-fold lower doses than either compound alone. These results demonstrate the potential for co-targeting the IGF system and EGFR in HNSCC.
Assuntos
Carcinoma de Células Escamosas/metabolismo , Neoplasias de Cabeça e Pescoço/metabolismo , Proteínas de Ligação a Fator de Crescimento Semelhante a Insulina/metabolismo , Receptor IGF Tipo 1/metabolismo , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Ensaio de Imunoadsorção Enzimática , Humanos , Immunoblotting , Ligantes , Fosfatidilinositol 3-Quinases/efeitos dos fármacos , Fosfatidilinositol 3-Quinases/metabolismo , Inibidores de Proteínas Quinases/farmacologia , Proteínas Proto-Oncogênicas c-akt/efeitos dos fármacos , Proteínas Proto-Oncogênicas c-akt/metabolismoRESUMO
Elevated vascular endothelial growth factor (VEGF) levels correlate with increased progression and poor prognosis of head and neck squamous cell carcinomas (HNSCC). VEGF expression is regulated by hypoxia and cytokines, including insulin-like growth factor-1 (IGF-1). In this report, we examined IGF-1 signaling and VEGF expression in SCC-9 cells. IGF-1 and the chemical hypoxia agent, cobalt chloride, each stimulated VEGF secretion and VEGF promoter activation. Cobalt chloride increased Hif-1alpha protein levels and HIF-1 dependent activation of the enolase promoter. IGF-1 increased these parameters only in the presence of cobalt chloride. IGF-1 stimulated PI-3K/Akt and Erk/MAPK pathways in SCC-9 cells, each contributing to Hif-1alpha expression and VEGF secretion. SCC-9 cells express the VEGF receptors Flk-1 and neuropilin-1, with VEGF treatment increasing VEGF promoter activity and VEGF secretion that was attenuated by the Flk-1 tyrosine kinase inhibitor, ZM 323881. These results demonstrate the presence of an IGF-1 regulated VEGF autocrine loop in HNSCC.