Transforming LEND leadership training curriculum through the maternal and child health leadership competencies.

The purpose of this article is to describe how the Maternal and Child Health (MCH) Leadership Competencies (v 3.0) were used to examine and improve an MCH Leadership Education in Neurodevelopmental and Related Disabilities (LEND) training curriculum for New Hampshire and Maine. Over 15 % of the nation's children experience neurodevelopmental disabilities or special health care needs and estimates suggest 1 in every 68 children is diagnosed with an autism spectrum disorder. Across the Unites States critical shortages of qualified MCH professionals exist, particularly in poor and rural areas. A continued investment in training interdisciplinary leaders is critical. The MCH Leadership Competencies provide an effective foundation for leadership training through identification of requisite knowledge, skills, and dispositions required of MCH leaders. This paper describes a three-step process, which began in 2010 and included utilizing the MCH Leadership Competencies as a tool to reflect on, develop, and evaluate the NH LEND leadership curriculum. Curriculum development was further supported through participation in a multi-state learning collaborative. Through a series of intentional decisions, the curriculum design of NH LEND utilized the competencies and evidence-based principles of instruction to engage trainees in the development of specific MCH content knowledge and leadership skills. The LEND network specifically, and MCH leadership programs more broadly, may benefit from the intentional use of the MCH competencies to assist in curriculum development and program evaluation, and as a means to support trainees in identifying specific leadership goals and evaluating their leadership skill development.

Geographical mapping of a multifocal thyroid tumour using genetic alteration analysis & miRNA profiling.

BACKGROUND: Papillary thyroid carcinoma (PTC) frequently presents as multiple tumour-foci within a single thyroid gland or pluriform, with synchronous tumours comprising different histological variants, raising questions regarding its clonality. Among the genetic aberrations described in PTC, the BRAF V600E mutation and ret/PTC activation occur most commonly. Several studies have investigated the genetic alteration status of multifocal thyroid tumours, with discordant results. To address the question of clonality this study examined disparate geographical and morphological areas from a single PTC (classic PTC, insular and anaplastic foci, and tumour cells adjacent to vascular invasion and lymphocytic infiltrate) for the presence of ret/PTC 1 or BRAF mutations. Moreover, we wanted to investigate the consistency of miRNA signatures within disparate areas of a tumour, and geographical data was further correlated with expression profiles of 330 different miRNAs. Putative miRNA gene targets were predicted for differentially regulated miRNAs and immunohistochemistry was performed on tissue sections in an effort to investigate phenotypic variations in microvascular density (MVD), and cytokeratin and p53 protein expression levels. RESULTS: All of the morphological areas proved negative for ret/PTC 1 rearrangement. Two distinct foci with classic morphology harboured the BRAF mutation. All other regions, including the insular and anaplastic areas were negative for the mutation. MiRNA profiles were found to distinguish tumours containing the BRAF mutation from the other tumour types, and to differentiate between the more aggressive insular & anaplastic tumours, and the classic variant. Our data corroborated miRNAs previously discovered in this carcinoma, and additional miRNAs linked to various processes involved in tumour growth and proliferation. CONCLUSION: The initial genetic alteration analysis indicated that pluriform PTC did not necessarily evolve from classic PTC progenitor foci. Analysis of miRNA profiles however provided an interesting variation on the clonality question. While hierarchical clustering analysis of miRNA expression supported the hypothesis that discrete areas did not evolve from clonal expansion of tumour cells, it did not exclude the possibility of independent mutational events suggesting both phenomena might occur simultaneously within a tumour to enhance cancer progression in geographical micro-environments within a tumour.