Learning from Graduate and Undergraduate Public Health Virtual Internship Experiences with State Title V Agencies During COVID-19, Summer 2020.

BACKGROUND: Since summer 2014, the National MCH Workforce Development Center has placed students from MCH public health graduate (Centers of Excellence and Catalyst) and undergraduate (MCH Pipeline) programs, all funded by the Maternal and Child Health Bureau, in summer internships with state and territorial Title V agencies. In 2020, due to the COVID-19 pandemic the Title V MCH Internship Program was offered virtually. PARTICIPANTS AND METHODS: This manuscript includes quantitative and qualitative data from 2017 to 2020 generated by both Title V MCH Internship student interns (n = 76) and their preceptors (n = 40) with a focus on a comparison between the 2020 virtual year and the 2017-2019 years. RESULTS: Evaluation data from the 2017 to 2020 Title V MCH Internship Program from both students and preceptors revealed the implementation of a robust and successful internship program in which students increased their confidence in a variety of team, mentorship, and leadership skills while gaining direct exposure to the daily work of state Title V agencies. However, students and preceptors identified more challenges during 2020 compared to previous years. CONCLUSIONS: The COVID-19 Pandemic was both a disruption and a catalyst for change in education. While there were clearly some challenges with the pivot to a virtual Title V MCH Internship Program in summer 2020, students were able to participate in meaningful internship experiences. This success can be attributed to the ability of the internship sponsor to engage in best practices, including extensive planning and provision of ongoing support to the students. Going forward, it is recognized that virtual internships may facilitate access to agencies in distant locales, eliminating issues related to housing and transportation. When both virtual and in-person relationships are available, those responsible for internship programs, including the Title V MCH Internship, will need to weigh these type of benefits against the potential missed opportunities students may have when not able to participate in on-site experiences.

Innovations in Maternal and Child Health: Pairing Undergraduate and Graduate Maternal and Child Health Students in Summer Practica in State Title V Agencies.

Objective As part of the National MCH Workforce Development Center, an innovative internship program placed MCH undergraduate and graduate students in summer practica in state Title V agencies. Graduate student mentoring of undergraduates and leadership and professional development training and support are key features of the program. The objective of this paper is to report on the results of the evaluation of the MCH Paired Practica Program in its pilot years, 2014-2016. Methods Students completed pre and post internship questionnaires which included closed as well as open-ended questions. In addition, the Title V state health agency preceptors completed a questionnaire at the end of each summer. Results Over the 3-year pilot project, a total of 17 teams participated. Students were from 6 of the 13 graduate Centers of Excellence in MCH programs in Schools of Public Health and two undergraduate MCH Pipeline Programs. There were 11 participating states. After the practicum experience, there was a significant increase in students' confidence in a number of measures related to working in complex, dynamic environments and in their ability to contribute to improvements in MCH population health. Students reported having more confidence in their ability to function effectively as an informal/formal MCH leader (p = 0.02), more confidence in their ability to contribute to improvements in MCH population health (p = 0.04), and being more prepared to enter the workforce after the practicum experience (p = 0.07), although there was no significant change in students' (n = 22) interest in seeking a job in a Title V agency or a community based organization with a MCH focus. Nearly 60% of the students did state at the posttest that they would likely seek additional education in MCH. Overall, the Title V preceptors (n = 14) were very positive about the program although in some instances there was less confidence in the knowledge and skills of the undergraduate students. Conclusion The MCH Paired Practica Program is a unique effort to go beyond the academic training of undergraduate and graduate MCH students to provide them with direct exposure to the field, as well as leadership, mentorship, and professional development training. While some challenges emerged related to differences in skills between undergraduates and graduate MCH students, participating students demonstrated clear improvements in their leadership skills including increased confidence in their ability to take initiative, provide opinions and feedback, to function informally or formally as leaders, and to contribute to improvements in MCH population health.

Mutation spectrum in the large GTPase dynamin 2, and genotype-phenotype correlation in autosomal dominant centronuclear myopathy.

Centronuclear myopathy (CNM) is a genetically heterogeneous disorder associated with general skeletal muscle weakness, type I fiber predominance and atrophy, and abnormally centralized nuclei. Autosomal dominant CNM is due to mutations in the large GTPase dynamin 2 (DNM2), a mechanochemical enzyme regulating cytoskeleton and membrane trafficking in cells. To date, 40 families with CNM-related DNM2 mutations have been described, and here we report 60 additional families encompassing a broad genotypic and phenotypic spectrum. In total, 18 different mutations are reported in 100 families and our cohort harbors nine known and four new mutations, including the first splice-site mutation. Genotype-phenotype correlation hypotheses are drawn from the published and new data, and allow an efficient screening strategy for molecular diagnosis. In addition to CNM, dissimilar DNM2 mutations are associated with Charcot-Marie-Tooth (CMT) peripheral neuropathy (CMTD1B and CMT2M), suggesting a tissue-specific impact of the mutations. In this study, we discuss the possible clinical overlap of CNM and CMT, and the biological significance of the respective mutations based on the known functions of dynamin 2 and its protein structure. Defects in membrane trafficking due to DNM2 mutations potentially represent a common pathological mechanism in CNM and CMT.

The exon 55 deletion in the nebulin gene--one single founder mutation with world-wide occurrence.

In 2004, Anderson et al. reported a homozygous 2502 bp deletion including exon 55 of the nebulin gene in five Ashkenazi Jewish probands with nemaline myopathy. We determined the occurrence of this deletion in a world-wide series of 355 nemaline myopathy probands with no previously known mutation in other genes and found the mutation in 14 probands, two of whom represented families previously ascertained by Anderson et al. Two of the families were not of known Ashkenazi Jewish descent but they had the haplotype known to segregate with this mutation. In all but two of eight homozygous patients, the clinical picture was more severe than in typical nemaline myopathy.

Nemaline myopathy with minicores caused by mutation of the CFL2 gene encoding the skeletal muscle actin-binding protein, cofilin-2.

Nemaline myopathy (NM) is a congenital myopathy characterized by muscle weakness and nemaline bodies in affected myofibers. Five NM genes, all encoding components of the sarcomeric thin filament, are known. We report identification of a sixth gene, CFL2, encoding the actin-binding protein muscle cofilin-2, which is mutated in two siblings with congenital myopathy. The proband's muscle contained characteristic nemaline bodies, as well as occasional fibers with minicores, concentric laminated bodies, and areas of F-actin accumulation. Her affected sister's muscle was reported to exhibit nonspecific myopathic changes. Cofilin-2 levels were significantly lower in the proband's muscle, and the mutant protein was less soluble when expressed in Escherichia coli, suggesting that deficiency of cofilin-2 may result in reduced depolymerization of actin filaments, causing their accumulation in nemaline bodies, minicores, and, possibly, concentric laminated bodies.