Development and delivery of justice, equity, diversity, inclusion, and anti-oppression concepts in entry-level health professional education: a scoping review protocol.

OBJECTIVE: The objective of this scoping review is to identify the frameworks, guidelines, and models used to develop and deliver justice, equity, diversity, inclusion (JEDI), and anti-oppression (AO) principles in mandatory, entry-level health care professional program curricula (EHCPPC). A secondary objective will be to examine how these frameworks, guidelines, and models are used. INTRODUCTION: Health inequities are perpetuated globally, as observed by the suboptimal quality of care and health outcomes among equity-deserving groups. An understanding of JEDI and AO concepts is necessary in health care settings to promote culturally safe and high-quality care; however, entry-level health care programs may lack adequate integration of content and/or delivery of these principles. This scoping review will summarize the international literature on frameworks, guidelines, and models used to develop and deliver JEDI and AO concepts in EHCPPC. INCLUSION CRITERIA: This review will consider articles that discuss frameworks, models, or guidelines included in EHCPPC that guide the development and/or delivery of JEDI and AO principles in any country. Studies will be considered if they were published from 2015 to the present and are in English. All study designs will be considered for inclusion. METHODS: This review will be conducted in accordance with the JBI methodology for scoping reviews. A search of MEDLINE (Ovid), Embase (Ovid), and CINAHL (EBSCOhost) will be conducted. Two or more independent reviewers will assess titles and abstracts, screen full-text studies, and extract data from included studies. Data from the included studies will be collated into tables or figures and described in a narrative summary. REVIEW REGISTRATION: Open Science Framework osf.io/ewqf8.

The exon junction complex component EIF4A3 is essential for mouse and human cortical progenitor mitosis and neurogenesis.

Mutations in components of the exon junction complex (EJC) are associated with neurodevelopment and disease. In particular, reduced levels of the RNA helicase EIF4A3 cause Richieri-Costa-Pereira syndrome (RCPS) and copy number variations are linked to intellectual disability. Consistent with this, Eif4a3 haploinsufficient mice are microcephalic. Altogether, this implicates EIF4A3 in cortical development; however, the underlying mechanisms are poorly understood. Here, we use mouse and human models to demonstrate that EIF4A3 promotes cortical development by controlling progenitor mitosis, cell fate and survival. Eif4a3 haploinsufficiency in mice causes extensive cell death and impairs neurogenesis. Using Eif4a3;p53 compound mice, we show that apoptosis has the most impact on early neurogenesis, while additional p53-independent mechanisms contribute to later stages. Live imaging of mouse and human neural progenitors reveals that Eif4a3 controls mitosis length, which influences progeny fate and viability. These phenotypes are conserved, as cortical organoids derived from RCPS iPSCs exhibit aberrant neurogenesis. Finally, using rescue experiments we show that EIF4A3 controls neuron generation via the EJC. Altogether, our study demonstrates that EIF4A3 mediates neurogenesis by controlling mitosis duration and cell survival, implicating new mechanisms that underlie EJC-mediated disorders.

The exon junction complex component EIF4A3 is essential for mouse and human cortical progenitor mitosis and neurogenesis.

Mutations in components of the exon junction complex (EJC) are associated with neurodevelopment and disease. In particular, reduced levels of the RNA helicase EIF4A3 cause Richieri-Costa-Pereira Syndrome (RCPS) and CNVs are linked to intellectual disability. Consistent with this, Eif4a3 haploinsufficient mice are microcephalic. Altogether, this implicates EIF4A3 in cortical development; however, the underlying mechanisms are poorly understood. Here, we use mouse and human models to demonstrate that EIF4A3 promotes cortical development by controlling progenitor mitosis, cell fate, and survival. Eif4a3 haploinsufficiency in mice causes extensive cell death and impairs neurogenesis. Using Eif4a3 ; p53 compound mice, we show that apoptosis is most impactful for early neurogenesis, while additional p53-independent mechanisms contribute to later stages. Live imaging of mouse and human neural progenitors reveals Eif4a3 controls mitosis length, which influences progeny fate and viability. These phenotypes are conserved as cortical organoids derived from RCPS iPSCs exhibit aberrant neurogenesis. Finally, using rescue experiments we show that EIF4A3 controls neuron generation via the EJC. Altogether, our study demonstrates that EIF4A3 mediates neurogenesis by controlling mitosis duration and cell survival, implicating new mechanisms underlying EJC-mediated disorders. Summary statement: This study shows that EIF4A3 mediates neurogenesis by controlling mitosis duration in both mouse and human neural progenitors, implicating new mechanisms underlying neurodevelopmental disorders.