Modeling for Fidelity: virtual mentorship by scientists fosters teacher self-efficacy and promotes implementation of novel high school biomedical curricula.

This small-scale comparison case study evaluates the impact of an innovative approach to teacher professional development designed to promote implementation of a novel cutting edge high school neurological disorders curriculum. 'Modeling for Fidelity' (MFF) centers on an extended mentor relationship between teachers and biomedical scientists carried out in a virtual format in conjunction with extensive online educative materials. Four teachers from different diverse high schools in Massachusetts and Ohio who experienced MFF contextualized to a 6-week Neurological Disorders curriculum with the same science mentor were compared to a teacher who had experienced an intensive in-person professional development contextualized to the same curriculum with the same mentor. Fidelity of implementation was measured directly using an established metric and indirectly via student performance. The results show that teachers valued MFF, particularly the mentor relationship and were able to use it effectively to ensure critical components of the learning objectives were preserved. Moreover their students performed equivalently to those whose teacher had experienced intensive in-person professional development. Participants in all school settings demonstrated large (Cohen's d>2.0) and significant (p<0.0001 per-post) changes in conceptual knowledge as well as self-efficacy towards learning about neurological disorders (Cohen's d>1.5, p<0.0001 pre-post). The data demonstrates that the virtual mentorship format in conjunction with extensive online educative materials is an effective method of developing extended interactions between biomedical scientists and teachers that are scalable and not geographically constrained, facilitating teacher implementation of novel cutting-edge curricula.

The Great Diseases Project: a partnership between Tufts Medical School and the Boston public schools.

Medical schools, although the gatekeepers of much biomedical education and research, rarely engage formally with K-12 educators to influence curriculum content or professional development. This segregation of content experts from teachers creates a knowledge gap that limits inclusion of current biomedical science into high school curricula, affecting both public health literacy and the biomedical pipeline. The authors describe how, in 2009, scientists from Tufts Medical School and Boston public school teachers established a partnership of formal scholarly dialogue to create 11th- to 12th-grade high school curricula about critical health-related concepts, with the goal of increasing scientific literacy and influencing health-related decisions. The curricula are based on the great diseases (infectious diseases, neurological disorders, metabolic disease, and cancer). Unlike most health science curricular interventions that provide circumscribed activities, the curricula are comprehensive, each filling one full term of in-class learning and providing extensive real-time support for the teacher. In this article, the authors describe how they developed and implemented the infectious disease curriculum, and its impacts. The high school teachers and students showed robust gains in content knowledge and critical thinking skills, whereas the Tufts scientists increased their pedagogical knowledge and appreciation for health-related science communication. The results show how formal interactions between medical schools and K-12 educators can be mutually beneficial.

Rhodopsin-mediated retinitis pigmentosa.

Retinitis pigmentosa (RP) is a genetically and phenotypically heterogeneous group of diseases that cause blindness. Mutations within the rhodopsin gene account for approximately 25% of autosomal dominantly inherited RP cases. Therefore, understanding the mechanisms causing rhodopsin-mediated RP has a significant health impact. To date, results from multiple labs indicate that rhodopsin-mediated RP pathogenesis does not share a common mechanism of degeneration. There is strong evidence that multiple mechanisms are involved, including protein misfolding, mislocalization, release of toxic products, and aberrant signaling. Development of effective treatments requires investigation of the mechanism involved in the different rhodopsin mutations. This chapter focuses on the mechanisms by which rhodopsin mutations cause retinal degeneration, as well as potential therapeutic strategies to treat the disease.

A novel form of transducin-dependent retinal degeneration: accelerated retinal degeneration in the absence of rod transducin.

PURPOSE: Rhodopsin mutations account for approximately 25% of human autosomal dominant retinal degenerations. However, the molecular mechanisms by which rhodopsin mutations cause photoreceptor cell death are unclear. Mutations in genes involved in the termination of rhodopsin signaling activity have been shown to cause degeneration by persistent activation of the phototransduction cascade. This study examined whether three disease-associated rhodopsin substitutions Pro347Ser, Lys296Glu, and the triple mutant Val20Gly, Pro23His, Pro27Leu (VPP) caused degeneration by persistent transducin-mediated signaling activity. METHODS: Transgenic mice expressing each of the rhodopsin mutants were crossed onto a transducin alpha-subunit null (Tr(alpha)(-/-)) background, and the rates of photoreceptor degeneration were compared with those of transgenic mice on a wild-type background. RESULTS: Mice expressing VPP-substituted rhodopsin had the same severity of degeneration in the presence or absence of Tr(alpha). Unexpectedly, mice expressing Pro347Ser- or Lys296Glu-substituted rhodopsins exhibited faster degeneration on a Tr(alpha)(-/-) background. To test whether the absence of alpha-transducin contributed to degeneration by favoring the formation of stable rhodopsin/arrestin complexes, mutant Pro347Ser(+), Tr(alpha)(-/-) mice lacking arrestin (Arr(-/-)) were analyzed. Rhodopsin/arrestin complexes were found not to contribute to degeneration. CONCLUSIONS: The authors hypothesized that the decay of metarhodopsin to apo-opsin and free all-trans-retinaldehyde is faster with Pro347Ser-substituted rhodopsin than it is with wild-type rhodopsin. Consistent with this, the lipofuscin fluorophores A2PE, A2E, and A2PE-H(2), which form from retinaldehyde, were elevated in Pro347Ser transgenic mice.