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Using an actionable research approach, researchers and practitioners can collaborate in research to inform advocacy for and development of interventions that seek to reduce inequality in educational outcomes. This process was used at an elite public university to examine the limitations of a summer bridge program and inform the development of an intervention model that provided comprehensive academic and social support for underrepresented students enrolled in engineering and, after a pilot test, other programs at the Midwest University (MU). This article discusses the process leading to the Engineering Academy bridge program, summarizes the research on the pilot test, and describes how the results were used by administrators to advocate for the continuation of the Engineering Academy. Currently, support from the National Science Foundation and MU’s general fund is being used to adapt the intervention for biology, math, and other fields at MU’s College of Liberal Arts. [ABSTRACT FROM PUBLISHER]

Recent studies have demonstrated the importance of local protein synthesis for neuronal plasticity. In particular, local mRNA translation through the mammalian target of rapamycin (mTOR) has been shown to play a key role in regulating dendrite excitability and modulating long-term synaptic plasticity associated with learning and memory. There is also increased evidence to suggest that intact adult mammalian axons have a functional requirement for local protein synthesis in vivo. Here we show that the translational machinery is present in some myelinated sensory fibers and that active mTORdependent pathways participate in maintaining the sensitivity of a subpopulation of fast-conducting nociceptors in vivo. Phosphorylated mTOR together with other downstream components of the translational machinery were localized to a subset of myelinated sensory fibers in rat cutaneous tissue. We then showed with electromyographic studies that the mTOR inhibitor rapamycin reduced the sensitivity of a population of myelinated nociceptors known to be important for the increased mechanical sensitivity that follows injury. Behavioural studies confirmed that local treatment with rapamycin significantly attenuated persistent pain that follows tissue injury, but not acute pain. Specifically, we found that rapamycin blunted the heightened response to mechanical stimulation that develops around a site of injury and reduced the longterm mechanical hypersensitivity that follows partial peripheral nerve damage - a widely used model of chronic pain. Our results show that the sensitivity of a subset of sensory fibers is maintained by ongoing mTOR-mediated local protein synthesis and uncover a novel target for the control of long-term pain states. [ABSTRACT FROM AUTHOR]