Making the Case for Global Engineering: Building Foreign Language Collaborations for Designing, Implementing, and Assessing Programs

Engineering programs must prepare students for a global engineering profession. In global markets, processes as well as products can be outsourced. Highly technical engineering work may be completed by large and diverse collaborations. Engineering students need to have foundational work in languages, cultural differences, and strategies for working with diverse colleagues. Historically only about 3% to 4% of engineering students pursue study abroad opportunities. Clearly, new and innovative programs must be devised to build global competency in undergraduate engineers. In working toward that end, the authors suggest that interdisciplinary collaborations between departments of foreign language and schools of engineering can be highly productive. To illustrate the benefits of such collaborations and to share the results of recent program assessments, this case study presents a conceptual model useful in program design and describes the evolution of a particularly intensive and effective program in global competency for undergraduate engineers

Primary cilia and SHH signaling impairments in human and mouse models of Parkinson’s disease

Parkinson’s disease (PD) as a progressive neurodegenerative disorder arises from multiple genetic and environmental factors. However, underlying pathological mechanisms remain poorly understood. Using multiplexed single-cell transcriptomics, we analyze human neural precursor cells (hNPCs) from sporadic PD (sPD) patients. Alterations in gene expression appear in pathways related to primary cilia (PC). Accordingly, in these hiPSC-derived hNPCs and neurons, we observe a shortening of PC. Additionally, we detect a shortening of PC in PINK1-deficient human cellular and mouse models of familial PD. Furthermore, in sPD models, the shortening of PC is accompanied by increased Sonic Hedgehog (SHH) signal transduction. Inhibition of this pathway rescues the alterations in PC morphology and mitochondrial dysfunction. Thus, increased SHH activity due to ciliary dysfunction may be required for the development of pathoetiological phenotypes observed in sPD like mitochondrial dysfunction. Inhibiting overactive SHH signaling may be a potential neuroprotective therapy for sPD