Incorporating Diversity, Equity, and Inclusion Content Into Bioengineering Curricula: A Program-Level Approach.

Diversity, equity, and inclusion (DEI) are interconnected with bioengineering, yet have historically been absent from accreditation standards and curricula. Toward educating DEI-competent bioengineers and meeting evolving accreditation requirements, we took a program-level approach to incorporate, catalog, and assess DEI content through the bioengineering undergraduate program. To support instructors in adding DEI content and inclusive pedagogy, our team developed a DEI planning worksheet and surveyed instructors pre- and post-course. Over the academic year, 74% of instructors provided a pre-term and/or post-term response. Of responding instructors, 91% described at least one DEI curricular content improvement, and 88% incorporated at least one new inclusive pedagogical approach. Based on the curricular adjustments reported by instructors, we grouped the bioengineering-related DEI content into five DEI competency categories: bioethics, inclusive design, inclusive scholarship, inclusive professionalism, and systemic inequality. To assess the DEI content incorporation, we employed direct assessment via course assignments, end-of-module student surveys, end-of-term course evaluations, and an end-of-year program review. When asked how much their experience in the program helped them develop specific DEI competencies, students reported a relatively high average of 3.79 (scale of 1 = "not at all" to 5 = "very much"). Additionally, based on student performance in course assignments and other student feedback, we found that instructors were able to effectively incorporate DEI content into a wide variety of courses. We offer this framework and lessons learned to be adopted by programs similarly motivated to train DEI-competent engineering professionals and provide an equitable, inclusive engineering education for all students.

Fostering Community and Inclusion in a Team-Based Hybrid Bioengineering Lab Course.

As cornerstones of biomedical engineering and bioengineering undergraduate programs, hands-on laboratory experiences promote key skill development and student engagement. Lab courses often involve team-based activities and close communication with instructors, allowing students to build connection and community. Necessitated by the pandemic, changes to class delivery format presented unprecedented challenges to student inclusion and engagement, especially for students from underrepresented minority backgrounds. Here, we present a multi-faceted approach for fostering inclusion and community-building in a hybrid bioengineering laboratory course. A basis for this project was an approach for team-based project work which allowed students to have hands-on experience in the lab and collaborate extensively with peers, while abiding by social distancing guidelines. Members of each student team worked together remotely and synchronously on a project. One team member executed the hands-on portion of each lab activity and the remote student(s) engaged in the project via online communication. The hybrid lab course was supplemented with interventions to further promote inclusivity and community, including instructor modeling on inclusion, team-based course content, attention to lab session logistics, and instructor communication. Students responded positively, as indicated by the median ratings in course evaluations for the four lab sections in the following categories concerning course climate (using a 5.0 scale): their overall comfort with the climate of the course (4.8 to 5.0), feeling valued and respected by lab instructor (4.8 to 5.0) and their peers (4.8 to 5.0), peers helping each other succeed in the course (4.5 to 5.0), and the degree to which the experience in the course contributed to their sense of belonging in engineering (4.2 to 5.0). When asked to describe aspects of the class that contributed to inclusivity towards differences, students cited a collaborative environment, course content on implicit bias and inclusivity, and an approachable teaching team. Overall, our approach was effective in fostering a sense of community and inclusion. We anticipate many of these initiatives can transcend instructional format to positively impact future lab course offerings, irrespective of modality. Supplementary Information: The online version contains supplementary material available at 10.1007/s43683-022-00081-4.

Attenuation of ephrinB2 reverse signaling decreases vascularized area and preretinal vascular tuft formation in the murine model of oxygen-induced retinopathy.

PURPOSE: EphB4 and ephrinB2 are known key regulators of retinal vascular development, but due to their capacity for bidirectional signaling, delineation of their individual roles in this process remains unclear. To better dissect out individual contributions, a model of proliferative retinopathy in mice with attenuated ephrinB2 reverse signaling was studied. It was hypothesized that endothelial ephrinB2 reverse signaling regulates hypoxia-induced capillary sprouting, as well as the pathologic formation of neovascular tufts in postnatal retinal microvascular networks. METHODS: Genetically manipulated mice with attenuated ephrinB2 reverse signaling (ephrinB2(lacZ/+)), along with wild-type (WT) controls, were exposed to oxygen-induced retinopathy (OIR), a postnatal model of proliferative retinopathy. At peak disease (postnatal day 18), microvascular networks were analyzed to examine intraretinal revascularization, capillary sprouting, and pathologic neovascularization responses. EphB4 and phosphorylated ephrinB protein expression patterns along retinal microvessels were also assessed. RESULTS: EphrinB2(lacZ/+) mice exhibited reduced hypoxia-induced revascularization (P ≤ 0.04) and reduced formation of neovascular tufts (P < 0.001), as compared with WT controls. Corresponding to the observed inhibition of retinal angiogenesis, ephrinB2(lacZ/+) retinas displayed an increased number of blind-ended capillary sprout tips (P < 0.02) and endothelial filopodial processes (P = 0.001). In WT and ephrinB2(lacZ/+) OIR-exposed retinas, ephrinB was confined to endothelial cells, with expression detected along angiogenic vascular processes including neovascular tufts and blind-ended capillary sprouts. CONCLUSIONS: EphrinB2 reverse signaling is a regulator of key processes during retinal vascularization and controls pathologic retinal angiogenesis through direct effects on capillary sprouting and endothelial filopodia formation.

Chronic whole-body hypoxia induces intussusceptive angiogenesis and microvascular remodeling in the mouse retina.

Currently, little is known about the response of the adult retinal microvasculature to hypoxia. To test the hypothesis that chronic systemic hypoxia induces angiogenesis and microvascular remodeling in the adult mouse retina, adult 10-week old female C57Bl/6 mice were exposed to 10% O(2) for 2 or 3 weeks. After hypoxia exposure, retinas were harvested, whole-mounted, and processed for immunohistochemistry. Retinas were stained with lectin, anti-smooth muscle alpha-actin antibody, and anti-NG2 antibody to visualize microvascular networks and their cellular components. Confocal microscopy was used to obtain images of superficial retinal networks. Images were analyzed to assess vessel diameter, vascular length density, branch point density, and the presence of vascular loops, a hallmark of intussusceptive angiogenesis. Both 2 and 3 weeks of hypoxia exposure resulted in a significant increase in the diameters of arterioles and post-arteriole capillaries (p<0.003). After 3 weeks of hypoxia, vascular length density and branch point density were significantly increased in retinas exposed to hypoxia as compared to normoxic controls (p<0.001). The number of vascular loops in the superficial retinal networks was significantly greater in hypoxia-exposed retinas (p < or = 0.001). Our results demonstrate, for the first time, intussusceptive angiogenesis as a tissue-level mechanism of vascular adaptation to chronic systemic hypoxia in the adult mouse retina and contribute to our understanding of hypoxia-induced angiogenesis and microvascular remodeling in the adult animal.

EphB4 expression along adult rat microvascular networks: EphB4 is more than a venous specific marker.

OBJECTIVE: EphrinB2 and EphB4 are considered to be markers of arterial/venous identity during embryonic development. However, the expression patterns of these arterial/venous-specific markers in adult microvascular networks remain unclear. The objective of this study was to characterize the cellular distribution of EphB4 expression along the hierarchy of unstimulated and remodeling adult rat mesenteric microvascular networks. METHODS: Mesenteric tissue was harvested from unstimulated and stimulated adult male Fisher rats, and stained for various combinations of EphB4, SM alpha -actin, NG2, and isolectin/CD-31. The distribution of EphB4 expression was compared to the cell-specific markers along arteriole, venule, and capillary segments for each mesenteric microvascular network (n = 32). Arterial/venous expression was also characterized in subcutaneous tissue and spinotrapezius muscle. RESULTS: Endothelial cells along both venules and arterioles stained positive for EphB4. EphB4 expression levels along capillaries correlated with capillary type, as the fluorescence staining intensity along capillary sprouts was significantly elevated in comparison to capillaries connecting arterioles and venules (mean intensity index = 25 for capillary sprouts; 6 for connected capillaries) CONCLUSION: The results suggest that EphB4 is not an arterial/venous-specific marker in adult rat microvascular networks, and provide new data suggesting that its elevated expression in capillaries is indicative of capillary sprouting.