Student presentations had been widely implemented across content areas, including health sciences education. However, due to various limitations, small-group student presentations in the classroom may not reach their full potential for student learning. To address challenges with presentations in the classroom, we redesigned the assignment by having students present and discuss online using VoiceThread, a cloud-based presentation and discussion tool. First-year students pursuing a Doctor of Dental Surgery degree were assigned into small groups to present physiology content and to discuss that content online. This assignment was similar to traditional student classroom presentations, with the exception that the entire assignment was conducted online. The primary purpose of this exploratory study was to investigate the impact of the online format on the discussion quality. Another purpose of the study was to examine students’ perceptions of using VoiceThread for presenting and learning, as well as the online interactions between the presenter and audience. Students posted a higher number of questions and comments than required by the assignment. The questions from students were also higher level questions, and the answers to these questions were more thorough compared with what we had previously observed in classroom presentations. The survey results showed that students preferred using VoiceThread for presenting, learning from other presentations, and discussing presentation content over performing this process in the classroom. Preliminary findings suggested that having dental students make presentations and hold discussions online might help address the challenges of student presentations in the classroom.

Many reports in dental education showed that student learning improved with the flipped classroom method. However, there are few reports that describe how different subsets of students may benefit from the flipped classroom. In this study, we investigated how students’ preference for the flipped classroom impacted their learning outcome. We used a flipped classroom module on the physiology of the autonomic nervous system taught to year one Doctor of Dental Surgery students to test the hypothesis that students who favored the flipped classroom performed better on assessment quizzes. The module was composed of pre-class activity, out-of-class assignment, in-class discussion, and two in-class quizzes. Quiz 1 was given after students self-studied the foundational content online through the pre-class activity, and Quiz 2 was at the end of the module. Students filled out a survey to report learning experiences and preferences. Fewer students scored below 75% on Quiz 2 than on Quiz 1. Students’ self-evaluated understanding of content significantly improved after finishing the assignment and discussion compared to finishing the pre-class activity alone. Moreover, students who preferred to learn through the flipped classroom scored higher in Quiz 2. Students with higher overall grades in the course preferred the flipped classroom more than low performers. Our results indicated that students favoring the flipped classroom method spent more time on the assignment, understood the content better, and performed better on assessments than students who prefer traditional lectures.

Background and Objectives: Nicotine is the most well-studied toxic substance in cigarette smoke and e-cigarette vape. However, smoke and vape are composed of other components that have a negative impact on health. The objective of this study is to investigate whether nicotine has a distinctive impact on molecular mechanisms in stem cells. Methods: The cellular impact of nicotine on the regenerative capacity of human dental pulp stem cells (DPSCs) and the microRNA (miRNA) profile was examined. Bioinformatic analysis was performed to identify miRNA-regulated cellular pathways associated with nicotine exposure. These pathways were then compared to those induced by cigarette smoke condensate (CSC). Results: Prolonged exposure to nicotine significantly impaired the regeneration of DPSCs and changed the expression of miRNAs. Nicotine upregulated the expression of hsa-miR-7977, hsa-miR-3178, and hsa-miR-10400-5p compared to vehicle control. Interestingly, nicotine did not change the expression of hsa-miR-29b-3p, hsa-miR-199b-5p, hsa-miR-26b-5p, or hsa-miR-26a-5p compared to the control. However, the expressions of these miRNAs were significantly altered when compared to CSC treatment. Further analysis revealed that nicotine was distinctively associated with certain miRNA-targeted pathways including apoptosis, ErbB, MAPK signaling, PI3K-Akt, TGF-b signaling, and Wnt signaling. Conclusions: Our work provides evidence on the distinctive miRNA signature induced by nicotine. The information will be important for identifying the unique molecular pathways downstream of nicotine from smoking and vaping in different individuals, providing a new direction for personalized disease prevention, prognosis, and treatment.

Our preliminary studies showed 17 β-estradiol (E2)-regulated Ca²⁺ homeostasis may play a role in enhancing nitric oxide (NO) production in endothelial cells. Here, we investigated whether the effect of E2 on intracellular calcium concentration ([Ca²⁺]_i) regulation in human endothelial cells (EA.hy926) was estrogen receptor (ER) dependent. Using PCR, we showed ERα but not ERβ was expressed in EA.hy926. To establish the role of ERα in E2-regulated Ca²⁺ homeostasis, ERα was down-regulated in EA.hy926 using siRNA (90 pmol) as determined by real time RT-PCR and Western blotting. [Ca²⁺]_i in Fura 2 loaded ERα knockdown cells and negative control knockdown cells was measured using spectrofluorometry. In the absence of extracellular Ca²⁺, inhibition of endoplasmic reticulum Ca²⁺-ATPase with thapsigargin (1 μM) caused a single Ca²⁺ transient response, indicating Ca²⁺ release from the store. Cells subjected to siRNA-mediated ERα knockdown treated with E2 (1 μM, 24 h) exhibited reduced TG-induced Ca²⁺ release compared to E2 treated negative control knockdown cells. Furthermore, a subsequent increase in extracellular Ca²⁺ concentration led to a robust increase in [Ca²⁺]_i which was significantly reduced in E2 treated ERα knockdown compared to E2 treated control cells. Our results indicated that ERα may contribute to E2-regulated Ca²⁺ homeostasis and subsequently NO production in endothelial cells. Supported by NHLBI.