ABSTRACT
The coronavirus disease 2019 (COVID-19) pandemic made it necessary for medical schools to restructure their curriculum by switching from face-to-face instruction to various forms of flexible learning. Flexible learning is a student-centered approach to learning that has received interest in many educational sectors. It is a critical strategy for expanding access to higher education during the pandemic. As flexible learning includes online, blended, hybrid, and hyflex learning options, learners have the opportunity to select an instruction modality based on their needs and interests. The shift to flexible learning in medical education took place rapidly in response to the COVID-19 pandemic, and learners, instructors, and schools were not prepared for this instructional change. Through the lens of the technology acceptance model, human agency, and a social constructivist perspective, I examine students, instructors, and educational institutions’ roles in successfully navigating the digital transformation era. The pandemic has also accelerated the use of advanced information and communication technologies, such as artificial intelligence and virtual reality, in learning. Through a review of the literature, this paper aimed to reflect on current flexible learning practices from the instructional design and educational technology perspective and explore emerging technologies that may be implemented in future medical education.
ABSTRACT
Purpose@#To evaluate changes in central macular thickness (CMT) and subfoveal choroidal thickness (SFCT) after phacovitrectomy over a 2-year period in idiopathic epiretinal membrane (ERM) patients. @*Methods@#The records of 52 idiopathic ERM patients (52 eyes) who underwent phacovitrectomy, without recurrence of the condition over a 2-year follow-up period, were reviewed retrospectively. Changes in CMT and SFCT, as measured by optical coherence tomography, were analyzed and compared with those of a normal control group over a 2-year period. @*Results@#The mean preoperative CMT and SFCT were 425.67 ± 84.67 and 257.56 ± 90.13 μm, respectively. Postoperative CMT was reduced significantly to 372.17 ± 45.26 μm at 1 year and 363.15 ± 47.35 μm at 2 years (p < 0.001). SFCT at 1 and 2 years postoperatively was significantly reduced to 238.85 ± 84.85 and 230.31 ± 87.95 μm, respectively (p < 0.001). In the control group, there was no significant change in CMT; however, the SFCT decreased by 11.09 ± 22.36 μm during the 2-year follow-up (p = 0.007). In contrast, in the patient group, CMT and SFCT decreased by 62.52 ± 71.45 and 27.25 ± 41.97 μm, respectively, showing a significant difference from the control group (p < 0.001 and p = 0.043, respectively). Both before surgery and at 1 year postoperatively, the thinner the CMT, the better the best-corrected visual acuity (BCVA) (p = 0.010 and p = 0.018, respectively). A better postoperative BCVA at 2 years was associated with a thinner CMT and better BCVA before surgery (p < 0.001 and p < 0.001, respectively). @*Conclusions@#Following a phacovitrectomy procedure, ERM patients showed significant reductions in both the CMT and SFCT at the 2-year follow-up.
ABSTRACT
PURPOSE: To determine the possible effects of chronic exposure of low dose benzalkonium chloride (BAK) on trabecular meshwork cells, and to characterize the pathways involved in the effects. METHODS: Trabecular meshwork cells were treated with 0.0005%, 0.00075%, 0.001%, and 0.0025% BAK for 10 minutes; then, the cells were transferred to a new medium for 24 hours. This process was repeated three times. Cell survival was assessed using the MTT assay to determine the non-apoptotic BAK concentration. Senescence-associated (SA)-β-gal staining was performed to compare quantitatively the cellular senescence of BAK-treated cells with the control group. Cells treated with BAK were analyzed by western blot to determine whether the expressions of cell cycle regulators were affected. RESULTS: Two concentrations (0.0005% and 0.00075%) showed persistent cell viability and were chosen for further experiments. After SA-β-gal staining, cells treated with 0.0005% and 0.00075% BAK showed 28% (± 2.08), 37% (± 2.08) increases in cellular senescence expression, respectively, when compared with control cells (p < 0.05). To identify the molecular pathways involved in cell cycle arrest via BAK, western blot analysis was performed on trabecular meshwork cells, resulting in decreased expressions of cyclin E/CDK2, and increased expressions of the upper stream control molecules, p53 and p21. CONCLUSIONS: Chronic exposure to low dose BAK accelerated cell senescence through cell cycle arrest. Because senescent cells of the trabecular meshwork can inhibit its outflow pathway function and ultimately worsen the glaucomatous process, long-term usage of topical glaucoma medications containing BAK should be conducted with caution.