Exploring student perceptions of their learning adaptions during the COVID-19 pandemic.

OBJECTIVE: With the shelter-in-place orders implemented during the COVID-19 pandemic, learning experiences abruptly changed from on campus to wholly online. This qualitative study explores the perceptions and attitudes of students as they adapted their study space, study time, and approach to learning. METHODS: One hundred five students enrolled in a doctor of chiropractic program were invited to participate in a survey to understand how shelter-in-place orders during the COVID-19 pandemic influenced their approach to learning. Fifty-two of 105 (49.5%) students completed the survey. The survey asked students to select their primary study strategy from a list of options and then prompted students to explain how the COVID-19 pandemic influenced their study space, use of technology, study time, and metacognitive cycle of planning, monitoring, and evaluating their approach to learning. A Thematic analysis of the participants' responses was performed. RESULTS: Nearly all study participants described a challenge in adapting their study space, study time, or approach to learning. Respondents reported that the use of technology did not change because assessments and resources were electronic before the pandemic. Respondents who selected high-impact study strategies such as self-quizzing or who demonstrated evidence of well-developed metacognition described a positive approach to learning more frequently than did respondents who selected low-impact study strategies such as repeated reading or who did not show evidence of metacognitive development. CONCLUSION: This study presents student perceptions related to promoting and developing self-regulated learning skills. Educators can use this information to understand the adaptations to changes in learning experiences that may promote successful learning.

Measuring the Level of Metacognitive Regulation in Graduate Health Sciences Students: What Is the Value of a Prompt?

Students with strong metacognitive and self-regulated learning skills will better adapt to the rigor of graduate health sciences education, and as professionals, they will be able to better manage unpredictable patient populations. In this observational study, we presented students with information about study strategy characteristics and used self-evaluation surveys to measure the level of the metacognitive skills planning, monitoring, and evaluating of study strategies in students in their first and second terms of a doctor of chiropractic program. Ninety-eight percent of students were willing to adopt new strategies and evaluate their effectiveness, and 75% of students were able to follow through with and maintain all or a portion of their new study plan. Within the self-reported data, we identified a continuum of passive to active learning strategy choices associated with variable levels of self-evaluation and follow through. Students reporting more active or high-impact learning strategies with positive motivators in their self-evaluations were more likely to follow through with and maintain a new study plan. These data suggest a need for educators to support and develop strategies to encourage a more robust student response to learning prompts. By both designing and modeling prompts on metacognitive and self-regulated learning in a positive environment, educators empower learners to apply these tactics to task specific work. Supportive interactions with the educator will incentivize learners to develop a better awareness of metacognitive regulation and make positive behavior changes in response to learning prompts.

Modulating T cell functions does not alleviate chronic inflammatory skin lesions in K5.TGF beta 1 transgenic mice.

To use mice with chronic hyperproliferative skin inflammation as psoriasis models, their thorough phenotypic and functional characterization is indispensable. Mice with keratin 5 promoter-controlled overexpression of latent human Transforming Growth Factor (TGF)beta1 within the basal epidermis (K5.TGF beta 1 mice) show a psoriasiform phenotype, but the underlying pathogenic mechanisms are not entirely clear. To elucidate the contribution of T lymphocytes to the pathogenesis in K5.TGF beta 1 mice, we used three complementary approaches: first, peripheral T cells were eradicated via systemic treatment with CD3- or CD4-depleting antibodies. However, this elimination did not alleviate the chronic inflammatory disorder. Second, bone marrow transplantation from transgenic mice into wildtype recipients and vice versa resulted in the expected reconstitution of both adaptive and innate immune system but had little effect on the cutaneous phenotype both in wildtype and transgenic chimeras. Third, based on the hypothesis that the disease course could be modulated by regulatory T cells (Tregs), we expanded Tregs in vivo using a superagonistic anti-CD28 antibody. While this treatment achieved a threefold increase in Foxp3-expressing Tregs, there was little, if any, effect on the chronic skin inflammation. We conclude from our findings that T cells play little, if any, role in the skin lesions of K5.TGF beta 1 mice.

A role for TGFbeta signaling in the pathogenesis of psoriasis.

Deregulation of transforming growth factor-beta (TGFbeta) signaling has been reported in human psoriasis. Our recent study using a keratin 5 promoter (K5.TGFbeta1(wt)) showed that transgenic mice expressing wild-type TGFbeta1 in the epidermis developed severe skin inflammation. Additional experimental data further support a direct role for TGFbeta1 overexpression in skin inflammation. First, we temporally induced TGFbeta1 expression in keratinocytes in our gene-switch TGFbeta1(wt) transgenic mice and found inflammation severity correlated with TGFbeta1(wt) transgene expression. Second, deletion of T cells in K5.TGFbeta1(wt) mice significantly delayed skin inflammation and associated epidermal hyperplasia/hyperkeratosis. Third, therapeutic approaches effective for human psoriasis, that is, Etanercept and Rosiglitazone, are effective in alleviating the symptoms observed in K5.TGFbeta1(wt) mice. Future studies will analyze specific mechanisms and identify key factors in TGFbeta1-induced skin inflammation. Our mouse models will provide a useful tool for understanding the molecular mechanisms of inflammatory skin disorders in which TGFbeta1 is overexpressed.

OX40-mediated differentiation to effector function requires IL-2 receptor signaling but not CD28, CD40, IL-12Rbeta2, or T-bet.

Ag-specific CD4 T cells transferred into unirradiated Ag-bearing recipients proliferate, but survival and accumulation of proliferating cells is not extensive and the donor cells do not acquire effector functions. We previously showed that a single costimulatory signal delivered by an agonist Ab to OX40 (CD134) promotes accumulation of proliferating cells and promotes differentiation to effector CD4 T cells capable of secreting IFN-gamma. In this study, we determined whether OX40 costimulation requires supporting costimulatory or differentiation signals to drive acquisition of effector T cell function. We report that OX40 engagement drives effector T cell differentiation in the absence of CD28 and CD40 signals. Two important regulators of Th1 differentiation, IL-12R and T-bet, also are not required for acquisition of effector function in CD4 T cells responsive to OX40 stimulation. Finally, we show that CD25-deficient CD4 T cells produce little IFN-gamma in the presence of OX40 costimulation compared with wild type, suggesting that IL-2R signaling is required for efficient OX40-mediated differentiation to IFN-gamma secretion.