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Objective: This study assesses the effectiveness of clinical simulation-based training in boosting self-perceived confidence for using upstander communication skills to confront racism, discrimination, and microaggressions (RDM). Methods: We conducted an observational cohort study with emergency medicine professionals at the 2023 Scientific Assembly of the American Academy of Emergency Medicine in New Orleans, Louisiana. The study featured a clinical simulation-based training on upstander communications skills session followed by small- and large-group debriefs. Participants completed pre- and post-training questionnaires assessing demographics and confidence in health equity competencies. This survey was used in a previous study with emergency medicine residents. Data were analyzed using an independent Student's t-test, with a significance threshold of 0.05. Results: Thirty-two individuals participated in the simulation-based training, and 24 completed surveys, with a 75% response rate. Most participants were non-Hispanic (24, 85.7%) and women (18, 64%), with racial demographics mostly White (8, 28.6%), Black or African American (8, 28.6%), and Asian (6, 21.4%). After the workshop, there was a notable increase in self-perceived ability and confidence in identifying RDM (from 7 ± 3.2 to 8.6 ± 1.6, p < 0.003), using upstander communication tools (from 6.1 ± 3.5 to 8.5 ± 1, p < 0.0001), and the likelihood of intervening in RDM situations (from 7.1 ± 3.3 to 8.8 ± 1.1, p < 0.0002). Conclusions: The clinical simulation-based training significantly improved participants' confidence and self-perceived ability to address RDM in simulated clinical environments. This training method is a promising tool for teaching health equity topics in clinical medicine.
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Background: Qualitative research explains observations, focusing on how and why phenomena and experiences occur. Qualitative methods go beyond quantitative data and provide critical information inaccessible through quantitative methods. However, at all levels of medical education, there is insufficient exposure to qualitative research. As a result, residents and fellows complete training ill-equipped to appraise and conduct qualitative studies. As a first step to increasing education in qualitative methods, we sought to create a curated collection of papers for faculty to use in teaching qualitative research at the graduate medical education (GME) level. Methods: We conducted literature searches on the topic of teaching qualitative research to residents and fellows and queried virtual medical education and qualitative research communities for relevant articles. We searched the reference lists of all articles found through the literature searches and online queries for additional articles. We then conducted a three-round modified Delphi process to select papers most relevant to faculty teaching qualitative research. Results: We found no articles describing qualitative research curricula at the GME level. We identified 74 articles on the topic of qualitative research methods. The modified Delphi process identified the top nine articles or article series most relevant for faculty teaching qualitative research. Several articles explain qualitative methods in the context of medical education, clinical care, or emergency care research. Two articles describe standards of high-quality qualitative studies, and one article discusses how to conduct the individual qualitative interview to collect data for a qualitative study. Conclusions: While we identified no articles reporting already existing qualitative research curricula for residents and fellows, we were able to create a collection of papers on qualitative research relevant to faculty seeking to teach qualitative methods. These papers describe key qualitative research concepts important in instructing trainees as they appraise and begin to develop their own qualitative studies.
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Aggregates of ß-amyloid peptide are found to occur in brains of AD patients and are formed upon sequential cleavage of the amyloid precursor protein by BACE1 and γ-secretase. Strategies inhibiting either peptide aggregation or the rate limiting enzyme BACE1 have been in demand for its implication in AD therapeutics. The present study is undertaken to mine compounds with dual ability. In this context, some natural compounds that were already predicted as BACE1 inhibitors by our group, were further tested for their activity as aggregation inhibitors. A pharmacophore model built with known antiamyloidogenic compounds was then applied for screening the natural compounds previously predicted as BACE1 inhibitors. Subsequently experimental validation by Thioflavin-T and Aß-GFP assay filtered four compounds genistein, syringetin, tamarixetin and ZINC53276039. Out of them, ZINC53276039 showed promising antiamyloidogenic activity to act as a potent inhibitor of aggregation. Interestingly, our previous study revealed syringetin and ZINC53276039 to be good BACE1 inhibitors while tamarixetin to be a moderate BACE1 inhibitor. These good to moderate BACE1 inhibitors with moderate to reasonable antiamyloidogenic activity might show potency in reducing the amyloid load of AD brains.
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Enfermedad de Alzheimer , Secretasas de la Proteína Precursora del Amiloide , Humanos , Secretasas de la Proteína Precursora del Amiloide/metabolismo , Ácido Aspártico Endopeptidasas/metabolismo , Enfermedad de Alzheimer/metabolismo , Péptidos beta-Amiloides/metabolismo , Precursor de Proteína beta-Amiloide/metabolismo , Flavonoides/farmacologíaRESUMEN
Stress response and checkpoint activation are the main determinants of cellular survival in adverse conditions. In Schizosaccharomyces pombe, these are controlled by the Mitogen Activated Protein Kinase Spc1 and the Cyclin dependent Kinase Cdc2 respectively. Cdc2 is regulated positively by Cdc25 and negatively by Wee1. Changes in Cdc2 activity can be sensed by Spc1 resulting in the modulation of mitotic timing by Spc1. Functional cross talks between cell cycle regulation and MAPK machinery during regulation of mitotic timing are well characterised but the presence of similar communication during stress response remains unexplored. In this study we report how the checkpoint activator kinase Wee1 can also influence the transcriptional response to oxidative stress. We show that deletion of Wee1 results in changes in gene expression of the cells, especially with respect to genes whose expression is known to be regulated by Spc1. These differences are seen in unperturbed cells as well as during oxidative stress. Moreover, such variations extend beyond what could be expected to occur due to the known enhanced Spc1 activity of these cells. This is the first depiction of the influence of Wee1 and consequently Cdc2 activity on transcriptional response to oxidative stress.
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Proteínas de Schizosaccharomyces pombe , Schizosaccharomyces , Schizosaccharomyces/genética , Schizosaccharomyces/metabolismo , Proteínas de Schizosaccharomyces pombe/genética , Proteínas de Schizosaccharomyces pombe/metabolismo , Proteínas de Ciclo Celular/genética , Proteínas de Ciclo Celular/metabolismo , Proteínas Quinasas Activadas por Mitógenos/metabolismo , Estrés Oxidativo , Proteínas Tirosina Quinasas/genética , Proteínas Tirosina Quinasas/metabolismoRESUMEN
Schizosaccharomyces pombe has been used as an excellent model for studying eukaryotic cell cycle regulation and stress responses. The bZIP transcription factors Atf1(ATF2 homolog) and Pcr1(CREB homolog) have been shown to be important for regulating the expression of genes related to both stress response and cell cycle. Pcr1 has in fact been implicated as a determining factor in the segregation of the cell cycle and stress response related functions of Atf1. Interestingly Atf1 and Pcr1 levels are known to vary during the cell cycle thus giving rise to the possibility that their relative levels can influence the periodic transcriptional program of the cell. Here we report our observations on the changes in transcriptome of S. pombe cells which have been genetically manipulated to create relative differences in the levels of Atf1 and Pcr1. These results highlight new information regarding the potential role of Atf1 and Pcr1 in orchestrating the integration of the transcriptional programs of cell cycle and stress response.
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The bZIP transcription factor Atf1 is a key player in the transcriptional programme of Schizosaccharomyces pombe cell cycle. It also controls both expression and degradation of mitotic cyclin Cdc13. Temporal regulation of these opposing functions of Atf1 is critical for fidelity of cell division. Our investigations revealed that an increase in the activity of mitogen-activated protein kinase (MAPK) Spc1 during mitotic exit and the consequent phosphorylation of Atf1 along with the prevailing high activity of cyclin-dependent kinase Cdc2 regulate Cdc13 degradation. Our results also indicate the possibility of a complex interplay between Cdc2 inhibitory kinase Wee1, the anaphase-promoting complex and Atf1 during mitotic exit. These observations provide evidence of new regulatory mechanisms of mitotic exit.