A Professional Development Workshop: Applying the Race and Culture Guide to Reduce Bias in Medical Teaching Cases.

Introduction: Clinical teaching cases are a cornerstone of health professions education programs, but cases historically have lacked diversity and have the potential to reinforce essentialism. In this article, we describe the creation, implementation, and feasibility assessment of a professional development workshop aimed at integrating an existing bias reduction tool into discussion and revision of teaching cases. Methods: Six 60-minute workshops were held introducing "The Race and Culture Guide for Editors of Teaching Cases" to different health profession education programs wherein all participants worked in small groups to critique and edit two sample teaching cases. To assess initial feasibility, facilitators completed a facilitator evaluation survey to capture experiences after the first three workshops. Due to positive feedback, workshops were continued, and participants completed a participant evaluation survey to understand learner impact. Results: Facilitators (n=6) identified the workshop as addressing an important need, highlighted the value in small-group format, and noted their ability to facilitate future sessions. Participants (n=18) rated the workshop as useful, effective at challenging biases, and would recommend the workshop to others. Conclusion: The purpose of this study was to understand the feasibility of implementing a discussion-based workshop integrating a bias reduction tool. Initial feasibility and acceptability assessments demonstrate that this workshop.

Neuronal dysfunction caused by FUSR521G promotes ALS-associated phenotypes that are attenuated by NF-κB inhibition.

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are related neurodegenerative diseases that belong to a common disease spectrum based on overlapping clinical, pathological and genetic evidence. Early pathological changes to the morphology and synapses of affected neuron populations in ALS/FTD suggest a common underlying mechanism of disease that requires further investigation. Fused in sarcoma (FUS) is a DNA/RNA-binding protein with known genetic and pathological links to ALS/FTD. Expression of ALS-linked FUS mutants in mice causes cognitive and motor defects, which correlate with loss of motor neuron dendritic branching and synapses, in addition to other pathological features of ALS/FTD. The role of ALS-linked FUS mutants in causing ALS/FTD-associated disease phenotypes is well established, but there are significant gaps in our understanding of the cell-autonomous role of FUS in promoting structural changes to motor neurons, and how these changes relate to disease progression. Here we generated a neuron-specific FUS-transgenic mouse model expressing the ALS-linked human FUSR521G variant, hFUSR521G/Syn1, to investigate the cell-autonomous role of FUSR521G in causing loss of dendritic branching and synapses of motor neurons, and to understand how these changes relate to ALS-associated phenotypes. Longitudinal analysis of mice revealed that cognitive impairments in juvenile hFUSR521G/Syn1 mice coincide with reduced dendritic branching of cortical motor neurons in the absence of motor impairments or changes in the neuromorphology of spinal motor neurons. Motor impairments and dendritic attrition of spinal motor neurons developed later in aged hFUSR521G/Syn1 mice, along with FUS cytoplasmic mislocalisation, mitochondrial abnormalities and glial activation. Neuroinflammation promotes neuronal dysfunction and drives disease progression in ALS/FTD. The therapeutic effects of inhibiting the pro-inflammatory nuclear factor kappa B (NF-κB) pathway with an analog of Withaferin A, IMS-088, were assessed in symptomatic hFUSR521G/Syn1 mice and were found to improve cognitive and motor function, increase dendritic branches and synapses of motor neurons, and attenuate other ALS/FTD-associated pathological features. Treatment of primary cortical neurons expressing FUSR521G with IMS-088 promoted the restoration of dendritic mitochondrial numbers and mitochondrial activity to wild-type levels, suggesting that inhibition of NF-κB permits the restoration of mitochondrial stasis in our models. Collectively, this work demonstrates that FUSR521G has a cell-autonomous role in causing early pathological changes to dendritic and synaptic structures of motor neurons, and that these changes precede motor defects and other well-known pathological features of ALS/FTD. Finally, these findings provide further support that modulation of the NF-κB pathway in ALS/FTD is an important therapeutic approach to attenuate disease.

High Prevalence of Diabetes Distress in a University Population.

CONTEXT: Diabetes distress is an affective condition that addresses an individual's frustrations, worries, and concerns about living with diabetes. It is associated with fewer self-care behaviors, suboptimal glycemic control, and lower quality of life (QOL). For these reasons, diabetes care guidelines recommend routine assessment of diabetes distress. OBJECTIVE: To assess diabetes distress in a university population. METHODS: This study was conducted using a descriptive, cross-sectional design. Researchers assessed diabetes distress and other psychosocial factors via an electronic anonymous survey among students, faculty, and staff at a large university in the Midwest. RESULTS: A total of 173 participants completed the survey (mean [SD] age, 35.1 [16.7] years), with 108 [62.4%] female and 142 [82.1%] white participants). Eighty-five participants had type 1 diabetes mellitus (T1DM), and 88 had type 2 diabetes mellitus (T2DM). Of the 85 T1DM participants, 23 (27.4%) reported high diabetes distress, and 27 (30.7%) T2DM participants reported high diabetes distress. Sixteen T1DM (18.8%) and 15 T2DM (17.0%) participants screened positive for severe depression. Severe depression was associated with high distress for both T1DM and T2DM participants (T1DM: χ2=28.845, P<.001; T2DM: χ2=20.679, P<.001). Participants with T1DM reported more frequent self-care behaviors (mean [SD], 62.3 [17.1] vs 52.2 [19.2]; P<.001), but lower diabetes QOL (63.3 [14.1] vs 68.5 [15.5]; P=.021) compared with T2DM participants. No differences were observed in depressive symptoms, diabetes self-efficacy, and coping styles. Linear regression models showed that high diabetes distress scores (standardized ß=.323, P=.025; standardized ß=.604, P<.001) were independently associated with higher hemoglobin A1C levels and lower diabetes QOL after controlling for depressive symptoms, age, and gender in T1DM participants. Similarly, high diabetes distress scores (standardized ß=.434, P<.001) were associated with lower diabetes QOL in T2DM participants after controlling for the same variables. CONCLUSION: High diabetes distress levels were associated with lower diabetes QOL for both T1DM and T2DM participants. These findings suggest that attending or working at a university may be associated with high diabetes distress scores and lower diabetes QOL. Additional research with a larger, more diverse sample from multiple universities is needed to confirm these findings.