RESUMEN
Objective: Volunteerism represents an important mechanism to promote resilience, empathy, and general well-being in medical students, a group that stands to benefit. Medical students report feelings of fatigue, burnout, exhaustion, and stress that correlates with poor academic performance, and significant decline in empathy over the 3rd year of both MD and DO programs. Volunteer motivations have been shown to mediate participant well-being. The relationship between medical student volunteer motivations and specific outcomes during the COVID-19 pandemic has not been addressed. Methods: We characterized features of medical student volunteers during the COVID-19 pandemic in 2020, including volunteering motivation using the Volunteer Functions Inventory, the types of activities in which they participated, and the physical, psychosocial, and emotional outcomes they experienced following volunteering. Results: Altruistic and humanitarian values-centric motivation predicts positive volunteering outcomes including increased resilience, ability to deal with disappointment and loss, and ability to cope with the COVID-19 pandemic. Values-centric motivation also increases volunteer empathy independent of educational stage. Values-centric participants were more likely to select volunteering activities with patient contact, which promotes student empathy and resilience. Conversely, career-centric motivation does not predict positive outcomes. These students are more likely to engage in research-oriented activities. Conclusions: The efficacy of integrating volunteerism into medical school curricula may be limited by professional pressure that manifests as career-oriented motivation. We propose that practical integration should promote altruistic and humanitarian values-centric participant orientation to the volunteering process, which is associated with enhanced recruitment, preservation of empathy, and additional positive volunteering outcomes of interest.
RESUMEN
Mutations in Cu/Zn superoxide dismutase 1 (SOD1) lead to Amyotrophic Lateral Sclerosis (ALS), a neurodegenerative disease that disproportionately affects glutamatergic and cholinergic motor neurons. Previous work with SOD1 overexpression models supports a role for SOD1 toxic gain of function in ALS pathogenesis. However, the impact of SOD1 loss of function in ALS cannot be directly examined in overexpression models. In addition, overexpression may obscure the contribution of SOD1 loss of function in the degeneration of different neuronal populations. Here, we report the first single-copy, ALS knock-in models in C. elegans generated by transposon- or CRISPR/Cas9- mediated genome editing of the endogenous sod-1 gene. Introduction of ALS patient amino acid changes A4V, H71Y, L84V, G85R or G93A into the C. elegans sod-1 gene yielded single-copy/knock-in ALS SOD1 models. These differ from previously reported overexpression models in multiple assays. In single-copy/knock-in models, we observed differential impact of sod-1 ALS alleles on glutamatergic and cholinergic neurodegeneration. A4V, H71Y, G85R, and G93A animals showed increased SOD1 protein accumulation and oxidative stress induced degeneration, consistent with a toxic gain of function in cholinergic motor neurons. By contrast, H71Y, L84V, and G85R lead to glutamatergic neuron degeneration due to sod-1 loss of function after oxidative stress. However, dopaminergic and serotonergic neuronal populations were spared in single-copy ALS models, suggesting a neuronal-subtype specificity previously not reported in invertebrate ALS SOD1 models. Combined, these results suggest that knock-in models may reproduce the neurotransmitter-type specificity of ALS and that both SOD1 loss and gain of toxic function differentially contribute to ALS pathogenesis in different neuronal populations.