RESUMO
BACKGROUND: Aimed at bridging the gap in continuing medical education (CME) resource availability in low- and middle-income countries (LMICs), the "Continuing Medical Education on Stick" (CMES) program introduces two technological solutions: a universal serial bus (USB) drive and the CMES-Pi computer facilitating access to monthly updated CME content without data cost. Feedback from users suggests a lack of content on tropical infectious diseases (IDs) and content from a Western perspective, which may be less relevant in LMIC settings. METHODS: This quality improvement project was intended to identify areas for improvement of the CMES database to better meet the educational needs of users. We compared the CMES content with the American Board of Emergency Medicine (ABEM) Exam content outline to identify gaps. The curriculum map of the CMES library, encompassing content from 2019 to 2024, was reviewed. An anonymous survey was conducted among 47 global users to gather feedback on unmet educational needs and suggestions for content improvements. All healthcare workers who were members of the CMES WhatsApp group were eligible to participate in the survey. RESULTS: The curriculum map included 2,572 items categorized into 23 areas. The comparison with the ABEM outline identified gaps in several clinical areas, including procedures, traumatic disorders, and geriatrics, which were represented -5%, -5%, and -4% in the CMES library compared with the ABEM outline, respectively. Free responses from users highlighted a lack of content on practical skills, such as electrocardiogram (ECG) interpretation and management of tropical diseases. Respondents identified emergency medical services (EMS)/prehospital care (81%), diagnostic imaging (62%), and toxicology/pharmacology (40%) as the most beneficial areas for clinical practice. In response to feedback from users, new content was added to the CMES platform on the management of sickle cell disease and dermatologic conditions in darkly pigmented skin. Furthermore, a targeted podcast series called "ID for Users of the CMES Program (ID4U)" has been launched, focusing on tropical and locally relevant ID, with episodes now being integrated into the CMES platform. CONCLUSIONS: The project pinpointed critical gaps in emergency medicine (EM) content pertinent to LMICs and led to targeted enhancements in the CMES library. Ongoing updates will focus on including more prehospital medicine, diagnostic imaging, and toxicology content. Further engagement with users and education on utilizing the CMES platform will be implemented to maximize its educational impact. Future adaptations will consider local relevance over the ABEM curriculum to better serve the diverse needs of global users.
RESUMO
One of the most extensively studied members of the Ras superfamily of small GTPases, Rac1 is an intracellular signal transducer that remodels actin and phosphorylation signaling networks. Previous studies have shown that Rac1-mediated signaling is associated with hippocampal-dependent working memory and longer-term forms of learning and memory and that Rac1 can modulate forms of both pre- and postsynaptic plasticity. How these different cognitive functions and forms of plasticity mediated by Rac1 are linked, however, is unclear. Here, we show that spatial working memory in mice is selectively impaired following the expression of a genetically encoded Rac1 inhibitor at presynaptic terminals, while longer-term cognitive processes are affected by Rac1 inhibition at postsynaptic sites. To investigate the regulatory mechanisms of this presynaptic process, we leveraged new advances in mass spectrometry to identify the proteomic and post-translational landscape of presynaptic Rac1 signaling. We identified serine/threonine kinases and phosphorylated cytoskeletal signaling and synaptic vesicle proteins enriched with active Rac1. The phosphorylated sites in these proteins are at positions likely to have regulatory effects on synaptic vesicles. Consistent with this, we also report changes in the distribution and morphology of synaptic vesicles and in postsynaptic ultrastructure following presynaptic Rac1 inhibition. Overall, this study reveals a previously unrecognized presynaptic role of Rac1 signaling in cognitive processes and provides insights into its potential regulatory mechanisms.
Assuntos
Hipocampo , Memória de Curto Prazo , Proteínas rac1 de Ligação ao GTP , Animais , Proteínas rac1 de Ligação ao GTP/metabolismo , Proteínas rac1 de Ligação ao GTP/genética , Hipocampo/metabolismo , Hipocampo/fisiologia , Camundongos , Memória de Curto Prazo/fisiologia , Terminações Pré-Sinápticas/metabolismo , Terminações Pré-Sinápticas/fisiologia , Transdução de Sinais , Masculino , Fosforilação , Neuropeptídeos/metabolismo , Neuropeptídeos/genética , Camundongos Endogâmicos C57BL , Plasticidade Neuronal/fisiologiaRESUMO
One of the most extensively studied members of the Ras superfamily of small GTPases, Rac1 is an intracellular signal transducer that remodels actin and phosphorylation signaling networks. Previous studies have shown that Rac1-mediated signaling is associated with hippocampal-dependent working memory and longer-term forms of learning and memory and that Rac1 can modulate forms of both pre- and postsynaptic plasticity. How these different cognitive functions and forms of plasticity mediated by Rac1 are linked, however, is unclear. Here, we show that spatial working memory is selectively impaired following the expression of a genetically encoded Rac1-inhibitor at presynaptic terminals, while longer-term cognitive processes are affected by Rac1 inhibition at postsynaptic sites. To investigate the regulatory mechanisms of this presynaptic process, we leveraged new advances in mass spectrometry to identify the proteomic and post-translational landscape of presynaptic Rac1 signaling. We identified serine/threonine kinases and phosphorylated cytoskeletal signaling and synaptic vesicle proteins enriched with active Rac1. The phosphorylated sites in these proteins are at positions likely to have regulatory effects on synaptic vesicles. Consistent with this, we also report changes in the distribution and morphology of synaptic vesicles and in postsynaptic ultrastructure following presynaptic Rac1 inhibition. Overall, this study reveals a previously unrecognized presynaptic role of Rac1 signaling in cognitive processes and provides insights into its potential regulatory mechanisms.