Disparities in Prehospital Non-Traumatic Pain Management.

Introduction: While prior research has identified racial disparities in prehospital analgesia for traumatic pain, little is known about non-traumatic pain. Using a national prehospital dataset, we sought to evaluate for racial and ethnic disparities in analgesia given by EMS for non-traumatic pain.Methods: We analyzed the 2018 and 2019 data from the ESO Data Collaborative, a collection of de-identified prehospital electronic health records from nearly 1,300 participating EMS agencies in the US. We included all transported, adult, non-traumatic encounters with a primary or secondary impression of a pain complaint, and we stratified encounters based on race and ethnicity as recorded by the EMS clinicians. We performed a mixed model analysis, modeling EMS agency as a random intercept and adjusting for age, sex, pain location, level of service, location of incident, and highest pain score. With non-Hispanic White patients as the reference group, we then evaluated the association between race/ethnicity and receiving any pain medication (acetaminophen, non-steroidal anti-inflammatories, or opioids), receiving opioid pain medication, and receiving pain medication within 20 minutes of EMS arrival.Results: We included 1,035,486 patients; 67.5% non-Hispanic White, 26.8% Black, 4.9% Hispanic, 0.5% Asian, 0.1% Native Hawaiian or Other Pacific Islander, and 0.2% American Indian or Alaska Native patients. 4.7% of patients received pain medications. Compared to White patients (5.1%), Black patients were less likely to receive pain medication (3.3%, aOR 0.7; 95% CI 0.7-0.7) and Hispanics were more likely to receive pain medication (7.6%, aOR 1.5; 95% CI 1.4-1.6). Black patients were also less likely to receive opioids (1.8% for Black v 3.0% for White, aOR 0.7; 95% CI 0.6-0.7), while Hispanic patients were more likely to receive opioids (4.9%, aOR 1.4; 95% CI 1.3-1.5). The odds of receiving pain medication within 20 minutes was lower for Black patients (aOR 0.9; 95% CI 0.8-0.95) but no different for Hispanic patients (aOR 1.0; 95% CI 0.9-1.1), when compared to White patients.Conclusion: Pain medication administration is uncommon for non-traumatic pain complaints. While Black patients were less likely than White patients to receive pain medications and receive pain medication within 20 minutes, Hispanics were more likely to receive pain medications.

Proteomics of Mouse Heart Ventricles Reveals Mitochondria and Metabolism as Major Targets of a Post-Infarction Short-Acting GLP1Ra-Therapy.

Cardiovascular disease is the main cause of death worldwide, making it crucial to search for new therapies to mitigate major adverse cardiac events (MACEs) after a cardiac ischemic episode. Drugs in the class of the glucagon-like peptide-1 receptor agonists (GLP1Ra) have demonstrated benefits for heart function and reduced the incidence of MACE in patients with diabetes. Previously, we demonstrated that a short-acting GLP1Ra known as DMB (2-quinoxalinamine, 6,7-dichloro-N-[1,1-dimethylethyl]-3-[methylsulfonyl]-,6,7-dichloro-2-methylsulfonyl-3-N-tert-butylaminoquinoxaline or compound 2, Sigma) also mitigates adverse postinfarction left ventricular remodeling and cardiac dysfunction in lean mice through activation of parkin-mediated mitophagy following infarction. Here, we combined proteomics with in silico analysis to characterize the range of effects of DMB in vivo throughout the course of early postinfarction remodeling. We demonstrate that the mitochondrion is a key target of DMB and mitochondrial respiration, oxidative phosphorylation and metabolic processes such as glycolysis and fatty acid beta-oxidation are the main biological processes being regulated by this compound in the heart. Moreover, the overexpression of proteins with hub properties identified by protein-protein interaction networks, such as Atp2a2, may also be important to the mechanism of action of DMB. Data are available via ProteomeXchange with identifier PXD027867.

Modeling Myotonic Dystrophy 1 in C2C12 Myoblast Cells.

Myotonic dystrophy 1 (DM1) is a common form of muscular dystrophy. Although several animal models have been established for DM1, myoblast cell models are still important because they offer an efficient cellular alternative for studying cellular and molecular events. Though C2C12 myoblast cells have been widely used to study myogenesis, resistance to gene transfection, or viral transduction, hinders research in C2C12 cells. Here, we describe an optimized protocol that includes daily maintenance, transfection and transduction procedures to introduce genes into C2C12 myoblasts and the induction of myocyte differentiation. Collectively, these procedures enable best transfection/transduction efficiencies, as well as consistent differentiation outcomes. The protocol described in establishing DM1 myoblast cell models would benefit the study of myotonic dystrophy, as well as other muscular diseases.