The response readiness tool: An instrument to measure knowledge, skills, and attitude after taking a stop the Bleed® course.

Stop the Bleed® is an emergency response course that offers a certificate of completion but no ending assessment. The purpose of this educational study was to develop and test the Response Readiness Tool (RRT) that measures learning of participants after taking Stop the Bleed®. The study used a pre-/post-test design to measure knowledge and attitudes, and a post-test only for skills.

Taking High-Fidelity Simulation to the Next Level: Nursing in Nontraditional Environments.

Nurse educators must prepare nursing students to be competent first responders and providers in nontraditional situations. We developed a course that provides in-depth experiential instruction in disaster nursing, remote/austere nursing, and global health. The Nursing in Nontraditional Environments course provides nursing students with the knowledge and skills to provide quality care to patients in environments outside traditional hospitals and clinics.

Implementing an approach to prevent life-threatening bleeding: Guidance on forming a campus initiative.

A community that is trained to respond to life-threatening bleeding can reduce the risk of death from trauma and violence. Stop The Bleed is a nationally recognized, free, 1-hour bleeding control training designed for laypersons. Implementing a campuswide Stop the Bleed initiative can be daunting, yet vital to creating a safe, prepared campus.

Cardiovascular involvement among collegiate athletes following COVID-19 infection.

Background: Recent studies suggest that the prevalence of cardiac involvement in young competitive athletes with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection appears to be low.

Aim: This study aimed to determine the prevalence of cardiovascular involvement in young competitive athletes.

Methods: In this single-center retrospective cohort study from one Division I university; we assessed the prevalence of cardiovascular involvement among collegiate athletes who tested positive for SARS-CoV-2 by polymerase chain reaction testing.

Prolonged treatment with pimelic o-aminobenzamide HDAC inhibitors ameliorates the disease phenotype of a Friedreich ataxia mouse model.

Friedreich ataxia (FRDA) is an inherited neurodegenerative disorder caused by GAA repeat expansion within the FXN gene, leading to epigenetic changes and heterochromatin-mediated gene silencing that result in a frataxin protein deficit. Histone deacetylase (HDAC) inhibitors, including pimelic o-aminobenzamide compounds 106, 109 and 136, have previously been shown to reverse FXN gene silencing in short-term studies of FRDA patient cells and a knock-in mouse model, but the functional consequences of such therapeutic intervention have thus far not been described. We have now investigated the long-term therapeutic effects of 106, 109 and 136 in our GAA repeat expansion mutation-containing YG8R FRDA mouse model.

Two new pimelic diphenylamide HDAC inhibitors induce sustained frataxin upregulation in cells from Friedreich's ataxia patients and in a mouse model.

Background: Friedreich's ataxia (FRDA), the most common recessive ataxia in Caucasians, is due to severely reduced levels of frataxin, a highly conserved protein, that result from a large GAA triplet repeat expansion within the first intron of the frataxin gene (FXN). Typical marks of heterochromatin are found near the expanded GAA repeat in FRDA patient cells and mouse models. Histone deacetylase inhibitors (HDACIs) with a pimelic diphenylamide structure and HDAC3 specificity can decondense the chromatin structure at the FXN gene and restore frataxin levels in cells from FRDA patients and in a GAA repeat based FRDA mouse model, KIKI, providing an appealing approach for FRDA therapeutics.

Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance.

Insulin resistance arises from the inability of insulin to act normally in regulating nutrient metabolism in peripheral tissues. Increasing evidence from human population studies and animal research has established correlative as well as causative links between chronic inflammation and insulin resistance. However, the underlying molecular pathways are largely unknown.

Structure and expression of the Huntington's disease gene: evidence against simple inactivation due to an expanded CAG repeat.

Huntington's disease, a neurodegenerative disorder characterized by loss of striatal neurons, is caused by an expanded, unstable trinucleotide repeat in a novel 4p16.3 gene. To lay the foundation for exploring the pathogenic mechanism in HD, we have determined the structure of the disease gene and examined its expression.