An Application of Social Marketing Theory to develop a social marketing campaign to address mental health literacy and help-seeking behavior among male college students

Male college students have been observed to have low mental health literacy and help-seeking behaviors. The purpose of this study was to apply social marketing theory to address mental health literacy among male undergraduate students in order to improve both mental health literacy and help-seeking behaviors. The current study employed qualitative methods involving key informant interviews among male undergraduate university students (n = 26). Participants were provided three vignettes representing a male college student presenting with anxiety, depression, or stress during the key informant interviews. The concepts from the key informant interviews were mapped onto the social marketing theory marketing mix (product, price, place, promotion). The social marketing mix identified methods to improve professional help-seeking behaviors (product) among male undergraduate students by reducing stigma, both perceived social stigma and self-stigma, as well as addressing masculine norms (price) in locations where students are comfortable, such as the university health center or the Internet (place), by connecting the physical signs and symptoms (promotion) to mental health concerns. Findings were translated into a targeted and tailored social marketing campaign implemented in male restrooms in the campus recreation center. Social marketing theory is a valuable tool for developing targeted and tailored social marketing programs for mental well-being among college students

Development of Evaluation and Capacity Building Plans for the Chapel Hill-Carrboro City Schools' Local Wellness Policy

Research shows that students who eat a healthy diet and regularly engage in physical activity show improved behavior and academic performance in schools. However, many children in North Carolina, and across the nation, are not healthy: rates of childhood obesity and overweight are high and continue to rise. Schools provide a unique opportunity for interventions to improve healthy eating and physical activity, and there is ample evidence to show that school-based interventions are effective in improving students' health. For this reason, in 2004, Congress mandated that all schools participating in the National School Lunch Program must develop and implement a Local Wellness Policy (LWP), as well as a plan to evaluate the policy. Our Capstone team worked with Chapel Hill-Carrboro City Schools (CHCCS) to design an evaluation plan to measure implementation of their LWP and a capacity building plan to increase CHCCS' ability to successfully implement the policy. First, we conducted a literature review to learn more about LWPs and their implementation across the country. Next, we created a process evaluation plan and a survey tool to collect information from stakeholders to measure LWP implementation annually. Throughout the project, we attended monthly meetings of the Healthy Schools Advisory Council (HSAC) to interact with stakeholders and update them on our progress. We assisted school nurses at three schools in applying for national awards to recognize their wellness efforts. Lastly, we created a capacity building plan to help the district improve its ability to fully and consistently implement the LWP. These Capstone deliverables expand CHCCS' capacity to evaluate the implementation of its LWP and use the results to make improvements, thus making progress toward the ultimate goal of improving student and staff health. As a result of this project, the Capstone team gained knowledge and experience in designing evaluations and writing clearly for a wide audience. By disseminating our deliverables through CHCCS and online in the form of a public Drop Box folder, the team added to the field of resources on LWP implementation, evaluation, and capacity-building, allowing future projects to use our deliverables to inform their own work.Master of Public Healt

Dynamics of cellular states of fibro-adipogenic progenitors during myogenesis and muscular dystrophy

Fibro-adipogenic progenitors (FAPs) are currently defined by their anatomical position, expression of non-specific membrane-associated proteins, and ability to adopt multiple lineages in vitro. Gene expression analysis at single-cell level reveals that FAPs undergo dynamic transitions through a spectrum of cell states that can be identified by differential expression levels of Tie2 and Vcam1. Different patterns of Vcam1-negative Tie2highor Tie2lowand Tie2low/Vcam1-expressing FAPs are detected during neonatal myogenesis, response to acute injury and Duchenne Muscular Dystrophy (DMD). RNA\ua0sequencing analysis identified cell state-specific transcriptional profiles that predict functional interactions with satellite and inflammatory cells. In particular, Vcam1-expressing FAPs, which exhibit a pro-fibrotic expression profile, are transiently activated by acute injury in concomitance with the inflammatory response. Aberrant persistence of Vcam1-expressing FAPs is detected in DMD muscles or upon macrophage depletion, and is associated with muscle fibrosis, thereby revealing how disruption of inflammation-regulated FAPs dynamics leads to a pathogenic outcome

HnRNP L represses exon splicing via a regulated exonic splicing silencer

Skipping of mammalian exons during pre-mRNA splicing is commonly mediated by the activity of exonic splicing silencers (ESSs). We have recently identified a regulated ESS within variable exon 4 of the CD45 gene, named ESS1, that is necessary and sufficient for partial exon repression in resting T cells and has additional silencing activity upon T-cell activation. In this study, we identify three heterogeneous nuclear ribonucleoproteins (hnRNPs) that bind specifically to ESS1. The binding of one of these proteins, hnRNP-L, is significantly decreased by mutations that disrupt both the basal and induced activities of ESS1. Recombinant hnRNP-L functions to repress exon inclusion in vitro in an ESS1-dependent manner. Moreover, depletion of hnRNP-L, either in vitro or in vivo, leads to increased exon inclusion. In contrast, the other ESS1-binding proteins, PTB and hnRNP E2, do not discriminate between wild-type and mutant ESS1 in binding studies, and do not specifically alter ESS1-dependent splicing in vitro. Together, these studies demonstrate that hnRNP-L is the primary protein through which CD45 exon 4 silencing is mediated by the regulatory sequence ESS1

Dependence-induced ethanol drinking and GABA neurotransmission are altered in Alk deficient mice

Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase that is expressed in the brain and implicated in alcohol abuse in humans and behavioral responses to ethanol in mice. Previous studies have shown an association of human ALK with acute responses to alcohol and alcohol dependence. In addition, Alk knockout (Alk −/−) mice consume more ethanol in a binge-drinking test and show increased sensitivity to ethanol sedation. However, the function of ALK in excessive drinking following the establishment of ethanol dependence has not been examined. In this study, we tested Alk −/− mice for dependence-induced drinking using the chronic intermittent ethanol-two bottle choice drinking (CIE-2BC) protocol. We found that Alk −/− mice initially consume more ethanol prior to CIE exposure, but do not escalate ethanol consumption after exposure, suggesting that ALK may promote the escalation of drinking after ethanol dependence. To determine the mechanism(s) responsible for this behavioral phenotype we used an electrophysiological approach to examine GABA neurotransmission in the central nucleus of the amygdala (CeA), a brain region that regulates alcohol consumption and shows increased GABA signaling after chronic ethanol exposure. GABA transmission in ethanol-naïve Alk −/− mice was enhanced at baseline and potentiated in response to acute ethanol application when compared to wild-type (Alk +/+) mice. Moreover, basal GABA transmission was not elevated by CIE exposure in Alk −/− mice as it was in Alk +/+ mice. These data suggest that ALK plays a role in dependence-induced drinking and the regulation of presynaptic GABA release in the CeA

COVID-19 Evidence Accelerator: A parallel analysis to describe the use of Hydroxychloroquine with or without Azithromycin among hospitalized COVID-19 patients.

BackgroundThe COVID-19 pandemic remains a significant global threat. However, despite urgent need, there remains uncertainty surrounding best practices for pharmaceutical interventions to treat COVID-19. In particular, conflicting evidence has emerged surrounding the use of hydroxychloroquine and azithromycin, alone or in combination, for COVID-19. The COVID-19 Evidence Accelerator convened by the Reagan-Udall Foundation for the FDA, in collaboration with Friends of Cancer Research, assembled experts from the health systems research, regulatory science, data science, and epidemiology to participate in a large parallel analysis of different data sets to further explore the effectiveness of these treatments.MethodsElectronic health record (EHR) and claims data were extracted from seven separate databases. Parallel analyses were undertaken on data extracted from each source. Each analysis examined time to mortality in hospitalized patients treated with hydroxychloroquine, azithromycin, and the two in combination as compared to patients not treated with either drug. Cox proportional hazards models were used, and propensity score methods were undertaken to adjust for confounding. Frequencies of adverse events in each treatment group were also examined.ResultsNeither hydroxychloroquine nor azithromycin, alone or in combination, were significantly associated with time to mortality among hospitalized COVID-19 patients. No treatment groups appeared to have an elevated risk of adverse events.ConclusionAdministration of hydroxychloroquine, azithromycin, and their combination appeared to have no effect on time to mortality in hospitalized COVID-19 patients. Continued research is needed to clarify best practices surrounding treatment of COVID-19