Promoting Health Literacy Among Adult ELLs Virtually During COVID-19.

The adult English language learner (ELL) population is often overlooked in health literacy discussions, which can result in perpetuating low health literacy and unfamiliarity with and low access to community resources. Health literacy interventions can reduce the impacts of social determinants of health. We examine the experience of a virtual health literacy educational course, Health in the English Language, for ELLs at Alaska Literacy Program (ALP), an Anchorage nonprofit. Our class was designed to help students navigate interactions with health care services, including medical care, pharmacy, health insurance, and nutrition resources. After 2 years of in-person teaching by university undergraduates, COVID-19 required a pivot to virtual instruction in Zoom in the summer of 2020. Instructors describe lessons learned and adjusting to student needs, community-building and personal connections, and the complexities of the topic of health literacy. ALP collaboration with university students continues to be a successful partnership to build health literacy capacity. Adoption of virtual instruction during COVID demonstrated the role that partnerships between nonprofits and university students can play to benefit all partners in the collaboration.

A Mechanism Linking Two Known Vulnerability Factors for Alcohol Abuse: Heightened Alcohol Stimulation and Low Striatal Dopamine D2 Receptors.

Alcohol produces both stimulant and sedative effects in humans and rodents. In humans, alcohol abuse disorder is associated with a higher stimulant and lower sedative responses to alcohol. Here, we show that this association is conserved in mice and demonstrate a causal link with another liability factor: low expression of striatal dopamine D2 receptors (D2Rs). Using transgenic mouse lines, we find that the selective loss of D2Rs on striatal medium spiny neurons enhances sensitivity to ethanol stimulation and generates resilience to ethanol sedation. These mice also display higher preference and escalation of ethanol drinking, which continues despite adverse outcomes. We find that striatal D1R activation is required for ethanol stimulation and that this signaling is enhanced in mice with low striatal D2Rs. These data demonstrate a link between two vulnerability factors for alcohol abuse and offer evidence for a mechanism in which low striatal D2Rs trigger D1R hypersensitivity, ultimately leading to compulsive-like drinking.