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Community as Medicine: A Qualitative Study of How Group Health Coaching and Social Connection Improve Mental Well-Being in Older Adults
(MDPI, 2026-02-17) Duplantier, Sally C.; Hayes, Michaela G.; Sanchez-Zaragoza, Noriah; Londoño, Angelina I.; Hamilton, Erykah; Markle, Elizabeth A.; Emmert-Aronson, Benjamin; Epidemiology, Richard M. Fairbanks School of Public Health
Background/objectives: Older adults in under-resourced communities experience high levels of social isolation, chronic illness, and reduced access to healthcare, which can undermine mental well-being. Open Source Wellness's Community As Medicine® (CAM) program is an evidence-based, community-delivered, clinically integrated program that combines trauma-informed, culturally-relevant, experiential group health coaching with social connection to improve mental and physical well-being. This qualitative study, conducted in early 2025, examined how participation in CAM supports mental well-being among older adults (age 65+) in under-resourced communities who are managing chronic physical and mental health challenges.
Methods: Semi-structured interviews were conducted with participants who completed CAM. Transcripts were analyzed using reflexive thematic analysis to explore relational and experiential processes associated with improved well-being.
Findings: Participants entered CAM with internalized ageist beliefs and low expectations for personal change. As they engaged in new behaviors, experienced successes, and observed similar progress among peers, they gained motivation, confidence, and a sense of control. Four interconnected themes appear to explain the mechanisms through which CAM supports mental well-being: (1) belonging and inclusion through trust and safety; (2) personal accountability through relational accountability; (3) self-efficacy through social learning and reciprocal support; and (4) agency through positive actions.
Conclusions: Findings suggest that CAM supports mental well-being by creating conditions that help older adults overcome internalized ageism and feel connected, capable, and in control of their lives. These results identify actionable strategies that community organizations and health systems can adapt to support mental well-being for older adults in under-resourced communities.
RIPK1 regulates β-cell fate via actions on gene expression and kinase signaling in a mouse model of β-cell self-reactivity
(Springer Nature, 2026-02-12) Contreras, Christopher J.; Mukherjee, Noyonika; Harris-Kawano, Arianna; Mather, Egan G.; Amarsaikhan, Nansalmaa; Davis, Christopher; Berryhill, Christine A.; Peyton, Madeline; Kundu, Debjyoti; Colglazier, Kaitlyn A.; Miller, Addison S.; Branco, Renato C. S.; Johnson, Travis S.; Angus, Steven P.; You, Sylvaine; Cai, Erica P.; Templin, Andrew T.; Medicine, School of Medicine
Type 1 diabetes (T1D) is characterized by autoimmune destruction of pancreatic β-cells, insulin insufficiency, and hyperglycemia. Receptor interacting protein kinase 1 (RIPK1) is a multifunctional regulator of cell fate with kinase and scaffolding functions, and we previously identified RIPKs as regulators of β-cell cytotoxicity in vitro. Here we report that Ripk1 expression is increased in islets from aged non-obese diabetic (NOD) mice and β-cells from T1D donors, suggesting that RIPK1 may drive cytokine- and autoimmune-mediated β-cell demise in T1D. Using NIT-1 β-cells derived from NOD mice, we observed that TNFα + IFNγ increases RIPK1 phosphorylation, caspase 3/7 activity, and cell death. In contrast, this cytotoxicity was blocked with small molecule RIPK1 inhibition or in Ripk1 gene-edited (Ripk1Δ) β-cells. Small molecule caspase inhibition studies and co-labeling of caspase 3/7 activation and cell death in single cells revealed protection from caspase-dependent and -independent forms of death in Ripk1Δ cells. RNAseq uncovered differential cell death-, immune-, and identity-related gene expression, and kinome profiling identified changes in MAPK, Eph, JAK, and other kinase activity associated with protection from cell death in RIPK1 deficient β-cells. Furthermore, in vitro co-culture assays and in vivo adoptive transfer experiments revealed that NIT-1 Ripk1Δ cells are protected from autoimmune destruction by splenocytes isolated from diabetic NOD mice. Collectively, our findings indicate that RIPK1 promotes β-cell demise in response to cytokine and autoimmune stress via actions on gene expression and kinase signaling. Therapeutics targeting RIPK1 may provide novel opportunities for the prevention or treatment of autoimmune diabetes.
Low intensity vibration with zoledronate reduces musculoskeletal weakness and adiposity in estrogen deprived female mice
(Springer Nature, 2026-01-21) Pagnotti, Gabriel M.; Trivedi, Trupti; Wright, Laura E.; John, Sutha K.; Murthy, Sreemala; Pattyn, Ryan R.; Willis, Monte S.; She, Yun; Suresh, Sukanya; Touray, Aji F.; Thompson, William R.; Rubin, Clinton T.; Mohammad, Khalid S.; Guise, Theresa A.; Medicine, School of Medicine
Aromatase inhibitors are widely used in the treatment of hormone-sensitive breast cancer, but their suppression of estrogen production accelerates bone loss, increases fracture risk, and negatively impacts muscle and fat metabolism. Here, we demonstrate that daily low intensity vibration, serving as a non-drug mimetic for exercise, protects musculoskeletal health in skeletally immature, female mice under complete estrogen deprivation. Subsequent improvements in vertebral bone density are paralleled by greater and leaner skeletal muscle mass and function alongside reduced fat accretion and circulating metabolites. In mature, estrogen deprived mice, vibration enhances weekly bisphosphonate treatment, improving bone density, cortical thickness, and mechanical resistance to fracture. These findings support the proposed hypothesis that low intensity vibration reduces musculoskeletal frailty in estrogen deprived mice, with stronger effects observed in younger cohorts, while in skeletally mature mice combination therapy with anti-resorptive treatment is necessary to suppress cancer-treatment induced musculoskeletal degradation.
High fat diet remodels the gene regulatory networks in the preoptic area
(Springer Nature, 2026-02-03) Lazaro, Olivia; Beimfohr, Caleb; App, Britany; Basu, Rashmita; Johnson, Travis S.; Flak, Jonathan N.; Biostatistics and Health Data Science, Richard M. Fairbanks School of Public Health
Diabetes is characterized by widespread dysfunction throughout the body due to chronic hyperglycemia. To offset the beta cell failure and insulin resistance through potentially intact mechanisms in the individual, the central nervous system is an intriguing target for restoring glycemic control. While the current generation of diabetes therapeutics operate, at least in part, by re-tuning the function of dynamic neural circuits that maintain energy balance, neurological markers for remission have not been established for metabolic disease in many parts of the brain that are involved in energy balance and glucose homeostasis. These remission modules could be then applied to lesser established brain regions and expedite the discovery of diabetes-related functions in additional regions. To meet this goal, we used a previously published hypothalamic single cell sequencing dataset from ob/ob mice in remission from diabetes due to FGF1 treatment and identified remission modules (i.e. clusters of genes) that can be used to locate the networks that are corrected with successful treatment. We applied the remission modules to a dataset using C57 mice from the preoptic area of the hypothalamus, a region with links to metabolic disease but little characterization. We identified markers in both excitatory and inhibitory neurons in the preoptic area and validated their expression in the preoptic area using RNA scope. Together, these studies establish a remission module in hypothalamic neurons that can be used to define key cell types and markers in the brain that are responsive to correction of glucose homeostasis.
Protein Intake in Hemodialysis Patients Should Be Higher than 1.2 g/kg per Day: PRO
(Wolters Kluwer, 2026) Biruete, Annabel; Kistler, Brandon M.; Medicine, School of Medicine