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We surveyed (September 9-17, 2021) students, staff, and faculty at the University of Minnesota, a large, highly vaccinated university, to evaluate whether the COVID-19 vaccine mandate increased self-reported vaccine uptake. Vaccine mandates have the potential to improve public health but should consider the context of implementation and costs associated with infringements on personal choice. Policymakers need to be equipped with data to inform decisions about vaccine mandates in light of contextual factors and potential backlash affecting public health interventions. ( Am J Public Health . Published online ahead of print August 29, 2024:e1-e6. https://doi.org/10.2105/AJPH.2024.307804).

Wildfires have become common global phenomena concurrent with warmer and drier climates and are now major contributors to ambient air pollution world-wide. Exposure to wildfire smoke has been classically associated with adverse cardiopulmonary health outcomes, especially in vulnerable populations. Recent work has expanded our understanding of wildfire smoke toxicology to include effects on the central nervous system and reproductive function; however, the neurotoxic profile of this toxicant remains ill-explored in an occupational context. Here, we sought to address this by using RNA sequencing to examine transcriptomic signatures in the pre-frontal cortex of male mice modeling career wildland firefighter smoke exposure. We report robust changes in gene expression profiles between smoke exposed samples and filtered air controls, evidenced by 2,862 differentially expressed genes (51.2% increased). We further characterized the functional relevance of these genes highlighting enriched pathways related to synaptic transmission, neuroplasticity, blood-brain barrier integrity, and neurotransmitter metabolism. Additionally, we identified possible contributors to these alterations through protein-protein interaction network mapping, which revealed a central node at ß-catenin and secondary hubs centered around mitochondrial oxidases, the Wnt signaling pathway, and gene expression machinery. The data reported here will serve as the foundation for future experiments aiming to characterize the phenotypic effects and mechanistic underpinnings of occupational wildfire smoke neurotoxicology., (© The Author(s) 2024. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

The harms accompanying disordered gambling are well documented. Additionally, there is growing attention to the harms that arise from people who gamble heavily but do not meet the criteria for a gambling disorder. Accordingly, there has been an increasing interest in the effectiveness of consumer protection tools for consumers of gambling products. Subsequently, there is a need to properly evaluate the evidence for their effectiveness. This review aimed to conduct a narrative synthesis of empirical studies to identify gaps, weaknesses, and strengths in the existing evidence for the effectiveness of harm minimisation tools available to people who gamble. This review includes studies published between January 2015 to July 2022 and comprises 55 peer-reviewed studies for final synthesis. Findings reveal that while more research is needed to examine the effectiveness of active and passive consumer protection tools, uptake of tools is low in part because users view them as tools for individuals already experiencing gambling harm as opposed to protective tools for all users. Research is needed to determine effective ways of communicating the value of consumer protection tools for gambling.

An increased risk of cardiometabolic disease accompanies persistent systemic inflammation. Yet, the innate and adaptive immune system features in persons who develop these conditions remain poorly defined. Doublets, or cell-cell complexes, are routinely eliminated from flow cytometric and other immune phenotyping analyses, which limits our understanding of their relationship to disease states. Using well-characterized clinical cohorts, including participants with controlled HIV as a model for chronic inflammation and increased immune cell interactions, we show that circulating CD14 + monocytes complexed to CD3 + T cells are dynamic, biologically relevant, and increased in individuals with diabetes after adjusting for confounding factors. The complexes form functional immune synapses with increased expression of proinflammatory cytokines and greater glucose utilization. Furthermore, in persons with HIV, the CD3 + T-cell: CD14 + monocyte complexes had more HIV copies compared to matched CD14 + monocytes or CD4 + T cells alone. Our results demonstrate that circulating CD3 + T-cell:CD14 + monocyte pairs represent dynamic cellular interactions that may contribute to inflammation and cardiometabolic disease pathogenesis and may originate or be maintained, in part, by chronic viral infections. These findings provide a foundation for future studies investigating mechanisms linking T cellmonocyte cell-cell complexes to developing immune-mediated diseases, including HIV and diabetes., Competing Interests: Declaration of interests The authors have no competing interests.

Background: Anorexia nervosa (AN) is associated with left ventricular (LV) atrophy and unexplained sudden death. Myocardial mechanics have not been well studied in adults with AN. Whether LV mass or illness duration, markers of AN severity, correlate with abnormal strain imaging is unknown., Methods: We performed a prospective study among patients hospitalized with severe AN (n = 29) [body mass index (BMI) < 14.5 kg/m 2 ] and sex/age-matched controls (n = 16) (BMI > 18.5 kg/m 2 ). LV ejection fraction (LVEF) was calculated via modified-biplane method and LV mass was derived using the truncated ellipsoid formula. Apical 2-, 3-, and 4-chamber images were used to generate regional strain mapping and global longitudinal strain (GLS). N-terminal brain natriuretic peptide (NT-proBNP) levels were measured and linear regression was used to determine independent predictors of strain., Results: Mean LVEF did not differ (65% ± 6.0 vs. 62% ± 4.4, p = 0.06), but LV mass was substantially reduced (61.6 ± 16.8 vs. 97.6 ± 19.1 g, p < .0001). GLS was similar (- 20.6 ± 3.8 vs. - 20.9 ± 2.8, p = 0.82), however, the basal strain was worse (-18.7 ± 4.8 vs. -21.9 ± 4.1, p = 0.03). Lower LV mass was associated with worsening GLS (r = - 0.40, p = 0.003), but not among controls (p = 0.89). Median (IQR) NT-proBNP (pg/ml) was higher in patients with AN [141 (59-257) vs. 35.5 (21-56.5) p = 0.0007]. Both increasing NT-proBNP and illness duration were associated with worsening strain patterns in AN (both p = .001)., Conclusions: While LVEF and GLS did not differ, regional strain variation was noted among patients with AN. Elevated NT-proBNP may reflect increased wall tension from LV atrophy. Whether strain heterogeneity can identify patients with AN, at risk for sudden death, requires further study., (© 2023. Japanese Society of Echocardiography.)

γδ T cells are resident in visceral adipose tissue (VAT) where they show an age-associated increase in numbers and contribute to local and systemic chronic inflammation. However, regulation of this population and mechanisms for the age-dependent accumulation are not known. In this study, we identified a progressive trend of γδ T cell accumulation in VAT over the lifespan in mice and explored physiological mechanisms contributing to accumulation. Using isochronic parabiotic pairs of wild-type (WT) and T cell receptor delta knockout (TCRδ KO) mice at young and old age, we confirmed that VAT γδ T cells are predominately a tissue-resident population which is sustained in aging. Migration of peripheral γδ T cells into VAT was observed at less than 10%, with a decreasing trend by aging, suggesting a minor contribution of recruitment to γδ T cell accumulation with aging. Since tissue-resident T cell numbers are tightly regulated by a balance between proliferation and programmed cell death, we further explored these processes. Using in vivo EdU incorporation and the proliferation marker Ki67, we found that the absolute number of proliferating γδ T cells in VAT is significantly higher in the aged compared to young and middle-aged mice, despite a decline in the proportion of proliferating to non-proliferating cells by age. Analysis of apoptosis via caspase 3/7 activation revealed that VAT γδ T cells show reduced apoptosis starting at middle age and continuing into old age. Further, induction of apoptosis using pharmacological inhibitors of Bcl2 family proteins revealed that VAT γδ T cells at middle age are uniquely protected from apoptosis via a mechanism independent of traditional anti-apoptotic Bcl2-family proteins. Collectively, these data indicate that protection from apoptosis at middle age increases survival of tissue-resident γδ T cells resulting in an increased number of proliferative cells from middle age onward, and leading to the age-associated accumulation of γδ T cells in VAT. These findings are important to better understand how adipose tissue dysfunction and related changes in the immune profile contribute to inflammaging among the elderly., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Mukherjee, Bruno, Oakes, Hawk, Stromberg, Cohen and Starr.)