March Mammal Madness is a science outreach project that, over the course of several weeks in March, reaches hundreds of thousands of people in the United States every year. We combine four approaches to science outreach – gamification, social media platforms, community event(s), and creative products – to run a simulated tournament in which 64 animals compete to become the tournament champion. While the encounters between the animals are hypothetical, the outcomes rely on empirical evidence from the scientific literature. Players select their favored combatants beforehand, and during the tournament scientists translate the academic literature into gripping “play-by-play” narration on social media. To date ~1100 scholarly works, covering almost 400 taxa, have been transformed into science stories. March Mammal Madness is most typically used by high-school educators teaching life sciences, and we estimate that our materials reached ~1% of high-school students in the United States in 2019. Here we document the intentional design, public engagement, and magnitude of reach of the project. We further explain how human psychological and cognitive adaptations for shared experiences, social learning, narrative, and imagery contribute to the widespread use of March Mammal Madness.

Particulate matter (PM) exposure is associated with the development of cardiopulmonary disease. Our group has studied the adverse health effects of World Trade Center particulate matter (WTC-PM) exposure on firefighters. To fully understand the complex interplay between exposure, organism, and resultant disease phenotype, it is vital to analyze the underlying role of genomics in mediating this relationship. A PubMed search was performed focused on environmental exposure, genomics, and cardiopulmonary disease. We included original research published within 10 years, on epigenetic modifications and specific genetic or allelic variants. The initial search resulted in 95 studies. We excluded manuscripts that focused on work-related chemicals, heavy metals and tobacco smoke as primary sources of exposure, as well as reviews, prenatal research, and secondary research studies. Seven full-text articles met pre-determined inclusion criteria, and were reviewed. The effects of air pollution were evaluated in terms of methylation (n = 3), oxidative stress (n = 2), and genetic variants (n = 2). There is evidence to suggest that genomics plays a meditating role in the formation of adverse cardiopulmonary symptoms and diseases that surface after exposure events. Genomic modifications and variations affect the association between environmental exposure and cardiopulmonary disease, but additional research is needed to further define this relationship.

Introduction: Previously, we discovered similar esophageal gene expression patterns in patients with systemic sclerosis and eosinophilic esophagitis where eosinophil/mast cell–targeted therapies are beneficial. Because systemic sclerosis and eosinophilic esophagitis patients experience similar esophageal symptoms, we hypothesized that eosinophil/mast cell–directed therapy may potentially benefit systemic sclerosis patients. Herein, we determine the association between esophageal mast cell quantities, gene expression, and clinical parameters in order to identify systemic sclerosis patients who may benefit from eosinophil/mast cell–directed therapy. Methods: Esophageal biopsies from systemic sclerosis patients and healthy participants were stained for tryptase, a mast cell marker, and associations with relevant clinical parameters including 24-h esophageal pH testing were assessed. Intra-epithelial mast cell density was quantified by semi-automated microscopy. Microarray data were utilized for functional and gene set enrichment analyses and to identify intrinsic subset assignment, a systemic sclerosis molecular classification system that includes inflammatory, proliferative, limited, and normal-like subsets. Results: Esophageal biopsies from 40 systemic sclerosis patients (39 receiving proton pump inhibition) and eleven healthy participants were studied. Mast cell numbers in both the upper esophagus ( rs = 0.638, p = 0.004) and the entire (upper + lower) esophagus ( rs = 0.562, p = 0.019) significantly correlated with acid exposure time percentage. The inflammatory, fibroproliferative, and normal-like intrinsic subset originally defined in skin biopsies were identified in esophageal biopsies. Although esophageal mast cell numbers in systemic sclerosis patients and healthy participants were similar, gene expression for mast cell–related pathways showed significant upregulation in the inflammatory intrinsic subset of systemic sclerosis patients compared to patients classified as proliferative or normal-like. Discussion: Esophageal mast cell numbers are heterogeneous in systemic sclerosis patients and may correlate with acid exposure. Patients with inflammatory intrinsic subset profiles in the esophagus demonstrate more tryptase staining. Mast cell–targeted therapy may be a useful therapeutic approach in systemic sclerosis patients belonging to the inflammatory intrinsic subset, but additional studies are warranted.

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