To Provide or Protect? Masculinity, Economic Precarity, and Protective Gun Ownership in the United States.

Protection is now the modal motivation for gun ownership, and men continue to outnumber women among gun owners. While research has linked economic precarity (e.g., insecurity and anxiety) to gun ownership and attitudes, separating economic well-being from constructions of masculinity is challenging. In response to blocked economic opportunities, some gun owners prioritize armed protection, symbolically replacing the masculine role of "provider" with one associated with "protection." Thus, understanding both persistently high rates of gun ownership in the United States (in spite of generally declining crime) alongside the gender gap in gun ownership requires deeper investigations into the meaning of guns in the United States and the role of guns in conceptualizations of American masculinity. We use recently collected crowdsourced survey data to test this provider-to-protector shift, exploring how economic precarity may operate as a cultural-level masculinity threat for some, and may intersect with marital/family status to shape gun attitudes and behaviors for both gun owners and nonowners. Results show that investments in stereotypical masculine ideals, rather than economic precarity, are linked to support for discourses associated with protective gun ownership and empowerment.

Database discrepancies in understanding the burden of mass shootings in the United States, 2013-2020.

Background: The United States experiences more mass shootings than any other nation in the world. Various entities have sought to collect data on this phenomenon, but there is no scholarly consensus regarding how best to define mass shootings. As a result, existing datasets include different incidents, limiting our understanding of the impact of mass gun violence in the U.S. Methods: We compared five datasets of mass shootings for each year included in five databases (2013-2020) and identified overlaps between each database's incidents. These overlaps and divergences between datasets persisted after applying the strictest fatality threshold (four or more) in mass shootings scholarship and policy. Findings: The datasets collectively include 3155 incidents, but the number of incidents included in each individual dataset varies from 57 to 2955 incidents. Only 25 incidents (0.008% of all incidents) are included in all five datasets. This finding persists even when applying the strictest criteria for mass shootings (four or more fatalities). Interpretation: Data discrepancies prevent us from understanding the public health impact of mass gun violence. These discrepancies result from a lack of scholarly consensus on how to define mass shootings, likely the downstream consequence of the politicization of gun violence research. We argue for a broad definition of a mass shooting and a government-supported data collection program to remedy these discrepancies. Such steps can improve the quality of research and support policy-making and journalism on the subject. Funding: This research was supported by the Pahl Initiative on the Study of Critical Social Issues, University of California, Santa Barbara.

"Husband, father, coward, killer": The discursive reproduction of racial inequality in media accounts of mass shooters.

Relying on more expansive criteria for defining "mass shootings" than much existing research, we examine a subset of a unique dataset incorporating 7,048 news documents covering 2,170 shootings in the United States between 2013 and 2019. We analyze the descriptive language used to describe incidents and perpetrators and discover significant racial disparities in representation. This research enables a critical examination of the explanatory frames utilized by news media to tell the public who mass shooters are and journalistic attempts to explain why they occur. Data were analyzed utilizing a mixed methods approach, relying on content analysis to inductively code emergent categories of descriptions of shooters and binary logistic regressions to analyze the preponderance of descriptive categories when comparing news articles reporting on shootings committed by differently racialized shooters. Our results confirm some recent research showing that mass shooters racialized as white are more likely to be described with kind and compassionate language. With our larger sample, however, we also find that mass shooters racialized as white are additionally more likely to be described with negative language as "bad" or "evil" in comparison to shooters of color. We discuss how these data demonstrate that media reports present a more complex picture of white mass shooters for the public than shooters of color.

MECP2-related pathways are dysregulated in a cortical organoid model of myotonic dystrophy.

Myotonic dystrophy type 1 (DM1) is a multisystem, autosomal-dominant inherited disorder caused by CTG microsatellite repeat expansions (MREs) in the 3' untranslated region of the dystrophia myotonica-protein kinase (DMPK) gene. Despite its prominence as the most common adult-onset muscular dystrophy, patients with congenital to juvenile-onset forms of DM1 can present with debilitating neurocognitive symptoms along the autism spectrum, characteristic of possible in utero cortical defects. However, the molecular mechanism by which CTG MREs lead to these developmental central nervous system (CNS) manifestations is unknown. Here, we showed that CUG foci found early in the maturation of three-dimensional (3D) cortical organoids from DM1 patient-derived induced pluripotent stem cells (iPSCs) cause hyperphosphorylation of CUGBP Elav-like family member 2 (CELF2) protein. Integrative single-cell RNA sequencing and enhanced cross-linking and immunoprecipitation (eCLIP) analysis revealed that reduced CELF2 protein-RNA substrate interactions results in misregulation of genes critical for excitatory synaptic signaling in glutamatergic neurons, including key components of the methyl-CpG binding protein 2 (MECP2) pathway. Comparisons to MECP2(y/-) cortical organoids revealed convergent molecular and cellular defects such as glutamate toxicity and neuronal loss. Our findings provide evidence suggesting that early-onset DM1 might involve neurodevelopmental disorder-associated pathways and identify N-methyl-d-aspartic acid (NMDA) antagonists as potential treatment avenues for neuronal defects in DM1.