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Anthropologists have long understood that a society's ideas about who or what is risky depend on how meaning and worth are attributed to objects, people, and processes in a given place and time. However, until recently, little consideration has been given to the ways race and other hierarchical relations of power and difference shape how risk is constructed and deployed in social life. This article explores how race and criminal status intersect to shape the perception and management of risk and vulnerability in the United States by chronicling the lived experience of one young African American man who was prevented from obtaining an emergency medical technician (EMT) license because of his felony convictions. His pursuit of the EMT license and a career in firefighting exposes how risk, as a purportedly value-neutral concept, builds on racialized ideas about threat and vulnerability and further entrenches racialized social exclusion. Whereas many have decried racism as an unfortunate by-product of actuarial practices, I argue that racism and antiblackness are among risk's core animating logics. Challenges to risk evaluations must therefore go beyond politics of deservedness, rehabilitation, and inclusion to confront the foundational premises of risk head-on. [ABSTRACT FROM AUTHOR]

This study investigated the presence of racial bias in mental health assessments among White trainees and clinicians using the shifting standards paradigm (Biernat, 2003) and the racial triangulation framework (Kim, 1999). A total of 181 White participants viewed one of three case vignettes, all of which were identical except for the race of a fictitious client named Karl. Participants completed a clinical impressions inventory (Gushue, 2004) and the internal causality subscale from the Causation Dimension Scale (Russell, 1982). Results indicated differences in examiner ratings based on Karl's race. Black Karl was rated as significantly less symptomatic, compared to White or East Asian Karl, consistent with the shifting standards paradigm (Biernat, 2003; Gushue, 2004). No difference was found in symptom severity ratings between White Karl and East Asian Karl. Symptoms were also more likely to be attributed to internal factors with Black Karl than with White or East Asian Karl. [ABSTRACT FROM AUTHOR]

ER network formation depends on membrane fusion by the atlastin (ATL) GTPase. In humans, three paralogs are differentially expressed with divergent N- and C-terminal extensions, but their respective roles remain unknown. This is partly because, unlike Drosophila ATL, the fusion activity of human ATLs has not been reconstituted. Here, we report successful reconstitution of fusion activity by the human ATLs. Unexpectedly, the major splice isoforms of ATL1 and ATL2 are each autoinhibited, albeit to differing degrees. For the more strongly inhibited ATL2, autoinhibition mapped to a C-terminal α-helix is predicted to be continuous with an amphipathic helix required for fusion. Charge reversal of residues in the inhibitory domain strongly activated its fusion activity, and overexpression of this disinhibited version caused ER collapse. Neurons express an ATL2 splice isoform whose sequence differs in the inhibitory domain, and this form showed full fusion activity. These findings reveal autoinhibition and alternate splicing as regulators of atlastin-mediated ER fusion., (© 2021 Crosby et al.)