"When Appearances Matter: A Taxonomy and Ethics for Demographic-Based Provider Requests".

Requests by patients for providers of specific demographic backgrounds pose an ongoing challenge for hospitals, policymakers, and ethicists. These requests may stem from a wide variety of motivations; some may be consistent with broader societal values, although many others may reflect prejudices inconsistent with justice, equity, and decency. This paper proposes a taxonomy designed to assist healthcare institutions in addressing such cases in a consistent and equitable manner. The paper then reviews a range of ethical and logistical challenges raised by such requests and proposed guidance to consider when reviewing and responding to them.

Human CFEOM1 mutations attenuate KIF21A autoinhibition and cause oculomotor axon stalling.

The ocular motility disorder "Congenital fibrosis of the extraocular muscles type 1" (CFEOM1) results from heterozygous mutations altering the motor and third coiled-coil stalk of the anterograde kinesin, KIF21A. We demonstrate that Kif21a knockin mice harboring the most common human mutation develop CFEOM. The developing axons of the oculomotor nerve's superior division stall in the proximal nerve; the growth cones enlarge, extend excessive filopodia, and assume random trajectories. Inferior division axons reach the orbit but branch ectopically. We establish a gain-of-function mechanism and find that human motor or stalk mutations attenuate Kif21a autoinhibition, providing in vivo evidence for mammalian kinesin autoregulation. We identify Map1b as a Kif21a-interacting protein and report that Map1b⁻/⁻ mice develop CFEOM. The interaction between Kif21a and Map1b is likely to play a critical role in the pathogenesis of CFEOM1 and highlights a selective vulnerability of the developing oculomotor nerve to perturbations of the axon cytoskeleton.