RESUMEN
Forensic anthropologists are often responsible for the management of long-term unidentified individuals. Others have contextualised these decedents-many of whom likely belonged to socially, politically, and/or economically marginalised groups in life-as part of a larger identification crisis in the US. However, there has been little discussion surrounding how this humanitarian crisis has manifested in academic institutions, where anthropologists often provide medicolegal consultation and act as long-term stewards of the unidentified. The Identification & Repatriation Initiative was created at the Forensic Anthropology Centre at Texas State University (FACTS) to recognise and investigate unidentified human remains in long-term storage. Our paper outlines common challenges that were encountered during our initial reassessment of unidentified cases at FACTS, emphasising the detrimental impacts of inconsistent procedures, loss of context, and case fatigue. It is likely that other academic institutions face similar challenges, and by highlighting these issues we hope to help initiate a larger conversation concerning ethical stewardship of human remains in these settings. By incorporating humanitarian perspectives into forensic casework, anthropologists in academia can better advocate for the long-term unidentified.Key pointsForensic anthropologists at academic institutions are qualified to act as consultants on forensic casework when requested by jurisdictional authorities and are often responsible for the long-term management of unidentified human remains.The long-term unidentified represent a vulnerable population and academic institutions are not exempt from calls for humanitarian approaches to identification.The Identification and Repatriation Initiative was created at the Forensic Anthropology Centre at Texas State University to acknowledge and investigate unidentified human remains in long-term storage.This paper considers possible ways for humanitarian action to be incorporated into academic settings and suggests anthropologists can better advocate for the unidentified through procedural standardisation, institutional and interagency collaboration and ethical stewardship.
RESUMEN
Mutations in hundreds of genes cause neurodevelopmental disorders with abnormal motor behavior alongside cognitive deficits. Boys with fragile X syndrome (FXS), a leading monogenic cause of intellectual disability, often display repetitive behaviors, a core feature of autism. By direct observation and manual analysis, we characterized spontaneous-motor-behavior phenotypes of Drosophila dfmr1 mutants, an established model for FXS. We recorded individual 1-day-old adult flies, with mature nervous systems and prior to the onset of aging, in small arenas. We scored behavior using open-source video-annotation software to generate continuous activity timelines, which were represented graphically and quantitatively. Young dfmr1 mutants spent excessive time grooming, with increased bout number and duration; both were rescued by transgenic wild-type dfmr1+. By two grooming-pattern measures, dfmr1-mutant flies showed elevated repetitions consistent with perseveration, which is common in FXS. In addition, the mutant flies display a preference for grooming posterior body structures, and an increased rate of grooming transitions from one site to another. We raise the possibility that courtship and circadian rhythm defects, previously reported for dfmr1 mutants, are complicated by excessive grooming. We also observed significantly increased grooming in CASK mutants, despite their dramatically decreased walking phenotype. The mutant flies, a model for human CASK-related neurodevelopmental disorders, displayed consistently elevated grooming indices throughout the assay, but transient locomotory activation immediately after placement in the arena. Based on published data identifying FMRP-target transcripts and functional analyses of mutations causing human genetic neurodevelopmental disorders, we propose the following proteins as candidate mediators of excessive repetitive behaviors in FXS: CaMKIIα, NMDA receptor subunits 2A and 2B, NLGN3, and SHANK3. Together, these fly-mutant phenotypes and mechanistic insights provide starting points for drug discovery to identify compounds that reduce dysfunctional repetitive behaviors.
