Keeping Campuses Safe: The College Crime and Consequence Conundrum

Recent cases of sexual assault and violence against women proliferate in intercollegiate athletics. Despite federal mandates under Title IX, universities may struggle to appropriately respond to such incidences due to fan bias and/or difficulty in prosecuting under the criminal burden of proof. As such, this article offers up the National Collegiate Athletic Association (NCAA) as an adjudicating body, which could appoint a tribunal to ensure safety on campus and just punishment for transgressors. Using retributive justice and procedural justice as theoretical frameworks, it is argued that the NCAA is best served to investigate instances of sexual assault and violence against women by studentathletes at member institutions. Further, the NCAA has the power to levy punishment against those found responsible for violence against women, leading to a zero-tolerance policy for sexual assault in college sport

Creating Change in Intercollegiate Athletics: The Sexual Assault Prevention Paradigm for Athletic Departments

In 2011, the Office for Civil Rights issued a “Dear Colleague Letter” instructing universities to take action regarding sexual assault on college campuses. Specifically, universities must better educate students on the prevention of sexual assault, in the hope of reducing violence against women. Previous research is inconclusive on the involvement of intercollegiate student-athletes in incidences of sexual assault; however, recent high-profile cases of sexual misconduct at universities indicate that student-athletes are not immune to this issue. The purpose of this study was to explore how sexual assault is viewed within the culture of intercollegiate athletics, including education, occurrence, and prevention. Through interviews with former intercollegiate athletes, three main findings emerged: (1) Participant Knowledge, (2) Sexual Assault Within the Context of College Athletics; and (3) Creating Change in Athletic Department Culture. Using grounded theory, these themes were combined to create the Sexual Assault Prevention Paradigm for Athletic Departments

Legal Implications of Conducting Background Checks on Intercollegiate Student Athletes

Non

Legal Implications of Conducting Background Checks on Intercollegiate Student Athletes

Non

Legal Implications of Conducting Background Checks on Intercollegiate Student Athletes

Non

Loss-of-function in RBBP5 results in a syndromic neurodevelopmental disorder associated with microcephaly

Epigenetic dysregulation has been associated with many inherited disorders. RBBP5 (HGNC:9888) encodes a core member of the protein complex that methylates histone 3 lysine-4 (H3K4) and has not been implicated in human disease. We identify five unrelated individuals with de novo heterozygous variants in RBBP5. Three nonsense/frameshift and two missense variants were identified in probands with neurodevelopmental symptoms including global developmental delay, intellectual disability, microcephaly, and short stature. Here, we investigate the pathogenicity of the variants through protein structural analysis and transgenic Drosophila models. Both missense p.(T232I) and p.(E296D) variants affect evolutionarily conserved amino acids located at the interface between RBBP5 and the nucleosome. In Drosophila, overexpression analysis identifies partial loss-of-function mechanisms when the variants are expressed using the fly Rbbp5 or human RBBP5 cDNA. Loss of Rbbp5 leads to a reduction in brain size. The human reference or variant transgenes fail to rescue this loss and expression of either missense variant in an Rbbp5 null background results in a less severe microcephaly phenotype than the human reference, indicating both missense variants are partial loss-of-function alleles. Haploinsufficiency of RBBP5 observed through de novo null and hypomorphic loss-of-function variants is associated with a syndromic neurodevelopmental disorder. Huang et al. report the first functional validation of candidate pathological variants in RBBP5. We present three truncating p.(K244Nfs*6), p.(W254*), p.(R307*) and two missense p.(T232I), p.(E296D) variants found de novo in affected individuals sharing phenotypes including microcephaly and short stature. RBBP5 is a core member of the COMPASS complex responsible for H3 lysine 4 methylation to activate developmental target genes (COMPASS complex adapted from Namitz et al., 2023). Differentiation of neural stem cells in humans and neuroblasts in Drosophila is conserved allowing for the study of neural development in the fly model organism (neural stem cell/neuroblast differentiation diagram adapted from Kim and Hirth, 2009). We used overexpression and rescue experiments to characterize the missense variants in the fly. Neural progenitor populations were evaluated in the larval brain and tissue specific phenotypes were quantified using adult eye and wing morphology studies. We identify that the truncating and missense variants are loss-of-function alleles. As additional patients are identified, the full phenotypic spectrum of RBBP5-related disorders will be elucidated. Created with Biorender.com. [Display omitted