Toward Positive Retention in Academic Libraries: A Conceptual Framework

It’s been nearly 25 years since ACRL and ARL named recruitment and retention of BIPOC librarians a priority for the profession, but the numbers have stagnated or even decreased. One reason for this could be that research on recruitment and retention in academic libraries tends to conflate these concepts and focus on recruitment, which can be more easily quantified. As a result, less attention has been paid to defining, measuring, and improving retention. Here, the researchers present a framework to better define the multiple dimensions of retention and how retention is related to organizational culture in academic libraries

Symphonic Wind Ensemble, video

Ensemble Performance videoSymphonic Wind Ensemble, video What A Wonderful World conducted by Duane CostonWednesday, october 8, 2025 at 7:00 p.m.Sonia Vlahcevic Concert HallW.E. Singleton Center for the Performing Arts922 Park Avenue | Richmond, Virgini

Flute Studio Recital, video

Studio Recital VideoFlute +1 Studio Recital, videowith Hope Armstrong Erb & Brent te Velde, pianoThursday, October 9, 2025 at 7:00 p.m.W.E. Singleton Center for the Performing ArtsSonia Vlahcevic Concert Hall922 Park Avenue | Richmond, Virgini

Investigating the Potential of Broccoli Seed Extract to Attenuate Morphine Tolerance

Opioids remain one of the most effective treatment strategies for managing severe and persistent pain. However, its long-term use leads to pharmacological tolerance, requiring progressively higher doses to achieve analgesia. This dose escalation increases the risk of life-threatening side effects and dependence, underscoring the urgent need for safe adjuncts to preserve opioid efficacy. Emerging evidence suggests that morphine tolerance is linked to intestinal inflammation and disruption of gut barrier integrity. Broccoli Seed Extract (BSE), rich in the bioactive compound sulforaphane, exhibits antioxidant and anti-inflammatory properties that may protect against these effects. We hypothesized that BSE could prevent the development of morphine tolerance by mitigating inflammation associated with chronic opioid exposure. To test this, an animal model was used with three groups (n=20 each): saline, chronic morphine + vehicle, and chronic morphine + BSE. All animals received four days of respective treatments followed by a morphine dose-response challenge on day 5. Analgesic response was assessed using the tail immersion assay, and the animals which were administered BSE showed a rightward shift in the dose-response curve compared to morphine + vehicle group but the difference did not reach statistical significance. To further explore the anti-inflammatory mechanism, T84 colon epithelial cells were pre-treated with BSE for 3 hours prior to exposure to an “inflammatory colon soup” prepared from chronically morphine-treated animal colons. BSE pre-treatment reduced IL-8 mRNA expression in T84 cells. Although reduction of morphine tolerance with BSE did not reach statistical significance in-vivo, inhibition of proinflammatory cytokine IL-8 expression in colonic epithelial cells suggest that anti-inflammatory effects of BSE may be modulated by the shift in gut microbiome due to chronic morphine. Harnessing such natural compounds may provide a novel, accessible strategy to enhance opioid safety and maintain pain relief in chronic pain management

S20, E01: Federalist 51 (Aired 9/5/2025)

Aughie and Nia discuss Federalist Paper 51, which lays out checks and balances in the proposed federal government. James Madison is the author of Federalist 51. Centinel 1, by Samuel Bryan, responds.https://scholarscompass.vcu.edu/civil_discourse/1281/thumbnail.jp

Exploring the Role of Transcription Factor Nrf1 in Autophagy and Inhibiting the Nrf1 Bounce-Back Response

Cells exposed to proteotoxic stress invoke adaptive responses aimed at restoring proteostasis. Our previous studies have established a firm role for the transcription factor Nuclear factor-erythroid derived-2-related factor-1 (Nrf1) in responding to proteotoxic stress elicited by inhibition of cellular proteasome. Following proteasome inhibition, Nrf1 mediates the synthesis of new proteasomes, thus enabling cells to mitigate proteotoxic stress. Here, we report that under similar circumstances, multiple components of the autophagy-lysosomal pathway (ALP) were transcriptionally upregulated in an Nrf1-dependent fashion, thus providing the cells with an additional route to cope with proteasome insufficiency. In response to proteasome inhibitors, Nrf1-deficient cells exhibited profound defects in inducing autophagy and clearing aggresomes. This phenomenon was also recapitulated in NGLY1 knockout cells, where Nrf1 is known to be non-functional. Conversely, overexpression of Nrf1 induced ALP genes and endowed the cells with an increased capacity to clear aggresomes. Overall, our results significantly expand the role of Nrf1 in shaping the cellular response to proteotoxic stress. Proteasome inhibitors, ixazomib, carfilzomib, and bortezomib, are FDA-approved and currently used in clinics to treat multiple myeloma and mantle cell lymphoma. However, over time, patients often develop resistance to proteasome inhibitors, rendering them less effective as a treatment. The transcription factor Nrf1 induces proteasome and autophagy-lysosomal pathway (ALP) genes in response to proteasome inhibition, thus making proteasome inhibitors less effective. To improve the efficacy of proteasome inhibitors, it is necessary to identify drugs that can attenuate the Nrf1-mediated bounce-back response. Here, we found that anthracyclines, such as doxorubicin, synergized with proteasome inhibitors. Anthracyclines were able to attenuate Nrf1 transcriptional activity and increase cancer cell death. Moreover, we found that anthracyclines inhibited Nrf1\u27s ability to bind to antioxidant response elements (AREs) of target genes for the proteasome and ALP. Interestingly, we also saw that aclarubicin, a non-DNA damage-inducing anthracycline, was also able to attenuate the Nrf1-mediated bounce-back response. Our work provides a mechanistic explanation of the synergy between anthracyclines and proteasome inhibitors in cancer cell lines, and these findings could lead to future preclinical and clinical studies for this combinational treatment

REPEAT EXPANSION IN MYOTONIC DYSTROPHY: Exploration of Genetic Modifiers of Repeat Instability

Congenital myotonic dystrophy (CDM), the most severe form of myotonic dystrophy type 1 (DM1), arises from rapid intergenerational expansions of CTG repeats in the DMPK gene. This study leverages the largest whole-exome sequencing (WES) cohort of CDM cases to date to elucidate genetic modifiers of repeat instability and contributors to clinical phenotype. Variant burden analysis, allele frequency comparisons, and permutation testing revealed the enrichment of rare variants in DNA repair and muscle integrity pathways, with MSH6, NEBL, and SGCG emerging as key candidates. Functional enrichment highlighted disruptions in mismatch repair (MMR), homologous recombination, and replication-associated processes, implicating these pathways in both germline and somatic instability. Two lines of evidence implicate MSH3 in CDM pathogenesis: a deleterious variant identified in a multigenerational pedigree cosegregating expanded DMPK alleles and demonstrating impaired DNA repair capacity in functional assays and a strong prevalence of an MSH3 haplotype (including the rs1650697 variant) previously linked to contrasting effects, delayed onset in Huntington’s Disease and earlier onset in DM1. Correlation analyses revealed a compelling dichotomy: rare MMR variants are associated with smaller expansions, predominantly in DM1 mothers, suggesting a germline influence; in contrast, replication stress-related genes correlated with larger expansions characteristic of CDM, reflecting somatic instability. These findings underscore two central themes: disruption of DNA repair machinery and compromised muscle integrity as potential modifiers of repeat instability and the CDM phenotype. Together, this integrative approach, which combines statistical enrichment, family-based variant sharing, and functional validation, advances the understanding of CDM pathogenesis and highlights MSH3, a known modifier of repeat instability, as a promising target for therapeutic modulation with distinct effects in CDM compared to other repeat expansion disorders

VCU Guitar Ensemble, video

VCU Guitar Ensemble, videodirected by David ToussaintTuesday, April 22, 2025 at 7:00 p.m.Recital HallJames W. Black Music Center1015 Grove Avenue | Richmond, VirginiaEnsemble MembersSimon BarrettMason BerdecioJosh HuddleNate JohnsonAidan McMullanRyelyn NordengAlex Turne

(Art) Education in the Afterlife of Massive Resistance: Constructing, Capturing, and Commodifying Racialized Disability in Virginia’s Student Assignment Practices, 1956-1966 and Present Day

This dissertation explores discursive functions of disability in pupil placement decisions in Massive Resistance Virginia, the relationship between disability and race that was constructed through these moves, and how these relationships surface in the reflections, perceptions, and pedagogy of a practicing art teacher, Nathan, who works at Arts High School (AHS), a Virginia specialty center high school. Under the umbrella of the Discourse Historical Approach, which relies on multiple, interdisciplinary data sources to explore how discourses evolve, I connect a robust archival analysis of historical data collected in the records of Virginia’s Pupil Placement Board (746 boxes, 1956-1966) with present-day demographics from Virginia schools, school district documents, and nearly 30 hours of interviews and classroom observations conducted in collaboration with Nathan. Utilizing a post-structural feminist interpretive framework that relies most heavily on Critical Disability Studies, Disability Critical Race Theory, and Critical Whiteness Studies, I trace historical throughlines from Massive Resistance to present-day. My findings expose how, during Massive Resistance and in present-day, the language of ability and disability functions to deny Black children (art) educational opportunities and solidifies historically-prevalent associations between Blackness and lack. I put forward a cycle of construction, capture, and commodification, suggesting that in Massive Resistance and present-day, such discourses construct a racialized understanding of disability that is captured by white parents and commodified to accrue additional resources for their already-privileged children, enacting metaphorical and literal harm on Black children and further reinscribing the construction of Black disability. This evidences what I call an afterlife of Massive Resistance in which present-day (art) education operates. I explore strategies of resistance, practiced during Massive Resistance and in present day, which make the movements of power visible and endeavor toward a constructive and collective politics. I conclude by discussing limitations of the study and directions for future research

Love Letter

I applied to graduate school to reconnect with and better understand my studio practice, acquire language, and to disrupt my known ways of making. Generally speaking, I see my practice as being about being seen, and unseen, and the pain and pleasure of being perceived. I’ve learned about my ways of being in the studio. I’ve come closer to speaking honestly about my relationship with my materials, processes, tools, how I value my own labor, and how this informs my work. I am grateful for the cascade of small epiphanies that came and left me while I worked in my studio, (I wish I’d written them down) and for the time I was given to take risks, explore new materials, processes, and to love my studio practice again