Hospital Re-admission, Length of Stay, and Chief Complaints of Patients Experiencing Housing Instability

https://digitalcommons.unmc.edu/emet_posters/1047/thumbnail.jp

Drivers and Mechanisms of Golgi Fragmentation as a Modulator of Disease

The Golgi apparatus plays a pivotal role in post-translational modification, trafficking, and secretion of proteins, ensuring proper cellular function. As a result, its fragmentation has been implicated in multiple pathological conditions, including alcohol-induced liver injury and prostate cancer (PCa). Despite its known impact on cellular homeostasis, the molecular mechanisms governing Golgi fragmentation remain to be clarified. Additionally, we have only just begun to understand the vast consequences of Golgi disorganization on disease progression. This dissertation investigates the drivers and mechanisms of Golgi fragmentation, with a focus on its role as a modulator of disease. Using both in vitro and in vivo models, I demonstrate that chronic alcohol exposure triggers Golgiphagy (a selective form of autophagy that degrades Golgi membranes) through downregulation of the Rab GTPase, Rab3D. The loss of Rab3D results in p230 extension and dissociation of NMIIB from the Golgi. Ultimately, NMIIB dissociation gives way for NMIIA to associate with the Golgi and promote autophagy of the Golgi membranes. This Golgi disorganization leads to endoplasmic reticulum (ER) stress by activating the activating transcription factor 6 (ATF6)-mediated unfolded protein response (UPR). Additionally, the glycosyltransferase MGAT3 loses Golgi localization, but its competitor MGAT5 remains. This results in abnormal integrin glycosylation and binding to Galectin-3, increasing cluster formation and retention on the plasma membrane (PM). In addition to MGAT5-mediated glycosylation, underglycosylated integrins arrive at the PM carrying high-Man glycans due to alternative trafficking. This non-canonical route bypasses the Golgi and depends on STIM1- and ORP5-mediated ER-PM contact sites, which are involved in relieving ER stress and maintaining Golgi architecture. The findings presented in this dissertation underscore a novel link between Golgi fragmentation, ER stress, and alternative protein trafficking routes, revealing how these pathways contribute to disease pathogenesis. I demonstrate that Golgi integrity can be restored by autophagy inhibition with hydroxychloroquine (HCQ) and ER stress inhibition by ATF6 depletion. Importantly, by restoring compact Golgi morphology, I have reduced tumor growth and progression of alcohol-induced liver injury. These results highlight Golgi disorganization as both a driver of pathology and a potential therapeutic target, offering new insights into the development of interventions for alcohol-related liver disease and aggressive PCa

Association Between Rurality of Residence and Initial Stage at Presentation of Oral Cavity and Oropharyngeal Squamous Cell Carcinoma

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Ventricular Tachycardia Ablation in Patients with Valvular Heart Disease

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Exercise Interventions and Physical Activity in Adult Blood Cancer Survivors: A Scoping Review

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Self-Removal of a Hypoglossal Nerve Stimulator: Challenges and Lessons Learned

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Indocyanine Green and Near-infrared Guided Surgery Publications: An Analysis of Conflict of Interest Statements and Industry General Payments

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Barriers to Medication-Assisted Treatment for Opioid Use Disorder in Prisons and Jails in the United States: A Comprehensive Literature Review

Background: The American Society for Addiction Medicine guidelines state that all FDA-approved medication for opioid use disorder should be available for all patients (CDC, 2024). Medication-assisted treatments for opioid use disorders, also known as medication for opioid use disorder (MOUD), are treatments that help diminish the physical symptoms of addiction to opioids. Currently, there are three FDA-approved medications to treat opioid use disorder: buprenorphine, methadone, and naltrexone (FDA, 2024). Despite being at an increased risk for opioid misuse and overdose, incarcerated individuals in the U.S. often do not have access to MOUD. This comprehensive literature review aimed to determine the prevailing barriers to MOUD programs in carceral facilities. Methods: A comprehensive literature search approach was conducted across five databases and scholarly search tools, resulting in 41,395 records from the initial search. The review followed systematic review principles and adhered to a modified Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 guidelines. A thematic review process using Zotero reference manager and modified MAPiT strategy provided additional analysis and insights, resulting in ten final studies to analyze. Results: Applying search refinement criteria of the research resulted in (n = 8) qualitative studies that gathered data through interviews, focus groups, surveys, or a combination of these methods—all included studies that identified at least two types of MOUDs. Half of the study settings included only jails (n = 5), less than half (n = 4) included unified jails and prisons, and only one study was limited to just a prison. Study participants in eight of the studies were representatives of the carceral settings, such as administrators, clinicians, or staff—two studies utilized incarcerated individuals as study participants. The identified barriers were categorized into four thematic groups: program, stigma, regulatory, and community barriers. Conclusion: Despite societal evidence supporting MOUD, many compounding and interdependent barriers such as policy, geography, staffing issues, and resources prevent carceral institutions from adopting best practices for opioid use treatment. Reducing these barriers to MOUD for incarcerated individuals would save thousands of lives every year from overdose

A Comparison of Scar Infiltration, Scar Deactivation, and Standard of Care for Treatment of Chronic, Post-Surgical Pain After Cesarean Section in the Primary Setting: A Comparative Effectiveness Trial

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