SOURCE 2026 | Program, Proceedings, and Highlights

A Rare Advanced Case of Hyperostosis Frontalis Interna in a Male Donor Lacking Atypical Sex Characteristics: A Cadaveric Case Study Quaid Hunt; Celine Cortes, PhD; Christian Heck, PhD Project Mentor(s): Celine Cortes, PhD Hyperostosis frontalis interna (HFI) is characterized by thick, bony nodules confined to the inner surface of the frontal bone. It is often identified incidentally on imaging or postmortem examination due to its often benign nature. HFI occurs most frequently postmenopausal females. In males, it has been associated with testicular atrophy, hypogonadism, or Klinefelter’s syndrome. Cases in males lacking these associations are rare. Here, we describe an advanced case of HFI in a male donor without physical correlates of sex hormone imbalance. HFI was discovered in a 96-year-old male donor during routine dissection at Central Washington University. Medical history was limited to cause-of-death: age- associated neurodegeneration. Osseous protrusions ranged from 1.89–3.87 cm in diameter and covered approximately 25–50% of the frontal bone internal surface. Given reported links between HFI and endocrine dysfunction, the testes were examined following standard scrotal dissection. The right testis measured 4.08 × 2.50 × 2.26 cm and the left 3.89 × 2.98 × 1.69 cm. No gross lesions or masses were observed. This case was classified as Type-C under the Hershkovitz system. Although prior studies associate HFI in males with hypogonadism or testicular atrophy, our findings suggest these relationships may be subtle. These findings support a potential association with long-term, age-related hormonal changes, not exclusively from gonadal pathology. Although our study is limited by an absence of detailed medical history, our findings are an important contribution to the understanding of HFI and underlying mechanisms driving its formation. Presentation Type: Poster Presentation (May 21, 9:30am–3:00pm) Keywords : Hyperostosis frontalis interna, cadaver, case study, endocrine, gonadal morphology SOURCE Form ID: 103 Phthalates are found in long-lasting flexible plastics including food containers, clothing, and more. Due to weak bonding, phthalates easily leak into our environment. Non-phthalates are a recent advancement, but are they still affecting us negatively in different ways, possibly worse than phthalates? This research aims to question the effects of non-phthalates on regeneration in planarian, and how caffeine may interfere. Regeneration is a process of reforming tissues, structures, and small or whole-body parts after an injury. Planaria are commonly studied for their ability for full body regeneration. Planaria have stem cells called neoblasts that accumulate at the site of injury forming a blastema 1-2 days later. Differentiation occurs 4-6 days after an injury, and eyespots and auricles will become more visible and mature. Regeneration is completed in 2-3 weeks in normal conditions. Studies have shown that Planarian regeneration rate increases with exposure to caffeine and decreases with exposure to phthalates such as Diethyl Phthalate, but what about caffeine and non-phthalates together? Studies have shown that specific the non-phthalate Acetyl Tributyl Citrate (ATBC) decreases glial cells regeneration, leading to neurodegeneration causing rapid aging in humans. Using sublethal concentrations of caffeine and ATBC, I studied head regeneration in planaria exposed to both chemicals separately and simultaneously. Regeneration was measured using blastema area measured with Image J, eyespots, and auricle development timing, and behavioral reactions. Using results from this research, we can understand the effects of non-phthalates on Planarian stem cells to better understand how other stem cells may respond to these chemicals. Planarian Regeneration with Non-phthalates and Caffeine Isabela Kincaid Project Mentor(s): April Binder, PhD

Presentation Type: Poster Presentation (May 21, 9:30am–3:00pm) Keywords: Biological Research, Regeneration, Non-phthalates, Caffeine SOURCE Form ID: 229

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