Students, faculty and postdocs from the University of Utah’s Biomedical Engineering department attended and participated in the annual Biomedical Engineering Society (BMES) national meeting from October 21st – 24th, 2026 in Orlando Florida!

The conference was a plethora of rich and stimulating knowledge and collaborative networking with over 2,500 presentations from students and researchers across the nation.  The conference featured specialized keynote sessions as well as poster and podium presentations.

11 graduate students, 4 undergraduate students and 2 postdoctoral researchers presented their research at BMES with the support of 5 BME faculty members. Continue reading to view BME’s contributions to this year’s conference through their presentation abstracts.

After transfemoral amputation, individuals commonly rely on passive prosthetic knees and ankles, which are unable to generate positive mechanical power during walking like biological joints. As a result, transfemoral amputees are not able to produce as much forward propulsion with the prosthetic limb  and must compensate by increasing the mechanical work produced by the residual hip. These compensatory gait mechanics have been associated with increased joint loading, pain, and the development of secondary musculoskeletal conditions such as osteoarthritis, which can further reduce mobility and quality of life. Active knee prostheses have the potential to improve forward propulsion and reduce hip compensation by supplying positive power to the lower limb.  However, it remains unclear how much positive knee assistance is required to produce meaningful biomechanical improvements. Therefore, the objective of this study is to assess the biomechanical effects of increasing positive energy injection at the prosthetic knee, in the form of knee flexion torque during late stance. We hypothesize that increasing levels of knee flexion torque during late stance will increase forward propulsion and decrease positive residual hip work.

There is a growing awareness that exposure to nature has innumerable health benefits, including improved mood, attention, and cognition. In this study, we sought to test whether nature-deprived hospital patients immersed in virtual reality (VR) nature environments experienced improvements in mood and affect. These patients were undergoing intracranial neuromonitoring for neurosurgical diagnosis and treatment for drug-resistant epilepsy. Critically, cortical and subcortical deep-brain recordings enable us to measure neural activity during immersion in VR nature. These recordings can help uncover neurophysiological changes during VR that could underlie variations in mood and perceived recovery and to bridge a longstanding gap in the field of environmental neuroscience.

Declining mental health remains one of the most prominent health crises in this generation; it is crucial to recognize the need for therapeutic development. By compounding the accessibility and efficacy of VR with the salutogenesis of immersion in nature, there is a potential to revolutionize therapeutic options for patients in long-term care. This study has implications for depression and anxiety and provides a deep understanding of the intracranial mechanisms of mood and affect.

Following vertebral fusion, many patients experience accelerated degeneration in vertebral segments that were not fused but are adjacent to the fusion. This phenomenon, known as adjacent segment disease (ASD), is well-documented in the lumbar and lower cervical spine regions, and is commonly believed to be caused by increased mechanical loading due to compensatory motion in unfused segments. However, little is known regarding the risk of ASD in patients who undergo fusion in the craniocervical junction (CCJ). Understanding the patterns of stress and force alterations that take place in unfused cervical segments after fusion in the CCJ can contribute to improved surgical planning for more effective and durable surgical outcomes.

Liver cancer is the third leading cause of cancer-related deaths worldwide, with hepatocellular carcinoma (HCC) accounting for 80% of cases. Early stages of HCC have a 70% 5-year survival rate, while advanced stages have less than 20%. Transarterial chemoembolization (TACE) is the standard of care for intermediate stage HCC in patients ineligible for surgical resection, though it has limited tumor penetration, non-target embolization, hypoxia-driven revascularization, and high recurrence rates. There is a critical need for injectable embolic systems that both occlude tumor feeding vessels and provide sustained, localized chemotherapy while minimizing systemic exposure. Silk-elastinlike protein polymers (SELPs) are recombinant, thermoresponsive, biodegradable polymers that undergo a sol-gel transition at 37°C, enabling deeper tumor permeation as a liquid embolic, ex vivo drug loading, sustained localized drug delivery, and reduced non-target embolization. SELP analogs differ in their silk and elastin motif compositions, which change their mechanical properties critical for embolic delivery. Ideally, viscosity should remain below 150 cP for injectability in clinical catheters, having rapid gelation at 5 minutes, and storage modulus should be at least 1X10⁵ Pa for vascular occlusion. Here we systematically evaluate three SELP analogs under bland and drug-loaded conditions to identify the optimal candidate for clinical TACE.

Conventional gait metrics (e.g., joint moments, angular displacements, and work) limit comparisons between commercial prostheses and biological limbs because these analyses typically rely on rigid-body joint mechanics. This is problematic because biological limbs have multiple articulating joints in multiple planes, whereas prosthetic designs can range from multiple articulating joints (i.e., biomimetic) to single elastic elements with no joints (i.e., non-biomimetic). This diversity in joint types can lead to inaccurate comparisons of joint-based metrics across disparate leg designs. Conversely, in typical engineering practice, single elastic elements are characterized by the displacement induced by an applied force and the resultant work done. Such an approach to analyze single elastic elements may be valuable for quantifying mechanical function across disparate legs (e.g., biological, biomimetic and non-biomimetic prostheses). By treating all structures distal to the shank as a single element, all leg-specific components, including joints, segments, and soft tissues, can be ignored, allowing a direct comparison of the entire leg’s forces, displacements, and work [1]. Thus, the purpose of this study is to compare distal-to-shank gait mechanics (ground reaction forces (GRF), centre-of-pressure (COP) displacement, and resultant work relative to the shank) using a single-segment analysis across different lower-limb types, including commercially available prostheses and biological limbs.

Pathology of the intervertebral disc (IVD) and associated back pain is a major healthcare concern in the US. Degenerative disc disease (DDD) is associated with increased inflammation and senescence in degenerating discs. Using genome wide CRISPRa screens, our lab identified a previously uncharacterized zinc finger protein, ZNF865, that regulates cell cycle, DNA damage, and senescence, and is reduced with age in patients with low back pain. Here we investigate the direct effects of ZNF865 regulation on senescence, DNA damage, degeneration and pain outcomes in a rat model both in vitro and in vivo.

DNA damage accumulation is a well-known marker of age-related diseases ranging from cancers to degenerative musculoskeletal conditions. DNA damage accumulation with aging is attributed to a combination of exogenous and endogenous sources of damage. Exogenous sources of DNA damage include prolonged exposure to UV light or chemical species. Endogenous sources include increased rates of reactive oxygen species due to mitochondrial dysfunction and pH decreases. Our lab has recently shown that cell populations isolated from patients undergoing treatment for low back pain display significantly elevated baseline levels of DNA damage relative to healthy cell populations. Furthermore, we have recently discovered the gene ZNF865 (BLST) as a key regulator of cellular senescence. Because cellular senescence has been shown to be a direct response to DNA damage accumulation in numerous pathogenic states, here, we elucidate BLST’s involvement in DNA repair pathways. Additionally, we demonstrate that CRISPR modulation of BLST in human nucleus pulposus (hNP) cells has a direct effect on DNA damage within the cell population. Further, because the intervertebral disc maintains a pH of approximately 7.1 in a healthy state, but drops to as low as 6.2 during degeneration, we demonstrate BLST’s ability to protect form low-pH induced DNA damage in an in-vitro model mimicking various stages of disc degeneration. Finally, we demonstrate BLST’s ability to rapidly repair exogenously damaged DNA upon exposure to UV radiation.

Benign paroxysmal positional vertigo (BPPV) is the most common cause of episodic vertigo, due to dislodged utricular debris becoming displaced into the lumen of 1 or more semicircular canal ducts (canalithiasis) either the long-arm (LA) or short-arm (SA). Once identified, a specific canalith repositioning maneuver (CRM) is performed to clear the lumen of the canal and move the debris into the utricular vestibule. Although CRMs have high success rates in resolving posterior canal (PC) canalithiasis of LA, patient-specific morphological differences, the ability to position the head in the targeted position, atypical BPPV, and multi-canal BPPV, in which particles appear in more than one canal simultaneously, can make diagnosis and treatment challenging. Three-dimensional (3D) simulations (Traboulsi and Teixido 2021, Aran-Tapia, Soto-Varela et al. 2024) have recently been applied to the design and evaluation of CRMs for the simultaneous treatment of all three ipsilateral canals (D’Albora Rivas, Teixido et al. 2020, Barreto, Yacovino et al. 2023, Cherchi 2025).  The purpose of this study is to compare the robustness of Epley CRM (standard of care for PC-BPPV) to a newly developed OMNI universal CRM (OMNI uCRM) for resolving ipsilateral multi-canal BPPV using a robust computational framework.

The tympanic membrane (TM) plays a significant role in efficient hearing and sound transmission through the middle ear (ME). Tympanometry is one of the standard clinical tests used to assess ME and TM function. During pressure-biased low-frequency loading, such as in 226 Hz tympanometry test, the TM is statically deformed before the low-frequency probe-tone stimulus is applied, which can alter its stiffness and mobility. Despite prior research into the mechanism of sound transmission through the ME, the impacts of TM’s unique material and geometric characteristics on its nonlinear behavior remain poorly understood. Our goal is to build a nonlinear finite element (FE) model of the ME to explore how nonlinear geometric stiffening, TM conical curvature, fiber recruitment, and the compliance of acoustic chambers shape TM responses to static pressure bias and low-frequency tone stimulation.

Despite the advancements and increased availability of conventional cancer therapies, many challenges remain, such as drug resistance, systemic toxicity, and recurrence. Identification of molecular regulators that support hallmarks such as tumor proliferation and invasion is crucial for the development of effective therapeutic strategies that address the limitations of traditional therapies and enhance therapeutic outcomes. ZNF865 is a 1056 amino acid-long protein with 20 unique ZNF and two transactivation domains identified by our team. Even though ZNF865 is widely expressed in all cell types, the function of this protein has not been investigated outside of our work. We have demonstrated that upregulation of ZNF865 leads to the repair of DNA damage, while downregulation leads to rapid DNA damage accumulation, which pushes cells into and out of senescence. Because dysregulation of DNA damage response and cellular senescence is recognized as a key mechanism in cancer progression, we hypothesized that ZNF865 may serve as a novel regulator of cancer survival. In addition, survival analysis of The Cancer Genome Atlas (TCGA) data showed that ZNF865 has significant effects on survival across multiple cancer types. We further investigated whether ZNF865 downregulation suppresses cancer cell colony formation, migration, and proliferation, thereby assessing its potential as a novel molecular target for cancer therapeutics.

Degenerative Disc Disease (DDD) is the leading cause of chronic lower back pain. Cellular senescence in the tissue drives the degradation of the extracellular matrix. The loss of proliferation capability due to senescence inhibits regeneration and contributes to the progression of the disease. Even though DDD is a main concern worldwide, current treatment options target only the symptoms rather than providing cellular and tissue restoration and healthy homeostasis. Recently, our team identified ZNF865 using genome-wide CRISPR screening as a regulator of cell cycle, DNA damage, and senescence in patient samples with DDD. ZNF865 is a 1056 amino acid-long protein with 20 unique ZNF domains and two transactivation domains, which is widely expressed in all cell types. We have demonstrated that upregulation of ZNF865 via CRISPRa increases proliferation, whereas downregulation via CRISPRi leads to rapid DNA damage accumulation and proliferation suppression across multiple cell types. Here, we investigate the effect of ZNF865 upregulation via delivery of ZNF865 mRNA using ionizable lipid nanoparticles (LNPs) in cells isolated from the intervertebral disc (IVD) of patients with DDD. LNPs are clinically translatable platforms that facilitate mRNA delivery and allow transient/tunable gene expression, avoiding the risks associated with viral vectors. We assessed whether increased ZNF865 expression via mRNA delivery can reverse senescence-associated phenotypes in human degenerative disc cells in vitro.

BMES 2026 was an excellent success with Utah BME faculty and students connecting and sharing research with scientist and fellow researchers across the nation.

BME’s Chair, Dr. Jessica Wagenseil was elated to participate this year and stated, “It was great for my lab to meet up in person as we currently have trainees both at the University of Utah and Washington University. I enjoyed attending my first conference as department chair and especially found the networking with other chairs to be useful in terms of learning different ways to run a productive and collaborative department.”

Here’s to BMES 2027!