Female athletes sustain anterior cruciate ligament (ACL) injuries at four to six times the rate of their male counterparts, a disparity that has been linked to hormonal fluctuations across the menstrual cycle. Estrogen, which surges in the days before ovulation, has been shown to suppress the activity of lysyl oxidase (LOX), the primary enzymatic cross-linker of collagen in ligament tissue. This suppression reduces ligament stiffness and tensile strength without any change in collagen content, suggesting a functional vulnerability that is mechanistically distinct from structural damage. While the effect of estrogen on LOX activity has been established, the intracellular pathways responsible for this regulation, the precise timeframe over which changes occur, and the role of progesterone in modulating or counteracting these effects remain poorly characterized. This study uses an engineered porcine ACL ligament model to investigate the individual and combined effects of estrogen and progesterone on LOX activity and ligament mechanical function. Fibroblasts isolated from porcine ACL tissue will be used to form three-dimensional constructs cultured across four hormone conditions: no hormone, estrogen only, progesterone only, and a combined estrogen and progesterone group. Constructs will be assessed for mechanical properties, LOX enzyme activity, LOX mRNA expression via qRT-PCR, and LOX protein abundance via western blot. Together, these measures will allow differentiation of transcriptional, translational, and post-translational hormonal effects. Findings from this study will advance mechanistic understanding of how sex hormones regulate ligament biology and may provide a biological foundation for future research into sex-based differences in connective tissue injury risk.

Caffeine is the most widely used stimulant in the world, yet many adults with attention-deficit/hyperactivity disorder (ADHD) report that it makes them feel sleepy rather than alert, a paradoxical response that has never been empirically tested. The present study investigates whether ADHD is in fact associated with caffeine-induced sleepiness, and, if so, whether this relationship is reflected in two stress-response hormones: cortisol and dehydroepiandrosterone (DHEA). While these hormones have previously been independently linked to caffeine and to ADHD, they have never been studied together relative to the unique relationship these two variables share. . Adult participants completed an online survey assessing ADHD symptom severity (Adult ADHD Self-Report Scale), caffeine use patterns, subjective caffeine-related symptoms including sleepiness, general daytime sleepiness (Epworth Sleepiness Scale), and mood. Participants also provided a saliva sample, which was assayed for cortisol and DHEA concentrations. Preliminary review of the data suggests that ADHD symptom severity may be associated with greater self-reported caffeine-induced sleepiness, consistent with prior anecdotal reports, although formal statistical analyses linking these symptoms to hormone levels are still underway. This research is the first to combine self-report and salivary biomarker data to examine the paradoxical relationship between caffeine and ADHD, and findings may help clarify whether hormonal stress regulation contributes to why caffeine affects some individuals with ADHD differently than others. Identifying a physiological basis for this phenomenon would have direct implications for how clinicians and individuals with ADHD understand and discuss caffeine use as a coping strategy.

Honey bees (Apis mellifera) are exposed to various stressors, which have contributed to a global increase in honey bee colony loss. Among these stressors, viral pathogens are a major contributor to the decline of honeybee colonies, most notably, Israeli acute paralysis virus (IAPV). There is limited existing knowledge about honey bee host-virus interactions. Related research about bumble bees’ (Bombus terrestris) host-virus interaction has shown there is a link between increased levels of juvenile hormone (JH) and greater IAPV viral activity. Juvenile hormones are an insect hormone that regulate development, reproduction, and behavior. Honey bees use juvenile hormone for various physiological changes, and express different levels of JH throughout different seasons. In this study, we will investigate the relationship between juvenile hormones and virus activity inside honey bees. In addition, how do viral load and mortality vary seasonally in honey bees. A longitudinal study was performed in which a timed injection trial was performed every month. The treatment groups of the trial are IAPV doses (low, medium, and high), topical applications (juvenile hormone and precocene), and control groups. During the experiment, mortality is monitored, and samples are gathered for future qPCR analysis.

Trauma-induced hemorrhage is one of the leading causes of preventable death globally, yet the clinical tools available to address it remain severely limited. Donor derived platelets, the current standard for treating hemorrhage related bleeding, face persistent challenges including short shelf life, strict storage requirements, risk of contamination, and chronic supply shortages that make them unavailable in many pre-hospital and resource limited settings. These limitations have motivated a growing field of research aimed at developing synthetic platelet alternatives: engineered particle systems designed to mimic the hemostatic functions of natural platelets without relying on donor blood. Natural platelets perform hemostasis through a coordinated sequence of adhesion, activation, and aggregation at the site of vascular injury, but replicating this complexity in a synthetic system has proven difficult. Despite significant progress, most existing synthetic platelet designs replicate only a single aspect of this process, and this narrow functional scope has constrained their therapeutic potential. A more integrated approach, one that simultaneously targets multiple stages of clot formation, offers a compelling path forward. The goal of this project is to develop and characterize a biodegradable microsphere platform surface functionalized with multiple hemostatic ligands, designed to engage the coagulation cascade at more than one point of intervention. By building a system capable of addressing hemostasis more broadly within a single particle construct, this work aims to advance the rational design of scalable, donor-independent hemostatic agents with meaningful potential for trauma care and surgical applications.