Undergraduate Research in Natural and Clinical Science and Technology Journal
The Undergraduate Research in Natural and Clinical Science and Technology (URNCST) [pronounced "earnest"] Journal is a leading open access, Scopus-indexed, and international peer-reviewed publication for undergraduate research. The journal publishes abstracts for undergraduate conferences and case competitions and promotes innovative undergraduate research education initiatives. Are you looking to gain or share undergraduate research opportunities? Join our 3k+ member international Facebook group community today!
Undergraduate Research in Natural and Clinical Science and Technology (URNCST) Journal
The Impact of Social Media on Vaccine-Related Legislation Following Measles Outbreaks
Introduction: Vaccine exemptions are on the rise in many states. Exemptions to vaccine requirements can lead to a breakdown in herd immunity, allowing viruses like measles to propagate easily through a population. In response to recent measles outbreaks, many states have passed vaccine-related legislation. Methods: This study seeks to describe the discourse on social media related to state’s vaccine-related legislation, and how it may influence the policy cycle. Specifically, social media data were retrospectively collected from four states: California, New York, Arizona and Texas to understand the interplay between public discourse on X and the outcome of each bill. Analyses were performed to determine if sentiment can be used to predict recent vaccine-related legislation and how legislators interact with the general public via X. Results: Sentiment analysis on discussion of vaccine-related legislation during the specified policy window, and a chi-squared analysis revealed that public sentiment as measured on X was not related to the outcome of the proposed legislation. Discussion: It seems that X is not a platform that influences the policy cycle regarding vaccine-related legislation, particularly the formulation stage where stakeholders can communicate alternative solutions Conclusion: While public sentiment on X does not seem to influence the outcome of vaccine-related legislation, it is interesting to further explore what actions can be taken by the general public that will substantially influence the outcome of legislation important to stakeholders.
Copyright (c) 2026 Carina Goodart, Elise Bolin, Amber McCord, Allie Smith https://creativecommons.org/licenses/by/4.0
A Multidataset Investigation of Resting-State and Event-Related EEG Correlates of Major Depressive Disorder
Introduction: Major Depressive Disorder (MDD) is a prevalent psychiatric condition which lacks reliable biomarkers for diagnosis and treatment. Electroencephalography (EEG) offers a non-invasive, cost-effective method to identify potential biomarkers of MDD. However, findings vary widely across studies due to differences in patient populations, analytic methods, and brain states. To investigate these issues, this study evaluates the consistency and reproducibility of EEG biomarkers of MDD across two datasets with both resting-state and task-based data. Methods: We analyzed EEG data from two publicly available datasets of healthy controls and MDD patients. The MODMA dataset provided resting-state EEG data; the Cavanagh dataset included both resting-state and task-based data. Spectral power was extracted for canonical frequency bands, and task-evoked components were computed from feedback-locked event-related potentials (ERP). Group-level comparisons and brain-behaviour correlations were assessed using t-tests, Spearman correlations, and FDR correction. Results: In the MODMA dataset, MDD patients showed increased beta power and reduced alpha power in frontal and temporal regions, with beta power having the strongest positive correlation with depression severity. In the Cavanagh dataset, spectral and ERP amplitudes did not differ significantly between MDD and control groups. Reward-Positivity (RewP) amplitudes were reduced in MDD patients, and time-frequency analyses showed altered theta and delta responses. However, none of the findings were significant after FDR correction. Cross-dataset comparisons revealed significant variability in spectral profiles, particularly in the beta band. Discussion: Our findings highlight the challenges in identifying consistent EEG biomarkers of MDD across datasets and brain states. While trends in beta power and RewP amplitudes aligned with prior literature, they failed to replicate across datasets or remain significant after FDR correction. These results suggest that commonly reported neural markers may not generalize well across populations. This also highlights the need for greater standardization and cross-dataset validation in EEG biomarker research for MDD. Conclusion: This study found limited consistency in EEG biomarkers for MDD across two datasets and brain states. Future research should investigate why spectral features like beta power show significance in some datasets but not others and assess how factors such as EEG hardware and recording conditions contribute to this variability.
Copyright (c) 2026 Kevin Sogoli, Muhammad Faiq Faizy, Roger Guirguis https://creativecommons.org/licenses/by/4.0
Investigating the Role of H3K27me3 Demethylation in VEGFA Gene Activation Following Acute Exercise in Human Skeletal Muscle
Skeletal muscle adapts to endurance exercise by tissular remodelling such as angiogenesis, the growth of novel capillaries, a response largely mediated by transcriptional activation of vascular endothelial growth factor A (VEGF). While VEGF expression is classically regulated by the hypoxia-inducible transcription factor (HIF), recent evidence in endothelial cells suggests that epigenetic mechanisms—specifically, the removal of the repressive histone mark H3K27me3—also play a key role in activating this angiogenic gene. It remains unclear however, whether skeletal muscle myocytes utilize similar chromatin-based regulation for VEGF transcription during exercise. This study proposal aims to determine whether acute endurance exercise in humans induces epigenetic remodeling at the VEGFA promoter in skeletal muscle through H3K27me3 demethylation, and whether this is accompanied by upregulation of histone demethylases. Recreationally active male and female participants will complete 60 minutes of treadmill running at 70–80% of their maximal oxygen uptake. Muscle biopsies will be collected from the vastus lateralis at baseline, immediately post-exercise, and 1- and 3-hours post-exercise. Chromatin immunoprecipitation followed by quantitative-PCR (ChIP-qPCR) will be used to assess H3K27me3 enrichment at the VEGFA promoter. VEGFA mRNA expression will be measured via real-time quantitative PCR, and protein expression of the histone demethylases JMJD3 (KDM6B) and KDM4B will be quantified by immunoblotting. Our hypothesized results include a time-dependent decrease in H3K27me3 enrichment at the VEGFA promoter post-exercise, with significant reductions at 1 and 3 hours. This will be paralleled by increased VEGFA mRNA expression and a rapid and sustained upregulation of JMJD3 and KDM4B protein levels. These results would suggest that myocytes may employ a conserved epigenetic mechanism, previously observed in endothelial cells, to regulate VEGFA expression in response to exercise-induced hypoxia. The coordinated reduction in H3K27me3 and upregulation of demethylases supports a chromatin remodeling model of angiogenic gene activation. This study would broaden our understanding of exercise-induced molecular adaptation by implicating histone modifications as regulators of VEGF expression in human skeletal muscle. Future work should investigate the cell-type specificity of these changes and their implications for long-term skeletal muscle remodeling to endurance exercise.
Copyright (c) 2026 Zita Suranyi https://creativecommons.org/licenses/by/4.0
The Dual Role of Microglial Synaptic Pruning in Autism Spectrum Disorder and Schizophrenia: A Literature Review
This review investigates the dual roles of microglial synaptic pruning dysfunction in Autism Spectrum Disorder (ASD) and schizophrenia. While ASD is characterized by insufficient synaptic pruning leading to synaptic overabundance, schizophrenia exhibits excessive pruning and synaptic loss. This review aims to synthesize current knowledge on these distinct roles and clarify their associations with divergent behavioral phenotypes, ultimately contributing to identifying new research questions and potential therapeutic targets. Peer-reviewed literature from 2000-2025 was identified and analyzed using open-access databases such as PubMed, Scopus, and Google Scholar. Articles were selected based on relevance to microglial synaptic pruning in mammalian models of ASD and schizophrenia, focusing on synaptic markers, electrophysiological recordings, and complement cascade expression. Exclusion criteria included non-mammalian models, primary focus on other disorders, opinion articles and editorials, and use of purely in vitro evidence. In ASD, findings consistently indicate increased synaptic density and immature dendritic spines, particularly in the prefrontal cortex (PFC), temporal lobe, and cingulate cortex, linked to sensory hypersensitivity and social deficits. Electrophysiological studies show network hyperexcitability and excitation/inhibition imbalance. The classical complement cascade's role is less clear, with evidence pointing to dysfunction in the CX3CR1- CX3CL1 signaling axis impairing pruning instead. Conversely, schizophrenia exhibits reduced synaptic density in regions like the PFC and hippocampus. Electrophysiological recordings reveal decreased excitatory postsynaptic currents and widespread hypoconnectivity. Strong evidence implicates excessive classical complement cascade activation, especially C4 gene variants, in driving synaptic loss in schizophrenia. These findings highlight a striking neurobiological opposition: ASD appears to involve too little pruning leading to overconnectivity, while schizophrenia involves too much, resulting in synaptic loss. These structural and functional disparities underlie distinct behavioral phenotypes. Crucially, this suggests that a "one-size-fits-all" approach to neurodevelopmental disorder treatment is likely ineffective. Therapies must be tailored to address the specific pruning imbalance present in each condition. Understanding these precise mechanisms is crucial for developing targeted therapeutic strategies and diagnostic biomarkers. Future research should investigate regional specificity of pruning dysfunction, explore the heterogeneity of microglial phenotypes, and develop human-relevant translational models to uncover novel treatments.
Copyright (c) 2026 Haley Willem https://creativecommons.org/licenses/by/4.0
Temporal and Spatial Dynamics of Enteric Glial Cell Involvement in Parkinson’s Disease: A Literature Review
Introduction: Enteric glial cells (EGCs) are critical regulators of gastrointestinal (GI) homeostasis and are implicated in early Parkinson’s disease (PD) pathogenesis. Disruption of EGCs can trigger gut inflammation and propagation of pathological α-synuclein (α-syn) to the central nervous system (CNS). Investigating both the temporal dynamics of EGC activity across stages and spatial differences among gut regions is essential to identify when and where their shift from protective to pathological roles occurs. This review addresses these dynamics to understand PD progression better and propose EGC-targeted strategies. Methods: A systematic search in May 2025 of PubMed and Google Scholar (Jan 2012–Apr 2025) yielded 842 articles. Prioritizing primary research on enteric glial cells in Parkinson’s disease and excluding reviews or unrelated studies, 26 articles ultimately met the inclusion criteria for this review. Results: Regarding temporal dynamics, animal models demonstrate that EGC activation and inflammation emerge in the prodromal phase, preceding motor deficits. Subacute toxin models exhibit variable glial stress responses, whereas chronic and protopathic models illustrate neurochemical remodeling and the potential spread of pathology from the ENS to the CNS. Spatially, animal studies indicate region-specific vulnerability: the gastric myenteric plexus exhibits early α-syn accumulation; the distal ileum and proximal colon display oxidative stress and neurotransmitter imbalances; and the sigmoid colon shows TRL4-mediated inflammation. In parallel, human clinical findings corroborate distinct regional alterations, particularly in the duodenum, characterized by reactive gliosis and α-syn aggregates, and the ascending colon, where elevated pro-inflammatory cytokines correlated with increased expression of reactive glial marker GFAP and the developmental marker Sox-10. Discussion: The results support the hypothesis of PD pathology originating in the gut, with EGCs playing a critical role. Understanding these dynamics could help develop region-specific, EGC-based biomarkers for early diagnosis in the prodromal phase and guide targeted interventions. Future research should incorporate longitudinal tracking of EGC activity, single-cell multi-omics, and targeted interventions in PD models to establish causality. Conclusion: EGCs respond to early gut dysfunction and influence subsequent PD progression. Their time and region-specific activation may explain not only GI symptoms but also PD pathology, suggesting possible biomarkers or treatment targets.
Copyright (c) 2026 Soyoung Kim, Jeongmin Park https://creativecommons.org/licenses/by/4.0
Reframing Skeletal Muscle Angiogenesis: A Determinant, Not a Consequence, of Hypertrophic Adaptation to Resistance Training
Introduction: Exercise-induced skeletal muscle angiogenesis is governed by regulators such as vascular endothelial growth factor (VEGF) and thrombospondin 1 (TSP-1) and is classically attributed to aerobic training. While aerobic exercise is well established as a key driver of capillary adaptation, the purpose of capillary expansion during resistance training remains unclear. This review evaluates angiogenic regulation and evaluates whether vascular remodeling functions as a permissive, active contributor to muscle hypertrophy. Methods: Literature was identified through PubMed, Scopus, and Google Scholar using terms related to skeletal muscle angiogenesis, resistance exercise, VEGF, and TSP-1with studies from 2015 onward prioritized alongside key seminal papers. As a narrative review, studies were selected for relevance to the research objectives rather than predefined inclusion criteria, allowing a comprehensive synthesis of mechanisms underlying vascular adaptation. Results: Endurance exercise stimulates angiogenesis through mechanical and metabolic signals, with myofiber-derived VEGF acting as the essential driver of endothelial activation and capillary growth. This response is shaped by fiber-type hypoxia, endothelial metabolism, and the VEGF and TSP-1 balance. Resistance exercise also engages VEGF-dependent pathways, and myofiber-specific VEGF deletion demonstrates that preserving the capillary network is necessary for full hypertrophic adaptation. Angiogenesis can precede or scale with muscle growth, and baseline capillarization strongly predicts hypertrophic potential, indicating that vascular remodeling functions as a permissive mechanism supporting adaptation. Discussion: Detraining rapidly shifts muscle toward an anti-angiogenic state, with early suppression of VEGF and increases in TSP-1 preceding controlled, partially reversible capillary rarefaction. Aging further limits angiogenic potential by reducing baseline capillarization and blunting VEGF responsiveness, producing a vasculature that is less plastic and less capable of supporting hypertrophic adaptation. Metabolic conditions such as obesity also disrupt this balance, as elevated TSP-1 creates an inhibitory endothelial environment even when VEGF expression is preserved. Conclusion: Overall, the literature shows that skeletal muscle capillarization is essential for functional adaptation, that VEGF and TSP-1 signalling governs exercise-induced angiogenesis, and that vascular expansion acts as a permissive driver of hypertrophy, a relationship that persists across detraining, aging, and obesity.
Copyright (c) 2026 Lily D. Bauman https://creativecommons.org/licenses/by/4.0
How do Dual GLP-1/GIP Receptor Agonists Differ from GLP-1 Agonists for Diabetes Management: A Systematic Review
Introduction: Type 2 diabetes is a chronic metabolic disorder driven by insulin resistance and impaired β-cell function. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have become central to diabetes management by improving insulin secretion, reducing glucagon, promoting weight loss, and lowering cardiovascular risk. Dual GLP-1/glucose-dependent insulinotropic polypeptide (GIP) receptor agonists, such as tirzepatide, represent an emerging therapeutic class designed to enhance metabolic outcomes by activating complementary incretin pathways. This review evaluates how dual GLP-1/GIP agonists differ from GLP-1 RAs in mechanism, efficacy, safety, and therapeutic potential. Methods: A systematic review was conducted using PubMed, Scopus, and the Cochrane Library to identify randomized trials, meta-analyses, and observational studies published from 2010 to 2025. Studies included adults with type 2 diabetes and directly compared dual GLP-1/GIP agonists with GLP-1 RAs. Primary outcomes were hemoglobin A1c reduction and weight change; secondary outcomes included safety, cardiovascular measures, and β-cell function. Results: Across phase 3 trials, dual agonists achieved greater reductions in hemoglobin A1c (up to 2.4%) and body weight (up to 22%) compared to GLP-1 RAs. These effects reflect synergistic actions on insulin secretion, glucagon suppression, appetite regulation, and adipocyte metabolism. Dual agonists also demonstrated higher rates of normoglycemia and durable glycemic control, with gastrointestinal side effects similar to GLP-1 RAs. Preliminary data suggest improvements in blood pressure, lipid levels, and inflammatory markers, although dedicated cardiovascular outcome trials remain ongoing. Beyond diabetes, dual agonists show therapeutic potential in obesity, obstructive sleep apnea, and steatohepatitis Discussion: Dual GLP-1/GIP agonists differ from GLP-1 RAs by activating two incretin pathways, resulting in superior glucose lowering, more pronounced weight reduction, and broader metabolic benefits. These advantages appear without added safety concerns. Distinct GIP-mediated effects on adipose tissue and central appetite pathways contribute to their enhanced efficacy. Conclusion: Dual GLP-1/GIP receptor agonists represent a major advancement over GLP-1 RAs by delivering deeper glycemic improvement and greater weight loss through combined hormonal activation. Pending results from cardiovascular outcome trials, these agents may reshape diabetes management, particularly for individuals requiring substantial metabolic improvement beyond what GLP-1 RAs alone can provide.
Copyright (c) 2026 Prisha Bhat https://creativecommons.org/licenses/by/4.0
Prognostic Features and Clinical Outcomes Across Breast Cancer Subtypes Defined by Hormone Receptor and HER2 Status: A Literature Review
Introduction: Hormone-responsive breast cancer biologically varies from hormone-unresponsive breast cancer in treatment response. Hormone-responsive breast cancers are characterized by estrogen (ER) and progesterone (PR) receptors that, upon activation, alter gene expression and promote tumor growth. The presence of these receptors highlights ideal targets for treatments that block or lower hormone levels. In contrast, hormone-unresponsive breast cancers lack these receptors, exhibit insensitivity to endocrine therapy, and display poorer prognoses. Understanding the differences between hormone-responsive and unresponsive breast cancer presents crucial implications for developing effective treatment strategies, improving patient outcomes. Methods: A literature review was conducted using PubMed to identify English-language, peer-reviewed studies published between 2014 and 2025 examining breast cancer subtypes based on ER, PR, and HER2 status. Clinical trials, population-based cohort studies, and subtype-specific analyses evaluating prognosis, metastatic potential, or treatment responsiveness were included. Fifteen studies met the inclusion criteria and were included in the qualitative synthesis. Results: Hormone receptor-positive tumours expressing ER and PR demonstrated the most favourable outcomes, with slower metastasis and lower proliferative activity compared to receptor-negative tumours. Triple-negative breast cancer (TNBC) demonstrated the most aggressive biological course, characterized by increased metastatic potential and reduced responsiveness to endocrine therapy. Evidence from recent clinical trials indicates that in advanced TNBC, therapeutic benefit is primarily limited to immunotherapy-based combination strategies. While HER2 expression reflects a more aggressive biology, its presence enables targeted therapeutic intervention associated with improved patient outcomes. Discussion: Differences in subtype biology, metastatic behaviour and treatment responsiveness highlight the importance of hormone receptor status and subtype classification in guiding the clinical management of breast cancer. Conclusion: Hormone receptor status is a strong determinant of prognosis and treatment responsiveness across breast cancer subtypes, with HR-positive tumours demonstrating more favourable outcomes and TNBC exhibiting the most aggressive disease course. These findings emphasize the need to refine therapeutic strategies and guide the development of effective treatment options and molecular targets to improve outcomes across all breast cancer subtypes.
Copyright (c) 2026 Justine Nicoll https://creativecommons.org/licenses/by/4.0
Systematic Review of Quality Improvement Interventions on Surgical Safety Checklists
Introduction: Postoperative mortality is a significant global burden, partially driven by preventable perioperative errors, caused by human factors that contribute to preventable harm. The World Health Organization’s Surgical Safety Checklist (SSC) was introduced to reduce preventable harm during surgery and to improve surgical outcomes. Despite it being implemented across many healthcare systems, compliance and effective use of the SSC remains inconsistent. This systematic review aims to synthesize recent evidence on quality improvement interventions (QII) that target SSC implementation, identify strategies, and evaluate their impact on checklist utilization and related outcomes. Methods: This systematic review was conducted in accordance with the Cochrane Handbook and reported following the PRISMA 2020 guidelines. A literature search was performed using MEDLINE and PsycInfo, which limited the studies to those published between 2015 and 2025. Data was extracted using a standardized form, and study quality was assessed using the Joanna Briggs Institute (JBI) Checklist for Qualitative Research. Results: 23 studies published between 2015 and 2025 were included in this systematic review. The studies varied in design, sample size, units of analysis, and were conducted across a broad range of surgical specialties. QII included educational and training initiatives, audit and feedback mechanisms, mentorship programs, simulation-based interventions, and the introduction of modified checklist tools. Most interventions targeted all three phases of the SSC. Improved checklist compliance was the most frequently reported outcome. Fewer studies evaluated patient-centered outcomes. Discussion: The findings indicate that QII are generally effective in improving implementation and the use of the SSC across diverse surgical settings. However, the evidence base is limited by heterogeneity in intervention types, outcome measures, and study designs, with most studies relying on observational or pre-post methodologies. The limited reporting of patient-level outcomes restricts conclusions regarding the direct impact of these interventions on postoperative morbidity and mortality. Conclusion: Quality improvement interventions are associated with improved implementation and use of the SSC across diverse surgical contexts. While these interventions consistently enhance compliance and team engagement, further high-quality research is needed to determine its impact on patient outcomes and to identify the most effective and sustainable strategies.
Copyright (c) 2026 Lovejeet Kaur Manger, Emma Zhang https://creativecommons.org/licenses/by/4.0
Autism Spectrum Disorder and Associated Gastrointestinal Issues
Introduction and Definition: Autism spectrum disorder (ASD) is a “collection of conditions regarding brain development”; it presents with a diverse spectrum of characteristics and severity. It is well documented that people with ASD face gastrointestinal (GI) issues at a much higher frequency than the neurotypical population. This can drastically reduce their physical quality of life as well as hinder many social situations. The etiology is complex with multiple factors centred around the gut-brain axis. Presentation & Impact: The GI issues faced by those with ASD commonly include nausea, chronic constipation, diarrhoea, gastroesophageal reflux disease (GERD), chronic flatulence, gut inflammation, ulcers, and more. These problems carry extra baggage as they often lead to further distressing reactions. For example, posturing, self-harm, and outbursts are regularly reported – especially as those with ASD struggle to articulate the pain/issue. In the long term, GI issues affect mood, learning, as well as sleep (which can exacerbate the previous behaviours, particularly aggression). From a social perspective, this can impede on the social life of those with ASD. Etiology: The gut-brain axis – the two-way influences between the gut microbiome and the brain – seems to be at the core of most GI issues. People with ASD often have gut dysbiosis: an imbalance in their gut bacteria. While there is an excess of pathogenic bacteria, there is a lack of beneficial ones as well as a decrease in bacterial diversity. Other issues commonly associated with ASD contribute to this: digestive enzyme deficiencies (such as absence of lactase), selective eating (for example, with eating sensory issues), medication, and more. The issue of selective eating itself causes many of the GI symptoms; an unbalanced diet can cause diarrhoea, constipation, reflux, and intestinal motility issues. Treatment & Management: Treatments are usually behavioural. For children, clinicians work with parents to incorporate more balanced meals. Therapy is also used to overcome sensory issues and mealtime-related anxiety. However, specific medications such as laxatives or probiotics can be administered to relieve persistent symptoms.
Copyright (c) 2026 Winston Tan https://creativecommons.org/licenses/by/4.0
The 2026 Women in Science and Engineering National Conference took place at the Westin Harbour Castle in downtown Toronto on January 17-18. It welcomed several hundred student, research, and industry participants across all STEM disciplines. Student delegates were invited to submit abstracts describing their research for publication in collaboration with URNCST. The resulting collection spanning life science, physical science, and engineering work is featured here. Echoes of Adversity: The Prevalence and Associations of Invisible Symptoms with Adverse Childhood Experiences, Attachment Style, Self-Compassion, and Care Preferences in People with Multiple Sclerosis. Caitlin Evran [1], Jillian Scandiffio [2], Robert Simpson [3] [1] University of Toronto St. George, Toronto, Ontario [2] St. Michael’s Hospital, Toronto, Ontario [3] Department of Neurology, St. Michael’s Hospital, Toronto, Ontario Undergraduate Author Email: Caitlin.evran@mail.utoronto.ca Multiple sclerosis (MS) is a chronic inflammatory neurodegenerative disorder characterised by the destruction of the sheath that insulates neurons in the central nervous system. Over 90,000 Canadians live with MS, one of the highest prevalences worldwide. People with MS (PwMS) tend to suffer from scarcely researched ‘invisible symptoms’ including vision problems, muscle weakness, tingling, numbness, bladder control problems, dizziness, and trouble with cognition. Many environmental and demographic factors are linked with disease onset, progression, and symptom severity, but recent studies suggest that there is an association between adverse childhood experiences (ACEs) and MS. Further research is urgently needed to explore this relationship in more detail, because if there is a high prevalence of ACEs in people with MS, this has important implications for health service design and delivery, meaning providers should be trained to deliver trauma-informed treatments that are effective in this population. Research Question: What is the prevalence of invisible symptoms in Canadians with MS, and how do these symptoms relate to ACEs, attachment style, compassion, and care preferences? Methodology: Quantitative surveys will be employed to measure invisible symptoms and ACE burden in up to 90,000 Canadians with MS, along with clinical and sociodemographic factors, stress, attachment style, patient satisfaction, and quality of life. Furthermore, qualitative interviews will be conducted with survey respondents reporting ACEs to explore their perspectives on how these experiences impact their MS symptoms, coping, and care needs. MS healthcare providers will also be interviewed to understand how they approach treating patients with invisible symptoms and ACEs, as well as how their education affects this. Conclusion: Findings will help shape policy and optimize the care of MS patients with invisible symptoms and ACEs. Given the highly diverse MS population in Canada, this study will be important locally, nationally and internationally. Base editing-mediated correction of a nonsense variant in congenital muscular dystrophy Emily Huynh [1] [2], Ryan Marks [1] [2], Emily Bell [1], Ronald Cohn [1] [2] [3], Evgueni Ivakine [1] [2] [4] [1] Genetics & Genome Biology Program, Research Institute, The Hospital for Sick Children, Toronto, ON, Canada [2] Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada [3] Department of Pediatrics, The Hospital for Sick Children, Toronto, ON, Canada [4] Department of Physiology, University of Toronto, Toronto, ON, Canada First Author Email: emilyhuy.huynh@mail.utoronto.ca Merosin-deficient congenital muscular dystrophy type 1A (MDC1A) is a neuromuscular disease caused by autosomal recessive loss-of-function LAMA2 variants, which encode the ⍺2 chain of laminin-211. Deficiencies in this structural protein compromise interactions between skeletal myofibers and the extracellular matrix, leading to myofiber instability and fatal muscle wasting. Adenine base editors (ABE) are CRISPR-derived genome editing tools that convert A-to-G by deaminating deoxyadenosine, however, their clinical translation has been limited by unintended RNA off-target effects and bystander editing. Here, we optimize components of ABE to treat patient-derived MDC1A fibroblasts with a LAMA2 nonsense variant. Primary fibroblasts were Sanger sequenced to confirm compound heterozygous LAMA2 p.R1029X/L1984Ffs*4 genotype. Various Cas9 orthologues, guide RNA (gRNA) spacer lengths, and TadA8e deaminases were screened to identify the most efficient components of ABE. This workflow involved gRNA cloning, lentiviral production and titration, and lentiviral transduction to patient-derived fibroblasts. LAMA2 editing efficiency of the nonsense allele was evaluated by Sanger sequencing. Functional rescue of laminin-⍺2 was assessed by Western blot analysis. Among the Cas9 orthologues, Staphylococcus aureus Cas9 (SaCas9) achieved the highest editing efficiency at 30%. TadA8e deaminase variant V106W demonstrated reduced RNA off-target effects and bystander activity while maintaining editing efficiency. Western blot analysis confirmed laminin-⍺2 rescue. These findings demonstrate that ABE are an efficient and clinically translatable strategy for treating LAMA2 nonsense variants, highlighting its potential as a gene editing therapeutic for up to 50% of pathogenic single nucleotide variants. Aperiodic monotile lattices for enhancing the crash resistance of EV battery packs Shin-Ling Lai MEng Student [1] [1] Institute of Aerospace Studies, University of Toronto, Toronto, Ontario, Canada Author Email: celina.lai@mail.utoronto.ca Architected cellular materials are widely used in energy–absorbing structures, yet their mechanical response is strongly determined by topology. Periodic lattices such as hexagonal honeycombs exhibit efficient load transfer but fail through directional buckling, leading to stress drops and localized collapse. In this work, we experimentally investigate an aperiodic “hat monotile” lattice as a topology-engineered alternative designed to disrupt continuous failure paths. Monotile and hexagonal specimens were fabricated by stereolithography and density-matched to ¯ρ ≈ 15% through analytical calibration of wall thickness and characteristic length. Quasi-static compression tests (ε˙ = 10−3 s−1) provided force–displacement and laser-based deformation data. Monotile lattices exhibited smoother stress–strain evolution and spatially distributed collapse, with deformation spread across many struts rather than concentrated in discrete crush band formation characteristic of the hexagonal topology. Normalized stress-strain curves (σ/σf (ε) and σ/E(ε)) revealed consistent peak and elastic behavior across repeats, while monotile response lacked catastrophic drops and absorbed deformation through gradual, multiorientation strut bending. Deformation images confirmed isotropic compaction in the monotiles versus crush bands in hexagons. Despite slightly lower peak stress, the monotile geometry provided more stable load transfer and reduced collapse localization. These findings offer the first experimental evidence that aperiodic monotile lattices achieve comparable strength to-weight performance while enhancing deformation uniformity, highlighting their potential for crash–tolerant battery Informing Resource Allocation Policies Through Equity-Aware Epidemic Modelling Grace Lin, BSc Student [1], Isabelle Rao, PhD [1] [1] Department of Mechanical and Industrial Engineering, University of Toronto, Toronto, Ontario, M5S 1A1 Undergraduate Author Email: grace.lin@mail.utoronto.ca Equitable allocation of resources like vaccines are a central challenge in epidemic response, particularly when disease burden is unequally distributed across population subgroups. Most existing research prioritizes efficiency, by minimizing infections or deaths, while giving less attention to the equity implications of these strategies. Real-world populations exhibit disparities in transmission risk and disease vulnerability, raising questions about how to allocate limited resources fairly. To address this gap, we aim to systematically characterize the equity-efficiency tradeoff and identify disparity contexts where equity goals become more or less costly. We developed a deterministic compartmental epidemic model based on an extended Susceptible Infected-Recovered framework, with two subgroups having heterogeneous transmission and mortality rates. We evaluated four equity-aware optimization strategies from the literature. For each disparity metric, we fixed one group’s parameter, varying the other’s across four values. We simulated these scenarios, recording the optimal allocation under each strategy and the resulting deaths and infections. Preliminary simulations show that the “cost of fairness”– the efficiency loss when shifting from an efficiency-optimal to a fairness-constrained solution– varies with the type of disparity and optimization strategy, with some approaches consistently yielding fairer but more costly allocations. Our findings contribute to growing research intersecting epidemiology and social equity. This work offers public health policymakers a clearer understanding of when equity goals can be pursued with minimal loss in overall health outcomes. Future work will extend this to stochastic models and real-world data, bridging the gap between theoretical insights and actionable epidemic response strategies. A dynamic crop selection tool for space-based food production Olivia Mendelson, M.Sc. Student [1], Mark Lefsrud, Associate Professor [1] [1] Department of Bioresource Engineering, McGill University, Sainte-Anne-de-Bellevue, Quebec, Canada H9X 3V9 Graduate Author Email: olivia.mendelson2@mail.mcgill.ca As human missions extend beyond Earth, reliable fresh food production methods are essential. Limited resupply opportunities and harsh environmental conditions place significant demands on closed-loop plant growth systems. To date, comprehensive model-based tools for crop selection that balance mission objectives and system capabilities remain limited. This research presents the development of a dynamic crop selection tool to support mission planning and increase the success of space-based plant production. The tool is built upon a database of candidate crops, incorporating key parameters such as nutritional composition and growth requirements (e.g., temperature, humidity, water, nutrients, light, and crop cycle length). User-defined inputs such as mission timeline, dietary needs, and environmental control capabilities are considered alongside the evaluation of mission priorities using multi-criteria decision analysis methods. This tool enables interactive comparison of crop options while estimating yield and resource consumption rates (e.g., oxygen production, carbon dioxide uptake, and water flows) to optimize plant production and ensure crew health. By supporting rapid assessment of biomass and nutritional trade-offs, this tool enhances the efficiency, adaptability, and success of space food production strategies. This tool can equally support food security initiatives in Northern Canada, where remote communities face resource limitations and environmental challenges analogous to those in lunar and Martian systems. Melatonin reveals anticancer potential via systems biology analysis on cancer cell Shivangi Roy [1], Adin Aggarwal, Kenneth W. Yip University of Toronto, Anticancer.ca Primary Author Email: shivangi.roy@mail.utoronto.ca Melatonin, a neural hormone secreted by the pineal gland that regulates circadian rhythms, has emerged as a potential anticancer agent. This study investigated melatonin's effects on cancer cell viability and its cellular mechanism of action via transcriptomic changes across multiple cancer types. In experimental studies, melatonin has been shown to play a key role in limiting cell proliferation by inducing apoptosis, generating free radical oxygen species to combat oxidative stress, and upregulating suppressor genes and survival pathways. Using the NCI60 dataset, 60 different human cancer cell lines were treated with melatonin at various concentrations; cell survival was measured using an SRB assay to determine half-maximal inhibitory concentration (IC50) values. Results revealed significant variations in cell line sensitivity to melatonin—renal cancer cell line 786-O demonstrated high sensitivity, while K562 myeloid leukaemia and SW620 colorectal cancer lines showed relative resistance. Melatonin also exhibited greatest potency against renal and CNS cancer cell lines, with 19 of 63 cell lines showing significant sensitivity. Transcriptomic analysis using the L1000 assay revealed that melatonin treatment produced gene expression changes like knockdowns of genes involved in cell cycle regulation and upregulation of apoptotic pathways. These genetic similarities extended to compounds with antioxidant properties, suggesting melatonin's anticancer effects operate through multiple molecular mechanisms including modulation of oxidative stress response. This study highlights melatonin's varied anticancer effects across different cancer types. Future research should focus on optimizing melatonin's therapeutic potential in animal models of sensitive cancers and exploring chronobiological intervention strategies for cancer prevention and treatment. Experimental demonstration of a confined two-locus CRISPR toxin-antidote gene drive Ruobing Feng [1], Andrea Y.N. Tan [1] [2], Jackson Champer [1] [*] [1] Center of Bioinformatics, Center of Life Science, School of Life Science, Peking University, Beijing, China 100871 [2] Division of Engineering Science, Faculty of Applied Science and Engineering, University of Toronto, Toronto, Ontario, Canada M5S 1A4 [2] Undergraduate Author Email: andrea.yn.tan@gmail.com Gene drive systems enable rapid spread of desired transgenes throughout populations. Advances in CRISPR-Cas9 technology have facilitated the construction of toxin-antidote gene drives, which utilize a CRISPR nuclease as the toxin to disrupt an essential wild-type gene, alongside a recorded version of the same gene as the antidote. Because these systems propagate by eliminating wild-type alleles rather than directly copying themselves like homing drives, they typically exhibit introduction thresholds. Here, we constructed a drive system targeting two essential but haplosufficient genes, sim and stg, using two different drives located at different genomic locations. Each drive targets the gene that the other rescues. The system showed high cleavage in individual crosses. When released into a multigenerational cage population above the introduction threshold, the drive successfully and rapidly modified the entire population; below this threshold, it was eliminated. However, due to inherent fitness costs in the drive construct, our experimentally determined introduction threshold (34%) exceeded the threshold predicted by idealized computational models assuming zero fitness cost (18%). Our findings indicate that two-locus CRISPR toxin-antidote drives represent promising tools for effective and regionally confinable population modification gene drive. From Rivers to Dinners: Tracing Microplastics Through Clams Sangeeta Vidyarthi [1], Shamsunnahar Suchana [1], Pedro Mena-Giraldo [1], Masashi Kaneda [1], Miguel Eduardo Felismino [2], Irene Gregory-Eaves [2], Nathalie Tufenkji[1] Department of Chemical Engineering [1], Department of Biology [2], McGill University Microplastics are a global research priority due to their toxicity, their ability to act as vectors for environmental pollutants, and their potential for bioavailability and bioaccumulation across food webs. As a result, microplastics released into aquatic environments can enter human systems through dietary exposure. This study focuses on bivalves, among the most heavily consumed seafood worldwide, as a critical link between environmental contamination and human exposure. Microplastics were extracted, characterized, identified, and quantified from the soft tissue of 36 soft-shell clams (Mya arenaria) collected across 11 sampling sites in the Saguenay and St. Lawrence rivers. Both physical characteristics (particle size, morphology, color) and chemical composition were analyzed to trace potential sources and assess environmental fate. Among the detected and confirmed microplastic particles, 40% were smaller than 1 mm. In terms of morphology, ~80% were fibers, and 30% were composed of synthetic polymers, compared with natural and non-synthetic materials. Among synthetic polymers, particular attention is drawn to polyvinyl fluoride (PVF), which was dominant. PVF is a high-risk fluoropolymer that is widely used in water-repellent clothing, yet it is rarely monitored in environmental studies. Finally, these findings are placed within the broader context of human health by summarizing current understanding of microplastic exposure and its potential biological impacts. Together, these results highlight the need for improved monitoring of overlooked polymer types in aquatic food systems.
Copyright (c) 2026 Zia Owens, Radia Salam https://creativecommons.org/licenses/by/4.0
7th Annual Neuro Health Awareness Conference (NHAC) Abstract Book
The Neuro Health Awareness Conference (NHAC) is an initiative organized by the University of Ottawa Multiple Sclerosis Club (UOMSC), a student-led organization committed to raising awareness about multiple sclerosis and broader neurological health through education, advocacy, fundraising, and community engagement. UOMSC works to create opportunities for students and the wider community to learn about neurological disorders, connect with researchers and healthcare professionals, and support individuals affected by these conditions. Through events like this conference, the club aims to foster meaningful conversations around brain health, neuroscience research, patient experiences, and innovation in care. The conference brings together students, researchers, clinicians, advocates, and individuals with lived experience for a day of keynote talks, panel discussions, and networking opportunities centered on neurohealth. In addition to promoting education and dialogue, the NHAC also supports an important charitable mission, with proceeds being donated to the MS Canada and the University of Ottawa Brain and Mind Research Institute to help advance multiple sclerosis support, neurological research, and innovation in brain health. By combining awareness, collaboration, and philanthropy, the conference reflects UOMSC’s dedication to making a meaningful impact both on campus and in the broader community.
Copyright (c) 2026 Jordan J. Yin, Maggie Divok, Gillian Kresan https://creativecommons.org/licenses/by/4.0
The 10th Annual CCNM Research Day: Student Research & Innovation in Naturopathic Medicine
The following are abstracts from the research competition at the 10th annual CCNM Research Day hosted by the Canadian College of Naturopathic Medicine in New Westminster, BC, Canada and Toronto, ON, Canada. The conference celebrates high quality student–faculty research collaborations, showcased as poster presentations.
Copyright (c) 2026 Prabhjot Chohan, Jensen Pletch, Faith Stoesz, Mariangela Bagnato, Monique Aucoin, Kieran Cooley https://creativecommons.org/licenses/by/4.0
Proceedings of the 2026 Queen’s University Undergraduate Bladder Cancer Case Competition
The Queen’s University Undergraduate Bladder Cancer Research Case Competition, organized by the nonprofit organization Queen’s Awareness of Bladder Cancer Club (QABC), provides university students with the opportunity to conduct research and raise awareness of bladder cancer. Guided by university student mentors with prior research experience, participants are introduced to the fundamentals of scientific analysis and academic writing while receiving personalized mentorship fostering both professional and personal growth. The 2026 program brought together students with interests in bladder cancer to learn from notable oncologists like Dr. Charles Graham and Dr. D. Robert Siemens, allowing students to pursue projects in bladder cancer. During the case competition, participants proposed research projects, which are presented in this abstract book as a reflection of their intellectual curiosity. Following the competition, a panel of professionals evaluated the student projects, providing expert feedback and selecting only the top-tier submissions for final recognition. By creating accessible and supportive pathways into research, QABC aims to bridge the gap between youth and scientific engagement, inspiring the next generation of researchers, healthcare providers, and innovators. Moving forward, the Research Case Competition will continue to grow and adapt, incorporating feedback from participants and mentors to strengthen its impact.
Copyright (c) 2026 Daniel Jafari, Alan Mourah, Gary Zhuo, Marco Kee https://creativecommons.org/licenses/by/4.0