CBR SUMMER STUDENTSHIP BOOKLET 2024
A COLLECTION OF SUMMER STUDENT EXPERIENCES
Welcome to CBR - LSI Research Day!
We’re so happy to welcome you to the 2024 CBR - LSI Reseach Day! This event celebrates the conclusion of the Summer Studentship Program & showcases the high quality research performed by talented undergraduate and medical students over the past four months.
This year marks the CBR’s 13th annual Summer Studentship Program. In the past few months, the summer students have enhanced their scientific & professional skills through their research projects, networking sessions and participation in various career development workshops. Event highlights include Lay Writing & Presentation Skills workshops, Journey to Grad School session, Canadian Blood Services’ netCAD Blood4Research facility tour & the return of the CBR Amazing Race! We hope these events, combined with hands-on research, have provided a well-rounded summer experience. A huge thank you to all postdocs, research associates, research technicians and other trainees for mentoring & supporting our students over the summer!
Congratulations to this year’s summer student cohort for all that they have accomplished! To our students: we hope you had an enjoyable & enriching experience. We can’t wait to see where your journey takes you next & we look forward to seeing everything you achieve! Best of luck!
Ed Conway, Mira Milutinovic, Kaitlyn Chuong CBR Admin Team
Research Day Program 2024
Investigating sleep disturbances as a risk factor & therapeutic target for dementia
Keynote Speaker: Dr. Brianne Kent
Department of Psychology, Simon Fraser University
A majority of patients with Alzheimer’s disease (AD) experience some form of sleep disruption, including nocturnal sleep fragmentation, increased daytime napping, decreased slow-wave sleep (SWS, stage N3), and decreased rapid-eye-movement sleep (REM). Clinical studies are investigating whether such sleep disturbances are a consequence of the underlying disease, and whether they also contribute to the clinical and pathological manifestations of AD. Emerging research has provided a direct link between several of these sleep disruptions and AD pathophysiology, suggesting that treating sleep disorders in this population may target basic mechanisms of the disease. We conduct translationally-focused research — bridging fundamental, preclinical, and clinical studies — to better understand the relationship between sleep and AD, with the overarching goal of preventing dementia and improving human health.
12:00 PM - 1:00 PM Registration & Lunch LSC West Atrium Reception
1:00 PM - 1:10 PM Director’s Remarks LSC 3
1:10 PM - 2:30 PM Student Oral Talks LSC 3
2:30 PM - 2:45 PM Neil Mackenzie Mentorship LSC 3 Excellence Award
2:45 PM - 3:15 PM Keynote Talk LSC 3
3:15 PM - 5:30 PM Poster Judging/Open Bar LSC West Atrium
5:30 PM - 7:00 PM Awards & BBQ Dinner LSC West Atrium
SUMMER STUDENT PROJECTS
IDENTIFYING REGULATORS OF PODO447 ANTIBODY BINDING IN CANCER CELLS
Aidan Gallant
Supervisor: Dr. Calvin Roskelley
Podocalyxin, a glycoprotein normally involved in kidney filtration, is overexpressed in cancer and is a marker for poor outcome in patients making it a potential target for treatment. Cancer cells express an aberrantly glycosylated form of podocalyxin, but what regulates the glyco-
sylation remains unknown. Our lab has generated an antibody, PODO447, selectively targeting the epitopes of the tumor-glycosylated form of podocalyxin, making it a candidate for a tumor-specific antibody therapeutic. In collaboration with the Wisnovsky lab we preformed a CRISPRi screen to find genes regulating the PODO447 epitope expression. Using the screen results I am generating knockdown cell lines of key regulating genes. Using flow cytometry and fluorescent microscopy, I am exploring how these genes influence podocalyxin expression and PODO447 binding in MDAMB-231 breast cancer cells. PODO447 regulators from this work have the potential to act as biomarkers for determining which patients may benefit most from podocalyxin targeting treatments.
CHANGES IN PROTEOME AND METABOLOME INDUCED BY GENDER-AFFIRMING HORMONE THERAPY
Alessia Palumbo
Supervisor: Dr. Leonard Foster
Gender-affirming hormone therapy (GAHT) is an under-researched area of study that impacts the health of transgender people on GAHT and translates into a lack of knowledge of the cellular and systems-level effects and changes caused by GAHT. The introduction of new sex hormones with GAHT is expected to impact protein expression and regulation of metabolic pathways in the body, leading to changes in secondary sex characteristics. In the immune system, sex differences are thought to be a result of both chromosomal and hormonal factors, leading to the hypothesis that people taking gender-affirming hormone therapy will have a unique proteome and metabolome. This project focuses on determining the effects of feminizing GAHT on B and T lymphocytes using both proteomic and metabolomic data.
ACQUIRED HEMOPHILIA A OUTCOMES AND EXPERIENCE IN BC
Andrew Johnston
Supervisor:
Dr. Shannon Jackson
Acquired Hemophilia A (AHA) is a rare bleeding disorder caused by the development of inhibitors (or antibodies) to the coagulation protein Factor VIII (FVIII), which can lead to life or limb-threatening bleeding. AHA has no genetic basis and can arise spontaneously or secondary to underlying autoimmune conditions and malignancies.
Treatment consists of costly hemostatic agents, long inpatient hospital stays, and strong immunosuppressive therapy (IST). Beyond this, specific data regarding mortality, relapse rates, and complications of therapy including infection is scarce as there is currently no disease registry or aggregate data collection in BC. Using retrospective data from AHA cases in BC between 2018 and 2023, we first determined a benchmark set of presenting clinical and laboratory metrics. This included baseline partial thromboplastin time (PTT), FVIII and inhibitor strength (titre), bleeding characterization, the use of IST and hemostatic agents in treatment, and the rates of remission, infection, and relapse. Using this data, we then began populating a prospective AHA database to lay the groundwork for quality improvement and improved health outcomes.
IMMUNOSUPPRESSIVE POLYMERS FOR TRANSPLANT PROTECTION
Anna Zandstra Supervisor: Dr. Jay Kizhakkedathu
Organ transplantation is challenged by immune system rejection and extreme side effects caused by the use of harsh systemic medications. The attachment of immunosuppressive polymers to endothelial cells can provide a localized treatment to avoid systemic effects, immune system rejection, and tissue injury. The endothelial glycocalyx is an external cell structure which maintains a barrier between immune cells to provide protection and maintain cell integrity. During organ transplantation, reperfusion of the newly transplanted tissues damages this protective layer, causing immune cell activation and consequent organ injury. Attaching linear polyglycerol (LPG) coupled with a sialic acid to the cell surface mimics the natural glycocalyx and enhances tissue protection from harmful immune responses. LPG provides a compatible and non-immunogenic structure to present sialyl lactose, which acts like the glycocalyx by binding immunosuppressive receptors on cells. This strategy should allow for improved organ acceptance and localized immunosuppression to improve transplant patient outcomes.
UNDERSTANDING THE STRUCTURAL AND KINETIC CHARACTERISTICS OF THE PBP2-PBP2A COMPLEX IN STAPYLOCOCCUS AUREUS
Ben Paetzel
Supervisor: Dr. Natalie Strynadka
The PBP2-PBP2a protein complex in Staphylococcus aureus has long been recognized as a critical entity in promoting high-level antibiotic resistance in certain strains of pathogenic S. aureus. This study will aim to characterize the three-dimensional structure of the PBP2-PBP2a complex through the use of X-Ray crystallography and cryo-EM. Additionally, the PBP2-PBP2a complex will be studied with a variety of both established and novel inhibitors, so as to provide further insight into the catalytic mechanism of PBP2-PBP2a.
UNVEILING THE MODE OF ACTION: GENERATING RESISTANT MUTANT STRAINS TO INVESTIGATE COMPOUNDS MECHANISMS
Houria Afshar
Supervisor: Dr. Yossef Av-Gay
This research project aims to elucidate the mode of action of two potent antimicobacterial compounds, against Mycobacterium bovis Bacillus Calmette-Guérin (BCG), a model organism for tuberculosis (TB). Both compounds demonstrate significant antimicrobial activity against BCG and Mycobacterium tuberculosis. The study employs a strategy of selecting resistant mutant strains through iterative exposure cycles to the compounds, followed by Whole Genome Sequencing (WGS) and comparative genomic and transcriptomic analyses. This approach aims to identify mutations in drug targets and elucidate molecular mechanisms of resistance, thereby revealing the compounds’ specific targets and pathways within BCG cells. Ultimately, this research enhances our understanding of antimicrobial mechanisms and supports the development of new therapeutic strategies against tuberculosis and related infectious diseases.
THROMBOTIC EVENTS IN PATIENTS WITH ERYTHROCYTOSIS BEING WITH TREATED SGLT2 INHIBITORS
Jackie Hagstrom
Supervisor: Dr. Wendy Davis
Sodium-glucose cotransporter-2 (SGLT2) inhibitors are a growing class of medication in Canada used to lower blood sugar in type 2 diabetes patients. SGLT2 inhibitors have been shown to cause secondary polycythemia in some patients, an increase in red blood cells as a result of an underlying condition that over-stimulates bone marrow. While specific hematocrit targets are used to reduce the risk of thrombotic events in polycythemia vera (PV), the risk of thrombosis in secondary polycythemia is less clear. The optimal management of erythrocytosis secondary to SGLT2 inhibitors is unknown. Diabetes patients often have other risk factors that affect thrombotic risk, while evidence suggests SGLT2 inhibitors contribute to a cardioprotective effect. This study reviews St. Paul’s Hematology outpatients to assess the incidence of SGLT2 inhibitor therapy among patients referred for erythrocytosis, frequency of PV testing, steps taken to reduce thrombotic risk, and the incidence of thrombotic events during the follow-up period.
ROLE OF SASH1 IN THE GENERATION OF HEMATOPOIETIC STEM CELLS
Khirad Hassam
Supervisor: Dr. Aly Karsan
Although hematopoietic stem cell (HSC) transplantation is a first-line treatment for many hematological diseases, patient fatality remains commonplace due to limited donor availability. HSCs can be generated in vitro via directed differentiation from pluripotent stem cells. However, these protocols are limited by safety concerns, poor reproducibility and low throughput. To become a feasible source of HSCs for clinical use, these protocols must be improved upon by identifying the extrinsic factors capable of driving HSC development, a process which occurs via an endothelial-to-hematopoietic transition (EHT). During embryogenesis, EHT is tightly spatiotemporally regulated by the specialized niche of the aorta-gonad-mesonephros (AGM). Our preliminary data indicates that cell extrinsic Sash1 signaling promotes EHT. In this work we characterized Sash1 wild-type and conditional knockout mouse models via flow cytometry and immunohistochemistry to identify the source of EHT-promoting Sash1 signals within the AGM microenvironment. We demonstrated that loss of Sash1 from within mesenchymal populations impairs EHT.
ANTI-PHOSPHOLIPID SYNDROME (APS) TESTING DISCREPANCY: A COMPARISON BETWEEN TESTING PLATFORMS USED IN VANCOUVER, BRITISH COLUMBIA
Lee Wang
Supervisor: Dr. Benjamin Lai
Anti-phospholipid syndrome (APS) is an autoimmune condition characterized by the presence of antibodies that target phospholipids and associated binding proteins, elevating risk of thrombosis, pregnancy complications, and other autoimmune manifestations. Anticardiolipin and anti-beta-2-glycoprotein-I are two such antibodies routinely tested during assessment of APS. However, discrepancies in testing results have been observed between the two available testing platforms used in the clinical setting in Vancouver: Phadia and BioPlex. In this mixed retrospective and prospective study, we aim to describe the prevalence of this testing discrepancy and elucidate clinical or biochemical markers that predict testing discrepancy. We further aim to clarify the impact of the testing discrepancy on diagnosis and risk stratification. The findings from this study may better inform patient assessment pathways for APS.
UNCOVERING ROLES OF ZONULA OCCLUDENS-1 (ZO-1) IN CHEMICAL SYNAPSE FORMATION IN C. ELEGANS
Madelyn Tisdale
Supervisor: Dr. Kota Mizumoto
Synapses allow for rapid information transfer between neurons, and their formation is guided by signaling molecules during development. Abnormalities in synapse patterning are linked to neurodevelopmental disorders like autism spectrum disorder and schizophrenia. The tight junction protein ZO-1 has well characterized roles in the formation of electrical synapses, which permit communication between neurons via direct ion flow. However, in chemical synapses which achieve this communication through release of neurotransmitters, ZO-1’s role remains unclear. To investigate this, I utilized the DA9 neuron in the nematode C. elegans as a model. In DA9, synaptic adhesion molecules regulate where synapses are formed, with the Wnt receptor Frizzled playing a contributing role. Interestingly, Frizzled and ZO-1 take on distinct localizations: ZO-1 where synapses are formed and Frizzled where synapses are not. Therefore I hypothesize that ZO-1 interacts with Frizzled to determine where synapses localize in the DA9 axon of C. elegans.
TOWARDS MEMBRANE PROTEOME PROFILING OF THE LIVER: DIET-INDUCED DYSREGULATION AND HYPOINSULINEMIA AS A COUNTERMEASURE
Mohammed Al-Seragi Supervisor: Dr. Franck Duong
Two-thirds of the druggable proteome is membrane bound; yet, large-scale initiatives aimed to define membrane proteins implicated in chronic liver disease have been challenging due to hydrophobicity & scarcity of the membrane proteome. Dogma-challenging research has also put forth that hyperinsulinemia is causal in priming liver disease, while hypoinsulinemia can reverse obesity & rectify fasting glucose in animal models. In light of this, we performed Peptidisc-based membrane proteomics to elucidate dysregulation of diet-guided liver disease, & decipher the molecular mechanisms that underlie the hypoinsulinemia-induced protective phenotype. In the diet-dysregulated liver, we noted aberrant trends in lipid metabolism & cholesterol homeostasis. With the analysis on the hypoinsulinemic liver, we noted marked upregulation in glucose utilization, lipid catabolism, & insulin signaling. Our results contextualize the role of the membrane proteome in liver disease, and the mechanisms by which hypoinsulinemia imparts a protective response, thereby informing novel therapeutics.
CELL 2 SPEC: SPATIO-TEMPORALLY RESOLVED SPARSE-CELL PROTEOMICS
Nadege Oger
Supervisor: Dr. Govind Kaigala
Cancer aggression and adverse treatment outcomes are linked to increased intra-tumoral cell heterogeneity. As a result, emphasis is being placed on analysis of spatial and temporal variability in solid tumor cell populations, to un-
derstand and predict disease progression as it undertakes metastasis. Current methods for proteomic analysis are incompatible with spatial non-targeted protein discovery, and collection of small phenotypic foci with low protein concentrations. We developed a technique for user-directed spatial and temporal analysis of mixed phenotype cells in culture, using a Microfluidic Probe to interface with Mass Spectrometry. Shear and chemical impacts for cell lysis were deconvolved, and chemical, volumetric and concentration targets were determined to avoid sample dilution. Following this, the effects of cell surface coating (collagen, fibronectin, serum) on lysis were studied. This workflow will facilitate our understanding of heterogenous proteomic expression pathways, and their implications on cancer migration and metastasis.
QUALITY OF LIFE IN HBH DISEASE, THALASSEMIA INTERMEDIA, AND THALASSEMIA
MAJOR: A COMPARATIVE STUDY
Nastaran Davilu
Supervisor: Dr. Ali Amid
This research addresses the gap in knowledge regarding the quality of life (QoL) outcomes in patients with HbH disease by conducting a comparative assessment with those having thalassemia intermedia and thalassemia
major. We are quantifying and comparing health-related QoL in children and adults using established instruments like the SF-36 or Pediatric Quality of Life Inventory. The study also examines disease-specific comorbidities and their impact on patients’ QoL. By recruiting 40 patients from comprehensive thalassemia treatment centers at St. Paul Hospital and BC Children’s Hospital, we are collecting clinical and laboratory data to analyze the dynamic nature of these diseases. The expected outcomes include valuable insights into the unique challenges and QoL outcomes associated with HbH disease, which will help tailor healthcare approaches to improve patient satisfaction and care.
OPTIMIZATION OF A SCRATCH ASSAY TO CHARACTERIZE ADENOSINE DEAMINASE 2 (ADA2) MEDIATED EFFECTS ON CELL GROWTH
Nathan Millward
Supervisor:
Dr. Kelly Brown
Deficiency of adenosine deaminase 2 (DADA2) is a rare childhood disease associated with a range of manifestations including blood vessel damage, hematological defects, and cytopenia. We know that DADA2 is caused by variants in the ADA2 gene that abrogate ADA2 enzyme activity, but none of the enzyme related role(s) of ADA2 proposed to date account for the varied clinical features of DADA2. Here, we develop a scratch assay to test the hypothesis that, similar to structurally-related growth factors in insects, human ADA2 is an extracellular growth factor. We show that a manual microplate-based scratch method and analysis of brightfield microscopy images with an ImageJ plugin can be used to measure growth rates of mammalian adherent cells engineered to stably express wild-type ADA2 and known ADA2 mutants. This will allow us to assess (i) the ability of ADA2 to support cell growth and (ii) whether this ability is lost with certain pathogenic variants.
EXPLORING MOLECULAR MECHANISMS OF INCREASED THROMBOTIC RISK IN TYPE 2 DIABETES
Paniz Ghavimi
Supervisor: Dr. Ed Conway
Patients with obesity and diabetes experience increased risk of blood clots, the cause of which remains unclear. High levels of CD248, a transmembrane glycoprotein expressed by adipocytes, are correlated with obesity and type 2 diabetes, while deletion in mice of vascular smooth muscle cell CD248 protects against blood clot formation. CD248 binds to the insulin receptor (IR), interfering with insulin-signaling, thereby contributing to insulin resistance. In the coagulation system, CD248 interacts with tissue factor (TF), increasing its activity to initiate clotting. We hypothesize that CD248 acts as a bridge between insulin-signaling and coagulation by interacting with IR and TF. I confirmed there is a direct interaction between the ectodomains of IR and TF by using purified proteins in a series of ELISA. Our plan is now to identify the binding sites using mutational analyses by microscale thermophoresis and the functional relevance. We hope these studies will uncover strategies for preventing thrombotic complications in individuals with insulin resistance and obesity.
MITIGATING THROMBO-INFLAMMATION ON BIOCOMPATIBLE SURFACES BY INHIBITING COMPLEMENT ACTIVATION
Parisa Javadian Supervisor: Dr. Ed Conway
The use of blood-contacting biomedical devices, such as heart valves and vascular grafts, is increasing. Despite advances in developing new biomaterial surfaces, blood exposure triggers host immune and thrombotic responses (thrombo-inflammation), compromising the devices’ long-term integrity. This project aims to leverage the understanding of blood-based proteolytic cascades to mitigate thrombo-inflammation on biomaterial surfaces which can be triggered by the activation of complement alternative pathway. My project involves a novel strategy whereby a complement inhibitor - a factor D aptamer - is conjugated to a polydopamine (PDA)-based coating. PDA provides an adhesive biocompatible coating, yet it triggers thrombo-inflammation. Binding a pegylated FD aptamer to the PDA surface via covalently bound thiolated anti-PEG antibodies will inhibit the activation of the alternative pathway of complement. Validation steps will be done by a combination of confocal microscopy, quartz crystal microbalance (QCM), and functional assays to confirm the inhibition of the alternative complement pathway.
PREDICTION OF AUTOIMMUNE HEMOLYTIC ANEMIA IN CLL - A POPULATION BASED STUDY IN BRITISH COLUMBIA
Rayan Ramadan
Supervisor: Dr. Heather Leitch
Autoimmune Hemolytic Anemia (AIHA) can be idiopathic or secondary to lymphoproliferative disorders (LPDs). The focus of our project is on identifying prognostic and predictive markers for AIHA secondary to chronic lymphocytic leukemia (CLL), the most common adult leukemia in North America. Identifying differences in presenting characteristics and long-term responses to treatment between CLL, CLL-secondary AIHA, and idiopathic AIHA patients can help guide more effective treatment choices for patients at risk of developing CLL-AIHA. We conducted a hospital-wide database search of all patients diagnosed with idiopathic AIHA, CLL, and CLL-AIHA between January 1990 and April 2024 at St. Paul’s Hospital. Clinical and laboratory data were collected at diagnosis and after each round of treatment. Bivariate statistics, univariate Kaplan Meier analysis, and multivariate cox-regression will be used to identify statistically significant prognostic markers for the development of AIHA in CLL patients, and predictive markers for AIHA patients’ response to treatment.
BRIDGING DIAGNOSTIC GAPS IN WOMEN’S HEALTH: SILICON PHOTONIC BIOSENSORS FOR MULTIPLEXED BIOMARKER DETECTION
Sajida Chowdhury Supervisor: Dr. Karen
Cheung
Current medical technologies offer accurate lab-based diagnostics & rapid, low-cost home tests, but a gap remains in providing information-rich data of lab-based tests in a widely accessible and rapid format. One gap is the quantification of fluctuating hormone levels that can impact biomarker measurements & clinical trials, fertility, and symptoms during menopause. Our team seeks to bridge this gap using silicon photonic (SiP) biosensors for decentralized, portable, or point-of-care diagnostics. SiP devices employ semiconductor fabrication techniques to create cost-effective, micro-patterned biosensor chips. Microring resonators on these chips use light to detect molecular binding on their surface by measuring resonance peak shifts caused by changes in refractive index. This technology can potentially integrate 10s to 100s of sensors on a mm-scale chip, & simultaneously detect multiple biomarkers, enhancing diagnostic accuracy & robustness. Our research involves validating assays for individual biomarkers & developing amplification techniques to detect targets that cannot be detected in a label-free manner (e.g., hormones).
THE ASSOCIATION OF HIV, AGE, SEX, & OTHER CHRONIC/LATENT VIRUSES WITH INFLAMMATION AND IMMUNE AGING
Simrat Binning
Supervisor: Dr. Hélène Côté
Human Immunodeficiency Virus (HIV) is a chronic, lifelong condition that attacks the body’s immune system by impairing the function and proliferation of CD4+ T cells. This leads to chronic immune dysregulation, causing persistent activation of the innate immune system and chronic inflammation in people living with HIV (PLWH), compromising their immune systems. As a result, PLWH experience age-related morbidities earlier than the general population. This phenomenon leads to accelerated immune aging in PLWH, as their immune systems work more intensely than those of unaffected individuals. To understand this accelerated aging, we are studying selected inflammation markers and their associations with sex, age, HIV status, and other viral infections. We aim to identify age- and/or sex-specific differences, and the role of other viruses in immune aging. This will facilitate the development of interventions and therapies tailored to specific needs of PLWH, and assist in predicting non-HIV co-morbidities risks in PLWH.
MODULATORS OF THROMBOINFLAMMATION ON THE VIRUS SURFACE
Susan Zhang Supervisor: Dr. Ed Pryzdial
Virus infection commonly affects the blood clotting system, which is integral to inflammation. These virus-hemostasis interactions broadly cause thrombotic, hemorrhagic and inflammatory diseases depending on the virus type, and can be attributed to an outer coat that the virus obtains from the host cell membrane, the envelope. The Pryzdial lab has established that tissue factor (TF), a host-encoded trans-membrane protein that acts as the main initiator of blood clotting and important cell signaling protein, is pirated by all enveloped viruses studied to date. TF is known to have modulating proteins that enhance its function, however whether these exist on the viral envelope is not known. Using purified oral herpes (HSV1) as a model enveloped virus, my project aims to identify TF-modulating proteins on HSV1 and investigate their contributions to clotting activity on the virus. Further characterizing viral TF activity will allow new broad-spectrum anti-viral targets to be developed.
INCIDENCE AND CLINICAL OUTCOMES OF SEVERE IMMUNE THROMBOCYTOPENIA PURPURA IN BRITISH COLUMBIA
Vivian Zhang
Supervisor: Dr. Hayley Merkeley
Severe immune thrombocytopenia purpura (ITP) is an autoimmune disease where platelet-attacking antibodies are produced, resulting in a platelet count of <30x109/L. Symptoms can include life-threatening bleeding. There is much that remains unanswered about ITP in BC. First, the incidence of ITP in BC is unknown. Second, the morbidity, mortality, and cost of caring for patients who are unresponsive to first-line treatments is unknown. Second-line treatments are required for those with persistent, steroid-unresponsive ITP, yet are often hard to access. Therefore, a retrospective chart review was done. Participants included adults 18 years or older with newly diagnosed ITP who received at least one dose of IVIG for severe ITP between 2018 and 2023. This project has broad buy-in from hematologists across all health authorities. The baseline data generated from the project is instructive for creating a prospective database to systematically follow these patients and provide better, evidence-informed care.
PROGRAM HIGHLIGHTS
The CBR recognizes the value of developing skills and experiences not only in the lab, but also outside of it. The Summer Studentship Program aims to provide opportunities for students to socialize, network, explore different career paths, and practice ssential skills like public speaking and communication.
Here you’ll find memories from some of the events that were held throughout the program, from skill workshops to socials, as well as student snapshots!
Workshops, professional development events & socials held were:
Welcome Orientation & Potluck
CBR Step Challenge
Lay Summaries Writing
Visual Communications
Journey to Grad School
CBR Amazing Race
netCAD Facility Tour
Research Day Rehearsal
CBR Research Day
PROGRAM IMPACTS & PAST STUDENT PERSPECTIVES
13 years
of program growth, research excellence & mentorship
16 students supported with CBR funding in 2024
200+ students supported since 2011
40+ principal investigators & research teams participating over the years
“The friendships I made and the connections I established will undoubtedly extend beyond the program’s duration. I will always cherish this experience.”
- Jiaqi Wu, Summer Student Alum 2023
“Getting to participate in a poster presentation really boosted my confidence and encouraged me to present at more conferences. This program has provided me with a platform to grow & realize my capabilities as a researcher.”
- Akilesh Shankar, Summer Student Alum 2023
“Research Day was an amazing opportunity for me & the summer students to showcase our projects, practice our communication skills, and receive recommendations and feedback.”
- Paniz Ghavimi, Summer Student Alum 2023
“This program nurtured my passion for research. I appreciated the emphasis on collaboration and discussion, which led to personal growth and a richer perspective on science.”
- Zechariah Noronha, Summer Student Alum 2023
MENTORSHIP EXCELLENCE
Mentorship is an integral part of the CBR and the Summer Studentship Program. Each year, the CBR recognizes an individual who has demonstrated an outstanding commitment to mentorship and the development of others, through the Neil Mackenzie Excellence Award.
Below are the 2024 award nominees, who have been recognized for their dedication to mentoring. The award recipient will be announced at Research Day. Congratulations to all!
About Dr. Neil Mackenzie: Neil was a postdoctoral fellow in Dr. Bromme’s lab at the CBR, who tragically passed away in a climbing accident at Joffre Peak in 2015. A dedicated and caring mentor, Neil’s encouraging and motivation words and actions were sincerely appreciated by all those whom he touched - colleagues, friends, and students. In honour of his legacy, the CBR has created an award to recognize dedicateed members who are making a difference.
Ahmed Kabil
Kerryn Matthews
Kevin Gonzalez
Michael Sutherland Nooshin Safikhan
Patricia de Benedet
Samantha Grist
Vivian Zhang
Loulou Cai
Joseph Sadden
KB Choi
SPECIAL THANKS & ACKNOWLEDGEMENTS
A special thank you to the LSI for partnering with us on this year’s Summer Studentship program & Research Day. Thank you to Dr. Leonard Foster, Sharda Muni & Deepali Mahajan for their collaboration over the summer!
We would like to thank our sponsors for their generous support, without whom the Summer Studentship Program & Research Day would not have been possible:
Neil Mackenzie Memorial Fund