We fund innovation in Manitoban health care.
The HSC Foundation is proud of the researchers we fund. The work they do ultimately leads to improved patient care at Manitoba’s flagship hospital. Research is the key to deepening our understanding of health matters, and often leads to new technology, medicine, or practices.
The HSC Foundation 2024 grants were awarded through four different competitions and applications were reviewed by experts in their fields from HSC.
Dr. Biniam Kidane, $70,000: “Curing without harming: A proteomic screening approach to identify biomarkers associated with respiratory failure in lung surgery patients”
Synopsis: More than 100 000 Canadians undergo lung surgery annually. Although lung surgery can cure many diseases of the lung, including lung cancer, patients are at risk of developing life-threatening complications following surgery. Since 2018, our research team has been performing a study and collecting samples on all lung surgery patients at the Health Sciences Centre. Our goal is to try and understand the practices that surgical teams can modify to make lung surgery safer. In collaboration with lung biologists and the Manitoba Centre for Proteomics and Systems Biology at the University of Manitoba, our research team is proposing a leading-edge approach to identify new diagnostic and therapeutic targets for acute lung injury. Our ultimate goal is to make lung surgery safer.
Dr. Abdullah Al Maruf, $70,000: “Pharmacogenetics of Selective Serotonin Reuptake Inhibitor-Induced Behavioural Activation in Children and Adolescents (PGx-SImBA)”
Synopsis: PGx-SImBA Major depressive disorder, anxiety disorders, and obsessive-compulsive disorder are amongst the most common mental health disorders in children. Antidepressants are frequently prescribed for these children. Although these medications are generally effective and safe, some children suffer from adverse effects. One such adverse effect is behavioural activation, characterized by hyperactivity, impulsivity, or irritability. Unfortunately, we do not currently know why some children develop these adverse effects while others do not. The proposed project aims to identify a panel of genetic variants that could assist clinicians in detecting children at-risk for developing this adverse effect.
Rhiza Regalado Lam Chew Tun, $20,000: “The prevalence of improved exocrine pancreatic function among cystic fibrosis pediatric patients age 2 years and older on cystic fibrosis transmembrane conductance regulator modulator drug therapies”
Synopsis: Majority of people with Cystic Fibrosis (CF) cannot digest and absorb what they eat. Pancreatic enzymes are prescribed to prevent diarrhea, failure to thrive, fat-soluble vitamin deficiencies and malnutrition. Thickening and scarring of intestines can happen with too much use of enzymes. There have been anecdotal reports that patients on modulator therapy may recover exocrine pancreatic function. Although we discourage patients from adjusting their own enzymes, patients and families continue to do self-adjustments. Presently, the cost for checking levels of pancreatic functions for CF patients on modulator therapies is not covered. This project will examine repeat pancreatic function testing to determine the need for continued enzyme replacement.
Courtney Marshall, $5,000: “Sex as a biological variable in immunomodulation of airway inflammation by Innate Defence regulator (IDR) peptides”
Synopsis: Asthma is the most common chronic respiratory disease affecting nearly 3 million Canadians. Around 15% of patients do not respond to available steroid therapies and represent the major burden of asthma accounting for annual healthcare costs of $2B. Also, common steroid therapies can increase the risk of lung infections, which can make asthma worse. New therapies are urgently needed that can alleviate steroid-unresponsive disease without compromising the ability to resolve infections. There is a clear sex bias in asthma, for example adult females experience greater disease severity and are more likely to develop treatment-unresponsive disease, compared to males. Traditionally, these sex-related differences were overlooked in preclinical studies. Effective development of new treatments must consider differences in disease and response to therapy between females and males. Specifically, how biological sex alters control of IL-33, which drives steroid unresponsive asthma, remains unknown. Previous studies in the Mookherjee lab have shown in female mice Innate Defence Regulator (IDR) peptides improve breathing, reduce immune cells in the lung and control cellular processes linked to steroid-unresponsiveness including controlling IL-33. However, due to the sex-related differences in asthma and in mouse models, sex as a biological variable in modulating airway inflammation must be considered and has yet to be defined. Therefore, the goal of this project is to use IDR peptides to investigate how sex impacts modulation of airway inflammation, including IL-33 and to define how IDRs modulate IL-33. Overall, this can allow for identification of novel therapeutic targets to control IL-33 while taking into consideration how this happens in females compared to males.
Mojdeh Matloubi, $5,000: “Investigating the role of airway epithelial cell-derived (AEC) Semaphorin3E in steroid-resistant neutrophilic asthma”
Synopsis: Asthma is a major health concern in Canada, while inhaled corticosteroids (ICS) are the first-line treatment for persistent asthma, some patients have a poor response to these drugs. This condition is known as steroid-resistant asthma (SRA), with type 2-low (neutrophilic) asthma being a major phenotype of SRA. Understanding the mechanisms behind this resistance is crucial for developing better treatments. Our research focuses on Semaphorin3E, a protein that our lab has found to reduce asthma severity in preclinical models. Sema3E decreases airway sensitivity, inflammation, and lung tissue scarring. Healthy human lungs naturally produce Sema3E, primarily from airway epithelial cells (AECs). However, in severe asthma cases, Sema3E levels are lower, correlating with decreased lung function, indicating its role in maintaining lung health. Using two chronic (type-2 high) eosinophilic and (type-2 low) neutrophilic asthma models, we aim to study the effects of AEC-derived Sema3E on asthma. We will also compare the impact of Sema3E with dexamethasone, and explore the combination of both treatments.
Dagem Yilma Chernet, $10,000: “Lung proteomic analysis of patients with postoperative respiratory failure after one-lung ventilation surgery”
Synopsis: When a person has lung cancer, and it is caught soon, doctors might do surgery to take it out. But this surgery can cause issues in the lungs. A serious disease that comes from this kind of surgery is called acute respiratory distress syndrome, in short terms ARDS. Even though it’s uncommon for this disease to occur, it can be critical to one’s life. When the doctors do surgery on the sick lung, the healthy lung is supplied with special air to keep the patient’s body working. So far, we have learned that problems can occur after such surgery. One of the reasons these problems happen is because these people often have weak lungs even before going through this surgery. Also, the air supply to only one of the lungs makes it even worse for these people. Our team wants to do a research project on this topic because we don’t fully know why these problems happen. We want to find new signals in the body that can tell us if someone will have these lung problems after surgery. These new signals come in the form of proteins. We will do this by looking at proteins in the fluids from the lungs and blood of people who had surgery. We will use a fancy tool called Mass Spectrometry to find these proteins. Our aim is to find the warning signs that might tell us who could have these serious lung problems after surgery. Our research is led by the lab space established at CHRIM. CHRIM has a theme called Biology of Breathing, in which our research falls within. CHRIM values research areas of lung issues that affect the lives of youth and families in the province. Through these themes and values, our research aligns with the missions and values of CHRIM
McKay Lowry, $10,000: “The role of epOMEs and DiHOMEs on the contractility of airway smooth muscle”
Synopsis: Asthma is a dangerous health problem. It causes coughing, wheezing, and the loss of breathing. These problems can lead to hospital visits or even death. It can be caused by allergies (dust, pollen, and pets), illnesses from bacteria or viruses, cold air, chemicals in the air, and even mysterious causes that can start at birth. Roughly 1 in 5 Canadian children under 14 suffers from Asthma. Knowing this shows the need for more research. This will help find new medicines for children with asthma. The human lung is an important part of the body. It helps to bring oxygen into the blood. This allows one to live a healthy life. Normally a healthy person will have their airways open. This is different from Asthma people who lose the shape of their airway from the growth of muscle. This muscle layer can squeeze easily when an Asthma person experiences an allergen. This can cause the airway to narrow leading to trouble in breathing. Research over the recent years has noticed molecules called ‘oxylipins’ in the lungs of Asthmatic people. Some groups of these ‘oxylipins’ play a huge role on the airway muscle. Some oxylipins cause the muscles of the airways to squeeze tight. Some can cause them to open. This shows that some can be dangerous in Asthma while some can be helpful. Our research for the next 2 years is looking at 2 different types of oxylipins called EpOMEs and DiHOMEs. We want to see how these oxylipins squeeze the airways to know if they are dangerous. We suspect that these molecules will cause the airways to close. This could be a possible problem in people living with asthma. We will experiment with these ideas within our lab located in the Children’s Health Research Institute. We have the hope of discovering new medicines for children living with Asthma.
Kaihim Wong, $12,500: “Designing a machine learning model using quantitative magnetic resonance imaging to predict lesion evolution”
Synopsis: Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (i.e., brain and spinal cord), lacking a known cure. Timely therapeutic interventions and treatments are crucial. However, the complexity of MS diagnosis stems from substantial variability in individual biological processes and patient symptoms. This imposes a heavier workload on clinicians. Routine magnetic resonance imaging (MRI) scan is widely adopted to generalize the diagnostic process. However, the information provided by routine magnetic resonance imaging (MRI) is limited by its ability to capture only a qualitative summary of brain lesions. Advanced MRI technique is a rapidly growing field in MS research. While these techniques are better at detecting subtle changes in brain structure and hold the potential to facilitate early diagnosis, they still have a lot of progress to make before doctors can use them in real-world medical settings. To accelerate the path to clinical maturity, the goal of this Ph.D. project is to utilize a group of advanced MRI measures and unlock the potential of MRI to predict lesion growth in MS. This involves the development and optimization of a predictive model using machine learning. But to reach the ultimate goal with a model with better prediction of lesion evolutionary pattern, the project will first address how unique these metrics are to each other and how are they relevant to predict lesion growth. Secondly, the project aims to see if the spatial information outside MS lesion is useful.
Alana Slike, $12,500: “The incorporation of automated phenotyping strategies and single cell sequencing data to identify genes, pathways and cells involved in age-related hearing loss”
Synopsis: Rett syndrome (RTT) is a severe neurodevelopmental disorder which primarily affects females and is characterized by loss of motor, coordination and communication abilities. Over 95% of individuals with RTT have a mutation in the MECP2 gene, resulting in the gene not functioning properly, leading to disease. However, variable severity is observed in patients with RTT. One possible explanation for this observation are modifier genes. Modifiers genes do not directly cause disease, but can alter the severity and age of onset of genetic diseases. In addition to explaining the variable severity seen in RTT, modifier genes may aid in the discovery of new treatment options. This is of particular importance in RTT, as there are limited treatment options for the disease. One recent study in mice found that a mutation in the FAN1 gene improved the health and life span of RTT mice. The FAN1 gene is involved in DNA repair and influences the age of onset of the neurodegenerative disease, Huntington’s disease. It is therefore the goal of this project to determine if the FAN1 modifier effect for RTT detected in mice, also has beneficial consequences in human RTT cells that resemble those found in the brain.
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