Experience

• 

  SixRing Inc.

  • Research Scientist Microbiologist

    • Jan 2023 - Present

• 

  SixRing Inc. A division of Fluid Energy Group

  • Calgary, Alberta, Canada

  • Research Scientist, Microbiologist

    • May 2022 - Dec 2022
    • Calgary, Alberta, Canada

• 

  University of Calgary

  • Canada
  • Higher Education
  • 700 & Above Employee

  • Postdoctoral Researcher (Biochemist/Microbiologist)

    • Mar 2022 - May 2022

  • PHD Student

    • May 2016 - Mar 2022

    During the course of my PhD, I was responsible for attempting to determine how the thermosensory diguanylate cyclase (TdcA) is able to regulate cellular processes in response to temperature shifts, through the production of c-di-GMP. Additionally I was, as a part of a collaboration, attempting to determine the mechanism by which TdcA is able to detect and respond to temperature changes. During this research, I was involved in research that lead to the filing of a patient based on TdcA. Additionally, I have developed thermosensory proteins using components of TdcA.

• 

  University of Calgary Departmant of Biological Sciences

  • Calgary, Alberta, Canada

  • Masters Student

    • Sep 2013 - Apr 2016
    • Calgary, Alberta, Canada

    In this project, I was looking at the mechanism by which the bacterial signaling molecule c-di-GMP was being produced in response to temperature changes in the bacterial pathogen Pseudomonas aeruginoisa. Here, we discovered that the responsible protein was the thermosensory diguanylate cyclase (TdcA), and this protein senses heat using a similar principle to the proteins that allow us to sense heat, using a newly discovered mechanism. I was responsible for characterizing the activity of TdcA.

• 

  University of Calgary, Department of Biological Sciences, Dr. Gerrit Voordouw's Lab

  • Undergraduate Researcher

    • May 2012 - Apr 2013

    During this project, I was attempting to understand the effects of a certain porin protein (Dvu0273) on the dissimilative sulfate reducing oilfield bacterium Desulfovibrio vulgaris. This protein transport was found to be important for transferring produces hydrogen sulfide gas out of the cell, allowing the organism to survive in sulfide enriched environments. This was done to provide a better understanding of the processes involved in oil well and source water souring.

• 

  Biological Sciences, University of Calgary in Sergei Noskov's Lab

  • University of Calgary, Calgary, Alberta, Canada

  • Research Assistant

    • May 2011 - Aug 2011
    • University of Calgary, Calgary, Alberta, Canada

    This project was a continuation my project in 2010. In this project, I was using molecular dynamics (MD) simulations and protein-drug docking simulations to determine how the drug cisapride could be rehabilitated, allowing for it to be reintroduced to the market to treat gastrointestinal disorders. During the course of my research I used MD simulations to map the interactions of cisapride with both the human Ether-à-go-go-Related Gene (hERG) potassium channel, as well as with its intended interactions with the human A2A adenosine receptor. With these simulations, as well as some protein-drug docking simulations, we were able to identify critical interaction points between cisapride and the hERG channel, and some possible solutions to reduce these interactions, while maintaining the wanted interactions with the wanted A2A adenosine receptor.

• 

  Biological Sciences, University of Calgary in Sergei Noskov's Lab

  • Research Assistant

    • May 2010 - Aug 2010

    In this position, I was trying to identify how different drug molecules interacted with the human Ether-à-go-go-Related (hERG) potassium channel, which is important for maintaining a steady heart rhythm in humans. When this channel becomes blocked by a drug, the subject has been shown to go into arrhythmia. In this study, I was responsible for setting up and running quantitative structure-activity relationship (QSAR) modelling simulations to identify the factors of the drugs that would cause the blockage of the channel, thus providing a model to better design medical drugs that are less toxic to humans. The goal of this project was to use generated models as a means of screening drugs that were taken off of the market due to hERG channel blockage risk and predict what alterations to the drug structure would be required to maintain the intended functionality of the drug within the body, while limiting the negative side effects of the drug. This helped increase our understanding of how the drug may be rehabilitated.