Between 2018-2020, I was a research assistant in the Roman Lab in the Graduate School of Public Health. The focal point of this lab’s research was understanding a disease known as Hereditary Hemorrhagic Telangiectasia (HHT). The disease is defined by arteriovenous malformation (AVMs), or direct connections between arteries and veins, which can occur in various tissues including mucocutaneous membranes, lungs, brain, and liver, and can lead to ischemia, stroke, or rupture of the fragile vessels. During my time, I assisted PhD candidates in doing histochemical and immunological staining procedures, dissection procedures, fish breeding, and fish sorting in order to understand how bmp10 mutant zebrafish–which produced a phenotype similar to the human (HHT) disease– demonstrates high-output heart failure. As a result of collaborative effort, our team found that zebrafish bmp10 mutants develop enlarged hearts, have high cardiac output, and experience volume overload in response to skin and liver vascular malformations, all of which leads to AVMs. The results of the paper were published in 2019.
More recently, I had worked on another project with another PhD candidate to characterize and understand mechanical forces and pathways that led to the localization of shunts–also called high flow AVMs–in one of three spatiotemporal locations during cranial vasculature development in the alk1 mutant zebrafish embryos. We proposed to characterize the haemodynamic changes that lead to shunt formations by using drug treatments that would modulate either the shunt size or location by impacting heart rate with norepinephrine bitartrate and triciane, or by modulating the biological transducer of cardiac mechanical force, Piezo1, with Yoda1 and GSMTx4. Unfortunately because of the pandemic, I was only able to participate in the Tricaine drug treatment experiments. As a result, I finished my research obligations by conducting a thorough literature analysis into the efficacy of the drug treatments, as well as the possible mechanical forces and pathways that could be responsible for modulating shunt formation in the alk1-mutant zebrafish embryos. The final submitted paper will be present in the papers section of this website.