Smith Agyingi, a fourth-year biomedical sciences student, will showcase his research on sickle cell comorbidities at the annual Experimental Biology Conference April 2-6 in San Diego. Agyingi, a native of Cameroon, West Africa, who moved to Rochester six years ago, has been testing how single nucleotide polymorphisms in the toll-interacting protein gene affect sickle cell comorbidities, complications and diseases that arise from sickle cell disease. In addition to his research, he serves as a mentor for RIT’s Collegiate Science and Technology Entry Program and plays piano and intramural soccer.
Question: What brought you to RIT?
Answer: Two major reasons why I chose RIT were that they offered me the best financial aid package of all the schools I wanted to attend and most importantly, they were one in very few well recognized schools in New York state with an exclusive major in biomedical sciences.
Q: Why did you choose your major?
A: I knew for sure I wanted to go to medical school after I graduate and the course requirements of this major exposes you not just to the contemporary biology and chemistry classes but also to some medical oriented classes like immunology, endocrinology and parasitology. I believe this will better prepare me for my career ahead.
Q: What made you decide to conduct research on sickle cell comorbidities?
A: I am African American, and sickle cell disease affects a large number of people from my ethnic group. The science world isn’t giving as much attention to this disease as it deserves. As if single sickle cell disease is not enough, this sickle cell polymorphism fosters susceptibility to several other complications including infectious diseases, which exacerbates the severity of disease pathophysiology in sickle cell patients. My hope is that the little knowledge I can add concerning the workings of this debilitating disease may help people understand why there is a poor immune response in patients and clarify infectious disease susceptibility.
Q: How did you conduct the research?
A: We thought that the susceptibility to several other infectious diseases, known as comorbidities, in patients with sickle cell disease was brought about by a polymorphism/mutation of the toll-interacting protein gene, which disrupts proper immune response. We used primarily two laboratory methods genotyping via polymerase chain reaction and the restriction fragment length polymorphism to analyze the genomic DNA of the control group and patients with sickle cell disease from Africa and the United States. We tested for the genetic diversity and haplotype frequency of this polymorphism.
Q: How has Professor Bolaji Thomas helped you with the research and influenced your education at RIT?
A: Dr. Thomas hasn’t only been very instrumental in my research and educational goals but also in helping me grow as an individual and understand life better. I would say he has been a great mentor in several aspects of my life. Quite honestly on several occasions during my research, my findings didn’t make any sense to me, which was always the perfect time to quit. On such occasions, he would give me those talks about the reality of life and how research can get a little frustrating sometimes. For some reason, he always seemed to put sense into those “not so great results” and he always had a way to make those results make sense. This didn’t just apply to research but with everything else.
Q: What are your findings?
A: Sickle cell disease comorbidities and high mortality are a huge burden for patients in Africa. We found that a “relatively significant” frequency of toll-interacting protein polymorphism in disease samples compared to controls. This by no means is the cause of high comorbidity rates in patients but we believe a major contributory factor. This is an extension of our previous work to examine the role of CD209 promoter gene and toll-like receptor polymorphisms among and between population and disease groups. More work in larger sample sizes needs to be done to confirm these findings.
Q: What is the next step in the research?
A: So far, from our research, we are certain there is a relationship between SCD comorbidities and the toll-interacting protein gene polymorphism. To follow up on these results, we will try to establish a clear mechanism through which these sickle cell comorbidities take hold, by specifically examining urinary tract infection and intestinal nematodes in both study groups.
Q: What does the opportunity to present your research at the Experimental Biology Conference mean to you?
A: It is an honor for my research to be deemed worthy and important enough to be accepted at a conference of that caliber. It is my hope that this work will encourage many more researchers to look into this neglected disease, which is affecting a great number of people worldwide.
Q: What do you hope to learn at the conference?
A: One thing I hope to achieve at this conference is to network with other researchers from a variety of institutions who share similar interests, both students and professionals. Hopefully, I may be able to find a laboratory where I could conduct research during my gap year or make new acquaintances that may be very resourceful in helping achieve my goals. Also this will serve a great opportunity to explore new scientific knowledge and career advancement opportunities and other resources that may be of interest to me now or a few years down the road.
Q: After graduation, what are your plans?
A: After I graduate in May, I plan on taking a year off before starting medical school in 2017. During that gap year, I will take my MCAT, put out applications to medical schools and do some more research, hopefully a continuation of my previous research and work.
Traci Turner compiles “Student Spotlight” for University News. Contact her at email@example.com with suggestions.