Marshall senior wins big for research with Tylenol
This article appeared in the Oct. 31, 2007, edition of the Charleston Daily Mail.
By Kelly L. Holleran
Daily Mail staff
HUNTINGTON -- Marshall University student Megan Neal smiles frequently and talks with a humble confidence about winning a $1,200 award for being considered the best undergraduate researcher in West Virginia.
She refuses to accept all the credit for the award, which she won for her part in a project that studies the correlations between acetaminophen and heart disease.
The award was bestowed in September at a Morgantown symposium sponsored by the West Virginia Experimental Program to Stimulate Competitive Research.
Eight graduate students have spent countless hours with Megan, a senior biology major, in a room tucked away in Marshall's Robert C. Byrd Biotechnology Science Center.
Their goal is to develop a new intervention for age-associated cardiac problems.
They have been working since the beginning of summer, testing the effects of acetaminophen on rats. Acetaminophen is a major ingredient in Tylenol.
The group uses a rat-aging model. When the rat reaches the equivalent of a human's 50 years, it starts to receive treatment.
The bottom line of what they are discovering is that acetaminophen is good for the heart. The researchers are concluding that acetaminophen manages the complex, chemical systems that dictate whether heart muscle breaks down or not.
With acetaminophen, they believe, the proper rhythm of the heart is more likely to hold up over time.
Getting to that conclusion is a complex lesson in biology.
The group tests the amount of microRNA in the rats before and after treatment. MicroRNA refers to single strands of coding with the job of regulating gene expression.
MicroRNA may be responsible for heart arrhythmias, said Eric Blough, an associate professor of molecular physiology at Marshall.
Megan, 21, and her fellow researchers have found arrhythmias may be caused by a decrease in the protein connexin 43, also known as CX43. Connexins, also known as gap joint proteins, are essential for many physiological processes, such as the regulation of cardiac muscle.
When the amount of CX43 in the heart decreases, the microRNA levels increase, Blough said. But acetaminophen appears to reduce the amount of microRNA, he said. The upshot is that CX43 levels increase, causing less of a chance for arrhythmias.
"If CX43 decreases, you lose the ability to properly regulate the heart's contractions," Blough said.
The nine students have taken on different roles in the project. Some work with the rats, ejecting microRNA from the muscle. Others study the tissue under microscopes.
Megan and her partner, Jackie Decker, look at the reactions of acetaminophen in tubes and determine the different levels of microRNA as the rats age.
Winning the statewide competition was no walk in the park for Megan, who is also busy serving as women's ministry director for Revolution Ministries, a campus Christian group, and as Supreme Court chief justice for Marshall's student government association.
For the research contest, students across West Virginia were invited to submit abstracts and posters.
Megan was one of about 20 picked to present a project during the symposium in Morgantown. She had to submit a one-page abstract and a poster and give an oral presentation.
She said she was just a little nervous for the oral part.
"It was just kind of like talking," she said.
Jackie Decker, Megan's partner, could not enter the competition because she is a graduate student. But Megan plans to give Jackie half of her winnings.
"She did half of it, too," Megan said.
Megan began working in the lab as a volunteer in January. That's when she stumbled upon the project she later was asked to join.
"She was a tremendous asset, her and Jackie, to look and develop that whole molecular aspect," Blough said.
Last summer Megan was awarded a $4,000 grant from an undergraduate research program that allowed her to spend more time in the lab. She also didn't have to worry about finding a summer job.
She is continuing her work on the project. She plans to use it as the capstone project that is required of Marshall undergraduates.
The researchers hope to expand and develop their initial findings.
Megan is applying to graduate school. She would like to work in the health sciences field, either in medicine or pharmacy.
Her initial interest in biology was sparked while she was a student at Triway High School in Wooster, Ohio.
"I've always liked the sciences, and I've always kind of wanted to go in the health field in some way," she said. "Going into biology is a pretty big step into getting into the health field."
She is proud to say she is part of the project.
"It's awesome to be a part of something that matters," she said. "I feel like I'm accomplishing something. It's not just coming in and sitting at a desk. This project may help people. It actually means something."
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Wednesday, October 31, 2007
Posted by Press Center at 2:10 PM
Labels: Blough , Daily Mail , Neal , STaR Symposium
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Your heart will be strong, but your liver...
J Toxicol Sci. 2007 Oct;32(4):401-9.
Changes of micro-RNA expression in rat liver treated by acetaminophen or carbon tetrachloride--regulating role of micro-RNA for RNA expression.
Fukushima T, Hamada Y, Yamada H, Horii I.
Drug Safety Research and Development, Nagoya Laboratories, Pfizer Japan Inc., Aichi, Japan.
Recently, microRNAs, involved in RNA interference, were discovered as new gene regulators, with little known about them in the field of toxicology. In this study, a toxic dose of acetaminophen or carbon tetrachloride was administered singly to male rats, and microarray analysis using mirVana miRNA bioarray was performed. Partial least squares-discriminant analysis of the microarray data revealed that the microRNAs expression was specifically changed by treatments at 6 hr after dosing. Furthermore, we focused on miR298 and miR370 among the microRNAs commonly affected by hepatotoxicants, because they were speculated to regulate an oxidative stress-related gene. From real-time RT-PCR analysis, microRNA expression was suppressed by hepatotoxicants at 6 and 24 hr. Regarding acetaminophen, the decreases were found even though there were no morphological changes in the liver at 6 hr. To investigate these 2 microRNAs in more detail, we measured their expression, WST-1 for mitochondrial function and LDH release for cell collapse in primary cultured hepatocytes exposed to several concentrations of acetaminophen for 3 hr. At more than 5 mM, the microRNA expression and WST-1 decreased, whereas LDH was unchanged. Therefore, the change in microRNA expression occurred at the time when mitochondrial function was damaged prior to cell collapse. From all the above findings, we conclude that microRNAs were affected by hepatotoxicants and that the changes were found in the early phase of toxicity. Thus, our data suggest microRNAs have an important role for toxicological mechanism and we proposed that the changes in microRNA expression might be key molecules for toxicity expression.
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