Lucas Goss

Lucas Goss
Mentor: Dr. Peter Adhihetty
College of Health and Human Performance
 
"I have always had a passion for science, so my freshman year I took a class called Science for Life. In the class researchers present their research projects and what they investigate. My faculty mentor, Dr. Peter Adhihetty, gave a presentation on mitochodrial biogenesis, it's complexities, and it's relation to various diseases. I immediately was fascinated and approached him about volunteering in his research lab. "

Major

Biology

Minor

N/A

Research Interests

  • Mitochondrial Biogenesis
  • DNA Mutation and Repair
  • Molecular Genetics

Academic Awards

  • University Scholars Award
  • HHMI Science for Life Undergraduate Research Award

Organizations

  • Pi Kappa Alpha Fraternity
  • UF HEROES Program
  • AMSA

Volunteer

  • Florida Diabetes Camp
  • Sidney Lanier Fitness and Research Program
  • Boys and Girls Club

Hobbies and Interests

  • Science
  • Exercise
  • Socializing

Research Description

Effect of aging and chronic heart failure on skeletal mitochondrial regulation in skeletal muscle
The purpose is to assess whether CHF alters skeletal muscle morphology (size of peripheral muscle tissue) and fiber-type young and old mice. A variety of experimental techniques will be employed to achieve these objectives including: 1) Western Blot Analyses (examination of proteins by gel electrophoresis), 2) Mitochondrial Enzyme Activities (assesses overall mitochondrial content and function in various tissues), 3) Immunohistochemistry (examination of muscle fiber type). Our preliminary data definitively confirms that mitochondrial dysfunction plays a role in CHF-induced muscle dysfunction in young animals but the effect of age on these underlying mechanisms is currently unknown. Thus, understanding the molecular and cellular mechanisms associated with CHF-induced muscle impairments and atrophy with age represents an extremely relevant clinical area of research that is currently understudied and underdeveloped. Furthermore, investigating the underlying cellular and molecular mechanisms responsible for CHF-induced muscle impairments and/or atrophy could reveal potential molecular targets and contribute to the development of future therapeutic interventions to combat CHF.