Faculty and their Research Interests in Molecular Medicine
Click on the faculty member’s name for a more in-depth description of their research
DEPARTMENT OF PHYSIOLOGY AND PHARMACOLOGY
Andrew D. Beavis, Ph.D.
University of Bristol, U.K., 1977
Mitochondrial bioenergetics and transport processes.
George T. Cicila, Ph.D.
University of Pennsylvania, 1986
My major interests are the inheritance of complex traits, with a focus on cardiovascular and related phenotypes. These include blood pressure, intrinsic aerobic running capacity, cardiac performance, and obesity. We are also studying a mutation that regulates the length of telomeres.
Jennifer W. Hill, Ph.D.
Northwestern University, 2003
I am interested in the hypothalamic homeostatic mechanisms controlling body weight and fertility and the interactions between them. My hypothesis is that the suppression of reproductive cyclicity during states of negative energy balance results from the action of circulating metabolic factors (such as leptin, insulin, ghrelin, glucose, LC-FAs or PYY3-36), in the hypothalamus. My experimantal approach includes use of timed, targeted genetic manipulation, such as tissue-specific gene deletion.
Terry D. Hinds, Jr., Ph.D.
University of Toledo, 2010
My lab focuses on the involvement of the heme oxygenase (HO) system and nuclear receptors in metabolic diseases, which includes obesity and diabetes as well as cancer.
Bina Joe, Ph.D.
Professor and Chair
Director of Center for Hypertension and Personalized Medicine
University of Mysore, Mysore, Karnataka, India, 1996
The focus of the Joe Lab is on the molecular genetics of complex traits. The current thrust area is on studying hypertension through a systems biology approach utilizing custom-genetically altered models of differential blood pressure.
Sivarajan Kumarasamy, Ph.D.
University of Madras, TN, India.
University of Toledo College of Medicine and Life sciences, OH
Nikolai Modyanov, Ph.D., D.Sc.
The overall objective of my research program is to identify the novel genes/genetic components involved in onset and development of hypertension. Studies from humans and experimental animal models proven that hypertension is closely linked with diabetes, obesity and renal failure. Hypertension can quietly damage the vital organs in the body for years before symptoms develop. The onset and progression of high blood pressure is complex and multi-factorial. Understanding this complex physiology is important, because it may provide insight into developing novel therapeutic strategy to treat patients with high blood pressure and its associated diseases.
Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russia, Ph.D., 1973
Russian Academy of Sciences, D.Sc., 1987
Research in my lab is focused on the molecular aspects of ion transport across biological membranes. These studies led to the recent discovery of a novel structural member of the mammalian X,K-ATPase ß-subunit gene family, designated ßm due to its exclusive expression in skeletal and heart muscles. Studies are underway to elucidate functions of this hitherto unknown, muscle-specific protein.
Nitin Puri, M.D., Ph.D.
Program Director of MSBS-MS
Ph.D.-New York Medical College, Valhalla, NY, 2010
M.D.-M.G.M Medical College, Indore, M.P, India, 1999
My research focus lies in the study of renin-angiotensin system (RAS) contributing to the development of cardiovascular-renal anomalies including, endothelial dysfunction, hypertension, ischemic heart disease and renal failure. We employ genetic models, like transgenic mice, to dissect the polygenic nature of these diseases. Our projects are guided by GWAS and the SNPs in the genes of the RAS. I am also interested in the contributions of redox mechanisms in the development of metabolic syndrome. We use human mesenchymal stem cells to examine the role of oxidative stress during the process of adipogenesis and in adipocyte function afterwards. Our focus is on the key cellular antioxidant, heme-heme oxygenase.
Edwin R. Sanchez, Ph.D.
University of Michigan, 1983
Regulation of steroid hormone receptors, with emphasis on the convergence of the heat shock, immunophilin and glucocorticoid receptor signal pathways.
John W. Turner, Jr., Ph.D.
Cornell University, 1970
Current research interests are focused on the development of a single-injection, multi-year controlled-release wildlife contraceptive vaccine to alleviate suffering faced by numerous species which are overpopulating fixed-size habitats and on assessment environmental stress due to chronically deteriorating habitats in wildlife and fishes via fecal cortisol measurement.
Guillermo Vazquez, Ph.D.
Associate Director of Center for Hypertension and Personalized Medicine
Universidad Nacional del Sur, Argentina, 1997
The focus of our research is on the role of Canonical Transient Receptor Potential
(TRPC) channels in endothelial dysfunction/inflammation associated to Molecular Medicine.
The repertoire of TRPC isoforms expressed in endothelium from different vascular beds,
signaling modulating channel function, and molecular/cellular outcomes of TRPC-mediated
Ca2+ entry, are some of the subjects of our studies.
DEPARTMENT OF MEDICINE
Alexei Fedorov, Ph.D.
Associate Professor, Director of Bioinformatics Laboratory
Institute of Molecular Genetics, Russian Academy of Sciences, Moscow, 1993
Origin and evolution of introns. Computer mining of novel genes. Prediction of constitutive and alternative splicing. Information content of genes beyond the coding meaning – codon bias and context-dependent codon bias. How are these biases created and maintained? Principles of genome organization.
Rajesh Gupta, M.D.
Northwestern University Feinberg School of Medicine, Chicago; M.D.
Steven Haller, Ph.D.
University of Toledo, Ph.D., 2012
Atherosclerotic renal artery stenosis (RAS) is the leading cause of secondary hypertension (renovascular hypertension) and an important cause of ischemic renal injury. Impaired renal function is one of the most important contributors to adverse cardiovascular events and survival in this population. The focus of my research involves identifying the molecular targets leading to the development of renal fibrosis and renal dysfunction in RAS.
Juan Jaume, M.D.
Chief of Endocrinology
National University of Buenos Aires, M.D.
David Kennedy, Ph.D.
Medical University of Ohio, Ph.D., 2006
The overall aim of my research is to develop a mechanistic understanding of the pathogenesis of accelerated cardiac and renal dysfunction during cardio-renal syndrome. Thus, we seek to identify novel mechanisms of cardiac and renal injury in order to aid and improve diagnostic, therapeutic, and preventive strategies in this high-risk population of patients. One of the primary scientific objectives of my laboratory is to understand the pathophysiology whereby endogenous counter-regulatory mechanisms become maladaptive and contribute to disease progression in patients with cardio-renal syndrome.
Jiang Tian, Ph.D.
University of Toledo, Ph.D., 2006
Research in my laboratory is focused on the molecular mechanisms of cardiovascular disease, with special emphasis on uremic cardiomyopathy. Cardiac dysfunction associated with chronic kidney disease and end stage renal disease is responsible for high cardiovascular mortality. Our laboratory uses a Na/K-ATPase alpha1 heterozygous knockout mouse and partial nephrectomy (PNx) model to study the relationship between Na/K-ATPase content, circulating levels of CTS and cardiovascular function. These studies have been funded by the National Clinical Research Program of American Heart Association and by the National Heart, Lung and Blood Institute.
DEPARTMENT OF ORTHOPEDIC SURGERY
A. Champa Jayasuriya, Ph.D.
Shizuoka University, Hamamatsu, Japan, 1997
My research areas are bone tissue engineering, regenerative medicine and biomaterials.
Beata Lecka-Czernik, Ph.D.
Institute of Biochemistry and Biophysics Polish Academy of Sciences, Warsaw, Poland, 1986
Previously, we have demonstrated that a class of anti-diabetic drugs TZD have adverse effects on bone by causing bone loss and affecting fracture healing in animal models. We have also showed that this process can be prevented by using slightly modified TZD drugs, which retain their beneficial anti-diabetic effects but are lacking adverse effects on bone. Currently, we are investigating molecular mechanisms by which TZDs induce bone loss and investigating the means by which diabetic bone status can be improved by using bone-specific gene and stem cell therapies, as well as pharmacological therapies.