Faculty and their Research Interests in Molecular Medicine
lick on the faculty member’s name for a more in-depth description of their research and publications.
DEPARTMENT OF PHYSIOLOGY AND PHARMACOLOGY
Jennifer W. Hill, Ph.D.
Associate Professor and Director of MOME Track
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 experimental approach includes use of timed, targeted genetic manipulation, such as tissue-specific gene deletion.
Ritu Chakravarti, Ph.D.
Associate Professor
Indian Institute of Technology-Delhi, India
Chakravarti lab is interested in studying auto-immune diseases, particularly in Non-Infectious
Aortitis (NIA). Both infectious and non-infectious reasons can result in inflammation
of blood vessel wall, a.k.a. aortitis. NIA is more prevalent in recent times. About
20% of aortitis patients develop thoracic aortic aneurysms that can rupture or dissect,
therefore, present a life-threatening condition. Histologically, vessel wall in NIA
shows infiltration of immune cells, thickening of adventitia & media with, quite often,
necrotic regions. No specific serological test exists for the diagnosis of aortitis.
Immuno-suppressors are popular choices to control clinical symptoms, but they don't
provide any curative effect. Absence of targeted therapy & serological markers to
monitor the disease activity, significantly limit the management strategies for aortitis.
Bina Joe, Ph.D., FAHA, FAPS (CV), ISHF
Distinguished University Professor and Chair
Director of Center for Hypertension and Precision 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.
Lauren Koch, Ph.D.
Associate Professor
The University of Toledo (formerly Medical College of Ohio), 1991
Research interests include development of animal models of health and disease, exercise science, biology of aging and evolution of complex disease
Nikolai Modyanov, Ph.D., D.Sc.
Professor
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.
John W. Turner, Jr., Ph.D.
Professor
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.
Professor
Associate Director of Center for Hypertension and Precision 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.
Matam Vijay-Kumar, Ph.D.
Professor
Director, UTMiCO
CFTRI, University of Mysore, India, 2000
A large body of my work focuses on intestinal inflammation, a hallmark of numerous gastrointestinal disorders. Understanding the mechanisms by which gut epithelial cells participate in the innate immune response will provide insight into the etiology of inflammatory bowel diseases (IBD). Our laboratory employs numerous innate immune deficient mice to delineate the interactions between host innate immunity and gut microbiota in IBD pathogenesis. Our current active project in the lab is investigating the role of neutrophil extracellular traps (NETs) in gastrointestinal pathophysiology.
An additional vein of my research pertains to the interplay between innate immune deficiencies and how it impacts gut microbiotal homeostasis. My research has demonstrated that TLR5 deficient mice develop hallmark symptoms of metabolic syndrome, such as obesity, Type II diabetes and liver diseases, which are absolutely microbiota-dependent. This finding was substantiated by our observation that transplanting the microbiota from TLR5 deficient mice into germ-free mice eventuates features of metabolic syndrome in the recipients. As a whole, my work in this area has advanced our understanding of how innate immune deficiencies results in microbiotal dysbiosis, and consequently, contribute to metabolic diseases. My lab slogan is ‘Gut Microbiota: We can’t live without or with it’.
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.
Assistant Professor
Northwestern University Feinberg School of Medicine, Chicago; M.D.
Research interests: acute coronary syndromes, peripheral vascular interventions, antiplatelet therapies, cardiorenal syndromes
Steven Haller, Ph.D.
Assistant Professor
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.
David Kennedy, Ph.D.
Associate Professor
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.
DEPARTMENT OF ORTHOPEDIC SURGERY
A. Champa Jayasuriya, Ph.D.
Professor, Director of Orthopedic Research
Shizuoka University, Hamamatsu, Japan, 1997
My research areas are bone tissue engineering, regenerative medicine and biomaterials.
Beata Lecka-Czernik, Ph.D.
Professor
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.