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[ PhD Program: Pathology Keyword: ]

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NameEmailPhd ProgramResearch InterestsPublications
Arendshorst, William email , , , , publications

We study mechanisms of cellular and molecular function as they control cardiovascular and kidney physiology in health and disease. We focus on G-protein coupled receptors and calcium signaling pathways of resistance arterioles that regulate vascular resistance in normal kidneys and pathophysiologically such as those of animals with genetic hypertension or animals with genes deleted. Measurements include renal vascular reactivity to neurohormonal agents and autacrine/paracrine factors combined with parallel investigation of receptor/calcium signal transduction in vascular smooth muscle cells in vitro.

Bellinger, Dwight A. email , publications

Research interests include atherosclerosis, thrombosis and von Willebrand’s disease. The role of von Willebrand factor in arterial thrombosis is being studied in atherosclerotic vessels to gain a better understanding of thrombosis and its possible prevention in people with coronary artery disease. Comparative pathology and the use of animal models in research are also the focus of some research efforts.

Braunstein, Miriam email , , , , publications

Our research focuses on understanding the virulence mechanisms of Mycobacterium tuberculosis, the bacterium responsible for the disease tuberculosis.

Cairns, Bruce A. email , , , , publications

The immune system of severely burned patients becomes extremely suppressed after injury. An overwhelming number of patients die from wound infection and sepsis. However, we are unable to graft these patients with skin from other donors as their immune system is still able to reject the graft efficiently. Our inability to cover the wound site leaves the patients further open to bacterial and fungal infections. Our laboratory investigates the translational immune mechanisms for these devastating consequences of burn within mouse models and burn patients. Focuses in the lab include  1) investigation of innate molecule control of both the innate and adaptive immune systems after burn injury, 2) Role of innate signaling to Damage Associated Molecular Patterns in Immune Dysfunction after burn / inhalational injury,focusing on  mTOR-mediated Immunomodulation 3) Using NRF2/KEAP1-Targeted Therapy to Prevent Pneumonitis and Immune Dysfunction After Radiation or Combined Burn-Radiation Injury and 4) Investigating sex-specific disparities in Immune Dysfunction after trauma / transplantation. ​

Chen, Xian email , , , , publications

Developing and applying novel mass spectrometry (MS)-based proteomics methodologies for high throughput identification, quantification, and characterization of the pathologically relevant changes in protein expression, post-translational modifications (PTMs), and protein-protein interactions.  Focuses in the lab include: 1) technology development for comprehensive and quantitative proteomic analysis, 2) investigation of systems regulation in toll-like receptor-mediated pathogenesis and 3) proteomic-based mechanistic investigation of stress-induced cellular responses/effects in cancer pathogenesis.

Church, Frank C. email , , , , , , publications

Our research is concerned with proteases and their inhibitors in various disease processes (thrombosis and cancer); our science tools are structure-activity, cell biology and signaling, pathobiology, immunohistochemistry, and in vivo models.

Clemmons, David R email , , , , , , publications

Cross-talk between insulin like growth factor -1 and cell adhesion receptors in the regulation of cardiovascular diseases and complications associated with diabetes.

Coleman, William B. email , , , , , publications

The research in our laboratory involves several major projects related to the molecular pathogenesis of human cancer and investigations related to the biology of liver stem-like progenitor cells, including (i) characterization of human liver tumor suppressor genes, (ii) analysis of genetic determinants of breast cancer, (iii) investigation of mechanisms governing aberrant DNA methylation in breast cancer, (iv) liver progenitor cell responses after toxic liver injury, and (v) transplantation of liver stem-like progenitor cells for correction of genetic liver disease.

Costello, Joe email , , , , , publications

The main research project is to determine the role of intercellular junctions in normal development, cell aging and cataract formation in human and animal lenses.

Crews, Fulton email , , , , , publications

Research in the laboratory focuses on mechanisms of neurodegeneration and regeneration, particularly stem cells in brain.

Doerschuk, Claire M email , , , , publications

We study host defense mechanisms in the lungs, particularly the inflammatory and innate immune processes important in the pathogenesis and course of bacterial pneumonia, acute lung injury/acute respiratory distress syndrome, and cigarette smoke-associated lung disease. Basic and translational studies address mechanisms of host defense, including recruitment and function of leukocytes, vascular permeability leading to edema, bacterial clearance and resolution.  Cell signaling pathways initiated by binding of leukocyte-endothelial cell adhesion molecules and molecular mechanisms underlying the functions of neutrophils are two particular areas.

Falk, Ronald J. email , , , publications

As the Director of the UNC Kidney Center, the scope of Dr. Falk’s research interests spans many disciplines, including molecular biology, immunology, genetics, pathology, cell biology, protein chemistry, epidemiology, pharmacokinetics and biostatistics. Dr. Falk is recognized world wide as a leader in research on kidney diseases related to autoimmune responses. He works closely with the basic research scientists within the UNC Kidney Center, including Dr. Gloria Preston, thus this research program provides an environment for Translational Research within the UNC Kidney Center.

Gulati, Ajay email , , , , publications

The work of our laboratory is focused on understanding interactions between the commensal microbiota of the gut and the host epithelium, particularly in the context of chronic inflammatory conditions such as inflammatory bowel diseases (IBD).  Specifically, we are interested in determining the mechanisms by which various susceptibility genes for IBD affect the structure and function of the intestinal microbiota.  In particular, we are exploring the mechanisms by which IBD risk alleles alter the function of intestinal epithelial cells including Paneth, goblet, and stem cells. We expect these studies will lead to the development of safer, patient-specific therapies for individuals with IBD.

Homeister, Jonathon W. email , , , , publications

Our research focuses on understanding the molecular and cellular mechanisms of leukocyte (white blood cell) trafficking and homing in vascular inflammation and immune responses. We are interested in the glycobiology of the Selectin leukocyte adhesion molecules and their ligands, and understanding the roles for these glycoproteins in the pathogenesis of inflammatory/immune cardiovascular diseases such as atherosclerosis and vasculitis. We are also interested in the mechanisms whereby the selectins and their ligands link the inflammatory response and coagulation cascade and thereby modulate thrombosis and hemostasis.

Huang, David email , , publications

Dr. David Huang is the director of the UNC Health Care Comprehensive Stroke Center and  the director of the UNC Stroke Trials Unit (STU).  He has research interests in developing new treatments for ischemic and hemorrhagic strokes .  The STU conducts a number of clinical trials testing novel treatments as well as studies investigating the pathophysiology of cellular injury resulting from stroke.

Jennette, Charles J. email , , publications

My research interests and diagnostic responsibilities center around nephropathology and immunopathology. My laboratory carries out basic, translational and clinicopathologic research on kidney diseases. I am most interested in pathogenic mechanisms and pathologic manifestations of glomerular diseases and vasculitis. A major current research focus is on elucidating the pathogenesis of vascular inflammation caused by anti-neutrophil cytoplasmic autoantibodies (ANCA).

Kakoki, Masao email , publications

My research aims at prevention and treatment of cardiovascular diseases and focuses on the identification of genes that confer susceptibility or resistance to the diseases with the use of genetically engineered mice. In collaboration with Dr.Oliver Smithies, I very recently developed a new method for altering gene expression by modifying 3’ untranslated regions in mice which enables fine-tuned modification of gene expression. I am now analyzing the phenotypes of several mouse models generated with this method.

Kaufman, David G. email , , , , , publications

Topic 1  We seek genomic targets for carcinogenesis among segments of DNA replicated in early S phase when cells are most susceptible to carcinogens.  We are mapping genomic sites replicated during early S phase, identifying origins of replication activated in this interval, and characterizing temporal sequencing of replication from these origins.  Topic 2  We are reconstructing differentiated and functional human endometrial tissue from epithelial and stromal cells interacting in culture.  We use these co-cultures to study development of endometrial cancer.

Kesimer, Mehmet email , , , , publications

The upper airways serve to clean inspired air from physical, chemical and pathological detritus that might damage the delicate peripheral airways where oxygen exchange is achieved. It is the heart of a powerful two tiered  innate immune system based upon a  layer of mucus that captures the incoming material that is moved over a bed of cilia. The system is called the muco-ciliary escalator.
Failure of this complex protective system is associated with a wide variety of diseases such as cancer and chronic inflammatory diseases. Biomolecules in mucus are split into two distinct groups, the first group being of globular type proteins between 6 kDa to 200 kDa and the second being of mucins which are large, space-filling glycoconjugates of 200 kDa to 100 MDa, with most of this mass being of carbohydrate in origin. Besides these biomolecules, mucus also contains secreted vesicles (exosomes) with innate immune properties. In chronic inflammatory lung diseases like cystic fibrosis (CF), chronic bronchitis (COPD) and asthma, mucus quantity and quality is altered and it is not efficiently removed from the lungs, causing airway obstruction, impaired gas exchange, bacterial colonization & infection and damage to lung tissue. The long term goal of our laboratory is to understand how this innate immune barrier is dynamically organized around the protective macromolecules under normal and pathological conditions. Currently, research in the Kesimer laboratory is focused on three main fundamentally important areas: 1- How mucins and globular proteins are organized within the airway mucosal barrier and how they are altered in disease pathogenesis, 2- How mucins are processed to mature after granular release for optimal function and how this progression is altered in chronic lung diseases, CF in particular, and 3- The role of extracellular vesicles in the airway mucosal barrier. Our laboratory is established with a wide range of state of the art biochemical, biophysical and proteomics methods including UPLC-Orbitrap mass spectrometry, atomic force microscopy, dynamic and static light scattering, and a variety of surface biophysics tools including QCM-D.

Kleeberger, Steven email , , , , publications

Genetic determinants of environmental lung diseases.

Koller, Beverly email , publications

We have used gene targeting to generate an animal model for the most common genetic disease in the Caucasian population, cystic fibrosis. We are continuing to characterize this animal and to modify it to produce a disease that more closely resembles human cystic fibrosis. A second area in which our lab is interested involves the study of the inflammatory processes involved in allergic responses, asthma, and arthritis. Our current efforts are aimed at generating animals deficient in various factors that are believed to be important in these diseases. By providing us with a better understanding of the immunological processes that underlie allergic responses, asthma and arthritis, these animals should help us to identify more effective treatments for these diseases.

Luebke, Robert email , , , , publications

My interests include immunotoxicant modes of action, developmental immunotoxicity, alternative models to screen and prioritize potential immunotoxicants and shared pathways of toxicity/susceptibility across systems and biological levels of complexity.  Recent projects include exploring the relationship between exposure to amphibole asbestos and the reported increases in systemic autoimmune disease in residents of Libby, MT, developing zebrafish-based alternative methods to screen for developmental immunotoxicants, and most recently, the effects of particulate and gaseous air pollutants on innate and acquired resistance to respiratory pathogens.

Mack, Christopher P. email , , , , , publications

My research goals are to identify the mechanisms by which environmental factors regulate smooth muscle cell phenotype and to define the transcriptional pathways that regulate SMC-specific gene expression.

Mackman, Nigel email , , , , publications

The major focus of Mackman lab is the procoagulant protein tissue factor. This is the primary cellular initiator of blood coagulation. We study its role in hemostasis, thrombosis, inflammation, ischemia-reperfusion injury and tumor growth.  LPS induction of the tissue factor gene in human monocytic cells and endothelial cells is mediated by various transcription factors, such as AP-1, NF-ĸB and Egr-1. More recently, we found that the phosphatidylinositol-3-kinase protein kinase B intracellular signaling pathway suppresses LPS activation of monocytes and endothelial cells.  We found that inhibition of either tissue factor or the downstream coagulation protease thrombin reduced infarct size in a rabbit model of cardiac ischemia-reperfusion injury. We showed that the tissue factor-thrombin pathway increased inflammation during myocardial ischemia-reperfusion injury by inducing chemokine expression and enhancing the recruitment of neutrophils. We have generated a number of mouse models expressing different levels of both mouse and human tissue factor. These mice have been used to provide new insights into the role of tissue factor in hemostasis and thrombosis. In 2007, we developed a new assay to measure levels of microparticle tissue factor in plasma. We found that elevated levels of microparticle tissue factor are associated with venous thromboembolism in cancer patients.

Maeda, Nobuyo N. email , , , , , , , publications

Our research is focused on the genetics and molecular pathology of complex multi-factorial conditions in humans – obesity, diabetes, hypercholesterolemia, insulin resistance, and hypertension.  These conditions underlie cardiovascular diseases, including atherosclerosis, the major cause of death and disabilities in North America. Our approach consists of experiments with mice carrying modifications in various genes important for the maintenance of vascular function, antioxidant defense, and metabolism.  We dissect how gene-gene and gene-environment interaction influences the pathogenesis of these common human conditions and their complications.

Maile, Robert email , , , , , publications

An overwhelming number of burn patients die from wound infection and sepsis. Our laboratory, along with Dr Bruce Cairns, investigates translational immune mechanisms within mouse models and burn patients. Focuses in the lab include  1) investigation of innate molecule control of both the innate and adaptive immune systems after burn injury, 2) role of innate signaling to Damage Associated Molecular Patterns in Immune Dysfunction after burn / inhalational injury 3) using NRF2/KEAP1-Targeted Therapy to Prevent Pneumonitis and Immune Dysfunction After Radiation or Combined Burn-Radiation Injury and 4) Investigating sex-specific disparities in Immune Dysfunction

Miller, C. Ryan email , , , , , , , , , , publications

My laboratory studies diffuse gliomas, devastating primary tumors of the central nervous system for which few effective drugs are currently available.  We utilize genetically engineered mice, cell culture, and human tumor model systems to explore the molecular pathogenesis of gliomas.  We utilize animal model systems to develop drugs and diagnostic markers for their individualized therapy.  Rotating students gain experience with multiple techniques, including cell culture, molecular biology, genomics, genetic lineage tracing, fluorescence microscopy, and digital image analysis.

Nagarajan, Uma M email , , , , , publications

Chlamydia trachomatis is the most common sexually transmitted bacterial pathogen that causes Fallopian tube inflammation and subsequent tubal infertility in women.  Our current research interest is to investigate the role of an innate immune responses to chlamydial infection and its role in genital tract pathology in a mouse model of genital infection.  Specifically, we are interested in delineating pathogen recognition by the host, signaling pathways that lead to the induction of innate immune cytokines in vitro and their downstream cellular effects in vivo.  We are specifically interested in understanding the contribution type I IFN, IL-1 activation, caspases and damage associated molecular patterns in pathogenesis. The identification of host molecules involved in amplification of the inflammatory response during infection, would serve as biomarkers and therapeutic targets to prevent reproductive sequelae in women infected with Chlamydia.

Nichols, Timothy C. email , publications

My research interests include the role of von Willebrand factor in thrombosis and atherosclerosis. Our current lab work focuses on the molecular biology of porcine von Willebrand factor.

Parise, Leslie email , , , , , , , , publications

The overall goal of our laboratory is to understand the molecular interface between cell signaling and adhesion receptors in blood diseases and cancer in order to develop novel therapeutic targets and approaches. One area of study is platelets because they become activated by cellular signals and adhere to each other and the blood vessel wall via specific adhesion receptors. These events can block blood flow, causing heart attacks and stroke, the leading causes of death in the US. Another area of research is sickle cell disease, since red blood cells in these patients are abnormally adhesive and also cause blood vessel blockages. A third area is cancer since cancer cells use similar cellular signals and adhesion receptors in tumorigenesis and metastasis. Our work involves a wide array  of technologies that include molecular, structural and cellular approaches as well as clinical/translational studies with human patients.

Pecot, Chad Victor email , , , , publications

The development of metastases is the cause of death in nearly all cancer patients, yet the mechanisms driving metastatic biology remain poorly understood. Also, few cancer therapeutics are being developed to specifically control this problem. My laboratory is interested in discovering novel mechanisms that drive metastatic biology, and in utilizing RNA interference (RNAi) strategies (such as nanoparticle delivery of miRNAs/siRNAs) to control this process. We will apply integrative analysis of large bioinformatic datasets, in vitro studies for mechanistic validation, and in vivo metastasis models to assess therapeutic efficacy of our RNAi approaches.

Sartor, R. Balfour email , , , , publications

Our long term goals are to better define mechanisms of chronic intestinal inflammation and to identify areas for therapeutic intervention. Research in our laboratories is in the following four general areas: 1) Induction and perpetuation of chronic intestinal and extraintestinal inflammation by resident intestinal bacteria and their cell wall polymers, 2) Mechanisms of genetically determined host susceptibility to bacterial product,. 3) Regulation of immunosuppressive molecules in intestinal epithelial cells and 4) Performing clinical trials of novel therapeutic agents in inflammatory bowel disease patients.

Serody, Jonathan email , , , publications

Our laboratory is involved in studies to determine the mechanisms and proteins involved in the migration of alloreactive and regulatory T cells to organs involved in graft-versus-host disease after stem cell transplantation using mouse models.

Smithies, Oliver email , publications

Correction of genes with mutant pathologies (gene therapy); construction of animal models of human genetic diseases to facilitate better studies of the resultant pathology and develop new modes of treatment.

Snider, Natasha email , , , , publications

Our lab has two areas of interest: the molecular basis of liver diseases and the biochemical mechanisms of disorders linked to intermediate filament gene mutations. We use biochemical, cell-based and in vivo approaches to identify potential disease targets and to understand their function and regulation. The major goal of our work is to promote the discovery of pharmacological agents that can slow or halt the progression of these diseases.

Tarran, Robert email , , publications

A critical component of airways innate defense is the thin liquid layer lining airway surfaces, the periciliary liquid (PCL), that provides a low viscosity solution for ciliary beating and acts a lubricant layer for mucus transport. Normal airways appear to be able to sense the PCL volume and adjust ion channel activity accordingly.  The long term goal of this laboratory is to understand how homeostasis of PCL volume occurs in airway epithelia under normal and pathophysiological conditions. Currently, research in the Tarran lab is focused on three main areas: 1) Regulation of epithelial cell function by the extracellular environment, 2) Gender differences in cystic fibrosis lung disease and 3) The effects of cigarette smoke on epithelial airway ion transport.  We utilize cell biological and biochemical techniques coupled with in vivo translational approaches to address these questions.

Taylor, Joan M. email , , , , , publications

The goal of our research is to identify signaling mechanisms that contribute to normal and pathophysiological cell growth in the cardiovascular system.  We study cardiac and vascular development as well as heart failure and atherosclerosis.

Tisch, Roland email , , , publications

Projects involve the study of cellular and molecular events involved in autoimmunity, and development and application of genetic vaccines to prevent and treat autoimmunity and cancer.

Troester, Melissa email , , , , publications

Dr. Troester’s research focuses on stromal-epithelial interactions, genomics of normal breast tissue, breast cancer microenvironment, and molecular pathology of breast cancer progression. She is a Co-Investigator on the Carolina Breast Cancer Study (CBCS), a resource including breast tumors from thousands of African American women, and she is PI of the Normal Breast Study (NBS), a unique biospecimen resource of normal tissue from women undergoing breast surgery at UNC Hospitals. Dr. Troester has extensive experience in integrating multiple high dimensional data types. She is chair of the Normal Breast Committee for the Cancer Genome Atlas Project where she is leading coordination of histology, copy number, mutation, methylation, mRNA and microRNA expression data. She has more than a decade of experience working with genomic data and molecular biology of breast cancer progression and has published many papers in the area of breast cancer subtypes, breast microenvironment, and stromal-epithelial interactions. She has trained four postdocs, 12 predoctoral students and several undergraduates.

Webster-Cyriaque, Jennifer email , , publications

A goal of the laboratory is to understand viral molecular pathogenesis in the oral cavity. We seek to understand the critical molecular interactions that occur between DNA viruses and the host that govern the development of oral disease.

Whang, Young E. email , , , , publications

My laboratory is interested in characterizing the role of cytoplasmic signal transduction pathways in regulation of androgen receptor activity and progression of prostate cancer.  Our studies have focused on HER-2 receptor tyrosine kinase and we have demonstrated that HER-2 activation stimulates androgen receptor activity and HER-2 inhibition inhibits androgen receptor transcriptional function at the level of recruitment to the androgen responsive enhancers.  These findings have led to the design and initiation of the protocol involving lapatinib, a clinical HER-2 inhibitor, in treatment of patients with prostate cancer.  More recently, we have demonstrated that activated Cdc42-associated kinase Ack1 promotes progression of prostate cancer via tyrosine phosphorylation of androgen receptor at Tyr-267 and Tyr-363 residues.  We are interested in further characterizing the role of tyrosine phosphorylation of androgen receptor in prostate cancer and development of Ack1 targeted therapy for clinical use.

Williams, Scott E email , , , , , , , , publications

Divisions and decisions in development and disease. The mammalian skin epithelium is an ideal model system to study fundamental questions in stem cell and cancer biology. It is accessible; it can be cultured, genetically manipulated and transplanted; and its resident stem cells possess unparalleled regenerative capacity. Our skin, unlike many other organs, undergoes continuous growth and turnover. In development and homeostasis, progenitors in the skin must balance self-renewal and differentiation programs. We have found that asymmetric cell divisions are a critical mechanism by which skin progenitors maintain this equilibrium. We are interested in studying how this asymmetry is controlled at a molecular level, and how division orientation impacts cell fate choices in normal and neoplastic growth. To facilitate these and other studies in diverse epithelia, we have developed a powerful functional tool, lentiviral in vivo RNAi, which allows us to rapidly perform functional studies on any gene in the intact mouse in weeks instead of years. Our broad goal will be to use this technique, in combinations of candidate and screening approaches, to dissect pathways that influence stem cell differentiation. I will be joining the Pathology Department in April, 2013 and am seeking passionate, open-minded, and interactive students for the summer and beyond.

Willis, Monte S. email , , , , publications

We are looking for talented and motivated individuals to join our research team. Dr. Willis’s lab investigates the molecular basis of genetic and lifestyle mediated cardiomyopathic disease (heart failure) using bioinformatics, molecular, and animal model approaches. We are seeking graduate students looking for an exciting and supportive research environment offering a diversity of experiences integrating cardiac phenotyping, mouse models of disease, molecular biology, and ubiquitin proteasome biology. Both national and international training experiences supported by the Leducq Foundation (http://fondationleducq.org/network/proteotoxicity-an-unappreciated-mechanism-of-heart-disease-and-its-potential-for-novel-therapeutics/) are possible,  depending on citizenship and interest in travel.

Wolberg, Alisa email , , , , publications

We investigate cellular, molecular, and biochemical mechanisms of blood coagulation.  Using in vitro, ex vivo, and in vivo models, we focus on mechanisms contributing to cardiovascular disease (heart attack, stroke, deep vein thrombosis), including the effects of plasma proteins, cells, and blood flow (shear) on blood clot biochemical and mechanical stability.  We have shown that abnormalities in blood protein and/or cellular function contribute to bleeding and clotting pathologies including hemophilia and thrombosis, and shown how hemostatic and antithrombotic therapeutics modulate clot quality.  Current efforts are focused on pathophysiologic mechanisms that result in bleeding or prothrombotic disease (e.g., cancer).  Our overall goal is to translate this knowledge into novel approaches for treating bleeding and clotting disorders.