The University of New Haven established the Lyme disease research group in 2005. To date, over 70 graduate students have received training in Lyme disease related research. The Lyme disease research group has identified an alarming increase in the co-infection rate in deer ticks, including discovery of novel co-infections such as mycoplasma and microfilarial nematode species. In the last several years the Lyme disease research group has received several extramural grants from the Lymedisease.org, Tick Borne Disease Alliance, Lyme Research Alliance, Lyme Disease Association, Charles E. Holman, Schwartz Foundation, Warman Family and Portman Foundation, which will allow the group to investigate novel ideas for Lyme disease research.
In the Fall of 2007, the our research group began one of the largest tick counting and Borrelia testing surveys in the North East (testing over 50 sites in Fairfield County). The uniqueness of this survey is that the tick collection is being conducted at school yards, public parks and playgrounds, to evaluate exposure of our children to tick borne diseases. We have collected ~2500 deer tick samples and tested ~1500 samples for Borrelia burgdorferi (Bb) infection. The overall Bb infection rate was 72%, ranging from 51%-94%.
The group also studies different forms of Borrelia bacteria to better understand how Borrelia can hide from the immune system and from different therapies. For example, our research group demonstrated that Borrelia is capable forming a protective layer around itself, called biofilm, which could render it very resistant to antibiotics and provide a logical explanation as to why extensive antibiotic treatment for patients with a tick-bite history could fail.
Our final goal is to better understand Borrelia survival mechanisms, and ultimately to provide new research information for the chronic Lyme debate.
Furthermore, our research group has held six National Lyme Disease Symposiums during the last several years (2006-2013) with over 200 attendees/symposium.
This work is to develop models of epithelial to mesenchymal transition (EMT) progression from clones of established breast cancer cell lines and correlate the behaviors to the expression and activation of cell attachment pathway proteins. For carcinomas the initial EMT is critical in the formation of a mobile population of cells potentially capable of establishing metastases. This transition step requires the change in expression and regulation of a host of proteins. These cells normally have very specific attachment to the neighboring cells that determine the tissue architecture.
By selecting subclones of established epithelial cell lines that have gained mesenchymal characteristics, we will have model systems that permit comparisons between the original epithelial state and the potentially more invasive state.
Proteins such as the integrin-linked kinase, cadherins, and integrins have been shown to play a role in EMT in systems where the expression is manipulated. This study will expand on this by looking at the proteins' expression and activity in cells that have spontaneously, or in response to various extracellular matrices, made the EMT.
My research focuses on cellular and molecular biology of reproductive immunology. The overarching theme of my research is the communication between different cell types, as well as the interaction of the immune and endocrine systems. During my doctoral work, I examined estradiol regulation of uterine stromal fibroblast-secreted keratinocyte growth factor (KGF) on the innate immune function of uterine epithelial cells. As a post-doctoral associate, I examined embryo implantation into the endometrium and the effect of trophoblast cells on the maternal immune system. In addition, I studied how ovarian cancer cells “educate” the host immune system (i.e., macrophages) to be tolerant and even support tumor growth.
My overall interest is in the role of protein kinases and protein phosphatases in oncogenesis. An understanding of how these proteins function not only gives us more information about how cancer develops, but these kinases and phosphatases also can be targets for anti-cancer therapy. We use many of the cell culture and molecular biology techniques that are taught in the labs at the University of New Haven to study the signaling pathways that regulate cancer cell growth and invasion. Currently there are two areas of focus in my lab:
Crosstalk between skeletal muscle and breast cancer cell lines
There seems to be a harmful recipricocal relationship between cancer cells and skeletal muscle. Patients with cancer often suffer from cancer induced muscle wasting. This calchexia is caused by both a depletion of nutrients and by cross talk between the cancer cell and the muscle cell. Conversely, muscle cells which may be proliferating or differentiating secrete factors that affect cancer cell growth and invasion. One of our research goals is to investigate the signaling pathways that are activated during these cancer/ muscle cell crosstalk.
Growth and invasion of non-HPV related cervical cancer
Most cases of cervical cancer are related to infection with the Human Papilloma Virus. However, a small number of cervical cancers are not associated with HPV infection, and I am interested in studying the signaling pathways that are activated in these cervical cancer patients.
Increasingly, humans are exposed to substances that may interfere with normal endocrine function. Whether exposure comes from the environment or from things like chemicals leaching out of plastic food containers, it is apparent that we are continually exposed to many different types of chemicals (some harmful, some inert, and some whose effects remain unknown). My research focuses on detection of contaminants that mimic human hormones and therefore affect the human endocrine system.
Currently, I make use of two strains of genetically-engineered yeasts that produce light (bioluminescence) when they detect substances that mimic human estrogen (female sex hormone) or androgen (male sex hormone), as well as a strain that decreases in light production in the presence of toxic substances. Increasingly, the public has grown aware of the potential harm of substances like bisphenol A (BPA) that may be found in plastics. I am generally interested in many areas of environmental science, especially in using biotechnology to help solve problems associated with cleaning up the environment. I am interested in projects that use the power of genetic engineering and/or molecular detection to answer questions about environmental issues. I am also specifically interested in the ecotoxicological effects of metal-nanoparticle complexes.
Dr. Pauline M. Schwartz is a Professor in the Department of Chemistry and Chemical Engineering. Her research interests include designing and exploring novel computational models of chemical systems. Current studies in collaboration with Dr. Carl Barratt are investigating prebiotic chemistry – the chemistry to generate the chiral building blocks necessary for life and the evolution of metabolic systems from simple chemical cycles.
Due to recent research advances at UNH, we now know that many different organisms can infect ticks and cause the symptoms of Lyme Disease. The goal of this project is to create a curated, web-based database to store genomic data for these organisms. The scope of the data will be two-fold. In addition to data generated at UNH, it will also store and organize data gleaned from the scientific literature and from collaborating institutions.