Research in the BMS department - by professor
My research has revolved around understanding the pathogenic mechanisms of Salmonella and Escherichia coli. Currently, I am focused on two areas of interest. My first project involves looking for additional genes necessary for Salmonella pathogenesis. Studies have shown that the genes involved in Salmonella pathogenesis are often found in specific areas known as pathogenicity islands. Salmonella Pathogenicity Island 1 (SPI-1) contain a large number of genes involved in the formation of the type III secretion system and other secreted effector proteins. Activation of this island allows for bacterial invasion of intestinal cells. A second critical island (SPI-2) is required for survival within macrophage after invasion. Due to the number of genes required for these processes, I have focused on the regulatory genes that control activation and repression of these islands in response to environmental signals. In the course of these studies I identified a repressor known as hilE, which represses the activation of SPI-1. Studies of the sequences around hilE suggest that this repressor falls in a 40 kb region of the chromosome that has all of the hallmarks of a pathogenicity island, yet very little is known about the function of the genes around hilE. Since its identification, we have created ten different polar mutations in open reading frames within this potential pathogenicity island. Work has commenced trying to analyze the effects these mutations have on Salmonella virulence by utilizing gene reporter, cell invasion, macrophage survival, bacterial adherence, and cell motility assays under various inducing and noninducing environmental conditions. Any effects on Salmonella invasion could then be further characterized by identifying how each of the mutations leads to changes in Salmonella invasion in response to an environmental signal.
My second project is looking for genes important for Escherichia coli biofilm formation under conditions that mirror its natural environment. Previous work has identified many genes needed for the activation and formation of a biofilm when the bacteria are grown under aerobic conditions. As E. coli is commonly found in the anaerobic conditions of the colon we are trying to identify regulator genes that are responsible for increasing or decreasing biofilm formation in response to oxygen. We have developed a biofilm assay to screen for biofilm formation that can be used under aerobic, microaerophilic and anaerobic conditions. Transposon mutagenesis allows the creation of random mutations within the chromosome that can then be characterized via the biofilm assay. This is an ongoing project which will hopefully find a variety of different regulators and will teach students a variety of microbiological and molecular techniques.
Professor Bergman’s research lab is a multidisciplinary lab that works in the disciplines of neuroscience, physiology, ethology, ecology, toxicology, histology, and pharmacology. Much of the research in the lab is accomplished using crayfish. Using crayfish for biomedical research may not seem immediately applicable when considering human health, but basic biomedical research it turns out is largely about understanding organisms and their interactions with other organisms. Humans as you know are extraordinarily complex on many levels, yet we only understand a small fraction of the interactions, structures, chemicals, and pathways in our bodies. Therefore, the best way to determine the effect of a drug or disease on a living system is to study it first in an animal system. Drugs, vaccines and treatments in human medicine are largely based on years of physiological research with animals. To that end, the crayfish lab studies sensory system physiology, neurochemical modulation of aggression, neurogenesis via social enrichment, operant conditioning/learning, pollution effects on sensory receptors and development, nociception, growth/molting, orientation strategies when finding food or mates, the interactions of various invasive crayfish species, and feeding behaviors. A student joining this lab can expect to become knowledgeable in the scientific fields of neuroscience, animal behavior, physiology, biomechanics, toxicology, ecology, chemistry, and molecular biology.
My research centers on the identification of processes necessary for regulation of genes that are involved in neural function in the fruit fly Drosophila melanogaster, using transgenic model approaches. One gene known to be necessary for communication between cells encodes the enzyme that synthesizes histamine, Histidine decarboxylase (Hdc). We are currently examining the role of the Hdc gene in establishing when and where the neurotransmitter substance, histamine, is synthesized and also what histamine may be contributing to with regards to central brain function and its consequences on behavior. As a result, projects in my lab range from molecular biology projects to behavioral projects.
Current Research Projects include:
1) Analysis of developmental and tissue-specific regulatory regions of the Hdc gene. Transgenic flies that contain a gene fusion between the upstream portion of Hdc (pHdc) and the enhanced green fluorescent protein (eGFP) have been generated to examine the expression control of the Hdc gene. We have determined that the upstream promoter region for the Hdc gene does induce eGFP expression in most histaminergic cells. Work investigating which cells throughout development are being marked with eGFP could be done. We are now beginning to constructing new transgenic flies, some of which will have an altered Hdc promoter region, that will enable a more exciting manipulation of histamine-containing cells in the fly’s brain.
2) Examination of labeled HDC protein processing in vivo. The genomic region encoding the HDC protein was engineered, being labeled with a FLAG peptide epitope, to allow the study of the HDC protein. Our intent is to identify the process of HDC protein maturation and cellular localization in vivo using these very specific and unique labels. My lab is now focused towards completion of the tissue and cellular localization of HDC, which may lead to new discoveries of tissues that may identified as expressing HDC and thus, likely contain histamine. Studies can be done in whole brain tissue, tissue sections from adult tissue, as well as larval gut tissue. Embryonic localization of HDC is currently something I would like to have someone complete, using this tool we have developed.
3) Determining the contribution of central brain histamine to behavior. We have identified an effect that a central nervous system histamine deficiency has on courtship behavior in flies. We will continue examining these effects, using engineered Hdc genes in transgenic flies. We are also investigating a number of other behavioral analyses to determine the contribution that histamine may make to these behaviors as well. One of the more recent projects involve examining the effect of histamine on spontaneous activity demonstrated in decapitated flies
4) Histamine and gut function. Recently, we found histamine in specific regions of the fly gut, suggesting there may be some function for histamine in gut function. We have shown that lack of histamine has an effect on the regulation of gut pH in the larva (see figure below). Currently, we are examining histamine gut localization with respect to identification of the cell type that may contain histamine in flies that specific cell types can be identified, using confocal fluorescence microscopy.
We are examining a molecule called GAP-43 which is a brain protein that is expressed in a wide variety of species including humans and has been shown to become biochemically altered in the process of learning and memory. Specifically, levels of phosphorylated forms of GAP-43 have been shown to increase following a controversial paradigm of learning and memory in several animals including rat, mouse and rabbit. We are interested to see if any differences in the profile of GAP-43 are associated with dementing illnesses that severely disrupt memory and learning. Since human brain tissue is difficult to obtain, we utilize brain tissue from a genetically altered mouse engineered to resemble Alzheimer’s disease, a human neurodegenerative disorder characterized by profound cognitive impairment. Therefore, to test the hypothesis that the profile of phosphorylated isoforms of GAP-43 are changed in the brains of a mouse used to model Alzheimer’s disease, GAP-43 will be examined by 1 and 2 dimensional SDS polyacrylamide gel electrophoresis. Isoforms of mouse brain GAP-43 will be detected by immunocytochemistry and silver staining and, further, quantified by computerized densitometry. Alterations in quantities of phosphorylated forms of GAP-43 might result from a pathological biochemical processes. Revealing molecular defects generates potential targets for the development of possibly more effective drugs to combat dementia.
My research focuses on the regulation of cell shape and stress responses in Candida albicans. This fungus is part of the normal human-associated microbial population, but it is also an opportunistic pathogen and remains the main causative agent of invasive fungal infections. Invasive candidiasis is now the fourth most frequent hospital acquired infection in the U.S and is associated with high morbidity and mortality rates. C. albicans lives in varied environments from the skin to the GI tract, and must be able to respond appropriately to these different conditions. Changes in cell morphology and accompanying alterations in surface protein components are important virulence traits and are key factors for the complex interaction between the fungal cells and the host immune system. We are particularly interested in understanding the contributions of different genes to the control of the yeast to hypha morphological transition. Current projects examine different components of this mechanism from adhesion and sensor proteins on the cell surface, to internal signaling proteins, to transcriptional regulators.
Our group uses the chicken and mouse embryo as model systems to determine how neural stem cell differentiation is influenced by intrinsic factors (such as gene expression) and extrinsic factors (such as factors secreted by other cells). The accessibility of the chick embryo to experimental manipulation allows us to screen for the effect of experimental manipulation on stem cell differentiation using quantitative PCR and anatomical approaches. With this approach, undergraduate and master's level students have determined that the basic helix loop helix protein Nato3 is sufficient to promote expression of markers for dopamine producing neurons. The clinical significance of this finding is that dopamine neurons are the target of degeneration in the pathophysiology of Parkinson Disease, so our current studies are focused on understanding the mechanism of this effect with the hope of informing therapeutic strategies towards this disease.
Additionally, our lab is using the same model system to analyze the effect of factors outside of the neural stem cell (cell-extrinsic factors) such as polyunsaturated fatty acids. These factors have been shown to be important signaling components in development and can affect stem cell differentiation in culture but have not been analyzed in the living embryo.
Xenopus laevis thymus – a model for assessing impact of environmental pollutants
The amphibian thymus gland may be an easily assessable surrogate indicator of the effect of endocrine agents. Endogenous (eg cortisol) and synthetic (eg dexamethasone, commonly used to treat inflammatory conditions) glucocorticoids have been associated with reduced organ size and programmed cell death of the cells of the thymus in mice. Interestingly, the commonly used pesticide Atrazine has shown similar endocrine disrupting effects and, like glucocorticoid alters immune function in Xenopus. Preliminary studies have shown that thymus reduction seen after exposure of tadpoles of Xenopus laevis to atrazine is glucocorticoid receptor-dependent; we have evidence that thymus involution is not correlated with apoptosis but associated with a decrease in autophagic flux. Given the role of this organ in the immune system and its utility as an easily detectable indicator, the overall aim of my current research project seeks to characterize the mechanism of atrazine-induced organ toxicity (ii) validate the use of the Xenopus tadpole thymus as a toxicological model for environmental pollutants. Immediate specific goals in the lab are to elucidate the cell death/ survival signaling cascades activated in response to atrazine, and its effect on tissue and organ architecture, and function.
My research program is somewhat unique in that there isn’t really an overarching disciplinary theme that all my work falls neatly under. My tendency is to seize on an interesting question (or set of related questions), recruit students to help answer it, then after a year or two move on to something (sometimes totally) different. Most of the projects in my lab, in one way or another, have employed molecular markers to infer past demographic and evolutionary events in populations of parasites and human pathogens. Past projects have looked at intragenic recombination in rotavirus, positive selection in viral hemorrhagic septicemia virus, and microevolution of rabies virus in Michigan bat populations. My students and I recently completed a project looking at the population dynamics of raccoon roundworm in West Michigan. And with colleagues in GVSU's Computer Science department, I recently collaborated on a project modeling Ebola diffusion in West Africa. Currently, my research students and I are studying social evolution among bacterial symbionts in an interesting tripartite system involving bacteria, nematodes, and insect hosts (some background here).
During the infectious process a battle ensues between the human host and the bacterial pathogen over access to various nutrients including metals. The focus of my research is to gain a better understanding of how bacteria acquire nutrients during an infection and how availability of various metals influence disease outcomes. One bacterial pathogen I am currently researching is the gastric pathogen, Helicobacter pylori which colonizes the stomachs of over half of the world’s human population and is the leading cause of gastric cancer. I am specifically interested in understanding how access to both iron and zinc regulate the cag type IV secretion system which is responsible for injecting host cells with the oncogenic protein, CagA. Furthermore, I am interested in identifying how environmental levels of zinc alter H. pylori flagella production and therefore influence the initial steps of colonization. In addition to studying H. pylori I also study the skin commensal Staphylococcus lugdunensis which is a coagulase-negative Staphylococcal species that has the potential to cause aggressive and progressive disease. Currently little is known regarding the molecular mechanisms deployed by S. lugdunensis that enable it to transition from a harmless component of the skin flora to a deadly pathogen. I am interested in identifying genes involved in metal acquisition and metal detoxification in S. lugdunensis.
I am actively involved in both laboratory and field research. My current lab-based projects include assessing various aspects of hominin (e.g. humans, two species of chimpanzee, their ancestors, and the extinct lineages of their common ancestor) evolutionary anatomy through dissection and non-invasive Magnetic Resonance Imaging (MRI). Currently, I have been examining the insertion of the pectoralis minor muscle in the chimpanzee (Pan troglodytes), as various interpretations of this attachment have been reported throughout the anatomical literature. Clarity of this issue is fundamental for not only understanding the evolutionary structural and functional pathway(s) of the muscle, but also for producing a better understanding the evolution of the hominin shoulder.
Another research area that I have focused on is assessing spatio-temporal variation of stress and developmental stability among extant and extinct mammalian taxa through fluctuating asymmetry (FA). The aim of this research area is to continue exploring the utility and advancement of FA to a variety of modern and prehistoric mammalian species. Deviations from symmetry in bilateral characters have achieved some prominence as measures of developmental (in)stability, revealing greater levels of asymmetry under adverse settings and mirrored target phenotypes under optimal extrinsic (environmental) and intrinsic (genetic) conditions. Increased FA has been associated with dietary, thermal, audiogenic and chemical stresses, but has been reported to decrease when genetic heterozygosity is elevated. Identifying the distribution and expression of FA among (paleo)species that have an extensive and well documented biological history (i.e. through time and space) provides a context for understanding how evolutionary processes and events potentially impact development.
My current paleobiological field research is situated within the Cradle of Humankind World Heritage Site, North-West Province, South Africa, at the fossil-bearing site of Luleche and in the adjoining Provence of Gauteng, at the fossil site of Hoogland. Notable excavations within the Cradle of Humankind and several in eastern Africa have produced rich samples of Pliocene and Pleistocene fossil mammals (including hominins), which have been a major source for interpreting our past. Such excavation and analysis of fossil assemblages from prolific sites has led to a wealthy and detailed understanding of a broader African paleolandscape. As important as these excavations are, the exploration of novel deposits, like Luleche and Hoogland, can only increase our understanding of the variability and richness of African (paleo)species, paleoecosystems, depositional processes, and evolutionary factors that existed in the past.
In my lab we investigate the mechanisms involved in the nonenzymatic biological oxidation/reduction (Redox) reactions that are closely involved in physiologic and pathophysiological mechanisms. The working hypothesis is that the formation of an organic redox complex is necessary for electron transfer to take place. My investigations center on elucidating and understanding the mechanisms involved. To accomplish this, my students and I will be implementing biological, biochemical, spectroscopic and electrochemical techniques to characterize and describe the mechanisms of organic redox complex formation and the resulting transfer of electrons.
My research is generally focused on studying of the impact of stressful, potentially pathological, conditions on blood vessel function. That work can involve studies of cells collected from vessels (cultured smooth muscle or endothelial cells) or of isolated blood vessels. Examples of conditions that students have addressed in my lab include: fatty acid exposure (omega 3 vs 6 and cis vs trans), contents of cell culture growth media (growth factor and glucose) and an acidic environment. As relative expression of vascular connexin (Cx) proteins reflects the healthiness of a vessel, I have used these proteins as markers of vascular cell responses to these conditions. In endothelial cells, increases in Cx43 expression reflect a reduction in the healthiness of a vessel whereas increases in Cx37 would occur in healthier vessels. At the cellular level, these Cxs play a role in regulation of cellular growth and apoptosis (which is why they indicate health, by affecting the balance between these pathways). I also work with blood vessels evaluating the role of changes in myosin light chain (MLC) phosphatase vs MLC kinase activity in the control of resistance vessel dilation to an acidic environment. While decreasing kinase activity has been presumed to dominate, the role of the phosphatase in regulating vessel relaxation remains to be resolved.
In addition to the specific areas above, my broad training in exercise and comparative physiology has provided me with the background to address many other questions. I would be happy to talk with a student about research questions that they might be interested in addressing. I have mentored many student projects for the honors college.
One emphasis in my lab has been to isolate the cells in the eye that die during glaucoma, and then test compounds that may protect them. This work has focused on examining the neuroprotective effect of drugs that selectively activate a specific type of nicotinic acetylcholine (ACh) receptor (the alpha7 nAChR), on retinal ganglion cells from the pig eye. We followed that project with the examination of a selective ‘positive allosteric modulator’ (PAM) of alpha7 nAChRs. More recently, we have explored the possibility that drugs originally developed for Alzheimer’s disease (AD) could be used for glaucoma. These AD drugs were originally designed to promote the amount of ACh released in the brain to compensate for the loss of cholinergic neurons during AD. We have shown that one such compound increases the release of ACh from the pig eye & appears to activate alpha7 nAChRs in a ‘mixed’ retinal cell culture system resulting in increased survival. New projects include retinal slice studies using the confocal microscope to determine which cells are activated by these ‘release enhancers’ and at what concentrations. In the future, we plan on examining these neuroprotective compounds in rodents to determine the extent of neuroprotection and the possibility of the proliferation of new cells in the mammalian retina.
Heart disease is the leading cause of death worldwide. According to the data published by American Heart Association in 2015, ~610,000 people die of heart disease in the United States every year-that’s 1 in every 4 deaths. Research in my lab focuses on understanding how a group of protein phosphatases called dual specificity phosphatases (DUSPs) regulate extracellular signal-regulated kinases 1/2 (ERK1/2) signaling in the heart. Recently we have identified DUSP8 as a critical regulator of ERK1/2 activity in the heart. Knockout of Dusp8 gene in mice leads to increased ERK1/2 activity, which protects the mice from progression towards heart failure in two surgery-induced disease models. Cardiac specific overexpression of DUSP8 in mice results in decreased ERK1/2 activity, ventricular dilation, and heart failure. These data suggest that targeting DUSP8 might be a therapeutic approach for heart disease. We are currently investigating whether knockout of both DUSP6 and DUSP8, two DUSPs specific for ERK1/2, will protect the heart from disease. In this study, we propose two specific aims as follows to study the effect on ERK1/2 signaling upon loss of DUSP6 and DUSP8 proteins in the heart. Specific aim 1: generation of knockout mice with loss of both Dusp6 and Dusp8 genes. Specific aim 2: determine the effect of loss of both Dusp6 and Dusp8 genes on MAPK signaling, myocyte proliferation, and cardiac function at both rest and stimulation conditions.
Dr. Lown’s research is mainly focused food access and justice in Michigan.
The Food Access in Michigan study (FAiM) is a five-year, multicenter study funded by the USDA. The project is a collaborative research effort across six universities including the University of Michigan, UM-Flint, MSU, GVSU, LSSU and UW-Madison. Additionally, each university has partnered with a community organization to work on a local urban agriculture intervention. The overall goal is to obtain a better understanding of food access and food insecurity across the state of Michigan. Students for this project are trained on taking 24-hour recalls, initiating/downloading accelerometers, measuring anthropometrics, conducting phone interviews with key informants and retailers, and conducting focus groups.
I am the co-PI on a project which examines the effects of Paleolithic Diet and HIIT exercise interventions on health markers. Students working on this project are trained on taking 24-hour recalls, and initiating/downloading accelerometers.
I am the PI on a project examining the impact of a new gleaning program on fruit and vegetable intake of low-income seniors. Students working on this project are out in the community surveying subjects at food commodity sites.
My lab group is continuing to study a renamed (1993) Bacillus bacteria (Paenibacillus) which is a facultative anaerobic, endospore-forming bacteria. These bacteria have been found in a variety of environments such as: soil, water, rhizosphere, vegetable matter, as well as clinical samples. The name indicates as much as the Latin word paene means almost, and so the Paenibacilli are literally almost Bacilli. The genus includes P. polymyxa, which is capable of fixing nitrogen a trait that the bacteria I have worked with in the past (Rhizobia fredii) and is used in agriculture studies. Our group is trying to better understand the metabolism and physiology of these bacteria focusing on possible bacteria viruses (phages) that interact with these strains. Our goal is to optimize both growth and culturing of this bacteria to combine with the phage work to study phage host/ interactions within this system.
I currently have two BMS majors working with me trying to optimize the growth of various Bacillus strains and a third student working on isolating viruses which will be able to infect and kill these bacteria.
The primary goal of our laboratory is to characterize the cellular and molecular mechanisms that regulate energy homeostasis and how disturbances in these regulatory mechanisms contribute to obesity. My lab is currently involved with the following project to address these long term goals.
Profiling Changes in Gene Expression in Response to Exercise & Aging
Obesity is a significant health concern as it is a major risk factor associated with increased morbidity and mortality from several chronic diseases including: cardiovascular disease, non-insulin dependent diabetes mellitus, some types of cancer, gallbladder disease, osteoarthritis, and hypertension. Despite the perception that the American public is increasingly concerned about consuming a healthful diet, the percentage of overweight individuals in the US continues to increase. Currently, 66% of adults over 20 years of age in the U.S. are considered overweight or obese. Current treatments for obesity are only moderately successful. Macroarrays and real time PCR are being utilized to profile changes in gene expression that occur in response to endurance training and aging in rats. Endurance training has been shown to result in consistent, but modest reductions in total fat mass, even when total body weight is not reduced. Aging, on the other hand, is consistently associated with an increase in fat mass. Developing a better understanding of the cellular adaptations that occur in adipose tissue in response to training as well as aging will allow a better definition of training protocols to maximize fat loss and may lead to the development of novel pharmacological treatments that maximize lipid oxidation and fat loss during physical activity or calorie restriction, and/or attenuate age associated increases in obesity.
Dr Nochera is interested in developing research with breadfruit not only as an alternative but also as a "functional food" product for the public. Other research interests include testing the reliability and validity of feeding tools for infants and adults and currently investigating DHA consumption in women of Hispanic origin.
The overall focus of my research is to investigate the role of estrogen signaling in the male reproductive tract with the goal of better understanding male fertility and infertility. Control of spermatogenesis and sperm production is hormonally regulated through the hypothalamic-pituitary-gonadal axis. Classically, testosterone and other androgens have been associated with the male, while estradiol and other estrogens have been associated with the female. However, the testes express functional aromatase and produce significant amounts of estradiol in addition to testosterone and males unable to produce estrogens are infertile. Results from my research, and other groups, reveal that estrogen receptor alpha (ERα) and beta (ERβ) are expressed within the testis and epididymis of multiple species. This indicates that the male reproductive tract in mammals is both a source and target for estrogen regulation. Additionally, estrogen receptors and aromatase are expressed by sperm throughout the reproductive tract suggesting that the sperm themselves are also a potential source and target for estrogen regulation. The mechanisms by which estrogen regulates sperm production and maturation remain largely unknown, but this knowledge is essential for further progress in understanding male fertility. Elucidating these mechanisms is the long-term objective of my research program. Active projects in my lab are investigating the effects of estrogen signaling during aging and the effects of endocrine disruption of the reproductive tract.
My research interests center around a functional, real-time measure of neurotransmission. Neurons send and receive information through chemical means, transducing electrical signals into chemical signals. These transmissions occur on a very fast time- scale, in the millisecond time frame.
One of the best methods for monitoring neurotransmission in real time is called Fast-Scan Cyclic Voltammetry (FSCV). Fast-scan because it is happening fast: every 100 ms; cyclic because it happens repeatedly; and voltammetry because it deals with voltage changes. In brief, when a carbon surface reaches a certain voltage, and a neurotransmitter is next to it, the neurotransmitter will oxidize (like metal rusting). You can measure this reaction and use it to look at changes in neurotransmitter concentration.
The goals of my lab: 1) continue to improve neurotransmitter recording techniques. 2) to classify and understand neurotransmission in the zebrafish brain. Zebrafish is a classic model system, allowing for genetic and environmental changes. 3) to record epinephrine release from pig adrenal glands. If various chemicals induce more or less epinephrine release from the adrenal gland, this is important information to consider in human treatments.
My research focuses on human craniofacial growth and development, with specific attention to the closure of cranial sutures. My current project is investigating the structure of non-human primate dura mater. The dura mater has been shown to be a source of genetic regulation of and mechanical influence on the closure of the cranial sutures. Both of the genetic and mechanical effects on suture closure may be related to the density and orientation of the regions of the dura deep to the cranial sutures. For instance, previous research in a rabbit model has indicated that the regions of the dura deep to the coronal suture does indeed contain a denser arrangement of collagen fibers when compared to the rest of the structure, which might provide increased genetic signaling and mechanical force to stimulate suture closure. In order to continue this line of investigation, my research students and I currently are in the nascent stages of a project to evaluate the density and orientation of collagen fibers in the dura mater of non-human primates. The organization of collagen in the dural section associated with the sutures could indicate a significant influence on the closure of cranial sutures. If the primate model yields positive results, we hope to move directly to human dura mater.
My scholarly interests these days are centered around running the GVSU plastination lab The lab processed it’s first specimens in the fall of 2013, and in the past 3 years we have produced more than 200 plastinated specimens (plastinates). The production of high quality plastinates begins with careful dissection of each specimen, and most of the dissections are carried out by undergraduates and a few graduate students. The specimens we produce are used primarily in courses taught by the BMS and BIO departments at GVSU, but we are also involved in producing plastinated specimens for several outside institutions, including several schools of veterinary medicine. Students in the lab will therefore be working with a wide variety of vertebrates, including humans. There are limited opportunities for participation, but I welcome anyone with a strong interest in vertebrate anatomy and a talent for careful dissection.
My primary research interest lies in understanding the ecological mechanisms that drove changes in community composition and structure throughout mammalian, specifically primate, evolution. In other words, I am interested in determining “why” and “how” mammalian groups arose, diversified, and went extinct by studying their interactions with their physical environment and with one another. In mammals, one of the most impactful species interactions is competition, and those species most likely to compete with one another are those who occupy the same ecological niche, or “role” in the community. In the fossil record, ecological niches can only be examined using the anatomical features preserved in fossil specimens, namely teeth and bones. As teeth are the point of contact between a mammal and its food, I use fossil teeth to reconstruct the dietary niches, and ultimately pattern of dietary competition, of mammals living in North America between 65 and 40 million years ago.
Students working in my lab have the opportunity to explore different aspects of mammalian evolution and dietary reconstruction through the study of dental anatomy. This process can include preparing dental molds for casting, casting dental specimens from these molds, curating molds and casts, mounting dental casts for microCT-scanning, and processing digital microCT scans and collecting two- and three-dimensional data using imaging software. Finally, students working in my lab also have the opportunity to conduct paleontological fieldwork in Utah.
My research focuses on the effects of hyperbaric oxygen therapy on the circulatory system. I am most interested in deciphering the changes in blood flow regulation within the vasculature upon acute exposure to hyperbaric oxygen. This area of research utilizes multiple experimental techniques including in vitro organ preparations, Western blotting, and biochemical assays. It is hoped that insight gained from these studies may lead to an improved understanding of the role of hyperbaric oxygen therapy in cardiovascular health.
I’m broadly interested in the evolution of locomotor diversity in primates. My research uses three-dimensional geometric morphometrics (analysis of shape in three dimensions) to examine patterns of postcranial variation in the forelimb and hindlimb of human ancestors. I am using this data to investigate the underlying processes that drive shape variation in the postcranial skeleton of primate (e.g., patterns of integration/modularity, potential ontogenetic shifts, functional constraints) and the environmental factors that could have been instrumental in past selective events. Students working with me have the opportunity to either dissect primate cadavers and collect data on patterns of musculature in living primates or to collect three dimensional data using computer rendered models of bony material.
My research focuses on using C. albicans as a model fungal pathogen. C. albicans is a frequently acquired nosocomial infection both within the US and worldwide. It is an increasingly common threat to human health as a consequence of AIDS, steroid therapy, organ and tissue transplantation, cancer therapy, broad spectrum antibiotics and other immune defects. These infections carry unacceptably high morbidity, mortality rates (30-50%) and important economic repercussions (estimated total direct cost of approximately 2 billion dollars in 1998 in US hospitals alone).
The objectives of my research are: (i) the application of state-of-the-art yeast cell biology and genetics to the study of Candida albicans pathogenesis and commensalism, (ii) the use of proteomics, genomics, and bioinformatics in the analysis of the lifecycle of C. albicans, (iii) studies of C. albicans virulence in vivo, and (iv) signal sensing and transduction particularly with reference to disease related and quorum sensing pathways in C. albicans.
My research focuses on the physiological and ecological drives for primate behavior in the wild. I aim to holistically understand how all aspects of primate biology work together at the organismal level to allow animals to successfully thermoregulate, communicate, mate, and forage for food. My current projects focus on: 1) how primates use behavior, hormones, and social mechanisms to maintain a stable body temperature under varying thermal conditions, and 2) how primates use the chemical composition of scent secretions to communicate information about food resources. There are opportunities in my lab for students interested in gaining experience in hormone analysis, behavioral observation methods, various thermal measurements, as well as international field work with wild monkeys.
My research interests involve understanding the supply and demand for oxygen in tissues such as skeletal muscle and brown adipose. To this end I use a variety of noninvasive techniques such as Doppler ultrasound, magnetic resonance imaging, and spectroscopy to study human research subjects across a range of ages (college-aged to octogenarians) and physical activity levels (sedentary to highly trained athletes). The goal of my research is to better understand the interplay between the demand and supply for oxygen by these tissues and the impact of chronic physical activity and different disease states.